lllllllllllllmiUlllllltllinnillilllUUllillllilllllMllllllllllllllHHHIIIIII ANTA BARBARA CLINIC Left common carotid artery Innominate artery / __- Left subclavian artery Right Ir.nomln.ite vein /j- Left inno ' X Sui-trior ven Vena a Pulmonary vein v Imonary artery Superior pulmo- nary vein FIG. 1A. The heart and great vessels, viewed from the front. (After Piersol.) T.eft pulmonary artery Superior left pulmonary vein Inferior left pulmonary vein Termination of left coronary vein Transverse brancil of left coronary artery Left ventricle Supeiior vena cava Superior right pulmonary vein Right pulmonary artery nferior riglit pulmonary vein Inferior vena cava Coronary sinus Right coronary vein Transverse branch of right coronary artery Posterior descending branch of right coronary artery * 'Middle cardiac vein Right ventricle Fiu. 1H. Same, from behind. (After Piersol.) DISEASES of the HEART AND AORTA BY ARTHUR DOUGLASS HIRSCHFELDER, M.D. ASSOCIATE IN MEDICINE, JOHNS HOPKINS UNIVERSITY WITH AN INTRODUCTORY NOTE BY LEWELLYS F. BARKER, M.D., LL.D, PROFESSOR OF MEDICINE, JOHNS HOPKINS UNIVERSITY 344 ILLUSTRATIONS BY THE AUTHOR SECOND EDITION PHILADELPHIA & LONDON J. B. LIPPINCOTT COMPANY COPYRIGHT, 1910 Bv J. B. LIPPIXCOTT COMPANY COPYRIGHT, 1913 BY J. B. LIPPINCOTT COMPANY Printed by J. B. Lippincott Company The Washington S'fuare Press, Philadelphia, U.S.A. TO MY FATHER Professor of Clinical Medicine, Leland Stanford Junior University AND TO atetoeHpjef f . father, ;jm,2D,, iULSD, Professor of Medicine, Johns Hopkins University CHIEFS OF THE CLINICS IN WHICH THE WORK WAS DONE,' WHO HAVE TAUGHT ME BY PRECEPT AND EXAMPLE HOW SCIENCE, ART, AND HUMANITY SHOULD BE WOVEN INTO PRACTICE OF MEDICIN-E THIS BOOK IS AFFECTIONATELY DEDICATED INTRODUCTORY NOTE THE researches in the great field of inner medicine have so multiplied in recent years that it has become highly desirable that we should have from time to time, in addition to the summaries of progress contained in the gen- eral text-books on practice, monographs which picture more completely the status of our knowledge in the several special divisions of the subject. In diseases of the circulatory system new methods of study have led to the discovery of many new facts, and a great many workers have been attracted during the last twenty years to this domain of cardiovascular inquiry. In the medical clinic at the Johns Hopkins Hospital, Dr. Hirschfelder has during the past few years occupied himself especially with such studies. The present volume is an attempt to epitomize the actual condition of the subject at the present time, as viewed from the standpoint of an active in- vestigator of extensive first-hand experience who has also a wide acquaint- ance with the literature of the physiology and pathology of the circulatory apparatus. The clearness and brevity of the presentation and the excellent arrange- ment of the material will, I am sure, appeal to students and practitioners of medicine. It is no easy matter adequately to combine the most recent results of anatomical, physiological, pathological, and clinical studies in a form which will satisfy the critical demands of the scientific investigator and at the same time be useful as a guide to the every-day practitioner. Especial attention has been paid in the volume to the practical facts of diag- nosis and treatment; in the more theoretical portions there will be found evidence of careful, critical sifting, and an appreciation of the distinction between what is essential and what non-essential for the more general reader. The bibliographic references make no attempt at completeness, but have been chosen with the idea in mind of permitting those who desire to do so to consult the most important, and especially the more recent, treatises, monographs, and original articles which deal with the various matters discussed. A notable feature of Dr. Hirschfelder's book is the liberality of illustra- tions; the majority of the figures are made from original drawings and tracings and are in pleasing contrast with the time-worn figures which pass from compilation to compilation. LEWELLYS F. BARKER. BALTIMORE, MAY 12, 1910. vn PREFACE TO THE FIRST EDITION IN the preparation of this book it has been the writer's aim to present side by side the phenomena observed at the bedside and the facts learned in the laboratory in order to show how each supplements the other in teaching us how to observe the patient and to direct the treatment. Many of the results obtained in the laboratory have not yet attained practical importance because they have been scattered through the literature and have not reached the eye of the clinician; but wherever the clinicians have looked to the laboratory or laboratory workers have looked to the clinic for verification or application of their theories the great pillars of progress have been raised. In accordance with this idea the clinical presentation in each chapter is preceded by an introductory section dealing with the experimental pathology and more fundamental principles of the subject, which has been used as a basis for frequent reference in the clinical dis- cussions. The trend of clinical observation during the past two decades has been toward more accurate study of disturbances of function and toward the introduction of mechanical methods for their observation, methods of precision which tend to supplement or supplant the older and simpler methods of physical diagnosis. Chief among these may be mentioned the study of blood-pressure, the graphic studies upon alterations in cardiac rhythm by means of the venous pulse, the outlining of the heart and vessels by means of the X-ray, and the phonographic recording of the heart sounds. Each of these subjects has been reviewed with special reference to the general principles upon which the method is based, in order to point out its applicability, its limitations, the character of information which it has yielded in clinical conditions, the conditions under which the same informa- tion may be gained by simpler methods, the conditions under which its employment is essential and those under which it is superfluous. The failure of the heart has been traced through its varying stages from the simple fatigue of the normal heart in exercise, through the stage of primary overstrain, to that of broken compensation, especial attention being devoted to the states of broken pulmonary compensation arising from failure of the left ventricle and of broken systemic compensation from failure of the right. xi xii PREFACE TO THE FIRST EDITION. The pathogenesis of cardiac symptoms is fully discussed, with their pathological physiology, occurrence, and the symptomatic treatment for their relief. The general methods of treatment in cardiac diseases, dietetic, phar- macological, gymnastic, hydrotherapeutic, and electrical, have been treated both as empirical procedures and as experimental methods to correct definite disturbances in the physiology of the circulation, especially changes in cardiac force, cardiac tonicity, and peripheral resistance. The chapters upon the individual organic lesions include discussions of pathological anatomy, pathogenesis, pathological physiology, as well as of symptomatology, course, notes of typical cases, diagnosis, treatment, and prognosis. Considerable attention is also paid to functional disturb- ances (valvular insufficiencies, etc.) which may bring about conditions similar to those resulting from organic changes or may accompany the latter. The Adams-Stokes syndrome seems so definitely associated with lesions of the auriculoventricular muscle bundles as to justify its classifi- cation among conditions due to organic lesions. The congenital heart lesions are viewed as disturbances in embryologic development in which primary malformations or states in fetal life have diverted the blood current, modifying the further course of development and producing concomitant secondary malformations. The effect of these lesions upon the adult circulation and their relation to cardiac overstrain in producing the syndrome of the morbus cceruleus are discussed, as well as the signs, diagnosis, prognosis, and treatment. Short chapters are devoted to the subjects of pregnancy in heart disease and the effects of trauma and wounds of the heart. Considerable space is given to the purely functional disturbances of cardiac action, especially to the physiological mechanisms by which many of them result from disturbances in distant organs as well as to the improve- ments resulting when these disturbances are corrected. A great deal of care has been bestowed by the writer in the prepara- tion of the illustrations, especially upon the cardiosphygmographic trac- ings, the diagrammatic representations of clinical conditions and of effects upon the blood flow in different parts of the circulation as well as in differ- ent stages of the disease. When necessary, figures have been borrowed from other sources, to whom due credit has been given. Since the aim of the book is not only to present the principal facts but to aid the reader in following out lines in which he is especially inter- ested, an adequate bibliography has been added to each chapter, embrac- ing the articles referred to in the text. Tt is a pleasant duty for the writer, in conclusion, to express his thanks to Professors Barker and Thayer for the privilege of using the clinical PREFACE TO THE FIRST EDITION. xiii material and records of the Johns- Hopkins Hospital, to Professor T. B. Futcher for that of the Johns Hopkins Dispensary, and to his father, Pro- fessor J. O. Hirschfelder, for the cases at the City and County Hospital of San Francisco; to Professor F. P. Mall and Drs. Knower, Retzer, and Evans in matters of anatomy and embryology; to Professors W. H. Howell, J. Loeb, and Dr. D. R. Hooker in physiology; to Professors W. S. Hal- sted, T. S. Cullen, and J. M. Slemons in matters of surgery, gyna3cology, and obstetrics; to Professors W. G. MacCallum and W. Ophiils, as well as to Major F. F. Russell, Dr. Lamb, and Dr. Gray, of the Army Medical Museum, for the use of pathological material; to Professor C. M. Cooper for the collection of radiographs; to Dr. Chas. S. Bond for his untiring labors in the preparation of photomicrographs; to Professor W. Einthoven of Ley den for the use of electrocardiograms; to Professor Max Broedel for his kind instruction and suggestions in matters of illustration; to Dr. Caroline B. Towles for her assistance in reading of proof as well as for many helpful suggestions; and to Miss Alberta E. Bush for her care in the technical matters pertaining to the manuscript and index. PREFACE TO THE SECOND EDITION SINCE the appearance of the first edition numerous advances have been made in the subject of cardiac disease of such importance that, in order to embody them in the text, several chapters have had to be rewritten and enlarged. The electrocardiograph, which has now assumed a role of primary im- portance in physiology, pharmacology, and clinical observation, has been discussed in detail as to theory, construction, and application. The study of the mechanism of the normal and pathological heart-beat by this method has thrown so much light upon the site of origin of the normal and abnormal heart-beat, the action of the cardiac nerves, and the paroxysmal tachycardias and the permanent irregularity that it has become a procedure of routine examination of heart cases in many medical clinics, and in the hands of Mackenzie, Cushny and Lewis has led the way to more exact methods for the use of digitalis. Other drugs which have merited consideration have come into use, and the chapters and sections upon treatment have been con- siderably enlarged. The studies of Haldane, Pembrey and Yandell Hender- son upon acapnia, and of Sir William Ewart upon CO 3 inhalations, have given a clinical importance to the investigation of CO 2 in the alveolar air of the lungs. The recent investigations upon syphilitic arterial disease and its frequency have made possible a more clear-cut classification of arterioscle- rotic conditions, and in the light of these the section upon the pathology of arteriosclerosis has been rewritten. It is a pleasant duty to the author to express his grateful appreciation of the cordial reception which the book has received at the hands of his medi- cal colleagues, to many of whom he owes his thanks for suggestions that have been helpful in the revision. To Dr. George S. Bond he is particularly in- debted for the preparation of the electrocardiograms used throughout the book, as well as to Dr. Milton C. Winternitz for many helpful suggestions and for the preparation of a number of photomicrographs. 2245 LINDEN AVENUE, JANUARY 10, 1913. CONTENTS PART I. GENERAL CONSIDERATIONS AND METHODS OF DIAGNOSIS. I. PHYSIOLOGICAL CONSIDERATIONS 1 II. BLOOD-PRESSURE AND BLOOD VISCOSITY 25 III. THE ARTERIAL PULSE 62 IV. THE VENOUS PULSE AND ELECTROCARDIOGRAM IN HEALTH AND DISEASE . . 70 V. X-RAY EXAMINATION 132 VI. PHYSICAL EXAMINATION. . 140 PART II. DISEASED CONDITIONS DUE TO DIFFUSE PATHOLOGICAL PROCESSES. I. PRIMARY CARDIAC OVERSTRAIN 177 II. PATHOLOGICAL PHYSIOLOGY OF EXERCISE, CARDIAC OVERSTRAIN, HEART FAILURE, AND COMPENSATION 185 III. SYMPTOMS OF CARDIAC DISEASE 203 IV. GENERAL PRINCIPLES OF TREATMENT OF FAILURE OF THE HEART 219 V. THE EFFECTS OF DRUGS IN CARDIAC DISEASE 233 VI. GYMNASTICS AND HYDROTHERAPY 267 VII. HYPERTROPHY AND ATROPHY 279 VIII. FATTY DEPOSITS IN AND ABOUT THE HEART 292 IX. AFFECTIONS OF THE MYOCARDIUM 302 X. ARTERIOSCLEROSIS 327 XI. VASOMOTOR CRISES AND THE ANGIONEUROTIC LESIONS 356 XII. SCLEROSIS OF THE CORONARY ARTERIES, AND ANGINA PECTORIS 366 PART III. DISEASED CONDITIONS DUE TO LOCALIZED LESIONS. I. ENDOCARDITIS 385 II. MITRAL INSUFFICIENCY 407 III. MITRAL STENOSIS 427 IV. AORTIC INSUFFICIENCY 450 V. AORTIC STENOSIS 471 VI. PULMONARY INSUFFICIENCY. . . 480 xvi CONTENTS. VII. TRICUSPID INSUFFICIENCY 486 VIII. TRICUSIMD STENOSIS 496 IX. MARRIAGE, PREGNANCY AND LABOR IN CASES OF HEART DISEASE 503 X. CONGENITAL HEART DISEASE 513 XI. HEART-BLOCK AND THE ADAMS-STOKES SYNDROME 553 XII. PERICARDITIS 578 XIII. WOUNDS OF THE HEART AND CARDIAC TRAUMA 611 XIV. ANEURISM . . 619 PART IV. FUNCTIONAL DISEASES WITHOUT ANATOMICAL LESION. I. PAROXYSMAL TACHYCARDIA .... 662 II. THYROID HEART 678 III. MISCELLANEOUS DISTURBANCES OF CARDIAC FUNCTION THE SO-CALLED "CARDIAC NEUROSES" AND "CARDIAC NEURASTHENIA". . . . 697 LIST OF ILLUSTRATIONS FIG. PAQB 1 . The heart and great vessels Frontispiece 2. Relations of the heart and great vessels, viewed from the front xxviii 3. The heart and thoracic viscera, viewed from behind xxviii 4. Sagittal section of the thorax, viewed from the right xxviii 5. Heart muscle-fibres 1 6. Section through the endocardium, showing section of the muscle-fibres 2 7. Curve showing the catalysis of hydrogen peroxide by mercury 2 8. Apparatus for perfusing the mammalian heart 4 9. The auricular end of the human heart, viewed from the right 6 10. The sinus region of the heart and the auriculoventricular bundle 7 1 1 . Diagram showing the arrangement of the strands of muscle-fibres in the ventricle 9 12. Apparatus for registering the volume of the ventricles 11 13. Diagram showing the events of a single cardiac cycle 12 14. Methods for demonstrating the movements of the heart valves 13 15. Volume curves of the ventricles at increasing pulse rates 14 16. Diagram showing the effect of varying venous pressures upon the volume of the heart, upon the rapidity of filling of the ventricles, and upon the position as- sumed by the mitral and tricuspid valves at the end of the first inflow into the ventricles 15 17. Diagram showing the condition of the heart with varying degrees of tonicity but with systolic output normal 16 18. Origin and course of the cardiac nerves, and cutaneous distribution of the corre- sponding branches 18 19. Curve of intraventricular and aortic pressures 25 20. Diagram showing the effect of compression upon various types of arteries 27 21. Types of manometer used for determining blood-pressure 27 22. Erlanger blood-pressure apparatus with Hirschf elder polygraph attachment 27 23. Auscultatory method of determining blood-pressure, as used with the Oliver apparatus 29 24a. Diagram showing arrangement of Erlanger apparatus 29 246. Curve taken with the Erlanger blood-pressure apparatus, showing the points of maximal and minimal pressure 29 25. Diagram showing the effect of varying degrees of compression upon the excursion of the arterial wall : 30 26. Diagram showing the maximal and minimal pressures in various parts of the circulatory system 35 27. Diagram showing effects of vasoconstriction, vasodilation, increased and decreased force of ventricular contraction upon the maximal and minimal blood-pressures and upon the form of the pulse 35 28. Diagram of apparatus for determining the rate of blood-flow through the human arm 37 29. Diagram showing the curve of blood-pressure during asphyxia 39 30. Diagram showing typical blood-pressures in various diseases 41 31. Hooker and Eyster's modification of v. Recklinghausen's method of determining the venous pressure in man 51 xviii LIST OF ILLUSTRATIONS 32. Determann's apparatus for determining the viscosity of the blood 59 33. Brachial pulse-curves taken with the Erlanger blood-pressure apparatus from the arms of two patients 63 34. Absolute sphygmograms, all of which correspond to the radial tracing above. ... 64 35. Significance of the pulse-curve 65 36. Diagram showing the time relations of ventricular volume and pressure curves to pulse tracings from the aorta, carotid and radial arteries 65 37. Three types of arterial pulse-curve corresponding to the same pulse-pressure and same pulse-rate 66 38. Effect of inhalation of amyl nitrite upon the pulse-form 66 39. Mercury manometer tracing from the carotid artery of a dog, showing rhythmic variations in blood-pressure and rhythmic increase in dicrotism 67 40. Diagram showing various forms of pulse-curve encountered clinically 67 41. Sites for recording the jugular and carotid pulsations 72 42. Apparatus for recording the respiration 73 43. V. Jaquet's cardiosphygmograph 73 44. Normal venous tracings 75 45. Diagram representing the various events in a cardiac cycle 75 46. Venous tracing showing absence of the c wave in a case of heart failure 77 47. Venous tracing showing auricular paralysis (absence of a wave) with large (x) depression 77 48. Venous tracing from a very slow heart, with loud third heart sound, showing the presence of the h wave 78 49. Tracing from the same person one hour later, after giving atropine and quickening the pulse 78 50. Showing a wave w occurring shortly before the a wave 79 51. Positive or ventricular type of venous pulse in tricuspid insufficiency, showing absence of the a wave 80 52. Positive or ventricular type of venous pulse in tricuspid insufficiency, showing absence of the a wave 80 53. Method of taking tracing from the oesophagus to show the contractions of the left auricle 81 54. CEsophageal and carotid tracings from a normal man 81 55. Photograph of the electrocardiograph laboratory or "heart" station of the Johns Hopkins Hospital 82 56. Edelmnnn's modification of Einthoven's string galvanometer 83 57. Edelmann's convenient switchboard and short-circuiting keys 84 58. Diagram showing main connections for the electrocardiograph 85 59. Normal electrocardiogram tracing 87 GO. Distribution of electromotive force in the body in the three principal leads or derivations 89 til. Normal electrocardiogram showing time relations to the venous and carotid pulse wave 92 62. Factors involved in the production of the normal electrocardiogram 92 G3. Diagram representing various types of irregular pulse 99 Ma. Respiratory arrhythmia 102 64'). Diagram; showing the relation of the afferent impulses in the vagus to the threshold of irritability of the medulla 102 Go. Venous tracings in heart-block. Partial heart-block (3 : 1 rhythm) during pres- sure on the vagus in a case of Adams-Stokes disease 104 GO. Venous tracings in heart-block. Complete heart-block in a case of Adams-Stokes 104 ccasional absence of apex impulse during inspiration simulating interventricular heart -block. . ... 105 LIST OF ILLUSTRATIONS xix 68. Alternating pulse in a case of paroxysmal tachycardia 106 69. Response of frog's ventricle to abnormal stimuli 107 70. Tracing from jugular vein and brachial artery in man, showing ventricular extrasystoles 109 71. Tracings from the jugular vein and brachial artery of a patient with trigeminal pulse 1 12 72. Volume curve of the ventricles, showing the dilatation which followed the entrance of an air-bubble into the right auricle 115 73. Extrasystoles with shortened conduction time, supposed to arise in the auriculo- ventricular bundle 115 74. Variations in conduction time in a case of mitral stenosis 115 75. Tracing showing absolute irregular with weak, ineffectual systoles 116 76. Diagram showing the alterations of rhythm which may cause a pulsus bigeminus 116 77. Perpetual arrhythmia of the ventricles 119 78. Diagram showing abnormal electrocardiograms and the structures in which they arise 124 79. Effect of arrhythmia on the circulation, blood-pressure, and volume of the ventricles 127 80. Radiograph of normal chest 133 81. X-ray shadows in different axes of the body 134 82. A simple form of orthodiagraph 135 83. Diagram showing the use of the orthodiagraph 135 84. Orthodiagraphic outline of normal heart, showing Moritz's conjugates 135 85. Movements of the heart leading to the protrusions and retraction during systole. 141 86. Rubber funnel for cardiographic tracings 142 87. Tracing from the apex impulse and carotid artery. Cardiograms obtained over a normal apex and over the fourth left interspace 142 88. Various forms of apex tracings 143 89. Areas of pulsation and retraction 144 90. Eddies producing thrills as illustrated by a stream of water 144 91. Goldscheider's orthopercussion 145 92. Percussion with the orthoplessimeter 146 93. Diagram to show the cause of unavoidable error in percussion of the cardiac outlines 147 94. Areas of cardiac dulness and flatness in a normal man 147 95. Cardiac outlines in a child of nine years 148 96. Diagrams illustrating the movements of the normal heart on change of posture from side to side, and in the various phases of respiration 149 97. Graphic records of the heart sounds 150 98. Diagram for representing the heart sounds in clinical notes 153 99. Choice of stethoscope bells 155 100. The "valvular areas" 156 101. The propagation of the heart sounds from valves to chest wall 157 102. Graphic records of the fetal heart sounds 158 103. Diagram illustrating the split sounds and gallop rhythms and their phonetic equivalents 159 104. Graphic record of a split pulmonic second sound 160 105. Graphic record of the third heart sound 161 106. Jugular and carotid tracings from a normal individual with a well-marked third heart sound 162 107. Forces supposed to be at work in the production of the third heart sound 162 108. Similarity between the production of voice sounds and the production of murmurs 164 109. Distribution of the accidental murmur 168 110. Graphic record of an accidental murmur 169 111. Diagram showing the relation of the more common simple murmurs to events of the cardiac cycle 170 xx LIST OF ILLUSTRATIONS 112. Cardiac dulness in v. Leyden's case upon his three successive admissions 181 113. Alterations of blood-pressure due to rapid lifting of light weights with the feet. . 186 114. Effect of walking on a level on patient with badly broken compensation 187 115. Effect of prolonged exercise upon the blood-pressure of men in various degrees of muscular strength 187 116. Rise of blood-pressure during Valsalva's experiment and during exercise 188 117. Semi-schematic drawing showing variations in size of the heart of a long-distance bicycle rider, as the result of a very long race 189 118. Effect of strain upon the dog's heart whose tonicity is good 191 119. Volume curve of a dog whose cardiac tonicity is low 192 120. Effect upon the volume of the dog's heart produced by clamping the descending thoracic aorta 193 121. Diagram showing changes in the circulation: I, normal; II, broken pulmonary compensation; III, broken systemic compensation; IV, both compensations fail; stases in lungs and veins 195 122. The two types of Cheyne-Stokes respiration in their relations to the blood-pressure curves 208 123. Legs of a patient with extreme oedema and tremendous ulcers 210 124. Curschmann's modification of the Southey tubes for draining cedema of the legs 211 125. Electrical record of afferent impulses travelling up the vagi 213 126. Insertion of the knife in venesection 222 127. Effect of venesection on the cardiac outline, showing diminution in size of right heart 223 128. Typical effect of venesection upon the circulation 223 129. Methods of administering oxygen and carbonic acid 230 130. Tracings showing the action of digitalis upon the dog's blood-pressure 239 131. Variations in blood-pressure in a patient under the influence of digitalis and nitroglycerin 240 132. Effect of digitalis on cardiac tonicity in the dog 241 133. Curve showing the effect of strychnine upon cardiac tonicity 251 134. Effects of drugs of the nitrite series upon the blood-pressure in man 256 135. Schott resisted movements 270 136. Hypertrophic, normal, and atrophic hearts 279 137. Photomicrographs of atrophic and hypertrophic heart muscle 280 lo>>. Heart of normal dog and of dog which has run for three months on a tread-mill . . 282 139. Areas of pulsation and reaction hypertrophy of the right and left ventricles 285 140. Diagram showing power of normal and hypertrophied (athlete's) heart at rest and during exercise, also that of a diseased heart 289 141. Distribution of fat in and about the heart : 292 142. Photomicrographs of fat deposits in the heart 293 143. An excessive deposit of epicardial fat 294 1 H. Infiltration along the course of the blood-vessels in subacute myocarditis; blood- vessels injected 303 1 }.">. Septic myocarditis with multiple abscesses in the heart wall 304 1 It;. Photomicrograph showing an abscess in the heart muscle 305 1 57. Orthodiagraphic outlines of the heart of a child during the course of a severe diphtheria. . 308 1 Iv Specimen shouirm a cardiac aneurism covered with pericardial adhesions 312 Chronic myocarditis fcardioselerosis) 312 Specimens showing chronic myocarditis 313 Hypertrophy of some muscle bundles in the auricle with atrophy (transparency) " 314 ( 'urve of blood-pressure in a case of chronic myocarditis, showing the high blood- --urc persisting until shortly before death. . -H5 LIST OF ILLUSTRATIONS xxi 153. Various types of arteriosclerotic lesions. (Schematic) 330 154. Types of aortic lesions .- 330 155. Syphilitic aortitis (atherosclerosis) with deposition of calcined plaques just above and upon the aortic valves 332 156. Arteriosclerosis of the descending aorta, showing atheromatous plaques 340 157. Tortuous radial artery 346 158. Retinal changes in arteriosclerosis (colored plate) 346 159. Effect of arteriosclerosis upon the circulation 347 160. Blood-pressure chart of case of typical vasomotor crisis 357 161. Blood-pressure chart showing a vascular crisis of the cerebral type 358 162. Diagram to illustrate the elimination of CO 2 by the blood in normal and scjerotic arteries 359 163. Thromboangitis obliterans and endarteritis obliterans 362 164. Hands and feet of a patient with thromboangitis obliterans, showing gangrenous ulcers and the stumps of amputated toes 363 165. Effect of ligation of a large coronary artery upon the blood-pressure 366 166. Sclerosis of a coronary artery, producing an area of infarction near the apex. . . . 368 167. Distribution of pain in attacks of angina pectoris 372 168. Distribution of attacks of pain and sensory disturbances] in a case of angina pectoris 373 169. Blood-pressure curve showing crises of hypertension during attacks of angina pectoris 374 170. Fibrinous deposit upon an aortic cusp one hour after mechanically injuring the valve 385 171. Mitral endocarditis showing large vegetations 386 172. Injection of chronically inflamed valves 386 173. Structure of the normal auriculoventricular valve 387 174. Photomicrograph of a specimen showing acute and subacute endocarditic lesions upon the mitral valve 388 175. Ulcerative and healed endocarditis 389 176. Temperature curve from a case of malignant endocarditis 391 177. Temperature curve from a case of simple acute endocarditis 391 178. Diagram showing relative frequency of the most important valvular lesions at various ages 398 179. Diagram showing the relative frequency of the various valvular lesions in cases of valvular heart disease 398 180. Regurgitant streams in organic and functional mitral insufficiencies 408 181. Diagram showing the volume and pressure curves under these conditions 410 182. Curve of intraventricular pressure in mitral insufficiency produced on a mechanical model 411 183. Diagram showing the effects of mitral insufficiency upon the circulation 412 184. Distribution of the murmur in mitral insufficiency 415 185. Cross section of the body showing how the thrill and murmur reach the chest wall 416 186. Radiograph of a patient with mitral insufficiency, showing horizontal enlarge- ment of the heart to the left 416 187. Diagram of Fig. ISO, showing the directions in which cardiac enlargement has taken place 417 188. Graphic records of the heart sounds, showing the systolic murmur 417 189. Human heart, showing mitral and tricuspid stenosis. Mewed from above. The auricles have been cut through 427 190. Diagram showing the changes in the circulation due to mitral stenosis 429 191. Volume of the ventricles in experimental mitral stenosis 430 192. Diagram illustrating the variations in the volume curve of the ventricles in increasing degrees of mitral stenosis 430 xxii LIST OF ILLUSTRATIONS 193. Diagram showing the direction of the stream entering the left ventricle through the stenotic mitral orifice 432 194. Cardiac outline and distribution of the presystolic rumble in mitral stenosis 433 195. Radiograph from a case of mitral stenosis, showing increase of the shadow due to the dilated left auricle 434 196. Diagram representing the shadows shown in Fig. 195 434 197. Graphic record of carotid pulse and heart sounds in mitral stenosis 434 198. Diagram showing the relations of the various sounds heard in uncomplicated mitral stenosis to events in the filling and emptying of the ventricle 435 199. Venous pulse of a patient with mitral stenosis during an attack of acute heart failure 436 200. Permanent arrhythmia in a case of mitral stenosis, showing persistence of the auricular contractions (a wave) upon the venous pulse 438 201. Specimen showing vegetations upon the aortic valves 450 202. Schematic, showing the various forms of lesion producing aortic insufficiency . . 451 203. Effect of aortic insufficiency in the mechanical model 452 204. Diagram of the circulation in aortic insufficiency 453 205. Diagram showing how the high cardiac tonicity hastens the equilibrium between aortic pressure, intraventricular pressure, and tonicity, and thus diminishes the amount of blood regurgitating 454 206. Effect of rupturing an aortic valve in a dog, showing a transitory dilatation followed by a permanent diminution in size 454 207. Area of cardiac dulness and distribution of the cardiac sounds and murmurs in aortic insufficiency 458 20S. Radiograph of a case of aortic insufficiency, showing elongation of the long axis of the heart 458 209. Diagram of Fig. 20S, showing the hypertrophy of the left ventricle 458 210. Direction of the primary regurgitant streams in aortic insufficiency 460 211. Relation of murmurs in aortic insufficiency to the cardiac cycle 461 212. Functional mitral stenosis in aortic insufficiency as demonstrated on the excised heart by Baumgarten's method 461 213. Variations in the form of the pulse-wave encountered clinically in aortic insuffi- ciency 462 214. Tracings from a dog with experimental aortic insufficiency, showing the con- version of a collapsing into an anacrotic pulse by clamping the descending aorta 463 215. Radial pulse tracings showing extrasystoles, probably of ventricular origin 464 21i). Specimen showing aortic stenosis. Viewed from above 471 217. Forms of stenotic aortic orifices 471 21 >. Carotid pulse and intraventricular pressure in experimental aortic stenosis 472 Diagram of the circulation showing the effect of aortic stenosis 473 Diagram showing the cardiac outline and distribution of the murmur in aortic stenosis 474 Murmur of aortic stenosis 475 Diagram showing the pulsus tardus and the anacrotic type 476 Pulse tracings from cases of aortic stenosis 476 Diagram of the circulation in pulmonary insufficiency 481 Distribution of the murmur in pulmonary insufficiency 482 The outline of a normal heart superposed upon that of a dilated heart, showing the enlargement of the tricuspid orifice 487 Diagram showing the changes in the circulation in tricuspid insufficiency 488 ions pulse nf patients with tricuspid insufficiency (positive venous pulse) 489 Venous pulse of another patient 489 Distribution of the murmur and cardiac outline in tricuspid insufficiency 491 LIST OF ILLUSTRATIONS xxiii 231. Cross section of the body, showing the paths of propagation of the murmur of tricuspid insufficiency 491 232. Tracings of liver pulsation 492 233. Systolic pulsation of the liver of patient W. H 493 234. Diagram showing the changes in the circulation in tricuspid stenosis 498 235. Cardiac outline and distribution of the presystolic rumble and snapping first sound in tricuspid stenosis 499 236. Very early stage in the development of the human circulatory system 513 237. Human embryo 4 mm. long (about the fourth week after fertilization), showing the further development of the heart and of the branchial or aortic arches. . 514 238. Heart of an embryo, slightly older than that shown in Fig. 237, showing the earliest stages in the formation of two auricular and two ventricular pouches. . 515 239. A diagram showing the interior of this heart 515 240. Schema to show the development of the arterial system from out of the primitive aortic arches 515 241. Heart of slightly older embryo, showing separation of aortic and pulmonary channels in truncus arteriosus 516 242. Still later stage, showing the complete division of the truncus arteriosus into pulmonary artery and aorta 517 243. Auricular end of the same heart 517 244. Development of the pericardial cavity 518 245. The circulation in the foetus just before birth 520 246. Pulmonary stenosis due to fusion of the cusps 523 247. Pulmonary stenosis due to a lesion of the infundibulum 523 248. Complete pulmonary atresia 523 249. Schema illustrating the genesis of pulmonary stenosis 524 250. Currents and lines of force in the embryonic heart which result from pulmonary stenosis and tend to produce patency of the septa and of the duct us arteriosus . 526 251. Three-chambered heart (cor biatriatum triloculare) produced by complete atresia of the pulmonary and tricuspid orifices 527 252. Diagram of the circulation in pulmonary stenosis and atresia 528 253. Dilatation and irregularity of the retinal vessels 531 254. Clubbed fingers 531 255. Distribution of the pulmonary systolic murmur of pulmonary stenosis 532 256. Direction of blood-streams and propagation of murmurs accompanying defect in the interventricular septum, pulmonary stenosis, and open ductus arteriosus . . 532 257. Distribution and character of the murmur due to a patent interventricular septum (Roger's murmur) 536 258. Open foramen ovale 538 259. Diagram showing a cross-section of the same 538 260. Openings between strands of muscle in the interauricular septum 539 261. Radiograph of a thirteen-year-old boy with patent ductus arteriosus and aneuris- mal dilatation of the ductus and pulmonary artery 543 262. Stenosis of the isthmus of the aorta above the ductus arteriosus, type of the new-born 545 263. Stenosis below the ductus arteriosus, adult type 546 264. Transposition of the viscera in embryo and adult 548 265. Transposition of the valves 550 266. Pulmonary artery with four cusps 550 267. Tracing of the apex beat in a case of Adams-Stokes disease 554 268. Partial heart-block (3 : 1 rhythm) produced by pressure upon the vagus in a patient with disturbed conductivity who was also subject to attacks of the Adams-Stokes syndrome 555 269. The right branch of the auriculoventricular bundle in the dog's heart 556 xxiv LIST OF ILLUSTRATIONS 270. Tracings from the carotid artery and the jugular vein of a patient with Adams- Stokes disease, showing stoppage of the ventricles and continuance of the auricular contractions during the attack 557 271. The Erlanger heart-block clamp compressing the auriculoventricular bundle. . . . 558 272. Effect of gradually tightening the clamp 558 273. Tracing from jugular vein and carotid artery in a case of complete heart-block after the syncopal attacks had subsided 561 274. Diagram representing the conditions found in the tracing Fig. 273 562 275. Heart of a patient showing calcifications which produced Adams-Stokes disease 563 276. Diagram showing the two types of ventricular stoppage producing the Adams- Stokes syndrome 564 277. Section of a luetic infiltration of the auriculoventricular bundle 564 278. Acute fibrinous pericarditis 580 279. Tuberculous pericarditis (cor villosum) 580 280. Diagram showing the relations of the pericardial and pleural frictions to the cardiac and respirator}' movements 582 281. The circulation in cases with pericardial effusion 586 282. Area of cardiac dulness from pericardial effusion 587 283 Positions of the heart in pericarditis with effusion 589 284. Radiograph of a patient with pericardial effusion 590 285. Sites for paracentesis pericardii and pericardiotomy 594 286. Specimen showing the two layers of pericardium united in some parts by long strands and in others by short bands of dense adhesions 598 287. Sections showing adherent pericardium 599 288. Anterior and posterior pericardial adhesions. (Semi-schematic) 600 289. Cardiac outline in adherent pericardium 603 290. Inspiratory and expiratory dropping of beats (Riegel's pulse and the pulsus paradoxus) in adherent pericardium, showing the position of the adhesions which bring the condition about 604 291. Radiograph of a case of adherent pericardium 605 292. Case of pericarditic pseudocirrhosis 607 293. Wounds of the left ventricle 612 294. Exposure o f the heart for suturing a wound 614 2'.t.">. Specimen of a large aneurism 619 296. Aneurism arising just above a sinus of Valsalva 622 207. Aneurism of the ascending arch and innominate artery 622 2'.lV Aneurism of the transverse portion of the aortic arch penetrating through the sternum 622 299. Aneurism of the descending aorta eroding the vertebrae 622 300. Sections through the wall of an aneurism 623 301. Composite figure showing the relations of various aneurisms to surrounding structures 626 302. Tracings of the ou' lines of ;m aneurism of the innominate artery, showing its growth and the formation of secondary prominences upon its surface" 627 30.'5. Method of inspecting for pulsations 630 301. Effect upon the circulation of interposing an inelastic and an elastic bulb along the course of an artery in a model of the circulation 632 305. Effect of aneurisms at various sites upon the blood-pressure, rate of transmission, and the form of the pul 0.024 per cent. + KC1 0.42 + NaHCO 3 0.01 to 0.03 + dextrose 0.1 per cent.). It is necessary to maintain the blood- pressure at 50-100 mm. Hg, and also the temperature 36 to 37. Kuliabko and others have revived excised human hearts many hours after death. Fibrillary contractions occasionally set in, but may be stopped by perfusing with KC1 1.0 per cent, for a few minutes instead of Locke's solution. The heart then comes to a stand-still and resumes beat- ing under Locke's solution. The study of the excised heart has been very useful both in testing the effect of drugs and in simulating conditions of disease; but the conditions of circulation are not exactly comparable to those within the animal, and the results should always be carefully checked upon the intact animal before assuming them to be normal or drawing any conclusions as to pharmaco- logical action. Myogenic and Neurogenic Theories. Whether the salts cr ions which maintain the rhythmicity of the heart-beat do so by acting directly upon the muscle tissue ( m y o g e n i c ), or whether the stimuli are first generated in nerve tissue ( n e u r o g e n i c ) and then transmitted to the muscle, is a question which has been disputed for centuries. And though the pendulum has repeatedly swung from one opinion to the other, this question cannot at present be answered. It is quite certain that all the extrinsic cardiac nerves can be removed without stopping the rhythmic contractions, and that the ganglion cells may be stimulated without materially affecting the rhythm (Gaskell). But the mohwork of muscle-fibres in the heart is so pi-nneated by a meshwork of fine nerve-fibres that it has been impossible to determine whether the impulse arises in the muscle-cells or in the nerve eudinus upon their surfaces. Win. His, Jr., has indeed shown that the heart of the chick embryo beats before nerve-fibres have entered it at all, but the FIG. 8. Apparatus for perfusing the mamma- lian heart. A, auricle; V, ventricle; TAMB., tambour; TIL, thermometer; MA\., manometer; G ASCII, gas check; Oi, tank of oxygen. PHYSIOLOGICAL CONSIDERATIONS. 5 possibility still remains that after once entering the heart the nerves may take the initiation of contraction away from the adult heart-muscle. More- over, the recent experiments of Carlson and of Magnus in allied fields give considerable evidence that such may be the case; so that, in spite of its im- portance for both the physiology and the pathology of the heart, neither the myogenic nor the neurogenic theory of the heart-beat has been finally proved. Maximal Contractions and Irritability. As Bowditch has shown, the heart liberates all its available energy at each contraction, which resembles in this way the explosion of gunpowder or the liberation of a spring by a trigger. Like the power of the spring, the strength of the cardiac contrac- tion depends upon the energy stored up. This energy seems to depend upon the regeneration of the contractile substance mentioned above by Howell. When the next contraction, normal or abnormal (extrasystole), occurs soon after the last (early in diastole), the contraction is weaker than the preceding, since it liberates less energy, but the contractile substance is again completely destroyed and requires another pause (compensatory pause (see page 107) to regenerate it. When it occurs late, the contrac- tion is of almost or quite original strength, and the stored-up energy is again liberated completely. Moreover, Erlanger has shown that the irritability of the heart increases progressively as diastole is prolonged and as the muscle becomes overloaded with the energy-producing substance. ORIGIN AND COURSE OF THE CARDIAC IMPULSE. The Sinus as " Pace=maker " of the Heart. In the frog, where the car- diac impulse travels slowly, it is very easy to see that it arises at the sinus venosus, which executes a contraction. This is followed by contraction of the auricle, the latter after an appreciable interval by a visible contraction of the small ring of muscle about the auriculoventricular ring (Bond), and this in turn by contraction of the ventricles. It is probable that the sinus initiates the cardiac rhythm, because it is the chamber which, when isolated, beats at the fastest rhythm in the blood- serum, and hence it becomes what Erlanger terms " the pace-maker of the heart." 1 Indeed, if the impulse from the sinus is blocked by crushing or by cooling the sino-auricular border, the impulses no longer reach the auricles, which must then contract by their own slower rhythm or not beat at all (sinu-auricular heart-block) . Anatomy of the Sinus Region in Mammals. In the mammalian embryo the sinus venosus or sinus reuniens exists as a separate chamber bounded by the mouths of the venae cavse, the interauricular septum, and the Eustachian valve, which at this stage of development is relatively large and almost com- pletely partitions it from the cavity of the auricle. As the heart grows, how- ever, the region about the Eustachian valves grows very little, and the sinus reuniens becomes incorporated in the cavity of the right auricle, so that in the adult it is represented by only a few bundles of smooth muscle-fibres lying indefinitely between the venae cava? and the auricle proper. In 1906 1 Under pathological conditions, and especially in the excised heart, the ventricle may become more irritable and may become the pace-maker (reversed rhythm). 6 DISEASES OF THE HEART AND AORTA. Wenckebach described one of these bands which crossed the veno-auricular junction from the superior vena cava to the upper surface of the right auricle and penetrated downward toward the coronary sinus. This was soon con- firmed by Keith and Flack, who stated: "Our search for a well-differentiated system of fibres within the sinus, which might serve as a basis for the inception of the cardiac rhythm, has led us to attach import- ance to this peculiar musculature surrounding the artery at the sino-auricular junction. In the human heart the fibres are striated, fusiform, with well-marked elongated nuclei, plexiform in arrangement, and embedded in densely packed connective tissue in fact, of closely similar structure to the Knoten. The amount of this musculature varies, depending upon how much of the sinus has remained of the primitive type; but in the neighborhood of the taenia terminalis there is always some of this primitive tissue found. Macroscopically the fibres resemble those of the a.-v. bundle in being paler than the sur- Systemic aorta Pulmonary aorta or artery Right auricular appendage Right ventricle, conus riosus Sup. pulm vein Inf. pulm. vein Fossaovalis surrounded by annulus Inferior vena cava . Orificeof coronary sinus, guarded byThebesianvalve Eustachian valve Depression receiving Thebesian veins Fie. 9. The auricular end of the human heart viewed from the right. (After Piersol.) rounding musculature, i.e., in being of the white variety. They can be dissected out on the superior vena cava in the region corresponding to the right venous valve and at the coronary sinus in the interval between it and the inferior vena cava and left auricle. Another remarkable point in connection with these fibres is the special arterial supply with which they are provided. These arterial branches, as noticed by Wenckebach, em- brace the sino-auricular junction. It will be seen that they come from both right and left coronary arteries and form what may be termed the 'sino-auricular arterial circle.' We might mention also that, in some of the pathological hearts cut by us, sections of this region appeared to show a definite increase in the amount of fibrous tissue present a fact of considerable importance, since we have found that the fibrous tissue of the Knoten and a.-v. bundle is sometimes increased in pathological hearts.'' These observations have been confirmed by Schonberg. W. Koch, de Witt. Cohn, Lewis and Oppenheimer, and a host of others. PHYSIOLOGICAL CONSIDERATIONS. 7 The Veno-auricular Junction. Schonberg studied the veno-auricular junction in a large number of normal and abnormal human hearts by means of serial sections, each series being composed of 300 to 800 sections. At a level 10 to 15 mm. above the entrance of the superior vena cava into the auricle (atrium) he found the usual structure of vein wall. Below this level the media is found to contain groups of striated muscle-fibres separated from one another by fat and connective tissue. These striated muscle-fibres arise in the vicinity of non-striated fibres but are never continuous with them. Bundles of these fibres % to 1 mm. in diameter run transversely across the vein toward the auricle, gradually converging into larger bundles, which are separated from one another by a tissue rich in lymph- and blood-vessels. In the angle (sulcus) formed between the auricle (atrium) and vena cava these bands of striated muscle become much thinner and contain numerous tortuous fibres resembling Purkinje fibres. In this region there is a considerable deposit of fat, lymphoid and connective tissue, forming a more or less definite border-line. The muscle-fibres of the auricle (atrium) are inserted in the connective tissue here. The connection between the musculature of the vena cava and that of the auricle is made by the numerous small bundles of striated muscle-fibres lying just beneath the endocardium, which pass across this junction and end in the fibres of auricular muscle. ''In the macro- umcULOVENTRICUUfl " BUNDLE. (HIS) SINO-AURICULAR NODE RIGHT BRANCH FIG. 10. The sinus region of the heart and the auriculoventricular bundle. (Schematic, constructed from the findings of Keith and Flack, Tawara and later investigators.) A, seen from the right. The broken line marks off the area corresponding to the region of the embryonic sinus. B, the same region seen from the front. CS, mouth of coronary sinus. scopic preparations it is almost always readily seen that the sulcus is bridged at its posterior lateral third by a muscle-bundle which ascends upwards and backwards from the auricle (atrium) to the superior vena cava, where it is strengthened by fibres from the circular musculature of the lower part of the vein. This bundle is also well seen microscopically, but numerous other smaller muscle bundles are seen as well. It corresponds quite well with that described by Keith and Flack, and Wenckebach. Schonberg found that the region of the sulcus is particularly rich in nerve-fibres, ganglion-cells, blood-vessels, and lymphoid tissue, and is therefore particularly liable to pathological infiltrations and cicatrizations. It is worthy of note that the sulcus noted by Schonberg does not repre- sent the sino-auricular junction but the veno-sinal junction. The strands of striated muscle which he describes are derived from the sinus. The sino- auricular (sino-atrial) junction, on the other hand, is actually situated within the body of the auricle (atrium). Role of the Sinus in Mammals. There is a considerable amount of physiological as well as anatomical evidence that in the adult mammal as well as in the amphibian this is the region in which the cardiac impulse arises. 8 DISEASES OF THE HEART AND AORTA. Knoll and also Fredericq have shown by graphic records that the right auricle begins to contract .01 to .03 second before the left auricle, and the latter as well as Langendorff and Lohmann demonstrated upon the excised heart that the left auricle ceases to contract when the right auricle is cut away from the septum. Erlanger and Blackman were able to constrict off the region of the venae cavae by a suitable clamp, and also by torsion of this part of the auricle, and obtained a slight degree of block (2:1) between the sinus and the atrial portions of this chamber by this means; but neither Hirschfelder and Eyster nor Erlanger and Blackman were able to produce such a sino- auricular block in the heart in situ. Erlanger has shown, however, that the tissue in this region responds more readily to induc- tion ducts than the rest of the auricle, showing a higher irritability. Quite recently Wybauw has shown, by means of the electrocardiogram, that the region of Keith and Flack's node becomes negative before any other part of the auricle; and this observation has been confirmed by Lewis. Lewis and, later, Wybauw have shown also that when artificial stimuli are applied to any other part of the auricle the resultant electrocardio- gram is atypical, but when it is applied to the node of Keith and Flack the electrocardiogram is normal. On the other hand, Flack himself clamped and destroyed the auriculoventricular node, Jager destroyed the entire region by actual cautery in the intact heart, and Magnus- Aloleben excised in the perfused heart without producing any appreciable effect upon the heart-rate other than an occasional very slight slowing. Lohmann, however, has found that if cotton soaked with formalin is applied to the region of the vena? cavae in rabbits, the rate of the heart becomes slow, and auricles and ventricles contract simultaneously (nodal rhythm). A. E. Colin and Kessel, on the other hand, have performed the latter experiment very carefully, and found that, although multiple incisions elsewhere in the auricle did not affect the rate, when the node-bearing area was entirely cut away the heart stopped entirely in ten out of sixteen experiments, and in two other experiments the rate fell 30 to 50 per cent. The stoppage after the excision lasted from 7 to 92 seconds, after which the rate gradually quickened but always remained slower than before the cut. The discrepancies between the results of the various observers are difficult to interpret, and further work on the subject is awaited. Course of the Impulse after Leaving the Sinus. From the sinus region the cardiac impulse travels to the walls of the auricles and gives rise to the auricular contraction. It is also propagated downward toward the ventricles, which it reaches about one-fifth of a second later. The discover}' of nerve-fibres (Tawara) and ganglion-cells (Wilson) in this bundle has raised the question as to whether the conduction occurs through nerve or muscle tissue. The preponderance of evidence seems to be in favor of the latter. In the frog Bond has been able to sec that the muscle-fibres of the auriculoventricular ring actually contract whenever an impulse passes from the auricles to the ventricles. V. Tabora has found that the vagi do not act upon the ventricles in mammals after the conduction has been completely cut off by means of an Erlanger clamp or by poisoning with digitalis. This observation is in opposition to the work of Carrey upon the terrapin's heart, using a similar method. He found the vagi active after clamping. Kent, His, Retzer, Braeunig, Keith, and Tawara have shown that the cardiac impulse is propagated from auricles to ventricles through the system of Purkinje fibres, which forms, a X whose shaft arises in the right auricle at or near the sinus, runs in the membranous septum (auriculoventricular bundle) downward to the muscle septum, where it divides into two branches which straddle the muscular septum and then pass to the right and left ven- tricles. Within these chambers the branches divide into numerous ramifi- cations which lie just beneath the endocardium and pass downward as a PHYSIOLOGICAL CONSIDERATIONS. 9 mesh work of light-colored translucent strands to the papillary muscles and walls of the ventricles. Occasionally instead of following tha walls they cross the ventricular cavity to the papillary muscle as isolated strands (mode- rator bands, T. W. King, Tawara) . COORDINATION OF THE CARDIAC CHAMBERS. Under all circumstances the contractions of both auricles and of both ventricles are almost synchronous, or under vagus stimulation or injury to the conduction system, the chambers of the right heart contract one or two hundredths of a second before those of the left. Even under these circum- stances the contractions are exactly similar in the two parts of the heart and there is no real dissociation. Biggs and Barker, Hirschfelder and Bond cut the left branch of the conduction system (His bundle), and found that the two ventricles continued to contract simultaneously and that extrasystoles produced in the one were communicated at once to the other. These obser- vations have been confirmed by Trendelenburg and Cohn and by Rothberger and Eppinger, who showed that the same thing was true for the right branch of the bundle. Rothberger and Eppinger have shown that, although the mechanical factors of the contraction are not altered, great changes occur in the electrocardiogram. Arrangement of Muscle=fibres in the Ventricle. This is not surpris- ing, on account of the peculiar arrangement of the muscle-fibres within the ventricle. It must be borne in mind that the heart is developed from the original cardiac tube, a vessel provided like other vessels with a longitudinal and a circular muscle coat. In the process of develop- ment this tube at first is twisted into a U shape, and the development of the in- terventricular septum transforms the U arrangement into more or less of a W, the arms of which are twisted as one might twist a rope or wring out a wet towel (Borelli, Mall). The final course of the muscle-fibres is rather complex, and, as stated by Mall, it " must be due to functional adaptation from the time the heart begins to beat." Borelli and the other workers who followed him, notably Haller, Wolff, Gercly and Ernst Heinrich Weber, rec- ognized the fact that the walls of the heart were composed of bundles of fibres encircling the ventricles, and Borelli found that those at the apex penetrated the walls to spread out within the cavity of the ventricles. Ludwig and, later, Krehl described what they believed was a very important bundle of fibres which surrounded the cavity of the left ventricle like a ring. They supposed that these fibres were the principal Fia. 11. Diagram showing the arrange- ment of the strands of muscle-fibres in the ventricle (modified from Mall). Pl'LM, pul- monary artery; MIT, mitral valve; TRIC, tricuspid valve; A \'B, auriculoventricular bundle; LV, left ventricle; RV, ri^ht ven- tricle. The sinospiral bands are shaded dark, the bulbospiral bands are light. 10 DISEASES OF THE HEART AND AORTA. factors concerned in squeezing the blood out of the cavity of the left ventricle, and hence designated them as the " driving apparatus " (Triebwerk). J. B. MacCallum, under Mall's direction, was able to show, however, that the heart of the pig's embryo could be unrolled like a scroll, and Knower found that the same was true of the hearts of man and all other adult mammals. Mall has continued these studies, and has found that the musculature of the two ventricles is composed of two distinct spirals, one running from the tricuspid or sinus portion of the heart to the apex of the right ventricle (sino- spiral), and the other from the aortic and mitral orifice to the apex of the left ventricle (bulbospiral). These two spirals are each composed of a deep and a superficial layer of fibres, which, as Ludwig demonstrated, run at right angles to one another, and they are connected with one another by the twisted strands which run from the papillary muscles of one ventricle to those of the other (Fig. 11). He found that Krehl's Triebwerk belongs to this sys- tem, and that it encircles the left ventricle like a spiral and not like a ring, and it does not have a separate existence. The system of auriculoventricular conduction fibres (Purkinje-Tawara system) is not derived from the muscular cardiac tube, like these ventricular muscular strands, but is derived from the fibres which lie in the loose meshes between the endocardial tube and the muscular tube, from which arise also the auriculoventricular valves and the papillary muscles. In the develop- ment of the interventricular septum these fibres are caught and pushed up by the latter. They therefore unite with the system of spiral fibres of the ventricles which run in the septum, not included in this structure, but rather superposed upon it, and straddle the septum like a man on horseback, whose head is the node of Tawara, whose body the His bundle in the membranous septum, and whose legs, the shafts of the bundle, pass down within the spiral, to enter the walls and papillary muscles like the feet within the stirrups. EMPTYING AND FILLING OF THE HEART, AND MOVEMENTS OF THE VALVES. The Presphygmic Period. The instant before the beginning of ven- tricular systole the mitral and tricuspid valves are open, while the aortic and pulmonic valves are closed. When the ventricular contraction begins, it at once raises the pressure within the ventricles above that in the auricles, causing the mitral and tricuspid valves to close with a snap. There is thus a short interval, the presphygmic (.07-. 09 sec.), at the very beginning of systole, during which all four valves are closed and movement of blood ceases in all four chambers. This period lasts until the pressure within tha ventricles rises above the arterial pressures (minimal pressure), after which the blood is driven out during the rest of systole. Marey has shown on mechanical models that the presphygmic period is prolonged in mitral insufficiency and shortened in aortic insufficiency; and Robinson and Draper have found it lengthened in cases of cardiac weak- ness. In extreme cases it may last .168 sec. In cases of arrhythmia the presphygmic periods of the weaker beats may be very much prolonged, and this may produce an effect upon the tracing which simulates prolonged con- duction time. PHYSIOLOGICAL CONSIDERATIONS. 11 FIG. 12. Apparatus for registering the volume of the ventricles. CARDIOM., cardiometer. Method of Recording the Volume Curve. Yandell Henderson has recorded the emptying and filling of the ventricles by means of a specially constructed cardiac plethys- mograph or cardiometer like that of Tigerstedt and Johannson. Henderson's cardiometer was made from an ordinary rubber ball, out of which a large window was cut and then closed hermetically by cementing on a curtain of rubber dam. In the centre of the rubber dam a hole was cut just large enough for it to fit air-tight in the auriculoventricular groove. The heart was then pushed in through the hole until the dam slipped into the groove. The changes of pressure within the air space surrounding the heart were communicated to a recording tambour through a glass tube cemented in the opposite surface of the ball (Fig. 12). Dr. Cameron and the writer have found it most convenient to have the recording tambour inverted, so that u p - strokes record systole and down- strokes diastole, while a general rise in the curve indicates diminution in volume, and a general fall indicates dilatation. W. G. MacCallum has controlled this method by recording the amount of blood flowing out of a tube whose proximal end is inserted into the aorta and whose distal end is elevated to a level corresponding to the diastolic pressure. The results obtained by this method indicate that the results obtained with the cardiometer have an error of not more than ten per cent., an accuracy sufficient for all experimental purposes. Outflow during Systole. By this means Henderson has found that during systole the ventricles do not empty themselves with a rush at the beginning of systole, but that the outflow continues quite uniform through- out at least nine-tenths of the latter period (outlasting the rise of the arterial pulse-wave) and begins to slow only toward the very end (slight rounding of the crest of the curve). At the cessation of outflow there is an instant during which the ventricular pressure is falling, in which no inflow takes place, but this is only one or two hundredths of a second and is difficult to estimate accurately. This instant corresponds to the dicrotic notch upon the aortic pulse-wave. Filling of the Ventricles. The ventricles then begin to fill at a rapid and uniform rate until they are almost completely distended. If the pulse-rate is rapid, the next systole takes place before the filling is as complete as possible, and cutting short the filling diminishes the volume of the heart; not only the total volume, but the amount of blood discharged at each systole (Fig. 13). Diastole and Diastasis. If, on the other hand, the heart rate is slow (Fig. 13), as after stimulation of the vagus, the influx begins at the same rate as before and continues uniformly for about two-fifths of a second (steep ascent of the curve) until the ventricles are distended, after which scarcely any blood flows into the ventricles no matter how long the interval to the next beat. The diastolic period is thus divided into two parts: (1) the phase of diastole proper during which filling of the ventricles takes place; (2) the phase of diastasis in which little or no filling occurs. The slower the heart the greater is the diastolic filling and the longer its duration. The greatest amount of output in unit time occurs at a rate which just allows the phase of diastolic filling to be complete but in which the next beat occurs before diastasis sets in. Any rate above or below this brings about some slowing of the circulation. 12 DISEASES OF THE HEART AND AORTA. AO R riC PRESSURE. Position of the Vahes and Diastole. Baumgarten (1S43) has been able to demonstrate upon the excised heart that the cusps of the mitral and triruspid valves are floated together by The influx of blood and the valves close spontaneously when the inflow ceases. The writer has been able to show that the occurrence of diastasis is not necessarily caused by the valves being closed, but by the faes not fill unless there is a slight positive pressure in the veins. The walls of the; heart are sufficiently rigid 14 DISEASES OF THE HEART AND AORTA. and are sufficiently provided with elastic fibres to resume their shape like a rubber ball, and, on the other hand, the pressure in the coronary arteries tends to hold them distended as though by a wire frame. 1 The heart muscle is quiescent and the heart walls are relaxed during the entire period of diastole, so that neither the most delicate recording levers nor the most sensitive galvanometers reveal the slightest signs of con- traction. Nevertheless, as will be seen, the degree of this diastolic relaxa- tion of the walls varies considerably under different circumstances depend- ent upon the tonicity of the heart muscle. This is shown by variations in the length of strips of cardiac muscle under a constant load, as well as by variations in the cardiac volume. Tonicity. T onicity may be defined as the resist- ance of the heart muscle to stretching in diastole; or, less accurately, as its diastolic rigidity. The force which stretches the heart walls in diastole is the pressure at which the blood enters the heart from the great veins, namely the venous pressure, so that with a high venous pressure (unless antagonized by a high FIG. l~). Volume curves of the ventricles at increasing pulse rates. The shaded zone indicates the amount of blood within the heart at each instant, the sketches at right and left indicating the size of the heart piotorially. The light broken line indicates the volume curve as it would appear if the heart rate were slow. (Kindness of the Interstate Medical Journal.) tonicity) they will be stretched considerably (dilatation), while with a low venous pressure comparatively little blood will enter and the heart will remain small. In all cases filling will continue until an equilib- rium is reached between the venous pressure and the cardiac tonicity, unless the heart rate is so rapid that the filling is interrupted by the next systole. A high tonicity will, however, antagonize a high venous pressure and prevent overfilling. Moreover, Howell and Donaldson have shown that the systolic output of tiie heart depends to a great extent upon the amount entering the latter from the great veins, and, hence, upon the venous pressure. If the venous pressure falls below a certain level, the heart fills incompletely, and the ven- tricles are unable to pump enough blood into the arteries to maintain the blood-pressure at the usual level. The rate of filling of the heart is accelerated (curve of filling steeper) (T'i'j;. Ki) when either the venous pressure is high or the tonicity is low; the H'or a detailed account of the various theories of the cardiac relaxation, with full bibliography, consult K. Ebstein, Die Diastole des Her/.ens, Ergebnisse der Physiol., V\ icsl)., I'.io I, iii, 2 Abth. PHYSIOLOGICAL CONSIDERATIONS. 15 filling is slowed (curve more oblique) when either the tonicity is high or the venous pressure is low. So that, as regards filling of the heart, a high tonic- ity is equivalent to a low venous pressure, and conversely, a low tonicity is equivalent to a high venous pressure (Fig. 16). Influences which affect tonicity may be studied objectively in isolated strips of cardiac muscle by means of their shortening or lengthening, or upon the intact heart by changes in the volume curve. VLNOUS PRESSURE: I VOLUME OF VENTRICLES FIG. 10. Diagram showing the effect of varying venous pressures upon the volume of the heart, upon the rapidity of filling of the ventricles (volume curve), and upon the position assumed by the mitral and tricuspid valves at the end of the first inflow into the ventricles. The figure to the left shows the valves remaining open, that in the middle shows partial closure (functional stenosis), that upon the right complete diastolic closure. The total volume of the heart at any given instant may be regarded as follows : Volume of heart = volume of heart walls + volume of blood within cardiac chambers. Volume of walls volume of muscle + coronary blood + lymph. (The two latter factors vary somewhat, though relatively slightly, the lymph increasing considerably in cardiac stasis.) Volume of blood within chambers = output at each systole -f- blood remaining at end of systole (residual blood). Residual Blood. The residual blood under g o e s g r e a t variations. In dilated- hearts it may attain to several times the amount 16 DISEASES OF THE HEART AND AORTA. of the systolic output (cf. Fig. 17), while in small hearts it may be only a fraction of the latter. The systolic output, on the other hand, may undergo equally large variations. The changes in tonicity may be measured by the volume of the heart at the end of diastole, i.e. when the filling is most complete, a large diastolic volume representing low tonicity (when venous pressure and pulse-rate are constant), a small volume indicating a high tonicity. Nature of Changes in Tonicity. Porter has found that a strip of heart muscle can be made to remain elongated (diminished tone), or can then be made to remain shortened when not receiving any stimuli whatever (in- creased tone). Several degrees of this permanent shortening can be super- posed on one another with great similarity to the tetanus of skeletal muscle (" tetanus of tone," Porter). Barcroft and Dixon have shown that the muscle FIG. 17. Diagram showing the condition of the heart with varying degrees of tonicity but with systolic output (amount of blood forced out per beat) normal. The volume at the end of diastole consti- tutes the index of tonicity which, at the end of systole, indicates the amount of residual blood. High venous pressure has the same effect as low tonicity. (Kindness of the Interstate Medical Journal.) when in tone gives off more C0 2 than when at rest, further supporting this view of the role of increase and decrease in tone. Factors Producing Changes in Tonus. F. B. Hoffmann has demon- strated that there are two separate sets of fibres in the frog's vagus. One set influences the heart-rate only (chronotropic effect) and also increases the si/e and force of contraction (augmentor effect) and also increases the cardiac tonus but does not affect the rate at all. This group of fibres is found only in the interauricular and interventricular septum (septal nerves) in the frog. In other animals the two groups of fibres pass side by side and cannot be dissociated, though it is frequent in weak stimulation of the vagus to find one effect occurring without the other. P. D. Cameron, in the writer's laboratory, has found that in dogs the intravenous administration of digitalis, strophanthus, nitroglycerin, and calcium salts increases cardiac tonicity. The effect of small (therapeutic) PHYSIOLOGICAL CONSIDERATIONS. IT doses of these drugs is exerted almost entirely upon the tonic fibres in the vagus, and fails to appear if the vagi have been cut or paralyzed with atro- pine. Larger doses, however, exert similar effects by direct action on the heart muscle. Atropine itself illustrates these effects by causing a primary depression of tonus as the vagi become paralyzed, which is followed by an increase in tonicity from direct action on the heart muscle. Potassium salts, asphyxia, formic acid, adrenalin depress tonicity. Aconite in therapeutic doses affects rate more than tonus in the dog. Since the exact volume of the heart cannot be determined clinically, the area of the cardiac shadow in diastole furnishes the best index of the tonus, especially when combined with study of the venous pressure. Com- paratively little investigation has been carried on in this field. Moritz and Dietlen have shown that exercise usually increases tonus in healthy persons. The study of tonus has also proved of value in the study of exercise and in the controlling of hydrotherapy and drug treatments, as well as in the study of myocardial insufficiency. ACTION OF THE CARDIAC NERVES. The nerve supply of the heart is derived from two sets of extracardiac nerves, the vagi connecting it with the medulla and the so-called accelerator nerves which connect it with the sympathetic system. These in turn divide into branches which run to the intrinsic ganglia of the heart itself, the course of these nerves and their relations to the rest of the central nervous system being indicated in Fig. 18. Each vagus and each accelerator is distributed chiefly over the corre- sponding half of the heart, but the free anastomosis of the cardiac plexuses permits the impulses from one side to spread more or less freely to the other, and only occasionally does a preponderance of effect upon one side of the heart become evident. (See page 18.) The vagi contain two sets of fibres, the afferent or sensory fibres, whose ganglion-cells are located in the ganglia and which carry the sensory impulses from the heart; and the motor or cardio-inhibitory fibres, whose cells are located in the nucleus and which carry the impulses down to affect the heart-rate. Afferent Impulses. As regards the afferent impulses, the tracings of Einthoven, Flohil, and Battaerd have demonstrated that a wave of electro- negativity passes upward at each heart-beat similar to the slower negative wave which accompanies each respiration (see page 213 and Fig. 125). The nature of the afferent impulses and their relation to cardiac symptoms are discussed on pages 213 and 214. Efferent Impulses. The efferent impulses which pass down the vagi are of various types: (1) Cardioinhibitory, which slow or stop the heart- beat by preventing the genesis of cardiac impulses. (2) Negatively dromo- tropic, which depress conductivity either by action on the His bundle or by depressing the irritability of the ventricles themselves. (3) Impulses which affect tonicity, sometimes depressing, sometimes increasing it. As Cameron has shown, paralyzing the vagi with atropine prevents the tonus changes resulting from the administration of most drugs. Right and Left Vagal Effects. Like the accelerators, each vagus acts upon the corresponding side of the heart, and certain differences between 2 18 DISEASES OF THE HEART AND AORTA. the action of the two vagi seem to be due to this localized action. In a series of experiments performed by the writer in collaboration with Dr. H. A. Stewart, in which the left vagus was the nerve usually stimulated, it was noted that vagal heart-block was produced with great frequency, and often over- shadowed the inhibitory effect upon the auricles; whereas in most physio- logical experiments, in which for greater convenience the right vagus is used, the inhibition predominates and the block is absent. Drs. G. C. Robinson and Draper have recently obtained similar results from pressure on the vagi in man. The right vagus usually slows the heart, the left induces block. FIG. 18. Origin and course of the cardiac nerves, and cutaneous distribution of the corresponding branches. (Schematic; modified from Douglas Powell and Gibson.) MOT SENS, nuclei of the efferent (motor) and afferent (sensory) fibres of the vagus; C 1, 2, 3, 4, 5, 6, 7, 8, and T 1, 2, 3, 4, 5, 0, 7, 8, cervical and thoracic (dorsal) spinal nerves and their cutaneous distribution; SCO, MCG, ICG, superior, middle, and inferior cervical ganglia; REC LAR, recurrent laryngeal nerve; C PL, cardiac plexus. A very extended series of experiments has recently been performed by Garrey upon the heart of the turtle. Garrey has found that when the vagi are stimulated with very weak stimuli, only the corresponding side of the heart is affected, but if the stimulation is stronger it affects both sides, the impulse then crossing to the other side of the heart within the cardiac plexus. The right vagus inhibits because it acts upon the right precaval and post- caval veins and the sinus which under ordinary circumstances beat twice as fast as the veins on the left and are the " pacemakers " of the heart; but if the right veins are slowed by cooling and the left veins accelerated by warm- ing, the left side of the heart may become the " pacemaker," and weak stimu- lation of the left vagus now produces slowing of the rate instead of block. PHYSIOLOGICAL CONSIDERATIONS. 19 Accelerator and Sympathetic Nerves. All the branches of the cervical and the upper four thoracic nerves give off rami communicantes which pass to the cervical and stellate ganglia. From these ganglia branches pass out down along the arteries and vena cava to the heart, constituting the second group of extracardiac nerves the so-called accelerator nerves. This term is applied because stimulation of the right annulus of Vieus- sens gives rise to a gradually-increasing quickening of the heart-rate which may amount to more than a doubling of the original rate. Pawlow has shown, however, that this action is not common to all the branches of those nerves, but is very much more marked in the case of the right than of the left annulus of Vieussens, probably because it supplies the sinus region of the heart. This fact has been confirmed by Bayliss and Star- ling, Reid Hunt, and others. Rothberger and Winterberg studied these effects with the electrocar- diograph, and from the form of the latter were able to demonstrate that : 1. Acceleration of the heart is a function of the right accelerator, or right annulus of Vieussens, probably because its fibres are distributed chiefly to the region of the embryonic sinus (sino-auricular node of Keith and Flack and neighboring regions). 2. Stimulation of the various branches of the right cervical sympathetic gave rise to an electrocardiogram typical of overaction of the right ventricle, and, conversely, stimulation of the left cervical sympathetic branches gave rise to electrocardiograms with inverted R and T waves indicating overaction of the left ventricle. 3. Stimulation of certain cardiac branches of the left cervical sympa- thetic gave rise to simultaneous contractions of the auricles and ventricles, by causing impulse to -arise in the atrioventricular bundle (nodal rhythm, cf. page 118), with or without the occurrence of tachycardia. Tonic Action of the Vagi and Accelerators. The recent studies of Ep- pinger, Falta, and their collaborators have shown that in many pathological and borderline conditions, especially those in which there is a disturbance in the glands of internal secretion, there is also an alteration of the balance which normally exists between the autonomic (vagi, phrenic and splanchnic) and the sympathetic nervous system; so that sometimes the influence of the former predominates (vagotonie) and sometimes the latter (sympathicotonie). Many cases of hyperacidity, bronchial asthma, ulcer of the stomach, and cer- tain forms of tuberculosis show manifestations of overaction of the vagi; while Basedow's disease and its formes frustes, as well as certain cases of diabetes mellitus, represent typical examples of overaction of the sympathetic system. In some conditions there occurs overaction, in others underaction, of both systems simultaneously. Eppinger and Hess have given the following tabulation of tonic nerve effects : Vagotonie. Sympathicotonie. Pupil Contracted Dilated Bladder Contracted Relaxed Cardia Contracted Relaxed Stomach Contracted Relaxed Pulse Slow Accelerated HC1 secretion Increased Diminished Glycosuria Diminished Increased 20 DISEASES OF THE HEART AND AORTA. Patients in whom there is overaction of the vagi show particularly marked effects from the administration of atropine (1 mg., gr. 1/60, sub- cutaneously, in men; 0.75 mg., gr. 1/75, in women) and pilocarpine (10 mg., gr. 1 6, subcutaneously, in men, 7.5 mg., gr. 1/8, in women). Those with overaction of the sympathetic are particularly sensitive to adrenalin (1 cc., 15 minims, of the 1 1000 solution, equal to 1 mg., gr. 1/60, of the crystalline substance, subcutaneously, in men; 0.75 cc., 12 minims, in women). Cardiac Plexus. The intrinsic nerves of the heart exist in the form of a plexus or plexus system grouped especially around the coronary vessels and their branches. The simplest form of intrinsic nerve supply is seen in the frog tadpole, where it has been studied by His, Jr. This observer found that the first ganglia pass out toward the heart as outgrowths from the vagosympathetic chain and lie on each side of the pulmonary vein, along which they gradually wander to the heart and come to lie between the layers of the interauricular septum. A second group of ganglia arises from the so-called intestinal branch of the vagosympathetic nerve and follows the. superior vena cava down into the heart to the sinus venosus, where it lies close to the pulmonary vein and anastomoses with the pulmonary plexus described above. This group of ganglion-cells forms the sinoauricular ganglion first described by Remak in 1848. From this ganglion the cells wander further down the septum, form- ing the t\vo septal nerves of Ludwig (1848), and each of these in turn ends in a ganglion (described by Bidder in 1852) at the auriculoventricular junction. From Bidder's ganglia one set of fibres passes down over the endothelial surfaces of the valves, to distribute themselves among the muscle-fibres of the ventricular walls; another passes over between the auricles and the bul- bus and distributes itself to the region of the bulbus and the walls of the auri- cles and ventricles. F. Hoffmann has cut these nerves away from the rest of the vagi and shown, that, while stimulation of the vagus fibres passing to the sinus and auricles caused slowing or stoppage of the heart, stimulation of the septal nerves caused no change in rate, but did cause an increase in the force of the ventricular beat and in the tonus of the walls (inotropic effect). An observation made by Cameron in the writer's laboratory has ren- dered it probable that similarly distributed fibres are present in the mamma- lian heart; for he found that substances (digitalis, strychnine and potassium, calcium) which cause increase or diminution in the tonus of the ventricular muscle of the intact heart no longer exert these effects in small doses when the vagi are paralyzed with atropine. B o t h v a g i and accelerators a r e n o r in a 1 1 y i n tonic a c t i v i t y . Reflex quickening of the pulse-rate, as from emotion, pain, sensation, and other reflex causes (Reid Hunt), and moderate exercise (Hering and Bowen), is due partly to diminution of tonic activity of the vagi, partly to direct stimulation of the accelerators (Hooker); while the acceleration after violent exercise is due to stimulation of the accelerators (Hering, Bowen). Acceleration upon mild exercise can also be obtained in patients whose vagi are made inactive by 0.5 to 1.0 mg. ( l \,, to 77 777=1^ v"~ I r = Efficiency of heart as a pump. In a normal individual this coefficient is 25 per cent, to 35 per cent. 38 DISEASES OF THE HEART AND AORTA. 2. After meals the maximal pressure and pulse-pressure are increased, also the pulse-rate, and the minimal pressure may be increased, but to a less extent. The circulation is accelerated. 3. After exercise the effect is the same as after meals, only more marked. When exercise is continued to the point of fatigue the pressures fall, the pulse-rate falls also, and the circulation is slowed (Schott, Masing, Cabot, Bowen). (See page 187.) 4. Upon sensory stimulation the vasomotor centre in the medulla usually responds by constricting the peripheral vessels, and the pressure, especially the minimal pressure, rises. The pulse-rate usually quickens also. There are great variations in the response of different healthy individuals to pain sensations. Dr. A. Berg, under the writer's direction, has tested the effect of pinching the ear upon the blood-pressure of healthy individuals, and has found in some persons a rise of blood-pressure amounting to 10 to 20 mm. Hg, in others no effect, in others a fall of about 10 mm. Too intense stimuli produce shock. Mental exertion has a similar effect a definite vasoconstriction setting in, which is shown by the shrinkage of the arm in a plethysmograph. Zabel has shown that the rise in blood-pressure is proportional to the amount of mental effort. For example, a theological student could translate a few lines of Ca?sar to which he was accustomed without any change in blood-pressure, while the calculation of 17 X 18 caused his blood-pressure to rise 21 mm. Hg (28 cm. H 2 O). On the other hand, a young merchant was able to do various calculations without change of blood- pressure, whereas an attempt at translation caused a rise of 16.5 mm. (22 cm. H 2 O). Cannon and de la Paz have demonstrated that the psychic rise in blood-pressure is due to a true psychic secretion of adrenalin, for they found in the cat that the blood obtained from a cannula which they introduced through the femoral vein up the vena cava to the level of the adrenal vein contained more adrenalin after the cat had been excited by the presence of a dog than it did when the cat was quiescent. They determined the amount of adrenalin by the inhibition of the rhythmic contractions of strips of perfused origin uterine muscle which occurs whenever adrenalin is added to the perfusion fluid in even infinitesimal quantities. 5. In sleep the opposite effects are seen: there is a general vasodilation and a fall in minimal blood-pressure (Howell, Brush, and Fayerweather). There is probably also a slight fall in maximal pressure. VARIATIONS IX BLOOD-PRESSURE UNDER PATHOLOGICAL CONDITIONS. ASPHYXIA AND THE EFFECT OF EXCESS OF COj. When the heart fails the circulation is slowed and the blood becomes incompletely aerated and overloaded with CO2 (f. Bohr). These conditions closely simulate the conditions present in asphyxia (Traube), or after breath- ing an atmosphere overladen with C02 (Klug has shown that the effect of these is quite similar). Experimental Asphyxia. The conditions as observed in experimental asphyxia somewhat foreshadow those due to accumulation of C0 2 from heart- failure. The blood-pressure changes in asphyxia have been most carefully studied by Konow and Stenbeck in Tigerstedt's laboratory, who found as- phyxiation in rabbits resulting in the following series of events: 1. At the beginning of asphyxia the vasomotor and cardiac centres in the medulla are stimulated, as is also the inhibitory centre. Blood- pressure rises and the pulse is slowed. (Cameron has shown that, on the other hand, the t o n i c i t y of the heart muscle promptly decreases with the first stage of asphyxia and remains diminished throughout.) 2. A.s asphyxia continues, the effect of slowing of the pulse exceeds that of the rise of pressure and the blood-pressure falls. 3. This condition slows the circulation still more, CO 2 accumulates in the blood, bathing the vasomotor centre, the latter stimulates the arterioles to still further constric- BLOOD-PRESSURE AND BLOOD VISCOSITY. 39 8 z\ tion, the vagus can no longer overcome these effects, and in spite of its continued action the pulse quickens and blood-pressure again rises. 4. The activity of the vasomotor centre diminishes while the vagus centre remains at maximal activity, and the pulse-rate again slows and blood-pres- sure again falls. 5. The vagus centre fatigues, the ac- cessory vasomotor centres in the spinal cord are again stimulated, and blood- pressure and pulse-rate again rise. 6. Conductivity of the heart dimin- ishes, occasional beats are dropped by the ventricle, blood-pressure and pulse-rate fall, and the animal dies at this stage unless respiration is promptly restored. Occasionally in asphyxia periodic changes in rhythm of the heart occur, such as have been described by Luciani in frogs and by Langendorff in cats. These irregularities occur when the vagi are sectioned as well as when they are active; this also occurs when the animal is made to breathe an excess of CO 2 (Klug). When, however, the vagi are inactive (cut), the rise of blood-pressure in asphyxia is continuous from the onset until the vasomotor centres fail (i.e., in the fourth stage). When the cervical nerves have been cut and the vagi are active, there is an immediate fall in both blood-pressure and pulse-rate; the rise in blood-pressure sets in much later when the accessory vasomotor centres in the spinal cord are stimulated, or the animal may die if these fail to respond. R \ \/ W FIG. 29. Diagram showing the curve of blood- pressure during asphyxia. (Schematic, illustrating the results of Konow and Stenbeck.) N, normal ; BP, blood-pressure ; PR, pulse-rate. BLOOD-PRESSURE IN VARIOUS DISEASES. Importance of Determining the Mechanism Producing the Change. Variations in blood-pressure occur not only in conditions of health but still more under pathological conditions. As will be seen, the mechanism which brings these changes about is not always a simple one, and the causal factor may not be affected by merely resorting to therapeutic methods which lower a high blood-pressure or raise a low one. It is therefore necessary for the clinician to investigate as far as possible the condition of the vasomotor nerves, the strength of the heart-beat, to determine also whether the blood is properly aerated, and learn whether the kidneys are performing their function properly, before proceeding to symptomatic treatment of high or low blood-pressure when the cause is in any way obscure. DISEASES WITH HIGH BLOOD-PRESSURE (HYPERTENSION). The following represents the typical blood-pressure findings in various diseases. In exceptional cases more extreme variations are seen. 1. Nephritis (discussed below), especially the chronic forms (maximal pressure 1GO to 220, minimal 120 to 100, pulse-rate 50 to 80). High blood-pressure is common in both 40 DISEASES OF THE HEART AND AORTA. parenchymatous and interstitial cases. Passler and Heineke found that in animals from which almost all the kidney substance had been removed, blood-pressure rose pari passu with the occurrence of signs of renal insufficiency in the metabolism. Excellent reviews of this subject have recently been published by T. C. Janeway and by Pearce. There seems to be a striking parallelism between continuous high blood-pressure and oversecretion of the adrenals, sometimes leading to an hypertrophy of the latter (see page 42). In acute nephritis the blood-pressure may not rise, but Buttermann reports a case of scarlatinal nephritis where a rise of 50 mm. heralded the onset of the nephritis. Here it is of diagnostic and prognostic importance. In uraemia blood-pressure rises at the beginning of the attack, but may gradually fall a few days before a fatal termination (Laqueur). Gradual fall in blood- pressure also accompanies amelioration. Engel finds that there is no rise in the mildest cases of nephritis, but that the rise of pressure runs parallel to the severity of the disease until the terminal fall sets in from cardiac weakness. 2. Arteriosclerosis. Increased blood-pressure (maximal 150 to 170, minimal 110 to 130, pulse 60 or over) is the rule in arteriosclerosis, though there are occasional exceptions where the maximal pressure does not exceed or even reach 110 mm. (Israel). (See also chapter on Arteriosclerosis.) 3. Lead Poisoning (plumbism). Acute and chronic forms are usually associated with high blood-pressure, as in arteriosclerosis, often with vasomotor crises. 4. Chronic Hypertrophy of the Heart from other causes, as in athletes, or as the result of smoking in excess, of compensated heart lesions, etc. (maximal pressure may reach 145 mm., minimal 90 to 110 mm., pulse-rate normal or increased). 5. Aortic Insufficiency is often but not always associated with high maximal pres- sure (maximal pressure 170 to 220 mm. Hg, minimal 60 to 140, pulse-rate usually increased, being even as high as 120). This is usually associated with arteriosclerosis. In young individuals, as in experimental aortic insufficiency in animals, the maximal pressure is usually little changed, the minimal pressure lowered (maximal 120 to 130, minimal 50 to 60, pulse-rate normal or increased). 6. Conditions associated with increased pressure in the cranial cavity (meningitis, apoplexy, cerebral thrombosis, frac- ture of the skull, intracranial hemorrhage, rapidly growing brain tumors, some cases of uraemia, Jacksonian epilepsy). Maximal blood-pressure may rise to 300 or 400 mm. Hg, minimal pressure to 160 or over, pulse-rate slow, 60 or under. Gushing has shown that when the intracranial pressure is raised above the blood-pressure, the ana?mia of the vasomotor centre brings about a tre- mendous vasoconstriction and action of the augmentor fibres in increasing the strength of the heart-beat. The blood-pressure rises in successive stages (Traube-Hering waves) until the mean pressure exceeds the intracranial pressure. The rise of blood- pressure expresses t h e need of the brain for blood; to coun- teract the vasoconstriction w i t h nitrites or other vaso- constrictors or by venesection only in creases the task of the heart. The only medical treatment which aids it at all is administration of atropine to paralyze the vagi, quicken the heart, and permit the pressure to rise more readily. Lumbar puncture helps somewhat by removing the excess of intracranial fluid. If this does not suffice, Gushing advises surgical interference in many cases, a flap of the skull being lifted temporarily in order to relieve the intracranial tension and to allow the blood-pressure to fall. This procedure is almost devoid of danger in the hands of a surgeon whose asepsis is perfect, but very dangerous if it is imperfect, and this point alone will often decide the advisability or inadvisability of the operation. 7. Attacks of Idiopathic Epilepsy are associated with very high blood-pressure and slow pulse. The blood-pressure falls within a few minutes after the fit, which assists to differentiate it from uraemia (Pilcz). 8. Vascular Crises. Pal has described an important group of cases associated with cripos of high blood-pressure due to vasoconstriction. Among these he classes unernia, certain cases of arteriosclerosis, especially with abdominal and cardiac symptoms, and BLOOD-PRESSURE AND BLOOD VISCOSITY. 41 especially the tabetic visceral crises with intense pain. He has shown that these as well as attacks of lightning pains are associated with marked vasoconstriction and rise in blood- pressure, and states that they are even relieved by the administration of nitroglycerin. He also classes angina pectoris, intermittent claudication, and Raynaud's disease under this head. 9. Attacks of Angina Pectoris. 10. Some Cases of Adams=Stokes Diseases between Attacks. Gibson reports a case with maximal pressure 270, minimal pressure 70, pulse-rate 27. The pressure may, however, never rise materially. During the attacks it always falls almost to zero (see page 553). 11. Exophthalmic Goitre (Graves's or Basedow's disease) is often accompanied by hypertrophy of the heart with increased maximal, 140 to 160 mm., minimal 90 to 110 mm., HYPERTENSION! NORMAL FIG. 30. Diagram showing typical blood-pressures in various diseases. Solid black, minimal pressure; striped shading, pulse-pressure; dot, pulse-rate. and pulse-pressure 30 to 50 mm., pulse-rate accelerated to 120 and over. In some cases of Graves's disease the pressure remains low (maximal 120, minimal 90). 12. The End of Pregnancy, the onset of labor, and the puerperium are accompanied by a slight (10-15 mm.) rise of maximal pressure with little change in minimal pressure (Siemens and Goldsborough; see Part III, Chapter IX). 13. Chronic Primary Polycythaemia. The increased number of rod corpuscles in- creases the viscosity of the blood, and thereby the work of the heart, besides arteriosclerosis is usually associated. On the other hand, as shown by W. Erb, Jr., increase in blood- pressure causes liquid to leave the vessels and thereby increases the viscosity of the blood further introducing a vicious cycle. 42 DISEASES OF THE HEART AND AORTA. 14. Cyanosis in Heart-failure with Broken Compensation, which occurs at some etagc in almost all failing hearts. The blood becomes overloaded with CO 2 , and vasocon- striction plus augmentation results as in asphyxia (see page 315). Usually the pulse is quickened, probably from fatigue of the vagus centre. This condition is of great clinical importance, since the high blood-pressure increases the work of the heart and accelerates its failure. Venesection, nitrites, digitalis, anything which accelerates the velocity of blood flow through the lungs, brings about improvement and lowering of the blood-pressure. CHRONIC HYPERTENSION. One of the most interesting and important conditions from the clinical stand-point, as well as from that of pathological physiology, is the condition of persistent high blood -pressure associated with hypertrophy of the left ventricle. As will be seen, this condition or syndrome is scarcely to be regarded as a single clinical entity, but more as a group of manifestations secondary to a variety of hetero- geneous clinical conditions, grouped together only for clinical convenience and for convenience in discussion of their pathogenesis and treatment. They are not associated with primary disease of the heart, but arise secondarily from diseases in other organs. For convenience of clinical designation, how- ever, they have been grouped under terms " chronic hypertension," " hyper- piesis " (Sir Clifford Allbutt) and " presclerosis " (Huchard); but these terms are usually applied to the high blood-pressure of chronic nephritis. Frequency of High Blood=pressure in Chronic Nephritis. A review of the cases of high blood-pressure in association with either arteriosclerosis or chronic nephritis which have come to autopsy from the Medical Service of the Johns Hopkins Hospital during the years 1905 to 1911 (total admis- sions 7,000) indicates strongly the relation of chronic nephritis to diffuse changes in the kidneys. Of thirty -nine cases of the two conditions in which the blood-pressure had been above 150 mm. Hg (Riva-Rocci wide cuff), only four were free from diffuse nephritic changes, and in none of these was the pressure above 190 mm. Hg, while in fifteen cases of chronic nephritis the blood-pressure ranged from 190 to 300 mm. Hg, eight being below and seven above 230 mm. Similarly T. C. Jane way has found that in 130 patients seen in private practice whose blood-pressures were over 200 mm. Hg, at least 105 (81 p?r cent.) were cases of outspoken chronic nephritis, most of the others being cases of aortic insufficiency. Cohnheim has shown that in cases of kidney stone and hydronephrosis, hypertension and cardiac hyper- trophy are also present, as they are in chronic nephritis. On the other hand, the blood-pressure is by no means always elevated in cases of chronic nephritis, as shown by the fact that it was below 135 mm. Hg in 6 out of 44 cases, and in other cases fell below this level after an initial period of elevation. The low blood-pressure is not always a terminal event even in cases with markedly impaired renal function, as is shown not only by the autopsy records, but also by the cases whose phenolsulphonphthalein excretion has been found by Rowntree and Geraghty to be greatly diminished during life. The chief other conditions in which very high blood-pressures are en- countered are those associated with increased intracranial pressure (menin- gitis, fracture of the skull, brain tumor, apoplexy, hemorrhagic meningitis) BLOOD-PRESSURE AND BLOOD VISCOSITY. 43 and aortic insufficiency. In the latter condition, though the maximal pres- sure is high the minimal is relatively low and the pulse-pressure is relatively large. In advanced Basedow's disease the blood-pressure is usually con- siderably elevated, though it rarely reaches 190 mm. and never towers to the extreme heights seen in chronic nephritis. In contrast to the latter con- dition the diastolic pressure is not extremely elevated and the velocity of the blood flow through the arm is very considerably increased (Hewlett and van Z waluwenburg) . Roughly speaking, the cases with blood -pressure permanently above two hundred millimetres of mer- cury are mainly those of increased intracranial pres- sure, chronic nephritis, and aortic insufficiency; those between one hundred and fifty and two hundred millimetres, besides these conditions are arterio- sclerosis, Basedow's disease, chronic polycythsemia, and high pressure stasis (Hochdruckstauung).* Possible Sources of Error. Just how much of the high reading of the sphygmo- manometer in chronic hypertension is due to actual elevation of blood-pressure and how much is due to the incompressibility of the arterial wall owing to increased tonus (see page 29) is difficult to determine. George Johnston, Savill and Russell have shown (see page 334) that in many of these cases there is great hypertrophy of the media of the peripheral arteries (see Plate X); and Russell claims that the increased tonus of the hypertrophied media imparts to the vessel wall a rigidity which makes it difficult to compress. He rather aptly compares the artery with thickened media to a thin-walled rubber tube, and he finds that such a tube of the same diameter as the radial artery may require a pressure of 150 mm. Hg to obliterate it. His suggestions have been confirmed with great care by Janeway and Park, who found that thickened arteries, especially when the muscular layer is rendered spastic by immersion in barium chloride, may require as much as 64 mm. Hg to collapse them, and that if the arteries were boiled it might require 154 mm. Hg. The actual dis- crepancies in human beings have not been studied on a large scale, but V o 1 h a r d has found the readings from a manometer inserted into one of the large peripheral arteries with a cannula prior to an amputation were 20 mm. H g lower than those obtained with the R i v a - R o c c i method. As the results by palpation at the wrist are 5-10 mm. Hg, this would indicate that the sphygmomanometric reading by the auscultatory method would have been 25-30 mm. Hg too high in this case, and it is by no means certain that this represented one of extreme grade. It is possible that, as Russell claims, this error may be doubled in certain cases, and that the high readings in this condition may be obtained when the actual blood-pressures, which are 60 mm. or more, lower. There is at present little conclusive evidence upon which to substantiate or to deny this claim. It is certain that when the diameter of the arteries is reduced by vasoconstric- tion, the resistance of their walls to compression is correspondingly increased, so that this factor probably plays a much greater role in producing errors in blood-pressure readings in conditions of vasoconstriction than in the normal state, or in states of arterial dilata- tion, such as are met with in aortic insufficiency. On the other hand, the tremendous degree of hypertrophy of the heart in these conditions furnishes good evidence that, though part of the high readings of (lie sphygmomanometer may be due to this error in the method, the greater portion is unquestionably due to a true elevation of the blood-pressure. Causes of High Blood=pressure in Nephritis. The cause of the high blood-pressure in chronic nephritis has been the subject of much discussion. Traube and Cohnheim believed that the diminution in the blood-channel through the kidneys rendered an increased blood-pressure necessary, i n *In many cases the periods of high blood-pressure may be transitory, coming on under strain and excitement. In these hypertension usually becomes permanent later. 44 DISEASES OF THE HEART AND AORTA. order-to maintain a sufficiently rapid blood flow through these organs; for, as Cohnheim put it, an excess of ex- cretable (harnfahige) substances in the blood readily brings this about. That the renal vessels were sclerotic and their walls thickened in chronic nephri- tis had been shown by George Johnson and by Gull and Sutton; but, as Cohnheim showed, mere cutting down of the pathway through the kidneys could not be the cause, for total ligation of both renal ar- teries was not followed by rise in bloo d-p r e s s u r e. Numerous writers following Cohnheim have believed that the hypertension was caused by the action of substances in the blood which are excreted by the healthy kidney but retained when the organ is diseased, notably urea, the purin bodies, and the ammonium salts. However, hypertension may occur in conditions in which the urea output is normal and in which the quantity present in the blood is not even as great as in a variety of other conditions. Similarly Erben has ascribed it to the non-coagulable nitrog- enous bodies (Reststickstoff) in the blood, among which the purin bodies, especially xanthin and hypoxanthin, seem sufficient to cause hypertension (Croft an). The relation of accumulation of these substances in the blood to hypertension does not seem to be a constant one, however (Strauss), and the theory requires some further proof. Certain it is, however, that reduction of the amount of kidney sub- stance alone is sufficient to bring about hypertension. J. Rose Bradford demonstrated that if more than half the substance of the healthy dog's kid- ney is removed the remaining portion secretes a very abundant and very dilute urine resembling that found in chronic contracted kidney. This find- ing was confirmed by P a s s 1 e r and H e i n e k e , who remove d m ore than a kidney and a half, bit by 1) i t , an d p r o - d need both hypertrophy of the heart and persist- e n t high blood-pressure, and these observations have been confirmed both by Sampson and Pearce and by Carrel and Janeway. The latter investigators reduced the renal substance by ligating successively sev- eral branches of the renal artery at long intervals; and found not only hyper- trophy of the ventricles of these dogs but also a rise in blood-pressure of over thirty millimetres of mercury. ( 'linical evidence, too, seems to confirm the results of these experiments, for Butter m a n n h a s e n c o u n t e r e d a rise of 50 m m . H g within 48 h ours after t h e o n s e t of n e p h r i t i s in scarlet-fever patients. The presence of an internal secretion of the k i d n e y has also been suggested by Brown-Sequard to explain the hypertension, and this investigator, as well as T i g e r s t e d t and Be r g - in u 11 n , has s h o w n t h a t a rise of bio o d - p r e s s u r e m a y be ]) r o d u c e d by injecting renal extract ('' renin "), although, us Pearce has found, this rise is both slight and inconstant. Ex- tracts of diseased kidneys show no striking difference from those of normal organs in this regard; so that it would appear that evidence in favor of this theory of renal internal secretion is insufficient to admit of its acceptance. Still another theory which has gained many advocates in recent years is that of a h y p e r s e c r e t i o n of adrenalin (adrenalin aemia) in BLOOD-PRESSURE AND BLOOD VISCOSITY. 45 these cases; and this theory has been supported by the observations of Josne, Vaquez and Aubertin, Wiesel, and others (see page 344), that in certain cases of hypertension and hypertrophy of the heart there was actual hyper- trophy of the adrenal cortex. The hopes of the adherents of this theory have been somewhat blasted by the fact that Cohn has found the same adrenal hypertrophy present in about an equal proportion of cases in which there was no hypertension or hypertrophy of the heart, and, on the other hand, that the latter conditions were by no means always accom- panied by hypertrophy of the adrenals. Physiological evidence also has pointed in the same way. Schur and Wiesel found that the serum of patients with hypertension caused contrac- tion of the pupil of the excised frog's eye (Ehrmann's reaction for adrenalin), and Frenkel has been unable to produce relaxation of the muscle of the mam- malian uterus profused with oxygenated Locke solution to which serum of such patients had been added. As the latter represents the most delicate and certain of the tests for adrenalin, its absence may be taken to indicate that in these cases there was no increased amount of adrenalin in the blood. It will appear from the foregoing that the hypertension of chronic nephritis still awaits satisfactory explanation. The high blood-pressure of chronic nephritis is almost certainly accom- panied by a tremendous vasoconstriction, for the diastolic blood-pressure also remains high, and, as Hewlett and van Zwaluwenburg have shown, the velocity of blood flow through the arm remains normal in spite of the increased pressure. On the other hand, the fact that the blood flow is not decreased might be construed as evidence that the blood-pressure is raised in order to keep up the velocity of flow, and that it is to be regarded as a compensatory mechanism to counteract the effect of the vasoconstriction. Arteriosclerosis and Hypertension. Hasenfeld has claimed that high blood-pressure and hypertrophy of the heart occur in those cases of arterio- sclerosis in which there are lesions in the splanchnic arteries or the aorta above the diaphragm, and Longcope and McClintock have shown that a distinct rise of blood-pressure may be produced in dogs whenever the supe- rior mesenteric artery is occluded. Marchand and Jores, on the other hand, find that lesions of these vessels are by no means always associated with cardiac hypertrophy and hypertension. Jores even goes so far as to claim that they occur almost exclusively in the cases with small red kidney. In this form he finds that the most striking change is an arteriosclerosis in the renal arteries beginning in the glomeruli and smaller vessels and gradually involving the larger branches (arteriocapillary fibrosis, Gull and Sutton). The autopsies made at the Johns Hopkins Hospital, however, do not bear out Jores's contention that the small red kidney is the only form associated with high blood-pressure and nephritis. If the patient does not die of intercurrent infection, heart-failure sets in in the course of a few years, with gradually developing dyspnoea, ana- sarca, hydrothorax, progressive dilatation of the heart, and relative tricuspid insufficiency. Effects of Chronic Hypertension upon the Circulation. When the blood-pressure remains elevated to the heights mentioned above, the work 46 DISEASES OF THE HEART AND AORTA. of the heart is considerably augmented. If this be calculated simpl}' as work of heart = maximal blood-pressure X pulse-rate, it will be seen that the latter may readily be more than doubled without bringing about any improvement in the circulation, and in the course of several years this overwork usually impairs the strength of the heart. When the pulse-rate becomes more rapid, which usually occurs as heart-failure sets in, the work of the heart may be increased, and a vicious circle is introduced. This is sometimes accompanied by a fall of blood-pressure shortly before death, but in many cases the pres- sure remains elevated until the end. Many of these patients are entirely free from symptoms for some years after the onset of the hypertension, and then begin with only occasional headaches, frequent micturition at night, and palpitation. Sooner or later a tendency to fatigue and lassitude sets in, and then the actual failure of the heart. In not a few of the cases the course is interrupted by the onset of uraemia, resulting in death. In patients with simple arteriosclerosis the blood-pressure rarely if ever rises to the heights reached in many cases of nephritis, and it is almost always well below 190 mm. Hg. The urine may contain albumin and casts, but the phenolsulphonphthalein excretion is undiminished (Rowntree and Ger- aghty). The symptoms are usually confined to those of circulatory failure, although headaches may arise from cerebral arteriosclerosis and nocturnal micturition may be due to impairment of the general circulation. Cerebral Hemorrhage and Hypertension. A considerable number of cases of chronic high blood-pressure are sooner or later associated with cere- bral hemorrhage, owing in part to the fact that mesarteritis of the cerebral vessels is particularly common in chronic nephritis, and in part to the fact that the high blood-pressure imposes a very severe strain upon the walls of the arteries and thus leads to their rupture. The rupture in turn leads to hemorrhage, and the pressure from the hemorrhage upon the surrounding tissue and the oedema of this injured tissue lead in turn to increased intra- cranial tension and thus to a further increase in the blood-pressure itself; so that a vicious circle is introduced: High blood-pressure. Cerebral hemorrhage. Moreover, as Cushing has shown, the mere una?mia of the brain leads reflexly to still further vasoconstriction until the blood-pressure is increased above the intracranial pressure so as to bring sufficient nourishment to the brain in spite of the local conditions. Treatment of chronic hypertension may be undertaken in two ways, cither by attempting to reduce the pressure directly by dilating the periph- eral arterioles with drugs of the nitrite series or vasotonin (yohimbin- urethane) or by attempting to alleviate the factors which lend to the vaso- constriction. The advisability of attempting to dilate the arterioles with nitrites or vasotonin depends upon whether the high blood-pressure arises incidentally or whether it is a phenomenon of physiological compensation. For example, in conditions accompanied by increased intracranial pressure, as C'ushing BLOOD-PRESSURE AND BLOOD VISCOSITY. 47 has shown, the vasoconstriction goes on until the blood-pressure rises above the intracranial pressure and the requisite amount of blood is shunted through the brain. If this vasoconstriction is antagonized by the action of nitrites and the vasoconstriction is prevented, the heart must be stimulated to far greater efforts in order to nourish the brain, and, if the treatment is pushed still further, the patient may suffer distinctly from the effects of cerebral anaemia. In the past decade, before this fact was recognized, the writer has seen this borne out in patients with apoplexy, whose general condition and mental condition were decidedly worse during periods when the pressure was reduced by nitrites than it was during those when the hypertension was not interfered with. On the other hand, as seen in some cases of vasomotor crisis, the vaso- constriction may also be merely an accessory phenomenon bearing no rela- tion at all to any physiological need, and the pressure is then raised merely in order to force the blood through the constricted arteries at its usual velocity. The exact mechanism which brings about the rise in pressure in chronic nephritis is not well understood, nor has it been conclusively proved whether this is a toxic or a compensatory phenomenon, though Janeway leans to the latter. Fellner believes that there is sometimes an over-compensation, in which a slight but not a great reduction of blood-pressure is beneficial. Whatever be the explanation, Matthews has shown that, though the hyper- tension can be reduced by comparatively small doses of nitrites in the early stages of chronic nephritis, these drugs become much less effective after the disease is far advanced. On the other hand, some benefit may be obtained by modification of the diet, especially, as Widal has shown, by reducing the amount of salt ingested. With the decrease in salt in the food, there follows in many cases a decreased need for water, for Erich Meyer has shown that the contracted kidney is unable to excrete more than a certain definite con- centration of salt in the urine; an excess of water is needed, therefore, to carry away the salt. Meats should be either entirely eliminated from the diet or taken but once a day, while bouillon and meat soups and the glandular organs (sweet- breads, liver, kidneys, spleen, lungs), which are particularly rich in purins, should not be taken at all. The patient should be made to live a life as free as possible from over- exertion and over-excitement, and he should take hot baths rather than cold ones, to dilate his arteries rather than constrict them more than is necessary. For the same reason IK; should be warmly clothed during the periods when the weather is at all cool. When these precautions are carried out, considerable respite may be obtained by the patient, and the readings of the sphygmomanometer may be lowered thirty millimetres or more during the course of the treatment, along with a general improvement in health and spirits. For the symptoms of cardiac weakness themselves, or in order to Avard them off, digitalis may be administered, either in the tincture or the more modern special preparations, or, on the other hand, be given as the infusion, Avhich is preferred by many clinicians for the treatment of this condition. 48 DISEASES OF THE HEART AND AORTA. In cases of chronic nephritis, however, the effect of digitalis is at best only palliative, for the agent, toxic or secretory, which has led to the hyperten- sion and the hypertrophy of the heart has already exerted an action quite similar to that of the drug itself; and the effect to be obtained is, therefore, but limited. PATHOLOGICAL CONDITIONS ASSOCIATED WITH LOW BLOOD-PRESSURE (HYPOTENSION). Although the occurrence of low blood-pressure is usually associated in the mind with the idea of a diseased heart, such is, as a rule, not the case. In fact, in most chronic diseases of the heart the maximal pressure is in- creased rather than decreased, as has been shown above. In one case of aortic insufficiency, for example, the writer found a maximal pressure of 150 and a minimal pressure of 110 two minutes before death, in spite of in- tense heart failure. A low blood-pressure is more commonly an index of fail- ure of the vaso motor centre than of the heart, and occurs in con- ditions where the strength of the heart is uninjured (Romberg and Passler, Hasenfeld and Fenevessy, Crile). Conditions in which low blood-pressure is found are: 1. Acute infectious diseases, except meningitis (where the blood-pressure is high from increased intracranial tension). Romberg and Passler have shown that bacterial poisons diminish the tonic activity of the vasomotor centre, and may even paralyze it. The strength of the heart is shown to be undiminished if the vasodilation is counteracted by adrenalin, compression of the abdominal aorta, etc. The blood-pressure falls because the arterioles are dilated and the outflow from the arteries is too rapid (maximal pressure 90 to 110, minimal pressure 50 to 90, pulse-rate increased, see table, page 41). The lowest blood-pressure is in t y p h o i d fever (Barach) and peritonitis, where the dilatation of abdominal vessels from the local inflammation add their effect to that of the cutaneous vasodilation. In typhoid fever the writer has seen maximal pressures as low as 65 mm. Hg (Riva-Rocci), although maximal 100 to 120 with minimal 60 to 90 is more common. Crile and Briggs have described rises in blood-pressure at the onset of per- foration due to splanchnic stimulation, but the writer has had two cases (one of which is mentioned by Briggs) in which inactivity of the vasomotor centre prevented this rise from occurring. In pneumonia the blood-pressure may not be changed much (maximal 110 to 130, minimal 90, pulse-rate 120); it may rise as mild asphyxia sets in, or it may fall very low from vasomotor paralysis. In diphtheria, scarlet fever, measles, acute rheumatism, and in fact in all other acute infectious diseases, the maximal pressure usually falls below 100 during the height of the fever (Weigort). 2. Phthisis. In this disease all ranges of blood-pressure may be found. John, Xau- mann, Burckhardt, and Stanton have found uniformly low pressures, 90 to 100 mm. with the Gaertner and Riva-Rocci apparatus, but this may arise from the pallor of the skin. Janeway found that variations of maximal pressure between 80 and 120 mm. Hg are com- mon in the same patient, and the writer's experience bears this out. The pulse-rate is usually rapid, 80 to 100 per minute. Peters finds that there is usually a rise of blood-pres- sure when improvement sets in, and a fall when the case is getting worse. 3. Shock. Goltz in 1863 found that if a frog were lapped upon the abdomen the heart stopped beating for a while and then resumed contraction, but the arteries were then pale and small and the circulation very much retarded. He found, on the other hand, that the abdominal veins were very full, and that the vasomotor nerves supplying the abdominal vessels were no longer active. He regarded this vasomotor paralysis as the cause of trau- matic shock, a view which was further applied to surgical shock by various clinicians, among them Keen. Mitchell and Morehouse (1S64), Lauder Brunton (1873), and Crile BLOOD-PRESSURE AND BLOOD VISCOSITY. 49 (1903). Acting upon this hypothesis, Crile attempts to counteract the vasomotor paralysis by putting a double-walled rubber suit upon the patient and inflating it until the pressure upon the abdomen and lower extremities compensates for the loss of vascular tone. The common practice of elevating the feet has, of course, the same effect. The conception that the vasomotor centre is paralyzed in shock is contradicted by the observations of Porter, who found that it was still active; and Seelig and Lyon have also shown that the peripheral vasoconstrictor nerves of the leg are in tonic activity during severe shock. Still further they have shown that the arteries of the retina are distinctly contracted during shock, and that various organs (kidney, etc.) removed during shock are relatively ansemic as compared with those removed with a normal circulation. Moreover, they found that the outflow from a cannula introduced into the femoral vein was only one-third as fast when the animal was in shock as when it was normal. Their observations seem to substantiate in every way the claim of Malcolm, on purely clinical grounds, that the trouble could not be due to dilatation of the peripheral vessels. More recently Yandell Henderson has expounded a new theory for the production of shock; He noticed that in experiments upon animals under artificial respiration shock occurred with great frequency in those animals in which the ventilation of the lungs had been excessive, and he was even able to induce death from shock by excessive ventilation or to retain a slow pulse-rate and a high blood-pressure by limiting the latter, in which the animals remained in good condition in spite of severe operative procedures. In this respect he was able to show that the ill effects of over-ventilation were due to the washing out of CO2 from the blood, bringing about the condition of acapnia, or low CC>2 in the blood, which Mosso had found to produce the syncope of mountain sickness, and which Haldane and his collaborators had found to be responsible for many conditions of weakness in man as result- ing from too rapid breathing.. Henderson believes that in most cases of surgical shock or clinical syncope the rapid breathing (hyperpncea) is the underlying factor, and that the sequence of events is as follows: (1) pain or emotion; (2) hyperpnoea; (3) overaeration of the blood (lowering of the CO2 content, acapnia), dilatation of the veins, accumulation of the blood in the latter and transudation of fluid into the tissues; (4) lowering of the pressure in the veins and hence diminished entry of blood into the heart; (5) fall in arterial pressure, accompanied by loss of arterial tone (vasodilation) ; (6) cerebral anaemia and syncope. Henderson's studies have also received clinical corroboration in the observations of Gatch upon anaesthesia. In studying the effect of nitrous oxide as an anaesthetic, Gatch found that by allowing the patient to rebreathe the air which he expired the patient's condi- tion remained much better than when the ordinary methods were used in which the expired air was rapidly removed. The amount of oxygen supplied had, of course, to be kept ade- quate, but the important difference lay in the fact that in spite of hyperpnoea the patient breathed in a mixture of O 2 and CO 2 . In many cases Gatch, like Henderson, was able practically to regulate the pulse-rate of the patient by regulating the amount of CO 2 in- spired; and by the use of judicious mixtures he has been able to operate upon patients with badly broken compensation without any ill effects. There is an accumulation of blood in the veins with depletion of the arteries (an arterial anaemia). In fevers the high temperature gives rise to a slight polypncea and also favors the evaporation of CO2 from the lungs, and Minkowski 1 and, later, Caspari and Loewy' 2 have found that the CO 2 content of the blood is lowered, as well as the O 2 . This would strengthen the resemblance between the circulatory failure of fever and that of shock according to Henderson's theory of acapnia. Wolff 3 has shown with the ferrooyanide test that the velocity of the circulation through the body is about 30 per cent, slower during fever than in health. Whether an occasional whiff of CO 2 or merely occasionally holding the breath will relieve the acapnia and restore the vascular tone in such cases remains to be proved. 1 Minkowski, O.: Ueber den Kohlensauregehalt des arteriellen Blutes beim Fieber, Arch. f. expor. u. Pharmokol., 1885, xix, 209. 2 Caspari, W., and Loewy, A.: Ueber den Einfluss gesteigerter Korpertemperatur auf das Verhalten der Blutgasen., Biochem. Ztschr., Berl., 1910, xxvii, 405. 3 Wolff, E.: Ueber die rmlaufsgeschwindigkeit des Blutes, Arch. f. exper. Path. u. Pharmakol., Leipz., 1885, xix, 265. 4 50 DISEASES OF THE HEART AND AORTA. 4. Collapse from various poisons, carbolic and salicylic acid, arsenic, phosphorus, drugs of the antipyretic series, etc., is due to the same cause failure of the vasocon- strictor centre and likewise is accompanied by low blood-pressure. 5. After extensive hemorrhage a fall of blood-pressure sets in (except after vene- section in some cases where a failing heart is relieved), owing to lack of blood to fill out the arteries. This is usually relieved by subcutaneous or intravenous NaCl infusion, or even by direct arterial transfusion (Crile). 6. In diarrhoea, dysentery, cholera, or after profuse vomiting, as from cancer of the stomach, intestinal obstruction, peritonitis, etc., when large amounts of fluid have left the body, the arteries may also be depleted of fluid and a very low blood-pressure result. This is also relieved by infusion. 7. In pleurisy, especially pleurisy with effusion, blood-pressure is uni- formly low. 8. Pericarditis is accompanied by low blood-pressure (maximum 100 to 120, mini- mum 70 to 90, pulse-rate increased) unless complicated by hypertrophy of the heart or some other factors. 9. Acute cardiac diseases of all types, which have not been preceded by chronic proc- esses and are not associated with marked cyanosis. Here the above-mentioned toxic action on the vasomotor centre is usually present if the endocarditis is of the infectious variety, and besides there is some weakening of the heart. The quickened pulse-rate prevents CO 2 from accumulating in the blood and the asphyxial rise in pressure does not occur. K. Weigert reports all ranges of pressure between 95 and 140 mm. Hg. 10. In chronic mitral stenosis the maximal and minimal pressures are usually normal or a little below normal, when the left ventricle does not hypertrophy; but this may vary considerably. 11. Chronic wasting diseases, cancer, chronic phthisis, anaemias, etc., are associated with brown atrophy of the heart muscle (see page 289) with weakened heart action, hence with lowered blood-pressure (10 to 20 mm. lower than normal, pulse-rate usually increased). BLOOD-PRESSURE IN THE VEINS. Various methods have been devised for the determination of the venous blood-pressure in man, the first being introduced by v. Basch and being but a slight variation of his arterial sphygmomanometer. A very similar apparatus has been constructed recently by Sewall, but this gives rather unsatisfactory results in practice. V. Frey and later Gaertner also determined the pressure by considering it equal to the height above the angle of Ludwig at which the veins of the hand could be seen to collapse. This method is not quite as good as the former. A considerable advance was made by v. Recklinghausen, who compressed the vein by inflating a small rubber capsule provided with a glass window in the top and a rubber-dam floor having a hole in its centre. This dam was coated with glycerin so as to insure perfect contact. It is then placed over a vein, preferably upon the back of the hand or wrist, and the system blown up until the vein can be seen to disappear, at which point the pressure is read off upon a water manometer. Eyster and Hooker have modified this chamber by constructing one of aluminum with the entire top of glass and the two ends concave so as to avoid pressure upon the veins, and their apparatus seems to give results concordant within 1 cm. II^O. They find that the normal venous pressure at the sterno- xiphoid articulation is 5-10 cm. H/). 1 It is increased by exercise and in cardiac cases with broken compensation, when it may rise to 27 cm. or over. When the veins arc not sufficiently distended at that level the hand may be lowered a known distance, the pres- sure read; and the distance lowered subtracted from the amount of the reading will repre- sent the venous pressure. In cases where phlebosclerosis is present no satisfactory deter- minations could be made. 1 These figures agree well with direct manometric determinations recently made in man by Moritz and v. Tabora (Verhandl. d. Kong. f. iunere Med., 1909, xxvi, 378). BLOOD-PRESSURE AND BLOOD VISCOSITY. 51 The pressure in the capillaries of vascular areas, especially of the lips, may be determined in the same way, using the point of blanching as the criterion. The study of the venous pressure is of undoubted importance as an index of accumulation of the blood in the systemic circulation and thus as an index of heart-failure. Moreover, it is the most important physiological factor bringing about variations in the volume of the heart; a high venous pressure causing dilatation, a low venous pressure causing diminution in volume (insufficient filling). This may prove to be an important factor in bringing about certain conditions in which there is " ar- terial anaemia " (shock, cardiac neurosis, etc.). THE PULMONARY CIRCULATION. Before birth the resistance in the vessels of the collapsed lung is greater than that in the sys- temic arteries, and hence blood, passes from the pulmonary artery to the aorta through the ductus arteriosus (Botalli). As the blood-pressure in young in- fants is SO mm. Hg (Trumpp), it must be assumed that the pulmonary pressure is somewhat greater than this. When the area of lung capillaries widens with the first inspiration, the resistance in the pulmonary vessels decreases very mark- edly. This decrease continues during the period of infancy until the lung is fully expanded. According to a number of observers (Beutner, Lichtheim, Open- chowski, Bradford and Dean, Plumier), the mean pressure in the pulmonary artery of rabbits, cats, and dogs varies from 6 to 35 mm. Hg. Wiggers has found that the maximal pressure in the pulmonary artery in dogs varies between 30 and 4 mm. Hg, the minimal between 5 and 12 mm., and the pulse-pressure between 22 and 41 mm. Since it is the difference of pressure between pulmonary artery air! pulmonary vein which drives blood through the lungs it may easily be seen how a slight rise of pressure in the latter lessens the flow. Work of the Right Heart. The pressure within the pulmonary artery and hence the work of the right heart varies within wide limits under experi- mental conditions. These variations are in part passive, due to passive stasis of blood within the pulmonary vessels, and in part may be the result of vasomotor changes in the pulmonary vessels. FIG. 31. Hooker and Eyster's modification of v. Recklinghausen's method of determining the venous pressure in man. 52 DISEASES OF THE HEART AND AORTA. The conditions in which the changes in pulmonary pressure arise pas- sively from changes in the left ventricle are the most common and are clin- ically the most important. Increased mean pulmonary pressure may arise : 1. When an increased amount of blood enters the right heart from the veins and is expelled into the pulmonary artery. 2. The pulmonary blood-pressure also undergoes rhythmic variations, falling during inspiration as a result of suction (as shown by de Jager) and rising during expiration. 3. When the left ventricle fails to pump an equal amount onward into the aorta, causing blood to accumulate in the pulmonary capillaries until these are overfilled and aid in increasing the resistance in this circuit. (The left ventricle acts upon the pulmonary circulation as a suction pump.) 4. Probably from constriction of the pulmonary arteries under the influence of vaso- motor nerves. Pulmonary Vasomotor Nerves. The existence of vasomotor nerves in the pulmonary artery, first suggested by Brown-Sequard (1870 to 1873) and later by Badoud, has been much disputed, but seems now to be proved. Francois-Fran ck has shown that stimulation of the lower cervical and upper five thoracic ganglia in the dog uniformly caused a rise of blood-pressure in the pulmonary artery, a fall of pressure in the left auricle, and an increase in the volume of the lungs, probably due to accumulation of blood on the arterial side of the capillaries. This rise in pulmonary pressure bore no constant relation to the pressure in the femoral artery, which sometimes rose and sometimes fell. This evidence strongly favors the existence of vasocon- strictor fibres. Fran?ois-Franck showed further that these same changes in pulmonary arterial pressure, left auricular pressure, and lung volume occurred reflexly when the central end of the femoral nerve or a proximal branch of the solar plexus was stimulated. This reflex, as he shows in a subsequent paper, may have important bearings in the production of certain cardiac symptoms and in influencing the course of cardiac diseases. Action of Drugs on the Pulmonary Circulation. Franc.ois-Franck's re- searches are very convincing. They have been confirmed by H. C. Wood, Jr., and others, and are accepted by as keen a critic as Tigerstedt; but Wood, Jr., and also Petit jean have found that all drugs exert a much less marked effect on the pulmonary circulation than on the systemic. Wiggers finds that adrenalin, digitalis, and strophan- thin increase the pulmonary arterial pressure and also increase both arterial and venous hemorrhage from the pulmonary vessels. The nitrites increase both under normal conditions but diminish both in the last stages of hemor- rhage. Ergotoxin sometimes raises and sometimes lowers pulmonary arterial pressure normally, but has little effect during hemorrhage. Under normal conditions it seems to diminish the pressure in the pulmonary veins. Chloro- form always diminishes both the pressure in the pulmonary veins and arteries and lessens hemorrhage from the lungs. Pituitary extract, however, according to the studies of Wiggers, exerts the most favorable action of all, for the in- flow of blood into the right heart is diminished, and pan passu with this a fall in pressure in the pulmonary vessels and a diminution of hemorrhage from the latter result, which is particularly marked in anaemic conditions. Pituitary extract would thus appear to be the drug indicated for the relief of pulmonary hemorrhage, especially in tuberculosis and congenital heart dis- ease. In mitral disease its use is more questionable, for the raising of the peripheral resistance in the systemic circulation may increase regurgitation BLOOD-PRESSURE AND BLOOD VISCOSITY. 53 or stasis in the pulmonary circulation. It must be admitted that accept- ance is not universal. The clinical importance of the problem renders it a matter of universal interest. It may be considered proved by Franc. ois-Franck's work that sensory stimuli, stimulation of the sympathetic nerves, asphyxia, etc., may cause the pulmonary arterial pressure to rise to about double its original height, and hence in chronic conditions may play an important role in bringing about hypertrophy of the right ventricle. Moreover, changes of pressure which are relatively small when applied to the left ventricle assume much greater proportions when applied to the weaker right ventricle, and appar- ently slight changes in the strength of this chamber may then be important factors in the mechanism of the circulation. Tonicity of the Right Ventricle. More important than the changes in pressure in the pulmonary artery are the changes in tonus of the right ven- tricle. Owing to the thinness of the wall, changes in tonicity affect this chamber much more readily than they do the left; overstretching of the fibres sets in more readily, and weakening of the right ventricle results more readily. These changes may have no direct relation to the changes in pul- monary arterial pressure. BIBLIOGRAPHY. BLOOD-PRESSURE. Huerthle, K.: Beitrage zur Haemodynamik, Arch. f. d. ges. Physiol., Bonn, 1891, xlix, 29. Porter, W. T.: A New Method for the Study of the Intracardiac Pressure, Jour. Exper. Med., N. York, 1896, i, 296. Vierordt, K. Quoted from Janeway. Marey, E. J. : Pression et vitesse du sang, Trav. du lab. de M. Marey, Par., 1876, ii, 306. Nouvelles recherches sur la mesure manometrique de la pression du sang chez 1'homme, ibid., 1878, iv, 126. V. Basch, S.: Der Sphygmomanometer und seine Verwerthung in der Praxis, Berl. klin. Wchnschr., 1887, xxiv, 181. Potain, F.: La pression arterielle de 1'homme a 1'etat normal et pathologique, Paris, 1902. Du sphygmomanometre et de la mesure de la pression arterielle chez 1'homme, Arch. de Physiol., Par., 1889, 5 Scr., i, 556. Tigerstedt, R.: Lehrbuch der Physiologic des Kreislaufs, Leipzig, 1893. Riva-Rocci, S.: Un nuovo sfigmomanometro, Gazz. med. di Torino, Turin, 1896, xlvii, 981. Hill, L., and Barnard, H.: A Simple and Compact Form of Sphygmomanometer or Arterial Pressure Gauge devised for Clinical Use, Brit. M. J., London, 1897, ii, 904. V. Recklinghausen, H.: Ueber Blutdruckmessung beim Menschen, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1901, xlvi, 78. Uskoff, L.: Der Sphygmotonograph, Ztsohr. f. klin. Mod., Berl., 1908, Ixvi, 90. Erlanger, J. : A Criticism of the Uskoff Sphygmotonograph, Arch. Int. Med., Chicago, 1912, ix, 22. Marey, E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Paris, 1881. Janeway, T. C.: The Influence of the Soft Tissues of the Arm on Clinical Blood-pressure Determinations, Arch. Int. Med., 1909, iii, 474 V. Basch, S.: Der Sphygmomanometer und Seine Verwendung in der Praxis, Berl. klin. Wchnschr., 1887, xxiv, 181. Martin, C. J.: The Determination of Arterial Blood-pressure in Clinical Practice, Brit. M. J., Lond., 1905, i, 865. Scholtyssek, A.: Arch. f. Physiol., Leipz., 1909, 323. Schmidt, M.: Ibid., 1909, 331. Russell, W.: Arterial Hypertonus Sclerosis and Blood-pressure, Phila., 1908. Herringham, W. P., and Womack, F.: Proc. Roy. Med. Soc. (Med. Sect.), Lond., 1908, ii, 37. Quoted from Janeway and Park. 54 DISEASES OF THE HEART AND AORTA. Janeway, T. C., and Park, E. A.: An Experimental Study of the Resistance to Compression of the Arterial Wall, Arch. Int. Med., Chicago, 1910, vi, 586. Hoover, C. F.: A Criticism of Blood-pressure Apparatus, J. Am. M. Ass., Chicago, 1910, Iv, 815. Howell, W. H.. and Brush, C. E.: A Critical Note upon Clinical Methods of Measuring Blood-pressure, Mass. Med. Society, 1901. Mosso, A. Quoted from Janeway. Masing, W.: Ueber den Verhalten des Blutdrucks des jugen und des bejahrten Menschen, Deutsch. Arch. f. klin. Med., Leipz., 1902, Ixxiv, 253. Erlanger, J., and Hooker, D. R.: An Experimental Study of Blood-pressure and of Pulse- pressure in Man, Johns Hopkins Hosp. Rep., Balto., 1904, xii, p. 145. Hirschfelder, A. D.: Some Observations upon Blood-pressure and Pulse Form, Bull. Johns Hopkins Hosp., Baltimore, 1907, xviii, 262. Brush, C. E.: Blood-pressure Observations for the Practising Physician, Am. Med., Phila., 1905, x, 97. Pal, J.: Ein Sphygmoskop zur Bestimmung des Pulsdruckes, Zentralbl. f. inn. Med., Leipz., 1906, xxvii, 121. A somewhat similar but much less accurate method is that of Oliver, G.: On Hiemomanometry in Man, Lancet, Lond., 1905, ii, 201. A New Form of Hamomanometer, Proc. Physiol. Soc., Lond., 1905, p. Ixix. V. Recklinghausen, H.: Unblutige Blutdruckmessung, Arch. f. exper. Pathol. u. Pharm- akol., Leipz., 1906, Iv, 375, 412. Eichberg, J.: The Factors in the Estimation of Blood-pressure, J. Am. M. Asso., Chicago, 1908, li, 1000. Gibson, G. A.: A Clinical Sphygmomanometer Yielding Absolute Records of the Arterial Pressures, Quart. J. M., Oxford, 1907, i, 103. The Arterial Pressure in Man. I. Meth- ods, Proc. Roy. Soc., Edinb., 1907, xxviii, 343. Sahli, H.: Die Sphygmobolometrie: cine neue f ntersuchungsmethode, Deutsch. med. Wchnschr., Leipz., 1907, xxxiii, 628. Janeway, T. C.: Some Observations on the Estimation of Blood in Man, with Special Reference to the Results Obtained with Newer Sphygmomanometers, N. Y. Univ. Bull. M. Sc., N. Y., 1901, i, 105. The Clinical Study of Blood-pressure, N. Y. and Lond., 1904. Pachon, V.: Oscillometre sphygmometrique a grande sensibilite et a sensibilite constante, Compt. rend, de la Soc. de biol., Par., Ixvi, 733. Bachmann, Geo. : The Measurement of Arterial Blood-pressure in Man, N. Y. M. J., 1911, Feb. 4. Bcndick, A. J.: A Xew Air-water Sphygmomanometer, J. Am. M. Ass., Chicago, 1911, Ivi, 1S73. Ettinger, N.: Auskultatorisohe Methode der Blutdruckbestimmung und ihr praktischer Wert., Wien. klin. Wchnsch., 1907, xx, 992. Fischer, J.: Die Auskultatorische Blutdruckmessung im Vergleich mil der oscillatorischen, U. S. W., Ztschr. f. dietat u. physik. Therap., Leipz., 100S, xii, 3S9. V. Westenrijk, N. M.: Ueber die Beziohungen der Tonmethode der Bestimmung des Max- imal und Minimal-Blutdrucks zu den iibrigen Methodcn und iiber die Bedeutung dieser Grossen, Ztschr. f. klin. Med., Berl., 190S, Ixvi, 465. Staehelin: Zur Koratkow'sche Methode der Blutdruckmessung, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1909, xxvi, 429. Lang, G., and Manswetowa, S.: Zur Methodik der Blutdruckmessung nach von Reckling- "hausen und KorotkofT, Deutsch. Arch. f. klin Med.. Leipz., 1908, xciv, 441. Gittings, J. C.: Auscultatory Bloov/fi6g) in contrast to the marked pulsation in disease (the -ira'/.^of of Hippocrates). Eristratus (B. C. 280) showed that the arteries near the heart beat before the arteries more distant from it. Aristotle and later Archigenes (first century after the Christian era) made numerous observations upon the pulse in various diseases, and the latter described and gave the name to the di erotic type in cases of fever, although he still believed that the arteries were filled with air. Galen (A. D. 131 - 202) demonstrated that the arteries were filled with blood and studied the influence of sex, age, climate, sleep, hot and cold baths upon the rhythm of the pulse. The old Chinese physicians also described the pulse and even made drawings to illustrate their sensory impressions a practice which did not begin in Europe until the time of Henri Fouquet in 1767. After Harvey's demonstration of the circulation of the blood (1628), the study of the pulse was resumed with renewed vigor and has continued to the present day. Examination of the Pulse. The characteristics of the pulse-wave are, as a rule, determined upon the radial artery, in which the arterial tension may be estimated as described on page 26, the wall of the artery being also rolled under the finger while the artery is empty, and thus the presence or absence of arteriosclerosis noted. The walls of a normal artery are barely, if at all, palpable; an atheromatous artery may feel like the trachea of a small animal (goose-neck) ; a diffusely sclerotic artery feels like a piece of thick-walled rubber tube. It is important to note the palpability of several arteries, since one of them ma} r escape a sclerotic process. All the blood must have been pressed out of their lumina and of the vense comites that accompany them before palpation is begun, or else normal arteries may appear to be sclerotic. The pressure is then relieved, and the tips of two or three fingers are pressed upon the artery until the pulse appears maximal (at about the minimal pressure), when the following characteristics are noted: (1) whether the artery (hence the pulse) feels large and dilated ( p u 1 s u s m a g - n u s) or small and constricted ( p u 1 s u s p a r v u s) ; (2) whether the pulse is hard (p uls us durus) or soft (pulsus moll is), i.e.. whether the minimal pressure is low or high; (3) whether the onset of the wave is sudden (pulsus color) or gradual (pulsus tardus); (4) whether the wave is sustained (an a erotic) or subsides suddenly under the finger ( c o 1 1 a p sing, w a t o r-h a m m o r , or Corrigan pulse) ; (5) the rate of the heart per minute (counted continuously during at least a half minute) ; (6) whether the rhythm is regular ( p u 1 s u s r e g u 1 a r i s ) or irregular (pulsus i r r o g u 1 a r i s). Clinical Sphygmographs. An instrument ( s p h y g m o g r a p h ) to record the pulse-wave graphically was first devised by K. Vierordt (1855), 62 THE ARTERIAL PULSE. 63 but it was not until 1860 that E. J. Marey devised a thoroughly practi- cal and accurate form, almost devoid of error, which is still in use. Marey's sphygmograph consists of a button (pelotte) pressed against the skin over the artery by means of a spring so as to receive the pulsations from the artery. It is held in place by a leather cuff, and it is most important that the pelotte remain exactly over and not to one side of the artery. The pelotte is surmounted by a vertical rod or screw which articulates by a movable joint with a long writing lever. The writing lever records the magnified pulse movements upon a surface of smoked paper held in vertical position by a brass upright and driven by a small piece of clock-work. A more compact and convenient form of sphygmograph is that of Dudgeon, in which the straight lever is supplanted by a double-jointed one which writes on a horizontal instead of a vertical strip of smoked paper. The tension of the spring pressing down the pelotte is roughly adjustable, which allows some variation in the pressure over the artery. V. J a q u e t has improved Dudgeon's apparatus by adding to it a small time marker recording fifths of a second. Another excellent form of sphygmograph is that devised by Roy and Adami, which, by means of a delicate adjustment, enables the observer to obtain a pulse record at exactly diastolic pressure. Unfortunately, it has never been placed on the market, and 4 hence has not been subjected to the test of general use, but any one who is interested in sphygmographs should certainly familiar- ize himself with their observations. FIG. 33. Brachial pulse-curves taken with the Erlanger blood -pressure apparatus from the arms of two patients, merely varying the pressure in the cuff. The figures indicate the pressures at which the curves are taken, those underlined indicating maximal and minimal pressures respectively. Errors in Sphygmography. In spite of the existence of these fairly satisfactory sphygmographs and of their wide use, discrepancies between the clinical observations and the tracings obtained are so great that Cabot refers to the sphygmograph as "an interesting little toy." The reason that it is not of value must be either that the apparatus itself is subject to inherent errors, or that, as Mackenzie states, "it was expected to give in- formation of a kind that it was incapable of supplying." Unfortunately, both are the case. Athanasiu, in investigating the accuracy of graphic recording devices, found that all sphygmographs which magnified the movement more than twenty times introduced ;i large inherent error, that of all the forms in use Marey's introduced the least error, while the Dudgeon apparatus and the Jaquet magnified it 130 times, introducing tremendous distortion from flinging large pulsations. On the other hand, the writer, D. Gerhardt, and Stewart have been able to show that not only the size but also the entire type of the pulse-curve obtained depends upon the pressure exerted upon the artery and other similar factors; the true form of the pulse- wave being obtained only when the pressure exerted by the sphygmograph is exactly equal 64 DISEASES OF THE HEART AND AORTA. to the pressure within the artery. Fortunately, this is the point at which the pulse excur- sion is maximal, and as all observers strive for the largest excursion, it is probable that most sphygmographic records are taken at about this pressure. The ideal apparatus is the one in which it is not merely probable but certain, and hence that of Roy and Adami is the only one which abso- lutely fulfils the requirements. The Absolute Sphygmogram. A very con- venient and instructive method of recording pulse tracings has been introduced by Sahli. Sahli transfers the pulse -curve to coordinate paper upon which the ordinates represent millimetres of mercury and the abscissae represent fractions of a second. The lowest point of the pulse-curve he marks at the level corresponding to the mini- mal blood-pressure, determined at the time with the sphygmomanometer; the highest point at the level corresponding to the maximal pressure; and maps out besides this the other main points of the pulse-curve (predicrotic fall and wave, dicrotic notch, summit of dicrotic wave, etc.) at heights and distances proportional to their occurrence upon the sphygmogram, but translated to this new scale of pressure and time. This curve he terms the absolute sphygmogram. FIG. 34. Absolute sphygmograms, all of which correspond to the radial trac- ing above. The figures to the left indicate pressures in mm. Hg. The absolute sphygmogram can also be read off from the ordinary sphygmogram by using the lowest point on the tracing as the ordinate of minimal pressure and as a base line for determining the pressure at other points, and calculating these from the proportion Ordinate of point : Total height of pulse-wave = Pressure at that instant (above minimal arterial pressure) : Pulse-pressure. Discrepancies between Feeling and Recording the Pulse. Not all the discrepancies between sensory impression and sphygmogram are the fault of the instrument. In the first place, there is no absolute uniformity in the minds of physicians as the standard to be applied to the individual pulse. Thus, the writer has seen one eminent clinician dictate a note, "pulse not collapsing," and another a few minutes later state that the same "pulse is collapsing in quality." The pulse had not changed, but the subjective criteria of the two men were slightly different. Again, between pulse palpation and sphygmogram there is a difference. It is very difficult, almost impossible, to determine just how long a pulse is sustained and how quickly it falls, since these judgments are based upon a sequence of events lasting for an interval of about one-tenth of a second, and changes both in time and in pressure must be con- sidered without the presence of any simultaneous standard for comparison. Psychologic- ally, such comparisons must be very fallible. Practically they are not as fallible as they appear, for the judgment is based not upon form or duration, unless the abnormalities are marked, as much as upon changes of pressure. What one really appreciates most in feel- ing the pulse is the amount of minimal pressure ("hardness" of the pulse) and the amount of the pulse-pressure (size of pulse), and only to a lesser extent the duration of the pulse- wave. Hence, the sensation due to a high pulse-pressure with a moderate diastolic pressure is often mistaken for that due to a collapsing pulse, though the form of the pulse- THE ARTERIAL PULSE. 65 FIG. 35. Significance of the pulse-curve. /, inflow into the artery from heart; O, outflow from the artery toward the periphery. wave may show that it is quite well sustained. In comparing the pulse sensation with the sphygmogram, one is therefore comparing two somewhat different standards, and this inherent difference must be taken into account. Significance of the Pulse=curve. Assuming, however, that one has ob- tained a correct tracing from the artery, what deductions are allowable ? It is evident that the artery expands somewhat under an increase in pressure (causing a rise in the pulse-wave) and contracts when pressure decreases (causing a fall in the pulse-wave). Further, the pressure in the artery in- creases or decreases, depending upon whether more blood enters it than can leave it at that instant (Fig. 35, I > O) or whether the reverse is the case (I < 0) . When the inflow exactly equals the outflow (I = O), no change of pressure occurs and a plateau results. The pulse tracing is merely the record of these events the record of the ratio that the inflow into the artery from the heart bears to the outflow toward the periphery at each instant of the cardiac cycle. The normal pulse-wave has the following forms: an upstroke more or less steep (percussion wave;, a rather acute summit, and sudden fall (predicrotic) followed by a very small rebounding wave (predicrotic wave), then another more gradual fall termi- nating in a small notch (dicrotic notch) which mar ks the end of systole (Marey, Huerthle), then a gradual fall during diastole. In the aorta the fall in waves is not as steep as in the radial artery, which indicates that the former reflects the conditions near the heart, the latter shows the conditions at the periphery (Marey) Relation of Pulse Form to Peri= pheral Resistance. There are three general types of pulse (Marey, Hirsch- felder) which may occur without any heart lesion whatever, and even in the same individual at the same maxi- mal and minimal pressures, though usually the maximal and minimal pres- sures vary with these conditions. (Fig. 36.) Type I c o r r e s p o n d s to m a r k e d peri p h e r a 1 dilata- tion, as after exercise, after meals, in shock, fevers, or in some m-rvous individuals with vasomotor instability. This is the collapsing type of pulse, rapid rise and rapid fall sometimes followed by a large dicrotic wave (see page 68). The rise is, however, about two hundredths of a second slower than normal, but this difference is not within the limits of perception. It P^IG. 3f>. Diagram showing the time rela- tions of ventricular volume and pressure curves to pulse tracings from the aorta, carotid and radial arteries. Time divisions in one-tenth sec- onds. (Schematic.) Dotted lines represent curves taken with high peripheral resistance. 66 DISEASES OF THE HEART AND AORTA. feels more sudden because it is sharply followed by the sudden fall. The fall in this type of pulse is almost complete before the end of systole, i.e., before the dicrotic notch which marks that point (Marey, Huerthle). no FlG 37 Three types of arterial pulse-curve corresponding to the same pulse-pressure and same pulse- rate. (Johns Hopkins Hosp. Bull, xviiij I, vasodilation; II, normal; III, vasoconstnction. In T y p e II only about half the fall occurs during systole. This corresponds to moderate degree of dilatation and is the type present in normal individuals. In T y p e III the wave soon rises to the summit and remains there, forming a sustained plateau (out flow = inflow) until the end of systole, when it gradually falls. This corresponds to peripheral constriction, preventing the outflow from the aorta from exceeding the inflow into it, as is the case where a normal degree of dilatation is present. The normal pulse in man may be converted into this type by compression of both femoral arteries (Marey) or of the ab- dominal aorta (Stewart). The mere increase of the blood-pressure is not a cause, because after exercise the blood-pressure is increased and yet the pulse becomes more collapsing than before. Fii;. 38. Kffert of inhalation of amyl nitrite upon the pulse-form. (After v. Kries.) Curves taken in succession. Vasodilation reaches its maximum at r and diminishes at d and e. Well- marked dicroti-m at d. and < indicate second- ar\ waves due to elasticity of the artery. These general outlines of the pulse- waves are further modified by smaller wave- lets due to the elastic vibrations of the artery wall, or to the rebound of the percussion wave at the periphery fv. Kries). The most important of these is the dicrotic wave following immediately upon the closure of the aortic valves and due either to a centrifugal wave from t li e blood impinging against them, or to a reflected c e n t r i p e t a 1 wave from t h e periphery toward the h e a r t ( v. Kries ). \\hichever theory may be correct, the essential fact remains that the dicrotic wave is a secondary one and is dependent upon arterial elasticity. V. Kries has shown that the dicrotic wave is most marked when the peripheral vessel.-, are consider- ably dilated, but not when they are dilated to their fullest extent (Fig. 3X). The other waves may occur upon either upstroke (anacrotic) or upon the downstroke (katacrotic, Fig. 38, a, h) and are designated accordingly. Small secondary waves of this THE ARTERIAL PULSE. 67 type are most marked when the pressure is high and the heart action strong (e.g., pulsus bisferiens), but their occurrence is often due to twitching of the tendons near the pelotte of the sphygmograph, and too great weight must not be attached to them. + FIG. 39. Mercury manometer tracing from the carotid artery of a dog, showing rhythmic varia- tions in blood-pressure and rhythmic increase in dicrotism. (Kindness of Prof. Abel and Dr. Rowntree.) The dicrotic wave increases at the points (D + ) at which the blood-pressure is lowest ( ) and the peripheral arteries are dilated. Time in seconds. Too much information should not be sought from the sphygmogram. All that should be looked for is whether the upstroke is sudden (p. celer) or gradual (p. tardus) ; whether the main fall in the wave begins early or late in systole, or not until the beginning of diastole; also whether the fall is quite or nearly complete before the end of systole. All possible mental reservations should be made for fling of the lever, incorrect appli- cations of sphygmograph, etc., before a judgment is made. THE PULSE-RATE. The normal pulse varies consid- erably in different individuals, being in general more rapid in those of small stature and slower in persons of larger stature, hence, more rapid in women than in men. It also varies considerably according to age, being dependent upon the relative tone of vagi and accelerators. The pulse-rate is also more rapid (tachy- cardia) in fevers, varying in general according to the temperature each degree Fahrenheit increase corresponds to an acceleration of about four to five beats per minute. C. D. Snyder, as the result of a long scries of experi- ments upon the heart-rate in different vertebrates, finds that the rate is influenced by temperature in the same degree as is the velocity of simple chemical reactions and follows the logarithmic formula _ 10 Coefficient of differ- _ /Rate at higher temperatures " higher lower r\o /~i ~~ I temperature temperature ence of rate for 10 t \R a te at lower temperature/ In typhoid fever there is often an exception, a temperature of 10;> to 10."> being accompanied by a pulse-rate of about 90 per minute, owing to a toxic stimulation of the FIG. 40. Diagram showing various forms of pulse-curve encountered clinically. Systolic portions of the curve are underlined. HY PER- DICROT, hyperdicrotic. G8 DISEASES OF THE HEART AND AORTA. TYPES OF PULSE IN VARIOUS DISEASES. The following types of pulse are associated with various pathological conditions and corresponding states of the heart and vessels. Type of pulse. 1 Shown in Fig. Characteristics. Clinical condi- tions in which it is most fre- quently observed. Blood-pressure associated with it. Vascular condition. Maximum. Minimum. Pulse- pressure. Normal .... 40 Sudden rise, sharp Normal individ- Normal Normal. apex, slight pre- uals dicroticfall; then | slow fall, small Some cases of aor- High Normal. . . Increased . Dilated. dicrotic wave. tic insufficiency gradual fall in di- astole A few cases of Normal or - - - Pulse-rate Dilated. fever d i m in - q u i c k - ished ened Anacrotic . 40 Sudden rise or Arteriosclerosis ; High High Slightlyin- Va s o c o n- slightly rounded chronic nephritis creased striction. plateau top last- or u n - ing almost to di- Some cases of aor- changed erotic notch tic insufficiency which is small; gradual diastolic Some normal indi- Normal . . . High Slightlydi- Va so con- fall viduals minished striction. Bisferiens . 40 Resembling ana- Arteriosclerosis; High High Increased Va s o c o n- erotic except chronic nephritis fetriction. that the' small predicrotic fall is Hypertrophied followed by rise heart acting equal or above strongly that of the per- cussion wave, making the sum- mit bifurcate Tardus 40 Gradual slow rise, Aortic stenosis ... Slightly or Elevated.. Increased Vasocon- percussion wave greatly or n o r - striction. oblique, summit elevated mal round, gradual fall Collapsing. 40 Steen rise, anex Aortic insufficien- 1^ o w or Increased Va so dila- sharp, sudden cy (water-ham- normal tion. steep fall, d i- mer or Corrigan crotic notch in pulse) lower half of curve often level , Fevers Normal or Normal or Normal or Vasodila- after the predi- low low increased tion. crotic wave Normal individ- Normal or Normal or Normal or Vasodila- uals, n e u r a s - low low increased tion. thenics Some cases of Increased Slightly in- Increased. Va so dila- Basedow's dis- creased tion. ease Dicrotic. . . 40 Collapsing in qual- Fevers, especially Normal or Normal or Normal or Vasodila- ity but ilicrotic typhoid subnor- s u b 11 o r- increased tion. wave very pro- mal mal nounced and pal- pable, as a small Normal individ- Increased Normal or Increased Va so dila- wave regularly uals during or increased tion. following soon after exercise after the percus- sion wave Neurasthenics, Normal or Normal. . . Increased Va so dila- after amyl ni- increased tion. trite or nitro- glycerin Hyper- 40 Diorotic wave oc- Any of the condi- Normal or Normal.. . Increased Vasodila- dicrotic curs at the foot tions in which increased tion. of the ascend- dicrotism may ing instead of occur, but witt descending limb more rapid pulse- rate. 'For forms of ii regular pulse see page 99. THE ARTERIAL PULSE. 69 vagus; while in meningitis the high intracranial pressure may bring the rate down to a great deal lower (50 to 60) and may cause irregularity. In tuberculosis the pulse is rapid even in the early stages. The pulse-rate is also accelerated in the anaemias, in neuras- thenia, Graves's disease, hysteria, shock and collapse, abdominal distention, peritonitis and other diseases of the abdominal viscera, and in numerous cardiac diseases. In fevers and in many other conditions of acceleration the pulse becomes extremely small and barely palpable on the one hand, and extremely rapid, barely countable on the other a small and ''running" pulse. Pulse-rates of over 160 per minute are not uncommon in fevers, while 200 or even 300 is reached in paroxysmal tachycardia. At these great rates the duration of systole is markedly shortened, as well as that of diastole (the period of systolic output falling from 0.26 sec. to 0.2 or even less). Slow pulse (bradycardia) (below 60 per minute) is observed especially in conditions with intracranial tension, in meningitis, in digitalis poisoning, chronic nephritis, chronic myocarditis, in convalescence from some fevers, especially diphtheria and influenza, and in Adams-Stokes disease. In the latter condition the auricles and ventricles are beating independently (see chapter on Adams-Stokes disease). BIBLIOGRAPHY. PULSE. Harvey, W. : Exercitationes anatomicae de motu cordis et sanguinis circulatione, Rotero- dami, 1671. For historical resume cf. Morrow, W. S.: "The Pulse," Reference Hand-book of the Medical Sciences, Phila., 1903, vi, 797. Vierordt, K.: Die Lehre vom Arterienpuls, Braunschweig, 1855. Ma rev, E. J.: Recherches sur 1'etat de la circulation d'apres les caracteres du pouls fournis par un nouveau sphygmographe, Journal de la physiol. de 1'homme, Par., 1860, iii, 241. V. Jaquet, A.: Studien ueber graphische Zeitregistrirung, Ztschr. f. Biol., Muenchen u. Leipz., 1S91, xxviii, N. F. x., 1. Roy, C. S., and Adami, J. G.: Heart -beat and Pulse-wave, Practitioner, Lond., 1S90, ' xliv, 81. 161, 241, 347, 412, xlv, 20. Athanasiu, J.: Methode graphique, Trav. Assoc. de 1'Institut Marey, Paris, 1905, p. 29. Hirschfelder, A. D.: Graphic Methods in the Study of Cardiac Diseases, Am. Jour. M. Sci., Phila., 1906, cxxxii, 378. Gerhardt, I).: Beitrage zur Lehre vom Blutdruck, Rindfleisch Festschrift, Leipz., 1907. Stewart, II. A.: An Experimental and Clinical Study of the Blood-pressure and Pulse in Aortic Insufficiency, Thesis, Edinb., 1907; also Arch. Int. Med., Chicago, 1908, i, 102. Salili, H.: L'eber das absolute Sphygmogram und seine klinische Bedeutung nebst kriti- schen Bemerkungen ueber einige neuere sphygmographische Arbeiten, Deutsch. Arch. f. klin. Mod., Leipz., 1904, Ixxxi, 493. Marey, E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Par., 1SS1. Huerthle. K.: Beitraae zur Haemodynamik, Arch. f. d. ges. Physiol., Bonn, 1891, xlix, 29. Hirschfelder. A. D.: Some Observations upon Blood -pressure and Pulse Form, Bull. Johns Hopkins Hosp., Baltimore, 1907, xviii, 262. A'. Kries. J.: Studien zur Pulslehre, Freiburg, 1892. Snyder, C 1 . I).: The Influence of Temperature upon the Rate of the Heart-beat in the Light of the Law for Chemical Reaction Velocity, Am. J. Physiol., Bost., 1906, xvii, 350. IV. THE VENOUS PULSE AND ELECTROCARDIOGRAM IN HEALTH AND DISEASE. THE NORMAL VENOUS PULSE. As has been seen, the study of the blood-pressure and of the arterial pulse conveys information regarding the strength of the heart-beat, the condition of the peripheral arteries, and the velocity which the heart is imparting to the blood stream. But it reveals the action of the left ven- tricle only, and what occurs in the other chambers of the heart must be sought for elsewhere. In studying the heart from the four stand-points of Engelmann, rhythmicity, irritability, conductivity, and contractility, it is necessary to obtain a knowledge of the origination of the impulses in or above the right auricle (atrium), of whether impulses other than those causing the normal rhythm are acting upon that chamber, of whether the right auricle (atrium) is itself contracting, and of whether all the impulses are being properly conducted to the ventricle. Our knowledge upon these points has been derived almost entirely from the study of the pulsation in the jugular vein. Visible Pulsation in the Veins. Pulsation over the veins is visible in SO per cent, of healthy individuals (Hewlett) and is as pronounced as that over the arteries, but it is different in character. The latter shows the force- pump, the former the suction-pump action of the heart. The pulsation over the arteries is quick, sharply localized, easily palpable, and the impulse is more marked than the collapse; that over the veins is diffuse, wavy, rarely palpable, and the c o 1 1 a p s e i s in ore marked t h an the i m - pulse itself. Further, the pulsations over the vein under normal con- ditions are exactly twice the number of those seen over the artery, and the first of the collapses is synchronous with the impact in the artery. Such a pulsation over the vein is known as the "physiological," "negative," or "double" venous pulse, in contradistinction to the other types of venous pulse to be described later. The pulsation over the veins is not, like the arterial pulse, to be seen in every vein in the body, though Morrow has shown that in dogs it can be detected by means of delicate manometers. To the eye and to the recording apparatus available upon man, it is appreciable only in the veins near the heart, the external and internal jugular, the cephalic, and the axillary. Occasionally it is also to be seen in the brachiocephalic and other veins in the arm. 1 The site where it is most easily and uniformly seen is in the right supraclavicular fossa, either over or just to the right of 1 Krieilreich thought that this pulsation was transmitted from the arteries through the capillaries to the veins, but such transmission probably never takes place and other explanations must be sought. 70 THE VENOUS PULSE AND ELECTROCARDIOGRAM. 71 the origin of the sternocleidomastoid. Sometimes it is a little more marked in the supraclavicular fossa at about the mammillary line where the exter- nal jugular vein enters the subclavian. The normal venous pulsation is rarely to be seen when the subject is standing or when propped up high upon pillows, but is most distinct after he has been in reclining posture for some minutes with a single pillow under his head and neck. In patients with venous stasis, on the other hand, it may be necessary for the patient to sit upright before any undulations appear. It must be borne in mind that the pulsation seen and recorded over the veins represents the alternate filling and collapse of the latter. The collapse, that is the obliteration of the lumen of the vein by the atmospheric pressure, is usually the most important factor. It is evident that a wave will occur during those periods in which the pressure within the vein is greater than the atmospheric, and a collapse will occur whenever it is less. If it is permanently less (negative) , the vein will remain collapsed ; if it is permanently a little greater, the vein will remain distended. In neither case will a pulsation be seen. The normal pulsation is best seen when the pressure in the jugular vein is alternating between a positive and a negative pressure during the different phases of the cardiac cycle. The elastic distention of the vein is not called into play. The elastic distention of the vein at systole occurs only at a much higher venous pressure, as in tricuspid insuffi- ciency. Occasionally, especially in chronic heart cases with phlebosclerosis, the veins stand out like large knotty cords, but no pulsation is to be discerned in them at all. The knotty appearance (Fig. 41) is due to the closure of the valves within the veins, the dilatations appearing just above the valves. Perhaps the closure of the valves prevents or dampens the pulsation, or perhaps the rigidity of the vessel wall prevents it from collapsing and filling. Normally the valves in the jugular do not close, but this closure is brought about by chronic venous stasis, just as it is in quadrupeds where back pressure results from the head being dependent. In such cases it is impossible to obtain any idea of the undulations nearer the heart. GRAPHIC RECORDS OF VENOUS PULSATIONS. A far more exact idea of the nature of the jugular pulsation can be obtained by recording it graphically than by mere inspection. With proper apparatus this is not accompanied by any difficulty, and a satisfactory record of both venous and carotid pulsations can be obtained in about the same time as a radial sphygmogram. For the interpretation of the venous tracing it is necessary to compare it with the other events of the cardiac cycle, which is accomplished by using the pulse-wave from some artery to fix the standard of time. In order to interpret the waves upon the venous pulse, it is necessary to record simultaneously the venous pulse and either the arterial pulse or the cardiogram, and to see at which point in the cardiac cycle each event will fall. Accordingly, all forms of apparatus (polygraph) for obtaining such records are arranged for taking at least two records simultaneously. In all of these the pulsation from over the vein is received in the same way, and the only difference in the various forms of polygraph lies in the method of obtaining the arterial tracing and in the form of kymograph used. Application of the Receivers. The pulsation in the jugular vein is recorded by holding over the skin above it a small glass funnel on special receiver (Fig. 41, r), which is connected with a Marey recording kymograph tambour. The movements of the skin are 72 DISEASES OF THE HEART AND AORTA. transmitted at once to the kymograph tambour and recorded by the lever. As a rule, the most favorable conditions are obtained when the patient is lying with head and neck supported on a single pillow that extends down just to the shoulders, with his head turned wel! to the right and the neck definitely flexed. In this way the right sternocleidomastoid is relaxed and a tracing over the pulsation from base of the internal jugular vein is trans- mitted to the skin. When this is not obtainable the junction of the external jugular vein with the subclavian should be tried in the same way. The funnel should be pressed against the skin just enough to make the contact air- tight without affecting the pulsation, but this is effected without any great dexterity, and oscillations due to the holding of the re- ceiver rarely appear upon the tracing. When they do so it is in the form of fine oscillations bearing no relation to the cardiac cycle and having a rate of from four to eight per second, in contrast to the much slower and larger movements in the veins. Such tracings should be discarded. In many cases the simple glass funnel is not as satisfactory as a receiving device introduced by Mackenzie (Fig. 41, c), con- sisting of a shallow metal pan 3 cm. in diameter with a tube leading off from it in the form shown in Fig. 41, one portion of the circumference being flattened instead of round in order to fit closely above the clavicle. It is convenient to have a small hole in the top of the pan so that it may be adjusted to the skin without moving the recording lever, and after adjustment is complete the hole is closed by placing KCIIVU FOR VtIN BEaiVlRFORARTlRY FIG. 41. Sites for recording the jugular and carotid pulsations. .-1, distribution of the veins (.-haded in black;, showing the sites for applying the jugular receiver (truncated) and the carotid receiver iconceatric circles); B, appearance of the valves within the jugular vein when closed by back pres- sure; C, receiver for jugular vein; D, spring tambour for recording the pulsation over the carotid artery. also stopped by covering with the finger, inside the sternocleidomastoid when the the finger over it. The tracing from the carotid artery is obtained in a similar way, using for ;-, receiver a small tambour surmounted by a button to fit over the artery (Fig. 41, D). A small hole in the top of this tamboui serves the same purpose as before and is The carotid artery is next to the skin just head is turned toward the corresponding side, the pulsation being most marked when the receiver is pressed heavily upon it. Comparison of Carotid and Jugular Pulsation. Since the jugular vein and the carotid artery are at about the same distance from the heart, the tracings from the latter must always be c o m p a r e d with the former in order to exclude waves which might have been transmitted to it from the artery, and also to indicate the relations of the venous waves to the cardiac cycle. 1 This comparison may be made by taking the jugular and the carotid tracings simul- taneously and comparing them with each other directly, 2 or, for the sake of convenience, 1 Where great accuracy is necessary the onset of the c wave must be compared with that of the apex beat. : It is not necessary that the levers be exactly superposed, but it is preferable to measure off the distance of the given point horizontally from the arc described by the lever at the beginning of the tracing (e.g., Fig. 44). This distance is then laid off upon the other curve in the same manner. Wherever the curve may begin the paper traverses the same distance upon both curves in the same time. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 73 FIG. 42. Apparatus for recording the respiration. RUB, rubber tube; GL, glass tube a carotid and a brachial or radial tracing may be made simultaneously, and the point at which the carotid wave begins marked off upon the latter. Then a jugular and a brachial tracing may be made, and the time that the carotid wave occurs before the brachial marked off before each brachial wave in this tracing, and these points then measured off upon the jugular tracing. This is often the simplest and quickest procedure. Respiration Recorder. It is often of importance to determine the relation of an arrhythmia to the phases of respiration. The simplest device for recording the latter consists of a piece of rubber tube (Fig. 42, RUB) connected with the tube to the recording tambours by a short L-shaped piece of glass tubing (GL) . A piece of string or tape is attached to the rubber tube, another to the glass tube. The apparatus is then put on so as to encircle the level of the nipples. The strings are tied tightly enough to just stretch the rubber tube during expiration. Inspiration then causes a downstroke of the levers, expiration an upstroke. Forms of Polygraph. Several forms of polygraph for clinical purposes have been devised to record these curves. Their relative value depends largely upon the delicacy of the tambours. The oldest form is the polygraph of Marey, consisting of an ordi- nary kymograph drum arranged to rotate horizontally with two Marey tambours to write upon it, so as to record simultaneously the curve from the jugular and carotid or jugular and cardiogram. This is fairly satisfactory, but in mechanical perfection some others are superior. Mackenzie has devised two forms of polygraph. The first, a simple Jaquet sphygmograph upon which a Marey tam- bour is mounted in addition so as to record the radial pulse and jugular or carotid, etc., simultaneously, the time being marked off in i seconds by a small clock-work as well. In the improved form of Mackenzie poly- graph, the levers bear ink pens and write upon an endless roll of white paper, so that a very long series can be obtained. The radial pulse is obtained by air transmission, which is a decided advantage. V. Jaquet 's cardiosphygmograph differs from the simple sphygmograph only in bearing in addition two Marey tambours whose double-jointed levers write just above the lever attached to the radial pclotte. One great objection to the Jaquet instrument is the inconvenience of adjusting the sphygmograph to the radial artery and keeping it adjusted during the entire observation, a factor which is very dis- concerting to both patient and physician and which prevents many important observations from being taken on restless patients. This difficulty is obviated in the writer's modification of the E r - 1 a n g e r b 1 o o d - p r e s s u r e apparatus (Fig. 22, page 27 ). in which two small Marey tambours and a time-marker are arranged to write above the lever of the blood- pressure apparatus. When the bag is inflated upon the arm, the brachial pulse is recorded by the lever of the blood-pressure apparatus and used as the standard instead of the radial FIG. 43. V. Jaquet's cardiosphygmograph. (Kindness of A. H. Thomas Co.) a, time marker (5 sec.); b, c, levers of tambours for recording venous tracing, carotid pulse, or cardiogram; d, lever recording radial pulse-wave. 74 DISEASES OF THE HEART AND AORTA. PLATE II. A. G. Gibson's clinical polygraph Mackenzie's endless roll ink-writing polygraph (as modified by Charles Dressier, Xew York) U^koff sphygmotonograph. (Kindness of A. H. Thomas Company.) THE VENOUS PULSE AND ELECTROCARDIOGRAM. 75 pulse. This entails no trouble and no expenditure of time, thereby saving much of the trouble given by the other methods, and permits a set of records to be obtained very quickly. It is also possible for the operator to work with one hand free and thus save the necessity of an assistant. The curve thus obtained from the jugular vein is shown in Fig. 44 and its relation to the other events in the cardiac cycle shown in Fig. 45. Recently, Uskoff has constructed a very compact form of this apparatus, bearing an Erlanger blood-pressure apparatus, a tambour for recording the height of the blood- SLOW FAST CAROTID JUGULAR FIG. 44. Normal venous tracings, a, wave due to auricular contraction; c, wave at onset of ventricular contraction (the vertical line c representing the beginning of the carotid pulse-wave); x, the bottom of the mesosystolic collapse; d time of dicrotic notch in the carotid; v, wave at end of systole; y, hollow at the end of the postsystolic collapse; t, d (Bard), telesystolic and protodiastolic waves described by Bard. (The z and y depressions are not lettered on all tracings.) pressure objectively, a tambour for apex or venous or carotid tracings, and an excellent time-marker. This seems to be a very good instrument of wide applicability, suitable to all the needs of the practitioner. A slight modification of the original Marey polygraph is still manufactured by the French instru- ment-makers, and, as the tambours which write horizontally are unex- celled for delicacy, this form is to be highly recommended. A. G. Gibson has devised an upright polygraph for taking a con- tinuous record in ink upon an end- less roll of paper. The size is not much larger than that of the Mac- kenzie, and the fact that the tam- bours are upright increases their delicacy considerably. This instru- ment is also provided with a time- marker and with excellent receivers which may be applied with straps and adjustable screws so that the receivers remain in place perma- nently and need not be held with the hands. These receivers, it may be added, may be purchased sepa- rately, and are a great addition to any form of polygraph. FIG. 45. Shaded portion of the cardiac cycle svstole of the ventricles. represents The choice of apparatus depends chiefly upon the delicacy of the tambours and upon the portableness of the apparatus. In the latter regard the Mac- kenzie ink-writing polygraph is particularly desirable, but in the former it is excelled by many. The possession of extremely delicate tambours enables 76 DISEASES OF THE HEART AND AORTA. the observer to proceed rapidly and to obtain beautiful and accurate records which would be impossible with ordinary apparatus. The horizontally writ- ing tambours of French manufacture are particularly delicate. THE MICROGRAPH. Crehore and Meara have employed for the registration of both pulsa- tions and heart sounds an instrument devised by the former and termed the micrograph. The pulsation is received upon an ordinary receiving tambour and transmitted by a rubber tube to the micrograph proper. This instru- ment consists essentially of a small pressure chamber surmounted by a more or less elastic diaphragm similar to that of a telephone. At the centre of the disk there is a small reflector, above which, and separated from it by a small air space, is placed a planocylindrical lens, convexity downward. This micrograph is placed upon the stage of a microscope and illuminated from above with monochromatic light, which gives rise to a series of light and dark concentric circles (interference rings) when looked at through the micro- scope. When a vibration is communicated to the diaphragm and the mirror moves toward or away from the lens, the movement of these interference rings greatly magnifies the movement of the diaphragm, and when these in turn are viewed under a magnification of 2000 diameters, the original move- ment is seen to be magnified 50,000 times. As the distance between two bands of light is readily determined in wave-lengths of the light used for illumina- tion, the amount of this movement can be readily calculated. The move- ments of the rings are recorded photographically by throwing them upon a slit in front of a rapidly moving photographic film. In order to obtain the correct curve, however, the curve obtained photographically must be plotted out upon coordinate paper with considerable labor, the ordinates represent- ing the amplitude of vibration, the abscissa the time. Laborious as this method may seem, it is extremely delicate, and it is possible that it may reveal many facts undiscovered by ordinary means. INTERPRETATION OF WAVES UPON THE VENOUS TRACING. The curve of venous pressure obtained clinically and in animals (Fred- ericq, Morrow, Hering, Theopold) corresponds exactly to those obtained within the auricles (Chauveau and Marey, Fredericq, Porter). The first w a v e (a) 1 in the venous pulse is due to the contraction of the right auricle, and disappears when the auricle is paralyzed. It occurs about one-fifth second before the contraction of the ventricle. The onset of the ventricular contraction is marked on the venous tracing by a small wave (c), caused in part by the pushing up of the tricuspid valve when the intraventricular pressure rises (Hirschfelder, 1. c., Bard, 1. c., Morrow, Cushny and Grosh), and in part by the flow of blood from the coro- nary veins, which, as Porter has shown, are forcibly emptied into the auricle at this instant (Sewall and Hirschfelder). Mackenzie thinks that it is due 1 Since Mackenzie's first nomenclature and lettering of the waves was introduced, a great variety of lettering and of designation by numerals has been used by different authors; but these serve to complicate rather than to simplify the question. The letters or numbers are merely symbols, and a single uniform system would be better than a Babel of terms. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 77 JUG. CAK. only to the carotid pulsation transmitted to the vein, but Morrow has obtained it after ligature of the carotid in animals. Besides the wave appears about oV second before the carotid wave in many cases (Hirschfelder, Bard). When the tracings are taken from the left jugular and right carotid, the c wave in the vein may be later than that in the artery, owing to longer time of trans- mission. The c wave is almost always present; but, as Bard has shown, it may be very small or entirely absent in hearts whose ventricles are failing (Fig. 46). The rise of the c wave is followed by a large fall (x), which may be the largest fall of pressure in the whole cardiac cycle. The exact mechanism by which this fall of pres- sure in the veins (and also in the auricles) is produced, and especially why it should sometimes represent the largest fall of pressure, is not clear. It is evident at this period of the cycle that several events are taking place: (1) relaxation of the auricle; (2) a certain amount of downward pull which the papillary muscles exert upon the tricuspid and mitral valves; (3) at each systole, as can be seen when the heart is exposed, the movements of the latter within the chest are exerting a pull upon the venae cavse, thus pumping their contents into the auricles; (4) the outflow of blood and the decrease in size of the heart during systole cause a slight increase in the negative pressure within the thorax which may be trans- mitted to the thin-walled veins. It is probable that neither of these factors FIG. 46. Venous tracing showing ab- sence of the c wave in a case of heart fail- ure. The tracing is otherwise normal. JUG., right jugular vein; CAR., left ca- rotid artery. Time in 5 seconds. FIG. 47. A. Venous tracing showing auricular paralysis (absence of a wave} with large (x) depression during ventricular systole between c and v. I*, t'-ame tracing, faster speed. alone is responsible for the fall (x depression), but that each is active. Cer- tain it is that auricular relaxation is not the sole cause, for as shown in Fig. 47 it may still be the largest depression in cases in which the auricle is par- alyzed. Dr. Peabody has called the writer's attention to a small wave which is frequently seen during midsystole, especially in tracings from vigorous hearts, occurring just at the base of the x depression, and which in many cases cannot be due to fling of the lever. The origin and significance of this wave are extremely uncertain. It may be really transmitted from the artery; or, as Dr. Peabody suggests, may be due to slight insufficiency of the papillary muscles studied by Sewall. 78 DISEASES OF THE HEART AND AORTA. The fall which leads to the x depression usually lasts until about the end of ventricular systole, d (instant of the dicrotic notch), after which it is followed by a large rise (diastolic wave of Porter; v or ventricular wave of Mackenzie; vs, ventricular stagnation (Ventrikelstauungswelle), Hering; telesystolic wave, t, Bard). This wave is very constant in its occurrence and is usually supposed to represent stagnation within the ventricle, lasting from the end of systole until the tricuspid valve opens; the fall v-y indicates the opening of the tricuspid valve. As Bard has shown, two undulations are occasionally found (t, d, t, telesystolic, occur- ring at the end of systole; and d, protodiastolic, occurring at the very beginning of diastole). Bard states that the wave t is coincident with the first secondary (predicrotic) wave of the arterial pulse, the second with the vibration of the ventricles due to the closure of the aortic valves, and Eyster has shown recently that the notch between the t and d waves upon the venous pulse indicates exactly the end of ventricular systole. FIG. 48. Venous tracing from a very slow heart, with loud third heart sound, showing the presence of the h wave. Max, maximal blood-pressure: Min, minimal blood-pressure. Sewall believes that the stagnation at the end of systole (when the upstroke of the v or t wave occurs before the end of systole) is due to a fatiguing or stretching of the papil- lary muscles, causing a slight tricuspid regurgitation at that instant; but in cases with no murmur in the tricuspid region this explanation needs confirmation. The rise upon the v wave outlasts the end of systole by about iV sec., which probably represents the time required to transmit this change of pres- sure to the veins. Most writers follow Mackenzie in believing that the upstroke of the v wave repre- sents stasis within the ventricle lasting until the tricuspid valve opens, but cardiometer tracings show that filling of the ventricles, or, at least, dilatation, begins at the instant systole ends. Chauveau's tracings of the movements of the heart valves also show that the tricuspid valve opens before the time at which the crest of the v wave appears, so that it is probable that this wave does not represent the very instant at which the tri- cuspid valve opens, but that when the period x-v exceeds the transmission time the interval represents a period during which the venous pressure remains greater than atmospheric pressure. Or it may last until a sufficient amount of blood has entered the ventricle to have relieved the venous engorgement which followed the cessation of the factors which had produced the x depression. The descending limb of the v wave continues as long as blood is rushing in to fill the ventricle (Henderson's period of diastolic filling), after which FIG. 49. Tracing from the same person one hour later, after giving atropino and quick- ening the pulse. The /t wave is absent. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 79 there is a gradual filling of the vein and a rise until the next auricular systole. In slow hearts Hirschfelder and A. G. Gibson have shown that the inflow into the auricles and the filling of the veins is no longer uniform but is inter- rupted by a well-defined wavelet (h, Hirschfelder; b, Gibson) which follows the v wave by a definite interval (Fig. 48, h). Both these writers indepen- dently ascribed this wave to the snapping together of the auriculoventricular cusps at the end of ventricu- lar filling in middiastole, and the former called attention to its corre- spondence with the onset of Henderson's period of diastasis. This fact is further borne out by the presence of a corresponding wave upon the tracing from the oesophagus (Fig. 54, h). This wave disappears when the pulse- rate becomes more rapid (Fig. 49). A. G. Gibson, Eyster, and the writer have occasionally seen a wave w in late diastole of slow pulse preceding the wave of auricular contraction (a wave) by a rather definite in- FIG. 50. Showing a wave w occurring shortly before the a wave. (From a tracing made in collaboration with Prof. L. F. Barker.) terval (Fig. 50). The distance from the h wave varies. This wave is assumed by the former writer to represent a contraction originating in the sinus region of the heart. How- ever, Hirschfelder has recently produced similar waves upon a mechanical model and proved that they are merely waves of elastic recoil of the venous wall. VISUAL EXAMINATION OF THE VENOUS PULSE. Some of these events in the cardiac cycle may be clearly distinguished with the naked eye. Upon looking carefully at the jugular pulsation in a normal individual and placing the finger upon the carotid artery the vein will be seen to fill twice (a wave and v wave) and to collapse twice (x depression and y depression) for each beat felt in the carotid artery (" presystolic-dias- tolic," " physiological," " negative," " double " venous pulse (Hirschfelder)). These waves may be timed less accurately with the eye, but, although, . as Mackenzie states, visual examination may save the examiner many unnec- essary tracings, it should not be relied upon in doubtful cases. For example, a simple mesosystolic collapse (like that shown in Fig. 44) with fibrillation of paralysis of the auricles may simulate a normal venous pulse. ABNORMAL TYPES OF VENOUS PULSE. Auricular Paralysis. Besides this normal (negative or double venous) pulse several other types of venous pulse are seen. In venous stasis and cardiac failure the auricles may soon become weakened and the a wave, due to their contraction, may disappear entirely (Figs. 47 and 51). ~\ . Frey and Krehl demonstrated that this takes place in animals when the venous pros- 80 DISEASES OF THE HEART AND AORTA. sure reaches 20 mm. Hg, and it may occur in man even when the electro- cardiogram shows an auricular wave (Lewis). Positive Venous Pulse. The ventricular type of venous pulse is met with when the heart-rate is regular in cases of tricuspid insufficiency and paroxysmal tachycardia, but is most frequently seen accompanying the absolute irregularity due to auricular fibrillation. In the latter case, as The- opold, Cushny and Edmunds, and Rihl have shown, the tricuspid valves JUG BRACII ma. 51. Positive or ventricular type of venous pulse in tricuspid insufficiency, showing absence of the a wave. VJD, right jugular vein; ACS, left carotid artery. probably close perfectly, but the ventricular form is due to stasis and the effect of small auricular movements. On the other hand, as Rihl has shown, tricuspid insufficiency may be present without a positive venous pulse. pv pv DV Information furnished by the Venous Pulse. It is apparent from the above description that the following facts are to be learned from the normal venous pulse-curve: (1) whether the au- ricle (atrium) is contracting, and whether each auricular (atrial) contraction is followed by a ventricular contraction; (2) the time required for the conduc- tion of the impulse from auricle (atrium) to ventricle (the inter- val a-c on the tracing, about i second in normal individuals conduction time); (3) whether or not the tricuspid valve is closing perfectly (shown by the fall or pressure during systole and the subsequent v wave). 1 In irregular pulses many more important facts are to be learned from the venous pulse, which will be discussed in connection with this disturbance of function. (ESOPIIAGEAL TRACINGS. The venous pulse tracing reveals the conditions prevailing in the right auricle (atrium) and the state of the tricuspid valve. A corresponding investigation of the state of the left auricle (atrium) and of the mitral valve was made possible by a method used in ani- mals by Frcderirq and in man by Sarolea (1S90), Minkowski (1906), Rautenberg (1907), FIG. 52. Positive or ventricular type of venous pulse in tricuspid insufficiency, showing absence of the a wave. JLG, right jugular vuin; BRACII, right brachial artery. Thi-', as has been shown by Mackenzie and by Rihl, is not absolute. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 81 Hewlett (1907), Joachim (1907), Lian (1909), Clerc and Esmein (1910). Minkowski calls attention to the fact that at the level of the seventh to the ninth thoracic vertebrae (about 35 to 37 cm. from the teeth) the left auricle is in contact with the oesophagus, and when one introduces a stomach-tube to this level it receives impulses from the left auricle alone. Accordingly, an ordinary stomach-tube is capped with a thin rubber finger cot, and the latter secured by winding a silk ligature sev- eral times around it. The stomach-tube is then swallowed by the patient until it extends down 35 to 37 cm. from the teeth. It is then connected with a Marey tambour whose oscil- lations record the contraction of the auricle and ventricle (Figs. 53 and 54). The fall in the wave occurs when the auricle moves away from the oesophagus, the rise when it is pressed against the latter by filling with blood. Under ordinary circumstances ventricular as well as auricular systole draws the auricle away from the oesophagus so that the falls and rises cor- respond to auricular and ventricular systole respectively. CEsophageal Tracing in Mitral Insuffi- ciency. When the mitral valve does not close (mitral insufficiency), blood is forced back into the auricle during ventricular systole, and, instead of a fall, there is a rise during systole.. Minkowski's method furnishes the means for obtaining the missing link in our knowledge of the cardiac impulse and the meaning of functional murmurs, but unfortunately the swallowing of the stomach-tube is so disagree- able to the ordinary patient and so dangerous in all very severe cases as to preclude its FIG. 53. Method of taking tracing from the oesophagus to show the contractions of the left auricle. The arrow points to the thin rubber bulb at the end of the ccsophageal tube. ST., stomach. CAROT. CESOPII. FIG. 5i. (Esophagcal and carotid tracings from a normal man. adoption into general use. Patients can, however, often bo trained to swallow the stomach- tube without difficulty, or a rubber tube of small bore may be substituted, and then very satisfactory results may be obtained. IXTRAXASAL TRACINGS. Mosso and also the writer have obtained very satisfactory cardiographic curves from the changes of air pressure' within the thorax. These may be obtained by placing in one nostril a cork perforated by a glass tube which is connected with the recording lever. The lips are closed and the other nostril is closed by pressure. Or, the tube may be placed in the mouth and both nostrils closed by pressure. The glottis must be open and the breath held. Curves thus obtained closely resemble the cesophageal tracings in normal indivi- duals, though the waves are smaller. THE ELECTROCARDIOGRAPH . In recent years another method for the observation of cardiac function, the study of the electrical variations accompanying the heart-beat, has at- tracted much attention, and has yielded so many results of both theoretical 6 82 DISEASES OF THE HEART AND AORTA. and practical importance that it has come almost to supplant the venous pulse tracing for the analysis of the arrhythmias. 1 Historical. The study of the electrical variations of the heart-beat is not new. Kolliker and Miiller in 1S55 found that each beat of the frog's heart was accompanied by a definite electric current, and numerous subsequent observers verified their findings. In 1887 Ludwig and his pupil Waller applied these findings to man, and discovered that the currents accompanying the beat of the human heart could be recorded by means of the capillary electrometer when electrodes were placed upon the precordial region. Their studies were extended by Einthoven of Leyden in 189.5, but he soon found that, although electrical curves (electrocardiograms) could be obtained in this way, the inertia of the cap- illary electrometer was too great to respond satisfactorily to the changes of 1/10000 to 1/3000 of a volt which are concerned in the heart-beat and that a more delicate method must be resorted to. In 1897 Ader invented a new type of galvanometer, now known as the string galvanometer or thread galvanometer, whose delicacy was almost sufficient for the purpose. This galvanometer depends upon the well-known fact that a current gen- erates a magnetic field acting at right angles to its course, which varies with the strength of the current, and which may thus exert a varying attraction or repulsion upon a second magnetic field in its vicinity. In Ader's instrument, which was designed for receiving FIG. 55. Photograph of the electrocardiograph laboratory or "heart station" of the Johns Hopkins Hospital. transatlantic dispatches, a copper or aluminum wire 100 cm. long and 0.2 mm. thick was used to carry the current. Einthoven (1903) constructed a much more delicate modification of this, in which the current from the body, which is thus varying in intensity, is carried upon a silver- coated quartz or a platinum filament about 3/i (.003 mm.) thick. This wire is so light that its weight is negligible, for it cannot bo weighed with the most delicate balances. It 'The entire literature of this subject up to 1910 has been collected and reviewed by Lewellys Y. Barker: Electrocardiograph}- and Phonocardiography, Johns Hopkins Hosp. Bull., Baltimore. HMO, xxi. 359. and Fr. Kraus and Ge. Fr. Xicolai: Das Elektro- kardiogramm des gesunden und Kranken Menschen, Leipz., 1910; other reviews of the literature are to be found in T. Lewis: Chapter on the Electrocardiograph in Mackenzie's Diseases of the Heart, 2d edition. W. B. James and II. B. Williams: The Electrocardiogram 5:i Clinical Medicine, Am. J. M. Sr., Phila. and X. Y., 1910, cxl. (144. A. D. Hirsdifelder: Recent Studies upon the Electrocardiogram and upon Change in the Volume of the Heart, Interstate M. J., St. Louis, 1911, xviii. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 83 is suspended between the poles of a very powerful electro-magnet with large cast-iron armatures. The movements of the thread are recorded by projecting its shadow under the magnification of a high-power microscope upon the slit of a specially devised camera, about six feet away. The film of this camera moves rapidly past the slit, and the oscillations of the thread are recorded as a curve. The time is indicated by the shadow of a time marker placed in front of the slit. The current is led off from the body from German silver electrodes which are padded with felt soaked in physiological salt solution (Fig. 58). Thus obtained it represents the difference of potential between the skin under two electrodes, and is generated by two elements. 1. The permanent difference of potential between these two differ- ent parts of the body, which is dependent upon local conditions of the skin and tissues and is quite independent of the cardiac cycle. This is known as the current of rest. 2. The oscillations due to the action current of the heart itself, the electrocardiogram proper. Since we are interested only in the latter, the current of rest is neutralized by pass- ing through the galvanometer a battery current exactly equal to it, but opposite in direc- tion, after which compensation the only current acting upon the galvanometer is that which accompanies the contraction of muscles. When the patient is quiet, the tonic con- B. A. Kindness of A. H. Thomas & Co. FIG. 56. Edelmann's modification of Einthoven's string galvanometer. A, the galvanometer with its magnets and microscope. B, the holder for the filament. tractions of the skeletal muscles play but a little role, and the action-current that is ob- served is seen to accompany cardiac contractions (Fig. 59). Contraction of the hand or foot muscles exerts a definite effect, which is much slower than the cardiac impulse; and the same is true of the wave accompanying deep inspiration. Einthoven has shown that it is by no means necessary that the patient be kept in the same room with the instrument, but that, on the contrary, the wards of the hospital may be connected by wires with the electrocardiographic laboratory and the patient thus examined without leaving his bed or even changing his position. The wiring in this case cannot be done on a grounded circuit, but requires double wires placed underground and very completely insulated. If this is done the electrocardiographic variations are com- municated very well to a great distance, Einthoven's own laboratory, in which the original work was done, having been located 1.5 kilometres (one mile) from the hospital in which the patients lay. With proper care even greater distances are feasible. In the short space between the wards and the laboratory of the Johns Hopkins Hospital no difficulties were encountered. In practice, the setting construction and setting up of an elcctrocardiogruphic outfit or "heart station" is a very laborious matter. The instruments themselves may be bought ready made at a considerable cost, but much labor must still be spent in installing them. 84 DISEASES OF THE HEART AND AORTA. Installation of the Electrocardiograph. Except the photo-registration apparatus, all the apparatus should be mounted on a heavy table 3x5 feet in size, which must be very steady to avoid mechanical vibrations of the string. A concrete pillar may also be used, especially if the laboratory is in the basement; but, best of all, according to James and Williams, who worked in a laboratory subject to great vibrations, is to allow the table to rest in a box of sand, which damps all the small vibrations. The use of the string galvanometer requires three separate electrical circuits, a circuit for the electric-light current for illuminating the filament, the circuit for charging w 'to :j it) ^B r KinJiu-ss of A. II. Thomas \- Ct. FIG. o7. Edelnaann's convenient switchboard and short-circuiting key: the electromagnets of the galvanometer, and the main circuit connecting the galvanometer and the patient. 1. The electric light-circuit must be capable of carrying over ten amperes of 110 or 220 volts for supplying a large arc lamp. For the installation of two galvanometers wires must be used which are capable of carrving between 20 and 30 amperes, or a double circuit installed. Arc lamps, such as are used for stereoptieons or moving pictures, suffice for all purposes, and an automatic feed for the carbons, though very convenient, is not indispensable. Just as for magic-lantern work, the lamp must be provided with a cooling chamber for water, having parallel glass walls at least two inches apart. By staining the water in this THE VENOUS PULSE AND ELECTROCARDIOGRAM. 85 cooler with methylene blue or some other fluid, it is possible to obtain an almost mono- chromatic light, which gives much sharper outlines to the shadows upon the film and greater contrasts than are otherwise attainable. THE STRING GALVANOMETER. A slight modification of Einthoven's original model may be obtained from the firm of Edelmann of Munich, the Cambridge Scientific Apparatus Co., of Cambridge, England, and Wertheim-Solamonson of Amsterdam. As stated above, it consists essentially of a fine filament of platinum or silvered quartz which is suspended between the two poles of a large electromagnet. The two poles of the electromagnets consist of large wire-wound soft-iron cores capa- ble of generating a field of 20,000 electromagnetic units (C. G. S.) per q. cm. Each core is FIG. 58. Diagram showing the main connections for the electrocardiograph. The heaviest lines (110-220 V) mark the electric light connections; the medium lines indicate the main circuit from right hand (RH), left hand (LH) or left foot (LF) of the patient through the galvanometer, showing the shunt through the rheostat (RHEOST). The galvanometer is shown between the two poles of the MAGNET, which is charged by the storage battery circuit (10 V). The connections for the compensating current, shown in the darkly shaded area; those for the standardizing current are shown in the lightly shaded area. The construction of the photo-registration apparatus is shown upon the right of the figure. penetrated by a large hole to accommodate a microscope to condense the light upon the filament and to magnify the image of the latter. The electromagnets are charged with a current from a ten-volt storage battery, which is provided with connections for recharg- ing, preferably from a direct street current. "Between the electromagnets there is a framework for holding the thread-carrier. The latter is a small separate holder consisting of an upright frame with binding posts at each end. The upper binding post is provided with a micrometer screw for adjusting the tightness of the filament and binder; thus each binding post is provided with two laterally acting micrometer screws for centring the filament between the lenses of the microscopes after its tautness has been adjusted. The Galvanometer Thread. The thread or filament which constitutes the main part of the galvanometer may be either of platinum or of quartz coated with silver, but in neither case should its diameter be greater than three microns (3/i). 86 DISEASES OF THE HEART AND AORTA. Platinum Filaments. The platinum filaments can be prepared from ordinary Wollas- ton wire, platinum wire coated with silver and then drawn out as fine as possible, by simply dissolving off the silver with dilute acid. This procedure, which at first blush appears extremely simple, is a matter of a good deal of technical difficulty: first, because the platinum core of the Wollaston wire is by no means uniform, and many samples may be used up before a piece ten centimetres in length can be secured; and, secondly, because the surface tension of the acid is strong enough to break many filaments as they are being lifted out of it. Indeed twenty or more bits of Wollaston wire may be used up before a single filament is obtained in this way, at least until one has acquired some degree of skill in the technique. The filaments are then soldered on to the ends of the thread-holder, which are first carefully coated with ordinary soft solder or Woods' metal, using acid-free zinc chloride solution or a solder paste as the flux. The solder coat is then softened once more and the end of the filament caught in it without allowing the latter to touch the soldering iron. Preparation of Quartz Filaments. Filaments of silver-coated quartz are, however, six or seven times more sensitive and are capable of being made much more tense than those of platinum. According to Wertheim-Solamonson, quartz filaments may be pre- pared in the following way: The operator sits with his back to the light, facing a screen of black silk. This silk curtain is hung a couple of feet above the head of the operator and passes obliquely downward to a horizontal bar above the opposite edge of the table, so as to catch all the fine filaments that may be blown off the quartz. By means of an oxygen-illuminat ing-gas burner he fuses a stick of quartz in the middle, draws it out rapidly, cuts it at its thinnest point, and bends the tapering portion in the flame to a right angle about 5 cm. from the end. The shaft of this L is then placed in the axis of the blast flame and in fusing it fine filaments will be found to be blown off onto the silk screen, es- pecially its upper portion. These filaments are taken up on a shaped bow of glass rod, to which they are sealed with melted rubber. The holder and thread are then immersed in a 5 per cent, solution of the double cyanide of silver and potassium and plated with a 10-20 micro-ampere current using a high graphite resistance (the current strength must be con- trolled with a very fine ammeter), gradually sinking them lower and lower in the fluid. They are then carefully removed and washed several times by dipping in distilled water. After this procedure, the ends of the filament are copper-plated by clamping a fine copper wire (cathode) against them and then immersing the other end in a very dilute CuSC>4 solution in a bath containing a copper strip (anode) also connected with the battery. When the ends are copper-plated, the filaments are soldered into the holders, as described above. Wertheim-Solamonson states that in this way he has been able to obtain excellent filaments with a thickness (including coating) of not more than 1.7^ (.0017 mm.) and a resistance of only 440 ohms. Inserting the String. The filament is then placed loosely in a temporary holder with which it can be carried to the holder of the galvanometer. Before doing so it must be stretched sufficiently taut in the holder by means of a mi- crometer screw. The filament is so thin that this is a matter of some delicacy. The fila- ment itself can barely be seen even in a strong light against a dark background, and when it is loose it can easily be broken by the breathing of the observer. When sufficiently tight for placing in the galvanometer, it will be moved only 2-3 mm. by a gentle zephyr, or by gentle breathing of a person about a foot away. It is then placed in the holder of the gal- vanometer and transferred to its place between the electrodes and just in front of the lenses of the two microscopes. This must be done with great care and all draughts or currents of air must be avoided. Care must be taken that no current is passing through the electromag- net s while the thread is being adjusted. Even if these are free from current, the adjustment must be carried out slowly, gradually tightening the screws and gradually sliding the holder in between the lenses to keep the filament from touching the latter and adhering to them. When the filament is brought between the lenses, it must be accurately centred. The light is turned on, the microscope lenses are focused so as to throw a sharp shadow of the thread on a screen, and the filament is adjusted by means of the centring screws to bring it to the exact centre of the magnetic field. This is attained when the thread is no longer pulled out to focus by making or breaking the circuit through the electromagnet, but the thread must be centred again whenever the degree of tautness is changed. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 87 Edelmann has also constructed a much smaller thread galvanometer, which may be used with either a permanent magnet or an electromagnet. The former was given an extended trial by the writer in collaboration with Prof. Barker and Dr. Bond, but, though it can be made to show all the waves of the normal electrocardiogram, the excursions are quite small, and even then the filament must be loosened to such a degree that it fails to record the fine wavelets of auricular fibrillation; and it cannot be recommended for clinical work. With the electromagnet, however, a field of 10,000 C. G. S. (of half the strength of that in the large galvanometer) may be obtained, and this is sufficient for most clinical purposes. The small galvanometer with electromagnet may still be used for clinical purposes in case expense precludes the pur- chase of the larger form; but the loss in delicacy must always be borne in mind. Electrical Connections in the Galvanometer Circuit. The essential portions of the con- nections with the galvanometer are made up of three distinct circuits, 1. The circuit from the electrodes on the patient through the galvanometer. 2. The compensating current through a cell and the galvanometer in the reverse direction. 3. The standardizing circuit to determine the excursion of the galvanometer. Electrodes. Einthoven originally immersed the hands or feet of the patient in large jars of physiological sodium chloride solution in which electrodes of zinc were placed, and these in turn connected with the galvanometer circuit. Later investigators, however, have found it more convenient to use large plates of German silver, about 15 x 25 cm., applied to the skin by tying about the limb over flannel pads soaked in 0.9 per cent, sodium chloride solution. Standardizing the Thread. For most purposes it has become conventional usage to employ strings of excursions standardized so that 1 millivolt gives an excursion of 1 centimetre. This adjustment is made before the electrocardiogram is taken, by throwing in a current of exactly 1 millivolt from the standardizing circuit and then adjusting the tightness of the thread until each make or break of this current gives an excursion of exactly 1 cm. After doing so the thread must be readjusted to the exact centre of the magnetic field. Procedure for Taking an Electrocardiogram. In proceeding to take an electrocardio- gram, the operator immerses the pads in salt solution, applies them to the right and left forearm and left shin of the patient, and then connects two of them with the binding posts of the galvanometer circuit. The electric lights are turned on and the shadow of the thread focussed upon the recording apparatus. The double connection is then made, which first throws the current into the electromagnet, and an instant later throws the galvanometer circuit, in i 111 J J. which the current is temporarily prevented from passing through the thread by keep- ing the short-circuiting key (0 resistance) in the rheostat. This and from one to ten others are then removed in order to see in which direction the body current (rest current, zero current, Nullstrom) is pass- UHCOMPENSATCD .,, ,. COMPLNSATCD ing; after which the Compensating Current FIG 59 ,_ NormaI e lectrooardia g ram tracing taken IS thrown in and by means ot the com- by the writer in collaboration with Prof. L. F. Barker mutator sent in the opposite direction. and Dr. G. S. Bond. The resistance plugs are removed grad- ually from the rheostat in the compensating circuit until the shadow of Ilie thread is brought back to its original position, after which more and more of the body current is shunted in by removing plugs from the rheostat on the main circuit, and the, shadow of the thread brought back to centre as before. These oscillations of the thread now corre- spond to each heart-beat, and the wavelets P, R, and T can usually be seen plainly. The arc light is once more adjusted carefully, the shadows focused, and the movement of the thread photographed. Photo Registration. The oscillations of the thread are recorded in the usual way by photographing its shadow upon a moving film at a distance of 1-2 metres from the galvanometer; but the great magnification of this shadow and the shortness of the 88 DISEASES OF THE HEART AND AORTA. exposure (less than T ^ second) give rise to certain technical difficulties. In the first place, as has been stated above, it is necessary to have an arc light of sufficient power, and small lights, such as are used for photomicrography or dark-field illumination, are inade- quate. An arc light with half inch or f inch carbons, such as is used for magic lanterns, represents the minimum illumination. In addition, it is necessary to obtain the sharpest possible shadow, for which the light must be focused sharply upon the thread with the condensing microscope and the image of the thread in turn focused upon the screen. Chromatic aberration, which, owing to long distance from the lens to screen is considerable, may be greatly reduced by using the methylene-blue color screen described above, which allows most of the blue and ultra- violet rays to pass through, and this gives a sharper and blacker shadow by limiting the refraction to the waves of shorter wave-length, with very little loss in photochemical power. The essential part of the photographic apparatus itself is a light-tight box with a slit, past which a film or strip of highly sensitized paper is rotated by means of a horizon- tally moving drum, a clock-work, or a motor. In the very elaborate apparatus which usually accompanies the electrocardiograph a film or roll of highly sensitized paper 75 metres long is held in a light-tight metal box and driven at any desired speed by an electric motor. A special lever is arranged so that the motor may attain a uniform speed before starting the film, and this in turn may be started before the exposure is made. The latter is accomplished by raising the shutter which covers a horizontal slit in the box. In order to concentrate all the light possible upon the slit, the latter is covered with a plano-convex cylindrical lens whose axis is horizontal, so that all the possible illumina- tion is obtained but the side-to-side movement is not altered. After passing the slit the film travels through a slit in the bottom of the box, to curl up in a second light-tight box below, where a plane-like blade running in a partition be- tween the two boxes cuts off the exposed from the unexposed film. Just before being moved, each film may be numbered, either by means of a disk perforated with holes to show the numbers, or else with a notched line made by signalling upon a telegraph key; these may be indicated by the number of movements made by the shadow of a signal mag- net, connected with a telegraph (make-and-break) key. A time-marking lever should also be placed in front of the slit. The time-marker may be an ordinary Jaquet chronograph recording fifths of a second or a signal magnet connected with an electrically-driven spring interrupter recording i or T ^JJ seconds. For very fast speeds a convenient time-marker recording T }n with the electrodes upon the right arm and left arm (Dl). B, Tracing taken with the electrodes upon the right arm and left leg (Dl'> C, Tracing taken with the electrodes upon the left arm and left leg (Do). The lowest line and the third line from the bottom represent signals, the second line from the bottom represents time in \ seconds. 92 DISEASES OF THE HEART AND AORTA. FIG. 61. Normal electrocardiogram showing the time relations to the venous and carotid pulse- wave. (After Einthoven.) It must be remembered, as Gotch and Florence Buchanan have pointed out, that these waves represent the difference of potential between the skin under the two electrodes. If both electrodes remain entirely free from charge, the curve remains at the base-line. But if both electrodes receive an electric charge of the same intensity (say, four milli- volts), the difference of potential between them remains zero, and the curve remains at the base-line (Fig. 62). It is a matter of empirical fact, shown by Kraus and Nicolai, that the contraction originating at the base of the right ventricle causes a wave exactly oppo- site in sign to that accompanying a contraction originating at the left apex, and it has been assumed by these writers that the ventricular part of the normal elec- trocardiogram represents the algebraic sum of two such almost equal and opposite currents, but that the R S wave, which occurs before the onset of the mechanical contraction, is caused by the impulse passing down the cells of the atrioventricular conduc- tion system. In conformity with this hypoth- esis, Xicolai found all the waves inverted in a patient with dextrocardia (see page 550) ; but, on the other hand, Gotch, Buchanan, Straub, and Samojloff found electrocardiograms simi- lar to those of mammals in frogs, snakes, and tortoises, in spite of the fact that these ani- mals possess but one ventricle. Florence Buchanan suggests that it may not be the separate ventricles, but the sepa- rate layers of muscle-fibres which arise in each papillary muscle. She suggests, moreover, that the R wave is produced by a slight asyn- chronism between the two ventricles, so that one ventricle only is acting during the instant in which the R wave occurs. This view is shared by Rothberger and Winterberg. Such an asynchronism has indeed been shown by Knoll, Fredericq, Stassen, Barker and Hirschfelder during vagus stimulation, and it is possible that even under normal conditions it may exist for a period long enough to just give rise to the deflection of the R wave. It must be admitted that neither of these theories has been proved and both await the confirma- tion of further experiment. As a matter of fact, ono occasionally meets with definite bifurcations of the R wave which seem to furnish support to this theory. And still further evidence is furnished by the electrocardiograms of Eppinger and Roth- berger from dogs, in which one branch of the His bundle was injured in which usually broad 7? waves were recorded. On the other hand, the R wave is not broadened by stimu- lation of the vagi nor in persons with slow hearts, as might be expected from the results of the above-mentioned observers. The validity of these hypotheses is, how- ever, rendered questionable by the fact that Eyster has obtained the R and T waves in typical form from isolated strips of terrapin's ventricle. Ii would appear, therefore, that, whatever be their cause, these waves are produced by a single contraction impulse and need not represent the algebraic summation of different elements, as Buchanan and others have claimed. The exact nature of the successive elec- trical phenomena which gives rise to the R, S, and T waves, however, remains unexplained uj) to the present, and there is little^basis even for speculation as to their mode of origin. Extracardiac Vibrations of the String. Although these waves and other waves to be discussed later are produced by the electrical variations of the FIG. 62. Factors involved in the normal electrocardiogram, according to the theories. (7) Ordinary diphasic variation in skeletal muscle of algebraic summation. The white and black areas (II and ///) indicate electrical changes going on in each of the ventricles or in different layers of ventricular muscle. The small diagram (/) at the left shows th:> connections of the electrodes in obtaining the tracing from skeletal muscle. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 93 heart, irregular and rapid vibrations are sometimes encountered which are superposed upon the main waves, and may be due to the following causes (James and Williams) : I. Induction from outside sources. 1. Neighboring strong electrical vibrations, such as the passage of elec- tric cars, etc. 2. Defective insulation. 3. Induction caused by hissing of the arc lamp. II. Muscular contractions. 1. Tenseness of the patient's muscles, which gives rise to a vibration of the string (Einthoven) at a rate of about 50 per second (Piper). This is especially common in persons who work with their hands (Strubell) . 2. Gross muscular movements, such as coughing, sneezing, movements of the hand, etc., which cause large irregular movements of the string, which can be readily distinguished from those due to the heart's action. The latter are easily recognized, but the finer vibrations might some- times be confused with those due to fibrillation of the auricles, except for the fact that they are merely superposed upon the other waves of the electro- cardiogram, whereas in fibrillation the P wave disappears entirely. The nonmuscular extraneous vibrations may, moreover, be recognized by taking a short control without connecting the galvanometer with the patient. Variations in the Form of the Electrocardiogram. Without considering the electrocardiograms accompanying abnormal contractions, to be discussed later in connection with the cardiac arrhythmias, several variations occur. Exaggerated P Wave in Mitral Stenosis. Although the P (or A) wave may diminish or disappear under the influence of vagus stimulation even when the auricles are still contracting actively, under other circumstances it may be markedly increased in size (Plate XI). This, as Samojloff has shown, is especially the case in compensated mitral stenosis, in which, accom- panying the hypertrophy and increased force of the auricles, the auricu- lar ( P ) wave may become definitely increased in height, though this is scarcely characteristic enough to warrant the diag- nosis of mitral stenosis from the form of the electrocardiogram alone. Change in Form of the Electrocardiogram Accompanying Change of Position of the Body. E i n t h o v e n and August II off in a n n have shown that alterations in the position of the heart within t h e b o d y , from c h a n g e i n p o s i t i o n o f t h e b o d y , inflation of t h e s t o m a c h , d i s p 1 a c e m e n t of the heart f r o m p 1 e u r a 1 e f f u s i o n , etc., c a u s e changes to take place in the e 1 e c t r o c u r d i o g r u in . In the former case the R (I) wave becomes smaller and N becomes larger; in the latter both R and S (Nicolai's / and J) become larger. Also somewhat arbitrary is the claim of Kraus and Xicolai that the size of the T wave is in some wav an index of the vigor of the contraction. 94 DISEASES OF THE HEART AND AORTA. True, they found that in many, though by no means all, cases of feeble heart action, this wave is small, absent, or inverted, and, on the other hand, that it may be large in hypertrophic hearts and in overacting hearts, in Basedow's disease, after exercise, etc., but many failing hearts retain a high T wave to the end, and in many otherwise vigorous persons the T wave may be small or even inverted. In hypertrophy of the right ventricle and also after stimulation of the vagus, the R wave becomes higher; in hypertrophy of the left ventricle it becomes inverted. Kraus and Nicolai have called attention to the fact that in nervous people, as well as in patients with mitral insufficiency, the S depression is very deep, so that they have termed it the Neurasthenikerzacke (neurasthenic notch) ; but Strubell has encountered this form in so many vigorous, athletic persons that this designation seems entirely too arbitrary. A very marked S depression has been obtained by Rothberger and Winterberg from stimu- lation of the right acceleratory nerve. And it is, of course, possible that in all these persons, whether from nervous excitement or exercise, the right accelera- tor may be stimulated, though by no means all have rapid pulse-rates. An exceptionally high T wave may also be obtained when the galvanom- eter thread is loose. Rothberger and Winterberg have also obtained peculiar deformations of the electrocardiogram by stimulating the various branches of the cervical sympathetic (accelerator) nerves, and have found a different form of electro- cardiogram for each branch of the ganglia stimulated, corresponding probably to an exaggerated effect localized in each case to a certain region of the heart wall. In general, stimulation of the right accelerator branches produced effects somewhat resembling those of the right ventricular hypertrophy, and those of the left suggested more or less hypertrophy of the left ventricle. (Fig. 78.) Stimulation of the vagi, on the other hand, as has been stated, usually causes a large R wave with diminution or disappearance of P and T. The inversions and changes in form due to hypertrophy of the two ventricles and to situs inversus will be discussed under these heads (pages 285 and 550). BIBLIOGRAPHY. VENOUS PULSE. Engelmann, Th. W.: Uebor den Unsprung der Herzbewegungen, Arch. f. d. gos. Physiol., Bonn, 1897, Ixv, 109. Morrow, \V. S.: Uebcr die Fortpflanzungsgeschwindigkeit des Venenpuls, Arch. f. d. pes. Physiol., Bonn, 1900, Ixxix, 4i2. The Rate of Propagation of the Venous Pulse, Canad. Roc. Sc., 1900, viii, 20."). Friodreich, X.: Uebcr den Venenpuls. Deutseh. Arch. f. klin. Mod., Leipz., 1865, i, 241. Maroy, E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Paris, 1SS1. Mackenzie. J.: The Venous and Liver Pulses, and the Arrhythmic Contraction of the Cardiac Cavities, Jour. Path, and Bacteriol., Kdinb. and Lond., 1893-94, ii, pp. 84 and 273. The Study of the Pulse and Movements of the Heart, London, 1903. Hirschfeldor, A. D.: Graphic Methods in the Study of Cardiac Diseases, Am. Jour. M. Sc., Phila., 1900, cxxxii, 378. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 95 Bachman, G.: The Interpretation of the Venous Pulse, ibid., 1908, cxxxvi, 674. Hay, J.: Graphic Methods in the Study of Heart Disease, Oxford and Lond., 1909. V. Jaquet: Cardiosphygmograph, Ztschr. f. Biol., Muenchen, 1901. Mackenzie, J.: Diseases of the Heart, Oxford and Lond., 1908. Uskoff, L.: Der Sphygmotonograph, Ztschr. f. klin. Med., Berl., 1908, Ixvi, 90. Crehore, A. C., and Meara, F. S.: The Micrograph; A Preliminary Report, J. Am. M. Ass., Chicago, 1911, Ixvi, 1549. Fredericq, L.: La seconde ondulation positive (premiere ondulation systolique) du pouls veineux physiologique chez le chein, Arch, intern, de Physiol., 1907. Historisch- kritische Bemerkungen ueber die von klinischer Seite neuerdings anerkannte Identi- tat der Venen- und (Esophaguspulsbilder mit den Vorkammerdruckkurven, Zentralbl. f. Physiol., Leipz. u. Wien, 1908, xxii, 297. Sarolea, Arch, de biol., 1890, x, 185. Clerc, A., and Esmein, C.: Etude critique de la pulsation oesophagienne chez 1' hommp, Arch, des malad. d. coeur des vaiss. et du sang., Par., 1910, iii, 1. Morrow, W. S.: Various Forms of the Negative or Physiological Venous Pulse, Brit. M. Jour., Lond., 1906, ii, 1807. The Venous Pulse, ibid., 1907, i, 777. Knoll, P.: Beitriige zur Lehre von der Blutbewegung in den Venen, Arch. f. d. ges. Physiol., Bonn, 1898, Ixxii, 317, 621. Theopold, P.: Ein Beitrag zur Lehre von der Arhythmia perpetua, Deutsch. Arch. f. klin. Med., Leipz., 1905, Ixxxii, 495. Marey, E. J. : La physiologic du sang a 1'etat physiologique et dans les maladies, Paris, 1881. Fredericq., L., 1. c. Porter, W. T.: Researches on the Filling of the Heart, Jour. Physiol., Camb., 1S92, xiii, 513. Bard, L. : Des divers details du pouls veineux les jugulaires chez 1'homme, J. de Physiol. et de Path, gen., Par., 1906, viii, 454. Hirschfelder, A. D. : Some Variations in the Form of the Venous Pulse, Bull. Johns Hop- kins Hosp., Bait., 1907, xviii, 265. Cushny, A. R., and Grosh, L. C.: The Venous Pulse, Jour. Am. M. Ass., Chicago, 1907, xlix, 1254. Mackenzie, J.: The Venous Pulse, Brit. M. J., Lond., 1907, i, 112. Sewall, H., and Hirschfelder, A. D.: Unpublished investigations. Peabody, F. W.: Personal communication. Sewall, H.: Safeguards of the Heart-beat, Am. J. M. Sci., Phila. and X. York, 1908, cxxxvi, 32. Hering, H. E.: Die Verzeichnung des Venenpulses am isolierten kiinstlich durchstromten Saugetierherzen, Arch. f. d. ges. Physiol., Bonn, 1904, cvi, 1. Chauveau and Marey: Quoted from Marey, La Circulation du Sang, etc. Gibson, A. G.: On a Hitherto Undescribed Wave in the Venous Pulse, Lancet, Lond., 1907, ii, 1380. Mackenzie, J.: The Interpretation of the Pulsations in the Jugular Veins, Am. Jour. M. Sc., Phila. and N. York, 1907, n. s. cxxxiv, 12. Rihl, J.: Ueber den Venenpuls nach experimenteller lesion der Trikuspidalklappe, Ver- handl. d. Kong. f. innere Mod., Wiesbaden, 1907, xxiv, 453. Gibson, G. A.: Certain Clinical Features of Cardiac Disease, Johns Hopkins Hosp. Bull., Bait., 1908, xix, 361. Eyster, J. A. E. : Unpublished observations. Hirschfelder, A. D.: Inspection of the Jugular Vein; Its Value and Its Limitations in Functional Diagnosis, J. Am. M. Assoc., Chicago, 1907, xlviii, 1105. V. Frey, M., and Krehl, L.: Untersuchungcn ueber den Puls, Arch. f. Physiol., Leipz., 1890, 31. Hewlett, A. W.: On the Interpretation of the Positive Venous Pulse, Jour. Med. Research, Bost., 1907, xvii, 19. Minkowski, O.: Die Registrierung der Herzbewegungen am linken Vorhof, Deutsch. med. Wochnschr., 1906, xxxii, 1248. Zur Deutung von Herzarrhythmien mittelst des cesophagealen Kardiograms, Ztsehr. f. klin. Med., Berl., 1907, Ixii, 371. Rautenberg, E.: Neue Methode der Registrierung der Vorhof spul.sat ion vom (Esophagus aus, Deutsche med. Wchnschr., Leipz. and Berl., 1907, xxxiii, 364. 96 DISEASES OF THE HEART AND AORTA. Young, C. I., and Hewlett, A. W.: The Normal Pulsations within the (Esophagus, J. M. Research., Bost., 1907, xvi, 427. Hirschfelder, A. D. : Observations on a Case of Palpitation of the Heart, Johns Hopkins Hosp. Bull., Baltimore, 1906, xvii, 299. Ader: Sur un nouvel appareil enregistreur pour cables sousmarins, Comp. rend. Ac. Sc., Par., 1897, cxxiv, 1440. Barker, L. F , and Hirschfelder, A. D.: The Effects of Cutting the Branch of the His Bundle Going to the Left Ventricle, Arch. Int. Med., Chicago, 1909, iv, 193. Barker, L. F., Hirschfelder, A. D., and Bond, G. S.: The Electrocardiogram in Clinical Diagnosis, J. Am. M. Assoc., Chicago, 1910, Iv, 1350. Buchanan, F. : Note on the Electrocardiogram, Frequency of the Heart-beat and Respira- tory Exchange in Reptiles, J. Physiol., Camb., 1909-10, xxxix, Proc. Physiol. Soc., p. xxv. Einthoven, W.: Ueber die Form des menschlichen Elektrocardiogramms, Arch. f. d. ges. Physiol., Bonn, 1895, Ix, 101. Ein neues Galvanometer, Ann. d. Physik, 1903, iv, Ser. xii, 1059. Ueber einige Anwendungen der Saitengalvanometers, ibid., 1904, xiv, 182. Le Telecardiogramme, Arch, internat. de physiol., Liege, 1906, iv, 132. Einthoven, W., and Vaandrager: Weiteres ueber das Elektrocardiogramm, Arch. f. d. ges. Physiol., Bonn, 1908, cxxii, 517. Eppinger, J., and Rothberger, J.: Ueber die Folgen der Durchschneidung der Tawara's- schen Schenkel des Reizleitungssystems, Ztschr. f. klin. Med., Berl., 1910, Ixx, i. Fredei'icq, L.: La pulsation du co3ur du chien est une contraction, etc., Arch, internat. de physiol., Liege, 1906, iv, 60. Gotch, F. : The Succession of Events in the Contracting Ventricle as shown by Electrom- eter Records, Heart, Lond., 1909-10, i, 235. Hoffmann, A.: Zur Kritik des Elektrokardiogramms, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1909, xxvi, 614. Kolliker, A., and M tiller, H.: Nachweis der negativen Schwankung am naturlich sich kontrahierenden Muskel, Verh. d. physikmed. Gesellsch., Wurzburg, 1855, vi, 528. Knoll, P.: Ueber Incongruenz in der Thiitigkeit der beiden Herzhalften, Sitzungsber. d. Iv. Akad. d. Wissensch., Math, naturw. Kl., Vienna, 1890, xcix, 31. Kraus, F., and Nicolai, G. F.: Ueber das Elektrokardiogramm unter normalen und path- ologischen Verhaltnissen, Berl. klin. Wchnschr., 1907, 765, 811; Das Elektrokardio- gramm des gesunden und kranken Menschen, Leipz., 1910. Piper: Ueber don willkiirlichen Muskeltetanus, Arch. f. d. ges. Physiol., Bonn, 1907, cxix, 301 ; Ztschr. f. Biol., Muenchen, 1908, 1, 393. Rothberger, J., and Winterberg, H.: Ueber die Beziehungen der Herznerven zur Form des Elektrokardiogramms, Arch. f. d. ges. Physiol., Bonn, 1910, cxxxv, 506. Samojloff, A.: Ueber die Vorhoferhebung des Elektrokardiogramms bie Mitralstenose, Muenchen. med. Wchnschr., 1909, Ivi, 1942. Stassen, A.: De 1'ordre de succession des diffcrentes phases de la pulsation cardiaque chez le chicn, Arch, internat. de physiol., Liege, 1907, v, 600. Strubell, A.: Zur Klinik des Elektrokardiogramms, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1909, xxiv, 623. Waller, A. D.: A Demonstration on Man of Electromotive Changes Accompanying the Heart's Beat, J. Physiol., Camb., 1887, viii, 229. Introductory Address on the Elec- tromotive Properties of the Human Heart, Brit. M. J., Lond., 1888. ii, 751. On the Electromotive Changes Connected with the Beat of the Mammalian Heart, Phil. Tr. Roy. Soc., Lond., 1889, 1890, clxxx, B, 169. Wertheim-Salamonson, J. K. A.: Anfertigung und Gebrauch diinner versilberten Quarz- fiiden, Ztschr. f. biol. Techn. u. Methodik., 1909, i, 35. For a more elaborate process see also Connegieter, II. G.: Leitendmachen diinner Quart zfaden durch Kathoden- zerstaubung mit nachfolgender galvanis cher Versilberung, ibid., 1910, ii, 21. Eyster, J. A. E.: Electrocardiogram Studies, read before the the American Physiological Society, Baltimore, Dec. 29, 1911. Judin A.: Zur Erklarung der Form des Elektrokardiogramms, Zentralbl. f. Physiol., Leipz. and Wien, 1908, xxii, 365. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 97 Morrow, W. S.: Various Forms of the Negative or Physiological Venous Pulse, Brit. M. Jour., Lond., 1906, ii, 1807. The Venous Pulse, ibid., 1907, i, 777. Knoll, P.: Beitrage zur Lehre von der Blutbewegung in den Venen, Arch. f. d. ges. Physiol., Bonn, 1898, Ixxii, 317, 621. Theopold, P.: Ein Beitrag zur Lehre von der Arhythmia perpetua, Deutsch. Arch. f. klin. Med., Leipz., 1905, Ixxxii, 495. Marey, E. J.: La physiologie du sang a 1'etat physiologique et dans les maladies, Paris, 1881. Fredericq, L., 1. c. Porter, W. T.: Researches on the Filling of the Heart, Jour. Physiol., Cam., 1892, xiii, 513. Bard, L.: Des divers details du pouls veineux les jugulaires chez l'homme, J. de Physiol. et de Path, gen., Par., 1906, viii, 454. Hirschfelder, A. D.: Some Variations in the Form of the Venous Pulse, Bull. Johns Hop- kins Hosp., Bait., 1907, xviii, 265. Cushny, A. R., and Grosh, L. C.: The Venous Pulse, Jour. Am. M. Ass., Chicago, 1907, xlix, 1254. Mackenzie, J.: The Venous Pulse, Brit. M. J., Lond., 1907, i, 112. Sewall, H., and Hirschfelder, A. D.: Unpublished investigations. Peabody, F. W.: Personal communication. Sewall, H.: Safeguards of the Heart-beat, Am. J. M. Sci., Phila. and X. York, 1908, cxxxvi, 32. Hering, H. E.: Die Verzeichnung des Venepulses am isolierten Kiintlich durchstromten Siiugetierherzin, Arch. f. d. ges. Physiol., Bonn, 1904, cvi. 1. Chauveau and Marey: Quoted from Marey, La Circulation du Sang, etc. Gibson, A. G.: On a Hitherto Undescribed Wave in the Venous Pulse, Lancet, Lond., 1907, ii, 1380. Mackenzie, J.: The Interpretation of the Pulsations in the Jugular Veins, Am. Jour. M. Sc., Phila. and X. York, 1907, n. s. cxxxiv, 12. Rihl, J.: Ueber den Venenpuls nach experimenteller Lasion der Trikuspidalklappe, Ver- handl. d. Kong. f. innere Med., Wiesbaden, 1907, xxiv, 453. Gibson, G. A.: Certain Clinical Features of Cardiac Disease, Johns Hopkins Hosp. Bull., Bait., 1908, xix, 361. Eyster, J. A. E.: F/npublished observations. Hirschfelder, A. D.: Inspection of the Jugular Vein; Its Value and Its Limitations in Functional Diagnosis, J. Am. M. Assoc., Chicago, 1907, xlviii, 1105. V. Frey, M., and Krehl, L.: Untersuchungen ueber den Puls, Arch. f. Physiol., Leipz., 1890, 31. Hewlett, A. W.: On the Interpretation of the Positive Venous Pulse, Jour. Med. Re- search, Bost., 1907, xvii, 19. Minkowski, O.: Die Registrierung der Herzbewegungen am linken Vorhof, Deutsch. med. Wochnschr., 1906, xxxii, 1248. Zur Deutung von Herzarrhythmien mittelst des o?sophagealen Kardiograms, Ztschr. f. klin. Med., Berl., 1907, Ixii, 371. Rautenberg, E.: Xeue Methode der Registrierung der Vorhofspulsation vom Oesophagus nus, Deutsche med. Wchnschr., Leipz. and Berl., 1907, xxxiii, 364. Young, C. L, and Hewlett, A. W.: The Xormal Pulsations within the (Esophagus, J. M. Research., Bost., 1907, xvi, 427. Hirschfelder, A. D.: Observations on a Case of Palpitation of the Heart, Johns Hopkins Hosp. Bull, Baltimore, 1906, xvii, 299. Einthoven, W.: Le telecardiogramme, Arch, internat. de Physiol., Liege, 1906, iv, 132. Weiteres ueber das Elektrokardiogramm, Arch. f. d. ges. Physiol., Bonn, 1908, cxxii, 517. (See also chapter on Alterations of Rhythm.) AXALYSIS OF ALTERATIONS IN CARDIAC RHYTHM. The irregularities in rhythm of the heart may be divided first into three classes: (1) arrhythmias, in which there is no discernible order in the occurrence of beats; (2) allorrhy t hmia s (altered rhythms), in which, though the rhythm is not regular, yet the irregular beats occur according to a certain regular system, so that the arrangement of these 7 98 DISEASES OF THE HEART AND AORTA. beats in one section of the trading can be prophesied from a knowledge of another; and (3) pararrhythmias (Wenckebach), in which two separate rhythms are going on in either the same chamber or in different chambers at the same time. ALLORRHYTHMIAS. A. Of extracardiac origin. I. Neurogenic (sinus arrhythmias), due to more or less rhythmic reflex stimuli passing through the vagi and accelerators (toxic, reflex from various organs, respiratory reflexes from lungs) . a. Associated with the phases of respiration. 6. Not associated with respiration Mackenzie's youthful type. II. Due to disturbances in the filling and empty- ing of the heart from traction upon the heart and great vessel s dropping of beats without heart-block, pulsus paradoxus and Riegel's pulse. B. Of intracardiac origin. I. Due to disturbance in the conduction of normal impulses dropping of beats. 1. Auriculo- (atrio-) ventricular block. 2. Sino-auricular block. 3. Interventricular (?) block (hemisystole). II. Disturbance of contractilit y pulsus alternans, and failure to open the aortic valves. III. Occurrence of beats in response to abnormal stimuli or increased irritability. 1. Extrasy stoles, in which irregular beat is brought on by a single ab- normal stimulus. -r 7 , . , f Right ventricular, a. Ventricular < y, , i ( Left ventricular. {Right auricular arising near the superior vena cava (normal site). i u *u u* -i arising elsewhere in the right auricle. Left auricular, c. Auriculoventricular, arising in the cells of the conduction system. 2. Paroxysmal tachycardia. 3. Absolutely irregular pulse (auricular fibrillation). I. SINUS ARRHYTHMIAS 1 (OR REFLEX ARRHYTHMIAS). Alteration in cardiac rhythm resulting from intermittent stimuli passing down the cardiac nerves constitutes one of the most common forms of cardiac 1 The term sinus arrhythmia has boon applied to these forms by Mackenzie because the impulse for each beat arises in the sinus region of the heart. Strictly speaking, this does not exclude extrasystolcs having their origin at the region of the sinus, although these THE VENOUS PULSE AND ELECTROCARDIOGRAM. 99 SINUS ARRHYTHMIA AURICULOVEN- TRICULAR HEART-BLOCK ALTERNATING PULSE AURICULAR EXTRASYSTOLE VENTRICULAR EXTKASY8TOLE AURICULO VEN- TRICULAR EXTRASYSTOLE ABSOLUTE ARRHYTHMIA (AURICULAR FIBRILLATION PAROXYSMAL TACHYCARDIA FIG. 63. Diagram representing various types of irregular pulse. The heavy white arrows indi- cate the site of origin of the disturbance of rhythm. The heavy white lines indicate the course of the ab- normal cardiac impulses. RESP, respiration; AL'R. auricle; A-V or A VH, auriculovenl ricular bundle; YEXT, ventricle; CAR, carotid pulse; VEX, venous pulse; SIX, sinus region of the heart; i'VC, JVC, superior and inferior venae cavas, respectively. 100 DISEASES OF THE HEART AND AORTA. PLATE IV A \ V Electrocardiogram of sinus arrhythmia (respiratory), with diagram showing the course of the impulses within the heart. 1 The white areas upon the diagram represent the sinoauric-ular node of Keith and Flack, and the auriculoventricular bundle. The black arrow indicates the course of the impulses. A, A-\ , V, impulses in the auricle, auriculoventricular bundle and ventricles, respectively. f EX. .SYS. KxtrasvPtole arising at the node of Keith and Flack (homogenetic), with diagram showing the course of the normal and extrasystolic impulses. 'The writer is indebted to D.-. GI.-O. S. Bon 1 for the preparation of the electrocardiograms used Throughout the book. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 101 allorrhythmias. As has been seen (Chapter III), alterations of the pulse-rate may result from any stimulation of any afferent nerve, from skin, muscles, mucous membrane, and viscera, or from stimuli arising in the vagal or accelerator centres in the medulla. As Reid Hunt and Hooker have shown, the reflex stimulation may cause a slowing on the pulse-rate through stimulation of the vagus centre, or, under other circumstances and especially when of a different intensity, it may cause an acceleration of the pulse's rate. Hunt has shown that this acceleration is due chiefly to momentary cessation of the tonic stimuli in the vagus; but Hooker proves that there is also a stimulation of the accel- erators. Such afferent or sensory stimuli may arise in the skin and muscles, but especially in the viscera and the serous and mucous membranes. Reflex stimulation of this sort may reach the medulla: 1. From cortical excitement (emotion or neurasthenia). 2. From intracranial pressure (meningitis, brain tumor, etc.). 3. Reflexes from nasal septum. 4. Reflexes from abdominal organs (uterus, stomach, intestines, prostate, enteroptosis). 5. Increased irritability from toxic agents (tobacco, tea, coffee). 6. Adhesions or tumors along the course of the vagus. Mode of Production. Francois-Franck and Koblanck and Roeder have been able to produce such an arrhythmia by stimulating the mucous mem- brane of the nasal septum at a point just opposite the middle turbinate bone, and Stadler and Hirsch have done so by stimulating the walls of the stomach and intestines. There is normally a reflex slowing of the heart during swal- lowing, and similar periodic slowing of the rate from stimulations of the vagus may account for many of the disturbances of rhythm in air-swallowers. Moreover, Einthoven has shown, by recording the electrical variations in the peripheral stump of the divided vagus, that, with each inspiration, afferent stimuli are passing up the vagus, and these may evoke reflex responses when the entire nervous system is abnormally sensitive. Occurrence. Neurogenic arrhythmias are particularly common in chil- dren and in young persons, and hence are designated by Mackenzie as the ''youthful type,'' but this is only because the cardiac, vasomotor, and respiratory centres are in more labile equilibrium in them than in normal adults. However, whenever the nervous system becomes more irritable, from the occurrence of visceral reflexes, emotions, or toxic influences (bacterial toxins, alcohol, tobacco, coffee, etc.). stimuli (like those passing up the vagus) which are normally subminimal become effective. Honce allorrhyth- mias of this type arise in nervous individuals and in the so-called functional cardiac diseases or cardiac neuroses (Part IV, Chapter III). Einthoven, Flohil, and Battaerd have shown that stimuli pass up the vagi at each respira- tory movement. These stimuli aro normally too feeble to bring about reflexes, but when the irritability of the nervous system is increased stimuli which are ordinarily subminimal rise above the threshold and give rise to reflex inhibitions and accelerations; so that in some cases there is a scries of slow beats associated with inspiration and a series of rapid beats in expiration (Fig. 64), while in others the slowing occurs during expiration and the rapid really belong in a different category, nor does the term neurngenic arrhythmia exclude neurogenic heart -block, nor, perhaps, extrasvstoles in cases of flatulence, etc. A thoroughly satisfactory term has not as yet been devised. 102 DISEASES OF THE HEART AND AORTA. beats are during inspiration. This latter type is often spoken of as normal, but in perfectly normal individuals the rate may be absolutely regular. Reissner has shown that the irregularity is sometimes of psychic origin; or, in other words, that the stimulus exciting the cardiac nerves may descend from the cerebral cortex instead of ascending by the usual paths of afferent stimuli. This psychogenic arrhythmia is not extremely uncommon. Indeed, the writer, whose pulse has been regular at all other times, experienced such an irregularity upon one occasion of intense anxiety lasting for several minutes. The pulse became regular as soon as the anxiety passed off; and has remained so for five years, in spite of a severe tonsillitis and tonsillectomy. As Reyfisch has shown, similar neurogenic allorrhythmias occur in meningitis and in conditions with increased intracranial tension and, as Eyster has shown, in association with Cheyne-Stokes RESPIRATION RADIAL FIG. 64a. Respiratory arrhythmia. Pulse Threshold stimulus NORMAL Respiratory Vagus Currents Fia. 64b. Diagram showing the relation of the afferent impulses in the vagus to the threshold of irrita- bility of the medulla. +, medullary irritability increased. The tracing shows the respiratory arrhythmia. breathing. Mackenzie has also shown that there are many other cases in which neurogenic irregularity is not associated with the phases of respiration. In these it may be either periodic or entirely intermittent. It is most im- portant that the exact mode of origin of such stimuli and its characteristics should be carefully studied, since this arrhythmia must be dif- ferentiated from those of myocardial origin. Sinus arrhythmias also arise frequently during the course of organic or functional cardiac weakness, and are very often superposed upon an extra- systolic irregularity, but in these cases they are to be regarded as extracardiac manifestations rather than as disturbances in the heart itself. It is only in rare cases and in these of extreme irregularity, in which they may impair the nutrition of the heart by interfering with the rapidity of blood flow through the coronary arteries in a diseased organ, that their presence can be regarded as of practical importance. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 103 Laslett, however, has reported a case of a woman aged forty in whom a sinus arrhythmia gave rise to graver symptoms. The periods of vagus inhi- bition were accompanied by prolonged pauses lasting several seconds and giving rise to syncope and a typical Adams-Stokes syndrome, although no waves suggesting auricular contractions could be made out on the venous pulse. After atropine the pulse-rate rose to 100 and remained regular for 24 hours. The patient was also subject to short periods of inhibition, during which syncope did not occur, but in which she experienced a sensation of precordial pain and constriction exactly like that which is so commonly felt by patients with the milder forms of sinus arrhythmia accompanying the so-called cardiac neuroses (as in the case of A. S. quoted on page 701). In these cases, though the relation of the allorrhythmia to respiration may be timed by palpation and inspection, a careful venous tracing should be made lest an extrasystolic irregularity be diagnosed when it does not actually exist. Characteristics of Sinus Allorrhythmias. The striking feature of these neurogenic disturbances of rhythm is that they are often characterized by instability of rhythm, by the occurrence of rhythmic changes in rate rather than by the interpolation of beats which differ from the others in character. The beats usually occur in short groups, the first beat of the slower group being the longest, the rate of the more rapid series showing a progressive increase. The last beat of the rapid series, with the vagal pause following it, may be taken for an extrasy stole; but, on examining the few beats preceding, it will be seen that this beat was not premature and not due to an abnormal stimulus. This is further demonstrated by the electro- cardiogram, which is in every respect normal, the only variations in form being shown by slight variations in the height of the P, R, and T waves. Moreover, the beats are usually of full and almost equal strength, thereby differing from the feeble beats of extrasystoles; and they do not occur, as do the latter, abnormally early in the cardiac cycle. It is an irregularity in rhythm rather than an irregularity in force, though a certain degree of the latter may be present through the action of the vagus on the heart. The rhythm usually becomes regular within half an hour after the hypo- dermic administration of atropine, .0005 to .001 Gm. (yyo to -gV gr.). This rule is not invariable. When long pauses alternate with short series of rapid beats, the force of the first large beat may be slightly below that of the smaller beats, as shown by tracings with the Erlanger apparatus at or near the maximal pres- sure. With extrasystoles the systolic pressure of the smaller beats is usually less than that of the regular (large) beat. In both cases, however, this de- pends upon too many factors (time at which the extrasystole occurs, amount of systolic output, amount of peripheral resistance, factors causing the extra- systole, etc.) to be regarded as absolute criterion for diagnosis. II. Respiratory (Pulsus paradoxus and Riegel's Pulse). As will be seen in the chapters on adherent pericardium (page G02) and enteroptosis, traction upon the aorta during respiration may prevent the heart from emptying itself and thus cause the dropping of a beat in the arteries. Or, on the other hand, traction upon the great veins may produce the same effect by preventing the heart from filling. When there are adhesions in the posterior mediastinum 104 DISEASES OF THE HEART AND AORTA. or when the diaphragm is low, this dropping occurs during inspiration (pulsus paradoxus, Kussmaul), whereas when there are adhesions between the heart and the anterior chest wall it may occur in expiration (Riegel). ALLORRHYTHMIAS HAVING THEIR ORIGIN WITHIN THE HEART. III. Allorrhythmias due to Failure to Conduct Impulses Generated Normally Heart=block. 1 Of this there are several types. (1) Auriculo- ventricular Heart-block. The more usual, or at least better known, A SEC. JUG. APEX BRACK. FIG. 65. Venous tracings in heart-block. Partial heart -block 3 : 1 rhythm) during pressure on the vagus in a case of Adams-Stokes disease. type of blocking the impulses is at the auriculoventricular junction. In In this type no change occurs in the origination of the cardiac impulse or in the contraction of the auricles (atria), but the conductivity of the impulse to the ventricle by the bundle of His is impaired. Such impairment may be FIG. GO. Venous tracings in heart-block. Complete heart-block in a case of Adams-Stokes disease. (a) functional, from overstimulation of the vagus, of which frequent examples are seen in every laboratory experiment. Clinically this may be seen also in the cases of digitalis poisoning and postfebrile bradycardia, especially after pneumonia and influenza, occasionally also in cases in which there is a tumor pressing upon the vagus. (6) Organic, from interrup- tion of the bundle of His. In this case the block may be increased by giving 1 A full discussion may be found in Part III, Chapter XI. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 105 atropine or anything else that quickens the heart, or it may not be affected, (c) There may be a combination of the two effects (v. Tabora, Gibson, Thayer), the conductivity of the injured Purkinje fibres of the bundle being still further diminished by the action of the vagus upon them, and this effect outweighing the favorable action in slowing the auricular rhythm. The block may be partial or complete, depending upon whether the ventricles still follow the lead of the auricles or initiate their own rhythm. Thus, in the partial block the ventricles may respond to only every second, third, or fourth, or even only every sixteenth contraction, or may sometimes respond to every second, sometimes to every fourth beat, etc. On the other hand, they may fail to contract at all over a considerable period (stoppage), during which syncope (Adams-Stokes syndrome), epileptiform seizures, or death may set in (Erlanger), or, after a stoppage of greater or less duration, they may begin to beat at a rhythm of their own, bearing no relation at all to the rhythm of the auricles (complete block). This consti- tutes the permanent bradycardia of Adams-Stokes disease. (2) Sino-auricular Block. Sino-auricular block may also occur, the cardiac impulse being generated as usual at the mouths of the great veins and coronary sinus in the region homologous with the sinus venosus of the frog, but may fail to be communicated to the auricles. Keith and Schonberg have shown that this could scarcely be the result of a localized lesion, and would therefore depend upon the difference in the properties and irritability of auricular and venous musculature rather than organic block. The presence of such APEX FIG. C7. Occasional absence of apex impulse during inspiration simulating intervcntricular heart-block. block is assumed by August Hoffmann in paroxysmal tachycardia, in which there is a sudden doubling or even quadrupling of the pulse-rate during the attacks, and by Hewlett in digitalis poisoning. Experimentally they have been produced by Erlanger and Black- man on the excised mammalian heart , but both Hirschf elder and Eyster and the former observers failed to do so in the heart in situ. Colin and Kessel (Heart, 1912, iii) have recently produced such a block by excising the sino-auricular node in the perfused dog's heart; and Eyster has produced it in morphine poisoning. Gibson assumes the existence of a similar block in a case of Adams-Stokes disease, which he cites, along with the block at the auriculoventricular junction. (3) Interventricular Block (Hemisystole). V. Ley den in 1808 reported a case of bigeminal pulso in which he assumed that one ventricle was con- tracting without the other. This case and other cases reported by the older writers, and the cases reported more recently by Kraus and Nicolai, Hewlett and Schmoll, probably also admit of a different explanation. True hemisystole, the contraction of one ventricle without the other, has never been produced experimentally, even by Biggs, Barker and Hirschfelder, Trendelen- 106 DISEASES OF THE HEART AND AORTA. burg and Cohn, Eppinger and Rothberger, who have cut the individual branches of the His bundle. In some of these instances, just as Knoll, Fredericq, Fauconnier, and Stassen had found for the intact heart under vagus stimulation, there was a very slight asynchro- nism ( T Ju to T jj(j sec.) between the contraction of the two ventricles. Eppinger and Roth- berger have found, however, that when one branch of the His bundle is cut, a character- istic change occurs in the form of the electrocardiogram, the ventricular part of which then resembles the form due to an extrasystole arising in the ventricle whose branch is intact. The R wave is sometimes broader than is found with ordinary extrasystoles, and the P wave is of course present in the usual place. Eppinger and Stoerck have demon- strated the value of this finding for clinical medicine by establishing the diagnosis of a patch of myocarditis affecting one branch of the bundle but not the other in two cases in which their correctness was proved by autopsy. It must be admitted, however, that the electrocardiogram in these cases does not differ very much from that found in simple hyper- trophy, and confusion with the latter is possible. The number of cases reported thus far is too limited to judge of the ultimate estimate of this criterion for diagnosis. IV. Diminution in Contractile Power Pulsus alternans. When the contractile power of the heart diminishes, or, more frequently, when the rate is increased to the point that the heart has some difficulty in carrying out effectual contractions, it is found that the alternate contractions are of different size, some larger, some smaller, giving rise to the condition known as pulsus alternans or alternating pulse. 1 This is especially common in the FIG. 68. Alternating pulse in a case of paroxysmal tachycardia. tachycardias associated with some weakness of the heart muscle, and especially with paroxysmal tachycardia; but w r herever it occurs it is an expression of disproportion between the rate and contractility of the heart (or, in Engel- mann's terminology, between the chronotropic and i n o t r o p i c influences). Experimentally this can be readily shown by throwing induction shocks into the heart at a rate which it can barely follow. A pulsus alternans invariably results (Hirsch- felder, Hering). After a few seconds or minutes the heart has gained its full contractility and the alternating character disappears, only to reappear when it begins to weaken. The same phenomenon is also seen in attacks of paroxysmal tachycardia (Fig. 68). Pul- sufl alternans is also present in some cases of angina pectoris (Mackenzie). It then indi- cates that the heart is in a weakened condition. V. Dropping of Beat Owing to Too Low Contractility. If the auricle be stimulated directly at a rate still more rapid, it can no longer follow every single stimulus, but occasionally one beat is dropped out, just as is the case in a partial heart-block, although the stimulus is being applied directly to the auricle, which intermits a little more rapidly, and it follows only alter- nate stimuli. If the irritability of the auricle be now suddenly increased, as by pouring warm salt solution over it, it will suddenly respond with a contraction to each instead of to alternate stimuli, or it may respond occa- 1 Extrasystoles, giving typical electrocardiograms, may occur midway between regu- lar heats and give rise to an alternating pulse. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 107 sionally to all and occasionally to only alternate stimuli, giving an allorrhyth- mia 1:1 + 2:1. Thus we may have allorrhythmias simulating partial heart- blocks on the one hand, and extrasystoles on the other, due merely to general decrease in the irritability of the entire musculature without any special disturbance in conductivity; and just such inotrophic and bathmotrophic variations may be responsible for many of the so-called veno-auricular heart-blocks, such as have been described by Hewlett and Wenckebach. IRREGULARITIES DUE TO THE GENESIS OF ABNORMAL IMPULSES. EXTRASYSTOLES. In the majority of all cases of cardiac arrhythmia and almost all of those associated with severe functional or organic heart disease, the disturbance of rhythm is due to the presence of beats which arise at an abnormal site within the heart. The simplest form of abnormal impulse is seen in the single abnormal beat (extrasystoles, Engelmann; premature systole, Marey, Mackenzie) which, as Marey has shown, sets in almost immediately when a single elec- trical or mechanical stimulus is applied to the heart at any instant of diastole. During the period of systole and dur- ing the instant before it, an external stimulus does not alter the cardiac rhythm, and the heart is said to be in its refractory period. Extrasystoles may arise in any part of the heart either as the result of definite external stimuli or as the result of some change, organic or functional, in the part of the heart wall where it arises. Such a condition is often brought about by overstretching of the heart wall as a result of inability of the chamber to empty itself, a con- dition which is readily brought about by clamping the aorta or by increasing the peripheral resistance, and which is very commonly met with in the ven- tricles when the heart is failing or the blood-pressure too high, in the left au- ricle in the severer grades of mitral stenosis or regurgitation (mitralized pulse). Extrasystoles may also arise in perfectly strong hearts with normal blood-pressure when the irritability of the latter is increased by some toxic action, such as nicotin, digitalis, or the more or less obscure nitrogenous sub- stances which are absorbed from the intestines during intestinal putrefac- tion. It is possible that they may also be produced reflexly from irritation of the gastro-intestinal tract; but, though extrasystoles are relatively common in otherwise healthy persons suffering from flatulence and tympanites, no Fio. 69. Response of frog's ventricle to abnormal stimuli. (After Marey.) Electric shock thrown into it at the instant marked by the nick in the base line and by the dotted line. 108 DISEASES OF THE HEART AND AORTA. one has as yet reported their production experimentally from stimulation of the gastro-intestinal tract, and the mechanism by which they arise in these cases is still obscure. Lewis has produced ventricular extrasystoles by ligating one of the descending branches of the coronary arteries, and a similar association with coronary sclerosis is sometimes noted clinically, but whether the extrasystole then arises as the result of weakening of the muscle and overstretching of the wall or from an increased irritability of the fibres undergoing localized asphyxia cannot be stated definitely. That the latter is not the case would appear probable from the fact that extrasystoles are not common in the correspond- ing stages of general asphyxia; and, moreover, other localized injuries, such as injury of the heart muscle by injection of alcohol, iodine, silver nitrate, etc., are not followed by extrasystoles (Barker and Hirschfelder). Extrasystoles of Neurogenic Origin. Quite recently Rothberger and Winterberg have been able to induce extrasystoles by stimulation of the left accelerator nerves, but only in animals whose cardiac irritability had already been greatly enhanced by intravenous injections of barium or calcium chloride. The latter required doses ten times greater than the former. Such extra- systoles probably are closely analogous to those met with clinically in persons suffering from indigestion. Physiologically the condition of the heart in which extrasystoles occur is one of increased irritability, of which there are several stages. Hirschfelder has shown that if the dog's heart muscle be stimulated with a very weak alternating current, no change in rhythm occurs; if the current be made stronger, occasional extrasystoles set in; if it be still stronger, there is a sudden acceleration of the rate, which rises at one bound to almost double the previous rate, and at some time after cessation of the stimulus subsides as suddenly to the original rate; while with maximal stimuli the contractions suddenly change from the ordinary coordinate systoles to a series of inco- ordinate worm-like contractions (fibrillary contraction or fibrillation), in which each fibre or group of fibres contracts by itself and the surface of the chamber appears like a mass of writhing earthworms. As regards irritability, therefore, the extrasystoles may be regarded as the first stage in the scale. This scale of intensity is seen more or less clearly in the action of certain heart poisons such as digitalis and aconite; and, moreover, finds its analogon in the realm of pure physical chemistry. Bredig and Wilke have found that a similar irregularity occurs in rhythmic chemical reactions, such as the catalysis of hydrogen peroxide by mercury, when the intensity of the current generating them is increased. The record from a slightly increased current at first resembles that due to single extra- systoles; a greater increase shows marked acceleration and irregularity. Extrasystoles may arise spontaneously in any part of the heart wall, in the right or left auricle, the right or left ventricle, or in the auriculo ventric- ular bundle. Indeed, as Lewis and Wybauw have proved, they may arise in various parts of the same chamber, and the site of origin may in many cases be identified by moans of the electrocardiogram. As a rule, the extrasystole occurs very early in diastole, and the heart is still in the refractory period when the next impulse should arise, so that the THE VENOUS PULSE AND ELECTROCARDIOGRAM. 109 latter is replaced by a long pause (compensatory pause). Occasionally, however, especially when the cardiac irritability is increased, the next impulse may set in at the regular time, and the compensatory pause may be omitted. Under these circumstances the extrasystole is said to be " interpolated." Ventricular Extrasystoles. Ventricular extrasystoles are always accom- panied by full bigemini and usually by a single large napping venous pulsa- tion of very characteristic appearance which sweeps upward over the sterno- cleidomastoid, while the normal beats and the auricular extrasystoles are usually accompanied by smaller double undulations which do not reach higher than the lower border of this muscle and are often barely visible. The jugular tracing of a ventricular extrasystole shows a relatively large wave, sometimes single and sloping, often in plateau form, and occasionally with a crest which is surmounted by a second smaller undulation, produced FIG. 70. Tracing from the jugular vein (V. J. D.) and brachial artery (A. B. R.) in man, showing ventricular extrasystoles. Time markings in g seconds. E, extrasystoles arising in the ventricle (not pre- 3 [ 5 4 2 X4 2 ceded by an a wave). Time of the bigeminus (regular systole + extrasystole + pause) = = ^ L - o o by the contraction of the auricle which takes place at its regular time, as though the ventricle were beating regularly. It is impossible to differentiate by means of the venous tracing between extrasystoles arising in the right ventricle and those having their origin in the left. In many cases this may be guessed at with more or less accuracy by a knowledge of the general con- ditions of stasis and lesions, extrasystoles accompanying aortic disease, the high blood-pressure of nephritis, etc., being usually left sided, those accom- panying mitral stenosis and congenital heart disease arising usually in the right. The definite differentiation between right ventricular and left ventricular extrasystoles can always be made by means of the electrocardiograph, which gives typical tracings (Kraus and Nikolai, Kahn), especially when taken in the second lead (D 2 , right hand to left foot). The curves thus obtained are simple diphasic variations. In right ventricular extrasystoles there is a very large upstroke, higher than that corresponding to the regular beats and of longer duration, followed by a slow fall to below the base line; while in the case of the left-sided extrasystoles the curve is the mirror image of the right, and starts off with a very deep depression below the line which is followed by a slower rise above it (Plate V). Occasionally extrasystoles arising sometimes in on ventricle and sometimes in the other may be met with in the same patient and even in different parts of the same tracing (Plate VI). If the extra stimulus be applied to the ventricle, the latter responds with a premature contraction, then usually but not always misses the next impulse from the auricle and pauses for a while, until the second impulse 110 DISEASES OF THE HEART AND AORTA. PLATE V. R P R P R R R P R pR EXSYS E.XSYS Kindness of Interstate Medical Journal. Tracing showing auricular extrasystoles arising from an abnormal site (heterogenetic), with diagram showing the course of the extrasystolic impulse. The P waveg of the extraaystoiea are inverted. LXS^S .. A A-V \L Tracing tak<--n in Dl, showing an extra=y=tolo ari.-ine in the right ventricle, with diagram. The extra svstole is followed bv a contraction of the auricles P wave) occurring at the usual time. THE VENOUS PULSE AND ELECTROCARDIOGRAM. Ill PLATE VI. l**"^***** <^ If \"?" A A-V X I v I T Kindness of Interstate Medical Journal. Tracing taken in D2, showing an extrasystole arising in the left ventricle, with diagram. .ELEXS Tracing taken in D2, showing one cxtrasystole arising in the right ventricle and one arising in the left ventricle. 112 DISEASES OF THE HEART AND AORTA. from the auricle reaches it. We have, therefore, a normal contraction, a premature contraction, and the subsequent pause (which together may be termed a bigeminus), lasting as long as two regular contractions. The bi- geminus may be spoken of as a ''full bigeminus" when it lasts through two full cardiac cycles, and a "shortened bigeminus'' when the duration of regular systole + ex t r asy s t o 1 e + s u bs e q u en t pause is less than two cardiac cycles. Auricular Extrasystoles. When, however, the extra stimulus is applied to the great veins or the auricle, the bigeminus lasts less than two cardiac cycles if the stimulus follows closely upon the regular contraction, and exactly equal to two cycles if it is applied late (Hirschf elder and Eyster). If the stimulus is applied early, the auriculo ventricular (atrioventricular) conduc- tion time (a-c) interval is slowed. Later in the cycle it is unchanged. JL'G. BRACH. FIG. 71. Tracings from the jugular vein and brachial artery of a patient with trigeminal pulse due to the regular occurrence of two auricular extrasystoles (E, E) after each regular systole. The o wave and general form of the venous pulse are the same for the regular and the auricu ar extrasystoles. The two forms of extrasystoles occur clinically and may be differentiated by the analysis of the venous pulse; the extrasystoles of auricular (atrial) origin often give rise to shortened bigemini, while ventricu- lar extrasystoles always cause full bigemini. In the tracings of auricular extrasystoles one can see the auricular wave before the ventricular even in the extrasystole; the ventricular showing a single large wave due to ventricular systole, sometimes with the notch due to the con- traction of the auricle from reversed conduction of the impulse. Occasionally ventricular extrasystoles can be distinguished on inspection by the large flapping ''single' pulsa- tion in the jugular vein which accompanies them, in contrast to the double venous pulse of the normal beats and the auricular extrasystoles (Hirschf elder). The electrocardiograms of auricular systoles do not show the large and striking variations that accompany ventricular extras3 r stoles. Indeed, when the extra stimulus arises in the vicinity of the superior vena cava, the waves accompanying the extra stimulus differ from the normal only in being a little lower and in the fact that they occur much earlier than the normal. When, however, the extrasystole arises at an abnormal site (ectopic impulses), such as the region of the inferior vena cava or the left auricle, the P wave is in- verted and somewhat modified in form. Auricular extrasystoles occur most commonly in the irregularities accom- panying mitral disease and in patients suffering from paroxysmal tachycardia THE VENOUS PULSE AND ELECTROCARDIOGRAM. 113 and paroxysmal irregularity during the intervals between attacks. In the latter case especially they are liable to arise at an abnormal site. It seems probable that in the latter groups the extrasystoles represent a lower degree of the hyperexcitability which finds its expression in the paroxysms. A further advance in the clinical study of extrasystoles ia due to the clinical use of the electrocardiogram by Einthoven and his pupils, and more recently by Kraus and Nik- olai, Hering, and Lewis. Einthoven called attention to the presence of certain very peculiarly formed electro- cardiograms obtained from irregularly acting hearts. Kraus and Nikolai were able to reproduce these abnormal waves by producing extrasystoles in dogs; and found that extra- systoles arising in the right and left ventricles respectively produced curves which were the inverse of one another (Plate VI). Kahn in Bering's laboratory has been able to confirm these findings in great part. However, he calls attention to the fact that they do not hold absolutely, and shows that stimuli applied to neighboring points in right and left ventricles, near the apex, may elicit electrocardiograms which differ only slightly from one another. Stimuli which Cause Extrasystoles. The question as to the nature of the stimulus which gives rise to extrasystoles in man is of the greatest practical importance, for many writers (especially Fr. Miiller) are of the belief that they never occur unless the heart muscle is diseased. On the other hand, Mackenzie, whose observations have been extended over a period of fifteen years, regards them as of no special significance either in prognosis or in influencing the patient's manner of life. He mentions having advised one of his patients to continue playing football in spite of his extrasystoles, and adds that the extrasystoles disappeared! Experimentally it has been shown by Knoll, Marey, Hering, and others that ventric- ular extrasystoles may be produced whenever either the left ventricle or the right is pre- vented from emptying itself (i.e., by clamping the aorta or the pulmonary artery). In man they are also most common in conditions in which there is a high blood-pressure and the heart is just beginning to fail (chronic nephritis, myocarditis, aortic insufficiency), and probably fails to discharge a sufficient amount of its contents. This probably acts as a stimulus for a second extrasystole, as is frequently seen (pulsus trigeminus). Ventricular extrasystoles are most common in hearts whose rate is slow and hence which discharge a large amount of blood. They are particularly common at the end of the first third of diastole when the filling of the ventricle is nearing completion. The ventricular fibres are stretched more or less by the influx, and in conditions of increased irritability the stretch- ing of the fibres may act as a stimulus and give rise to the extrasystoles. Similar conditions are observed with reference to the auricle. Dr. Cameron, in the writer's laboratory, observed an instance of permanent bigeminal pulse in a dog due to the presence of a bubble of air in the right auricle. The air had entered from a hypodermic syringe during an intravenous injection. When the bubble was massaged out of the auricle the bigeminal pulse disappeared. It seems not improba- ble that mural thrombi may play a similar role, though it is certain that this is not always the case. Auricular extrasystoles may also be produced experimentally by causing a s t e n o- sis at the auriculoventricular orifices (Hirschf elder). Clinically they occur quite com- monly in mitral disease and most frequently begin at the time of the v wave, the very in- stant in the cycle at which the auricle is most distended (Fig. 71). Nevertheless, it must be confessed that much remains to be learned regarding the nature of the stimulus or stimuli, and the actual functional significance of extrasystoles. Palpitation with Extrasystoles. Extrasystoles are very frequently associated clinically with cardiac hypersesthesia in the form of palpitation, so that many clinicians erroneously regard all irregularities with palpitation 114 DISEASES OF THE HEART AND AORTA. as extrasystolic. However, it is possible that this hypersensibility about the heart may have some causal relation, since Hornung has shown that extrasystoles in the dog are most readily produced by stimulating in the vicinity of the cardiac nerves auriculo(atrio)ventricular and interventricular grooves and that they cannot be produced after cocainizing the epicardium. As stated above, Rothberger and Winterberg have produced them by stimulation of the cervical sympathetic branches, and stimuli along the sympathetics may also be responsible for their occurrence in cases of gastro-intestinal disease. It is certain that they are often brought on by constipation and flatulence in certain persons, but whether there is a myocardial lesion already present in these cases is a still open question. Ineffectual Contractions. AVhen the extras} T stole occurs early in diastole, the heart may not have recovered from the effect of the last systole sufficiently to generate a' forcible contraction. The aortic valves are not opened. The aortic second of the extrasystole disappears and the sounds change from 1234 12, etc.. to 123 -12, etc. By beating time to the regular beats it is sometimes possible to note that the total rhythm is unchanged by occasional ventricular extrasystoles. Such extrasystoles cor- respond to impulses on the apex and jugular tracings but not on the carotid. The variations in the force of the extrasystoles or in the beats of the absolutely irregular pulse are great. Occasionally, especially when the extra- systoles occur early in the cardiac cycle and there is a high peripheral resist- ance, the intracardiac pressure may not reach the aortic pressure and the aortic valves are not opened. The systole has been ineffectual (Frustrane Contractionen, Hochaus and Quincke). The compensatory pause after these may be so long and the circulation may be so poor that actual syncope simu- lating the Adams-Stokes syndrome (W. B. James) may take place in the interval between the regular beats. On the other hand, a great deal of cardiac energy has been expended without opening the cardiac valves and without propelling any blood. This increases the cardiac fatigue. Bigeminal and Trigeminal Pulses due to Extrasystoles. Very common forms of extrasystolic irregularity are those in which the extrasystoles recur after each regular beat; thus we may find every beat followed by a single extrasystole and compensatory pause, so that the pulse beats occur in pairs separated by pauses (pulsus bigeminus), or there may be two extrasystoles following regularly after each regular systole (pulsus trigeminus), as in Fig. 71. These may be of either the auricular or the ventricular type, dependent upon the site of the origin of the irregularity or of the so-called auriculo(atrio) ventricular type referred to below. As stated above, it is sometimes difficult to differentiate the auricular extrasystolic groups from the youthful type of arrhythmia, but this may usually be accomplished by the use of a sufficiently large close of atropine. As Hering has shown, ventricular extrasystoles frequently disappear under atropine or any other influence by which the pulse-rate is accelerated, so that the normal stimuli fall in at about the periods at which the abnormal stimuli would have fallen. The form of the venous pulse in ventricular extrasystoles is, however, characteristic. Auriculo(Atrio) ventricular Extrasystoles. It is also claimed by Hering and Rihl, Mackenzie and Wenckebach, Lohmann, Schmoll, Mackenzie and THE VENOUS PULSE AND ELECTROCARDIOGRAM. 115 Morrow, and others that extrasystoles may arise in the Purkinje cells of the conduction system, and that such extrasystoles are char- acterized by a shortening in the conduction time (a-c interval on the venous pulse), for the impulse is conducted simultaneously in both directions. VOLUME OF VENTRICLES BLOOD-PRESSURE SECONDS FIG. 72. Volume curve of the ventricles, showing the dilatation which followed the entrance of an air-bubble into the right auricle. (Kindness of Dr. Cameron.) The extrasystoles drive very little blood into the aorta. DIL, dilatation. Cushny has found the same thing in dogs poisoned with aconite, and Hirschf elder has repeatedly produced them in hearts whose excitability was increased by faradization. Rothberger and Winterberg have found that such extrasystoles give rise to a characteristic electrocardiogram with a very small P wave which occurs just before the R. Correspond- FiG. 73. Extrasystoles with shortened conduction time, supposed to arise in the auriculoventricular bundle. ing to the two ventricles, extrasystoles arising in the two branches of the bundle give absence of the P wave, a rather small R, and an inverted T. Gaskell has shown in frogs that if the tissue at the auriculoventricular junction was touched with a probe a series of extrasystoles set in both auricles and ventricle. And Bond has been able to watch this process in the frog, in which he could see the auriculoventricular FIG. 74. Variation in conduction time (a-c) in a case of mitral stenosis. muscle fibres contract first, and this was followed by the contractions of auricles and of the ventricle, which contracted at apparently the same instant. In mammals it cannot be decided whether the fibres of the conduction system conduct or merely contract, but extra- systoles in which auricles and ventricles contract simultaneously (nodal extrasystoles) are occasionally met with. Lohmann also observed them persisting after the tissue in the 116 DISEASES OF THE HEART AND AORTA. vicinity of the His bundle had been stimulated. In a later investigation upon the excised heart Lohmann poisoned the region of the venae cava? by means of cotton soaked in form- alin. He then sometimes saw extrasystoles set in spontaneously. The auricles and ven- tricles sometimes contracted simultaneously, sometimes there were ventricular extrasystoles. ASEG. JUG. APEX BRACH. FIG. 75. Tracing showing absolute irregular with weak ineffectual systoles (/, 7, 7) which do not open the aortic valves. S, onset of ventricular systole. Numerals refer to duration of cardiac cycle in tenths of a second. The venous pulse is of the ventricular type. Upon the clinical side there is little positive evidence. Peculiar extra- systoles often occur between attacks of paroxysmal tachycardia, but occa- sionally also in cases with simple valvular lesions. Keith has found patches of fibrous myocarditis in the vicinity of the His bundle in cases which had CAR. A-V BLOCK SIXO- AURICULAR BLOCK VAGAL SLOWING In,. 70. Diagram showing the alterations of rhythm which may cause a pubus bigeminus. The arrows indicate the incidence of stimuli ori. shown these extrasystoles, and thinks that they irritated the cells in the vicinity, but such scars are very common, and elsewhere in the heart are not known to act as irritative lesions. Moreover, the writer has never been able to produce them by pressure upon the bundle with an Erlanger clamp, injection of mercury into the left branch of the bundle, etc. So that in spite THE VENOUS PULSE AND ELECTROCARDIOGRAM, 117 of the interest in the subject it must be admitted that the occurrence of extrasystoles with shortened conduction time cannot be as yet regarded as absolute proof of a lesion near the His bundle, but only to heightened excita- bility of the latter. Prognosis and Treatment of Extrasystoles. From the stand-point of prog- nosis and treatment patients with extrasystoles may be divided into two groups: 1. Extrasystoles in otherwise normal hearts. 2. Extrasystoles in weak or overworked hearts. The pressure of occasional extrasystoles in an otherwise healthy person whose blood-pressure is normal and who does not become especially short of breath upon exercise may be entirely disregarded. As has been stated, they are particularly common when the pulse-rate is slow and may entirely disappear when the pulse-rate is quickened by atropine, nitroglycerin, or even by exercise. Mackenzie, indeed, cites the case of a young professional football player who, though otherwise healthy, was troubled by occasional extrasystoles and had been condemned by various physicians to a life of invalidism on this account, whose heart became regular again as soon as he began to enter into the heat of a game, which he played in his best form without the slightest inconvenience. The extrasystoles in themselves under these conditions do not demand treatment, unless they are accompanied by palpitation which distresses the patient, and in that case avoidance of excitement and fatigue and of an over- loaded stomach, temporary abstinence from tea, coffee, alcohol, and tobacco (and, if necessary, the administration of bromides may be resorted to), is the rule in young persons with otherwise normal hearts. In those cases which are secondary to flatulence, constipation, and gastro-intestinal fermentation, the pulse may become regular as soon as these conditions are remedied. If these do not suffice, small doses of digitalis may be given, but larger doses are more likely to increase the irritability of the heart, and hence the occurrence of extrasystoles, than to depress it. On the other hand, in persons with valvular disease or with high blood- pressure the presence of extrasystoles may be regarded as an indication that the ventricles are not driving out blood well at each systole, and therefore they may be a forerunner of impending danger. This is especially true when the number is increased by exertion and accompanied by dyspnoea. More- over, it must be borne in mind that Lewis has produced ventricular ex- trasystoles by ligating the descending branch of one of the coronary arteries; and the occurrence of extrasystoles as the result of coronary disease, especially in elderly individuals, must always be borne in mind ; but neither the presence of coronary sclerosis nor of any organic lesion whatever can be diagnosed from the presence of ventricular extrasystoles. In weakened or overworked hearts, regardless of the definite anatomical diagnosis, the presence of extrasystoles constitutes a definite indication for digitalis and the usual treatment of cardiac overstrain. Various Types of Allorrhythmia which may Result in a Bigeminal Pulse. It must be borne in mind that the bigeminal pulse is not pathognomonic of any single disturbance of function, but may occur in any of the following conditions (Fig. 76): (1) recurring ventricular extrasystoles; (2) recurring auricular extrasystoles; (3) recurring auriculo ventricular extrasystoles; (4) 118 DISEASES OF THE HEART AND AORTA. recurring slight auriculoventricular heart-block, the ventricle failing to follow every third beat; (5) recurring sino-auricular block (?), the auricles failing to respond to every third impulse; (6) recurring vagal prolongation of every alternate diastole. Similar conditions hold for the trigeminal pulse except that two extrasystoles or regular beats are interpolated before the pause. AURICULAR FIBRILLATION (ABSOLUTE ARRHYTHMIA; DISORDERLY RHYTHM; PULSUS IRREGULARIS PERPETUUS; PAROXYSMAL IRREGULARITY). One of the commonest and most characteristic forms of arrhythmia is that which is seen in many old cases of mitral stenosis and myocarditis in which the pulse has become permanently irregular. The beats come in groups in which no order is discernible; an irregularity in force and rhythm devoid of definite relation to the phases of respiration or of indications of heart- block, and free from the pairs of trios and associated beats which are charac- teristic of extrasystolic arrhythmias. No two parts of the curve resemble one another, and, in contrast to the extrasystolic arrhythmias, weak beats may follow the longer pauses just as well as strong beats. On this account it was termed "Absolute arrhythmia" or "Disorderly rhythm" by Mackenzie, and, on account of its frequency among the cases of persistent arrhythmia, the desig- nations "Pulsus irregularis perpetuus" (Hering), "Arrhythmia perpetual" (Gerharclt), and "Perpetual arrhythmia" (Hewlett) were applied to it also. The patients are usually, but by no means always, weak, cyanotic, and subject to shortness of breath upon the slightest exertion. Their jugular veins are full and, owing to the increased venous pressure, stand out prominently across the sternocleidomastoid, showing the pouches above the venous valves. Often there is little or no pulsation, but in many cases a "single" venous pulse may be made out with one impulse accompanying the pulse in the carotid. When a tracing of the venous pulse is taken, this wave is seen to be of the ventricular type, a single plateau or an M-shaped crest throughout ven- tricular systole, with no indications whatever of an auricular contraction (a wave absent). Occasionally, as in Fig. 47, there is no positive pulsation, but the midsystolic (x) depression becomes so deep as to represent the most prominent wave upon the tracing. Tracings taken from the oesophagus in this form of arrhythmia show only the contractions of the ventricle (Hewlett, Clerc and Esmein). The exact nature of this form of arrhythmia was long a matter of doubt. Mackenzie, at first, relying upon the absence of the a wave and the general form of the pulse, believed that the auricles were absolutely paralyzed, and that the impulse no longer arose at the usual site but in the tissue of the His bundle at the node of Tawara; and accordingly he designated this form of arrhythmia as "Nodal rhythm." Later he thought that the auricles and ventricles were contracting, and hence the wave of auricular contraction superposed upon the c wave could not be made out. In support of this view, he presented the findings in a number of autopsies, by Keith, of patients who had died with this form of arrhythmia in which there were sclerotic myocardial lesions (supposed to be irritative) in the vicinity of the His bundle. Cushny and Edmunds, and Hewlett, as the result of experiments upon dogs, suggested that this form of irregularity might result from fibrillation THE VENOUS PULSE AND ELECTROCARDIOGRAM. 119 of the auricles; but no real support was given to this view until 1909, when Rothberger and Winterberg and Lewis showed that the electrocardiogram in such cases assumed a very characteristic form, upon which the two ventric- ular waves (R and T) are well marked, but the single presystolic (P) wave is absent, and replaced by a series of undulations irregular in size, in form, and in rate, and taking place continuously throughout systole and diastole of the ventricle. The average rate of these fibrillar contractions varies from about 450 to about 1000 per minute; the slower ones being larger and approaching more nearly to forcible contractions, the rapid ones smaller and feebler and approximating a condition of absolute paralysis. Moreover, exactly the same form of electrocardiogram and exactly the same irregularity could be produced in dogs when the auricles were caused FIG. 77. Perpetual arrhythmia of the ventricles. (After Jolly and Ritchie.) Tie small wavelets (a) are due to auricular fibrillations. to fibrillate by faradization or other means, and this form of electrocardio- gram corresponded to no other known condition. These fibrillations, as is seen from the electrical variations, are accom- panied by impulses which may pass down the His bundle and stimulate the ventricles, but which do so at a rate too fast for the latter to follow, and hence they respond to only occasional stimuli. In the dog this may give rise to either a regular rate at about doubled velocity or to an absolute arrhythmia, but in man the electrocardiograph shows that auricular fibrillation always brings about an irregular rhythm. Fibrillary contractions of the auricle are, as Cushny and Edmunds and Rihl have shown, too feeble to produce any definite waves upon the venous pulse and hence the latter assumes the ventricular type, often shewing small undulations during diastole (Fig. 77). The ventricular type of venous pulse, on the other hand, does not always correspond to an auricular fibrillation, but, as Lewis has shown, whenever a ventricular pulse accompanies a perfectly regular rhythm in man, the electrocardiograph shows that the auricle is still contracting (P wave present). 120 DISEASES OF THE HEART AND AORTA. The finer and coarser forms may have some clinical significance, for the coarser type occurs, as a rule, in cases in which compensation is established or nearly so, while the type of finer contractions is more common in cases with badly broken compensation. Occasionally, indeed, a reversion from the finer to the coarser type of contraction occurs in the same patient, accompany- ing improvement in the clinical condition, but it is doubtful whether this manifestation may be regarded as of importance in prognosis. The. presence of auricular fibrillation does not exclude the other forms of disturbance, but it may be accompanied by sinus arrhythmias, extrasys- toles, and even heart -block in the same patient. Although auricular fibrillation gives rise to the most common form of perpetual irregularity, it is by no means always perpetual. Cases are frequently encountered, especially in incipient heart-failure of mitral stenosis or myocardial insufficiency, in which the irregularity sets in only occasionally, often arising suddenly and subsiding suddenly, as is the case with true paroxysmal tachycardia, with which it is closely associated (see page 669). The rate remains rapid and irregular for a period which may vary from a few minutes to hours, days, or weeks, during which the patient usually feels weak, often a little light-headed or giddy, and with a feeling of flutter- ing in the chest and sometimes definite precardial oppression, and shortness of breath on slight exertion. The attacks may at any time subside suddenly and spontaneously to the regular rate which is normal for the patient, whose health and vigor are then suddenly restored, just as is the case in idiopathic paroxysmal tachycardia. Occasionally, as in a case reported by Lewis, true paroxysmal tachycardia passes into this form of arrhythmia, a transition which in to strange, since, as Hirschfelder has shown, the functional disturbances are clearly allied, and indeed seem to represent a difference of degree of hyperirri- tability rather than an essential difference in mode of origin. Moreover, as Lewis and Fox have shown, paroxysms of absolute irregularity usually become more and more frequent, more and more prolonged, and finally merge into a condition of permanent irregularity, whereas paroxysmal tachycardia may persist for decades without increase in severity or impairment of the general health and without definite association with any organic lesion. Anatomically the usual lesions of myocarditis are found in these cases, but in addition Schonberg, Keith and Joy Mackenzie, and Hedinger have never failed to find lesions in the superior vena cava at the veno-auricular junction (node of Keith and Flack). In view of the fact that from a physio- logical stand-point the condition corresponds merely to a condition of hyper- irritability of the auricular tissue, it is still questionable whether all cases correspond to definite lesions of the myocardium. As regards treatment, the cases of auricular fibrillation with perpetual arrhythmia and myocardial weakness represent the conditions in which the most favorable actions of digitalis are to be obtained. (Edens, Cushny, Windle). The beneficial effect of digitalis in these cases lies largely in its stimulat- ing action on the vagi, which still act on the fibrillating auricle, as has been shown by stimulating those nerves directly in dogs (Hirschfelder) and by direct pressure upon the neck in man (Wenckebach). Moreover, as Cameron has shown, digitalis in therapeutic doses markedly increases the THE VENOUS PULSE AND ELECTROCARDIOGRAM. 121 PLATE VII. \ \ Absolute arrhythmia due to auricular fibrillation of the coarse type, with diagram showing the origin and transmission of the impulses. mam \W\ 'Mil' IT \ Absolute arrhythmia due to auricular fibrillation of the fine typ", with diagram showing the origin and transmission of the impulses. 122 DISEASES OF THE HEART AND AORTA. tonicity of the heart muscle, and thus tends to prevent the overfilling of the ventricles which results from the arrhythmia. Still further, by increasing the force and raising the blood-pressure it increases the blood flow through the coronary vessels (Bond) and thus improves the nutrition of the cardiac muscle. There is a certain proportion of cases in which the irritability of the ventricle is already extreme and the rate rapid, in which digitalis has little or no beneficial effect, and in some cases may even be harmful. These are chiefly the cases in which the vagi have already lost their power to slow the heart, and in which the ventricle is already in a state of hyperirritability, perhaps contracting entirely independently of the impulses that pass down from the fibrillating auricle (i.e., in which there is a condition of auricular fibrillation and heart-block and ventricular tachycardia). In dealing with the paroxysmal arrhythmias we are confronted with two distinct problems: 1, to ward off the attack; 2, to abort it after it has arisen. The first step in the prevention of the attack lies in a careful study of the factors (reflexes from diseased organs, abdominal distention, excesses in Baccho et venere, overexertion, worry and emotional excitement, etc., seem to bring them about) and the removal of these as far as possible. The next is to institute a general tonic treatment of the circulatory system, with graded exercises, baths, and regular life, to bring the patient up to his maximum of general bodily vigor. If the heart is dilated or the patient shows signs of circulatory weakness between the attacks, small doses of digitalis may be resorted to. If the attacks are frequent or increasing in frequency, the patient should be put on absolute rest for some time (see p. 219), for, as can readily be shown in experimental fibrillation, each attack increases the irritability of the auricle and renders the heart more susceptible to the next. During the attack itself, absolute rest and small quantities of milk or very light food constitute the first essential. Aromatic spirits of ammonia may be taken at the very beginning of the attack. If the paroxysm bids fair to last more than a few hours, one or two large doses of digitalis, digalen, or digipuratum may be given promptly, or strophanthin may be given intra- muscularly or intravenously. The prognosis in cases of auricular fibrillation depends chiefly upon the allied lesions and functional power of the heart. Fox's observations indicate that unless great care is taken paroxysms of arrhythmia are liable to become increasingly frequent and lead to permanent irregularity and death within a few years; but, on the other hand, it is sometimes possible, by careful avoid- ance of the repetition, to bring the heart back to its normal irritability and save the patient from further attacks, as was done for the soldiers of the Civil War by da Costa long before the nature of the arrhythmia was known. More- over, even when once established and permanent, the mere presence of an absolute arrhythmia need not be an alarming symptom. About three years ago the writer was consulted by a medical student, twenty-three years of age, who had always been quite healthy up to the previous summer, when, after an attack of tonsillitis and heavy work as summer honor officer in a hospital, he began to feel rather weak, easily fatigued, and short of breath on exertion, and noted that his pulse was irregular. Venous tracings showed an absolute arrhythmia without a trace of a wave, and an average rate of about 80. The heart was otherwise normal, and, though rather THE VENOUS PULSE AND ELECTROCARDIOGRAM. 123 too stout and easily fatigued, the patient's condition seemed otherwise good. Dieting and exercise until his weight was reduced from 196 to 179 pounds brought about a considerable improvement in his general condition, and, though his pulse has never become regular, he has passed through an attack of appendicitis and the strain of a subsequent operation, as well as another year and a half's work as surgical house officer in a busy hospital, without any recurrence of cardiac symptoms. Dr. Mackenzie has noted similar persistence of absolute arrhythmia, and believes, also, that, as long as the functional capacity of the heart is not interfered with, the persistence of auricular fibrillation need not be regarded as of grave significance. However, patients in whom this is the case are in the minority, and in the greater number the onset of a permanent auricular fibrillation is to be regarded as the first step in the vicious circle: Permanent A arrhythmia \ Weak and Slow irritable heart circulation ^^ Impaired nutri- p tion of heart cells PARARRHYTHMIAS. In some of the allorrhythmias separate rhythms may be noticed in the different chambers, either conducted to one another and interfering peri- odically, or not conducted (heart-block). Wenckebach, who first called attention to this, has proposed the name pararrhythmia for these forms. The simplest example of this would be the bigemini. Another ex- ample would be seen if, without loss of conductivity, spontaneous contrac- tions would occur in the ventricles as the usual slow rate, and these go on simultaneously with the regular beats following the auricles, though with occasional pauses due to interference. Cushny has shown this to occur in digitalis poisoning, and it is. not improbable that it may explain many other- wise undecipherable arrhythmias, though little work has been done along these lines up to the present. DIFFERENTIAL DIAGNOSIS OF ARRHYTHMIAS BY ORDINARY PHYSICAL EXAMINATION. In spite of the elaborate apparatus necessary for exact functional analy- sis of the arrhythmias, a very fair idea of their nature in any given case can be obtained by the ordinary methods of physical examination. A sinus arrhythmia may in most cases be diagnosed by the fact that it is usually composed of a series of 2-4 short beats alternating with a series of 2-4 long ones. The venous pulse is either absent or normal in appearance; and the veins of the neck are usually rather empty, often barely discernible, and there is little or no irregularity in force, discernible to the palpating finger or made out by the dropping of a few of the beats as the pressure is raised in a blood- 124 DISEASES OF THE HEART AND AORTA. pressure cuff upon the arm. Moreover, in most cases they are accentuated in deep inspiration or in deep expiration but disappear when the breath is held. The serial character of the beats is made out better in listening over the heart than in palpation at the wrist. In the irregularities due to pericardial adhesions (pulsus paradoxus and RiegePs pulse) there may be irregularity in force and not in rhythm, the veins of the neck dilate in one or the other phase of respiration, and this corresponds to the period when the pulse is smaller or entirely absent. The existence of heart -block can always be suspected when the pulse- rate is below 42. The diagnosis can frequently be made from the presence of more than two pulsations over the jugular vein for each beat in the carotid, y YL.ACCEL. ! I A/dLr'ww. iwSu^ FIG. 78. Diagram showing abnormal electrocardiograms and the structures in which they arise. R.ACCEL, electrocardiogram resulting from stimulation of the right accelerator nerve; P, S, T waves increased, R wave diminished. L.ACCEL, effect of stimulating the left accelerator; P and R waves diminished, S wave increased, T wave inverted. .1. FIBRILL, auricular fibrillation, P wave absent, replaced by numerous small undulations. .St'P V.C.EXSYS, right auricular extrasystole arising in the vicinity of the lower end of the superior vena cava (especially in the vicinity of the Keith-Flack node): all the waves normal. I\F V.C.EX SYS, right auricular extrasystole arising in the vicinity of the inferior vena cava; P wave inverted. L.A.EXSYS. extrasystole arising in the left auricle; P wave inverted. R V.HYPERT, hypertrophy of the right ventricle, all the waves normal, but R wave increased. L. T . HYPERT, all waves, but especially the R wave inverted; or 5 wave increased. R V EX .?}'.*, extrasystole arising in the right ventricle, showing an absence of the P wave, and an abnormal ventricular wave, consisting of a large initial wave followed by a depression and a second smaller wave. LV EXSYS, extrasystole arising in the left ventricle, showing a large initial depression followed by a large -low wave. A-V EX.^YS, extrasystole arising in the node of Tawara or the His auriculoventricular bundle, accompanied by synchronous contraction of auricles and ventricles, showing absence of the P wave and slightly abnormal ventricular wave.-. R .4-1" B. electrocardiogram due to a myocardial lesion affecting the right branch of the auriculo- ventrirular bundlr>: /' wave normal, other waves resembling those due to a left ventricular extrasystole. L A-V B. electrocardiogram due to a myocardial lesion affecting the left branch of the auriculoven- trirular bunrtschritte in der Diagnostik der Herz- krankheiten, Deutsch. med. Wchnschr., Leipz., 1908, xxxiv. 13. Hunt. R.: Direct and Reflex Acceleration of the Mammalian Heart, Am. J. Physiol., Bost., 1S99, ii, 395. Hooker. D. R.: May Reflex Cardiac Acceleration Occur Independently of the Cardio- inhibitory Centre? ibid., 1907, xix, 417. Mackenzie, J.: The Study of the Pulse and Movements of the Heart, Lond., 1903. Franoois-Franck, Ch. A.: Contribution a 1'etude experimentale des nevroses reflexes d'ori- gine nasale. Arch, de physiol. de 1'homme. Par., 1889, 5 ser.. i. 538. Contribution a 1'etude de 1'innervation vasodilatatrice de la muqueuse, ibid.. 1889. i. Koblanck and Roeder. H.: Experimented Untersuchungen zur reflektorischen Herz- arhythmie, Arch. f. d. ges. Physiol., Bonn, 1908, cxxv, 377. Stadlcr, E., and Hirsch, C.: Meteorismus und Kreislauf, Mitth. a. d. Grenzgeb. d. Med. u. Chir., Jena, 190(3, xv, 449. Reyfi.sch: Klinische und experimented Erfahrungen ueber Reizungen des Herzvagus, Berl. klin. Wchnschr., 1905, 1468. Reissner, O.: Ueber unregelmassige Herztfitigkeit auf psychischer Grundlage, Ztschr. f. klin. Med., Berl., 1904, liii. 234. Einthoven, W., Flohil, A., and Battaerd, P. J. T. A.: On Vagus Currents Examined with the String Galvanometer, Quart. Jour. Exper. Physiol., Lond., 1908, i, 243. Eystt-r. J. A. E.: Clinical and Experimental Observations upon Cheyne-Stokes Respira- tion. Jour. Exper. M., Xew York and Lancaster, 1906, viii. 565. Kussmaul. A.: Ueber schwieliege Modia-stino-pericarditis und paradoxen Puls, Berl. klin. Wchnschr., 1S73, x, 433, 445, 461. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 129 Riegel, F.: Ueber extrapericardiale Verwachsungen, ibid., 1877, xiv, 657. Keith, A., and Flack, and Schonberg: See Chapter I. Hewlett, A. W. : Digitalis Heart Block, J. Am. M. Assoc., Chicago, 1907, xlviii, 47. Erlanger, J., and Blackman, J. R.: A Study of the Relative Rhythmicity and Conduc- tivity in Various Regions of the Auricles of the Mammalian Heart, Am. J. Physiol., Bost., 1907, xix, 125. Hoffmann, Aug. : See chapter on Paroxysmal Tachycardia. Hirschfelder, A. D., and Eyster, J. A. E. : Extrasystoles in the Mammalian Heart, Am. J. Physiol., Bost., 1907, xviii, 222. Kraus, Fr., and Nikolai: Ueber das Elektrokardiogramm unter normalen und patho- logischen Verhaltnissen, Berl. klin. Wochnschr., 1907, 765, 811. Kahn, R. H.: Ueber das Elektrokardiogramm kiinstlich ausgeloster Herzschlage Zentralbl. f. Physiol., Leipz. and Vienna, 1909, xxiii, 444. Hewlett, A. W.: Heart Block in the Ventricular Walls, Arch. Int. Med., Chicago, 1908, ii, 139. Biggs, L. N. H.: Investigation of the Bundle of His in Rabbits' Excised Hearts Perfused with Locke's Fluid, Brit. M. J., Lond., 1908, i, 1419. Barker, L. F., and Hirschfelder, A. D.: The Effects of Cutting the Branch of the His Bundle Going to the Left Ventricle, Arch. Int. Med., Chicago, 1909, iv, 193. Cohn, A. E., and Trendelenburg, W.: Untersuchungen zur Physiologic des Uebergangs- blindels am Saugetierherzen nebst mikroskopische Nachpriifung, Arch. f. d. ges. Physiol., Bonn, 1910, cxxxi, 1. Eppinger, J., and Rothberger, J.: Ueber die Folgen der Durchschneidung der Tawara- scher Schenkel des Reizleitungssystems, Ztschr. f. klin. Med., Berl., 1910, Ixx, 1. Eppinger, J., and Stoerck: Zur Klinik des Elektrokardiogramms, ibid., 1910, Ixxxi, 157. Fauconnier: Sur 1'onde de contraction de la systole ventriculaire, Arch, internat. de physiol., Liege, 1907, v, 122. Knoll, Philip: Ueber Incongruenz in der Thatigkeit der beiden Herzhalften, Sitzungsb. d. k. Akad. d. Wissensch. Math-naturw. Cl., Vienna, 1890, xcix, 31-53, 6. Fredericq, Leon: La pulsation du cceur du chien est une onde de contraction, etc., Arch. internat. de physiol., 1906, iv, 60. Stassen, M.: De 1'ordre de succession des differentes phases de la pulsation cardiaque chez le chien, Arch, internat. de physiol., 1907, v, 600. Von Leyden, E.: Ueber ungleichzeitige Kontraction beider Ventrikel, Arch. f. path. Anat., 1868, xliv, 365. Kraus, F., and Xicolai, G. F. : Ueber die funktionelle Solidaritat der beiden Herzhalften, Deutsche med. Wchnschr., 1908, xxxiv, 1. Aschoff, L., and Tawara, S.: See chapter on Acute Myocarditis. Hirschfelder, A. D.: Observations upon Paroxysmal Tachycardia, Johns Hopkins Hosp. Bull, Bait., 1906, xvii, 337. Hering, II. E.: Ueber Herzalternans, Mlinchen. med. Wochnschr., 1908, Iv, 1417. Mackenzie, J. : See chapter on Angina Pectoris. Wenckebach, K. F.: Beitriige zur Kenntniss der menschlichen Herztatigkeit, Arch. f. Physiol., 1906; 1907, i. Lewis, T. : The Experimental Production of Paroxysmal Tachycardia and the Effects of Ligation of the Coronary Arteries, Heart, Lond., 1909-10, i, 98. Hirschfelder, A. D.: The Functional Disturbances in Paroxysmal Tachycardia, Arch. Int. Med., Chicago, 1910, vi, 380. Recent Studies upon the Electrocardiogram and upon the Changes in the Volume of the Heart, Interstate M. J., St. Louis, 1911, xviii, 557. Bredig, G., and Wilke, D.: Erregung und Beeinflussung katalytischer Pulsationen (lurch elektrische Strome, Bioc. Ztschr., Berl., 1908, xi, 67. Lewis, T.: Galvanometric Curves Yielded by Cardiac Beats Generated in Various Areas of the Auricular Musculature, The Pace-maker of the Heart, Heart, Lond., 1910, ii, 23. Lewis, T., Oppenheimer, B. S., and Oppenheimer, A.: The Site of Origin of the Pace-maker of the Mammalian Heart-beat; The Pace-maker of the Dog, ibid., 1910, ii, 147. "Wybauw: Sur le point e d'origine de la systole cardiaque dans I'oreillelte droite, Arch, in- ternat. de physiol., Liege, 1910, x, 78. 9 130 DISEASES OF THE HEART AND AORTA. Rothberger, C. J., and Winterberg, H.: Ueber die experimentelle Erzeugung extrasystolis- cher Tachycardie durch Acceleransreinzung, Zentralbl. f. Physiol., Leipz. and Wien, 1911, xxv, 189, and Arch. f. d. ges. Physiol., Bonn, 1911, cxlii, 461. Engelmann: Ueber die Leitung der Bewegungsreize im Herzen, Arch. f. d. ges. Physiol., Bonn, 1894, Ivi, 149. Ueber die Ursprung der Herzbewegungen, ibid., Ixv. Cushny, A. R., and Matthews, S. A.: On the Effects of Electrical Stimulation of the Mam- malian Heart, Jour. Physiol., Camb., 1897, xxi, 214. Hirschf elder, A. D. : Inspection of the Jugular Vein; its Value and its Limitations in Func- tional Diagnosis, Jour. Am. M. Assoc., Chicago, 1907, xlviii, 1105. Lewis, T. : Single and Successive Extrasystoles, Lancet, Lond., 1909, i. Miiller, Fr. : Nervous Affections of the Heart, Arch. Int. Med., Chicago, 1908, i, 1. Mackenzie, J.: Diseases of the Heart, Lond., 1908. Knoll, Ph.: Ueber die Veranderungen des Herzschlages bei reflectorischer Erregung des vasomotorischen Nervensystems, sowie bei Steigerung des intracardialen Drucks iiberhaupt, Sitzungsber. d. k. Akad.d. Wissensch., Wien, Abth. Ill, 1872, Ixv-lxvi, 195. Marey: La circulation du sang a 1'ctat physiologique et dans les maladies, Par., 1881. Hering, H. E.: Zur experimentellen Analyse des unregelmassigen Herzschlages, Arch. f. d. ges. Physiol., Bonn, 1900, Ixxxii. Ueber continuierliche Herzbigeminie, Deutsch. Arch. f. klin. Med., Leipz., 1904, Ixxix, 175. Ergebnisse experimenteller und klin- ischer Untersuchungen ueber den Vorhofvenenpuls bei Extrasystolen, Ztschr. f. exper. Path. u. Therap., Berl., 1905, i, 26; also his pupils. Rihl, J.: Experimentelle Analyse des Venenpulses bei den durch Extrasystolen verur- sachten Unregelmassigkeiten des Saugethierherzens, ibid., 1905, i, 43. Pan, O.: Ueber das Verhalten des Venenpulses bei den durch Extrasystolen verursachten Unregelmassigkeiten des menschlichen Herzens, ibid., 1905, i, 56. Hirschfelder, A. D.: The Volume Curve of the Ventricles in Experimental Mitral Stenosis and its Relation to Physical Signs, Johns Hopkins Hosp. Bull., Bait., 1908, xix, 319. Mackenzie, J.: The Extrasystole, Quart. J. M., Oxford, 1908, i, 481. Gerhardt, D.: Beitrag zur Lehre von den Extrasystolen, Deutsch. Arch. f. klin. Med., Leipz., 1905, Ixxxii, 509. Hoffmann, Aug.: Arhythmie des Herzens, Deutsch. med. Wchnschr., Leipz., 1906, xxxii, 1682. Ueber die Entstehung der Extrasystolenirregularitat, Miinchen. med. Wchn- schr., 1907, liii, 1987. Dehio, K.: Einfluss des Atropins auf arhythmische Herztatigkeit, Deutsch. Arch. f. klin. Med., Leipz., 1894, lii, 97. Hering, H. E.: Experimentelle Untersuchungen ueber Herzunregelmassigkeiten an Affen, Ztschr. f. exper. Path. u. Therap., Berl., 1906, ii, 525. Hering, H. E., and Rihl, J.: Ueber atrioventrikulare Extrasystolen, ibid., 1906, ii, 510. Gaskell, W. H.: The Properties of Cardiac Muscle, Schafer's Text-book of Physiology, Lond., 1900, ii. Lohmann, A.: Zur Automatic der Briickenfasern des Herzens, Arch. f. Physiol., Leipz., 1904, 431; and Supplbd., 265. Ueber der Funktion der Briickenfasern an Stelle der grossen Venen die Ftihrung der Herztatigkeit beim Siiugetiere zu tibernehmen, Arch. f. d. ges. Physiol., Bonn, 1908, cxxiii, 628. Mackenzie, J.: Inception of the Rhythm of the Heart by the Ventricles, Brit. M. J., Lond., 1904, i, 529. Abnormal Inception of the Cardiac Rhythm, Quart. J. M., Oxford, 1907, i, 39. Mackenzie, J., and Wenckebach, K. F.: Ueber an der Atrioventrikulargrenze ausgeloste Systolen beim Menschen, Arch. f. Physiol., Leipz., 1905. Rothberger, J., and Winterberg, H.: Ueber die Beziehungen der Herznerven zur atrio- ventricularen Automatic (nodal rhythm), Arch. f. d. ges. Physiol., Bonn, 1910, cxxxv, 559. Schmoll, E.: Paroxysmal Tachycardia, Am. J. M. Sc., Phila. and X. York, 1907, cxxxiv> 662. Mackenzie, R., and Morrow, W. S.: Cardiac Arrhythmia due to Extrasystoles Originating in the Bundle of His, Am. J. M. Sc., Phila. and X. York, 1908, cxxxv, 534. Cushny, A. R.: See chapter on the Action of Drugs. Hering, H. E.: Ueber die haufige Kombination von Kammervenenpuls mit Pulsus irreg- ularis perpetuus, Deutsch. med. Wchnschr., Leipz., 1906, 213. THE VENOUS PULSE AND ELECTROCARDIOGRAM. 131 Gerhardt, D.: Arhythmia perpetua des Puls, Deutsch. med. Wchnschr., Leipz., 1907, xxxiii, 448. Hewlett, A. W. : On the Interpretation of the Positive Venous Pulse, J. M. Research, 1907-8, xvii, 119. Clinical Observations on Absolutely Irregular Hearts, J. Am. M. Ass., Chicago, 1908, li, 655. Theopold, J.: Ein Beitrag zur Lehre von der Arhythmia perpetua, Deutsch. Arch. f. klin. Med., Leipz., 1907, xc, 77. Hering, H. E.: Das Elektrocardiogramm des Pulsus irregularis perpetuus, ibid., 1908, xciv, 205. Mackenzie, J.: The Study of the Pulse and Movements of the Heart, Edinb. and Lond., 1902; Diseases of the Heart, 2d Ed., N. Y., 1910. Clerc, A., and Esmein, Ch.: Etude critique de la pulsation cesophagienne chez 1'homme, Arch, de mal. d. cceur, etc., Par., 1910, iii, 1. Lewis, T.: Auricular Fibrillation: A Common Clinical Condition, Brit. M. J., Lond., 1909, ii, 1528; Auricular Fibrillation, Heart, Lond., 1910, i, 306. Rothberger, J., and Winterberg, H.: Vorhofflimmern und Arythmia perpetua, Wien. klin. Wchnschr., 1909, xxii, 1091. Winterberg, H.: Studien liber Herzflimmern, Arch. f. d. ges. Physiol., Bonn, 1909, cxxviii, 471. Radasewsky: See chapter on Chronic Myocarditis. Ueber die Muskelkrankungen der Vorhofe des Herzens, Ztschr. f. klin. Med., Berl., xxvii. Schonberg, S.: Ueber Veranderungen im Sinusgebiete des Herzens bei chronischer Arhythmie, Frankf. Ztschr. f. Path., 1908, ii, 153. Miiller, G.: Ungewohnliche Dilatation des Herzens und Ausfall der Vorhofsfunktion, Ztschr. f. klin. Med., Berl., Ivi, 520. Quincke, and Hochhaus, J.: Ueber frustrane Herzcontractionen, Deutsch. Arch. f. klin. Med., Leipz., 1894, liii, 414. James, W.: Clinical Study of Some Arrhythmias of the Heart, Am. Jour. M. Sc., Phila. and N. York, 1908, cxxxvi, 469. Hirschfelder, A. D.: Contributions to the Study of Auricular Fibrillation, Paroxysmal Tachycardia, and the so-called Auriculo (Atrio)-ventricular Extrasystoles, Johns Hopkins Hosp. Bull., Bait., 1908, xix, 322. Hoffmann, A.: Neue Beobachtungen ueber Herzjagen, Deutsch. Arch. f. klin. Med., 1903, Ixxviii, 39. Cushny, A. R., and Edmunds, C. W. : Paroxysmal Irregularity of the Heart and Auricular Fibrillation, Am. Jour. M. Sc., Phila., 1907, cxxxiii, 66; and Studies in Pathology, Quatercentenary Public., Aberdeen Univ. Engehnann, 1. c. Trendelenburg, W.: Untersuchungen ueber das Verhalten des Herzmuskels bei rhythm- ischer elektrischer Reizung, Arch. f. Physiol., Leipz., 1903, 271. V. X-RAY EXAMINATION. The discovery of the X-rays by Rontgen in 1895 introduced a new era in cardiac diagnosis. By this means we can now actually see the heart, observe its outlines with accuracy, and note the changes of position and of contour with different phases of respiration, and even to a certain extent the changes from systole to diastole. All these data, when obtained with proper precautions, are absolutely accurate, and have greatly supplemented the observations made by percussion. 1 METHODS OF EXAMINATION. Most of the facts desired in the study of the circulatory system with the X-ray may be gained by means of inspection with the fluoroscope, a screen of barium platinocyanide or calcium tungstate which is rendered luminous wherever the X-rays strike it. A tube of low vacuum ("soft tube") should be used, one which shows the bones of the hand black without re- vealing their internal structure, and the tissues of the hand a fairly dark gray. The patient's chest wall should be at least 50 cm. from the screen. Recently the usual distance has been increased to 2 M. (64 ft.)- at which the rays are almost parallel. It is sometimes best to interpose a lead screen, with adjustable opening, between the patient and the tube in order to cut off all the rays except those emanating from a small part of the anticathode, thereby securing the greatest possible definition of focus. Indeed, Immelmann found greatest definition when the opening in the lead screen was only 1 cm. Often a lead cylinder (Albers-Schoenberg) is very satisfactory. It is also important that no large objects be placed near the cathode, as rays striking these may also generate secondary rays which affect the fluoroscope or photographic plate and thus blur the outline of the original image (Walter). For securing sharp images it is preferable to keep a number of tubes with vacua of different degrees which may be interchanged, rather than change the vacuum in each tube. Changing the latter shortens the life of the tube by heating the platinum target and causing the latter ultimately to become bent, so that the rays are not reflected uniformly from its surface. The X-ray image is a true shadow formed by the cutting off of rays and not by their refraction, and the shadow is magnified in proportion as the object is nearer to the tube or farther from the fluoroscopic screen. 1 Examinations with the X-ray require a very special technic, for which the student is advised to consult the special text-books upon the subject, especially: Albers-Schoenberg: Die Rontirentechnik, Hamburg, 1906. Gocht, II.: Handbuch der Rontgenlehre zum Gebrauche fur Mediziner, 2te Aufl. Stuttgart, 1903. Williams. V . 11.: The Rontgen Rays in Medicine and Surgery. New York, 1903. Beck, C.: Rontgen-ray Diagnosis and Therapy. Kassabian: Rontgen Rays and Electro-Therapeutics, Phila., 1909. 132 X-RAY EXAMINATION. 133 In fluoroscopic examination it is most important for the observer to accustom his eyes to the darkness before turning on the current. It is a well-proved physiological fact that the longer the sojourn in darkness the greater the delicacy of vision. Hence the exami- ner's vision is improved by closing or blindfolding his eyes or by going into a dark room some ten or fifteen minutes before the patient; and the examining room should be lighted only enough to permit the patient to undress and assume the proper position. The exami- ner may also keep his head under a dark hood or wear heavily smoked glasses during this time so as to accustom his eyes to the darkness. In looking over the areas of light and shadows each region should be studied carefully and in detail, the size and shape of the shadow, the clear- ness of the outline, and the distribution of areas of half shadows as well as of full shadows. Not of least importance are the so-called pulmonary figures, the half-tone shadows of pulmonary vessels, of bronchial glands, and of strands of adhesions. 1 Not only the full shadows but especially these half shadows should be examined with care, for an interpretation not apparent at first may become clear after a few minutes' observation. Radiographers are, moreover, in the habit of looking at the fluoroscope through half- closed eyes in order to intensify the contrast. This may be further intensified by the use of dark glasses. The writer has also found it very useful to look at the shadow or skiagraph through a biconcave lens which at once sharpens the contours and intensifies the contrasts. Often an area may be indefinite during quiet breath- ing or expiration and become quite definite on forced deep inspiration, or it may become so by simply turning the patient so that the rays pass through his body in a different direction. These and similar precautions, like a care- ful physical examination, reveal the unsuspected, and distinguish the skilled examiner from the unskilled. The Cardiac Shadow. The heart shadow thrown upon a screen at the front of the chest is shown in Fig. 81. It will be noted that the outline of the shadow closely resembles the area of relative dulness on percus- sion, except that the former extends upward over the manubrium sterni, where it is due to the presence of the latter and of the great Vessels FIG. 80. Radiograph of normal chest. (After /. , i i T .1 i v. Ziemmsen and Rieder.) Tube behind the chest and not oi the heart. In the second p kte in front. left inters p ace the s h a d o w of the pulmonary artery is seen, and in the second right that of the aorta. Occasionally a small prominence is seen to the left of the sternum arising at the arch of the aorta. This is sometimes mistaken for an aneurism, but if the patient be turned a little it will be seen to be due to the curving of the aorta (Holzknecht) . Oblique Illuminations. Much can be learned by turnini: the patient about and examining him in several planes, as was first performed by v. Criegern and Holzknecht (1. c.), and later by Rieder, who suggested the 1 See chapter on Adherent Pericardium. 134 DISEASES OF THE HEART AND AORTA. following cardinal directions (Fig. 81): (1) dorsoventral ; (2) ventrodorsal; (3) sagittal from right; (4) sagittal from left; (5) from right posterior to left anterior; (6) from left posterior to right anterior; (7) from left anterior to right posterior; (8) from right anterior to left posterior. FIG. 81. X-ray shadows in different axe.* of the body. (Modified from Holzkreeht. The arrows show the direction of illumination and position of the tube corresponding to the shadow. A f > aorta; PA. pulmonary artery; LA. left auricle; RA, right auricle; LI", left ventricle; RV, right ventricle. In 3 there is a metal sound in the oesophagus. By the examination in these planes every part of the heart can be brought into view, even the left auricle, which escapes observation in almost all other methods of examination but appears quite clearly when the tube is placed at the back or behind the right scapula. The oblique and trans- verse examinations should never be omitted. X-RAY EXAMINATION. 135 THE ORTHODIAGRAPH. The shadow of the heart and vessels upon the screen or plate is hvays larger than the objects themselves. In order to obviate this when measuring out the heart F. Moritz devised an instrument known as the orthodiagraph (Fig. 82). FIG. 82. A simple form of orthodiagraph. (After Gillet.) FIG. 83. Diagram showing the use of the ortho- diagraph. 1, first position; 2, second position; P, pencil; FLUOR, fluorescent screen. In the orthodiagraph the fluorescent screen and X-ray tube are fixed upon each arm of a large L T -shaped frame in such a way that the patient may stand or lie between the two arms of the U and the rays thus pass through his body to the screen. At the point upon the screen which is exactly opposite to the centre of the anticathode or target of the tube, a small hole is pierced, and a skin pencil is fixed in place here so that the site of this spot can be marked upon the body of the patient. The whole t'-shaped frame bearing the tube and fluoroscope is movable in two directions by any one of a variety of mechanisms, so that the perpendicular ray can be brought opposite any desired point. A series of points corresponding to the exact con- tour can thus be marked off, and when these are joined with lines the exact outline of the heart is repre- sented. As shown by Fig. S3, this furnishes a means of determining the size of the heart or any organ with absolute accuracv. FIG. 84. Orthodiagrnphic outline of normal heart, showing Morit7,'s conjugate*. MR, midline to right border (greatest distance); ML, midline to left border; L, oblique longitudinal; Q, transverse; numerals indi- cate centimetres. The outlines and mobility of the heart thus obtained are discussed on page 147. It is also possible with the fluoroscope to watch the individual con- tractions of the heart and to note the changes in size due to systole and 136 DISEASES OF THE HEART AND AORTA. diastole, but this is very difficult and can rarely be done with satisfactory accuracy. On the other hand, the contractions of the auricles can be seen with considerable definiteness, and dissociation of rhythm, heart-block, can often be diagnosed in this way by simple inspection (Kraus, Gibson). PERMANENT RADIOGRAPHS. For obtaining permanent photographs a " medium soft " tube (Moritz scale W 6 B W 5) is used in connection with a Wehnelt electrolytic inter- rupter and an induction coil with proper self-induction yielding a 40 to 60 cm. spark. The patient is laid upon a table with the tube above or below him, as is most suitable to the purpose of the examination. In order to absolutely immobilize him it is well to support the shoulders upon sand bags. He may also be examined standing by immobilizing the shoulders to prevent blurring of the picture. Skiagraphs of the chest made with very short exposures have proved particularly valuable, since they give greater definition (Rieder). Teleroentgenography. Recently the need for the orthodiagraph Has been obviated to a great extent by taking permanent radiographs at a distance of 150 to 200 cm. from the patient, in which the rays are so nearly parallel that the shadow of the heart is never more than 5 mm. larger than the heart itself, and the individual borders are not displaced more than the thickness of an ordinary chalk line (2 mm.) (Koehler). Such radiographs are, of course, much more objective records and preserve many more details than are furnished by the orthodiagraphic outlines, and are in this respect much more valuable, and the need of an expensive and cumbersome apparatus is also removed. If satisfactory pictures are not obtained in this way, it may be necessary to back the plates with an " intensifying screen " (Verstarkungsschirm) of calcium tungstate, etc., exactly similar to the screen of the fluoroscope, which intensifies the action of the rays upon the plate. By the use of such intensi- fying screens it has been possible to obtain satisfactory radiographs of the thorax with exposures of 1/10 to 1/20 sec. (Rieder and Rosenthal) or even 1/100 sec. (Dessauer). Dessauer has found that these can be made if the tube is strongly illuminated (anticathode red) before the plate is exposed, especially if an unusually large anticathode is placed in the tube. The expo- sure takes place through a slit in a lead disk which is rapidly rotated by a motor in front of the plate. Weber has devised an apparatus whereby such instantaneous photographs may be taken at any given phase of the cardiac cycle, and has obtained very interesting pictures in this way. His method for obtaining this instant in the cycle, which depends upon the use of a selenium cell, is very elaborate and cumbersome, and a much simpler and more satisfactory solution of the same problem can be obtained by using a slight modification of the apparatus devised by Hirschfelder and Eyster for obtaining a series of induction shocks at exactly the same phase of the cardiac cycle. This apparatus consists of two part, the first being a sphyemograph tambour arranged to give an electric contact when its lever is lifted in systole, and the second consisting of a X-RAY EXAMINATION. 137 clockwork device arranged to rotate for a definite period after the sphygmograph contact has been made, after which it sets off a second electric contact operating either the X-ray coil or a shutter in front of it so as to give an instantaneous exposure at the instant desired. The first part of the apparatus differs somewhat from the original apparatus of Hirsch- f elder and Eyster in the manner in which the contact is made, for in their experiments systole was recorded by the downstroke of the lever, which was allowed to dip into a pan of mercury, while in the clinical sphygmographs systole is recorded by an upstroke. In order to use the clinical sphygmograph or the ordinary tambour for this purpose, one of the bright metal parts should be well wrapped with the end of an elsewhere insulated copper wire to be used in the circuit. The second contact consists of a piece of platinum wire or foil which is bent in such a way that when mounted and fastened upon the sphygmograph by means of thread or rubber bands the sphygmograph lever will just touch it on the up- stroke and leave it on the downstroke. This contact should be insulated from the metal parts of the tambour by interposing a piece of paper, fibre or rubber, and it should be con- nected with a piece of insulated copper wire so that the upstroke of the lever may close a circuit through the two wires leading from the tambour, while the downstroke breaks it. The second or clockwork part of the apparatus consists of a set of wheels driven by a spring in the usual manner. One of these wheels bears a small outrigger which is caught by the lever from an electromagnet when the circuit through the latter is open, and released when the lever is moved by closing the circuit. When this magnet is connected with the wires from the sphygmograph tambour this represents the instant of systole. Upon the axle of the same wheel or a second wheel of the clockwork there is set an arm bearing a platinum wire which is just long enough to dip into a small pan of mercury fixed to the base-board but insulated from it. The arm is adjustable on the axle so that the arc through which it moves from the time the outrigger is released until it reaches the mercury may be varied at will. A binding post is made to connect with the metal work of the clockwork and another to connect with the mercury pan, so that when the arm dips into the latter a second circuit is closed, and this circuit may be arranged to operate the X-ray exposure. It is preferable to have the X-ray tube inclosed in a metal box and to allow the above-mentioned contact to close a magnetic circuit operating a photographic shutter of metal placed in front of the tube. Each upstroke of the sphygmograph lever thus sets the clockwork in motion, giving rise to an electric current which passes through the latter at any desired instant later in the cardiac cycle. This exposure may be repeated an indefinite number of times always at the same instant after the onset of systole, so that the summated exposures upon the plate have the same effect as a single instantaneous photograph at the same instant, only much more intense. By taking a series of such plates at successively later instants in the cardiac cycle a scries of pictures which are practically kinetoscopic can be readily obtained. Rontgen Kinematographs. Levy-Dorn, Eykman, and Dessauer and Grocdel have taken kinematographic pictures of the heart-beat. In Groedel's apparatus designed for this purpose a series of 24 plates, each provided with an intensifying screen, are pushed one after another into place by the rotation of a spiral, one turn of which represents a dis- tance of one centimetre. As in Dessauer's instrument, the exposure takes place through a slit in a lead disk which is rotated by the same belt as the spiral and at the same speed. The changing of plates occurs automati- cally during the period when the film is covered by the disk, the exposed plate being shoved into a padded box below before the new one is pushed into place. Kinetoscopic pictures have not yet come into general use, but promise to open a new field for the study of the heart. Stereoscopic Radiographs.- Still better also than the study of single plates are stereoscopic pictures, which can be made by taking two pictures with the tube moved 6.0 cm. laterally between exposures. In order to secure the best results, the two exposures should occur before the 138 DISEASES OF THE HEART AND AORTA. patient has had time to move, and hence a special apparatus should be used for automatic moving of the tube and changing of plates. The plates are then viewed in the Wheatstone stereoscope. Stereoscopic radiographs do not have the flat appearance of ordinary radiographs, but all the organs stand out plastically, showing themselves in perfect perspective and thus establishing the spacial relations of each shadow to the neighboring organs. It becomes easy to determine whether an object is located in the anterior, middle or posterior portion of the chest and whether an object like a tumor, aneurism, or mass of glands is pointing backwards or forwards... By obtaining a clearer view of the form of the object and the relations of the surrounding shadows, it is often possible to determine that a certain shadow which upon the single plate cannot be distinguished from a solid mass is actually made up of conglomerate smaller masses, and thus mediastinal tumors and fused tuberculous glands can often be distinguished from aneurisms with much greater definiteness than is possible upon the single plate. Similarly the plastic appearance causes strands of adhesions to stand out more clearly and facilitates their differentiation from ordinary lung figures. In some cases it is possible even to differentiate pleuritic de- posits from intrathoracic structures by this means. So great, indeed, are the advantages of the stereoscopic over the ordinary X-rays that in all doubt- ful cases the former should be resorted to, and the last word upon the diagnosis has not been said until this has been done. BIBLIOGRAPHY. Rontgen, W. K.: A New Form of Radiation, Science, N. York and Lancaster, 1896, X. S. iii, 726 and 729. Barker, Geo. .: The Rontgen Rays. Memoirs by Rontgen, Stokes, and Thompson, X. Y. and Lond., 1S99. Michelson, A. A.: Theory of the X-ray, Am. Jour. Sc., 1896, 4th ser., i, 312. Rowland, II.: Xotes of Observations on the Rontgen Rays, ibid., 1896, 4th ser., i, 247. For details regarding the secondary rays see: Walter, B.: Physikalisch technische Mitteilungen, Fortschr. a. d. Geb. d. Rontgenstrah- len, Hamb., 1900, i, 82. Faulhaber: Ueber eine durch Sekundarstrahlung bedingte Erseheinung auf Rontgen- platten, ibid., 1903, vi, 93. Holzknecht, G.: Die rontgologische Diagnostik der Erkrankungen der Brusteingeweide, Hamb., 1901. Das radiologischc Verhalten der normalen Brustaorta, Wien. klin. Wohnsohr., 1900. Cotton, W.: Some Principles and Fallacies of X-ray Interpretation, Practitioner, Lond., 1906, Extra Xo. on X-rays, 100. v. Criegern: Ergebnisse der Untersuchung des menschlichen Herzens mittolst fluores- cirenden Schirmes, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1S99, xvi, 302. Rieder, II.: Die Untersuchung der Brustorgane in verschiedemm Durchleuchtungsricht- ungen, Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamb., 1902-03, vi, 115. Moritz, F.: Ueber die Be.stimmung der wahren GrOsse von Gcgenstanden mittels des Rontgenverfahrens, Miinchen. med. Wchnschr., 1900, xlvii, 590, 902. Ueber ortho- diagraphische Untersuchungen am Herzens, ibid., 1902, xlix, 1. Ueber Tiefenbe- stimmungen mittels des Orthodiagraphcn und deren Yerkiirzungen bei der Orthodia- graphie des Herzens zu ermitteln, Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamb., 1904, vii, 169. Levy-Dorn: Schutzmaassregeln gegen Rontgonstrahlcn und ihre Dosirung, Deutsche med. Wchnschr., Berl. und Leipz., 1903, xxix, 921. X-RAY EXAMINATION. 139 For numerous forms of orthodiagraphs of Moritz and Albers-Schoenberg (1. c.), but what seems to the writer to be the most convenient and simple form is the apparatus de- scribed by: Gillet: Ein Orthorontgenograph einfacher Konstruction, Forthschr. a. d. Geb. d. Rontgen- strahlen, Hamb., 1906, x, 114. For the examination of the heart cf. also Moritz, F. : Einige Bemerkungen zur Frage der perkutorischen Darstellung der gesammten Vorderflache des Herzens, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxvii, 276. Dietlen, H.: Ueber Grosse und Lage des normalen Herzens und ihre Abhangigkeit von physiologischen Bedingungen, ibid., 1906, Ixxxviii, 55. Levy, M.: Ueber Abkiirzung der Expositionszeit bei Aufnahmen mit Rontgenstrahlen, Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamb., 1897, i, 75. Rieder, H., and Rosenthal, J.: Ueber Moment-Rontgenaufnahmen, Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamb., 1900, iii, 100. Rieder, H. : Neue Ausblicke auf die weitere Entwicklung der Rontgendiagnostik, Miin- chen. med. Wchnschr., 1908, Iv, 381. Koehler, A.: Teleroentgographie des Herzens, Deutsche med. Wchnschr., Leipz., 1908, xxxiv, 186. Dessauer, F.: Instantaneous Radiography in Less than 1/100 of a Second; a New Method of Radiography, Med. Rec., N. Y., 1909, Ixxv, 890; and Rontgen Moment Aufnahmen, Miinchen. med. Wchnschr., 1909, Ivi, 1075; also Rontgen Aufnahmen in weniger als 1/100 Sekunde, Ztschr. f. Elektrol. u. Rontgen., Leipz., 1909, xxv, 1095. Groedel, F. M.: Die Technik der Rontgen Kinematographic, Deutsche med. Wchnschr., Berl., 1909, xxxv, 434. Hirschfelder, A. D., and Eyster, J. A. E.: Extrasystoles in the Mammalian Heart, Am. J. Physiol., Bost., 1907, xviii, 222. Weber, A.: Eine Methode zur Darstellung von Herzmoment Aufnahmen in verschiedenen Phasen der Herz Revolution, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1910, xxvi, 673. VI. PHYSICAL EXAMINATION. While it is impossible to enter into a treatise upon physical exami- nation, a few points which are of special importance in cardiac cases may be discussed. General Appearance. The general appearance of the patient, expres- sion and color, are of great importance. The position which he naturally assumes in bed, the presence or absence of dyspnoea and orthopncea, the general degree of nervousness or dulness are all to be noted. The typical appearance of the cardiac patient (cardiac fades) is characterized by an anxious expression, bright eyes with moist, glistening conjunctiva?, cheeks full rather than sunken as in the abdominal facies, and as a rule a tinge of cyanosis about the lips. There are two main types: (1) the mitral (or mi t rot r icuspid) facies, with rosy, flushed cheeks, dilated capillaries, and cyanosis (most commonly seen in mitral stenosis); and (2) the aortic facies, with pale, often sallow, rather sunken cheeks, bright eyes, moist conjunctive, and slight cyanosis of lips and fingers. To these might be added (3) the subicteric facies of broken compensation, with pallor, subicteric conjunctive, and cyanosis of the lips. Nasopharynx. The tonsils and posterior nasopharynx should always be carefully examined. The former are the chief portals of entry for the germs of rheumatism, while adenoids and affections of the nasal septum may of themselves induce cardiac arrhythmia, and may also be an important contributing factor in the attacks of asthma in organic heart disease. Ophthalmoscopic Examination. The eye-grounds should always be examined when arteriosclerosis (page 260) or congenital heart disease (page 438) is suspected. Neck. In the neck especial attention should be directed to the visible throbbing of the carotids, the fulness of the neck, and the size and consist- ency of the thyroid gland (page 689), the presence of thrills and murmurs over vessels or thyroid, or a tracheal tug (page 631). The jugular pulsation is discussed in full in Part I, Chapter IV, page 70. Chest. The form of the chest is of considerable importance, not only as regards kyphosis. but particularly as to its fulness or flatness (see Part III. Chapter III). In recording this, the width of the costal angle should be noted, and the general obliquity of the ribs in quiet expiration should be designated by noting the vertebral spines which are on the same level with the sternoxiphoid articulation (normally at the level of the eighth thoracic spine) (page 702). It should be noted whether the chest in quiet breathing ap- proaches more nearly to the position of expiration, flat chest, or to that of inspiration. Pulsations, bulgings, heaving, or retractions of the ribs or interspaces, as well as the presence of abnormal shocks and thrills, should of course be noted. Abdomen. In the abdomen the important features to be noted are presence or absence of ascites, enlargement of liver (systemic 140 PHYSICAL EXAMINATION. 141 stasis), pulsation of the liver, systolic impulse (tricuspid insuffi- ciency), systolic retraction (dilated or hypertrophied right ventricle), the nature and the time of epigastric pulsation (systolic elevation being trans- mitted from the abdominal aorta, systolic retraction indicating dilated hypertrophied right ventricle). A palpable spleen of cardiac origin points to infarction, septic or thrombotic. When aneurism or arterio- sclerosis is suspected the course of the abdominal aorta should be mapped out by deep palpation with both hands, one above each side of the aorta and that vessel between them (page 648) . The genitalia should of course always be examined for signs of gonor- rhoea and lues, urethral smears for the former and a Wassermann reaction for the latter being made whenever possible. Extremities. Upon the extremities the presence of oedema and arthritis, acrocyanosis or pallor, and the size, consistency, and uniformity of the brachial, radial, femoral, popliteal, and dorsalis pedis arteries are the chief points of importance. THE CARDIAC IMPULSE. Mechanics of the Cardiac Impulse. The apex itself, as shown by Ludwig and Dogiel, does not move appreciably up or down during systole; and, as Hesse has demonstrated, the transverse diameter of the heart shortens more than the longitudinal. The chief movements which lead to the production of the apex impulse are due more to the systolic erection of the heart upon the great vessels than to its diminution in size. If one watches the exposed heart of a dog, cat, or rabbit, it is seen to execute two move- ments in systole: (1) the general contraction affecting chiefly the transverse diameter of the heart, and (2) a twisting about of the apex from left to right and forwards. This torsion of the apex is the resultant of the several lines of traction exerted by the muscu- lature of the right and left ventricles upon the base of the aorta and pulmonary artery, and modified by the pivoting of the heart against the vertebral column and by the shifting of its centre of gravity owing to variation in its liquid content. The tendency of this move- ment is to push the apex of the left ventricle against the chest wall, while the left wall of the left ventricle and the right (anterior) wall of the right ventricle move inwards toward the septum. Wherever in man these walls are in contact with the chest wall these inward movements give rise to retraction of the interspaces above them. The surface of the thin-walled right ventricle moreover is actually pulled inwards during systole, so that there may actually be an indentation of its surface which still further contributes to the systolic retraction. Protrusions and Retractions. A variety of protrusions and retractions of the interspaces may be seen to occur with each cardiac contraction. Graphic records of the impulse have been taken by means of the polygraphs described above, the receiving funnel being placed over the area of pulsation exactly as for a jugular or carotid tracing. Tracings can be made either with a rubber- Fid. 85. Movements of the heart leading to the protrusions and retraction during sys- tole. Forces shown by the arrows. 142 DISEASES OF THE HEART AND AORTA. covered spring tambour like that used for the carotid, or with an open funnel ; the former exerting pressure upon the apex, the latter merely recording the com- pression or rarefaction of the air in the funnel due to the impulse. The writer also finds that a funnel, made from a soft rubber stethoscope tip stoppered tightly with a perforated rubber stopper penetrated by a glass tube and bearing a rubber tip, is very satis- r factory (Fig. 86). The movements seen may be divided as: (1) Lifting of the entire precordium, which results, especially in flat-chested individ- uals or in those with very large hearts, from the systolic erection of the heart as a whole as it pivots against the vertebral column behind and pushes against the chest wall in front. This is usually seen in hearts which from any cause whatever are beating heavily, though it is most marked over large hearts. (2) The normal type of apex beat consists of a large protrusion synchronous with and lasting throughout the duration of ventricular systole (Fig. 88. I, s-d), usually preceded by a small presystolic wavelet (a-s), due FIG. 86. Rubber funnel for car- diographic tracings. APEX CAROTID APEX 3t..is.9cM cd c dsd c d cd cd cd cd cd cd cd 4TH LEFT INTERSPACE JUGULAR FIG. 87. A, tracing from the apex impulse and carotid artery: c. time of carotid wave; d, time of dicrotic notch. Upper line give.* the time in \ sec. B. cardiogram obtained over a normal apex. C and D. cardiogram over the fourth left interspace 5 cm. from costal margin (systolic retraction), from the same individual as B. to systole of the auricles. The large ventricular wave is followed by a fall in early diastole, coincident with the fall in intraventricular pressure. After this fall there is sometimes a small upstroke of the lever (passive protrusion of the apex by the inrushing blood) which may terminate in a small protodiastolic wavelet (;>). This protodiastolic wavelet corresponds PHYSICAL EXAMINATION. 143 to the shoulder upon the cardiac plethysmogram at the end of ventricular filling (page 11), and is particularly marked in cases in which a third heart sound can be heard (Thayer) . In cases with hypertrophy of the left ventricle the protrusion is usually very forcible and heaving throughout systole dome-like protru- sion, choc en dome (Bard). Occasionally, however, especially when there is some hypertrophy of the. right ventricle, the systolic protrusion may not last throughout ventricular systole, but may be represented by only a momentary protru- sion, followed by a retraction during midsystole (Fig. 88, III). Such a beat, which really represents the algebraic sum of the systolic protrusion over the left ventricle and the systolic retraction over the right, may be in. IV. FIG. 88. Various forms of apex tracings. I. Normal, showing presystolic (auricular) wave a, systolic plateau s-d, and the curve of ventricular filling d-p, ending in the protodiastolic wavelet p. II, Normal apex beat showing only systolic elevation. III. "Mixed" type of impulse showing an elevation followed by a retraction during the period of systole. IV. Systolic retraction. Apex formed by the right ventricle. V. "Mixed" type of apex beat showing protrusion during auricular systole and retraction during systole of the ventricle. termed admixed" type of apex beat. In other mixed types there may be protrusion during auricular systole (presystolic protrusion) followed by retraction during systole of the ventricle (systolic retrac- tion). The right ventricle plays the leading role in the production of such an impulse. (3) Systolic retractions over the entire right ven- tricle (third, fourth, fifth left interspaces between the parasternal line and sternal margin) when this chamber is h y pert r o p h i e d or contracting strongly, sometimes also in second left interspace (Mackenzie). Occasionally, especially in cases of mitral stenosis, the presence of a systolic retraction of the interspaces over the right ventricle and a systolic protrusion over the apex gives the cardiac impulse the w a v y appearance of a peristalsis. In reality, however, the two move- ments are synchronous. It is not a peristalsis but a see -saw movement. 144 DISEASES OF THE HEART AND AORTA. (4) Systolic impulse in the second right interspace in aortic insufficiency. (5) Systolic impulse in the second left interspace (pulmonic area) in pulmonary insufficiency or vigorous contract ion of the right ventricle. (6) Systolic retraction at FIG. 89. Areas of pulsation and retraction. , protrusion: . retraction. CAR. carotid artery: Jl'G. jugular vein; CEPH, cephalic vein; AO. aorta; PA, pul- monary artery; RV, right ventricle; APHD, apex with high diaphragm; AP, apex; LIV.TR.IXS, liver-pulsa- tion in trieuspid insufficiency; LIV. HYP. RV, liver- retraction with hypertrophy of right ventricle. the apex in adherent peri- cardium or when the apex is formed by an hypertrophied right ventricle. (7) Systolic retrac- tions in the interspaces beyond the apex (left axilla) due to negative pressure over those areas of lung produced by con- traction of a very large heart or to pleuropericardial adhesions. (S) Retraction of the xiphoid process or ribs from traction of costopericardial a d h e s i o n s during systole (Broad bent's sign). (9) Systolic i m pulses in various abnormal sites due to aneurisms, tumors, or tortuous sclerotic arteries. FIG. 90. Eddies producing thrills as illustrated by a -^treani of water. Arrows show lines of force. The large arrow indi- cates the pressure at the point of palpation. PALPATIOX. Palpation of the precordium and thorax is undertaken with a view to determine. (1) the force of the apex impulse; (2) the presence and force of any diffuse heave; (3) the intensity of the shock accompanying the heart sounds: (4) the presence and distri- i bution of "thrills"; (o) the presence, dis- tribution, and character of other pulsations. Thrills. Corrigan (1837) and, later, Marey showed that thrills maybe imitated by producing a constriction in a rubber tube attached to a water faucet. It will be seen that this causes the stream to asMime a corkscrew form. giving rise to eddies, tuists. and node.- below the constriction. These tend to produce zones of constriction and dilatation in the tube itself and thus set it into vibrations which are palpable as thrills and audible as murmur-. Above the constriction there are no eddies, hence neither thrills nor murmurs. The thrill is best transmitted in the direction of the stream producing it. It disappears when the constriction becomes too great or the pressure fails too low. and increases with the force of the stream (blood-pressure). PERCUSSION. It is of the greatest importance to determine the exact outline of the heart. As has been seen, this is done most accurately by means of the orthodiauTaph ipa.ire 135), but under ordinary clinical conditions this is not available and the cardiac area is outlined by percussion. PHYSICAL EXAMINATION. 145 In determining the area of cardiac dulness it is important to map out, (1) the area of cardiac dulness, or, more accurately, the relative cardiac dulness; (2) the area of absolute dulness or cardiac flatness. RELATIVE CARDIAC DULNESS. In mapping out the area of relative cardiac dulness it is important to begin percussion as far away from the heart as possible, and then to approach the heart, marking the points at which the very first change of note can be recognized as the heart is approached. In this way one obtains an absolutely resonant note as long as the plessimeter finger is over lung tissue, and a sharp contrast to this as soon as one percusses over the borders of the heart; whereas, if one were to begin percussion over the heart and percuss outward there would be a gradual change of note, becoming more and more resonant, until it finally faded into the perfect resonance over the lung. Choice of Methods. In outlining the cardiac area one has the choice of several methods: (1) Direct or immediate percussion by tapping the chest wall directly with the finger-tips of one hand. (2) Heavy indirect or mediate percussion. (3) Medium-light percussion. (4) Lightest audible percussion (threshold percussion of Ewald, Goldscheider, Curschmann and Schlayer). (5) Palpatory percussion (Ebstein) by note too low to be FIG. 91. Gold- heard at all. scheider's ortho- (6) Orthopercussion (Goldscheider) (Fig. 91), distal per phalanx of the plessimeter finger held perpendicular to the chest wall. (7) I n s t r u mental percussion with a mechanical plessimeter, the blow being struck by either the finger or a hammer. In selecting the method of percussion it should be borne in mind that the vibrations of heavy percussion are readily communicated to neighboring areas of lung, while those of the lightest percussion are readily absorbed by the neighboring lung tissue and hence are best transmitted by the clear lung tissue in the axis of the stroke. The resonations of the lightest strokes pass through the entire thickness of the lung (Goldscheider). Moreover, it is a well-known law of sense-perception that the softer the initial sound the easier it is to detect variations in it. Indeed, de la Camp goes so far as to recom- mend light direct percussion through a single layer of blanket laid upon the chest as the most accurate method of outlining the cardiac dulness. Moritz, Diction, de la Camp, Goldscheider, Curschmann and Schlayer, and a number of other writers have compared outlines made by the various methods of percussion in hundreds of cases with those obtained by the orthodiagraph, while Simon has marked out his outlines by percussion upon the intact cadaver with pins and then tested his accuracy upon opening up t IK; thorax. All these; o b s e r v e r s a r e u n a n i in o u s i n advocating very light percussion for outlining the left border of the heart, but Moritz prefers a rather heavy pulpatory percussion for the right border. Moreover, the sensations which percussion imparts to the finger are more delicate!}- graded for a light stroke 1 than for a heavy one, since the 10 146 DISEASES OF THE HEART AND AORTA. pressure of a heavy blow somewhat dulls the sensibility of the finger-tips, and in this way also a light stroke is more satisfactory. The oft-made claim that a light stroke does not penetrate deep enough for mapping out the right border of the heart, though seeming plausible, is not warranted by experience. On the contrary, the writer has observed that those clinicians who rarely make out at all the area of cardiac dulness which lies to the right of the midline were usually those who used heavy percussion. Avoidable Errors in Percussion. The exact method used is a matter of individual preference and practice. The essentials for all forms are: (1) a loose wrist, loosely held finger-joints, and a short sharp blow with immediate elastic recoil; 1 (2) firm pressure of the plessimeter finger against the chest wall, especially in the interspaces. In the writer's experience the important point is not the method used but the care in discriminating the first slight differences in note and sensation. The errors of percussion so frequent among students and even experienced physicians are far more frequently due to in- ability to detect differences in note than to inability to elicit them. This inability to detect slight differences was due in most cases to a precon- ceived notion as to the intensity of change obtainable. The observer usually expected a greater change and permitted his ear to neglect the lesser, although once his attention was called he was perfectly able to detect it. Special Methods of Percussion. The method of choice varies somewhat with the purpose. For ordinary purposes very light direct percussion is quite satisfactory, or ordi- nary threshhold percussion with barely audi- ble note. Where accuracy is important, as in determining the mobility of the heart or of the lung borders, Goldscheider's or- thopercussion or J. O. Hirschfelder's ort ho plessimeter is preferable. Goldscheider believed that orthopercus- sion was so delicate that dulness was given only by bodies directly in the axis of the plessimeter phalanx and that in this way the plane of an oblique surface could be detected but exj>erience shows that this is rarely possible. It succeeds much more frequently when the orthoplessimeter (Fig. 92) is used; so that a resonant note may be obtained when the shaft is pointed parallel to the heart surface, a dull note when it is pointed towartl the heart. Unavoidable Errors in Percussion Outlines. In outlining the heart by percussion the right and left borders present different problems. The right border is situated deeply and recedes at once from the chest wall, so that it represents the first point at which dulness could be obtained. The left border is superficial and convex and the convexity sometimes follows the curve of the ribs in the left axilla. Accordingly it may happen that in round narrow chests or in persons with large hearts the left ventricle may almost fill the left half of the thorax. The curve of the ribs follows the wall FIG. 92. Percussion with the orthoplessi- meter. A. J. O. Hirschfelder's orthoplessimeter and its mode of application. B. Supposed line of transmission of the percussion impulse from the orthoplessimeter. RES. resonant percussion note. 1 Some persons are possessed of a loose wrist at once, others acquire it only after loni: practice. For the latter the writer recommends the following exercise practised two to five minutes daily: Hold the wrist as loosely as possible, then vibrate the forearm very rapidly to and fro from the elbow until the hand shakes about like a flail upon the loose wrist too fast for the eye to follow its movements. The improvement in percussion fol- lowing this exercise is very gratifying. PHYSICAL EXAMINATION. 147 V FIG. 93. Diagram to show the cause of unavoidable error in percussion of the cardiac outlines. P P, outline on percussion; O O orthodiagraph outline. of the left ventricle and the latter may remain near the chest wall through- out the axilla. The outer border of dulness may thus be obtained not over the apex but over the posterior wall of the left ventricle. In persons with narrow chests or much enlarged hearts the area of dulness (Fig. 93, P- -P) ex- tends around the heart and not merely across the trans- verse diameter (O- -O). The transverse diameter ( - - ) corre- sponds accurately to the point mapped out with the orthodiagraph. Accord- ingly there may be a discrepancy of several centimetres between the percus- sion and orthodiagraph estimations of the distance from the midline to the left border. In a very large series of cases Moritz found his percussion (light percussion for the right border, threshold percussion for the left) to be correct for the right border in 86 per cent., for the left in 70 per cent. When the dulness reaches far around the axilla, this discrepancy may be reduced sev- eral centimetres by stretching the tape out to the left and projecting the outer border of cardiac dulness perpendicularly upon it and measuring this projection. DIAMETER OF THE CARDIAC AREA. In mapping out the area of cardiac dulness the position of the apex is given, designating the level of rib or interspace during quiet respiration, and the number of centimetres to ^^^H the left ^^M and 94) I : the midline (Figs. 84 (ML). The level of upper border at the left sternal margin is given and also the distance to the right of the midline (MR) in the fourth right interspace. The acuteness or obtuseness of the angle formed between the hepatic and the cardiac dulness ( c a r d i o - hepatic angle, angle of Ebstein) is also noted. In addition to this Moritz and Diction call attention to the importance of recording the two diagonal di- ameters of the heart (longitu- dinal, L, from apex to the aortic angle of the dulness, and transverse, Q, from the cardiohepatic angle to the upper left border, as shown in Fig. 84). Normal figures for these conjugates according to Dietlen are: FIG. 94. Areas of cardiac dulness and flatness in a normal man. The outer fine line represents cardiac dul- ness; the inner heavy line represents cardiac flatness. 148 DISEASES OF THE HEART AND AORTA. Height of individual. , Men. Women. i Cm. Feet and In. | MR. Cm. ML. Cm. Ciii. Q. Cm. Cardiac area. Qcm. MR. Cm. ML. Cm. T Ciii. Q. Cm. Cardiac area. Qcm. 145-154 4.75. 3.5 7.0 12.5 0.7 95 3.5 8.1 12.7 9.4 93 155-164 5.15.5 4.1 8.7 13.S 9.9 109 3.5 8.4 13.2 9.7 101 165-174 5.55.9 4.2 8.8 14.1 10.3 116 3.8 8.5 13.4 9.9 105 17 5- is? 5.96.2 4.4 9.1 14.8 10.7 127 Dulness in Children. In children the heart is proportionately larger and lies more transversely than in adults. Sawyer found the apex outside the mammillary line in (53 per cent, of 500 young children. Veith has shown that the cardiac shadow in children extends exactly twice as far to the left as to the right of the midline (ML : MR 2 : 1). Changes in the Relative Dulness. The relative proportions of the various conjugates undergo quite typical changes in various forms of heart disease. In weakening of the right heart, in tricuspid insufficiency, and tricuspid stenosis the conjugate MR is increased (dulness increased to the right); in hypertrophy of the left ven- tricle and in mitral insufficiency, dulness increases to the left (MR. increased), while in the latter condition as well as in mitral stenosis the oblique transverse diameter (Q) is increased. In aortic disease there is lengthening of the long axis (L). Cardiac Flatness. The area of ab- solute dulness or cardiac flatness repre- sents the portion of the heart which is not covered by lung (Figs. 93 and 94). It forms a triangle which varies very much in size and bears no relation to the size of the heart (Schieffer and Weber). It is best mapped out by very light percussion, beginning over in the fifth left interspace at the left sternal margin, percussing lateralward and upward, passing from the absolute flatness to the area of impaired resonance instead of in the opposite direction. By this procedure the tran- sition from absolute flatness to slight resonance occurs suddenly, whereas on percussing in the opposite direction the change of note occurs gradually. Variations in the Area of Flatness. In the primitive mammals (dog and cat) the heart does not lie in close apposition to the chest wall, but is slung rather loosely between the folds of the mediastinum and com- pletely covered by lung. There is no area of flatness. This same condition is met with in many otherwise normal persons, especially in the long flat- chested, and in those who have extremely movable hearts or general mo- bility of all the viscera (visceroptosis, enteroptosis, page 702). En tire absence of cardiac flatness is also found in the exact opposite type of chest, in the barrel-chest patients with emphysema, in 95. Cardiac outlines in nine vears. PHYSICAL EXAMINATION. 149 whom the exaggerated efforts at inspiration have caused the lungs to be sucked in gradually between the heart and the chest wall. On the other hand, the area of cardiac flatness is often enlarged in persons with flat, rhachitic, or tuberculous chests. In hypertrophy of the right ventricle the area of flatness is enlarged and the right border becomes oblique, extending downward to the right margin of the sternum, often interrupted by step-like protrusions (Kroe- nig). In pericardial effusion it extends well into the fifth right interspace. Changes in Size of the Heart. As seen in the investi- gations upon cardiac volume, the size of the heart, and hence the area of cardiac dulness, is subject to a physiological in- crease when the heart is slow and decrease in size when it is rapid (Henderson, see page 9). This decrease in size is especially noticeable in certain cases with rapid hearts, like paroxysmal tachycardia when there is no heart failure nor vasodilation (Hoffmann, Dietlen). An in- crease in size may be associated \vith a slow pulse or with in- spiration, hypertrophy of the heart, or with a pathological dilatation. The physiological condition should first be con- sidered before assuming the pathological. Changes in Position of the Heart. (1) Upon changes in posture. Normally changes in posture are accompanied by considerable changes in the position of the heart. The apex may move 3-5 cm. when the patient turns from one side to the other, always moving towards the side which is lower. On standing a similar but less marked change occurs. .Moritz, and, later, Dietlen have shown that the area of the cardiac shadow is from ten to thirty per cent, smaller on standing than on lying down. The latter observer confirms Erlanger and Hooker in stating that the pulse-pressure, and hence the systolic output of the ventricles, diminishes correspondingly. FIG. 90. Diagrams illustrating the movements of the normal heart on change of posture from side to side (A), and in the various phases of respiration (B). Solid black line, normal cardiac outline in quiet breathing; dotted line (/?), cardiac outline with patient lying on right side; broken line (), cardiac outline with patient lying on left side; EXP (horizontal shading), outline in expiration; /.V.S'P (vertical shading), cardiac outline in inspiration. The movements shown in these figures represent the upper limits of normal mobility. 150 DISEASES OF THE HEART AND AORTA. The diminished filling of the heart is due also to the fact that the pressure under which the blood enters it in diastole (venous pressure) is lower upon standing than upon lying down. In some people extreme mobility (6-8 cm.) of the apex is found (wan- dering heart) a condition often associated with cardiac neurasthenia and palpitation, and even paroxysmal tachycardia. Changes in position of the diaphragm, upon expiration, inspiration, or intestinal flatulence, also affect the position of the heart, especially upon standing, so that in expiration or flatulence the apex is pushed up and the heart lies more trans- versely, while in inspiration the apex falls and the heart lies more nearly in the long axis of the body (Fig. 96). As can be readily shown with Henderson's cardiometer, the former position interferes with the cardiac filling and hinders the circulation, while the latter position facilitates both. The amount of change of position of the apex is normally about 1-2 cm. AUSCULTATION. CHARACTER AND TIME OF THE HEART SOUNDS. The beat of the heart is accompanied by two definite sounds ordinarily likened to the syllables " dub-lub " or " ta-ta," the first sound accompany- 12 12 ing systole, the second occurring just at the beginning of diastole. SPECIAL METHODS FOR THE STUDY OF HEART SOUNDS. The Telephone Stethoscope. S. G. Brown has devised a telephone relay by means of which it is possible to intensify the telephone currents twenty-fold, or using two relays in tandem four-hundred-fold. Such instruments may prove of value for demonstrating FIG. 97.- CAROTID PHONOGRAM Iraphic records of the heart sounds. (Kindness of Prof. Einthoven.) Each vertical division represents .02 sec. heart sounds to a whole amphitheatre, or, as Barker suggests, for enabling permanent records of the heart sounds to be made upon a graphophone for use in medical society demonstrations or in the teaching of physical diagnosis. It has already been used for auscultation of the heart at long distance, and the heart sounds of a patient have been heard by physicians a hundred miles off (from London to the Isle of Wight). Graphic Methods of Recording the Heart Sounds. The first method for recording the heart sounds was introduced by Donders (ISoG) and revised by Martins (1SSS), who merely beat the time of the sounds upon a receiving tambour and recorded the movements of the lever. With a little practice it was possible for the observer to time the beats with a con- siderable degree of accuracy, though never sufficient to be absolutely reliable. II u e r t h 1 e was able to catch the sounds upon a microphone and to record the duration of the telephonic currents either by means of a frog nerve muscle preparation PHYSICAL EXAMINATION. PLATE VIII. 151 Diagram showing the connections for taking graphic records of the heart sounds by means of the Einthoven galvanometer; MICROPH, microphone suspended upon a Julius suspension; GALV, gal- vanometer; RHEO, rheostat; PHOTO, photoregiatration apparatus. The telephone induction coil is shown upon the right of the figure. 100 SEC> lumuiiiHiiiiiiHiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiniiiiiiiifmiHiiiniiimiiiiiiiiuuiiitituiuiiuniiiiiiuiiiiiiiiiiiiiiiiniiH SOUNDS JUGULAR Record showing the third heart sound and its relation to the venous pulse. (Redrawn from the original curves kindly loaned by Professor Eyster.) Compare with Figs. 45 anil 97. 152 DISEASES OF THE HEART AND AORTA. or by means of an electromagnet, but his method never became practical. Holo- w i n s k i and M a r b e have also obtained records of a change in Newton's rings and of the vibrations of a sensitive flame respectively, but none of these have been of real value. Einthoven and Geluk were the first to make really satisfactory records, by catch- ing the sounds from a stethoscope upon a microphone and leading the currents through a capillary electrometer whose movements were photographed. Since the introduc- tion of the string galvanometer in place of the capillary electrometer, this method has passed into every-day use, and excellent records of normal and abnormal heart sounds have been obtained which throw a good deal of new light upon the problems of auscultation. The heart sounds must be recorded in a quiet room, in which the microphone must be kept absolutely stationary, free from the slightest vibrations. In order to do this, it must be clamped firmly upon a plate which is suspended from the ceiling by three fine wires (Julius suspension) and made stable by heavy weights (40-50 pounds). The stetho- scope is connected with the microphone by means of a long, thin-walled rubber tube. About two feet from the microphone, the rubber tube is connected with one arm of a brass Y tube fixed firmly to the wall. A second arm of the Y tube is connected with an open rubber tube, whose lumen can be regulated with a screw clamp in order to prevent mechanical vibrations of the chest wall from reaching the microphone. The third arm of the Y is connected with the tube leading to a small (1 J4 in.) glass funnel or stethoscope bell, which is either held directly on the thorax or fixed in a special ^-shaped holder against which the patients may lean without giving rise to vibrations. The tube and funnel as well as the microphone must be absolutely quiet in order to record the sounds, free from external vibrations. The microphone itself is now connected with the primary coil of a telephone circuit, the secondary of which passes through shunts bearing a rheostat and the string galva- nometer. A special switch must be employed to keep the galvanometer out of the circuit at the instant that the primary current is made and broken. A galvanometer which gives 1 cm. excursion per millivolt (standard delicacy for elec- trocardiograms) is entirely too delicate for recording the heart sounds, and the thread must be either very much tightened or the smaller form of galvanometer used. Weiss and Frank have devised instruments of a differ- ent type, in which no microphone is used, but in which the vibrations of a membrane set in motion by the heart sounds are magnified and recorded photographically. O . Frank places a small mirror upon a condom membrane stretched across the mouth of a small funnel. A beam of light is thrown obliquely upon this mirror and reflected upon the slit of a photo-registration apparatus. The funnel is connected with the stetho- scope as for the Einthoven apparatus, and the oscillations are photographed. Unfortunately, Frank's curves represent a combination of phonogram and cardio- gram, and are therefore not entirely satisfactory for many purposes, although the rapid vibrations due to the heart sounds are so characteristic that they can scarcely be confused with the much slower vibrations due to the heart's movements. Weiss' phonoscope, which is a much more delicate instrument, and, accord- ing to its author, more sensitive even than Einthoven's, consists essentially of a closed chamber containing a funnel 1 cm. in diameter. The mouth of the funnel is covered with a film of soap-bubble, in the centre of which rests an L-shaped order of capil- lary glass tubes, whose movements are magnified with a microscope and are projected upon a photo-registration apparatus. The soap film may last three hours. Gerhartz, who has made use of the same apparatus, finds that membranes of collodion may be substituted for those of soapsuds and are much more permanent and easier to use. Condom membrane is far less sensitive. Still more delicate than this is the micrograph of Crehore (page 76). Reproduction of the Heart Sounds. Weiss and Joachim have successfully repro- duced the original heart sounds from the cardiophonographic curves by cutting out the curve upon a piece of cardboard and passing it rapidly between an arc light and a photo-sensitive selenium cell. Wherever the high points of the curve cut off the light the conductivity of the selenium coll changed and a telephone current was produced PHYSICAL EXAMINATION. 153 This method was very satisfactory, but it is necessary to make use of a selenium cell of very low resistance (less than 300,000 ohms). The resistance of the ordinary cells is too great for the purpose. Clinical Diagram for Heart Sounds. In many text-books the heart sounds are represented graphically in various ways, but it seems to the writer that the best is to indicate the occurrence of the sounds directly upon a simple diagram which indicates the relation to the auricular and ventricular contractions, as shown in Fig. 98. 1 CAUSES OF THE HEART SOUNDS. First Sounds. Harvey states that " when there is the delivery of a quantity of blood from the veins to the arteries, a pulse takes place which can be heard within the chest." Laennec (1819) was the first to describe the character of the sounds. He regarded the first sound as due to ventric- ular systole, though he thought the second to be due to the contraction of the auricle. In 1836, C. J. B. Williams and a committee of the British Medical Association investigated the heart sounds experimentally. He believed that the first sound was largely of muscular origin, like the contraction sound of skeletal muscles, because it could be heard upon the excised heart even when the auriculoventricular valves CARDIAC CYCLE HEART SOUNDS- 12 12 FIG. 98. Diagram for representing the heart sounds in clinical notes. Upper curve represents the events of the cardiac cycle, the small auricular contraction followed by the larger ventricular con- traction. Lower line represents the heart sounds. True heart sounds are represented by solidly shaded blocks, whose height indicates their intensity and whose breadth indicates their duration. were held open with the fingers, but the second sound could not be heard unless the aortic or pulmonic valves closed. This view was substantiated by Ludwig and Dogiel; but Sibson and Broadbent found that in the exposed heart of the ass the first sound begins with a sort of rumble, which disappears when the blood flow is shut off by tying the venae cavse. This r u m b 1 e they ascribe to the movement of the auriculo- ventricular valves. Graphic records of the heart sounds by Einthoven, Flohil, and Battaerd have shown that the first sound in man begins at the beginning of ventric- ular systole and lasts .07 to .10 sec. It is loudest at its v e r y beginning, is decrescendo in character, and is almost completed before the aortic valves o p e n , i.e., before the heart had begun to pump blood into the aorta. The first sound is followed by the short pause, which usually lasts .15 to .25 sec., and 1 Thus in cases of mitral stenosis (see page 434) the first sound may be short and tapping in character, though tracings show the systole to be of duration no less than that met with in the absence of tapping character (Hirschf elder) , 154 DISEASES OF THE HEART AND AORTA. which is then followed by the second sound. Einthoven's results have been confirmed in man by the records of Weiss and Joachim, Hess and Frank, as well as by Prof. Barker, Dr. Bond, and the writer. In the dog, R. H. Kahn has shown that the duration of the first sound is exactly coincident with the period during which the intraventricular pressure is rising, while the dura- tion of the short pause is exactly coincident with the systolic plateau. Sahli and other clinical observers believe that the first sound at the aortic area begins later than that at the apex and is due to the rush of blood from the ventricle into the aorta, but graphic records seem to indi- cate that the sounds in the two areas are synchronous, and begin before the aortic valves open. However, the first sound heard on listening in the suprasternal notch is often split; and it is possible that the latter portion of this sound is due to just such a forcible distent-ion of the aorta. The valvular element of the sound is probably brought about when the valves are thrown into tension by the ventricular systole. The normal valves give no sound at all when they open spontaneously. 1 There is no evidence to indicate that the normal sound is brought about to any extent by eddy currents as are thrills or murmurs, nor does systole of the auricles produce any portion of the normal first sound (Einthoven). Hess and Frank believe that the movement of the heart within the chest and perhaps against the chest wall (systolic erection) may be an impor- tant factor in the production of the first sound. This might explain why the heart sounds are occasionally inaudible in emphysematous persons in whom the organ is separated from the chest wall by a layer of lung. On the other hand, this factor is shown to play only a minor role by the fact that the first sound may be heard in its normal intensity in the exposed and even the suspended dog's heart. Second Sound. The second sound has been shown by C. J. B. Williams and the British Commission to accompany the closure of the aortic and pulmonary valves, to be modified when these valves are injured, and to disappear when they are held against the vessel wall. It lasts about .05 second. It is loudest when the blood-pressure is high, when the valves are thicker and more rigid than normally, or when the vessel walls are more elastic than usual, the intensity varying at different times of life and under patho- logical conditions. METHODS OF AUSCULTATION". Monaural Stethoscope. The monaural stethoscope, introduced by Laennec, is a simple wooden tube surmounted by a flat disk acting as an ear-piece and resonator. The tube is pressed against the chest and the ear laid upon the disk, so that the observer receives at once the sound and the thrill in the wood transmitted directly. Obviously this method accentuates the notes of low pitch which are nearest to the essential tone of the instru- ment (and constitute most of the normal sounds), as well as those of relative 1 Both the valves and the cardiac walls are at that time extremely lax and the val- vular opening is almost equal to the diameter of the ventricular chamber. PHYSICAL EXAMINATION. 155 loudness, which cause it to vibrate mechanically. Hence it is particularly adapted to the detection of presystolic and other rumbling murmurs, and is the method used almost exclusively outside of the United States. Binaural Stethoscope. In the United States the binaural stethoscope is in more general use. This consists essentially of a small receiving bell, which is placed upon the chest wall, and from which two tubes lead off to small rubber ear-pieces which fit tightly into the external auditory meatus. The most important essentials in these three forms are, (1) a bell composed of various materials ivory, wood, celluloid, or hard rubber provided with a sufficiently large air space at the tip (Emerson) ; (2) ear-pieces perfectly fitting the ear of the individual. It is safe to say that more errors of auscul- tation result from poorly fitting ear-pieces than from real inefficiency on the part of the listener. (3) In stethoscopes in which the ear-pieces are held in the ears by a spring this should not exert excessive pressure lest it produce sounds within the ear from the pressure on the drum. There are three main forms of binaural stethoscope: (1) those with rigid tubes (Gannett's), (2) those with soft rubber tubes, (3) those with soft rubber tubes, flat bells, and a small elastic disk of metal or celluloid to act as a resonator (Bowles). Of these three forms it may be said that the rigid tubes certainly convey the sounds somewhat better, but this is often more than compensated for by the better fitting of the ear-pieces in stethoscopes with soft BAD GOOD rubber tubes. In stethoscopes with disks certain sound waves, and particularly those of high pitch (soft blowing mur- murs), are accentuated, while other sounds may be relatively suppressed. Moreover, any movement of skin or hair over the FIG. 99. choice of stethoscope bells. disk may give rise to a sound simulating a friction, and this source of error must be carefully excluded. Hair should be moistened, and a small bell should be used with perfect approximation to the skin throughout its circumference. Alteration of Sounds by Pressure. Emerson has shown that many murmurs, especially presystolic and snapping sounds, are diminished or obliterated by pressure with the stethoscope, while certain others are inten- sified by pressure, and that this is dependent upon the pitch of the sound and not upon the site of its production. It is therefore important for the observer to listen carefully, first with the lightest possible pressure upon the stethoscope and then with gradually increasing pressure. He should do this consciously and as a matter of routine, rather than allow such sounds to escape him or stumble upon them by accident. Moreover, since the monaural and binaural stethoscopes each intensifies different sounds, both should be used in any important or dubious case before the examination is concluded. Differential Stethoscope. This consists of an ordinary binaural stetho- scope in which each ear-tube leads to a separate 1) el lor funnel. If one bell is placed over the mitral area and the other over the aortic, the observer is able to listen with one ear to the sounds produced at 156 DISEASES OF THE HEART AND AORTA. the two areas at the same time, and to use the more normal sound as time marker for the other. By squeezing the tube or lifting the bell, it is possible to diminish either sound at will. " VALVULAR AREAS IN AUSCULTATION. The various cardiac sounds are best heard over certain definite locations corresponding more or less to the structures in which they arise, but par- ticularly to the course of the blood current and to their mode of origin (Fig. 100). Thus the sounds produced in the left ventricle are best heard at the apex; those produced at the aortic orifice, though produced behind the ster- num, are heard just to the right of it in the second interspace; the pulmonary sounds are carried to the second left interspace at the sternal margin; while the sounds from the right ventricle are heard over the entire body of the sternum, over the greater part of the area of absolute dulness, and over the base of the ensiform cartilage. Abnormal sounds, murmurs, etc., have, however, a different distribution, which will be discussed later. Normally the first sound at the apex and everywhere else below the third rib is louder than the second sound. It is also of longer duration than the latter (.08 second as compared to .05). Over the aortic and pulmonic areas it becomes somewhat fainter, be- gins a trifle later, and is of longer duration than over the apex. The second sound is then louder than the first. The second sound at the sec- ond left interspace (pulmonic sec- ond) is usually louder than that over the second right (aortic sec- ond) up to the age of 25 to 30, when the latter becomes the louder (Cabot). 1 This varies greatly in different individuals. Mere changes in blood-pressure are not sufficient to account for all these conditions, since the pressure in the pulmonary artery is never more than half that in the aorta, but proximity to the sternum, greater elasticity of the walls, etc., combine to bring about the relative loudness of the second pulmonic sound, and therefore any further increase in pressure in either artery alters the relation of the two sounds to each other, increased pulmonary pressure increasing the pulmonic second, increased general blood-pressure increasing the second aortic, etc. The progressive thickening of the aortic semilunar valves after thf age of 30 also contributes to the intensity of the sound. Other Sites for Auscultation. Boy-Tcissier has also recommended auscultation in the s 11 p r a sternal not c h , pressing the bell of the stethoscope as far down behind the manubrium as possible. In this way he states that he can hear aortic diastolic murmur Fir,. 100. The "valvular areas." 1 Directly over the exposed aorta the sound is louder than over the exposed pulmonary artery. .Thayer.) PHYSICAL EXAMINATION. 157 FIG. 101. The propagation of the heart soundg from valveg to chest wall. A, course of tl H, propagation of the sounds at the level of the fourth and fifth intcrapu waves within the heart C, propagation of the heart sounds at the level of the second interspaced 158 DISEASES OF THE HEART AND AORTA. not otherwise audible. He thinks that he is also better able to distinguish the character of aortic systolic murmurs. The method has never gained general usage, and the writer is unable to find in it any of the advantages claimed by Boy-Teissier. The chief value of suprasternal auscultation is found in persons whose heart sounds are feeble or inaudible over the precordium. It must be borne in mind, however, that the mitral murmurs are not well transmitted to this region, and that the first sound heard there is frequently redupli- cated or split. Another form of auscultation not in general use is the auscultation through the stomach-tube, introduced as for a tracing from the left auricle. This method, first used by A. Hoffmann in 1892, has been revived by Gerhartz, but, though it might throw some light upon the nature of an occasional mitral murmur, it is in general difficult and very inconvenient to carry out; and in many cases at least the murmurs are no better heard than over the chest wall. Nevertheless where it is important to know whether a murmur is conducted back into the left auricle, a positive finding by this would be conclusive. EMBRYOCARDIA. Ordinarily the diastolic pause between sounds is longer than the sys- tolic period, and the interval between the second sound of one cycle and the first sound of the next is longer than the interval between the first and second sounds of the same cycle. However, when the heart-rate is very rapid, the diastolic pause may become shortened to about the same interval as that between the first and second sounds (long pause = short pause), so that the sounds succeed one another at uniform inter- 2 12 i Fir;. 102. Graphic records of the fetal heart .-ounds. (.After Weiss and Joachim.) vals like the ticking of a clock. This rhythm is heard normally over the fetal heart and hence has been termed embryocardia or fetal rhythm. It also occurs in adults when the rate is very rapid (120 and over), and hence under conditions in which the heart is under an abnormal strain (see page 305), as in fevers with high temperature, acute heart failure, and acute overwork of a chronically diseased heart, also in cases of paroxysmal tachy- cardia and allied conditions. Its absolute significance is simply that of the rapid heart-rate to which it corresponds. ACCESSORY HEART SOUNDS. REDUPLICATED SOUNDS AXD GALLOP RHYTHMS. Reduplicated Sounds. Occasionally one or the other of the two normal heart sounds is replaced by two clear sounds, or, in other words, there is a reduplication. This reduplication may occupy the place of either the first or the second sound, and, as already noted by Skoda, it may seem to be PHYSICAL EXAMINATION. 159 due to, (1) splitting of the normal sounds into two distinct portions, or (2) pressure of an accessory sound besides the normal sound, being in the latter case presystolic (before the first sound) , protodiastolic (shortly after the second sound) ,or mesodiastolic (in mid-diastole). The relation of groups 1 and 2 to one another and to the cardiac cycle is shown in Fig. 103. IVTRAVENTRICULAR PRESSURE VOLUME OF VENTRICLES PRESYSTOLIC GALLOP SPLIT FIRST SOUND SPLIT SECOND SOUND PROTODIASTOLIC GALLOP TC-LUB DUB K-LUBOUB I! SHE LUB DUB-L FIG. 103. Diagram illustrating the split sounds and gallop rhythms and their phonetic equivalents. As to the causation of these abnormal sounds, little definite is known. A great deal of the indefiniteness which permeates the enormous literature upon the subject is due to the failure of the writers to distinguish clearly between the different forms with which they are dealing. The presystolic and protodiastolic forms are grouped under one head regardless of their relations to mechanism or etiology; it is mainly due to the writers of the French school under the leadership of Potain that the differentiation has reached even its present stage of development. L. Bard, of Geneva, has recently given an excellent analysis of the subject from this stand-point. According to Bard, the two main groups of accessory sounds are: (1) The presystolic gallop reduplication (ta-ta-tat) or ta ta tat, to which the term 1 2 gallop rhythm should be limited, most commonly met in nephritics with cardiac hyper- trophy and in other heavily beating hearts. (2) The protodiastolic sound til ta ta (lub-dub-da), called by Bouillaud bruit de rappel, "sound of recall" or "cliastolic echo," frequently heard at the apex in mitral stenosis. Bard thinks that the above-mentioned accessory sounds are to be regarded as merely the exaggeration of vibrations normally present but normally inaudible. Split Sounds. The sounds (tlat-tat; tat-tatl) are characterized by the absolute similarity and short interval between the two portions, and may be due either to slight asynchronism of the two ventricles (C. J. B. Williams, 1836, Skoda, Gibson, 1874) or slight separation of two parts of the ven- tricular sound, which are of different origin but ordinarily fused. As has been seen, the ventricular sound contains both a valvular (auriculo ventric- ular) and a muscular element, and perhaps also an element due to the stretching of the walls of the aorta. Bard thinks that variation in either the muscular or the valvular element might give rise to their separation into two sounds. The question of asynchronism of the two ventricles which arises in this connection is one which was long without an experimental basis, but the recent observations of Stassen, Kraus and Nikolai, and Hew- lett indicate the possibility that it may occur clinically. Stassen, in Fredericq's labora- tory, has recorded asynchronous contractions of the two ventricles when the latter were recovering from vagus inhibition, and also witli ventricular extrasystoles produced during periods of vagus inhibition. The writer lias on one occasion heard a split first sound in an animal in which the contractions of both ventricles were being recorded with myocardio- 160 DISEASES OF THE HEART AND AORTA. graphs. The ventricular contractions were slightly asynchronous. In a number of other instances in which no split first sound could be heard the contractions were absolutely synchronous. Eppinger and Stoerck have confirmed these observations (see page 106). The splitting of the first sound is best heard over the base and body of the heart, in contrast to the accessory sounds which are best heard at the apex (see below). As to the splitting of the second sound, this likewise may be due to slight asynchronism of the two ventricles, or to the fact that even without this the semihmar valves may not close at exactly the same instant. It is often possible, by passing the stethoscope along the second right and left interspaces, to determine which second sound lags behind. It must be added, however, that, as Bard himself states, no accurate knowledge of either the split sounds or the accessory sounds can be gained until they are registered graphically by cardiophonographic methods along with simultaneous venous, arterial, or cardiographic tracings, so that their APEX PHONOGRAM T J-j SECONDS 1 PRE. 1 SYST. A 2 B Fir.. 104. Graphic record of a split pulmonic second sound. (After Weiss and Joachim.) PRE., presystolic rumble; SYST.. systolic murmur; 1, first heart sound; 2 A, B, two parts of split second sound (.04 sec. apart i. exact relation to the cardiac cycle may be determined. So rapid is the sequence of the sounds that in an individual case the differentiation between split and accessory sounds is often difficult. Reduplication of the First Sound from Pericardial Adhesions. Reduplication of the first sound is also heard in a number of cases in which old pericardial and pleural adhesions are found at autopsy (Sewall), which may be easily understood to give an abnormal sound in systole. Just how commonly this group occurs has not been determined statistically, but under these conditions it need not signify any disturbance of function. Presystolic Gallop Rhythm. As regards the accessory sounds, the great majority of writers take the view suggested by Exchaquet in 1S75 and Johnson in Is70 that the first sound of gallop rhythm (presystolic sound) is due to the vigorous systole of the auricle, a view which is further supported by the studies of Kriege and Schmall (1S!)1), Friedrich Miiller fl'.Xttji. (i. ('. Robinson (H)()S), and others. According to Miiller, Marey believe* 1 that the extra sound was produced by the auricle sending blood into a defectively emptied ventricle, a view which has been revived by Sewall. Moreover, the writer has been able to show on the excised heart that when the ventricles are distended under a slight positive pressure the auriculo- ventricular valves may open along only a small extent of their line of clos- ure. This gives rise to a slight functional stenosis at the point where 1 they actually open, a fact which may account for the audible auricular con- traction. Miiller considers that the extra tone may be dependent upon a PHYSICAL EXAMINATION. 161 delay in the time between the auricular and ventricular contraction, pos- sibly due to lowered conductivity in the atrioventricular bundle of His, and when the two contractions are abnormally separated two sounds instead of one are produced. Tracings, however, do not usually show delayed conduction. All these writers base their views upon the fact that the sound appears to be pre- systolic in time and that in many cases a well-marked auricular wave may be seen upon the cardiogram at a corresponding point of the cycle. It must be added that this is also seen in many cases in which there is no gallop rhythm, and that it seems to be dependent more upon the prominence of the apex impulse in the interspace facilitating the record than it does upon the existence of the sound. However, this wave is often quite as prom- inent in the curves (protodiastolic sound) in which no presystolic sound was heard as in those used to illustrate the gallop rhythm itself. The proof is therefore insufficient, but that does not mean that the theory is necessarily wrong. It is not at all improbable that the forcible contraction of an overloading auricle may give an audible sound just as it does when forcing blood through a narrowed orifice (presystolic rumble), but this has not yet been proved and will require careful investigation with the cardiophonograph. The possibility of functional mitral stenosis like those mentioned on page 461 must also be borne in mind. Another explanation for the phenomenon is that the sound occurs during the ven- tricular systole, as suggested by H. Chauveau, who thought it due to the tension of the auriculoventricular valves. His apex tracings, however, are not carefully timed and might quite as well be interpreted as evidence of the auricular sound. The numerous reviews of the literature, such as those of Obrastow, Pawinski, Robin- son, shed no further light upon the subject. Clinically, the presystolic gallop rhythm is usually met with in cases with rapid hypertrophied hearts which are under a slight overstrain, as in the classical group of chronic nephritis, chronic cardiac disease, aneurism, cases with arteriosclerosis, exophthalmic goitre, mitral stenosis, and acute fevers. Occasionally it is heard in normal individuals (Krehl). It seems in most cases to accompany slight overwork of the heart, but its me- chanical and physiological significance is still not clear. Protodiastolic Gallop Rhythm. Third Heart Sound. The role of the protodiastolic sound (bruit de rappel, diastolic echo) seems to be more definitely established. Though already heard by Bouillaud in 1835, in mitral stenosis, its occurrence was emphasized by Duroziez (1874) and by Sansom (1881), who term it the "opening snap" of the mitral valve, indi- cating that it was brought about by the opening of the stiffened valve. Barie (1893) and Thayer (1906) called attention to its occurrence in normal individuals. In 1907 the writer observed this sound in a normal individual with a slow and vigorous heart, whose venous pulse showed a peculiar extra wave (Fig. 106, h) which follows the inflow of blood into the ventricle (as indicated by the normal v wave, Fig. 106, page 162). The writer also called attention to the fact that this wave bore a close relation to the end of the rapid filling of the heart (or diastole proper) upon the volume curve of the ven- tricles, and that Henderson had claimed that at this time the mitral valves and t risen pi d. were closed by the elastic recoil of the heart walls. That this actually takes place and is 11 FIG. 105. Graphic record of the third heart sound. (Kindness of Prof. Einthoven.) 162 DISEASES OF THE HEART AND AORTA. dependent upon a high venous pressure can be shown on the dead heart by pouring water into the ventricles from a beaker after the auricles have been cut off in the manner devised FIG. 106. Jugular and carotid tracings from a normal individual with a well-marked third heart sound, showing a large h and a smaller preauricular wave (w). ? indicates a small wave in middiastole following the h wave, occasionally found though perhaps an artefact. by Baumgarten (1843). If the water is poured from just above the valves they merely float out a little toward the middle of the orifice; if from the height of about 10 cm. they float into apposition; if from 50 cm. above they are left tightly closed when the flow ceases. These observations have been confirmed recently by C. Lian in Francois-Franck's labora- tory. Hirschfelder also suggested that this clos- ure of the valves may be sudden and vigorous enough to cause a sound. 1 The relation of this sound to this portion of diastole seemed quite definite by comparison with a graphic record of this sound made at about the same date by Einthoven (Fig. 105), which shows it to occur 0.18 second after the second sound. This ex- planation has also been supported by A. G. Gibson and Professor Thayer. The tracings of Robinson, who was investigating the subject from a different stand-point, have also shown the constant presence of the h wave upon the venous tracings accompanying this sound. Rob- inson and Thayer have also shown that it accom- panies a wavelet p upon the cardiogram in early diastole (Fig. 88, I, page 143), probably due to the filling of the ventricles. They find this wave upon the cardiogram in almost all cases of pro- todiastolic gallop rhythm, and regard it as char- acteristic of the latter. Thayer has demonstrated that it cannot be an artefact, since it is often both visible and palpable. Ven- ous tracings made from animals by Eyster along with the volume curves of the ventricles show that the foot of the h wave, or more exactly the trough of the depression, marks the end of the rapid diastolic filling, and his graphic records of the heart sound show that the third sound occurs at this instant. The sequence of events would be as follows: The end of systole is marked by the second heart sound and by the fall in the cardiogram. The tricuspid and mitral valves open almost instantaneously, but a period of about i 1 : second is required before the fall of pressure is transmitted to the jugu- lar vein and the pressure begins to fall (v-y collapse). The inrush of blood into the ventricles VOL FIG. 107. Forces supposed to be at work in the production of the third heart sound. Diastolic closure of the auriculoventricular valves. Dotted lines indicate the direction of inflow. Black arrows indicate the recoil waves tending to push the cusps together. ; The assumption of such a slapping together of the auriculoventricular valves at the end of ventricular filling is not at all incompatible with the fact that a small separation (1-3 mm. i may reappear between them in the latter part of diastole, when the accumulation of blood in the auricles has become sufficient to just force the cusps apart (page 461). PHYSICAL EXAMINATION. 163 rapidly distends the latter until they reach their full distention, at which the inflow ceases and the cusps of both mitral and tricuspid valves slap together (closing slap in diastole). The end of this inflow may be accompanied by a slight recoil or similar movement of the ventricle, giving rise to the small wave and shock noted at this moment. The intensity of this recoil is probably dependent to a great extent upon the elasticity (elastic tissue) of the ventricular walls; hence its absence in old persons. Windle and Eyster have shown that the third heart sound may be present without the h wave or the h wave without the third sound. This is not surprising, for the valves may slap together neither suddenly enough nor hard enough to cause a sound though they may cause a wave. The sound may be present without the wave, for the recoil wave may be damped by dilating auri- cles; or the cusps may close suddenly along the greater part of, but not the entire line of, closure and give a sound but not a wave. A priori, according to this explanation a protodiastolic sound should be heard in slow hearts because in them the ventricular walls are distended to their full extent early in diastole; in cases of aortic insufficiency because of the high intraventricular pressure which tends to slap the cusps of the valves together early in diastole; in mitral stenosis owing to the peculiar events in the filling of the ventricle (vide page 12), and perhaps in cases in which there. is a large amount of residual blood in the ventricle (dilata- tion) which tends to diminish and shorten the period of inflow. These represent the chief conditions in which it is actually heard. Thayer states that it can be heard at the apex in about 30 per cent, of normal individuals lying upon the left side. By decades its frequency was as follows; First decade heard in 58.9 per cent.; second decade 84.4 per cent.; third decade 50.9 per cent.; fourth decade 42.3 per cent.; fifth decade 14 per cent.; sixth decade and after 0. It seems to occur in practically every condition, especially in cases with slow hearts, and seems to bear no definite relation to cardiac weakness. MURMURS. MECHANICAL FACTORS IN THE PRODUCTION OF MURMURS. As has been seen above (page 144), when a narrowing occurs in the lumen of an elastic-walled tube through which liquid is flowing, eddies are formed which set the walls of the tube into vibration and give rise to a pal- pable thrill. Accompanying the thrill a blowing sound known as a " mur- mur" may be heard over the tube; which, like the thrill, is heard much better below the obstruction than above it, and is transmitted in the direc- tion of the flow. The character of a murmur depends upon the width of the orifice at which it is produced, upon the nature of the walls of the orifice, upon the velocity and tension under which the fluid passes through it, and upon the direction in which the flow occurs. In this way a valvular orifice may be compared to the larynx with its vocal cords. When the cords are lax and wide apart, the air moving over them in even forced respiration gives no sound; when the cords are approximated a little but still held loosely, it gives a whispered "ch" sound, and when they are held very tense true vocal sound is heard. Similarly, no sound can be heard over the excised heart when the fluid regurgitates through an absolutely patent mitral orifice (Fig. 108) ; if one of the chordae tendinea' be stretched and the regurgitation takes place through u small slit whose walls 1 In the light of these facts it is difficult to comprehend why Windle heard the third sound in only 2 per cent, of his cases. 164 DISEASES OF THE HEART AND AORTA. are flabby (relative insufficiency, Fig. 108), a soft low blowing murmur will be heard (the smaller this orifice the higher pitched and more distinct the murmur); while if some more or less hard irregular body, like calcified vegetation, is situated at the orifice, this acts more or less as a resonator, increases the sound, and may even give it a roaring or a squeaking (musical) character. 1 B FIG. 108. Similarity between production of voice sounds and the production of murmurs. (Kindness of the J. Am. M. Asso.) A, B, C, vocal cords ; D. E, F, auriculoventricular valves; G. H, I. aortic and pul- monic valves. A (high note), D, G, small leaks producing high-pitched murmurs; B (low note), E, H, larger leaks producing low-pitcned murmurs ; C, F, I, very large leaks, producing no murmurs. Occasionally murmurs become so loud as to be heard several feet away from the chest or even across the room. Such murmurs are usually systolic in time and are often due to calcified vegetations, arterial plaques, or aortic or mitral stenosis. As in the larynx, the character of the sound produced at a valvular orifice is due not only to the size and shape of the orifice, but also to the tenseness of the walls and velocity of blood flow through it, and hence is largely dependent upon the height of the. blood-pressure. All these factors, both the widening of the leak and the decreased force of the beat, explain the fact that as the heart weakens under the influence of the lesion the murmur may actually disappear, CHARACTER OF MURMURS. Murmurs may be roughly divided into the following classes: (1) Direct mur- murs host transmitted in the direction. of the blood flow, as from stenoses or calcified plaques: 1 2i Resrurgitant murmurs due to a flow in the direction opposite to the 1 Musical or squeaking murmurs are sometimes due to the presence of tense mod- erator bands stretching across the ventricular cavity and resounding like banjo strings, although usually these bands do not cause murmurs at all. Very frequently they arise in dilated right ventricles in association with functional tricuspid and perhaps functional pulmonary insufficiencies. They are usually systolic, but sometimes diastolic in time. They are often cardiopulmonary. PHYSICAL EXAMINATION. 165 usual blood flow (as in mitral and aortic insufficiencies); 1 (3) To-and-fro "machinery" murmurs which occur in both systole and diastole in congenital heart lesions; (4) Rum- bling murmurs. Of these 1, 2, and 3 are more or less blowing or roaring in character; while the rumbling murmurs are devoid of this character, and are rumbling or echoing, more like a series of heart sounds which vary in intensity (mitral stenosis, Flint murmur) than like murmurs due to the passing of a stream through an orifice. Brockbank claims that these may be produced upon a model by means of a stream flowing through a conical valve from apex to the base of the cone. The mechanism of the production of such murmurs is still very obscure, and further researches are necessary before satisfactory elucidation can be given. Transmission of Murmurs from the Auriculoventricular Valves. Regurgitations at the mitral and tricuspid orifices, however, give rise to systolic murmurs which are trans- mitted loudly in two ways : in the direction of the regurgitant stream, and also in a direction exactly opposite to the latter. In the cases of mitral insufficiency the regurgitant stream through the mitral valve strikes the posterior wall of the left auricle and imparts its vibrations to the chest wall in the lower left interscapular region. In this area a systolic murmur is readily heard in thin-chested individuals, but even in them it is not so loud as the systolic murmur heard over the apex and in the left axilla near the apex, which is con- ventionally accepted as the characteristic sign of mitral insufficiency and which is heard in many cases of mitral insufficiency in which the murmur at the back cannot be made out. Similarly in tricuspid insufficiency the regurgitant stream impinges against the wall of the right auricle, which is distended so that the regurgitant stream should strike against its wall near the right border of cardiac dulness, and hence the murmur should be heard at its maximum far to the right of the sternum. Though a loud murmur is heard in this area in occasional cases, the most common site of maximal is between the sternum and the parasternal line or the sternum and the apex, that is, over the right ventricle. In both mitral insufficiency and mitral stenosis, therefore, the murmur is conducted loudest for- ward over the ventricle, though the blood impact of the regurgitant stream takes place in the opposite direction. No explanation for this apparently paradoxical condition was given until the writer, in 1910, suggested that the vibrations set up in the valves by the regurgitant streams might be propagated a long the chord se tendinese and the papillary muscles to the walls of the ven- tricles, and thus transmitted to the chest walls. In favor of this theory was the fact that the points at which the murmurs of mitral and tricuspid insufficiency are heard loud- est correspond closely to the insertions of the anterior papillary muscles in the walls of the right and left ventricles. At the writer's suggestion the matter was subjected to experi- mental test by W. T. DeSautelle and E. G. Grey (Arch. Int. Med., 1911, viii, 734). These investigators studied the intensity of the murmur produced in the dead pig's heart by the passage of a stream of water allowed to flow from a pressure bottle into the ventricles and to pass out of them through a leak at the auriculoventricular valves, which they pro- duced either by cutting the cusps or by sewing upon the latter "vegetations" made from masses of knotted cord. They then listened over the entire surface of the heart and found that the murmur was maximal over the insertion of the valves about the auriculoventricular ring and also over the areas which corresponded to the bases of the papillary muscles. When the papillary muscles were cut away from the heart wall, the murmur over these areas became greatly diminished in intensity, although over any other areas on the walls removal of any portion of its thickness tended to increase the intensity of the murmur. On the other hand, they found that when they sewed the base of a papillary muscle which had been severed from its normal attachment on to some new area of the ventricular wall, and even unon the interventicular septum, the murmur immediately became maximal at that 1 Mitral and tricuspid regurgitant murmurs may be transmitted along the papillary muscles (see page 418). 166 DISEASES OF THE HEART AND AORTA. point. The murmur due to the regurgitant stream was thus proved to be carried in the direction opposite to the regurgitation by transmission along the chordae tendinese and papillary muscles. It is probable that the same mechanism assists in conducting vibrations to the apex from the aortic valves and from the impact of streams of aortic regurgitation which strike upon the anterior cusp of the mitral valve. "ACCIDENTAL," "H.EMIC," AND " CARDIOPULMONARY " MURMURS. Murmurs over the heart without the presence of valvular lesions are so common that autopsy evidence led Laennec to the erroneous belief that murmurs (bruits de soufflet) were of no diagnostic importance whatever. Such murmurs are designated by various terms : "Haemic," on the assumption that they are always due to ana?mia, hydrsemia, or other changes in the quality of the blood; "Functional" or "inorganic," because they are not associated with organic lesion; "Cardiopulmonary" or "cardiorespiratory," on the assumption that they arise in the lung above the heart and not in the heart itself; and "Accidental," since they are not asso- ciated with any discernible alteration in form or function. These terms are not mutually exclusive; but, since the term "functional" has been used to desig- nate conditions in which there is actual leakage owing to muscular weakness, and since "inorganic" should include both "functional" and "accidental," the term "accidental" appears to be the one most generally useful. Thus, one murmur may be said to be an accidental murmur of hsemic origin, while in another case the accidental murmur may be of cardiopulmonary origin. Occurrence of Accidental Murmurs. Potain, who has made the most extensive inves- tigations upon the subject, found such murmurs in one-eighth of all the patients seen in his hospital service. It was present in almost all his cases of Basedow's disease (exophthalmic goitre). In chlorosia the frequency was 50 per cent.; in rheumatism, measles, and scarlet fever, 20-25 per cent.; in typhoid, 16 per cent.; in pulmonary affections, 5-10 per cent. These murmurs were common in subjects in the first three decades of life, reaching maxi- mum frequency at the ages from 20 to 30, and gradually decreased in frequency after the age of 30. For description of the murmurs Potain divided the precordium into the follow- ing regions: 1. About the apex (apical zone); 2. Above the apex (supra-apical); 3. Lateral from the apex (para-apical); 4. In front of the infundibulum and conus arteriosus of the pulmonary artery (pre-infundibular) ; 5. A zone between the pre-infundibular region and the apex (left prevent ricular); 6. An area behind the sternum (sternal region); 7. A region behind the xiphoid (xiphoid region). The murmurs are most common in the region lying between the pulmonary area and the apex (Potain's left ventricular region), that is, in the region above the right ventricle and the interventricular septum. Character of Accidental Murmurs. T h e s e murmurs usually are soft and blowing, and often seem rather super- ficial. They v a r y greatly when the patient changes his position. Sometimes they are best heard when the patient is lying do\\n and diminish or disappear entirely when he stands or sits up; sometimes they appear only when the patient's position is vertical and disappear on his lying down. They also vary with the phases of respiration. Time of Accidental Murmurs. As regards their occurrence in the cord in c cycle, accidental murmurs are most commonly systolic in time, though occasionally diastolic. Potain calls attention to the fact that mur- mur- may occupy either the whole of systole (holosy st oli c) or only PHYSICAL EXAMINATION. 167 a portion of it. The latter may occur only at the very beginning of systole (protosystolic), so that they accompany or replace the first heart sound. Or, they may be heard in midsystole (mesosystolic), in which case they follow the first sound but are separated from the second sound by the short pause, which is then somewhat shorter than usual. Or, they may occur at the very end of systole (telesystolic) and end, without interruption, in the second sound. According to Potain, the murmurs of mitral and tricuspid insufficiency are heard throughout the entire duration of systole, & view which is confirmed by the graphic records of Einthoven and Weiss and Joachim. The accidental murmurs, however, are con- fined to only a portion of systole. Potain believes that, as a rule, they are entirely mesosystolic; while Weiss and Joachim, from both auscultatory and graphic evidence (Fig. 110), believe that they also accompany and modify the first sound though they do not replace it; in other words, that they occupy both the proto- systolic and the mesosystolic portions of the systole. Sahli states that accidental murmurs never occupy the very end of systole (telesystolic, Potain; prediastolic), but Potain has shown that though such murmurs are rare they occur occasionally. Accidental diastolic murmurs are also rather common, and may occur either in the aortic region, behind the sternum, or along the upper left border of cardiac dulness. Occasionally they are heard at the apex. They are usually short superficial puffs following a well-marked second sound and lasting during only a short portion of early diastole. Differential Diagnosis of Accidental Murmurs. Potain gives the following points in which other murmurs differ from the cardiopulmonary. 1. Pulmonary Stenosis: loud, rough holosystolic murmur, maximum in second left interspace, transmitted toward left clavicle; always accompanied by a thrill. The accidental murmur is soft, often mesosystolic, devoid of thrill. 2. Pulmonary Insufficiency: diastolic murmur maximum in second left interspace; pulmonic second sound absent or diminished. The accidental diastolic murmurs very rarely have their maximum in the second left interspace. 3. Aortic Stenosis: rough holosystolic murmur, maximum in second right interspace, propagated toward right clavicle; accompanied by thrill. The heart is hyper- trophied. The accidental or cardiopulmonary murmur in this region is more superficial, soft, and changes on change of position. 4. Anaemia: murmur very similar to that of aortic stenosis, but the thrill is less marked and the heart is small or dilated rather than hypertrophied. 5. Aortic Insufficiency: murmur commences exactly at the beginning of the second sound and almost entirely fills diastole; whereas the cardiopulmonary diastolic murmur follows the second sound, often after a short intervening pause (i.e., the murmur is mesodiastolic). Both aortic and accidental murmurs are of wide distribution, embracing the entire precordium, and varying greatly with change of position. ft. Patent Septum of the Ventricles: holosystolic murmur loudest at the third >-ft interspace; rough, always accompanied by a thrill; whereas the accidental and cardiopulmonary murmurs are not. 7. Mitral Insufficiency: murmur holosystolic, usually rather rough, maxi- mum at the apex. The cardiopulmonary murmur may have its maximum two or three centimetres lateralwards from the apex; and this is usually associated with a systolic retrac- tion at the apex. 8. Tricuspid Insufficiency: murmur maximum over sternum and xiphoid process. There is an increased area of flatness (hypertrophy of ventricles). This murmur is also increased by leaning forwards so as to throw the heart against the chest wall. 168 DISEASES OF THE HEART AND AORTA. Nature and Causation of Accidental Murmurs, The facts mentioned above apply to a large number of cases in which murmurs have been heard during life, but in which no leaks and no lesions of the heart were demon- strable at autops3 r . A large variety of factors have been mentioned to explain these accidental murmurs: Haemic Murmurs. Bouillaud was the first to call attention to the fact that mur- murs were more readily produced in the less viscous blood of anaemia than under normal conditions; a fact which was subsequently verified by Cohnheim; but Bouillaud himself realized that, though ansemia might give rise to some of the accidental murmurs, there were many cases in which it could not be a factor. The blood counts made in later decades have entirely substantiated Botiillaud's conserva- tism. However, numerous observers from Bouillaud's time to the present have adhered to the " ha?mic " origin of the accidental murmurs. Sahli goes so far as to state that they may in reality be only venous hums transmitted to the ventricles, though he does not explain why they should be systolic in time. Even though this explanation is inadequate, it is certain that in cases of grave ansmia such trans- mitted murmurs do arise. They are heard very loudly over the aorta and second right interspace, but are loud, rough, and superficial, quite different from the gentle blow of the usual accidental murmurs. Functional Insufficiency of the Auriculoventricular Valves, especially of the mitral, was supposed by Xaunyn to be the chief cause of the accidental murmur in the pulmonary area. Xaunyn believed that this murmur was transmitted from the left auricle directly to the pulmonary artery and thence to the chest wall in the pulmonary area. However, in these cases the murmur may not be heard at all in those areas in which the definite mitral and tricuspid murmurs are best heard. Functional insufficiency of the tricuspid valve has also been assumed, but this is rendered improbable by the fact that these murmurs have a very different distribution from those of the tricuspid and are rarely heard over the xiphoid process. In dogs the writer has found accidental murmurs very common; but, in contrast to the murmurs in tricuspid or mitral insufficiency, these accidental murmurs cannot be heard over the right or left auricle. In man also they are not heard over the region of the right auricle, even when the patient is made to lean forward and the walls of that chamber are thus pressed against the chest wall. Functional Stenosis of the Pulmonary Artery and Infundibulum has been assumed by Luethje in order to explain the production of systolic murmurs in the pulmonary area. It is true that the pulmonary artery makes a sharp bend just behind the second left inter- space; and also, as Romberg and others have shown, that often the accidental murmur is increased by pressure with the stethoscope. Against this view are the softness of the murmur, the absence of a thrill, and the fact that it is not transmitted toward the left shoulder, but is well heard over the right ventricle. Moreover, in dogs the accidental mur- mur may persist in practically every position in which the heart may be held. Eddy Currents %vithin the Ventricles. Hilton Fagge has called attention to the fact that eddy currents may arise within the ventricles, as the blood passes between the papillary muscles and the trabecuhr carnse. However, W. M. Dunn and YV. S. Bennett, in the writer's laboratory, have studied this question experimentally upon the dead pig's heart through which a stream of water was allowed to flow from a pressure bottle. They found that such a stream flowing into the heart from the right auricle and out through the pulmonary artery gave rise to just such a murmur over the conus arteriosus, but that this murmur persisted even after the eddy currents were altered by cutting away the papillary muscles and the columnar carnesc. On the other hand, they found that the murmur was due largely to the direct impact of the blood stream upon the walls of the conus and that a similar stream which arose in the left ventricle impinged upon the septum ventriculorum just behind the infundibulum and wa,s transmitted to the latter. These murmurs were loudest over the infundibulum at the time that the blood stream was most rapid (i.e , in midsystole, which corresponds to the instant of the accidental murmur) and it was most intense when the viscosity of the blood and the peripheral resistance were low. All these factors corre- spond to conditions which seem to accompany the accidental murmur clinically, but though suggestive they cannot be accepted as a complete explanation of the latter without further proof. PHYSICAL EXAMINATION. 169 Similar to this view is the old-time assumption that accidental blowing as well as musical murmurs indicated the presence of a moderator band across the chamber of the right ventricle, but this is not borne out by autopsy experience. Cardiopulmonary Factors. Laennec in 1826 wrote: "In certain persons the pleurae and the anterior borders of the lungs extend in front of the heart and cover it almost entirely If one examines such a person when his heart is beating more forci- bly than usual, the diastole of the heart, compressing these portions of the lungs and forcing the air out of them, alters the breath sounds in such a way that it imitates a blowing murmur or the sound of wood file. But with a little skill it becomes easy to distinguish this sound from a cardiac murmur. It is more superficial; one hears the normal heart sounds be- low it; and it disappears almost entirely when the patient is made to hold his breath for a few moments.'' 1 Physiological experiments have borne out Laennec's claim that the lung moves to and fro with each cardiac cycle (Buisson, Voit, van der Heul, Landois, Meltzer), but have demon- strated that the most sudden movement of the air accompanies the rarefaction of the air within the lung during systole, rather than its extrusion during diastole. The cardiopulmonary murmurs formed the subject of an exhaustive study from 1865 to 1894 by Potain, many of whose data have been given above. Potain controlled the findings by auscultation with carefully made cardiograms and experimental studies and found that: 1 . The cardiopulmonary murmurs are loudest and most frequent in those regions (infundibulum and vicin- ity of the pulmonary artery) where the movement of the heart is greatest. '2. They occur in regions and in phases of the car- diac cycle at which the car- diogram shows retractions of the interspace (areas of negative pressure with sudden expan- sion of the lung). Hence, the systolic murmur is most common over the infundibulum and right ven- tricle, over which there is usually a systolic retraction (see page 143 and Fig. 89). If the retraction (fall in the cardiogram) occurs in the middle of systole, the murmur is found to be mesosystolic; if at the end of systole, the murmur is telesystolic; if the fall is in diastole, the murmur is diastolic. Indeed Potain encountered several cases in which the form of the cardiogram changed upon alteration of the position of the patient; and corresponding to the period of greatest retraction the murmur over the area changed from mesosystolic to diastolic. This is a surprising confirmation of the theory of cardiopulmonary murmurs. There can indeed be no doubt that cardiopulmonary murmurs are frequent, and that they form a very considerable proportion of "accidental" murmurs. Besides the blowing murmurs referred to above, it is probable that many of the so-called "musical'' or "squeak- ing" murmurs are of cardiopulmonary origin, and are really piping rales produced by the FIG. 109. Distribution of the accidental murmur. 1 ''Chez quelques sujets, les plevres et les bords anterieurs des poumons se prolongent au-devant du cceur et le recouvrent presque entierement. Si Pon explore un pareil sujet au moment oil il eprouve des battements du coeur un pen energiques, la diastole du ccrur comprimant ces portions du poumon et en exprimant Pair, alt ere le bruit de la respiration de manic-re a ce qu'il imite plus ou moins bien celui d'un soufHet donne par le cunir lui- meme: il est plus superficial; on entend au dessous le bruit naturel du cu'iir; et en recom- mandant au malade de retenir pendant quelques instants sa respiration, il diminue beau- coup ou cesse presque entierement." 170 DISEASES OF THE HEART AND AORTA. to-and-fro movement in the lung during either phase of the cardiac cycle. Other rales of cardiopulmonary origin more closely resembling the sonorous and crepitant ralea of respiration are also very common along the margin of the left lung. Moreover, the breath sounds themselves are frequently modified by the cardiac movements, giving rise to the so- called cog-wheel type of breathing; in which inspiration is interrupted by a series of small clicks and pauses coincident with and due to the effects of cardiac contractions upon the air in the lungs. The cog-wheel type of breathing is often associated with slight changes in the overlying lung and is thus often a premonitory sign of pulmonary tuberculosis. Differentiation between Cardiopulmonary and other Accidental Mur- murs. However, in spite of the frequency of cardiopulmonary murmurs, it is probable that Potain erred in ascribing all accidental or non-valvular murmurs to this origin. In the first place, many such murmurs are audible over the area of cardiac flatness several centimetres from the lung borders, when breath sounds which are of equal loudness over the lung cannot be CAROTID PHONOGRAM FIG. 110. Graphic record of an accidental murmur. (After Weiss and Joachim.) heard at all at these sites. Secondly, the murmurs can be well heard directly over the exposed dogs' hearts when the lung has been entirely retracted, and when valvular insufficiencies and stenoses can be absolutely excluded. For the present, therefore, it must be admitted that there are still many uncertainties in the differentiation between cardiopulmonary and other accidental murmurs. The diagnosis of the former must be confined to murmurs of distinctly superficial quality which are heard loudest over the lung bor- ders and are absent or much diminished over the area of cardiac flatness, and which vary with change of position. The diagnosis may be considered as rendered probable if the area over which the murmur is heard moves toward the sternum in inspiration and away from it in expiration, corresponding to the movement of the marginal strip of lung. If the reverse is the case and the area of intensity extends lateralward in expiration and recedes toward the sternum in inspiration, the murmur is more likely to arise within the heart. Imitations of the Heart Sounds. A remarkably accurate method for imitating the heart sounds, reduplications, and rough or blowing murmurs has been used for the past three years by the writer's colleague. Dr. Charles W. Larned. This is carried out by placing the palm of the observer's hand tightly over his ear, and then tapping upon the elbow with the finger tij>s of the other hand. The blow must be struck with loose finger-joints. Its force can be varied to suit variations in the loudness of the sound. Dull and distant sounds may be imitated by light blows of the finger or by raising the palm of the hand from the ear, snapping sounds by pressing the hand tightly upon the ear and executing a sharp stroke. Blowing murmurs are reproduced by a gentle stroking of the PHYSICAL EXAMINATION. 171 elbow. Dr. Henry Lee Smith has modified this procedure by striking the blows directly upon the back of the hand, instead of the elbow, a method by which sharper and more snapping sounds can be produced. He is able to give a very accurate reproduction of the presystolic rumble and snapping first sound of mitral stenosis by bringing all the four fingers down upon the knuckles or metacarpals in as rapid succession as possible, a manoeuvre which is best executed by a quick pronation from the elbow. The blow struck with the index ringer (snapping first sound) should be somewhat louder than the rest. While these methods are excellent for demonstrating to one student at a time, they cannot be used for demonstrating to a whole group simultaneously. For this purpose the writer has resorted to the somewhat cruder method of executing the same taps and strokes upon the top of a derby or even a soft felt hat. This imitation is not quite so accurate, and the snapping and rumbling quality are not reproduced, but nevertheless it enables the instructor to point out the salient features to all and to illustrate their main variations and relations to the events of the cardiac cycle. INTRAVENTRICULAR PRESSURE VOLUME OF VENTRICLES MITRAL SYSTOLIC AORTIC SYSTOLIC AORTIC DIASTOLIC PRESYSTOLIC FIG. 111. Diagram showing the relation of the more common simple murmurs to events of the cardiac cycle. Solid black bars indicate the heart sounds. Vertical parallel lines reaching to the base indicate blowing or rough murmur. Wavy vertical lines not reaching to the base indicate a rumble. The exact method for the reproduction of each sound or murmur can thus be indi- cated schematically by designating the finger to be used (I = index, M = middle, R = ring finger, L = little finger) and the accent of the sound'. Time intervals may be shown by dashes, and rapid succession of the split sounds by bracketing the corresponding letters. Murmurs are indicated by stroke. Thus: F I = Normal first sound at the apex; I I' = Normal first sound at aorta; stroke I' = Mitral murmur; I (I'M) = Split second sound; (IM I)=Split first sound; (I-M' I) = Presystolic gallop; I I'-M = Protodiastolic gallop; I stroke I = Mesosystolic murmur; LRMF I = Presystolic murmur; I stroke = Diastolic blowing murmur replac- ing second sound; I I stroke = Diastolic murmur following the second sound; LRMI' stroke I = Presystolic systolic murmur of mitral stenosis; Gentle to-and-fro nibbing of skin = Pericardial friction. Relations of the Simple Murmurs to Events of the Cardiac Cycle. The relations of the simple cardiac murmurs to the contractions of the cardiac chambers, as well as to the filling and emptying of the ventricles, is shown in Fig. 111. The mechanism of their production will be discussed in detail in connection with the valvular lesions to which they correspond. It will be seen, however, that the mitral systolic murmur begins coincident ly with the first heart sound before the blood flows into the aorta, and that it continues throughout systole; that the aortic systolic murmur follows the first sound and is loudest in midsystole; that the aortic diastolic murmur is loudest in early diastole, when the filling of the heart and the regurgitation are most rapid; and that the presys- tolic rumble is produced by the inrush of blood into the ventricles during auricular systole. 172 DISEASES OF THE HEART AND AORTA. SINGLE MURMURS. Time. Character. Phonetic * equivalents. Distribution. Clinical condition. 12 i j Presvstolic . . . Rumbling, occasion- ftat-ta; trs t-at; tr- Apex onlv, lower Mitral stenosis ; tri- ally blowing r-rub-dub precordium be- cuspid stenosis. 1 2 tween parasternal line and sternum a 2 Sv^tolic Blowing or roaring. Enters into or re- shush-dub; ssh-dub; jjje-dub; faf-tam Over body of heart, at apex and to ax- Mitral insufficiency ; tricuspid insuffi- places as well as illa, often at back. ciency. follows first sound. Over lower ster- Uniform or decres- num and neigh bor- cendo ing precordium Bl w" 1 2 1 ! taf-dub lit d SI ' t foUou'S first sound; uzsc right interspace; aortic stenosis; con- has a crescendo thrill also in ves- genital heart lesion. character in mid- sels of neck. Not systole and decres- so loud at apex cendo in late sys- tole i ; 1 ! Similar in character lu.isch-dub; taf-dub: 2d left interspace Pulmonary stenosis. to aortic systolic and to left of ster- congenital heart le- murmur taf-tarn num (thrill). Else- sion, aneurism. where over chest (thrill) i : 1 ! Mesosystolic or tel- Soft blowing, uni- lupff-dub; taf-tat; Over en tire precord- Functional, accident- es\>tolie \predi- form or decres- 1 2 ium, esp. 2d and al, or anaemic mur- astolic.i cendo luff -dub 3d left interspace. mur. Anaemic fever; Varying with neurasthenia etc. - change of position. sometimes organ- Not transmitted ic (?). beyond apex Diastolic Blowing lupd-sh?h; tam-taf: At 2d rib near ster- Aortic insufficiency, lup-dush; lup-shsh nal margin: loud- est over sternum at level of 2d left interspace and in the latter near the sternal margin I At 2d left inter- Pulmonary insufSci- space and right ency. sternal margin : a 1 > o to right of sternum At 2d left interspace With no other marked and sternal margin signs of valvular in- sufficiency. Abnor- mal murmur (Potain, Graham, Steele 1 . Mid-diastolic, . Rumble lub-t closely imitate the cardiac sounds when the consonants are prolonged a- much as possible. COMBINED MURMURS. Time. Character. Phonetic equivalent.-. Di.-tribution. Clinical condition. ftafta^h; tr-r-rub- Blow loudest at 2<1 Vegetation al aortic : right and 2d left in- valve, aortic insuf- du.-h ter^paoes; at apex ficiency. Sometimes, an tal heart lesions. slush-dush; slush- Over the entire pre- Fibrinous pericarditis, cordium. especial-] dush-da Accompanies both Pleuropericardial . heart sounds and both breath sounds Crepitant; small ex- plosive rales ly over the area of absolute dulness; increased by pres- sure with stetho- scope Over relative cardi-J Pleuropericarditis. ac dulness only; scratch simultane- ous with respira- tion as well as cardiac cycle. In- creased by pres- sure with stetho- scope Over relative cardi- ac dulness only Emphysema. Inter- stitial emphysema. VASCULAR SOUNDS AND MURMURS. Arterial. Besides the murmurs transmitted from the heart, murmurs also occasionally arise in the arteries themselves. A systolic murmur and an audible first sound (pistol-shot tone) may be produced by pressure with the stethoscope over the arteries, but without exerting a definite pressure it may often be found accompanying the dilatation of markedly pulsating arteries, as in aortic insufficiency and with dicrotic pulses, etc. The eddies arising in an aneurism usually give rise to a rough or blowing systolic murmur which may be transmitted for a considerable distance along the arteries. In aortic insufficiency a double murmur (sytolic and diastolic) may be heard over the arteries (Duroziez). Venous. A sound is heard over the jugular vein, especially over the jugular bulb just above the clavicle, in cases of marked anaemia, chlorosis, etc. (Camac). The murmur is humming or roaring in character and occurs during both systole and diastole (humming-top murmur, "bruit du diable," etc.). Weiss and Joachim have registered the sound and have shown that it never ceases. As shown by Cohnheim the anaemic blood flows more rapidly than does normal blood, probably owing to its lower viscosity; and both these factors facilitate the production of a murmur. However, it has not yet been shown that the murmur is loudest at those periods of the cardiac cycle during which the flow in the veins is most rapid. 174 DISEASES OF THE HEART AND AORTA. MURMURS AS AN AID TO DIAGNOSIS. It is evident from what has gone before, as well as from the consensus of medical practice, that auscultation furnishes a most important means of diagnosis of cardiac lesions. It is equally evident that each abnormal sound may be associated with any one of several clinical conditions, which must be still further differentiated from one another, not only by the mur- mur but by its distribution, transmission, and variations, but particularly by the other methods of physical examination, graphic methods, and X-ray examination. The examiner should not content himself with a simple desig- nation of the lesion, but should become fully conversant with the disturbance of function in all parts of the circulatory system, and with its remote secondary effects. BIBLIOGRAPHY. PHYSICAL DIAGNOSIS. Herz, M.: Herzmuskelinsuffizienz durch relative Enge des Thorax Oppressio Cordis, Ver- handl. d. Kong. f. inn. Med., Wiesbaden, 1908, xxv, 292. Selling, T.: Untersuchungen des Perkussionschalles, Deutsch. Arch. f. klin. Med., Leipz., 1907, xc, 163. Miiller, Fr.: Studies in Percussion, paper read before the Johns Hopkins Hospital Medical Society, Mar. 21, 1907. De la Camp, O.: Zur Methodik der Herzgrossenbestimmung, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1904, xxi, 208. Curschmann, H., and Schlayer : Ueber Goldscheider's Methode der Herzperkussion, Deutsch. med. Wchnschr., Leipz., 1905, xxxi, 1996. Ebstein, W.: Zur Lehre von der Herzperkussion, Berl. klin. Wchnschr., 1876. Goldscheider: Untersuchungen ueber Perkussion, Deutsches Arch. f. klin. Med., Leipz., 1908. xciv, 480. Moritz, F. : Einige Bemerkungen zur Frage der perkutorischer Darstellung des gesammten Vorderflache des Herzens, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxvii, 276. Dietlen, H.: Ueber die Grosse und lage des normalen Herzens und ihre Abhangigkeit von physiologischen Bedingungen, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxviii, 55. Die Perkussion der wahren Herzgrenzen, ibid.. 1906, Ixxxviii, 286. Simon, A.: Die Schwellenperkussion des Herzens an der Leiche, ibid., 1906. Ixxxviii, 246. Hoffmann, A. : Die paroxysmale Tachycardie. Dietlen, H.: Orthodiagraphische Beobachtungen ueber Veranderungen der Herzgrosse bei Infektionskrankheiten, exsudative Perikarditis und paroxysmale Tachykardie, Miinchen. med. Wchnschr., 1908, Iv, 2077. Williams, F. H.: Rontgen Rays in Medicine and Surgery. Sawyer. J.: Brit. J. Child. Dis., 1909, 525, quoted from the Arch, des malad. du coeur et " des vaisseaux. Par., 1910, iii, 385. Schieffer and Weber, A.: Die Perkussion der absoluten Herzdampfung und deren Werth fur die Bestimmung der Herzgrosse, Deutsches Arch. f. klin. Med., Leipz., 190S, xciv, 466. Veith, A.: Ueber orthodiagraphische Untersuchungen bei Kindern im gchulpflichtigen Alter. Jahrb. f. Kinderh.. Berl.. 1908. Ixviii. 205. Sahli, II.: Lehrbuch der klinischen Untersuchungsmethoden. Harvey. Wm : De mom cordis. William?. C. J. B.: Rep. Brit. Assor. Adv. Sc.. Lond.. lS3f>. p. 269. Ludwic. C., and Dogiel. A. S.: Ber. d. k. suchs. Gesellsch. math. nat. Cl., Leipz., 1869, x\. s(X Sibson and Broadbent: In Sibson's Medical Anatomy. 1S69. p. 89. Emerson, C. P.: The Effect of Pressure of the Stethoscope on Intrathoracic Sounds, Bull. Johns Hopkins Hosp., Baltimore, 1908, xix. 49. PHYSICAL EXAMINATION. 175 Smith, A. H. : On the Use of the Differential Stethoscope in the Study of Cardiac Murmurs, Med. Rec., N. Y., 1895, xlviii, 121, and Trans. Asso. A. Phys., Phila., 1896, x, 86. Cabot, R. C. : Physical Diagnosis. Boy-Teissier : L'auscultation retrosternale dans les maladies cardio-aortiques, Marseilles meU, 1892, xxix, 303; Rev. de m6d., Par., 1892, xii, 169. Hoffmann, A.: Ueber oesophageale Auskultation, Centralbl. f. klin. Med., Leipz., 1892, xiii, 1017. Gerhartz, H.: Zur Frage des Stethoskops, Deutsch. Arch. f. klin. Med., Leipz., 1907, xc, 501. Bard, L.: Du bruit de galop de 1'hypertrophie du cceur gauche, Sem. med., Paris, 1906, xxvi, 229. Also De la multiplicite anormale des bruits du coeur, ibid., 1908, xxviii, 3. Kriege and Schmall: Ueber den Galopprhythmus des Herzens, Ztschr. f. klin. Med., Berlin, 1891, xviii. Miiller, F.: Ueber Galopprhythmus des Herzens, Miinchen. med. Wchnschr., 1906, liii, 785. Marey, E. J. : La Circulation du sang a 1'etat physiologique et dans les maladies, Par., 1881. Sewall, H. : On a Common Form of Reduplication of the First Sound of the Heart, Contrib. Sci. Med. (Vaughan), Ann Arbor, 1903, 29; also, A Common Modification of the First Sound of the Normal Heart Simulating that Heard with Mitral Stenosis, Am. J. M. Sc., 1909, cxxxviii. Robinson, G. C.: Gallop Rhythm of the Heart, Am. J. M. Sc., Phila., 1908, cxxxv, 670. Chauveau, H.: Etude cardiograph! que sur la mecanisme du bruit de galop, Thesis, Paris, 1902. Pawinski, J. : Die Entstehung und klinische Bedeutung des Galopprhythmus des Herzens, Ztschr. f. klin. Med., Berl., 1907, Ixiv, 70. Duroziez and Sansom: Quoted from Bard. ' Hirschfelder, A. D.: Some Variations in the Form of the Venous Pulse, Bull. Johns Hopkins Hosp., 1907, xviii, 265. Einthoven, W.: Ein dritter Herzton, Arch. f. d. ges. Physiol., Bonn, 1907, cxx, 31. Gibson, A. G.: Upon a Hitherto Undescribed Wave in the Venous Pulse, Lancet, Lond., 1907, ii, 1380. Thayer, W. S.: On the Early Diastolic Heart Sound (the So-called Third Heart Sound), Bost. M. and S. J., 1908, clviii, 713; Further Observations on the Third Heart Sound, Arch. Int. Med., Chicago, 1909, iv, 297. Eyster, J. A. E.: Studies on the Venous Pulse, J. Exper. M., N. Y. and Lancaster, 1911, xiv, 594. Potain: La Clinique medicale de la Charite, Par., 1894. Laennec, Bouillaud, Hilton Fagge: Quoted from Potain. Luethje: Quoted from Brugsch and Schittenhelm, Lehrbuch klinischer Untersuchungs- methoden, Berl., 1908. Buisson, Voit, van der Heul, quoted from Mcltzer, S. J. : On the Nature of Cardio-pneu- matic Movements, Am. J. Physiol., Bost., 1899, i, 117. Also, Saunders, G. : Cardio- pulmonary Murmurs, Edinb. M. J., 1897, N. S., i, 522. Stengel, A.: The Significance of Systolic Murmurs over the Apex and Base of the Heart, Cleveland J. M., 1898, iii, 191; and Foshay, P. M.: A Case of Cardiopulmonary Murmur Illustrating the Importance of Differentiation, ibid., 1901, vi, 236. Putnam, J. J. : The Clinical Associations and Significance of the Cardiopulmonary Murmur, Tr. Ass. Am. Phys., Phila., 1903, xviii, 157. Brown, S. G. : Abstracted in the Scientific American, 1910, cii. Donders: Quoted from L. Hill, Schiifer's Text-book of Physiology, Edinb. and Lond., 1900, ii. Martius: Graphische Untersuchungen ueber die Herzbewegung, Ztschr. f. klin. Med., Berl., 1888, xiii, 327, 453, 558. Einthoven, W., and Geluk, M. A. J.: Registrirung der Herztone, Arch. f. d. ges. Physiol., Bonn, 1894, Ivii, 617. Huerthle, K. : Ueber die mechanische Registrirung der Herztone, ibid., 1S95, Ix. 263. Holowinski, A.: Physikalische Untersuchung der Herztone, Ztschr. f. klin. Med., Berl., 1901, xiii, 186. Einthoven, W., Flohil, A., and Battaerd, P. J. T. A.: Registriruag der menschlichen Herztone, Arch. f. d. ges. Physiol., Bonn, 1907, cxvii, 461. 176 DISEASES OF THE HEART AND AORTA. Marbe, K.: Registrirung der Herztone mittelst russender Flammen, Arch. f. d. ges. Physiol., Bonn, 1907, cxx, 205. Roos, E.: Ueber die objective Aufzeichnung der Schallerscheinungen des Herzens, Ver- handl. d. Kong. f. innere Med., Wiesbaden, 1908, xxv, 643. Frank, O., and Hess, O.: Ueber das Cardiogramm und den ersten Herzton., Verhandl. d. Kong. f. innere Med., Wiesbaden, 1908, xxv, 285. Weiss, O.: Das Phonoskop, Mediz. naturw. Arch., Berl. and Vienna, 1908, i, 437. Weiss, O., and Joachim, G.: Registrirung und Reproduktion der menschlichen Herztone und Herzgeriiusche, Arch. f. d. ges. Physiol., Bonn, 1908, cxxiii, 341. Hess: Entstehung der Herztone, Deutsche med. Wchnschr., Leipz., 1908, xxxiv, 1611. Kahn, R. H. : Weitere Beitriige zur Kenntniss des Elektrocardiogrammes, Arch. f. d. ges. Physiol., Bonn, 1909, cxxix, 291. The whole literature is reviewed in detail by Barker, L. F.: Electrocardiography and Phonocardiography, A Collective Review, Johns Hopkins Hosp. Bull., Baltimore, 1910, xxi, 358; and also by Weiss, O.: Das Phonoskop eine Vorrichtung zur Analyse und Registrirung schwacher Schallqualitaten, Med. naturew. Arch., Berl. and Wien, 1907, i, 437. Weiss, O.: Die Seifenlamelle als Schallregistrirende Membran im Phonoskop, Ztschr. f. biol. Techn. u. Methodik, Strassb., 1908, i, 49; Zwei Apparate zur Reproduktion von Herztonen und Herzgerauschen, ibid., 1908, i, 126. Gerhartz, H.: Die Aufzeichnung von Schallerscheinungen ins besondere die des Herz- schalles, Ztsch. f. exper. Path. u. Therap., Berl., 1908, v, 105; Herzschallstudien, Arch. f. d. ges. Physiol., Bonn, 1909, cxxxi, 509. PART II. i. PRIMARY CARDIAC OVERSTRAIN. IT has long been known that heart failure may arise from simple over- strain of the heart without the intervention of any actual cardiac lesions. This condition usually remains acute and ends in rapid recovery, but it may also become chronic and reduce the patient to lasting invalidism. In its worst form such a purely functional weakening of the heart may result in death. This conception was first introduced by Stokes in 1854, and was con- firmed later by studies of Clifford Allbutt, A. R. B. Myers, and Peacock in England, and da Costa in America. Their articles were collected, trans- lated into German, and published, along with an excellent monograph upon the subject, by Johannes Seitz, of Zurich, in 1875, bringing them to the cognizance of the German writers. In 1886 v. Leyden added important contributions. In 1S98 the matter was subjected to clinical experiment by Theodor Schott, whose conclusions have been disputed by a host of later and more careful observers. The most interesting, extensive, and complete of all these papers are those of da Costa, based upon several hundred cases occurring among Union .soldiers of the Civil War. It is impossible to do justice to these studies in a brief abstract. His presentation is so complete and so nearly a model of clinical study for its time that the reader is urged to consult the original publication. CLINICAL CASES. A very typical case of da Costa's series is illustrated by the following history. CASE I. Irritable lieart, chiefly from hard service; recovery. Wm. Henry H., private 6Sth Pennsylvania Vol., admitted into the Turner's Lane Hospital in Philadelphia, November 2, 1863, having just returned from a furlough. He enlisted in August, 1862, at the time in good health, though he had suffered occasionally from rheu- matism. He did a great deal of hard duty with his regiment. Some time before the battle of Fredericksburg, he had an attack of diarrhoea; after the battle, he was seized with lancinating pains in the cardiac region, so intense that he was obliged to throw himself down upon the ground, with palpitation. These symptoms frequently returned while on the march, were attended with dimness of vision and giddiness, and obliged him often to fall out from his company and ride in the ambulance. Yet he remained with his regiment until July 4, 1863, when he was wounded at the battle of Gettysburg. The wound healed in about one month: but the cardiac symptoms became worse, and violent palpitations ensued upon the slightest exertion, sometimes also whilst in bed, obliging him to rise. There was soreness in the cardiac 12 177 178 DISEASES OF THE HEART AND AORTA. region, and a constant dull pain. The impulse was extended, slightly jerky, 96, and of irregular rhythm, some beats following one another in rapid succession; the first sound was feeble, the second very distinct. The man did not look sick. Height 5 feet 7 inches; measured 31 inches around the chest one inch below the nipple; he did not smoke; chewed tobacco in moderation. The patient did not improve under aconite; but under digitalis the impulse became quiet and 78, and on March 23, having previously dona duty as orderly, he was detailed on police duty, and his treatment stopped. The heart continuing to act regularly, he returned to his regiment May 3, 1864. Another case, quoted from v. Leyden, illustrates the various phases of the malady very well. CASE II. Carl Timm, butcher, aged 30. Family history negative. Syphilis ten years before, quiescent for several years. Otherwise always healthy. Performed military service for 5 years without any trouble. In the fall of 1880 became a butcher in the Charite Hospital where he had to lift and chop sides of beef weighing 200 Ibs. The first symptoms appeared suddenly on the afternoon of December 30, 1880, during an ordinary day's work, when he felt a severe pressure in the pit of the stomach, preventing him from taking a deep breath and causing him to stop in his work. At this time he noticed palpitation and irregularity of the heart. For several days after this he did no heavy work and then felt well. When he tried to do heavy lifting again the same pain and sensation of pressure returned, and though he continued his work he was compelled to stop for breath from time to time. On Feb. 17, 1881, the pain became very intense and he entered the hospital on Feb. 21. Physical Examination. Patient is a very well-built young man, well muscled, well nourished but not fat. Complexion florid but healthy looking. No dyspnoea or cyanosis. Moderate oedema of lower extremities. Patient complains only of palpitation of the heart. The pulse is strikingly irregular so that it is im- possible to count. The radial arteries are small, blood-pressure apparently low. The cardiac impulse is intense, vibratory, and very irregular. Apex impulse is in 5th left interspace 2 cm. beyond mammilla ry 1 i n e , well marked, read- ily palpable. Cardiac dulness begins above at 3d rib, extending below to 6th rib, and reaching just to the right of the sternum. Heart sounds are feeble and unequal but clear. Lungs clear. Liver and spleen are not enlarged. Urine 500 c.c., sp. gr. 1023. no albumin. Ordered rest in bed, ice-bag over heart, infusion of digitalis every 2 hours. Within a few days symptoms and oedema had subsided, but the irregular heart action persisted. By March 20 he was well enough to be discharged, with the following note: Apex beat 0.5 cm. to left of mammillary line; first sound at apex loud and ringing, second sound distant but clear; pulse irregular; examination otherwise negative. This represents the first stage of his illness, in which the following features are noteworthy: 1. A very strong and perfectly healthy young man suffers from heart failure as the immediate result of overstrain. The first attack came on suddenly while at work and passed off soon, but attacks recurred whenever the patient did heavy work, and he was compelled to enter the hospital. 2. Physical findings: heart dilated especially in the longitudinal axis, weak apex beat (dilatation of left ventricle), great cardiac irregularity. 3. Relatively rapid improvement after rest in bed and digi- talis. 4. The heart then returned to almost normal size, but the irregu- larity in rhythm persisted. Second Stage. Patient returned to his old work in spite of warning, and within two months oedema of the legs had again set in and he was confined to bed for eight weeks more. Returning to work again, he could perform only very light labor, and very soon returned once more to the hospital for seven weeks, with still more marked oedema. Once more these disturbances disappeared after rest and PRIMARY CARDIAC OVERSTRAIN. 179 digitalis, but thereafter the slightest work caused palpitation and the feeling as though there were a tight cord about the chest. He also felt pain in the region of the liver. At this point he re-entered the hospital. Pulse 180, small, irregular. Face flushed, no cyanosis. Expression depressed. Skin normal; oedema of feet and legs. Gangrene of big toe of right foot. Respiration a little rapid, dyspnoea only on exercise, but while walk- ing he often stops to catch his breath. Occasionally he has attacks of dyspnoea lasting about 10 minutes, beginning with a feelirg of pressure in the region of the heart. He then feels as though hot liquid were pouring from the heart upwards to each side of the neck. Physical Signs. A pex beat in 6th left interspace in anterior axillary line, soft and easily compressed. Heart therefore much enlarged, sounds clear and fairly loud, action markedly irregular. Liver enlarged and tender. Ordered rest in bed, digitalis, morphine at night. Patient became much better within twenty-four hours, pulse then 68 per minute. The attacks of dyspnrea almost disappeared. Urine 1300, sp. gr. 1020. Within six days all cardiac symptoms had dis- appeared. March 11: Pulse 52. Feels well, no pain. Apex beat in 5th left interspace 3 cm. beyond mammillary line, moderately forceful. Heart sounds clear but irregular. He still occasionally has feeling of pressure in chest. Features of second stage: 1. Dilatation of heart much more marked than before. 2. Very rapid and very irregular heart action. 3. Definite attacks of pain in heart and feeling of pressure (anginoid in character), with radiating pains in shoulder and arm. 4. Swell- ing of liver (failure of right heart). 5. Return to almost normal under treatment, diminution in size of left ventricle. 6. Intercurrent affections: small infarct of lung, pressure gangrene of great toe, recovered from. Third Stage. Returned to the hospital in July, 1885 (two years later). He has been able to do very little since last admission. Now much emaciated, face thin, ap- pears depressed. Cheeks and lips slightly cyanotic. Respiration dyspnoeic and stertorous. Xo orthopnoea. Moderate cedema of shins. Cardiac impulse seen in 5th to 7th left interspaces, apex beat felt in 7th in axillary line, forcible. Heart rate about 132, irregular. Cardiac dulness 19 cm. from left sternal margin. (Upper limit of cardiac dulness as before begins at 3d rib.) Liver readily pal- pable. Sounds loud, more or less short but no murmur. Did not remain in hospital, but on October 4, 1885, was brought in again in collapse. Marked cyanosis, extremities cold, oedema of legs up to knees. Heart as before, sounds still clear. Pulse 150. Liver a hand's breadth below costal margin. Ordered digitalis, also camphor subcutaneously, tea with cognac. At midnight collapse more marked, very marked dyspnoea and cyanosis; threw himself to and fro, groaned loudly. Pulse not palpable, not revived by camphor or ether injection. At 2 A.M. became quiet; stertorous breathing set in at 3 A.M.; died quietly at 3.15 A. M. Autopsy. Marked oedema of legs. Both lungs slightly retracted, slightly adherent over apices. Pericardium distended, little fluid. Heart markedly enlarged (more than twice the size of patient's fist), especially in the longitudinal axis. Left ventri- cle more dilated than right. Distance from insertion of pulmonary artery to apex 13 cm., to right border of heart 10 cm. Length of left ventricle 15 cm. Little epicardial fat. Valves normal, aortic valves close perfectly. Papillary muscles well devel- oped, some trabecula: flattened and undergoing fibrous changes. A fibrous patch is seen on the interior surface of the left ventricle. Endocardium otherwise delicate, showing some yellow areas of fatty degeneration of the endocardium and papillary musclos. Cut surface of heart muscle shows cloudy swelling. Left auricle markedly di- lated. Right ventricle appears pale with spots of yellow. Lungs, oedema of bases. Liver, markedly enlarged; definite nutmeg liver. Kidneys, large, dark red, harder than normal. Microscopic examination shows extensive fatty degeneration of muscle-fibres, but only in the inner layers. No interstitial changes, no changes in blood-vessels or nerves of the heart. Here and there the interstitial strands of connective tissue appeared thicker than normal but without cellular infiltration. 180 DISEASES OF THE HEART AND AORTA. ETIOLOGY. In da Costa's 200 soldiers, well-marked fever preceded the overstrain in 17 per cent.; diarrhoea (among which there may have been many mild cases of typhoid fever) 30.5 per cent.; hard field service, particularly exces- sive marching, 38.5 per cent.; wounds, injuries, rheumatism, scurvy, ordi- nary duties of soldier life, and doubtful cases 18 per cent. Contrary to the belief of many observers, tobacco did not seem to be an etiological factor in his series. Allbutt gives the following etiological factors of cardiac overstrain: gymnastics, rowing, Alpine climbing, long-distance running, intense fits of anger or emotion, sexual excesses. Overstrain is very frequent among miners, metal workers, carriers of heavy burdens, blacksmiths, moulders. Morton Prince calls attention to the development of cardiac dilatation under severe mental strain, as in a civil service examination. Anaemia and chlorosis (Henschen), apparently mild illnesses, intestinal disturbances, acute alcoholism, and febrile diseases (Dietlen) are also frequent causes. Sexual excess is an important factor, especially in men; but its effects are usually more marked in hearts already weakened from other diseases or from valvular lesions than in perfectly healthy hearts. Myers, Allbutt, and Schott have shown that tight belts, uniforms, and corsets displace the heart upward, embarrass its action, and predispose to overstrain. Indeed Myers found that cavalry soldiers with tight belts suffered more from long rides than infantry from marching the same dis- tance. SYMPTOMS, SIGNS, AND CLINICAL COURSE. The chief symptoms are dulness, excitability, nervousness, loss of sleep, loss of appetite, restlessness, buzzing in the ears, vertigo, muscse volitantes, palpitation of the heart, usually very severe and often asso- ciated with a feeling of pressure or constriction over the chest. This may be very distressing, but does not, as a rule, cause the patient to remain absolutely still nor give him the fear of sudden death, though da Costa mentions cases in which the precordial distress was great enough to cause soldiers to fall to the ground in the midst of battle. Pain over the precordium and the left shoulder, occasionally down the arm, increased on inspiration and on coughing. Dull headache, dizziness, especially on bending over, sleep- lessness, indigestion, tympanites, and diarrhoea are common. The patient often wears an anxious expression and there are usually pallor and more or less cyanosis. Pulse is usually small, feeble, rapid, and often irregular. The c a r d i a c i m pulse may be barely or not at all visible, but on percussion the area of relative cardiac dulness is usually found to be enlarged considerably to the left both downward and upward, and often also to the right as well. This corresponds to the dilatation of the left ventricle and of both auricles (i.e., diameters MR and ML, Fig. 84, are much increased). On the other hand Katzenstein has shown that in just these cases the impulse may he exceptionally strong and impart a heaving to the whole chest, even though the heart be much dilated, failing, and devoid of the slightest trace of hypertrophy. A systolic retraction is usually seen over the greater PRIMARY CARDIAC OVERSTRAIN. 181 part of the precordium of these overworking hearts (Fig. 89), corresponding to the con- traction of the right ventricle (page 143). Occasionally in rapid and irregular hearts this appearance is somewhat puzzling and has led some clinicians to dictate notes of " delirium cordis" where this condition was not present at all. 1 The area of relative cardiac dulness is much enlarged (Fig. 112), especially to the left, both downwards, corresponding to the dilata- tion of the ventricle, and upwards, corresponding to the auricle. In more severe cases, especially with marked cyanosis, the dulness is enlarged also to the right from dilatation of the right auricle. Occasionally this dilatation may have passed off before the patient has been seen by the physician and only the other symptoms and signs persist, but it is safe to assume that it has been present at an earlier stage of the disease. The heart sounds may be either very distant and feeble or very short and sharp, corre- sponding to the two types of cardiac impulse. They are usu- ally unaccompanied by mur- murs, but in an irregular heart may be of uneven intensity. The second pulmonic is usually the loudest sound heard. The clearness of the first sound is often altered by a reduplication, especially in rapid hearts, or by the presence of a soft blowing systolic murmur, which is usually loudest over the pulmonic or tricuspid area, but occasionally also heard to the anterior axilla. These sounds do not always but may sometimes corre- spond to the presence of functional insufficiency of the mitral valve (vide page 409), in other cases to anaemia. It is, however, extremely difficult or sometimes impossible to decide absolutely whether such an insufficiency is present. The pulse is usually rapid, ranging from 80 to 160 per minute, small, and weak, in many cases irregular in both force and rhythm. In less severe cases there are only occasional extrasystoles (Schott) ; in the more advanced there is an absolutely irregular rhythm which persists even after the rate slows. There is often persistent tachycardia without dyspnoea, lasting for even weeks or months. Clinical Course. In some cases, however, all the signs and symptoms of overstrain may be present without any irregularity whatever, but often associated with a rapid and regular pulse. Occasionally the pulse may be regular only while it is rapid, but becomes irregular as the rate diminishes. In many cases no murmurs or other signs of valvular insufficiency are FIG. 112. Cardiac dulness in v. Leyden's case upon his three successive admissions (I, II, III). 1 The term delirium cordis is used rather indefinitely to designate conditions varying between extreme irregularity with tachycardia and true fibrillation of the heart. The onset of the latter is, however, not consistent with the existence of life. 182 DISEASES OF THE HEART AND AORTA. encountered, while in still others a relative or functional insufficiency of the mitral or tricuspid valve results from the cardiac dilatation, with some embarrassment of the heart resulting therefrom in addition to the original failure. Systolic (functional) murmurs are heard in these areas, and the stasis is still further increased by the regurgitation of blood. The oedema becomes extreme, hydrothorax may set in, and death soon results. As in the case of da Costa's patient under discussion, the progress may be stayed somewhat by occasional treatment and rest. If the latter is sufficient and the disease not too far advanced, the patient's life may be saved. The liver, as in Case II, enlarges when the condition becomes severe and tricuspid insufficiency has set in. Its edge is then smooth and varies in consistency from being rounded and so soft as to be palpable only with the side of the index finger to almost board-like hardness. It is always smooth. In severe cases jaundice may be present and the liver may pulsate. The abdomen is often distended with gas, a factor which contrib- utes largely to the cardiac discomfort by pushing up the diaphragm. In the later stages of heart failure ascites may be present. The g e n i t a 1 i a show oedema only in the later stages of the disease. The lower extremities are often oedematous, the swelling first mani- festing itself about ankles and shins. The urine during the period of heart failure is usually scant, less than 900 c.c. (30 ounces) for 24 hours, owing to diminished rapidity of blood flow. It is then of high specific gravity (1020 and over), and often contains albumin and casts. In extreme stasis numerous epithelial, coarsely and finely granular, and hyaline casts are seen in every field of the microscope. Blood. The blood picture may vary from a moderate ana?mia to a real polycythsemia, dependent upon the condition of the patient before the over-exertion. The sputum may be scanty and mucous, or profuse, frothy, and albuminous, dependent upon the relative strength of the right and left ventricles. In rare cases haemoptysis results during the exertion from engorgement of the pulmonary capillaries. Transitory Cardiac Dilatation. A particularly instructive series of cases studied with modern methods are those reported by Hornung (1908). Among 1100 cases which he watched with the X-ray during the past seven years he has met with a number who usually showed perfectly normal hearts but were subject to acute dilatation after overstrain. This was particularly frequent in persons who had used alcohol to excess, in those who had recently suffered from infectious diseases, and in anaemic indi- viduals. The attacks of dilatation are brought on by fright, high altitudes, excitement, over-exertion, etc. Sexual ex- citement might be added to this list. Hornung returns to the old view of Seitz, Allbutt, and v. Leyden, that cardiac overstrain with acute dilatation is much m ore c o m m o n than might be supposed from the work of Moritz and his pupils. For a long period, however, he may be expected to be more subject to other attacks than before, although by care he may remain free from them. Just how long this susceptibility may last varies with each case, PRIMARY CARDIAC OVERSTRAIN. 183 but da Costa has shown us that after carefully sparing the patient from all severe effort for weeks or even months, he may again perform even such severe efforts as are entailed on cavalry charges and forced marches without injury and may lead a life of perfect health. The other side of the picture is shown by v. Leyden's case. This man returned to work in spite of the discomfort. The latter became worse, and after bearing it for three months he entered the hospital with a heart already dilated and permanently irregular, and with w r ell-marked oedema of the limbs. Definite heart failure had set in. From this he recovered under- rest and treatment with digitalis. His heart resumed almost normal size, his oedema disappeared. The circulation once more returned to almost normal, but one permanent injury had been done for which the treatment was of no avail. The heart action had become irregular and remained so. The commencement of permanent absolute irregularity in rate (pulsus irregularis perpetuus) (see Part I, Chapter IV) at this stage is a very com- mon occurrence in overstrained hearts, and seems to be one of the most important factors in determining the subsequent course of the disease (see page 179). When the irregularity persists it adds its own mechanical effects on the circulation to those already present and increases the overstrain. When a life of strenuous muscular work is continued by such a patient the result is inevitable. Strain follows strain, and the condition brought about by the first failure is exaggerated with each successive day's work. The attacks of pain and pressure in the thorax (anginoid attacks) increase in severity and frequency. The heart dilates more and becomes corre- spondingly weaker. Blood stagnates in the veins, first in the more depend- ent portions, causing oedema of the ankles, shins, thighs, genitalia, then enlargement of the liver and ascites from stasis in the portal system, finally oedema of the face and arms. The heart dilates still more; the mitral and tricuspid orifices no longer close. After each attack he is less vigorous than before, and greater care must be taken to avoid exertion. For the manual laborer such a life may be at once impossible and intolerable, but the litterateur, the scholar, the scientist, and the man of affairs may be saved for years to a life of quiet but none the less useful activity in spite of a considerable degree of cardiac break-down. DIAGNOSIS. The diagnosis of primary overstrain of the heart is not always simple. It is always a question not of whether the heart has been overstrained but of whether this weakening is primary, and whether the heart was perfectly healthy before the effort was made. If the heart, muscle, or valves were in any way diseased before the effort, the overstrain may be considered as secondary to that lesion. Accordingly the diagnosis rests upon the pre- vious history, upon the nature, duration, and sequela; of previous infec- tious diseases, upon the degree of arteriosclerosis, and upon the general health of the patient before the onset of the trouble. Latent myocarditis, fatty degeneration, and arteriosclerosis are par- ticularly difficult to exclude. A mild grade of myocarditis may have given no symptom whatever in daily life, but become apparent when exercise is violent. A mild grade of arteriosclerosis is practically universal among 184 DISEASES OF THE HEART AND AORTA. persons past middle age, but if considerable efforts had been made without symptoms of cardiac insufficiency these may be disregarded. When symp- toms of heart failure occur suddenly in a robust individual during or after some intense muscular or nervous effort, acute cardiac dilatation and over- strain may usually be diagnosed with certainty, but, like hysteria among the nervous diseases, it should be arrived at only after a process of careful exclusion. BIBLIOGRAPHY. Stokes, W.: Diseases of the Heart and Aorta, Dublin, 1854. Allbutt, T. Clifford: The Effect of Overwork and Strain on the Heart and Great Blood- vessels, St. George's Hosp. Rep. (Lond.), 1870, v, 23. Da Costa, J. M.: On the Irritable Heart; a Clinical Study of a Form of Functional Cardiac Disorder and its Consequences, Am. J. M. Sci., Phila., 1871, Ixi, 17. Medical Diagnosis, Phila., 1864. Also, Observations upon Heart Diseases in Soldiers, etc., Mem. U. S. Sanitary Commission, Washington, 1867, ch. x, p. 36. Maclean, W. C.: On the Diseases of the Heart in the British Army and the Remedy, Brit. M. J., Lond., 1867, i, 161. Myers, A. R. B.: Etiology and Prevalence of Diseases of the Heart among Soldiers, London, 1870. Peacock, T. B.: Lectures on Diseases of the Heart, Med. Times and Gaz., Lond., 1873, ii, 1, 57, 113, 169, 221, 319, 349. On Some of the Causes and Effects of Valvular Dis- eases of the Heart, Lond., 1865. Seitz, Joh.: Die Ueberanstrengung des Herzens, Berl., 1875. (A monograph by the author containing translations of the articles of Allbutt, da Costa, and Myers.) V. Leyden, E.: Ueber die Herzkrankheiten in Folge von Ueberanstrengung, Ztschr. f. klin. Med., Berl., 1886, xi, 105. Schott, Th.: Zur acuten Ueberanstrengung des Herzens und deren Behandlung, Wies- baden, 1898. Hornung: Beitrage zur Frage der acuten Herzerweiterung, Berl. klin. Wchnschr., 1908, xlv, 1769. Henschen, S. E.: Ueber die Herzdilatation bei Chlorose und Ansemie, Mitth. a. d. med. Klin, zu Upsala, 1898, p. 27. Katzenstein, J.: Dilatation und Hypertrophie des Herzens, Miinchen, 1903. II. PATHOLOGICAL PHYSIOLOGY OF EXERCISE, CARDIAC OVER- STRAIN, HEART FAILURE, AND COMPENSATION. PHYSIOLOGY OF EXERCISE. It is evident from the foregoing examples that muscular efforts which lead to cardiac overstrain are in themselves merely the exaggeration of ordinary exercises. To understand these effects it is necessary first to understand those of ordinary exercise. McCurdy has classified exercises as 1. Exercises of speed, like running, chest weight exercises, etc., in which the individual movements require little effort, but the main effort lies in the rapidity with which they are repeated. 2. Exercises of en durance, as in long-distance running, prolonged walk- ing, forced marches, etc., in which the movements are neither difficult nor especially rapid and the element of strain sets in only with the onset of fatigue. 3. Exercises of strain, as lifting heavy objects, wrestling, etc. Exercises of Speed. The cases of cardiac overstrain reported by All- butt and da Costa represent overstrain from exercises of endurance; those by v. Leyden and Miinzinger represent exercises of strain. Masing, Erlanger and Hooker, Dawson and Eyster, and Gordon have investigated the effect of exercises of speed such as rapid weight- lifting, running, etc., upon man. The three last named have found that in individuals in training, whose circulation is least affected, mild exercise causes either no change or else a fall of blood-pressure. Tangl and Zuntz also found this in horses and a similar period, though of short duration, in dogs running on a tread-mill. In all muscular work an increased amount of CO 2 is given off from the muscles and acts as a hormone l which sets into play the following physio- logical mechanisms: 1. Vasodilation in the muscles, diverting four or five times as much blood through this channel (Chauveau and Kaufmann). 2. Acceleration of the heart, at first through diminution in the vagus action, and in the later stages of prolonged severe exercise chiefly through stimulation of the accelerators (Hering, Bowen). 3. Vasoconstriction, especially in the splanchnic vessels, which tends to counteract the effect of the vasodilatation in the muscles. 4. Stimulation of the augmentor fibres, and perhaps also of the heart muscle, directly, causing an increased force of contraction (higher maximal pressure) and an increased systolic output (higher pulse-pressure). Stimulation of the augmentor fibres also, as a rule, causes increased cardiac tonicity. 1 Hormone, a substance generated in one part of the body which circulates in the blood, reaches and sets into activity another organ, thus playing the role of a "chemical messenger." (Cf. Starling, E. H.: On the Chemical Correlation of the Functions of the Body, Lancet, Lond., 1905, ii, 391, 423, 501, 579.) 185 186 DISEASES OF THE HEART AND AORTA. The heart of the trained athlete is habitually throwing out an amount of blood suited, not to the needs of the moment, but to the needs of the periods of exercise to which he has accustomed himself. The systolic output is above normal when the exercise (and hence the increased production of CO,) is slight. The heart is thus able to take care of the excess CO, production in exercise without increasing its output; and hence the vasodilatation in the muscles is the only factor influencing the blood- pressure. When the exercise becomes severe the other mechanisms begin to play a role. In n o r m a 1 but not trained young men Masing found that upon lifting and lowering a weight with the feet the blood-pres- sure (maximal) and pulse-rate rose at once to a con- stant height, where they remained until the exercise ceased. They then fell almost immediately to the original level. The EXERCISE EXERCISE FIG. 113. Alterations of blood-pressure due to rapid lifting of light weights with the feet. (After Masing, Deutsches Arch. /. klin. Med., vol. bcxiv.) A. Noimal young man. B. Man aged 68. writer has found that the minimal pressure rises also, but less than the maximal, the pulse-pressure being increased. In middle-aged persons Masing found that the pressure rose higher, and on cessation of the exercise required several minutes to reach the original level; while in very old persons the rise was still greater and neither pressure nor rate returned to normal for a considerable period. The response is proportional to the effort. When exercise is continued in normal young persons and the organism readapts itself to the effort (the "second wind" setting in), blood-pressure and pulse-pressure again fall to a fairly constant level (Dawson and Hatfield). This probably explains why the heart -rate of well-trained Marathon racers is sometimes slow at the finish. In animal experiments it finds its analogy in the improved cardiac action observed as a result of clamping the thoracic aorta, and represents the response of the heart to a strain which is not excessive. T h o weaker the individual or the more severe the e x e r c i s e t h e m o r e p r o in incut become factors 2, 3, a n d 4. the greater the rise of blood-pressure and the creator the pulse-rat e. The slowness at which conditions return to normal is more or less proportional to the exertion and the fatigue. It is also true that for a given amount of exercise performed in a given time the amount of CO, formed is least when it is done with least effort bv trained individuals and increases when the effort becomes marked. PHYSIOLOGY OF EXERCISE. 187 Zuntz and Schumburg have shown upon German soldiers that a certain short march used up only 554.8 calories of energy when the subjects were fresh, but required 635.5 calories when they were fatigued. This is prob- ably due to the fact that with the increase in effort accessory muscles are called into play, many of which contract and give off C0 2 without mate- rially improving the execution of the exercise. FIG. 114. Effect of walking on a level on patient with badly broken compensation. (After Cabot and Bruce, Am. J. M. Sc., cxxxiv.) FIG. 115. Effect of prolonged exercise upon the blood-pressure of men in various degrees of muscular strength. The arrows indicate the point at which symptoms of exhaustion set in. COM- PENSATED, compensated heart lesions; FAIL- ING, broken compensation with heart failure. Up- per margins of bands, systolic pressures; lower, diastolic. Exercises of Endurance. The point at which an exercise of speed becomes converted into an exercise of endurance is more or less relative and depends chiefly upon the condition and the training of the individual. The most typical exercises of endurance, the forced march, the long-dis- tance runs (Marathon races), and long-distance bicycle races, have been carefully studied by Zuntz and Schumburg, Blake and Larrabee, Dietlen and Moritz, and R. T. Abercrombie. In these exercises the least changes occur in the best-trained individuals in whom the amount of effort put forth is least or least prolonged. The pulse-rate of the men who finished in the Marathon races at Boston showed sur- prisingly little increase, the greatest rise during the race of 1900 being from 76 before to 144 after; but the average rate after the race was 103 (Blake and Larrabee). There was frequently a moderate grade of irregularity. Zuntz and Schumburg found similar effects. The blood-pressure after the race was usually found to be a trifle lower than before the start 3 though it varied greatly in different individuals. J. Barach has recently obtained similar results with the Erlanger apparatus upon another set of trained Marathon racers; although the orthodiagraph showed dilatation of the heart in all. Quite different are the results in long-distance races run by amateurs. Dr. R. T. Abercrombie has recently made a careful study of the condition of contestants in a twenty-mile road race before and immediately after the race. Before the race the average blood-pressures with the Erlanger apparatus were: maximal 120-130, minimal 75-80; pulse-rate 80. Immediately after the race the pulse was in almost every instance too feeble to be counted, as were also the heart sounds; and neither these nor the blood-pressure could be satisfactorily estimated until one-half hour after the finish, when the pulse-rate was usually about 120 per minute, the maximal pressure about 75-100 mm. Hg. The heart sounds were still' 188 DISEASES OF THE HEART AND AORTA. rapid and feeble. Nevertheless all of these men felt quite well, and were able to enjoy a cold plunge immediately after the examination. Within an hour after the finish they were all feeling quite active. The blood-pressure was usually found to be lower than be- fore the start, but this varied greatly in individual cases. 1 Not all the results of endurance tests are as mild as these. During the amateur athletic contests in the United States the past five years there have been several cases of permanent heart failure following directly upon overstrain in long-distance runs. As in da Costa's series, the persons whose hearts were injured were usually boys under twenty who were poorly trained and whose hearts were not fitted for the strain put upon them. As regards the metabolism during such exercise Zuntz and Schumburg, and also A. Loewy and L. Zuntz, found that both the amount of CO, given off per minute and the respiratory quotient were markedly lessened (CO 2 falling from 802.3 c.c. to 743.0 c.c. per minute; respiratory quotient falling from 0.855 to 0.780) at the end of the exertion, though the O, used was unchanged. This is due to formation of intermediate oxidation prod- ucts, sarcolactic acid, 3-oxybutyric acid, etc., the pressure of whose salts may add to the fatigue. Moreover, the lessened output of CO 2 indicates a lowCO 2 content of the blood (acapnia), and, as Henderson has shown, this in turn causes dilatation of the veins and causes the blood to gradually leave the arteries, stagnate in the venous reservoir (see page 31), and thus diminish the rapidity of the blood flow. Corresponding to the variations in rapidit}' of blood flow, the urine is increased in amount during mild exercise, decreased during severe exer- cise. After boat races and after the Marathon races it often contains albumin, casts, and even traces of blood, probably as a result of stasis or high pressure in the renal veins and capillaries. Exercise of Strain. The effect of exercises of strain, lifting, etc., is totally different. McCurdy, Bruck, and others have shown that these exercises cause a far greater rise of blood-pressure than do the exercises of speed; and, on the other hand, the pulse-rate does not rise rapidly but is at first either slowed or unchanged. The rise in blood-pressure is greater in arteriosclerotics, old per- sons, and weak individuals for the same amount of work than in well- developed normal individuals. In per- sons already suffering from broken compensation, on the other hand, the heart absolutely fails to respond with increased effort, and may be so greatly weakened by the strain that the blood- pressure may fall. All the factors which are called into play by the hormone action of CO 2 in exercises of speed and of endurance are also acting in exercises of strain; but. since the latter are usually intermittent or of short duration, their effects are at first overshadowed by others which are more intense. 1 O. S. Lowsley (Am. J. Physiol., 1911, xxvii, 446) has found that the more severe the exercise the longer the systolic pressure remains subnormal after it is over. FIG. 116. Kise of blood-pressure during Valsalva's experiment and during exercise. Normal individual. (Schematic, after Bruck.) ARTERIOSCLER, curve of blood-pressure in man with arteriosclerosis performing the same exercise. PHYSIOLOGY OF EXERCISE. 189 In carrying out any exercise involving muscu- lar strain the individual involuntarily closes his glottis and executes an attempt at forced expira- tion. The result of this is a tremendous increase in intrathoracic pressure, which hinders the outflow of blood from the right ventricle as well as the inflow into the right auricle. The result of these two factors is dilatation of the right ventricle and stasis in the systemic veins, which is still further shown by the cyanosis of the face and distention of the veins that accompany all such exercises even in trained athletes. The venous stasis is further increased by the sudden squeezing out of blood from the large masses of skeletal muscles, which are being forcibly contracted simultaneously, as well as from the vessels of the splanchnic area. The high pressure within the lungs stimulates the sensory endings of the vagus, which in turn reflexly stimulate the motor nucleus of the vagus and the vasomotor centre in the medulla and cause both slowing of the pulse and rise of blood-pressure. The general result is the same, but less marked when the Valsalva experiment only (forced expiration with glottis closed) is carried out, and depends very largely upon this factor. SIZE OF HEART AFTER EXERCISE. Diminution in Size in Healthy Hearts. Examined with the X-ray the auricles are seen to dilate greatly, but the ventricles do not, as a rule, show any dilatation whatever. This again is a question of tonus, and here FIG. 117. Semi-schematic drawing showing variations in size of the heart of a long-distance bicycle rider, as the result of a very long race; reconstructed from the orthodiagraphic outline. A. Before the race. B. Immediately after the race, showing the gieat diminution in size of the heart. C. Four weeks later. (After Moritz and Dietlen, Munchen.med. Wchnschr., 1908, Iv.) also the latter factor seems to determine whether dilatation shall set in or not. All exercises when sufficiently severe lead to dilatation of hearts whose myocardium has suffered injury, especially during the course of infectious diseases (da Costa, Zuntz and Schumburg, de la Camp, Moritz and Dietlen) or during the first few weeks following them. On the other hand, Schott has claimed to have seen cardiac dilatation in healthy wrestlers and bicycle riders as a result of short wrestling bouts. This fact has been disputed by a number of observers who have carefully controlled the more or less subjective find- ings of percussion by outlining the heart with the orthodiagraph. The following exercises have been studied: bicycle riding, by Mendelsohn, Albu, Beyer, Schieffer, Dietlen and Moritz; marching, by Zuntz and Schumburg, Albu and Caspari, Balders, Heichelheim and Metzger; football playing, by F. Pirk and by Solig; ski running, by Henschen; wrestling, by Levy-Dorn, Selig, Mendl and Selig; swimming, by Kienbock, Selig and Beck. The results of these observations quite uniformly confirm those of de la Camp in showing that exercise, even to the point of exhaustion and 190 DISEASES OF THE HEART AND AORTA. fainting, does not bring about cardiac dilatation in otherwise healthy men. In most cases the X-ray and orthodiagraph show an actual diminution in the volume of the heart l (see Fig. 117). De la Camp also found that healthy dogs could run upon a tread-mill until they dropped from exhaustion with- out causing dilatation of the heart; whereas the hearts of dogs which had been poisoned with phosphorus and which were in a state of mild fatty degeneration dilated greatly from the same exercise. Dilatation and Myocardial Injury. On the other hand, Hornung, who has watched the course of 1100 cases of weak heart with the X-ray, states that in such persons acute dilatations (demonstrable with the ortho- diagraph) are very common as the result of slight overstrain. It may require comparatively little strain to bring this about. For example, he cites the case of a woman with a weak heart who acquired a dilatation by taking a short cut instead of a gradual ascent while climbing a hill (OertePs Terrainkur). The dilatation lasted for several days and gradually passed off. Persons whose hearts are in this labile equilibrium are liable to have repeated attacks. But the cardiac condition rarely stands still. It grad- ually becomes either better or worse, according to the treatment and the mode of life of the patient. Thoracic and Abdominal Constriction as a Factor in Cardiac Over= strain. A high diaphragm due to tight belts or corsets is one of the most important factors which predispose to cardiac overstrain. This was already shown by A. R. B. Myers in 1867. Myers observed that certain cavalry regiments in the Indian Army were particularly subject to cardiac over- strain and to chronic cardiac disease, even more so than the infantry regi- ments which were doing more arduous work under the same conditions of climate and diet. He noticed that the uniforms of this cavalry regiment were very tightly belted and had tight cuirasses compressing the chest. Upon experimentation he found that the men in this regiment, when not wearing their uniforms, were quite as strong as those of other regiments in the service. He also found that the same men were able to withstand much greater exertion in the same uniforms if only the belts were worn looser. This has been shown with somewhat greater exactness by Th. Schott. Schott demonstrated with the orthodiagraph that wrestlers could withstand much greater exertion before the onset of acute dilatation or of cardiac symptoms if they wore no belts than if they were tightly belted. This is, of course, not surprising, and is simply another way of demonstrat- ing the every-day experience of most healthy women that they can do more work without a corset or with a loose one than when wearing one that is tightly laced. The reason for this is twofold. The belt interferes with the respira- tory movements of the abdomen and diaphragm, and hence diminishes the rhythmic alternation of positive and negative pressures, of force-pump and suction-pump action, in one of the largest of the vascular reservoirs, thus 1 The syncope (cerebral amemia) under these conditions is probably due to the exactly opposite condition, diminished cardiac filling and hence diminished c a r d i a c output; arterial anaemia due to rapid pulse-rate in a heart whose tonicity is increased. (This condition is fully discussed in the chapters on Paroxysmal Tachycardia and Miscellaneous Heart Diseases.) PHYSIOLOGY OF EXERCISE. 191 diminishing the rapidity of blood-flow. Moreover the viscera are pushed back and the diaphragm is pushed upward by the belt, and this causes the heart to assume a more transverse position, in which kinking of the great veins, the aorta, and the pulmonary artery sets in, and both the filling and the emptying of the heart are impeded. This mechanism is readily demon- strated upon the exposed heart of the living animal. A comparatively slight upward or downward displacement of the heart from its natural posi- tion may cause tremendous fall in blood-pressure and interference with the work of the heart. PHYSIOLOGICAL FACTORS BRINGING ABOUT DILATATION. The diminution in the size of the heart which w r as found so uniformly by the above-mentioned observers seems to be due, in part, to diminished filling of the ventricles when the heart is rapid, but chiefly to the fact that the cardiac tonicity was increased by the strain. 1 This clinical observa- tion has its analogue in experimentation on animals. 0. Frank has shown that, other things being equal, a moderate increase in intraventricular pressure acts as a stimulus and causes an increase in the force of the next beat. If the pressure is raised further it reaches an optimum; but if it VOL. B. P. FIG. 118. Effect of strain upon the dog's heart whose tonicity is good. Volume curve (VOL.) and blood-pressure curve (B.P.) of an animal whose heart is in good condition. Descending thoracic aorta clamped at the moment indicated by the arrow. Momentary dilatation followed by a diminution in size. The heart becomes smaller than before the clamping. Tonicity is increased (T ). Blood- pressures maximal and minimal are also increased. becomes too high the force of contraction becomes much weaker than if there were no load at all. There is a similar effect upon cardiac tonicity. Hirschfelder has shown that if the thoracic aorta of the dog is clamped the ventricles at first dilate rapidly and the systolic output diminishes. If the heart is in good condition the systoles soon begin to increase, the excess of blood is pumped out of the ventricular cavities in systole, and on the other hand, in spite of the high pressure in the veins, less blood enters the ventricles than before. 1 It is possible that acapnia (page 49) may play a role under these conditions. 192 DISEASES OF THE HEART AND AORTA. The amount of blood which enters the ventricles depends upon two factors: 1. As Ho well and Donaldson have shown for the excised heart, and Roy and Adami for the dog's heart in situ, it is more or less propor- tional to the venous or intra-auricular pressure. 2. Roy and Adami, Hirschfelder, Cameron, and others have shown that it is also dependent upon the cardiac tonicity, being greater when tonicity is low (dilatation) and least when tonicity is high. It is therefore evident that a heart whose tonicity is high will withstand a comparatively high venous pressure with- out dilating, whereas when the tonicity is low it readily overfills. Several factors contribute toward diminishing the strength of an over- filled heart: 1. With the increase of the cubical contents and the internal surface of the ventricles the mechanical work necessary to exert a normal VOL. B. P. FIG. 119. Volume curve of a dog whose cardiac tonicity is low. Clamping the aorta is followed by permanent dilatation and only a slight momentary increase in blood-pressure. The systolic output i~ diminished, owing to inability of the heart to force the usual quota of blood against the increased resistance. pressure is increased (Roy and Adami). 2. In the dilated heart the blood flow through the coronary arteries and hence the nutrition of the cardiac walls is diminished (Hyde). Moreover the dilatation of the ventricles may or may not be permanent, dependent upon the tonus of the heart muscle (Hirschfelder, Cameron). If the latter is low the dilatation remains and increases, whereas if it is high the increased pressure acts as a stimulus. It is usually a high venous pressure which keeps the heart dilated and a low tonir'ity which permits it to remain so. Since the venous pressure is certainly highest in the exercises of strain, it is not surprising that permanent heart trouble arising in previously healthy persons as a. result of primary cardiac overstrain is particularly common among persons (butchers, porters, stevedores, etc.) who lift the heaviest weights. EFFECT OF THE STRAIN' UPON" THE HEART. The response of the heart to a muscular exertion which just fatigues may be of three grades: 1. The heart becomes smaller or the cardiac outlines are unchanged tonicity high (normal hearts). 2. There is a transitory dilatation (after acute infections and in hearts with myocardial or some other cardiac disturbance). 3. The overstrain leads to perma- nent injury of the heart, often with permanent arrhythmia (chronic car- PHYSIOLOGY OF EXERCISE. 193 diac overstrain, myocardial changes). These three conditions find their analogues in the effects of clamping the thoracic aorta upon the volume of the ventricles (Fig. 119). As has been seen in the cases quoted above, the repetition of the strain is quite as important a factor in heart failure as is the overstrain itself. Even a heart with extremely low tonicity will, in most cases, recover and gradually return to normal volume after the strain has been removed, but during the period when it is still dilated it is much more susceptible to a further overstrain. On the other hand, after a sufficient period of rest it regains its former volume and still later its former tonicity, and once more reaches its original strength. That this is probably the case in man also is shown by the fact that Poynton did not regard an occasional overstrain Fro. 120. Effect upon the volume of the dog's heart produced by clamping the descending tho- racic aorta. Ascent of curve = diminution in volume; descent = dilatation. 1, normal and vigorous heart; 2, slightly weakened heart with diminished tonicity; 3, very weak heart with much diminished tonicity. as of any special significance in boys, provided it w'ere followed by a period of sufficient rest. Moreover, Meylan has found that the lives of oarsmen upon the Harvard boat-crews were somew r hat longer than the average for normal individuals, in spite of the fact that albuminuria and other signs of cardiac overstrain, are quite common just after such races. Indeed not a single case of cardiac disease developed among the 1.12 oarsmen of his series, which comprised members of the intercollegiate crews from 1S52 to 1802. There was only one case in which enlargement of the heart was noted and one case of irregularity, but neither of these inconvenienced the patient. These individuals, in contrast to cases like that of v. Leyden, had rested sufficiently between the periods of strain, and the second strains had not been imposed upon their hearts until long after their strength and tonicity had returned to normal. In v. Leyden's case and other cases of permanent 13 194 DISEASES OF THE HEART AND AORTA. heart failure, the heart was still dilated at the time of renewed strain. This condition seems to determine the border-line between heart failure and recovery. The border-line conditions may therefore be summarized as follows: Dilatation of the heart during or after exercise represents a pathological, though not a very infrequent, condition in which the heart has overstepped its limits. The condition usually recedes and leaves no traces unless the heart is again overstrained while still in a dilated condition. As regards the anatomical changes induced by the condition of over- strain, Roy and Adami have shown that, when the dog's heart begins to fail after clamping the aorta, stasis occurs in the coronary veins and the heart muscle becomes oedematous. This oedema is especially marked in the regions which are richest in connective tissue, the auricles and the auriculoventricular valves. They believe that when the strain is con- tinued the ceclema is replaced by infiltration, the infiltration by connective tissue, and that fibrous myocarditis results. Indeed, a fibrous myocarditis (cardiosclerosis) is a common autopsy finding in cases of long-continued cardiac overstrain in which there has been no severe infectious disease to account for the lesion. On the other hand, Fleisher and Loeb and Pearce have found exactly the stages mentioned by Roy and Adami in animals in the various stages of adrenalin myocarditis (see page 304). BROKEN CARDIAC COMPENSATION. As long as the heart is able to maintain a certain velocity of blood flow throughout the circulation, the latter may be said to be compensated; but when the blood stagnates to such a degree as to give rise to the signs and symptoms of stasis, compensation may be said to be broken. There are two forms of broken compensation. When the blood stag- nates in the systemic veins from failure of the right side of the heart, the condition may be termed broken systemic compensation; when stasis occurs in the lungs because the left side of the heart is not acting as strongly as the right , broken pulmonary compensation results. Each of these two forms brings with it a characteristic group of symptoms: The broken systemic circulation (usually designated simply as "broken compensation") manifests itself in the signs and symptoms which are seen in tricuspid insufficiency breathlessness, cyanosis, oedema, begin- ning in the feet and legs, enlargement of the liver, and systolic pulsation of the liver and veins, etc. Broken pulmonary compensation is accom- panied by the signs and symptoms of an acute severe mitral insufficiency- intense respiratory disturbance, dyspnoea, cough, occasionally pulmonary hemorrhage, and the sputum containing the characteristic cells of passive congestion (Herzfehlerzellen) . Broken Systemic Compensation. From the physiological stand-point, the cardinal features of broken systemic compensation are dilatation and weakening of the right ventricle, dilatation and paralysis of the right auricle, increase 'n CO., and decrease in (), in the venous blood, functional insufficiency of the tricuspid valve, rise in venous pressure (often to as high as 20 mm. Hg) (Fig. 121, III). The signs are cyanosis, engorgement and systolic pulsation of the veins, enlargement of the liver, ceclema of the BROKEN CARDIAC COMPENSATION. 195 feet and legs, and sometimes venous stasis in the medulla, vasoconstriction. high blood-pressure, and dyspncea of medullary origin. Broken Pulmonary Compensation. The characteristics of broken pul- monary compensation are dilatation and weakening of the left ventricle, dilatation and usually paralysis of the left auricle, rise of pressure and stasis in the pulmonary veins, engorgement of the pulmonary capillaries, and "erection" of the lung tissue (v. Basch) (Fig. 121, IV). Welch has shown that when the stasis is very intense, pulmonary oedema sets in. V. Basch and his pupils have applied this idea to the milder pulmon- ary manifestations and have shown that a moderate erection of the lung tissue brings on cardiac dyspnoea and leads to bronchitis and cough. His pupil, Kauders, has shown that the position of the diaphragm is affected reflexly by the amount of blood in the lungs, congestion causing the diaphragm to descend, depletion causing it to ascend. It is thus usually lower than normal in mitral lesions, higher in pulmonary and tricuspid. NORMAL ii BROKEN PULMONARY COMPENSATION III BROKEN SYSTEMIC COMPENSATION IV FAILURE OF BOTH VENTRICLES FIG. 121. Diagram showing changes in the circulation. I, normal; II, broken pulmonary com- pensation; III, broken systemic compensation; IV, both compensations fail; stases in lungs and veins. AO, pressure in the aorta, PA. (Compare with Fig. 26.) V. Basch also believed that the congestion of the lungs causes the elastic- ity of the lungs to diminish and to become so rigid as actually to diminish the respiratory expansion, but the experiments of D. Gerhardt have thrown doubt upon this phase of his conclusions. As regards the changes of pres- sure and the distribution of the blood, however, v. Basch's conclusions have been confirmed, not only by Gerhardt in Germany but by W. G. MacCallum and McClure in America. In badly weakened hearts both forms of broken compensation may be present, sometimes features of one, sometimes of the other, predomi- nating. Functional Valvular Insufficiency in Broken Compensation. Although it has not been absolutely proved, it seems almost certain that the occur- rence of broken compensation from acute dilatation is accompanied by a functional insufficiency of the tricuspid or the mitral orifice which may be of transitory duration. Indeed this functional insufficiency of the tri- cuspid valve in heart failure is much more common than organic lesion of 196 DISEASES OF THE HEART AND AORTA. the valve, and in long-standing cases is accompanied by actual stretch- ing of the tricuspid orifice (T. W. King, G. A. Gibson, Mackenzie, Keith). T. W. King, in 1837, demonstrated that such functional insufficiencies occur at the triscupid valves, and even that they were dependent upon the tonic it y of the ventricular fibres; since the valves which had been in- sufficient a few hours after death held water perfectly after rigor mortis had set in (quoted in full on page 486). These observations have been confirmed and extended by G. A. Gibson, Frangois-Franck, Mackenzie, Friedreich, Marey, Hirschfelder, Keith. Hering demonstrated the same phenomenon for the mitral valve in rabbits, but found that in dogs the mitral valve did not leak even after clamping the aorta. Stewart and the writer have been able to demonstrate the occurrence of such an insuffi- ciency of the mitral valve when the aorta was clamped, in dogs whose aortic valves had been rendered insufficient. In man Morton Prince and Broadbent have noted the presence of transitory mitral systolic murmurs (sometimes transmitted to the axilla) in men who were being subjected to the strain of civil service examinations, and in cases with similar signs Minkowski has obtained tracings from the oesophagus which have the form characteristic of mitral insufficiency. In the earlier stages of cardiac overstrain the dilatation of the auricles is a more or less passive phenomenon which exerts little influence upon the circulation, but in the more severe stages it may play a leading role. Auricular Fibrillation and Arrhythmia in Cardiac Overstrain. Condi- tions which affect tonicity and filling of the ventricles have a still greater effect upon the tonicity and filling of the auricles. It was demonstrated by Ludwig's pupils, Waller (1878) and v. Frey and Krehl (1890), that when the ventricles began to fail, the auricles soon became overloaded with blood and ceased to contract visibly when the pressure reached 15-20 mm. Hg. As a rule this does not affect the cardiac rhythm, but Hirschfelder has shown in dogs that when this is brought about by narrowing the mitral orifice, an absolute irregularity (disorderly rhythm) may set in without any coordinate contractions carried out by the auricles. The contractions of the auricles under these circumstances do not give rise to any (a) waves upon the venous pulse, which is of the ventricular type; a'id when the latter furnished the sole criterion of cardiac activity it was believed that these chambers were either not contracting at all or were merely originating impulses without active contrac- tions, as Biedcrmann had shown for skeletal muscle. Lewis has shown with the electro- cardiograph that the latter occasionally takes place (P wave present upon the electrocardio- gram with (a) wave absent from venous pulse) while the pulse remains regular, but when irregularity sets in there are either extras ystoles or auricular fibrillation. The latter, and especially the finer type of auricular fibrillations, represent the more severe forms of cardiac failure. Arrhythmia. Whatever may be the origin of the arrhythmia it is very common in severe overstrains. This not infrequently arises in the course of valvular lesions as well, as Mackenzie has proved. The case cited on page 436 gives an example of such an irregularity arising during such an attack and subsiding a few days later after rest and digitalis. Five days later the rhythm became regular and the auricles were contracting once more. When the overstrain is more protracted the auricular contraction may remain absent for weeks and even months, and most frequently, if it has persisted for a considerable length of time, j>ermanent changes set in in the musculature of the sinus region (Keith, Schonberg), and regularity is never regained. The pulse has become permanently irregular (pulsus irregu- laris perpetuus, arrhythmia perpetua). As has been seen on page 127, the arrhythmia BROKEN CARDIAC COMPENSATION. 197 itself slows the blood stream and the diseased condition of the sinus prevents the heart from compensating for this by a greater number of contractions. The velocity of the circulation is thus self-limited. Only a certain amount of CO 2 per minute can be taken care of and any excess brings on overstrain. Changes in Venous Pressure. Changes in pressure in the systemic veins, which show how well the right ventricle is pumping, often afford an excellent index of the break in systemic compensation, rising from normal pressure of 5-10 cm. H 2 to a height of 20 or 25 cm. It usually rises when the patient's condition becomes worse and falls as improvement sets in (Hooker and Eyster). The arterial pressure, on the other hand, is affected by too many factors to show characteristic changes. It may be kept up until shortly before death, by asphyxia of the medullary centres and resultant vaso- constrictor and augmentor stimulation; or, on the other hand, when this mechanism is not brought into play, the arterial pressure may be low and the pulse may be small and weak. CARDIAC FAILURE WITH A SMALL HEART. There is another form of failure of the circulation which sometimes occurs as the result of exertion, even in trained athletes. This form is accompanied by pallor, a small rapid pulse, and sometimes even by syncope. However, as Dietlen and Moritz have shown, it is not accompanied by a dilatation of the heart, but, on the contrary, the latter is smaller than normally. It is a failure of the rest of the circulation rather than of the heart. It must be admitted that this condition has not attracted much attention, and but little can be said of the mechanisms involved. The pallor, small pulse, and small heart, however, are features which are also common to the condition of shock and the cardiac neuroses. In these conditions, the important mechanical factors are the accumulation of blood in the dilated abdominal veins, giving rise to a low venous pressure, the diminished filling of the heart, and consequently the diminished output into the aorta. The symp- toms are symptoms of ''arterial anaemia." The causal factor in bringing about this condition may be dilatation of the veins. In the case of exercise this veno- and vasodilatation may result either reflexly from dis- turbed digestion, or, perhaps, as Henderson suggests for somewhat similar conditions, it may set in when the rapidity of breathing exceeds that necessary to aerate the blood, even to meet the increased needs of the body. Under these conditions CO, leaves the lungs, and hence also the blood, a little too rapidly, acapnia results, and, as its first effect, allows the veins to dilate (see page 49). The blood thus stagnates in the veins. As a matter of fact, Kraus, Zuntz and Schumburg, and also A. Loewy have shown that at this stage of exercise less CO 2 is given off from the lungs than before, and the respiratory quotient CO, is lessened. They believe that oxidation is less at this stage and hence less CO 2 is present in the blood. In other words, from a totally different stand-point, and years before Henderson's experi- ment, it was rendered probable that a state of acapnia is present at the stage of fatigue in exercises of endurance, and therefore that the mechanism which he observed to be active in acapnia is largely responsible for this form of circulatory failure. FUNCTIONAL TESTS OF CARDIAC EFFICIENCY. It is evident from the facts discussed above that the most important question in the functional study of heart failure is to determine accurately the border-line between fatigue and overstrain, to distinguish between the nor- mal and the pathological. Various tests have been devised for this purpose. 198 DISEASES OF THE HEART AND AORTA. 1. Postural Change in Pulse-rate. The rise in the pulse-rate which oc- curs when the patient stands after lying down is of some importance. Under normal conditions the acceleration is not more than twenty beats per minute, the average acceleration for normal individuals being seven. However, this depends upon many factors, one of which is the length of time during which the patient has lain down, his state of mental excitement or quiet, etc. The psychic element plays a particularly important role in this test. 2. Contraction of Antagonistic Muscles. Herz has introduced another procedure, the self-checking or self-antagonizing test (Selbsthemmungsprobe). He counts the pulse over a period long enough to assure a reasonably constant rate per minute. The patient is then made to sit down and very slowly flex and extend the right forearm, putting, all the while, his full attention upon the movement, but contracting simultaneously the flexor and extensor muscles of the arm, and attempting to antagonize his own move- ment with as much force as possible. This converts the exercise into a mild exercise of strain. Herz states that in normal individuals this causes no change in pulse-rate, while in those with feeble hearts the pulse-rate is s 1 o w e d 5-20 beats per minute. (Per- haps this is due to the more vigorous expiratory effort which accompanies this procedure in persons with diseased hearts.) Cabot and Bruce have repeated Herz's observations, and find that they are correct in at least a certain number of cases, but they are unwilling to subscribe to his general rule. The writer also has found a number of perfectly strong and healthy individuals who give Herz's pathological reaction. 3. Rise of Blood=pressure on Constricting the Femoral Arteries. Marey (1881) demonstrated that in normal individuals the blood-pressure rose when both femoral and both brachial arteries were compressed. Katzenstein found that on com- pressing both femoral arteries alone, in Blood-pressure Pulse-rate Normal individuals Rose 5-15 mm Fell. Compensated cardiac lesions Rose 15-40 mm Unchanged or fell. Slight cardiac insufficiency Unchanged Unchanged or rose. Very weak hearts Fell Fell. Hoke and Mende and others have repeated Katzenstein's observations, and find that, though these results hold true in general, the method is unreliable as a test and in bad cases is too dangerous for use. 4. Rise of Blood=pressure upon Exercise. Another method, introduced by Graupner, of Nauheim, depends upon the rise of blood- pressure which occurs during exercise. Graupner found that, as Masing had shown, mild rapid exercise, such as walking up and down stairs rapidly, etc., caused a rise of blood-pressure in normal individuals but a fall of pressure in those with failing hearts. His observations have been repeated on a considerable series of patients by Baur (also of Nauheim). Baur used the stationary bicycle as a test, regulating the effort by applying a loaded brake to the wheels. He found that in normal individuals there was at first a rise of 5-10 mm. Hg, and later a fall of 5-10 mm., while in insufficient hearts there was a fall of 5-20 mm. Hg. The limit of performance of the latter was 45-300 Kg. of work, however, only a small fraction of that which could be done by the normal individuals. Cabot and Bruce also have repeated and confirmed Griiupner's observation, and believe that it will prove of assistance as an aid in functional diagnosis. 1 That a close relationship exists between the increase in blood-pressure and the increase in tonicity (stimulation of augmentor fibres), which results from strain put upon the heart, may be seen from the curves of Hirsch- felder and Cameron in the dog's heart (quoted on page 191, and shown in Figs. 118 and 119). It is probable that, in most cases, rise of pressure cor- responds to increased systolic output and concomitant increase in tonicity. It must be realized, however, that in some cases the rise may be secondary to stimulation of the vasoconstrictor centre from medullary stasis or asphyxia, and then may represent an unfavorable condition. 1 According to C). S. Lowsley, if the systolic blood-pressure remains subnormal for more than an hour and a half after the end of the exercise, the latter has been too severe. FUNCTIONAL TESTS OF CARDIAC EFFICIENCY. 199 Several objections may be made to the value of this test: 1. G. A. Gordon in G. A. Gibson's clinic and also Professor Dawson, in collaboration with Professor Eyster and also with Mr. Hetfield, have shown that the blood-pressure in trained athletes falls during mild exercise exactly as it does in broken compensation ; also that it falls when the "second wind" is acquired and while the person's functional power is increasing rather than decreasing. 2. As already shown by Masing, the greatest rises of blood-pressure occur in old and feeble persons, whom the exercise brings near to the border-line of cardiac overstrain. 3. In persons in whom the fall in blood-pressure occurs as a result of the test exercise, the general symptoms, respiratory distress, cyanosis, etc., to say nothing of the decrease in the size of the pulse, tachycardia and arrhythmia resulting, are more than sufficient evidence that the patient's strength has been overtaxed. 4. These simpler clinical manifestations are more delicate indices and are less ambig- uous signs than are the changes in blood-pressure. The recent studies of Schott, de la Camp, v. Criegern, Hornung, Moritz and his pupils, taken in conjunction with the physiological experiments of Frank, Hirschfelder, and Cameron, indicate that the only true numerical criterion of cardiac efficiency is whether a given strain causes it to diminish in size (increase in tonicity=stimu- lation) or to dilate (decrease in tonicity = overstrain). Functional studies upon the border-land between functional suffi- ciency and cardiac failure are of the most fundamental importance, and all the facts added to our knowledge of the subject are of the greatest value in adding to our understanding of the subject. Observation versus Estimation. However, it must be admitted that, in order to be decisive, all these tests usually have to be pushed to a point at which the appearance, sensations, and signs of the patient are in them- selves perfectly characteristic of cardiac insufficiency, and at which, for diagnostic purposes, a little common-sense observation is at least as unam- biguous as observation with elaborate apparatus. This does not mean that exercise tests are unimportant. On the contrary, they are of the greatest value; and no change in the patient's mode of living during convalescence or during after-life should be undertaken without them. But their impor- tance depends more upon the care with which the physician watches the gen- eral appearance and condition of the patient, the rapidity with which he recovers from the exercise, 1 his general condition, and whether nervousness, irritability, cough, or insomnia has set in during the twenty-four hours following it, than in the numerical changes which occur at the moment of exercise. The symptoms to be looked for as evidence of overwork are dis- cussed in more detail in the instructions for giving Schott exercises (page 269). These are subtler manifestations resulting from smaller changes than may be detected by even the most refined observations by mechanical methods, and which are less easily masked by ambiguities. Moreover, it must be realized that any one form of exercise furnishes data which may depend as much upon the condition of the skeletal muscles as upon the heart. The blacksmith with a diseased heart may be able to do more work than the book-keeper with neurasthenia, and yet under the conditions in which he lives, even if not under the strength test arranged for the average man, the blacksmith's heart may be failing. 1 Lowsley's criterion (the return of the systolic pressure to normalj should be taken into account. 200 DISEASES OF THE HEART AND AORTA. Relation of Functional Test to Mode of Life. In diagnosis, prognosis, and therapy, the testing of functional insufficiency is a matter of sociology as well as physiology. The important question is not what the patient can do in a gymnasium, but what he can do and what he can not do in every-day life. Each man must be fit for his own mode of life or must be made to change it. His cardiac power must be studied with reference to that mode of life rather than with reference to a rigid scheme. Probably the most thorough system of routine functional testing ever instituted was that resorted to by J. M. da Costa during the Civil War before he permitted his convalescents from cardiac overstrain to return to active duty with their regiments. He subjected them first to light camp duties, then to guard duty, then to provost duty, and later made them run frequent races comparable to charges upon a battlefield each test commensurate with the mode of life which the patient was about to live. Step by step he ascertained the endurance of his patients without overstraining them, and thus obtained a series of permanent cures which stands as a worthy monu- ment to one of the most careful and brilliant of American clinicians. BIBLIOGRAPHY. PATHOLOGICAL PHYSIOLOGY OF CARDIAC OVERSTRAIN. McCurcly, J. H.: Effect of Maximal Muscular Effort on Blood-pressure, Am. J. Physiol., Bost., 1901, v, 95. Masing, E.: Ueber das Verhalten des Blutdrucks des jungcn und des bejahrten Menschen bei Muskelarbeit, Deutsch. Arch. f. klin. Med., Leipz., 1901, Ixxiv, 253. Erlanger, J., and Hooker, D. R., vid. p. 54. Dawson, P. M., and Eyster, J. A. E.: Unpublished observations. Gordon, G. A.: Observations on the Effect of Prolonged and Severe Exertion on the Blood- pressure in Healthy Athletes, Edinb. M. J., 1907, xxii, N. S., 53. Tangl, F., and Zuntz, N.: Ueber die Eimvirkung der Muskelarbeit auf den Blutdruck, Arch. f. d. ges. Physiol., Bonn, 1898, Ixx, 544. Kaufmann, M.: Recherches experimentales sur la circulation dans les muscles en activite physiologique, Arch, de Physiol., Par., 1892, 5 ser. iv, 27S. Chauveau, A., and Kaufmann, M.: Compt. rend. Acad. des sc., Par., 1SS6, Nov. 29, and May 10, 25, June 20, 1887. Hering, II. E.: Ueber die Beziehungen der extracardialen Herznerven zur Steigerung der Herzschlagzahl bei Muskelthatigkeit, Arch. f. d. ges. Physiol., Bonn, 1895, Ix, 429. Bowen, W. P. : The Pulse-rate as Modified by Muscular Work, Contrib. Sc. Med., dedicated to V. C. Vaughan, Ann Arbor, 1904. Dawson and Het field: Unpublished observation. Zuntz and Schumberg: Studien zu einer Physiologie des Marches, Berl., 1901. Hough, Th.: On the Physiological Effects of Moderate Muscular Activity and of Strain, Science, Lancaster, 1909, X. S. xxix, 484. Blake, J. B., and Larrabee, R. C., Scannell, D. D., Tileston, W., Emerson, W. R. P., Strong, L. W., and Conollv, J. M.: Observations upon Long-distance Runners, Bost. M. and S. J., 1903, cxlviii, 195. Abercrornbie, R. T.: Personal communication. Dietlen, II., and Moritz, F.: Ueber das Verhalten des Herzens nach langdauernden und anstrengendem Radfahren, Miinchen. med. Wchnschr., 190S, Iv, 4S9. Loewy, A.: Die Wirkung ermudender Muskelarbeit auf den respiratorischen Gasstoss- wechsel, Arch. f. d. ges. Physiol., Bonn, xlix, 405. Zuntz, L.: Untcrsuchungen ucber den Gasweehsel und Energieunsatz des Radfahrers, Berl., 1899. Bruck. E.: Ueber den Blutdruck bei plotzlichen starken Anstrengungen und beim Val- Falva'schen Versuch nebst, Bemerkungen ueber die hierbei eintretenden Verander- ungen der Herzgrosse, Deutsch. Arch. f. klin. Med., Leipz., 1907, xc, 171. FUNCTIONAL TESTS OF CARDIAC EFFICIENCY. 201 De la Camp, 0.: Experimentelle Studien ueber die acute Herzdilatation, Ztschr. f. klin. Med., Berl., 1904, li, 1. EFFECT OF BICYCLE RIDING ON THE HEART. Mendelsohn, A. A., Albu, Beyer: Quoted from Moritz and Dietlen and Kienbock, Selig, and Beck. Moritz, F.: Ueber Herzdilatation, Miinchen. med. Wchnschr., 1905, lii, 681. Moritz, F.: Zur Frage der akuten Dilatation des Herzens durch Ueberanstrengung, Mi'm- chen. med. Wchnschr., 1908, Iv, 1331. Schieffer: Ueber Herzvergroesserung infolge Radfahrens, Deutsch. Arch. f. klin. Med., Leipz., 1907, Ixxxix, 604. Dietlen, H., and Moritz, P\: Verhalten des Herzens nach langdauerndem Radfahren, Munchen. med. Wchnschr., 1908, Iv, 489. MARCHI XG. Zuntz and Schumberg, I.e.; Albu and Caspari, Balders; Heichelheim and Metzger: Quoted from Kienbock, Selig, and Beck. FOOTBALL PLAYING. Pick, F., Schig: Quoted from Kienbock, Selig, and Beck; also Gordon. CLUB SWINGING. Gordon, G. A.: Observations on the Effects of Prolonged and Severe Exertion, Edinb. M. J., 1907, X. S. xxii. SKI RUNNING. Henschen: Quoted from Kienbock, Selig, and Beck. WRESTLING. Schott, Th.: Acute Overstraining of the Heart, J. Am. M. Assoc., Chicago, 1907, xlviii, 1423. Levy Dorn, Selig, Mendl and Selig: Quoted from Kienbock, Selig, and Beck. SWIMMING. Kienbock, Selig, and Beck: Untersuchungen an Schwimmern, Munchen. med. Wchnschr., 1907. liv, 1427. Frank, O.: Die Dynamik des Herzmuskels, Ztschr. f. Biol., Munchen. , 1895, xxxii, 370. Howell, W. H., and Donaldson, F.: Experiments on the Heart of the Dog with Reference to the Maximum Volume of Blood sent out by the Left Ventricle in a Single Beat and the Influence of Variations in Venous Pressure, Arterial Pressure, and Pulse-rate upon the Work done by the Heart, Phil. Tr. Roy. Soc., Lond., 1884, Pt. i. 139. Roy, C. S., and Adami, J. G.: The Failure of the Heart from Overstrain, Brit. M. J., Lond., 1888, ii, 1321. Contributions to the Physiology and Pathology of the Mammalian Heart, Phil. Tr. Roy. Soc., Lond., 1892, clxxxiii, 199. Hirschfelder, A. D.: Recent Studies on the Circulation and their Importance to the Prac- tice of Medicine, J. Am. M. Ass., Chicago, 190S, li, 473. Cameron, P. I).: Physiological and Pharmacological Studies upon Tonicity of the Mam- malian Heart, Thesis, Edinburgh, 1908. Hyde. I.: The Effect of Distention of the Ventricle on the Blood Flow through the Walls of the Heart, Am. J. Physiol., Bost.. 1898, i, 215. Meylan, G. L.: Harvard University Oarsmen, Harvard Grad. Mag., 1904. xii. 302. 543. Welch, W. H.: Zur Pathologic des Lungenodems, Virchow's Arch. f. path. Amu., Berl., 1878, Ixxii, 375. Sahli, H.: Zur Pathologic des Lungenoedems, Ztschr. f. klin. Med., Kcrl., 1SSS. xiii. 4S2. Zur Pathologic und Therapie des Lungenoedems, Arch. f. cxper. Path. u. Pharmakol., Leipz.. 1885, xix. 433. Klinisch-experimentelle Untersuchungen aus dem Laboratorium von S. v. Basch, Berl., 1891, vol. i; 1892, vol. ii: 1896. vol. iii. Vol. i. Grossmann, M.: Das Muscarin- 202 DISEASES OF THE HEART AND AORTA. Lungenoedem, p. 7 (also Ztschr. f. klin. Med., Leipz., 1887, xii, 550). V. Basch, S.: Ueber eine Function des Capillardrucks in den Lungenalveolen, p. 49; Pathologie der cardialen Dyspnoe, p. 53. Grossmann, M.: Experimentelle Untersuchungen zur Lehre vom acuten allgemeinen Lungenoedem, p. 80 (also Ztschr. f. klin. Med., xvi). Bettelheim, K., and Kauders, F.: Experimentelle Untersuchungen ueber die kiinstlich erzeugte Mitralinsufficienz und ihren Einfluss auf Kreislauf und Lunge, p. 144. V. Basch, S.: Ueber Lungenschwellung und Lungenstarrheit, p. 171; Zur Lehre von der cardialen Dyspnoe, p. 183; Ueber Lungenschwellung bei der cardialen Dyspnoe des Menschen, p. 198. Kauders, F.: Ueber einige Experimente zur Lehre yon der Cardialen Dyspnoe, p. 211. Vol. ii. Zerner, Th. J.: Ueber den Einfluss der Digitalis auf die Respiration, p. 19. Grossmann, M.: Ueber Stauungshyperaemie in den Lungen, p. 30. Kornfeld, S.: Experimenteller Beitrag zur Lehre vom Venen- druck bei Fehlern des linken Herzens, p. 126. Vol. iii. Hegglin, C.: Experimentelle Untersuchungen ueber die Wirkung der Douche, p. 1. Zerner, Th. J.: Klinisch- experimentelle Untersuchungen ueber die cardiale Dyspnoe, p. 77. Buday, K.: Ueber die Herzfiillung wahrend des Lebens urid nach dem Tode, p. 106. Winkler, F.: Experimentelle Studien ueber die Funktionelle Mitralinsufficienz, Ztschr. f. klin. Med., Berl., 1899, xxxvii, 456. Gerhardt, D.: Ueber die Compensation von Mitralfehlern, Arch. f. exper. Path. u. Phar- makol., Leipz., 1901, xlv, 186. MacCallum, W. G., and McClure, R. D.: On the Mechanical Effects of Mitral Stenosis and Insufficiency, Trans. Ass. Am. Phys., Phila., 1906, xxi, 5; and Johns Hopkins Hosp. Bull., 1906* xvii. Hering, H. E.: Zur experimentelle Analyse des unregelmassigen Pulses, Arch. f. d. ges. Physiol., Bonn, 1900, Ixxxii, 1. Minkowski, O.: Zur Deutung der Herzarhythmien mittelst des oesophagealen Kardio- gramme, Ztschr. f. klin. Med., Berl., 1906, Ixii. Prince, M.: Physiological Dilatation and the Mitral Sphincter as Factors in Functional and Organic Disturbances of the Heart, Am. J. M. Sc., Phila., 1901, cxxi, 188. Broadbent. Quoted from Prince. Waller: Die Spannung in den Vorhofen des Herzens wahrend der Reizung des Hals- markes. Arch. f. Physiol., Leipz., 1878, 525. V. Frey, M., and Krehl, L.: Untersuchungen ueber den Puls, ibid.. 1890. p. 31. Biedermann, W.: Elect rophysiology. transl. by F. A. Welby, Lond., 1896. Kraus, Fr.: Die Ermiidung als Mass der Constitution, Bibliothec. Med. Cassel. Abth. D., 1897, Heft 3. Stephens: Blood-pressure and Pulse-rate as Influenced by Different Positions of the Body. J. Am. M. A.ssoc., Chicago, 1904, xliii, 955. Herz. M.: Eine Funktionspriifung des Kranken Herzens, Deutsch med. Wchnschr., Leipz., 1905, xxxi. 215. Cabot, R. C., and Bruce, R. B.: The Estimation of the Functional Power of the Cardio- vascular Apparatus, Am. J. M. Sc.. Phila. and X. York, 1907. cxxxiv. 491. Ma rev. E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Paris, 1SS1. Katzenstein: Ueber eine neue Funktions priifung des Herzens. Deutsche med. Wchnschr., Leipz. and Berl., 1905, xxxi, 695. Hoke, E., and Mende. J.: Ueber die Katzensteinsche Methode zur Priifung der Herz- kraft. Berl. klin. Wchnschr., 1907, xliv, 304. Levy: Ueber Kraftmessung des Herzens, Ztschr. f. klin. Med.. Berl., 1906. Ix. 74. Fellner. B.. and Riidinjrer. C'.: Beitrag zur Fimktionsprufting des Herzens, Berl. klin. Wchnschr.. 1907. xliv. 417. 475. Gniupner: Die Messung der Herzkraft. Miinchen. 1905. Baur. Fr.: Zur Bestimrnung der Leistungsfahigkeit de> tresunden und kranken Herzens durch Muskelarbeit, Verhandl. d. Kong. f. inn. Mepite of vasoconstriction of marked increase in force of heart-beat in spite of empty- ing of vascular system and of relaxation of peripheral vessels. Quite independently of the-e changes the right border of cardiac d ni- ne < s recedes one or more centimetres toward the sternum, the venous pressure should fall, and the general condition should improve (cf. Fig. 127 and case on paire 317). Contraindications to Venesection. However, it must be borne in mind that venesection can do harm as well as good. Gushing lias shown that in conditions with increased intracranial tension, among them apoplexy, the 1 Heubner lias shown that two-thirds of the viscosity of the blood is due to the cor- puscles, hence venesection cannot fail to reduce the viscositv. TREATMENT OF FAILURE OF THE HEART. 223 FIG. 127. Effect of venesection on the cardiac out- high blood-pressure is a phenomenon of physiological compensation, whick is necessary in order to maintain the circulation through the medulla. In conditions with long-continued high blood-pressure, especially chronic nephritis, this may also be the case. In these conditions venesection with a view to lowering the arterial pressure is contraindicated; but in these, as in other conditions, it is still the procedure of choice to relieve pulmonary cedema or acute dilatation of the right heart. The venesection should be carried only to the point of relieving the venous stasis, not to that of low- ering the arterial pressure. 1 DIET. Rest for the gastro-intestinal tract is quite as important for the heart as is rest for the mus- cles. Erlanger and Hooker have line - showing diminution in size of right heart. (Case of G. G.) Solid line indicates cardiac outline before ShOWn that an increase in pulse- venesection, broken line after venesection. pressure becomes manifest within a few minutes after the beginning of the meal, reaches its maximum within one or two hours, and, as a rule, declines somewhat more slowly. It seems to pass off within one or two hours after the maximum has been reached. The pulse-rate is always distinctly increased with the ingestion of meals. .... The product P. P. X P. R., representing the velocity, follows the curve of the pulse- pressure," hence the velocity of flow and the work of the heart are increased. Accord- ingly, the diet should be light, just enough to keep the patient nourished without ever giving him a sense of fulness or to allow gas to form in the stom- ach and intestines. Distent ion of the stomach pushes up the diaphragm and causes the heart to lie more transversely in the thorax, embarrassing its action, causing a diminution in the systolic output and an increase in the pulse-rate. Xot infrequently this is also associated with onset of precordial pain and constriction. Accordingly a very light diet is necessary for the patient suffering from heart failure. The 1 a c t o - 1 V. Tabora (Verhancll. d. Kong. f. innere Mod., 1909, xxvi, 382) finds that venous stasis can be relieved by placing tourniquets about both arras and both legs as well as by venesection. BEFORE VENESECTION AFTER VENESECTION FIG. 128. Typical effect of venesection upon the circu- lation. Arrows indicate change in blood-pressure. 224 DISEASES OF THE HEART AND AORTA. cereal diet is the best, consisting mainly of milk, eggs, custards, junket, toast, zweiback, and crackers. The numerous prepared cereal foods contain large amounts of bran and other substances which leave bulky fecal residues. If given in large quantities, they keep the bowels full, push up the diaphragm, and thus embarrass the work of the heart, though in some persons this is counterbalanced by their purgative action. Meat should be given sparingly, partly because the purin bodies (xanthin, hypo-xanthin) tend to raise the blood-pressure and increase the work of the heart, and more particularly because the meat fibres are relatively slow in digestion. For this reason it is better to take the proteid food in the forms mentioned above. Finely hashed Hamburg steak, lamb chops, or chicken are the best forms of meat. Liquid and Salt. Liquids should be limited to 1500 c.c. (three pints) a day in cases where oedema is present, since an excess of liquid ingested causes further accumulation of cedema as well as bringing on a slight overfilling of the blood-vessels, and thereby increasing the work of the heart. Salt should also be withheld from the food as far as possible, since "\Vidal and Javal, Strauss and Richter have shown that it is a contributing factor in the production of cedema, and Barie reports good results from the diminution of XaCl in the diet in diseases of the circulation. Barie recommends the following articles as a basis for a diet low in sodium chloride: Type I Unsalted bread 500 Gm. (18 oz.), raw meat 400 Gm. (14 oz.). butter 80 Gm. (2^ oz.). sugar 100 Gm. (3* oz.). Type II Pota- toes 1000 Gm. (32 oz.), raw meat 400 Gm. (14 oz.), butter SO^Gm. (2i oz.), sugar 150 Gm. (5 oz.). Sample Diet. An excellent diet for severe heart cases, which may at least serve as a basis for other variations, is the following, slightly modified from that used for cardiac cases in the wards of the Johns Hopkins Hospital: 8 A.M. Cereal, soft egg. toast, milk 200 Gm. (vi oz.). 10 A.M. Milk 200 c.c. (vi oz.), soft egg, crackers. Dinner (noon). Soup, chicken, potatoes. 4 P.M. Milk 200 c.c. (vi oz.). Supper, G P.M. Milk 200 c.c. (vi oz.), soft egg. crackers, prunes. 1 9 P.M. Milk 200 c.c. (vi oz.), bread. Limited Milk Diet. In cases of broken compensation with extreme cedema great success has sometimes been attained by limiting the diet to GOO to s()0 c.c. of milk in 24 hours (Karell, Hoffmann. Jacob and Hirsch- feldi. oven in cases in which all other therapeutic measures have failed. Professor Barker has occasionally obtained excellent results by increasing the proteid intake upon this diet through the addition of nut rose to the milk. However, striking results with this method are by no means the rule, and it is to be used with caution. Alcohol. A very little alcohol, either as wine, or as brandy or whiskey, may !> allowed to persons accustomed to its use. Beer is less advisable. ' ; IT is important to avoid jrivinj: stewed fruits which contain much acid, such as peaches and apricots, aloiiir with the milk, as the digestion of patients with broken compensation is very easily disturbed, and an attack of vomiting places a considerable strain on the heart. TREATMENT OF FAILURE OF THE HEART. 225 since it carries with it large quantities of liquid and often disturbs the digestion as well, whereas, wine, whiskey, or brandy in small quantities improves it. Against this is balanced the deleterious effect of alcohol upon the heart muscle. Large quantities tend to produce fatty degeneration of the latter. Whether small quantities have any such effect in the individual case is uncertain, but it must be borne in mind that the injured organ is much more susceptible to deleterious influences than is the healthy organ. It is a safe rule that, in persons not already addicted to its use, brandy or whiskey be given only in doses which serve as carminatives, and not in doses intended for stimulation. Even the psychic effect may often be secured as well by small doses as by large ones. One point in favor of alco- hol in man as against animal experimentation lies in the fact that in such persons it greatly increases the sense of well being and removes psychic depression and worry. The latter may be especially straining upon the heart, and hence every effort should be made use of to ward it off, especially during certain crises; but it should be borne in mind that the patient may easily become dependent upon the drink to arouse his spirits and in this state more harm than good is done. The greatest judgment should be used in the administration of alcohol even in small quantities, and it should even then be reserved for crises when the stimulation of every fibre is all-impor- tant. On the other hand, alcohol should never be withdrawn suddenly from persons addicted to its use, since this procedure often precipitates an attack of delirium tremens, but moderate doses (whiskey 15 c.c. or oz. every four hours) should be given. Tea and Coffee. Whether tea and coffee should be given depends largely upon the patient. In some persons these cause marked general nervousness, sleeplessness, tremor, and even palpitation and irregularity; 1 others have established a tolerance such that no effect at all is produced. The caffein itself is an excellent cardiac tonic of the digitalis order, and where its effects on the nervous system are not manifest it may prove an excellent adjuvant to the treatment. (A cup of coffee or of strong tea contains about 0.1-0.2 Gm., 1^ to 3 gr.; the pharmacological dose of pure caffein being 0.05 to 0.25 Gm.) As a rule it is safer to remove them from diet, but in this as in all other rules individual exceptions can be made. Tobacco should not be used under any circumstances. Besides the ner- vous symptoms, it produces vasoconstriction, and often irregularities, palpita- tion, and even precordial pain. Hence it is particularly to be avoided in cases of cardiac disease. PURGATION. In patients with cardiac disease, and especially in those with broken compensation, the question of purgation assumes unusual importance. In these patients purgation seems to have a threefold beneficial action: first, by eliminating the products of waste and putrefaction, to which they are particularly sensitive; secondly, by relieving the distention of the bowels from gas which tends to push up the diaphragm and to embarrass the heart by placing it in a more transverse position; and thirdly, by removing fluid from the body through the bowels. This last effect is probably of con- 1 Coffee from which the caffein has been removed may be used with impunity. 15 226 DISEASES OF THE HEART AND AORTA. siderable importance, since Askanasy, Kast, and others have shown that broken compensation is accompanied by hydra?mic plethora. Hydra?mic plethora causes a rise in venous pressure and a dilatation of the heart (Roy and Adami, Cameron), thus embarrassing the circulation. Moreover, in broken systemic compensation the venous stasis also affects the kidneys and diminishes the excretion of fluid, so that the bowel becomes an impor- tant accessory channel of elimination. It is therefore the hydragogue purgatives which are indicated in cardiac failure and not merely the pur- gatives which increase peristalsis. In most cases the best method of procedure is to start movement of the bowels with calomel in either large single doses (0.3-0.6 Gm., grs. v-x) or in small divided doses (.006 Gm., gr. T V half-hourly). The dose of calomel should always be accompanied by a small dose of bicarbonate of soda (0.3-0.6 Gm.. gr. v-x) to avoid disturbing the digestion. Still more certain purgation is obtained by giving a single dose of calomel and rhubarb in equal quantities (0.3 Gm., gr. v), given at night. In all cases the calomel should be followed by a saline purgative the next morning. Epsom salt or some aperient water is preferable to Seidlitz powders or effervescent citrate of magnesia, partly because of the action of the organic acids upon the residium of calomel, but chiefly because the carbonic acid in the drug distends the bowels and pushes up the diaphragm, thus embarrassing the action of the heart. However, Epsom salts and aperient waters sometimes cause nausea, and in such cases the advantages gained from the mildness of the Seidlitz powder may outweigh its deleterious effects. After constipation has been overcome purgation with salines should be continued vigorously until the oedema has completely disappeared. Just how vigorously this purgation should be maintained is a matter of some dispute. Some clinicians, who regard presence of fluid as the most dele- terious factor, believe that the best results are obtained with ten to fifteen fluid stools in twenty-four hours, with the elimination of two or three litres by the bowel. Most observers, however, believe that the beneficial advan- tages of such extreme purgation are more than counterbalanced by the strain which they place upon the patient, not only by disturbing his rest, but also by causing a considerable rise of both arterial anil venous pressure with each movement of the bowels. Indeed, each effort at stool constitutes atypical Yalsalva's experiment, which, as has been seen (Fig. 116, p. 188), is accompanied by tremendous rises in blood-pressure and in weakened hearts by acute dilatation. Mr. AY. I-!. Dandy has shown that the rise of arterial pressure during the act of defecation is from 30 to .">0 mm. Ilg. and Mr. ('. ('. Cody has found a corresponding rise in the venous pressure. These observations are sup- ported by the fact that sudden death at stool is by no means uncommon in cases of cardiac disease, especially in cases of aortic insufficiency, and occiii's even when the movements have 1 been kept soft by daily purgation with salts. In this, as in most other therapeutic procedures, extreme measures are to lie avoided and treatment >hould be directed to secure a few easy bo\vel movements without too much disturbance to the patient. In many cases one or two compound cathartic pills (colocynth, jalap, gamboge, and TREATMENT OF FAILURE OF THE HEART. 227 calomel) at night and a dose of Epsom salts or aperient water in the morn- ing maintain just the correct number and quality of stools. Compound jalap or compound licorice powders are also useful from time to time. In stubborn cases elaterium or a drop of croton oil may be resorted to, but should be used with extreme caution. On the other hand, cascara, aloes, strychnine, belladonna, castor oil, phenolphthalein, and the other purgatives which purge by increasing peri- stalsis, are of less value in the stage of broken compensation, since they do not deplete the portal system nor relieve the hydraemia, though they are satisfactory enough when compensation has been reestablished. MASSAGE. Massage of the muscles brings about a dilatation of their capillaries and thus lowers the resistance through this part of the circulation. In this respect the effect is similar to that of exercise, but, as very much less C0 2 is given off, the velocity of the blood strain does not have to be in- creased. The blood-pressure falls and, in contrast to the effect of exercise, the strain upon the heart is diminished. It is, therefore, not surprising that in most patients suffering from poorly compensated cardiac disease, massage of the limbs should furnish considerable relief. When the heart is not too severely weakened, the effect upon the circulation of lymph also facilitates the absorption of oedema. Massage of the abdomen alone has been recommended by Cautru and Studzinski, and the latter has reported excellent results in twenty-two cases. The treatment was usually accompanied by fall of blood-pressure, owing to the dilatation of the abdominal vessels. Besides this effect, however, abdominal massage also tends to prevent constipation and to dispel accumulations of gas, both of which effects furnish considerable relief for the cardiac condition. Vibration of the Precordium. Besides these more general forms of mas- sage, Zabludowski, Selig, and Rimbach state that considerable benefit may be obtained for precordial pains, mild angina pectoris, and other sensory disturbances about the heart, by gentle vibratory massage or mechanical vibration over the precordium. The vibrations should be carried out either with the balls of all four fingers of the right hand or with the soft pad of the mechanical vibrator, and should be begun under gentle pressure well out in the lower left axilla, gradually passing upward and inward over the precordium until the entire cardio-aortic area has been covered. Selig and Rimbach have made use of this method in cases of dilatation of the heart, which they studied by means of the orthodiagraph. In these cases they claim to have obtained not only relief of the subjective symptoms but actual diminution of the dilatation as the result of the vibratory massage. Rimbach states that his observations were controlled by Dr. Bussenge and Prof. Steyrer, but the results of a greater number of cases must be awaited before this effect upon cardiac dilatation can be regarded as general. ELECTRICITY. Faradization of the precordium and left arm, and particularly the use of sinusoidal currents over these areas, may be considered as a form of counterirritation which may prove very efficient in relieving precordial paiii 228 DISEASES OF THE HEART AND AORTA. and discomfort; but care should be taken not to use currents of so great a severity as to produce real pain. A somewhat different effect is that secured by Prof. J. 0. Hirschf elder in patients of angina pectoris (see page 383) by applying the galvanic current with a large anodal pad (4 cm. in diameter) over the vagus in the neck and a large cathode (6-12 cm. in diameter) over the precordium. He recommends gradually increasing the current to 20 milliamperes for five minutes, changing the anode to the other side of the neck and repeating. The relief obtained under this treatment warrants its further trial. High=frequency Currents (d'Arsonvalisation). Many writers, especially of the French school, incline to the use of high-frequency currents (d'Arson- val), especially in cases of arteriosclerosis, Raynaud's disease, and other con- ditions involving the peripheral circulation. It seems to bring about dilata- tion of the peripheral vessels and fall of blood-pressure, as has been reported by Zimmern and Riffaut. Marque has reported excellent results in a very stubborn case of Ray- naud's disease treated by high-frequency currents over the lower cervical and upper thoracic vertebras, and Zimmern and Riffaut claim a beneficial effect upon the circulation in endarteritis obliterans. Except in Raynaud's disease, in which the effects upon the spinal centres and ganglia are to be considered, there seems to be no reason for regarding it as very different from other means of securing intense dilatation of the cutaneous vessels. SURGICAL MEASURES FOR THE RELIEF OF HEART FAILURE. For patients whose hearts are beating so heavily against the chest wall that this factor alone seemed materially to increase the work of the heart, Alexander Morison, in 1897, advised cutting the ribs over the heart, and thus allowing the organ free movement. This operation was carried out at his suggestion in 1908 upon a patient with aortic insufficiency, who obtained thereby considerable relief from palpitation ar.d precordial pain. The same operation (cardiolysis) was devised independently by Brauer, in 1904, for the relief of pericardial adhesions, in which it has been employed with great success (see page 608). G. A. Gibson has also found some relief following thoracostomy in a patient with mitral stenosis and adhesions between the outer layer of peri- cardium and the chest wall but not involving the pericardial cavity itself. The second operation might also be performed in cases of extreme flat- ness or narrowness of the chest (oppressio cardis, cf. page 700), provided the heart was so cramped as to give rise to symptoms of severe cardiac weakness that could not be relieved by other means. The results thus far from thoracostomy are sufficiently good to justify its use for the relief of costapericardial adhesions (see page 608), but in other forms of cardiac failure it should be resorted to only after unusual considera- tion of all factors. INHALATION' OF OXYGEN. Leonard Hill and Flack have shown that inhalations of oxygen greatly increase the endurance of men and animals when performing muscular work. TREATMENT OF FAILURE OF THE HEART. 229 This applies, however, only when the work reaches the point of strain. For example, he found that it had no effect in increasing the speed of race-horses running on a level track, whereas ordinary work-horses pulled a load uphill, when fatigued and then given an inhalation of oxygen, more rapidly and with less exertion than they had done when fresh to the task. Similarly, little effect was noticed upon the ability of athletes to perform the exercises to which they had been trained; but, on the other hand, the endurance of untrained men was greatly increased. The effect of oxygen inhalations, even on a trained man working to the full limit of his endurance, was tested by Flack upon Wolffe, the English Channel swimmer. Flack accompanied the swimmer in a small boat. When he became fatigued and about to give up the effort, Flack allowed him to inhale oxygen occasionally, with the result that from a condition of exhaustion he was able to swim for several hours further without dyspnoea or cardiac distress. Mackenzie has made use of this method in the treatment of cardiac disease, and has found that in some cases it gives a certain amount of relief, especially for restless nights; though the relief was neither as great nor as universal as he had anticipated. Sir Clifford Allbutt and Herz have also used it with good results. Mackenzie makes use of Hill and Flack's method of inhaling the con- centrated oxygen from under a mask, which can be made extemporaneously by inserting the patient's head into a lady's hat-box, cutting out one side so as to fit around the neck. A more convenient mask may be made from a piece of light mackintosh, near one margin of which a piece six inches square is cut out and replaced by gluing on a piece of transparent celluloid to cover the face. This margin of the mackintosh is held tightly around the head with an elastic band, while the lower border is slightly packed around the neck. The oxygen is led into it through a rubber tube. The writer, however, pre- fers to use a simple fountain syringe as an inhaler, allowing the patient to place the funnel end of the syringe over his mouth and nose while the rubber tube of the syringe is connected with the glass tube of the wash-bottle through which the gas is led (Fig. 129). Hill finds that for this purpose the most convenient manner of securing oxygen is by generating it from a gasogen containing oxylithe (Na 2 O 3 ), from which the gas is generated by contact with water, and is stored in a 15-litre gas-bag. Sodium perborate may be substituted for the oxylithe. INHALATION OF CARBON DIOXIDE. As early as 1899, Sir William Ewart, believing that the beneficial effect of the Nauheim baths was due largely to the inhalation of the carbonic acid which floated in the air above the water, recommended the inhalation of this gas by patients as a preliminary to the Nauheim treatment, and reported considerable benefit from its use. He found it particularly serviceable in the attacks of cardiac dyspnoea of aortic insufficiency and of mitral disease, in cases of precordial pain, and in angina pectoris. In cases of Cheyne-Stokes breathing, as well as in cardiac asthma, Eyster, Pembrey, and Allbutt recommend the inhalation of oxygen containing two or more per cent, of carbon dioxide to regulate breathing and prevent the onset of acapnia. 230 DISEASES OF THE HEART AND AORTA. For convenience of administration Ewart recommends obtaining the carbonic acid by allowing it to bubble off from the ordinary carbonated water obtained from a soda siphon. The latter is squirted into a pressure bottle, as shown in Fig. 129, where it may be kept and gradually given to the patient. The writer finds it still more convenient simply to allow the patient to squirt the soda water gradually into a Mason jar or into a fountain syringe in the manner described above, and to allow him to breathe with, his mouth immedi- ately above the mouth of the jar or the funnel of the >syringe. Care must be taken that his mouth and nose should not entirely cover the latter, lest the patient inhale too high a concentration of carbon dioxide. If he only gradually A H D Fir,. 129. Methods of administering oxyen and carbonic acid. A, Mackenzie's mask method, O- oxygen cylinder. B, administration of oxygen through a fountain syringe. C, Ewart's method of admin- istering CO:, showing the soda syphon, COi receiving bottle, and the pressure bottle (HuO). D, direct me'.hod of inhaling COs out of a Mason jar. places his mouth over the inhaler, however, this is not liable to occur, as he quickly becomes aware of an unpleasant sensation when the concentration of the gas is too high. INHALATION OF RAREFIED AIR. In cases of failure of the right heart in stenosis and mitral insufficiency, and also in some cases of failure of the left heart, Kulm has advocated dimin- ishing the resistance in the pulmonary circulation by the use of his suction mask. This device is a small tightly fitting mask about the size of a chloro- form musk which is held over the face by a strap around the head, so that it fits air-tight about the mouth and nose. It is provided with two valves, one allowing the air to enter the mask, the other allowing it to leave 1 . By regulating the pressure at which the inspiratory valve opens, it is easy to bring about any desired rarefaction of the air within the mask, which the patient should use for several hours a day. When the mask is applied it gives rise to a certain amount of dyspnoea, which may be somewhat annoy- TREATMENT OF FAILURE OF THE HEART. 231 ing and in the more severe cases may entirely preclude its use. After the patient has learned to accommodate his breathing to suit the new conditions, however, this element disappears. The patient should begin by using the mask for a few minutes at a time and then gradually increase the period and the frequency of application until he is using it for many hours a day. Albrecht recommends that the rarefaction of the air in the mask should not be greater than 3 mm. Hg, but, as this is almost one-third of the negative pressure in the thoracic cavity, and in view of the low mean blood-pressure in the pulmonary arteries, its effect would naturally be considerable. Indeed, Gerhardt has shown experimentally that such a diminished pressure greatly increases the rate of blood flow through the lungs, and has shown that it causes the lungs of a dog to become engorged with blood. Kuhn, Morelli, Bruhl, Zabel, Albrecht, and Gerhardt claim excellent results' from the use of this suction mask in patients with heart disease, espe- cially in mitral stenosis (Morelli) ; and it is worthy of a more extended trial. Not satisfied with the result of simple suction of the lungs in inspiration, Albrecht adds a spring upon the expiration valve of the mask, so that expira- tion must be forced at a slightly positive pressure, thus massaging the lungs by the change of pressure between the inspiration and expiration. Kuhn, however, apparently with good reason, objects that this imposes too great a strain upon the patient, and prefers the simple inspiration of rarefied air with expiration at the atmospheric pressure. The use of the suction mask is also of value in the treatment of the ansemia which is a frequent concomitant of cardiac disease, since, as Kuhn and others have shown, it acts like high altitudes in stimulating the forma- tion of red blood-corpuscles. Kuhn has also shown that the continued use of the suction mask leads to a gradual increase in the chest capacity, particu- larly in the type of long flat-chested individuals whose thorax is normally held in the position of exaggerated expiration (see page 702) . BIBLIOGRAPHY. GENERAL PRINCIPLES IN THE TREATMENT OF CARDIAC DISEASES. Erlangor and Hooker. Quoted on page 54. Winternitz and da Silva. Quoted from Buxbaum, Lehrbuch der Hydrotherapie, Leipz., 1903. Widal, F., and Javal, A.: La cure de dechloruration; son action sur 1'cedeme, sur 1'hydra- tation et sur 1'albuminurie ti certaines periodes de la nephrite epitheliale, Bull, et mem. Soc. Med. d. hoi), de Par., 1903, 3 s., xx, 733. Widal, F., and Lcmierre: Pathogenic de certaines cedemcs brightiqucs; action du chlorure de sodium ingere, ibid., 1903, 3 ser., xx, 678. Widal, F.: Die Kochsalzentziehungskur in der Brightschen Krankheit, Verhand. d. Kong. f. innere Med., Wiesbaden, 1909, xxvi, 43. Strauss, H. : Zur Frage der Kochsalz und Fliissigkeitszufuhr bei Herz und Xierenkranken, Tlierap. d. Gegenwart, Berl.-Wien, 1903, X. F. v. 433; Symposium on Therapeutics, Med. News, N. Y., 1903, Ixxxiii, G73; also Die Chlorentziehung bei Xieremmd Herz- wassersucht, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1909, xxvi, 91. Die Chlorentziehung bei Xieren- und Herzwassersucht, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1909, xxvi, 91. Richter, P. F.: Experimentelles ueber Xierenwassersucht, Berl. klin. Wchnschr., 1905, xlii, 3S4. 232 DISEASES OF THE HEART AND AORTA. Barie, E.: The Dechloridation Treatment in Diseases of the Heart, Internat. Clin., Phila. r 1906, 16th ser., i, 26. Cf. also Symposium in Verhandl. d. Kong. f. innere Med., Wiesb., 1909, xxvi. Karell, quoted from Romberg. Hoffmann, F. A.: v. Leyden's Handbuch der Ernahrungstherapie, 1898, i, 579. Jacoby, L.: Ueber die Bedeutung der Karellkur bei der Beseitigung schwerer Kreislauf- storungen und der Behandlung der Fettsucht, Miinchen. med. Wchnsehr., 1908, Iv, 839. Hirschfeld, F.: Die Karell'sche Milchkur und die Unterernahrung bei Kompensations- storungen, ibid., 1908, Iv, 1587. MASSAGE AND ELECTRICITY. Cautru, F. : Action du massage cardioabdominal sur le travail relatif du coeur, Rev. de therap. med.-chir., Par., 1909, Ixxvi, 73; and Bull. gen. de therap., Par., 1909, clvii, 127. Studzinski: Zur Frage der Bauchmassage bei Herzkrankheiten, Zentralbl. f. innere Med., Leipz., 1909, xxx, 641. Zabludowski, J.: Technik der Massage, 2d ed., Leipz., 1903. Selig, A.: Klinische Beobachtungen ueber Herzvibration, Therap. Monatsh., Berl., 1907, xxi, 204; and Berl. klin. Wchnsehr., 1907, xliv, 804. Rimbach: Orthodiagraphischer Xachweis der Einwirkung der Herzmassage auf die Grosse des Herzens und die Weite der Aorta, Verhandl. d. Kong, f . innere Med., Wiesbaden, 1908, xxv, 329; and Discussion by Selig. Hirschfelder, J. O.: Personal communication. Zimmern, A., and Riffaut: Note sur un malade ayant presente sous 1'influence du courant de haute frequence (lit condensateur) un abaissement notable de la pression aterielle, Arch, d'electric. med., Bordeaux, 1909, xvii, 803. SURGICAL. Gibson, G. A.: The Relief of Cardiac Enlargement by Surgical Methods, Edinb. M. J., 1910, N. S., v, 293. Morison, A.: On Thoracostomy in Heart Disease, Lancet, Lond., 190S, ii, 7. Hill, L., and Flack, M.: Oxygen in Muscular Exercise and as a Form of Treatment, Brit. M. J., Lond., 1908, ii, 967. Mackenzie: Diseases of the Heart, N. Y., 1910, 2d ed., p. 278. Allbutt, Sir T. C.: Article on Diseases of the Circulation in Musser and Kelly's Modern Treatment, Phila., 1911. Herz, M.: Sauerstoffbehandlung bei Herzkrankheiten, Prager med. Wchnsehr., 1909. Ewart, W.: On the Prebalnear Treatment of Heart Disease by Inhalations of CO->, and on the Uses of the Inhalations in Cardiac Dyspnu-a and Anginoid Pain, Brit. M. J., Lond., 1S99, ii, 1178; A Simple Method for the Therapeutic Inhalation of Carbonic Acid Gas, ibid., 1911, ii, 805. Kuhn, E.: Die Amvendung der Lungensaugmaske bei Lungen Kranken, Blutarmut, Asthma, Herzschwaehe, und Schlaflosigkeit, Zusammenfassende Ergebnisse aus der Literatur und Praxis, Therap. Monatsh., Berl., 1910, xxiv, 487; also Die Behandlung der Herzschwachezustanden und Stauung im Venengebiete durch ncgativen Druck in der Brusthohle, Yerhandl. d. Kong. f. innere Med., Wiesbaden, 1911, xxviii, 206. Albrecht, E.: Ueber einseitige Druckanderung der Lungenleft als Hilfsmittel fiir Diagnose und Therapie von Herzerkrankungen, ibid., 1911. xxviii. 201. Gerhardt, I).: Discussion of foregoing papers, ibid., 1911, xxviii, 208. Morelli. Ueber die wirkung der Kuhnsche Lungensaugmaske bei Herzkrankheiten, Ztschr. f. klin. Med., Berl., 1909, Ixvii. Bruhl, W.: Ueber die Einatmung verdunnter Luft in ihrer Wirkung auf den Kreislauf und das Herz, Thesis, Marburg, 1911. Zabel, quoted from Kuhn. V. THE EFFECTS OF DRUGS IN CARDIAC DISEASE. It does not lie within the scope of this work to enter into a detailed discussion of the pharmacology of the drugs used. The reader is referred to the text-books upon this subject, especially Cushny, A. It.: A Text-book of Pharmacology and Therapeutics, Philadelphia and New York. Sollmann, Torald : Text-book of Pharmacology. Hatcher, R. A., and Wilbert, M.: The Pharmacopeia and the Physician, Chicago, 1907 (published by the American Medical Association). Meyer, H. H., and Gottlieb, R.: Die experimentelle Pharmakologie also Grundlage der Arzneibehandlung, Berl., 1910. Brunton, Sir T. Lauder: Collected Papers on Circulation and Respiration, Lond. and N. Y., 1907; and Therapeutics of the Circulation, Lond., 1908. The drugs used in the treatment of cardiac disease may be of value through their action on the following systems: I. UPOX THE HEART MUSCLE digitalis, strophanthus, strychnine, squills, caffeine. II. UPON" THE PERIPHERAL VESSELS constrictors: camphor, strychnine, adrenalin, ergot, digitalis, nicotine (tobacco), caffeine; dilators: amyl nitrite, nitroglycerin, sodium nitrite, erythrol tetranitrate. 1. ACTING UPON* THE CARDIAC NERVES. A. Slowing the heart through stimulation of the vagus: aconite, digitalis, strophanthus, sometimes strychnine and caffeine, nicotine, veratrum viride, muscarin, very large doses of potassium salts, bile salts, blood in jaundice. 13. Increasing the heart-rate through paralyzing Hie vagi: atropine, cocaine, amyl nitrite and other nitrites. C. Increasing rate through stimulation of accelerators: adrenalin, amyl nitrite, and other nitrites. D. Paralyzing accelerators: apocodein. 2. DIMINISHING VENOUS PRESSX:HE AND STASIS BY DEPLETING PORTAL SYSTEM: purgative series, especially calomel, the saline and the vegetable purgatives. 3. DRUGS WHICH INCREASE THE TONICITY OF THE CARDIAC MUSCLE in pharmaco- logical doses: digitalis, strophanthus, strychnine, amyl nitrite, nitroglycerin, calcium chloride (transitory effect). 4. DRUGS WHICH DECREASE TONICITY: potassium salts, chloroform, formic acid, salt infusion, ether, adrenalin. Tonicity is practically unaffected by small doses of aconite, though slightly diminished by larger ones. DIGITALIS. Foremost among the drugs used in treatment of circulatory diseases are the preparations of digitalis, introduced into medical practice by Wither- ing in 1785. He says of it: "In the year 1775 my opinion was asked concerning a family receipt for the cure of the dropsy. I was told that it had long been kept a secret by an old woman in Shropshire, who had some- times made cures where the more regular practitioners had failed. . . . The medicine was composed of twenty or more different herbs, but it was not very difficult for one conversant in these subjects to perceive that 233 234 DISEASES OF THE HEART AND AORTA. the active herb could be no other than the foxglove. ... I soon found the foxglove to be a very powerful diuretic. . . I use it in ascites, ana- sarca, and hydrops pectoris." He then cites the results obtained in the treatment of over 100 cases, many of which would be worthy of modern therapeutics. Drugs of Digitalis Series. 1 Digitalis, strophanthus, apocynum, convallaria majalis, squill (scilla), erythropholoeine, helleborein, antiarin (antiaris toxicara). DIGITALIS consists of the dried leaves of Digitalis purpurea collected from the plant at the commencement of the second year's growth. It should not be kept more than one year. Average dose pulv. digitalis =0.05 Gm. (1 grain). PREPARATIONS. DOSE. Gram. English. Fluidextractum digitalis 0.05 TT\, 1 Kxtractum digitalis 0.01 gr. 1/5 Infusum digitalis (1.5 r c digitalis +10% alcohol + 15 c e cinnamon water) 8.00 3 ii Tinctura digitalis 1.00 n\,xv (10% f crude digitalis in dil. alcohol) A very satisfactory form for administering digitalis and a purgative at once is Addi- son's (or Xiemayer's) pill, made up according to the following prescription: Pulvis digitalis! .. n r 111- -ii /- tltl U.O III . X 'ulvis scilur. . j Hydrarg. chloridi mit 0.08 gr. 1 1/4 M. fiat in pil. x sen capsulas x. Sig. One pill every three hours. The calomel may be increased to gr. x, or may be replaced by blue-mass (massa hydrarg.) or gray powder (hydrargyrum cum creta) in capsules. The efficacy of Addison's pill depends upon the care taken to secure an active prepa- ration of digitalis in making it. Moreover, its action may be uncertain, owing to the fact that a certain amount of digitalis is eliminated with the stool without having been absorbed. DERIVATIVES OF DIGITALIS. Digitoxin the most active substance derived from digitalis, producing all the digitalis effects; soluble in alcohol; insoluble in water, except in the presence of digitonin. Prepared in soluble form with digitonin under the trade name "Digalen" (Cloetta). "Digalen," dose 1 c.c. Dirjilnlin (digitalinum verum Kiliani) a white amorphous glucoside, less toxic than digitoxin but otherwise resembling it in physical properties and pharmacological action. Dose 2-6 mg. (gr. ^-J,). _ Roughly, digitoxin is six times more potent than an equal weight of digitalinum verum (Fraenkel). Digitalin "German" amorphous powder, soluble in water and alcohol; a mixture of pure digitalin, digitalein, and digitonin. Dose 2-6 mg. (gr. ^o-'in). Digitalein and digitonin are other somewhat similar substances, the latter of which is a saponin-like body which has little pharmacological action. Digipuratum (Extractum digitalis depuratum), prepared free from digitonin accord- ing to Gottlieb's formula, contains digitoxin and digitalin, and is soluble in alkalies but insoluble in water and in acids. It is said to be less prone to produce nausea than the oilier digitalis preparations and is of very constant strength. STROPHANTHTS the ripe seeds of Strophanthus Kombe. Tinctura strophanthi, 10 per cent, of the drug in 65 per cent, alcohol. Dose 0.5 c.c. (n\,viii). STANDARDIZATION' OK DIGITALIS PRKPARATIONS. T h e . c h i e f point to 1> e c o n s i d e r e d in t h e c h o i c e of digi- talis {> r e p a r a t i o n s is t o o b t a i n a p r e p a rat i o n of u n i f o r in s t r e n g t h . Digitalis leaves even of the second year's growth vary greatly in the amount 1 A very full discussion of these drugs is given in Cushny's article. THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 235 of the active principles which they contain, as well as in the stability of the latter, for the leaves contain enzymes which break up the digitalis glucosides. In order to obviate this the leaves must be dried at a moderate heat, and kept in a dry, dark place. In order to keep the leaves permanently Max Winckel has devised a process whereby these enzymes are said to be completely destroyed. Age in itself is not always an objec- tion, for Hale has found leaves over eight years old, kept in a paper bag, which were of about the same strength as recently purchased leaves. The strength of digitalis preparations may be estimated either chemically or by their action on animals. The chemical assay is based on rather uncertain quantitative determinations of the digitoxin, and does not always show a parallelism to the activity of the drug, since the latter may also be due to the digitalin and digitalein contained. The action of the drug on animals may be tested in several ways, and among different observers there is still some uncertainty as to which method should be pursued. The activity may be tested on frogs, in which the action is mainly on the heart muscle, or on mammals, in which, as in man, the central nervous system is also brought into play. In frogs the activity has been tested upon the excised heart, the exposed heart (Focke), and upon the intact animal. The latter seems not only easiest but most satisfactory. Hough- ton (of Parke, Davis & Co.) recommends using as a standard the dose per gramme of frog which kills the animal in twelve hours after injection into the dorsal lymph-sac. Worth Hale, in a very exhaustive study, decides in favor of the method of Famulener and Lyons, in which the standard dose (per gram me of frog) is that which, when injected through the mouth into the anterior lymph- sac, brings the ventricle to a condition of permanent sys- tole at the end of exactly one hour. This method is the easiest to carry out, and requires only a small number of ordinary and healthy medium-sized frogs about 30 G. (one ounce) in weight. Each assay should cost about fifty cents. Dose of digitalis when diluted to tincture strength, per gramme of frog, 0.024-0.030 mg. Hatcher prefers cats, for strophanthus at least, using as his criterion the dose of strophanthin (diluted io'oo with 0.6 per cent. NaCl) which will kill a cat within an hour after intravenous injection. He finds the end reaction very constant (variation not over 3 per cent.) and believes that the action in mammals upon both heart and central nervous system corresponds more closely to the effect on man than does that upon the frog. The "frog unit" (Froschoinheit) is, however, in more general use, and is certainly practicable for any druggist. In case the latter does not standardize the drug himself, he should purchase his preparations only from manufacturing chemists who have already standard- ized them physiologically. For the history of digitalis and its uses see: Brunt on, T. Lauder: On Digitalis, with some Observations on the Urine (Thesis presented to Edinburgh University, 1866), Lond., 186S; also Collected Papers on Circulation and Respiration, 1st ser., Lond. and N. Y., 1907, p. 30. Winckel, Max: Ueber den Wert der frischc-n Folia Digitalis und ihre Konservierung, Muenchen. mod. Wchnschr., 1911, Iviii, 575. Hale, Worth: Digitalis Standardization and the Variability of Crude and of Medicinal Prepa- rations, Bull. No. 47, Hyg. Lab. U. S. Pub. Health and Mar. Hosp. Serv., Wash., 1911. Pratt, J. H.: The Potency of Digitalis Preparations, Boston M. and S. J., 1910, clxiii, 279. Famulener and Lyons: Proc. Ass. Am. Pharm. Ass., 1902, i, 415, quoted from Hale. Hatcher, R. A., and Bailey, H. C.: Tincture of Strophanthus and Strophanthin, J. Am. M. Assoc., Chicago, 1909, lii, 5; and Hatcher, R. A.: Note on Strophanthin, ibid., 1910, liv, 1954. STROPHANTHUS. According to the United States Pharmacopoeia, strophanthus is prepared from the ripe seeds of .strophanthus kombe; but Wilbert states that the latter is practically out of the market and is largely replaced by strophanthus hispidus and stro- phanthus gratus. The active principle of strophanthus kombe and strophanthus hispidus is strophanthin (methylouabain), while that of strophanthus gratus, the probable source of "crystalline strophanthin/' is ouabain, a substance twice as toxic as strophanthin. A closely related substance, acocanthcrin, derived from the wood of the acocanthacese, is dimethylouabain and is about one-fourth as toxic as ouabain. 236 DISEASES OF THE HEART AND AORTA. SQUILL. The sea-onion (scilla maritima) deprived of its dry membranaceous outer scales and cut into thin slices. Dose, 0.05-0.2 G. (gr. i to iii) in pills. Acetum scillae (U.S. P., B.P.). Dose 1-2 c.c. (n\. xv to xxx). APOCYNUM CANNABIXUM (the dried rhizome of Canadian hemp). Fluidextractum apocyni, U.S. P. (extract made in 10 per cent, glycerin, 60 per cent, alcohol, and 30 per cent, water). Dose 1 c.c. (n\ xv). COXVALLARIA. The dried rhizome and roots of Convalleria majalis (lily of the valley) . Dose 0.5 G. (gr. viii). Fluidextractum convallarise. Dose 0.3 c.c. (rt\viii). EUOXYMUS (U.S.P.), EUONYMI CORTEX (B.P.). The bark of the roots of the Wahoo. Euonymus atropurpureus, U.S. P., Extractum Euonymi 0.05 to 0.2 G. (gr. i to iii) B.P. Extractum enonymi siccum 0.05 to 0.15 G. (gr. i to iii). Other drugs having a similar action but not in the Pharmacopoeia are: Erythrophlocum, the bark of the casca or sassy bark (erythrophlceum guiniense). Helleborus niger (the Christmas rose) not the white hellebore; the pheasant's eye (adonis vornalis); the upas (Antiaris toxicaria), the Acocantheria, Thevetia grandiflora, and coronilla; also substances isolated from the skin of frogs (phrynin Faust) and bufagin (Abel and Macht). Derivative and Active Principle. Strophanthin (methyl ouabain) a white crystalline glucoside of constant composition and action, soluble but undergoing decomposition in water. Hence best prescribed in dilute alcohol. EFFECT OF DIGITALIS ON THE NORMAL HEART. Fraenkel and Schwartz and also Cloetta have shown that in therapeutic doses digitalis has no effect upon the normal heart, either in affecting the strength of the beat or in bringing about hypertrophy. Neither has it any effect upon the perfectly compensated, undilated heart with a valvular lesion. Its chief effects are seen in dilated hearts whose myocardium still retains some reserve power and in cases of auricular fibrillation. In the severest stages of cardiosclerosis and fatty degeneration it may stimulate the fibres beyond the limit of their power, and thus do actual harm, and even hasten the end. GENERAL ACTION OF DIGITALIS. Drugs of the digitalis series affect the heart through their action on three separate structures, the vagi, the cardiac muscle, and the vasoconstrictors. There is some evidence that the action of digitalis 1 upon the heart muscle is due to a definite chemical combination with the latter, uniting, as Schlio- mensun has claimed, with the phosphatid fraction (cuorin). Karaulow has shown that the digitonin is detoxified by cholesterin, but that digitoxin, digitalin, and strophanthin are not. Action of Therapeutic Doses. In ordinary therapeutic doses by mouth the effect of digitalis does not assert itself for 24 to 72 hours, though it may set in immediately after intravenous or very soon after intramuscular injections. In bringing about the usual therapeutic effects the pulse-rate becomes slower (Withering), the contractions larger and more forcible (Traube and Lauder Brunton), and the tonicity of the heart muscle is increased (Cushny, Cameron), so that the quantity of residual blood in the ventricles is dimin- ished and dilatation of the heart is lessened. 1 For convenience the action of digitalis as prototype of the digitalis series i.s discussed in detail, and the differences in the actions of the various members of the series will be discussed later. THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 237 Very often, as H. Turnbull in Mackenzie's clinic has pointed out, a sinus or neurogenic arrhythmia (instability of rhythm) sets in from inter- mittent action of the over-stimulated vagi, so that the originally rapid rate of the heart may change to a slow one with irregularity in which short series of rapid beats alternate with short series of slow ones, showing a normal (" double ") venous pulse. The beneficial action of the digitalis is brought about through increasing the force of the heart-beat and the tonus of the muscle, the one leading it to drive out more blood with each beat, the latter preventing it from over- filling in diastole, both effects tending to diminish dilatation. The effect of digitalis upon the coronary circulation is somewhat uncer- tain, for Oswald Loeb found that it diminished the blood-flow through the coronary vessels in the excised heart; but G. S. Bond, in the writer's labora- tory, demonstrated that with the heart in situ the flow is increased after digitalis and strophanthin throughout the period during which the general blood-pressure is elevated. These effects are produced chiefly through stimulation of the vagus, and may be prevented in animals by a section of the vagi (Traube and Lauder Brunton) and by the administration of atropine (Cameron). In animal experiments, and usually, but not always, in human beings, there is a moderate rise in blood-pressure, due (Blake, 1839, Traube, 1861, and Lauder Brunton, 1866) in part to constriction of the peripheral arteries. In man this rise in blood-pressure may or may not be present, and, as Mackenzie states, excellent results may be obtained in many cases without any change in the blood-pressure whatever. Toxic Effects. While these effects represent the favorable action of digitalis, larger doses give rise to real disturbances in the heart's action. These effects fall into four categories : (1) Weakening in the contractile power of the heart, as shown by the onset of a pulsus alternans. (2) A partial or complete blocking of the impulses passing from auricle to ventricle (digitalis heart-block) ; and (3) The genesis of abnormal contractions (extrasystoles) , auricular fibrilla- tion; or (4) Of a rapid heart-rate arising independently in the ventricle (ventric- ular tachycardia). Dependent upon a variety of conditions, either of these effects may predominate, or both may coexist, especially in the severer degrees of poisoning. The mildest of all these effects, the onset of an alternating pulse (pulsus alternans), gives no clinical manifestations save a slight feeling of general weakness corresponding to a diminution in the strength of alternate beats of the heart, which are well shown upon the sphygmogram. Cases of this sort have been reported by Guillaume and Mackenzie, in the former of which it was associated with occasional blocking of impulses at the auriculo ven- tricular bundle. Heart-block resulting from large doses of digitalis have been reported by Cushny, v. Tabora, and Erlanger in animals, and by Mackenzie, Hewlett, and Rihl in man. The stage most frequently encountered clinically is a sudden halving of the ventricular rate and pulse-rate without change in the 238 DISEASES OF THE HEART AND AORTA. rate of the auricles (2 : 1 rhythm) as shown by the venous pulse or electro- cardiogram. This represents a state of partial block, which in most cases may be promptly relieved by injection of atropine 0.5 to 1.0 mg. (gr. 7*3- to ^V) and passes off soon after the digitalis is discontinued. In animal experi- ments with larger doses the block becomes complete and can no longer be re- lieved by atropine, for not only the vagus (especially the left vagus) but also the fibres of the His bundle have been acted on by the poison. Mackenzie has encountered a number of cases in which the administra- tion of digitalis gave rise to absolute arrhythmia with auricular fibrillation. While these phenomena are going on at the supraventricular levels of the heart, changes are also taking place in the properties of the ventricular muscle itself, which manifests a gradually increasing tendency toward initiat- ing an independent rlrythm. The first manifestation of this condition is the onset of ventricular extra- systoles. Ritchie and Cowen believe that the latter arise on account of in- creased pressure within the ventricle during diastole, especially in slow hearts, just as they may arise when the aorta or pulmonary artery is clamped; and that the undue irritability of an enfeebled heart tends to increase this tend- ency. Some doubt is thrown upon this theory by the experiments of Brand- enburg, Straub, and di Cristina, who have shown experimentally that digi- talis actually tends to diminish the cardiac irritability and that stimuli which give rise to extrasystoles before the injection of digitalis are ineffectual after it. Another theory, which is very suggestive but by no means proved, has been advanced by Cushny. Cushny has supposed that the occasional extra- systoles represent the periodic manifestations of an independent rhythm arising in the ventricles themselves, just as is seen in complete block. Ac- cording to this view, the condition would correspond to a pararrhythmia in the sense of Wenckebach. Both the impulses from the auricles and those arising in the ventricles are conceived as effective, but the one which becomes active first at the end of the refractory period gives rise to the next beat. This stage of digitalis action, like all severe forms of arrhythmia, is accom- panied by a- corresponding retardation of the circulation, so that, unless com- pensated by still further vasoconstriction, a fall in blood-pressure ensues. The volume of blood driven out need not be diminished for all beats, but is diminished for the small irregular ones, partly because on account of an increased tonicity less blood enters the ventricles in diastole and partly because the beats themselves are weaker (both the systolic output and the residual blood arc diminished), and thus the velocity of the blood flow through the body becomes slower. The onset of either of these disturbances, whether heart-block or the extrasystoles, shows that the action of the drug has been too severe, the extrasystoles being, as a rule, less disconcerting than the heart-block. Both, as a rule, pass off within a day or two after the drug 1ms been discontinued; although palpitation, which is one of the most distressing features accompany- ing extrasystoles, may persist, a great deal longer. In the third stage of digitalis action, termed by Cushny the stage of inco- ordination, a complete block occurs betAveen the auricles and the ventricles, probably owing to a toxic action upon the fibres of the His bundle. The auricles still beat very slowly under the influence of the vagi, but the ventricles THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 239 beat at an independent rhythm. As the action of the drug becomes more and more pronounced, this rhythm tends to increase in rapidity, so that the condition of the heart at this stage may be summarized as auricular inhi- bition, complete heart-block, and ventricular tachycardia. While this repre- sents the end stage of digitalis poisoning as seen in animals, it is not commonly observed in man, but a case has been reported recently by Hewlett and Bur- ringer in which this form of irregularity was encountered shortly before death in a man who had received rather large doses of digitalis, apocynum, and strophanthus. In frogs and in cold-blooded animals the ventricle never relaxes and the heart ceases beating tightly contracted in systole; but in mammals, perhaps owing to asphyxia of the muscle, the great increase in tone is lost shortly before death, and the heart dies in diastole, unless, as Gottlieb has shown, large doses of calcium are given along with the digitalis. /WVWVWWVWW1 ABODE FIG. 130. Tracings showing the action of digitalis upon the dog's blood-pressure. (After Cushny.) .4, normal; B, therapeutic stage, with increased blood-pressure and moderate slowing of the pulse, but quickened blood-flow; C, excessive inhibition, causing low blood-pressure and slowed circulation; D, still further slowing, with slight arrhythmia; E, third stage, irregularity with further rise of blood pressure from excessive vasoconstriction. Effect on the Blood=Pressure. T he rise of b 1 o o d - p r e s s u r e due to digitalis is in part duo to t h o increase d f o r c e a n d o u t put of t h e h cart, i n p a r t to t h o c o n s t r i c - t i o 11 of the p e r i ]) h r e a 1 and, especially, the abdomi- nal blood-vessels. The velocity of blood flow (as shown by product of pulse-pressure X pulse-rate ! ) is usually increased when this effect is brought about (Fellner, Fraenkel). Strophanthus causes less vasocon- striction than digitalis, and hence usually affects the minimal pressure less than the maximal, but increases the velocity of blood flow without causing so great a strain upon the heart. Unfortunately, the preparations of stro- phanthus are less reliable for continuous action. 1 Janeway has reported cases in which digitalis produced great improvement without increasing P. P. X P. K. Considering the error which may be involved in this calculation, such exceptions are not surprising (see page 35). 240 DISEASES OF THE HEART AND AORTA. Occasionally it is found that both digitalis and strophanthus actually lower the maximal blood-pressure. This occurs especially in the cases where the circulation through the medullary centres is impaired by venous stasis or arteriosclerosis, or failure of the heart, and the high blood-pressure is merely the result of general reflex vasoconstriction from the ischaemia of the centre (high-pressure stasis). When the force of the heart is increased and the blood passing through the centre is better aerated, the vasoconstrictor influence is no longer ex- erted and the general blood-pressure then falls. Effect of Digitalis on Tonicity. C 1 i n - ically the most important action of digitalis is its effect upon the tonus of the cardiac muscle, in preventing and in overcoming dilatation, and it is in dilated hearts that the bene- ficial action of digitalis is most pronounced. Francois-Franck (1882) demonstrated that the administration of digitalis did away with the transitory functional tricuspid in- sufficiency which resulted from stimulation of the vagus. Cushny and Cameron have shown marked increase in tonicity, as shown by diminution in cardiac volume. More- over, Cloetta has demonstrated that the prolonged administration of digitalis pre- vents the heart from dilating in experi- mental aortic insufficiency (positive intra- ventricular pressure during diastole). The hearts of animals which have been treated with digitalis are smaller and stronger than those which have not been so treated (see page 467). Colbeck, Gossage, and others have also emphasized the importance of this effect on cardiac tonus. 240 230 220 210 200 190 180 170 160 FIG. 131. Variations in blood-pres- sure in a patient under the influence of digitalis and nitroglycerin. MAX, maxi- mal hloi id-pressure; 3//.V, minimal blood- pressure; I'P, pulse-pressure; PPXPR, pulse-pressure X pulse-rate; DISC. DIG- ITALIS, discontinue digitalis. RELATION OF PULSE-PRESSURE TO SYMPTOMS IN ONE OF FRAENKEL'S CASES. Time. Blood-pressure Max. Min. Pulse. Pulse-pressure Urine in X Pulse-rate. 24 hours. Jan. 27, 10.30 208 i 200 10.40 2S6 200 10.4.5 11. 00 Jan. 2S 200 150 r>040 7490 1 mg.strophanthin intravenously Diuresis begins 1000 Dyspnoea increasing. Pulse feels larger. 80 7904 BfioO Xo feeling of const ric- I I tion. Sleeps well. Jan. ol (Edema almost disappeared. Feb. 1 ... (Edema completely disappeared. I Patient makes uninterrupted recovery with no further medication. THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 241 SQUILLS AND STROPHANTHUS. The other members of the digitalis series which are of the greatest clinical importance are strophanthus and squills. The latter is of some value in patients whose stomachs do not tolerate digitalis, for it exerts a very similar action upon the heart, but has less tendency to produce nausea and vomiting. It is also given along with digitalis and calomel in Addison's (Niemeyer's) and Mackenzie's pills, the latter of which is preferable on account of the smaller dosage. Strophanthus possesses all the actions of digitalis except that it causes considerably less vasoconstrictions than the latter, and consequently strength- ens the heart without imposing so much strain upon it. VASOCONSTRICTION VOL. LEG VOLUME OF VENTRICLES There has been a great deal of discussion regarding the activity and toxicity of strophanthus preparations, and a number of cases of strophanthus poisoning have been reported on the one hand and of comparative inactivity on the other. This uncertainty of action, as Hatcher and Bailey have shown, is due to the fact that strophanthin, the active principle, is absorbed very irregularly from the digestive tract; so that under certain circumstances several doses may be entirely unabsorbed in the intestine, and under others may be ab- sorbed with fulminant rapidity and four or five times the usual dose may suddenly become active. When injected intravenously or intramuscularly, however, strophanthus acts with great regularity, and in a very large scries of experiments by Hatcher and Bailey to determine the toxicity of strophan- thin the limit of variation was three per cent. Albert Fraenkel has shown that very striking effects may be obtained clinically within a few minutes after the intravenous injection of 0.5 to 1 mg. 242 DISEASES OF THE HEART AND AORTA. (gr. -jJo to Tl V) of amorphous strophanthin (of Boehringer or Merck), or about one half that dose of the crystalline strophanthin (Thorns) (ouabain?). 1 An example of Fraenkel's remarkable therapeutic effects may be quoted here: Patient, aged 57, male, admitted to Strassburg Hospital November 17, 1905, Had rheumatic fever in 1S69 and again in 1SS6. Palpitation when at work, and occasional swelling of legs since 1000. Drinks considerably. Present Condition. Considerable o?dema of legs, thighs, and scrotum. Moderate ascites. Dulness and diminished breath sounds over right base. X-ray shows heart shadow enlarged to left and right: dynamic dilatation of aorta. Pulse irregular, 104 per minute, maximum pressure 180. Pulv. folia digitalis 0.1 Gm. (H gr.) three times a day brought pulse down to 86 in 4 days, to 76 in 6 days, increasing diuresis from 2000 to 4500 and 5800 respective!}-. Another attack of pain in joints on December 1 ; left clinic "improved" on December 11. Returned January 25, 1900. (Edema as before; ascites marked abdomen 108 cm. in circumference. Liver palpable four fingers' breadth below costal margin. Spleen pal- pable. Dulness and diminished fremitus over base of right lung. Heart dilated more than before; impulse not palpable; first sound at apex reduplicated; second accentuated, espe- cially over pulrnonic area. Slight gallop rhythm. Heart action rapid and regular. Marked orthopncra and very distressing cough. Patient has had no sleep for several nights. The following table shows the effects of the intravenous administration of strophan- thin upon his blood-pressure, urine output, and symptoms. The product of pulse-pressure and pulse-rate furnishes a very rough index of the velocity of blood-flow. Fraenkel's observations have been confirmed by Otfried Muller, Fleisch- mann, Bailey, and a host of others; and strophanthin may be said to have passed the experimental stage and to have reached general clinical use. It may be given either as one or two single doses intravenous!}', or, when pro- longed action is desired, particularly when digitalis is not well borne, it may be given in small daily doses (\ to % nig. crystalline strophanthin, Thorns) injected very deep into the muscle. The .site of injection must also be massaged for a few minutes after the injection. As a rule, the intravenous injection of strophanthin does not cause any discomfort to the patient; but if the injection is not made directly into the lumen of the vein and any of the fluid enters the wall or the perivascular tissues, it may give rise to considerable pain. Occasionally the injection mav be followed bv a severe chill and transitorv fever. CLINICAL APPLICATION OF DRUGS OF THE DIGITALIS SERIES. Although it is probably true, as Wenckebach has put it, that '' every man has his own way " of using digitalis, it may be said in general that digitalis should be given for di hit at ion of the ventricles and fibril- lation of the auricle^. As was already sho\\ n by Withering, it is the drug par excellence for ascites, anasarca, and broken compensation; and, when these conditions arc; met 1 Difficulty is oft on encountered in making an intravenous injection, either because the vein is small or because it slips under t lie needle. In order to obviate this, ,]. J. \Yatson suggests anchoring the vein by transfixing it with an ordinary sewing needle thrust through the skin and the wall of the vein and partly out through the skin. The hypodermic needle may then be inserted rear'ily into the vein, the injection made without difficulty, and par- ticularly without escape of strophanthin into the peri vascular tissues. THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 243 with, its prompt use may lead to almost unhoped-for improvement. In these cases it acts in part by its direct action on the heart, increasing the strength of the beat and tonicity of the heart muscle, and in part by improv- ing the circulation through limbs and kidneys and by its diuretic action, all of which become important factors in removing oedema. Owing to the marked effect in increasing cardiac tonicity, digitalis and its congeners also find their usefulness in all cases of permanent or transitory dilatation of the heart before the trouble has gone on to an actual break, whether of long standing or acute. There is no reason to wait for loss of compensation. Dilatation, in itself, accompanied as it is by a tendency to easy overstraining, represents a condition of lowered tonicity and is best treated by digitalis.' No better examples of this can be cited than the excel- lent results obtsined by Da Costa in the overworked soldiers of the Civil War, whom digitalis and rest promptly returned to their normal strength. In valvular disease digitalis is not required when the lesion is fully com- pensated and the patient free from symptoms, but it should be used vigor- ously whenever symptoms present themselves even in transitory attacks. In chronic valvular disease with broken compensation its action cannot always be prophesied, for in certain cases the expected effect may be entirely absent. This, as Mackenzie, Lewis, and Windle have shown, is especially true in cases of mitral stenosis with rapid, regular heart-rate, in which most probably the vagi are paralyzed and atrophied and in which the action of digitalis on ventricular tonicity is of minor importance. The experiments of Cloetta and Gelbart would indicate that in early aortic lesions, even when apparently compensated, a prolonged treatment with digitalis, lasting several months, increases the strength of the heart and does much to safeguard it against overstrain. It is most important, however, to guard against any great cumulative action of the drug in such cases. After the first few days of treatment the single doses should be small, and the pulse should be carefully watched for the onset of bradycardia or arrhythmia. Digitalis in Arrhythmia. As has been seen (page 669 J, the usefulness of digitalis depends upon the nature of the arrhythmia. In cases of respira- tory arrhythmia it is not needed unless the heart is definitely dilated, and indeed it tends to exaggerate this form of arrhythmia itself through its action upon the vagi. The action in heart-block will be discussed in a later chapter (page 574), but in general it may be stated that digitalis is definitely contraindicated in partial heart-block or in cases with delayed conduction (a-c interval OQ the venous pulse or P-R interval on the electrocardiogram prolonged). In complete block, however, where the impulses from the auricles and the influ- ence of the vagi no longer reach the ventricle, the experiments of Erlanger with digitalis and the clinical experience of Bachmann with strophanthin and of Hewlett and Barringer with digitalis indicate that drugs of this series increase the automaticity of the ventricle and thus tend to prevent the cessa- tion of the pulse. Up to the present, however, too few cases of this sort have been reported for the exact sphere of its usefulness and its limitations, its indications and contraindications, to be definitely defined, and in all such cases the drug should be used with caution. 244 DISEASES OF THE HEART AND AORTA. In cases of alternating pulse digitalis is usually indicated to increase the force of the contractions, of which the alternating is in itself an expression of weakness. Though extrasystoles from increased irritability may be brought on by digitalis, extrasystoles in a dilated heart are usually relieved by it in propor- tion to the relief of the dilatation. It is in the absolute arrhythmia from auricular fibrillation (arrhythmia perpetua, formerly designated by Mackenzie as " nodal rhythm "), however, that digitalis exerts its most favorable influence (Mackenzie, Lewis, Gushing, Edens, Windle). In this condition it has the same action as pressure on the vagus (Wenckebach). It does not remove the irregularity, except when this is in itself of transitory duration; but it slows the rate of the ventricles, either indirectly through inhibiting the fibrillation of the auricles which are the pacemakers, or by depressing the conductivity of the His bundle so that the feebler impulses generated in the auricles no longer reach the ventricles and only the greater stimuli become active. It is only in rare cases, formerly termed by Mackenzie " essential bradycardia " or " nodal bradycardia," that this blocking becomes complete, but in the ordinary cases, slow irregular heart-rate following the administration, the impulse for each contraction of the ventricles still arises in the auricles. Mackenzie, Lewis, and Windle have shown that the beneficial action is greatest when the pulse-rate is rendered extremely slow (50 to 60 per minute). In order to obtain this result large doses may have to be administered for a considerable period of time, and the patient may entirely miss the benefits if half-hearted therapy is resorted to. Windle estimates that from five to eight drachms (20 to 30 c.c.) of the tincture may have to be adminis- tered in fifteen-minim (1 c.c.) doses during a period of about ten days before the maximal slowing sets in. With very large doses, such as four or five minims (0.3 c.c.), of the fluid extract (equivalent to forty or fifty minims of the tincture) the same result may be obtained in two or three days, but the patient's condition must be carefully watched to avoid passing the limit of his tolerance. Certain patients whose heart muscle has undergone too great degen- eration do not react at all to the drug, and the rapid irregular heart-rate continues in spite of its use; but until the drug has been pushed to its limits it is very difficult to foretell whether one is dealing with a patient who would respond to a sufficient dose or one in whom response is no longer possible. In contrast to the effects obtained in broken compensation from valvular disease, which depend upon increased tonicity and increased force of con- traction, the effects obtained in auricular fibrillation, which depend chiefly upon the slowing of the heart and the partial blocking of the impulses, do not outlast the period of administration, but the tachycardia, dyspnoea, and weakness are often resumed within a couple of days after the digitalis is stopped. The drug must, therefore, be continued even after the patient is up and about, and the amount then given is determined by permitting the patient to vary his own dose to find out the one at which he feels most vigorous. THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 245 CHOICE OF PREPARATIONS AND MODE OF ADMINISTRATION. So many preparations of digitalis and its congeners are constantly being placed upon the market that some difficulty may be encountered in the selec- tion of the preparation best suited to the occasion, as well as in its mode of administration. Albert Fraenkel, Mackenzie, and Worth Hale have shown that a good tincture which has been standardized physiologically (see page 235) is about as satisfactory and as permanent as any of the more elaborate and costly preparations. 1 As Fraenkel has stated, the effect depends more upon the quantity of dose than upon the kind of drug used. The most common method is that of giving 1 c.c. (fifteen minims = 0.1 Gm. or gr. iss of the powdered digitalis) every four hours until the physio- logical effect (slowing of the pulse, etc.) has been obtained; but with such small doses it may require a considerable period of time to bring about the result. Mackenzie always continues the drug until the patient experiences nausea, which he regards as evidence that the physiological effect is being obtained. He then slightly diminishes the dose so as to remain within the limits of the patient's comfort. Albert Fraenkel gives several large doses (2 c.c. = ti\,xx of the tincture, equivalent to 0.2 Gm. or grs. iii of the powdered leaves) every four hours in order to insure a prompt initial effect, and then, to prevent cumulation, follows these with smaller doses, 0.5 c.c. (n\,vii, equivalent to 0.05 Gm. or one grain of the powdered leaves). This method has the advantage of com- bining prompt action with avoidance of sudden overdosage, and, for this rea- son, is of particular value where the patient is not continually under the eye of the physician. After obtaining the initial effect the latter can then vary the dosage to meet the exigencies of the case. In persons constantly under the supervision of the physician, particu- larly in patients with auricular fibrillation and in those whose heart muscle does not appear to be extremely degenerated, the writer has found it more satisfactory to prescribe " 0.3 c.c. (5 minims) of the fluid extract (equivalent to 3 c.c., fifty minims, of the tincture) three times a day until the pulse-rate has fallen below 80, when it should be discontinued by the nurse without special order," so as to prevent too great cumulation. These large doses insure prompt action, usually bringing the pulse-rate back to normal within two or three days, but their effects should be carefully watched, to keep the patient from passing into the toxic stage. In many cases recently in which very quick action is required this procedure has been supplanted by the use of strophanthin intravenously. PRECAUTIONS AND METHODS OF ADMINISTRATION. Flavoring. G a s t r i c disturbances, such as nausea and v o m i t i n g , occasionally result from the administration of digitalis preparations or deriva- tives. This is in part due to the direct irritating action upon the gastric mucous membrane and in part to the extremely unpleasant taste and after-taste of the drug. In order to obviate the former the drug should always be given in a large 1 J. H. Pratt (Boston M. and S. J., 1910, clxiii, 279) finds the digitalis of Cesar and Loretz the most active and constant. 246 DISEASES OF THE HEART AND AORTA. quantity (at least half a tumbler) of water. The intensely disagreeable taste of the digitalis and strophanthus preparations may be disguised by the addition of bitter orange peel (tinctura aurantii amari) , compound tincture of either gentian or cardamom, or tincture of quassia or calumba. It may also be given in albu- min water flavored with lemon so that its taste is barely noticeable. Sir Clifford Allbutt recommends that it be given in an iced drink. The use of any of these disguises frequently minimizes the gastric disturbances resulting from the drug, though vomiting of central origin finally results (Hatcher). Rectal Administration. When the gastric symptoms persist in spite of these precautions, the drug may be administered per rectum, being given in 100 c.c. physiological salt solution with a little starch. This method is very satisfactory (Janeway). Dr. Finley informs the writer that he has seen the pulse-rate slowed and the patient's condition greatly improved within two hours after the administration of digitalis per rectum, whereas the effect rarely follows administration by mouth in less than twenty-four hours. Intramuscular and Intravenous Administration. In order to insure very rapid and certain absorption, digitalis tincture or the more elaborate prepara- tions, such as digitalin, digalen, or digipuratum, may be injected into the gluteal or lumbar muscles. The injection should be very deep and the site should be massaged vigorously for ten or fifteen minutes afterwards in order to insure absorption, for if the injection remains unabsorbed it acts as an irritant and not only intense pain but the formation of a large abscess may result. It may also be injected into the vein under the usual aseptic precautions. Period of Administration. In the administration of digitalis it is impor- tant to obtain a definite effect and yet not to push the drug beyond the first stage of its activity, that of slowing and increase in size of the pulse, and to avoid the onset of the second stage, i.e., of irregularity. Since different hearts vary in their susceptibility to digitalis, and since, on the other hand, the drug begins to act only after twenty-four hours and may have a cumula- tive effect, tins task is by no means easy. To avoid the onset of toxic effects various routine methods may be resorted to. Thus, Professor Osier and other authorities recommend giving the drug in " courses " consisting of eight doses of 15 minims of the tincture (0.1 Gm. or IV gr. digitalis) every four hours. The course is to be repeated if necessary. It may be said that this method often falls short of the effect or brings it about too slowly. The writer has found it very satisfactory to order " 0.3 c.c. (5 minims) of the fluidextract three times a day until the pulse-rate reaches 80, when it should be discontinued without the necessity of a special order." Albert Fraenkel suggests giving several strong doses equivalent to 0.1 Gm. (2 gr.) of powdered digitalis (about twice the usual dose, 2 c.c. or 30 minims of the tinctura digitalis) to insure prompt effect (slowing of the pulse), and thereafter drop- ping to steady dosage of .03 Gm. (I gr., 0.5 c.c. , or 7-V minims of the tincture) to prevent cumulative but retain the therapeutic effect. This seems to be the most satisfactory method, since it insures not only the immediate but a permanent effect. Indeed, in many chronic cases " the strength of the heart begins to fail a short time after leaving off the digitalis. Here the continuous use of digitalis (0.05 Gm. or 1 gr. digitalis), as recommended by Kussmaul, Naunyn, and Groedel, for months and even years, has an admirable effect in keeping the cardiac activity at its necessary height " (Romberg). THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 247 Derivatives of Digitalis. Although, as Fraenkel has shown, the purified glucosides of digitalis have no great advantage over the crude drug, they have enjoyed considerable vogue. Digitalin, the glucoside first introduced into practice, still enjoys a certain favor. The ordinary digitalin, or " German digitalin" of commerce, is a very variable product, and it is only the purified digitaline or digitalinum verum of Kiliani which is worthy of recommendation. Of late digitalin has been largely replaced by digitoxin, especially in the form of the digitaline Nativelle granules (pure digitoxin), which are warmly recommended by Mackenzie and the French writers, and as Cloetta's "diga- len " (soluble digitoxin) or in Gottlieb's the digitonin-free digipuratum (digi- talis purified from digitonin). The claims that the former substance does not act upon the stomach and also that it is a preparation of great stability have both been largely repudiated, and Hale and others have found that the samples of digalen on the market are about as liable to deterioration as an ordinary digitalis preparation. Otfried Miiller has found that the intravenous injection of 1 c.c. (15 minims) of digalen has no influence upon the vasomotor nerves of the arm in man, as shown by the plethysmograph, and very little effect upon the blood- pressure. He believes that its action is similar to that of strophanthin intra- venously, only that it is less powerful and less rapid. Albert Fraenkel, on the other hand, regards this as merely a matter of dosage, but believes that strophanthin, owing to its more definite chemical composition, can be gauged more accurately. In digipuratum, a preparation introduced into practice by Gottlieb and Hoepffner in 1908, the aims sought for in the preparation of digalen seem to have been realized to a much greater extent, as is indicated by the favorable comments of Mueller and Clemens in Germany, Tissot in France, Szinnei in Austria, and Boos and his associates in America. Boos and Hale testify as to its permanency, and Boos, Newburgh, Marx, and Lawrence state tnat they have used it in over two hundred cases at the Massachusetts General Hospital without producing nausea, vomiting, or unfavorable cumulative action in a single case. The writer's experience, however, does not bear this out. Digipuratum is usually administered, as Hoepffner suggested, in courses of twelve tablets of 0.1 Gm. (gr. iss) each four tablets the first day, three the second day, three the third day, and two the fourth day, after which the dose of one or two tablets daily is regularly instituted according to the exi- gencies of the case. STROPHANTHIN. Where rapid intense action is required, as in a badly failing heart in which an immediate result is required, strophanthin or ouabain is the drug of choice, and should be administered intravenously, beginning with a dose of 0.5 mg. (gr. y^j ) of the amorphous strophanthin, or 0.25 mg. (gr. y-J,,-) of the crystalline ouabain may be repeated within an hour if no effect has been noted. Care must be taken to be certain the patient has not been taking digitalis before the injection, lest, as Fraenkel has observed, a sudden cumula- tive action set in whose consequences may be grave or even fatal. Otfried Miiller has seen a cerebral hemorrhage set in in a patient with chronic nephritis 248 DISEASES OF THE HEART AND AORTA. following an intravenous injection of strophanthin, and Fraenkel warns against its use in cases of chronic hypertension for fear of throwing too sudden a strain upon the heart. On the other hand, hearts whose muscles are in good condition may have a much greater tolerance for strophanthin; and Liebermeister has given as much as 4 mg. (gr. y 1 -) in twenty-four hours to patients with pneumonia without any ill effects. In ordinary cases the intravenous or intramuscular injection of strophan- thin is reserved for emergencies, and especially to cover the period during which no effect could be expected from the administration of digitalis by the mouth, so that in most cases the oral administration of digitalis may begin at once, allowing its effects to begin about the time that those of the strophan- thin wear off. In patients whose condition is very grave, however, and especially in those in whom absorption from the intestinal tract is uncertain, it is better to rely entirely upon the strophanthin and make daily intra- muscular injections of a single dose, leaving the digitalis off altogether until the period of emergency of uncertainty is over. DIGITALIS AND THE NITRITES. As has been stated, the drugs of the digitalis series strengthen the force of the heart-beat and increase its tonicity, and thus enable the dilated heart to empty itself better into the blood-vessels and prevent it from overfilling during diastole. This in itself usually suffices to return the circulation to its normal state, but in many cases, especially in acute cedema of the lungs and in failure of the left ventricle, with hypertension, and especially in the attacks of cardiac asthma of aortic insufficiency, it is advisable to lighten the burden upon the heart still further by dilating the peripheral arteries. The best drugs for this purpose are those of the nitrite series (amyl nitrite, nitroglycerin, sodium or potassium nitrite, erythroltetranitrate), whose action will be discussed in detail in a later section. In using these drugs in conjunction with those of the digitalis series it must be remembered that the heart does its best work when the general blood-pressure is high enough to maintain a good blood flow through the coronary arteries and the respiratory centre in the medulla, and that, owing to varying degrees of arteriosclerosis and arterial elasticity, the optimum will be different in each individual. Nevertheless a certain amount of relief may be afforded to the majority of cases provided care is taken not to pass below the optimum. It must be remembered, moreover, that for cases of increased intracranial pressure, apoplexy, cerebral sclerosis in which the vaso-constric- tion and high blood-pressure are the result of an attempt at physiological compensation, this optimum pressure may lie at a very high level, and at- tempts to reduce the blood-pressure may actually do harm. However, in the more acute conditions of high pressure, high-pressure stasis, reflex eleva- tions of pressure, vasomotor crises, etc., these phenomena are not compensa- tory but accessory reflexes, and to relieve them lessens the work of the heart without disturbing any essential condition; so that lowering the peripheral resistance may relieve the burden on the heart almost as much as increasing the strength of the latter, and the optimum is attained when both are accom- plished at once. This desirable condition is further enhanced by the fact that, as Cameron has shown, amyl nitrite and nitroglycerin augment the tonicity THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 249 of the heart muscle, and thus add their effect to that of the digitalis; the more so since, in accordance with a well-known pharmacological principle, the effect of two drugs exerting the same action administered simultaneously is greater than the sum of the two components acting separately. The ideal combination of these drugs for speed, harmony, and intensity of action is the injection of strophanthin and nitroglycerin simultaneously, for the former exerts little action upon the peripheral vessels and both sub- stances unfold their action at about the same period after injection. In attacks of cardiac asthma, particularly in cases of aortic insufficiency, this combination of drugs may give great relief. Their action may further be strengthened by venesection and inhalation of oxygen, according to the method of Hill and Mackenzie, for in cases of severe heart failure the best results are obtained by firing all the weapons of defence in one broadside. In this way the excess of residual blood is pumped out of the dilated heart and the latter allowed to return to normal volume. It is at the normal volume that the heart pumps to best advantage. If it is still possessed of any recuperative power, it is enabled then to assert itself, far better than if the same measures were applied singly at long intervals, so that the dilated heart is depleted a little by one measure, allowed to refill to the original degree before the next is applied, responds a second time to a slight degree but insufficient, and, still working at a disadvantage, again becomes dilated as it was before the beginning of treatment. Contraindications to Digitalis. However valuable the substances of the digitalis series may be in the above-mentioned conditions, there is a con- siderable group of cases in which they are useless or positively harmful. This is especially true for hearts in acute intoxications, either from acute infectious diseases or from the action of poisons or from acute fatty degenerations from other causes. In these conditions digitalis usually fails to exert its characteristic responses; partly because the disturbance in the circulation lies chiefly in the peripheral vessels rather than in the heart itself; partly because the vagi are less active than normally so that the drug cannot exert its action through this channel; and partly because the degenerated heart muscle is sensitive to further strains upon it. On the other hand, the acutely degenerated heart muscle seems hyper- sensitive to digitalis and readily passes into the toxic stages of digitalis action (see page 300). This may be analogous to the fact, demonstrated by Loeb and Fleisher, that two toxic substances acting simultaneously may produce degenerations of the heart muscle which could not be attained by either of them acting alone, for the toxic agent giving rise to the degeneration repre- sents one of these factors and the digitalis represents the other. Clinical experience is in harmony with these results, as the cases cited on pages 307 and 309 bear witness; and in such cases the drugs of the digitalis series if given at all must be administered with extreme caution. Another condition in which these substances are contraindicated, as stated above, is partial heart-block, for digitalis is likely to bring on complete block suddenly and with it there is danger of an attack of the Adams-Stokes syndrome. The question of the advisability of digitalis in complete heart- block is still an open one and is discussed on pages 573 and 574. 250 DISEASES OF THE HEART AND AORTA. HALLUCINATIONS FROM DIGITALIS. Another toxic effect of digitalis lies in the production of mental symp- toms, delirium and delusions, through its action on the central nervous system (Duroziez, Hall, see page 216). The onset of these symptoms there- fore constitutes a contraindication to continuing the drug. STRYCHNINE PREPARATIONS. Strychnine (strychnina) is an alkaloid obtained from nux vomica. Tinctura nucis vomieip contains 2 per cent, extract of nux vomica and is assayed to contain 0.1 per cent, strychnine. It is useful more as a stomachic bitters than as a cardiac stimulant. Dose, 1-2 o.c., lo to 30 minims. Strychninae sulphas contains 5 molecules of water of crystallization and 78 per cent, of strychnine, soluble in 3 parts of water. Average dose, 0.0015 Gm. ( T V S r -)- Strychnina; nitras is soluble in 42 parts of water and 120 parts alcohol. Dose, same as sulphate. PHARMACOLOGICAL ACTION OF STRYCHNINE. There are many cases in which the circulation is beginning to show some signs of slight weakening and yet where it does not seem necessary to use digitalis. In these cases other drugs are resorted to, in America usually strychnine, 1 in Germany usually camphor; both apparently yielding good clinical results. It must be added, however, that according to most pharmacologists strychnine has no effect whatever upon the heart and pro- duces the rise in. blood-pressure only by the vasoconstrictor action. Effect on Cardiac Tonicity. Dr. P. D. Cameron has recently investi- gated the subject under the writer's direction, and has found in the dog that strychnine in doses of .00003 Gm. per kg. or TJUTT gr. per lb., corresponding to .002 Gm. (ijV gr.) hypodermically for a man, always produces an increase in tonicity of the heart muscle, though without affecting the force of the beat or markedly changing maximal pressure. Mean and minimal pressures are usually slightly increased (by 10-15 mm. Hg) and pulse-rate a little slowed. Larger doses increase the systolic output, raise the blood-pressure, slow the heart, and increase the tonicity. Clinical Effects. In view of the wide-spread and often indiscriminate use of this drug, it is important to realize exactly its clinical use before pre- scribing it. As has been stated, strychnine stimulates both vasoconstrictor and vagus centres, hence raises the blood-pressure and slows the pulse-rate. Those effects, however, have been observed mainly in animals, and few exact clinical studies have been made upon man in connection with observa- tions of the change of blood-pressure. Briggs and Cook, who were most enthusiastic over the use of the drug, did not obtain rises of blood-pressure exceeding 10 mm. Hg from doses of 1 to G mg. (irV to yV gr.) and in no case slowing of the pulse. Cabot and F. P. Drayer, on the other hand, failed to note any changes whatever in many cases. The writer has made a considera- ble number of observations, determining the blood-pressure with the Erlanger 1 In view of the wide use of strychnine in heart diseases in English-speaking countries, it is quite striking that this drug is not mentioned in connection with therapy of the cir- culatory system in such extensive German text-books as those of Romberg and Heinz. THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 251 apparatus. He injected strychnine in doses which rose to 15 mg. (J Gr.) hypo, without obtaining any effect upon maximal or minimal pressure, pulse- rate, or rate of respiration, and from single doses scarcely any increase in reflexes. These tests were made upon hearts which were not dilated, and hence no effects upon tonicity could be noted. Since the rank and file of English and American physicians entertain an almost superstitious belief in the efficacy of this drug, it is evident that effect in each case should be controlled by blood-pressure determinations. BEFORE AFTER BEFORE AFTEH VobfME OF VENTRICLES SECONDS I II FIG. 133. Curve showing the effect of strychnine upon cardiac tonicity. (Experiment by Dr. Cameron.) Lettering as in Fig. 132. Fig. I shows increase in systolic output and maximal blood-pressure. Fig. II shows increase in tonicity, with a diminution in the systolic output and a fall in the minimal, but no change in the maximal blood-pressure. The effect upon tonicity is the most constant effect of the drug. Cameron's experiments upon animals have shown that a distinctly beneficial effect upon tonicity may be obtained with but little change (5-10 mm.) in the maximal blood-pressure, but that often when these change's are very slight the effect may be much more distinctly shown by a rise in the mean or minimal pressure. Both should be carefully watched in cases in which strychnine is given, and the dose should be sufficient to be effective. If no effect is obtained it should be discarded for some more potent drug. 252 DISEASES OF THE HEART AND AORTA. INDICATIONS FOR STRYCHNINE. It is probable that strychnine is of particular value in the disturbances of respiration following extreme heart failure, such as Cheyne-Stokes breath- ing, cardiac asthma, etc., as claimed by Eyster; and in such cases it should be given whether digitalis is being administered or not. By virtue of its stimulating action upon the vasomotor centre, strych- nine is particularly indicated in cases in which this centre is beginning to fail. This is particularly the case in all infectious diseases, in many cases of neurasthenia, in mild shock, in some cases of anaemia, asthenia, and in many convalescents. Strychnine should be used not to replace digitalis, but may be given as a prophylactic to prevent the heart muscle from wear- ing itself out upon a relaxed vascular system. When the heart muscle once shows signs of giving way, when marked cardiac dilatation, etc., have set in, its period of usefulness is over. Small doses of digitalis will then do the same work better and will do more. It is also valuable when given along with digitalis. The value of strychnine again becomes manifest in the later stages of heart failure through its action as a stimulant for the respiratory centre. Eyster believes that it is particularly useful in warding off Cheyne- Stokes respiration and also in the treatment of the latter. It is probably still more useful in cardiac asthma, more as a prophylactic measure in main- taining the activity of the respiratory centre than in stopping individual attacks; and it may also prove of value in warding off the distressing dreams that result from mild asphyxia during sleep, as well as the attacks of tachy- cardia and other unpleasant conditions which may occur as the result of waking " with a start " (asphyxia during sleep). CAMPHOR. Camphor is a white substance, soluble in alcohol, ether, and chloro- form, whose structural formula is CH 2 - -CH- -CH 2 C(CH 3 ) 2 CHo C - - CO CH 3 Average dose 0.12 Gm. (2 gr.). best given as linimentum camphora? (camphorated oil), which contains 20 per cent, of camphor dissolved in cotton-seed oil. Average dose 0.75 to 2.0 c.c. (20 to 45 minims), available for hypodermic use or by mouth. Spiritus camphonr, a, 10 per cent, .solution of camphor in alcohol. Dose 1 c.c. (15 minims). Camphor, like strychnine, is a stimulant to the vasomotor centre, but, according to Cameron, does not seem to have so pronounced an effect on tonic- it y . Like strychnine it also varies in its effects on different individuals. Some persons require doses twenty times as large as do others before an effect sets in, especially when the drug is given by mouth. Camphor is most important for its use in shock. It is given deeply into the muscles in order to avoid subsequent inflammations. It is not so valuable for continuous use. As recently shown by Winterberg, Seligmann, and Gottlieb and Magnus, camphor has also a very distinct action upon the heart muscle, causing the fibril- lating exercised heart to revive from fibrillary contractions. After camphor has been ad- THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 253 ministered to a dog the ventricle (in situ) can be thrown into fibrillary contractions by weak faradic stimuli and yet recover. On the other hand, a direct therapeutic effect upon the heart muscle in man has not yet been proved. CALCIUM SALTS. Calcium chloride and other salts of calcium have been recommended recently as cardiac stimulants by Lauder Brunton and other English clinicians. Although the action of calcium upon the excised heart is indisputable, its effect upon the heart in situ has been supposed to be too transitory to be of practical value. The writer has been unable to find any effect upon the maximal and minimal blood-pressures and pulse-rates of a number of cases of typhoid fever who were receiving calcium lactate in sufficiently large doses to hasten coagulation. Sladen also found in a large variety of cases that calcium lactate had no effect upon pulse-rate or blood-pressure. On the other hand, in animals calcium chloride has an effect, especially upon tonicity, which closely simulates that of strychnine. Injec- tion of considerable quantities directly into the cavities of the heart revives that organ as nothing else appears to do. The writer has found that in some cases dogs' hearts that had actually stopped beating and even lost their mechanical irritability revived to such an extent as to resume a regular rhythm with a moderately high blood-pressure. The matter is, however, still in the experimental stage. CAFFEINE. From the results of experiments upon animals, caffeine would take rank next to digitalis in cardiac therapy. Like digitalis it acts upon the cardiac muscle, increasing the size and force of the contraction; like digitalis it has a vasoconstrictor action, and raises the blood-pressure by bringing about constriction of the peripheral blood-vessels. It is therefore particularly valuable in conditions of collapse and shock. In this regard it is more reliable than camphor (Romberg) or strychnine. On the other hand, caffeine does not exert a constricting action upon the coronary arteries (O. Loeb), and hence is not contraindicated in cases of coronary sclerosis. Upon the pulse-rate caffeine exerts a variable effect, in relatively small doses (0.1 Gm., 2 gr.) slowing the pulse by stimulating the vagi, in larger doses accelerating. The acceleration is apparently due to direct action upon the heart muscle, since it occurs also in the excised heart when caffeine is added to the Locke's solution. However, as regards the effects of a given dose, there is the greatest variation among different individuals, some persons being extremely sensitive to small doses, others extremely resistant. Even in the same individual tolerance varies. Thus a considerable degree of tolerance may be developed by the constant use of coffee, so that three or four cups (0.15 to 0.2 Gm., 3 to 5 gr. caffeine) a day may be taken with no symptoms whatever. Thus, in a case under the writer's ob- servation, after several months of absolute abstinence from coffee, marked palpitation, tachycardia, and sleeplessness resulted from a single cup in twenty-four hours; a few weeks later one cup and after a few months two cups could be taken without any apparent effect. Unfortunately, the therapeutic use of caffeine is often accompanied by palpitation, sleeplessness, and even nausea, vomiting, vertigo, and delirium, which occur with particular ease in cases with cardiac disease. In using caffeine one is therefore usually in a dilemma between a hypersensitiveness and an habituation. Unfortunately, the palpitation and discomfort usually set in at about the same point as the therapeutic effects, or even curlier; but there are certainly many cases in which this is not the case, and in which caffeine is a valuable therapeutic agent. THEOBROMINE. Theobromine has a much less effect upon the cerebral cortex and upon the vasomotor centre than caffeine, but has a very strong diuretic action. As shown by O. Loeb it possesses a much more powerful action in dilating 254 DISEASES OF THE HEART AND AORTA. the coronary arteries of the excised heart. Upon the heart in situ its action does not seem to be pronounced. Indeed, G. S. Bond, in the writer's labora- tory, has been unable to detect any effect upon the outflow from the coronary veins as the result of intravenous injection of agurin (theobromine sodium acetate). The stimulating action of theobromine upon the heart muscle, though not as intense as that of caffeine, is still very marked. It has there- fore been recommended as a cardiac stimulant, particularly by the French clinicians, who found it of considerable value in the weak hearts of fatty individuals. Kaufmann and Pauli, Brewer and v. Leyden recommended the use of theobromine in attacks of angina pectoris (stenocardia). Pineles advises theophyllin. Pal has found that theobromine is occasionally useful in the treatment of vasomotor crises, but that it often fails in cases where iodine and potassium thiocyanate help. Romberg is not able to detect any beneficial action of theobromine apart from its diuretic action. In using theobromine it is pref- erable to use those compounds which are free from salicylates, since this radical has a certain depressant action upon the heart and an irritant action on the kidneys. Acettheobromin sodium (''agurin'') and acettheocin sodium are therefore preferable to theobromine sodium salicylate " diuretin "). ACONITE. PREPARATIONS. A o o n i t u m , the dried tuberous root of aconitum napellus, collected in autumn, and yielding not less than 0.5 per cent, aconitin. Dose 0.05 Gm. (1 gr.). T i n c t u r a a c o n i t i . U. S. P., now represents 10 per cent, of the crude drug, formeily stronger. It is the most certain and most stable of all the aconite preparations. Dose 0.6 c.c. (10 minims). Aconitina, the crystalline alkaloid. Dose 0.00015 Gm. (0.15 mg. or AT gr.). It is so irritating that it is usually preferable to prescribe the simple tincture of aconite, since this is assayed according to the last pharmacopoeia. Pharmacological Action. Aconite has three pharmacological actions upon the circulatory system: (1) it stimulates the vagus promptly and to a high degree; (2) it diminishes the size and force of the cardiac contraction, and also accelerates the heart when this organ is liberated from the action of the vagus centre; (3) it slightly stimulates the vasomotor Centre in very small doses. However, it also diminishes the activity of the respiratory centre, and may thus bring on dyspnoea. In experimental aconite poisoning in animals Cushny has been able to produce a number of rather unusual types of alterations of rhythm, sudden changes in the rhythm of the whole heart of varied character, with heart-block, pulsus alternans, auricular, ventricular, or auriculoventricular extrasystoles, paroxysms of tachycardia resembling the idiopathic paroxysmal tachycardia of man, and reversal of rhythm in which the cardiac impulse arises in the ventricles and travels up to the auricles. In the latter case the ventricles may beat twice as fast as the auricles (reversed rhythm with partial block). Therapeutic Uses. When carefully given in therapeutic doses aconite slows the heart by stimulation of the vagus, and has little action upon the heart muscle. It is therefore of value in the acceleration of the pulse in fevers, wh !,' the In-art muscle itself needs no stimulation and the heart needs slowing. THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 255 Owing to the variability of the tincture under the old pharmacopoeia, the use of aconite has fallen into disrepute, and enough time has not elapsed since the adoption of the last pharmacopoeia (1900, adopted in 1905) for its real utility in physiological therapeutics to have been investigated. There is no doubt that it is of value in many cases of tachycardia, especially those of nervous or postfebrile origin. Da Costa, in 1864, found it of some value for the tachycardia of acutely overstrained hearts, but particularly useful when given with digitalis. This combination contains two drugs; both stimulate the vagi, the one tends to diminish, the other to increase the force of cardiac contraction. The recent observations of Price, quoted by Cushny, indicate, however, that, in ispite of its action on the vagus, aconite alone does not affect the heart-rate of patients with auric- ular fibrillation who respond readily to digitalis, and it is an open question whether the results obtained with aconite cannot in all cases be obtained better with other drugs. ADRENALIN. Adrenalin (suprarenin, epinephrin) , the active principle of the suprarenal gland, is also used occasionally to raise blood-pressure by its constricting action upon the peripheral blood-vessels and slight stimulating action upon the heart, but its action lasts only from one to two minutes, and hence it is of little value, except to tide over a sudden failure until some other drug can become active. In cases of temporary failure of the circula- tion, however, a very slow continuous injection of 9oo"o~o to TOTJOT solution of adrenalin may be made into the vein and the blood-pressure thus raised for a considerable time without bringing about any cumulative action (Straub) . Under these circumstances the drug may also exert some stimulating digitalis- like action upon the heart itself, which may enable its contractions to regain their force ERGOT. Ergot has been recommended by some writers for its vasoconstrictor action exerted through stimulation of the vasomotor centre. It also stimu- lates the vagal centre. Cronyn and Henderson have found that these effects are very uncertain when the drug is given by mouth, but occur quite uni- formly when it is given intravenously. Since this is rarely necessary, the use of ergot may be confined to patients with vasomotor failure, in which, like adrenalin, it is used as a last resort. NITRITES AND NITROGLYCERIN. PREPARATIONS. (PHARMACOPOEIA!,, V. S. P.) Amyl nitrite (amylis nitris), a liquid containing about SO per cent, of amyl nitrite. Average dose 0.2 e.c., 3 minims (inhaled). Usually to be had in pearls, each pearl contain- ing one dose. Ni t rogly ccrin CH 2 ONO2 CIIONOo CHoOXO 2 is sold in tablets of varying size, usually one tablet containing TOO gr. (O.G nig.). How- ever, in tablet form the nitroglycerin is liable to undergo more or less rapid deterioration and hence administration in this form is unreliable. It is best given as spirit us glycerylis 256 DISEASES OF THE HEART AND AORTA. MIX. HOURS nitratia (spiritus glonoini), a 1 per cent, solution of nitroglycerin in alcohol, which should be freshly prepared from a 10 per cent, stock solution. Initial dose 0.05 c.c. (1 minim.), increasing if necessary 1 minim at a time. Sodii nitris (sodium nitrite), NaXQj, a white fused mass, very deliquescent and slowly becoming oxidized to sodium nitrate on exposure to the air, thus becoming useless. Dose 0.06-0.12 Gm. (gr. i-ii). There are also several non-pharmacopoeial nitrates which are very satisfactory. Erythrol tetranitrate, CH 2 ONO 2 -CHONO 2 - CHONO;>-CH 2 ON0 2 , has about the same action as nitroglycerin, except that it acts more slowly (action lasting three to four hours). Sold as tablets, each containing .03 Gm. (^ gr.). Dose one or two tablets every four to six hours. In the cases in which the writer has used it erythrol tetranitrate has been very efficient and satisfactory. ACTION OF THE NITRITES. In practical therapy the nitrites are drugs of great importance. In animals they are found to act upon the muscles and nerves of the blood- vessels to bring about an intense vasodilatation, thereby diminishing the resistance to blood flow and lessening the resistance to the action of the heart. As far as can be judged from the studies of O. Loeb, they do not influence the vasoconstrictors of the coronary arteries unless present in concentration which is absolutely toxic to heart muscle. G. S. Bond has found that the outflow through the coronary yems Q f normal dogS is decreased . rather than increased by nitro- glycerin and amyl nitrite. It is there- fore questionable whether these drugs even bring about dilatation of the coronary arteries, as has been supposed from their efficacy in angina pcctoris. The relation of the various nitrites to one another as regards rapidity of action is shown in Fig. 134. The effect of amyl nitrite sets in within a minute and passes off within five minutes; that of nitroglycerin lasts from about the seventh to the twentieth minute after administration, sodium nitrite from the fifteenth to the thirty-fifth, while erythrol tetranitrate begins to exert an effect only after about fifteen to thirty minutes, but this continues for three to four hours. Amyl Nitrite. Hewlett has recently made a careful clinical study of the effects of amyl nitrite Inhalation, and found, (1) an immediate fall of maximal pressure, average 13 nun. Hg, lasting less than forty seconds, and accompanied by a less fall of minimal pressure and an increase of pulse-rate. This is followed by a secondary rise (about 28 mm.) of maximal pressure to considerably above the original height, accompanied by a less marked rise of the minimal pressure and by a return of pulse-rate to the normal. These changes in blood-pressure correspond to an i n c r e a s e d sys- tolic o u t p u t and increased force of heart-beat (augmentor effect), and Hewlett was able to see with the fluoroscope that, ''as the action of the heart slowed down the excur- sions of the left ventricle became wider by fine-half centimetre, but they soon returned to normal.'' In other words, besides being a vasodilator amyl nitrite is a very active cardiac stimulant, more rapid than any except adrenalin. These FIG. 134. Efforts of drugs of the nitrite series upon the blood-pressure in man. (Schema representing the findings or Hewlett and -Mat- thews.) MIX, minutes. THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 257 findings accord well with the results of Cameron on dogs, that nitroglycerin both in- creases cardiac output and cardiac tonicity to a marked degree. Relaxation of the peripheral blood-vessels under the influence of the amyl nitrite, as shown by the plethysmograph, was present throughout all Hewlett's experiments in spite of the peculiar variations of blood-pressure. The vasodilatation reaches its maximum within the first minute and very gradually subsides after the second, but a definite effect is still noticeable ten or twelve minutes after. In older persons Hewlett found that the pulse- rate often did not change, probably owing to the absence of the tonic activity of the vagus. The following represent typical effects in normal men as obtained in the very careful clinical investigations of Hewlett and Matthew: Dose. Time when action begins. Average fall in B. P. Maximal fall occurs in Duration. Amyl nitrite (Hewlett) 15 sec. 20 mm. 1 min. 10 min. Nitroglycerin .05.! c.c. (gr. i ij) 1 min. 28 4^- min. i hr. Sodium or potassium nitrate .15 Gm. (gr. ij) . Erythrol tetranitrate .03-.06 Gm. (gr. }-i) . . . Manitol tetranitrate .06 Gm. (gr. i) 5 min. 5 min. 12 32 35 35 14 min. 22 min. 100 min. Nitroglycerin. As to nitroglycerin, there is tremendous variation in its effects upon different individuals, A. Loeb having reported a case of collapse after 0.6 mg. (iJa gr.), whereas J. Stewart has given 20 grains a day to a single patient. In some cases it is impossible to obtain a fall of pressure with any ordinary doses. The writer's experience agrees with that of Matthew, that the effects are often lacking in cases of nephritis in which blood-pressure has persisted for some ( time. To this might also be added a certain group of arteriosclerotics in which the renal symptoms do not pre- dominate, although it is possible that arteriosclerotic changes may be present in the kidney. In Prof. J. 0. Hirschfelder's wards it was customary to begin with a dose of 1 gtt. (-jV c.c., ^ minim) every half hour, increasing 1 gtt. at every third dose until palpitation, headache, or buzzing in the ears warned that the physiological limit had been reached. The next dose was then omitted and a permanent dosage of 1 gtt. less than the dose last given was then kept up. In some cases as much as 1 c.c. (15 minims) of the 1 per cent, solution was given every half hour with only the mildest subjective symptoms, the average permanent dose being 0.3 to 0.6 c.c. (5 to 10 minims). The effect of these doses is very variable. Effect on the Circulation. A fall in minimal blood-pressure is the most constant, usually accompanied by a rise in pulse-pressure, and the maximal pressure sometimes rising, sometimes falling. Hewlett thinks that there is combined dilatation of the blood-vessels and increased systolic output of the heart. In a series of observations upon the fluctuations of blood-pressure after the administration of these drugs, made with the Erlanger apparatus independently of and some years before those of Hewlett, the writer had noticed effects quite similar to those above mentioned. There seems no doubt, therefore, that, as stated by Hewlett, the beneficial effects of the nitrites in man are due to something more than a simple vasodilatation, and indeed it is possible that the latter may play often even a minor role. Certain it is that in many cases they are ideal drugs to relieve the work of the heart over short periods when the blood-pressure is not already too low to admit of their use. However, it must be borne in mind that individual susceptibilities 258 DISEASES OF THE HEART AND AORTA. vary, and the patient should be tested with amyl nitrite, whose effects can be controlled, before any other nitrite should be given. When used over long periods of time, moreover, the production of met haemoglobin in the blood may be brought on (shown by the spectroscope, or by a chocolate tint in the blood), which is distinctly harmful and a sign for immediately stopping the use of the drug. VASOTOXIX (YOHIMBIX-URETHAXE). Franz Miiller and Bruno Fellner have recently taken advantage of the vasodilator action of the salts of yohimbin to introduce a derivation of the latter into medical practice. In order to obviate the aphrodisiac action and the effect upon the respiratory centre, they have combined yohimbin nitrate with urethane, by which they claim a definite double salt of yohim- binurethane is formed, to which they have given the trade name of v aso- tonin. The claim that "vasotonin" represents a definite chemical combi- nation, rather than a mixture of the two drugs, has been sharply criticised by Spiegel and cannot be regarded as definitely settled. On the other hand, Miiller has shown that the physiological effects of yohimbin are greatly changed by the presence of the urethane, so that the desired effect of removing the aphrodisiac and respiratory effects seems to have been accomplished. Miiller has shown experimentally upon animals that it lowers the blood- pressure by producing dilatation of the blood-vessels of the limbs and also a certain amount of dilatation in the blood-vessels of the brain, but that the vessels of the splanchnic area are constricted. He showed by means of the cardiometer, as Cameron had shown for the nitrites, that in ordinary doses it increases the tonicity of the heart muscle. His results were at once applied clinically by B. Fellner in a series of fifteen cases. Fellner found that in man the subcutaneous administration of 1 c.c. (15 minims) of vasotonin (containing 10 mg. yohimbin nitrate or 8 mg. yohimbin) exerted about the same effects as Miiller had observed in animals, and gave rise to a dilatation of the arteries with a fall of maximal blood- pressure often amounting to 50 mm. Hg. The minimal blood-pressure was affected to a less degree; the pulse-pressure usually diminished. With a single injection daily or even upon alternate days these effects persisted and in many cases gave the desired result. His observations have been confirmed by Staehelin and by Rosendorff . Fellner recommends the drug in the following classes of cases: 1. Transitory hypertension, such as attacks of angina pectoris, various forms of asthma, vasomotor crises and conditions of increased vasomotor irritability, intermittent claudication, etc. 2. More lasting hypertension, as in arterioscleroses, the toxic hyper- tension of lead and nicotine poisoning, and also in chronic nephritis. Aneurism might also be added to this list. As regards the clinical phase of the question, it must be said that, regard- less of whether vand., 1911. i. Wenckebach, K. F.: Discussion on the Effect of Digitalis on the Human Heart, ibid., 1910, ii, 1600. Hoepffner, C.: Gesichtspunkte fur die Einfiihrung des Extraktum Digitalis depuratum, Mvinchen. med. Wchnschr, 1908, Iv, 1774. Mueller, ibid., 1908, Iv, 2651. Hewlett, A. W.: Digitalis Heart -block, J. Am. M. Assoc., Chicago, 1907, xlviii, 47. v. Tabora, D.: Ueber experiment elle Erzeugung von Kammersystolenausfall und Disso- ciation durch Digitalis, Ztschr. f. exper. Path. u. Therap., Berl., 1906, iii, 549. Erlanger, J.: Ueber den Grad. der Vaguswirkung auf die Kammern des Hundeherzens, Arch. f. d. ges. Physiol., Bonn, 1909, cxxvi, 77. Rihl, J.: Klinischer Beitrage zur Kenntniss der Ueberleitungsstorungen von der Bildungs- statte der Ursprungsreize zum Vorhof., Deutsches Arch. f. klin. Med., Leipz., 1908. xciv, 286. Ritchie, W. T.: Discussion on the Effects of Digitalis on the Human Heart, Brit. M. J., 1910, ii, 1609. Gottlieb, R. : Ueber einige Digitalisfragen, Therap. Montash., Berl., 1911, xxv, 9. Watson, J. J.: A Method of Fixation of Vein to Facilitate the Introduction of a Xeedle for Intravenous Injections, J. Am. M. Ass., Chicago, 1911, Ivii, 383. M tiller, Ot fried: Ueber die Herz und Gefasswirkung einiger Digitaliskorper bei gesunden und kranken Menschen, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1909, xxvi, 364. Fleischmann, P. : Ueber intravenose Strophanthintherapie bei Verwendung von g-Strophan- thinum crystallis (Thorns), ibid., 1909, xxvi, 369. Bailey, H. C. : A Clinical Study of Crystalline Strophanthin, J. Pharm. and Exper. Therap., Baltimore, 1909-10, i, 349. Cloetta. M.: Ueber den Einfluss der chronischen Digit alisbehandlung auf das normale und pathologische Herz, Arch. f. exper. Path. u. Pharmakol., Leipz., 1908, lix, 209. Gelbart: Ueber den Einfluss der Digitalis auf frisch entstandenen Herzfehler, ibid., 1911, Ixiv. 167. Bachmann, G.: Sphygmographic Study of a Case of Complete Heart -block; a Contribu- tion to the Study of the Action of Strophanthus on the Human Heart, Arch. Inst. Med., Chicago, 1909, iv, 238. Gibson, A. G.: A Contribution to the Knowledge of the Action of Digitalis on the Human Heart. Quart. J. M., Oxford, 1908, i, 173. Lewis. T.: Brit. M. J.. 1910, ii, 1670. Cushnv. A. R.: The Therapeutics of Digitalis and its Allies, Am. J. M. So.. Phila. and X. Y., 1911, cxli, 469. Clemens: Fortschr. d. Med., 1908. xxvi, 1057. Tissot: Folia Serol., 1909. iii. 1. Szennci, J.: Ueber die Wirkung des Extr. Digitalis depuratum (Digipuratum) auf das cardiovaskulare System, nebst Bemerkungen auf die Wirkung der Digitalis, Therap. Monatsh., Berl., 1910. xxiv. 427. Boos, W. F.. Xewburgh, L. H., and Marks. H. K.: Experiences with Digipuratum, Bost. M. and S. J.. 1910, clxii, 173; also The Use of Digipuratum in Heart Disease, Arch. Int. Med.. Chicago, 1911. vii, 55 1. Boos. W. F., and Lawrence, C. H.: The Xewer Heart Remedies, Interstate M. J., St. Louis, 1911, xviii, 648. THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 263 Fleisher, M. S., and Loeb, Leo: Experimental Myocarditis, Arch. Int. Aled., Chicago, 1909, iii, 78. Gottlieb, R., and Sahli, H.: Herzmittel und Vasomotorenmittel, Verh. d. Kong. f. inn. Med., Wiesbaden, 1901, xviii, 21. Boehm: Untersuchungen ueber die physiologische Wirkung der Digitalis und des Digi- talins, Arch. f. d. ges. Physiol., Bonn, 1872, v, 153. Schmiedeberg, O. : Untersuchungen ueber die pharmakologisch wirksamen Bestandtheile der Digitalis purpurea, Arch. f. exper. Pathol. u. Pharmakol., Leipz., iii, 16. Fraenkel, A., and Schwartz, G.: Ueber Digitaliswirkung an Gesunden und an kompen- sierten Herzkranken, ibid., 1908, Ivii, 188. Fraenkel, Alb.: Vergleichende Untersuchungen ueber die Kumulativwirkung der Digi- taliskorper, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1903, li, 84. Ueber Digitalis- wirkung an gesunden Menschen, Mxinchener med. Wchnschr., 1905, Hi, 1537. Die physiologische Dosirung von Digitalispraparaten, Ther. d. Gegenwart, Berl., 1902. Bemerkungen zur internen Digitalismedikation, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1874, iii, 16. Beitrage zur Kenntniss der pharmakologischen Gruppe des Digitalins, ibid., 1882, xvi, 149. Cloetta, M.: Einfluss der chronischen Digitalisbehandlung auf das normale und patholo- gische Herz, Therap. d. Gegemv., Berl., 1908, xlix, 437. For the standardization of digitalis preparations, consult: Sowton, S. C. M.: Some Experiences in the Testing of Tincture of Digitalis, Lancet, Lond., 1908, clxxiv, 310. Hatcher, R. A.: Tincture of Strophanthus, J. Am. M. Assoc., Chicago, 1907, xlviii, 1177. Edmunds, C. W. : ibid., 1907, xlviii, 1744; but particularly Edmunds, C. W., and Hale, W.: The Physiological Standardization of Digitalis, Bull. No. 48, Hyg. Lab. U. S. Pub. Health and Mar. Hosp. Serv., Wash., 1909. DlGITOXIN. Koppe: Untersuchungen ueber die pharmakologische Wirkung des Digit oxins, Digital- eins, und Digitalins, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1874, iii, 274. V.Starck: Zurtherapeutische VerwendungdesDigitoxins, Mimchen.med. Wchnschr., 1897. Cloetta: Ueber Digalen (Digitoxin solubile), Mtinchen. med. Wchnschr., 1904, li, 1466. Ueber die Kumulativwirkung des Digitalis, ibid., 1906, liii, 2281. V. Kehle: L'eber den therapeutischen Werth des Digalens, Therap. Monatshefte, 1906. Fraenkel, Alb.: Abhandlungen zur Digitalistherapie. II. Zur Frage der Kumulation, besonders beim Digalen, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1907, Ivii, 123. DIGITALIN. Kiliani: Archives de Pharmaeie, 1892-1899. Deuchor: Ueber die Wirkung des Digitalinum verum bei Cirkulationsstorungen, Deutsch. Arch. f. klin. Med., Leipz., 1896, Ivii, 1. Vid. also Fraenkel, cited above. STROPHANTHUS. Fraser: The Action and Use of Digitalis and its Substitutes, Brit. M. J., Lond., 1885, ii, 904. Note on Tincture of Strophanthus, ibid., 1887, i, 151. Popper: Ueber die physiologische Wirkung des Strophanthins, Zeitschr. f. klin. Med., Berl., xvi, 97. Fraenkel, Alb., and Schwarz: Ueber intravenose Strophanthintherapie bei Herzkrankon, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1907, Ivii, 79. Hatcher, R. A., and Bailey, H. C. : Tincture of Strophanthus and Strophanthin, J. Am. M. Assoc., Chicago, 1909, Iii, 5. Osier, William: The Principles and Practice of Medicine, New York, 1901. Francois-Franck, Ch. A. : Quoted on page 405. Colbeck, E. H.: Dilatation of the Heart, Lancet, Lond., 1904, i, 990. Gossage, A. M.: The Tone of the Cardiac Muscle, Proc. Roy. Soc. Med., Lond., 1908, i, 144. Hirschfelder, J. ().: Unpublished observations. Hewlett, A. W.: Digitalis Heart-block, J. Am. M. Assoc., Chicago, 1907, xlviii, 47. 264 DISEASES OF THE HEART AND AORTA. Dmitrenko, L. F.: Ueber die klinische Bedeutung der Digitalis- Allorrhythmie, Berl klin Wchnschr., 1907, xliv, 392, 432. Bering, H. E.: Ueber kontinuierliche Herzbigeminie , Deutsches Arch. f. klin. Med., Leipz., 1904, Ixxix, 175. Da Costa, v. Leyden, see page 184. Fellner, B.: Klinische Beobachtungen ueber den Wert der Bestimmung der wahren Puls- grosse (Pulsdruckmessung) bei Herz und Xierenkranken, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxviii, 36. Janeway, T. C.: The Use and Abuse of Digitalis, Am. J. M. Sc., Phila. and N. York, 1908, cxxxv, 781. STRYCHNINE. Heinz, R.: Handbuch der experimentellen Pathologic nnd Pharmacologie, Jena, 1905. Cook, H. W., and Briggs, J. B.: Clinical Observations on Blood-pressure, Johns Hopkins Hosp. Rep., Bait., 1903, xi, 451. Cabot, R. C. : Measurements of Blood-pressure in Fevers before, during, and after the Administration of Strychnine, Am. Med., Phila., 1904, viii, 31. Drayer, F. P.: Personal communication. Eyster, J. A. E.: Personal communication. CAMPHOR. Huebner: Ueber die Wirkung des Kampfers auf die Leistung des Froschherzens, Arch' cl. Heilk., Leipz., 1870, xi, 334. Harnack and Witkowski: Pharmakologische Untersuchungen ueber das Physostigmin und das Kalabarin, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1876, v, 401. Maki: Ueber den Einfluss des Kampfers, Kaffeins, und Alkohols auf das Herz, In. Diss., Strass., 1884. Passler, H. : Experimentelle Untersuchungen ueber die allgemeine Therapie der Kreislaufs- storungen bei acuten Infektionskrankheiten, Deutsch. Arch. f. klin. Med., Leipz., 1899, Ixiv. Winterberg, H.: Ueber die Wirkung des Kampfers, Arch. f. d. ges. Physiol., Bonn, 1903, xciv, 455. Seligmann: Zur Kreislaufwirkung des Kampfers, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1905, lii, 333. Gottlieb, R., and Sahli, H.: Herzmittel und Vasomotorenmittel, Verh. d. XIX Kong. f. innere Med., Wiesb., 1901. ACONITE. Matthews, S. A.: A Study of the Action of Aconitin on the Mammalian Heart and Cir- culation, J. Exp. Med., Baltimore, 1897, ii, 593. Cushny, A. R. : The Irregularities of the Mammalian Heart Observed under Aconitine and on Electrical Stimulation, Heart, Lond., 1909-10, i, 1. Da Costa, J. M.: On Irritable Heart, Am. J. M. Sci., Phila., Ixi, 17. Hirschfelder, A. D. : Observations upon Paroxysmal Tachycardia, Bull. Johns Hopkins Hosp., Bait., 1906, xvii, 337. ADRENALIN. Straub, W.: Die pharmakologische Grundlagen der Adrenalintherapie, Miinchen. med. Wchnschr., 1911, Iviii, 1388. CAFFEINE. Wagnor: Experimentelle Untersuchungen ueber den Einfluss des Kaffeins auf Herz und Gefiissapparat, In. Diss., Berl., 1885. Glupe: Ueber die Wirkung der Kaffeinsalze bei Herzkrankheiten, In. Diss., Berl., 1884. Cushny and van Xaten: On the Action of Caffein on the Mammalian Heart, Arch. int. de Pharmacodyn., 1901, ix, 169. Cushny, A. R.: A Contribution to the Pharmacology of the Mammalian Heart, Brit. M. j", 1S9S, i, 1068. THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 265 Fraenkel: Klinische Untersuchungen ueber die Wirkung von Kaffein, Morphium, Secale cornutum und Digitalis auf den arteriellen Blutdruck, Deutsch. Arch. f. klin. Med Leipz., 1889-90, xlvi, 542. Bock: Ueber die Wirkung des Kaffeins und Theobromins auf das Herz, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1900, xliii, 367. CALCIUM SALTS. Brunton, T. Lauder: Use of Calcium Salts as Cardiac Tonics in Pneumonia and Heart Disease, Brit. M. J., 1907, i, 616. Stark, J.: Calcium Salts as Cardiac Tonics, Lancet, Lond., 1907, i, 1701. Barr, J. : On the Use of Calcium Salts as Cardiac Tonics in Pneumonia and Heart Disease, Brit. M. J., Lond., 1907, i, 717. Sladen: Personal communication. Boggs, T. R. : Variations in the Calcium Content of the Blood Following Therapeutic Measures, Johns Hopkins Hosp. Bull., Baltimore 1908, xix, 201. NITRITES. Brunton, T. L. Quoted on page 253. Hewlett, A. W.: The Effect of Amyl Nitrite Inhalations upon the Blood-pressure in Man, J. Med. Research, Bost., 1906, xv, 383. Cameron. Quoted on page 201. Matthew: Vasodilators in High Blood-pressure. Quart. J. M., Oxford, 1909, ii. Loeb, A.: Klinische Untersuchungen ueber den Einfluss von Kreislaufsaenderungen auf die Urinzusammensetzung, Deutsches Arch. f. klin. Med., Leipz., Ixxxiv, 579. Stewart, J.: Tolerance to Nitroglycerin, J. Am. M. Ass., Chicago, 1905, xliv, 1678. POTASSIUM IODIDE. Potain: La clinique medicale de la Charite, Par., 1894. M tiller, O., and Inada: Zur Kenntniss der lodwirkung bei der Arteriosklerose, Deutsche med. Wchnschr., Leipz., 1904, xxx, 1751. Determann. Quoted on page 61. Koranyi, Loeb and Githens. Quoted on page 259. POTASSIUM THIOCYANATE. Pauli, W.: Ueber lonenwirkung und ihre therapeutische Verwendung, Mtinchen. med. Wchnschr., 1903, 1, 153. Pal, J.: Die Gefasskrisen, Leipz., 1905. SAJODIN. Kuttelwascher, W.: Erfahrungen mit Sajodin, Prager med. Wchnschr., 1907, 546. Vigorelli, A.: Alguni Esperimenti golla Sajodina, Poliambulanza di Milano, 1908, No. 10, quoted from Zentralbl. f. d. ges. Physiol. u. Path. d. Stoffw., Berl., 1909, N. F., iv, 639. SALVARSAX ("606"). Hering, H. E.: Experimentelle Erfahrungen ueber die letale Dosis der sauren Losun^, voii Ehrlich-Hata 606. Miinchen. med. Wchnschr., 1910. Camus, J. and L.: Recherches experimentales sur le "606," Paris medical, Dec., 1910, quoted from Sieskind. Hoke, E., and Rihl, J.: Experimentelle Untersuchungen ueber die Beeinflussung der zir- kulationsorgane und der Atmung durch das Salvarsan, Verhandl. d. Kong. f. innere Med., Wiesb., 1911, xxviii, 242, and discussions by Hering, Schreiber, Nicolai, and Benario. Sieskind, R.: Das Verhalten des Blutdrucks bei intravenoser Salvarsaninjektionen, Miin- chen. med. Wchnschr., 1911, Iviii, 568. 266 DISEASES OF THE HEART AND AORTA. Ehrlich, P. v.: Die Salvarsantherapie, Ruckblicke und Ausblicke, Miinchen. Med. Wchnschr., 1911, Iviii, 1. Martius, K.: Ueber Todesfalle nach Salvarsaninjektionen bei Herz und Gefasskrankheiten, ibid., 1911, Iviii, 1067. Spiethoff, B.: Salvarsan bei Syphilis, ibid., 1911, Iviii, 192. Wechselmann and Nicolai: Action du dioxydiamidoarsenobenzol d'Ehrlich sur le coeur, Arch, des Malad. du ccEur et des vaiss., Par., 1910, iii, 730. Kromayer: Chronische Salvarsanbehandlung bei Syphilis, Deutschen med. Wchnschr., Leipz., 1911, xxxvii, 1547. VASOTONIN. Miiller, Fr., and Fellner, B.: Ueber "Vasotonin," ein neuesdruckherabsetzen des Gefass- mittel, Therap. Montash., Berl., 1910, xxiv, 285. Miiller, Fr.: Enviderung auf die Bemerkungen des Herrn Prof. L. Spiegel im Juliheft dieser Zeitschrift, ibid., 1910, xxiv, 439; Ueber Vasotonin, Zweite Erwiderung an Herrn Prof. L. Spiegel, ibid., 1910, xxiv, 546. Spiegel, L. : Ueber Vasotonin, ibid., 1910, xxiv, 365; also Nocheinmal das "Vasotonin," ibid., 1910, xxiv, 544. Heubner, W.: Zur Vasotoninfrage, ibid., 1910, xxiv, 549. Staehelin, R.: Erfahrungen mit Vasotonin, ibid., 1910, xxiv, 477, 521. Rosendorff : Ueber Erfahrungen mit Vasotonin, ibid., 1911, xxv, 148. VI. GYMNASTICS AND HYDROTHERAPY. GYMNASTICS. FUNDAMENTAL PRINCIPLES. During recent years gymnastic exercises have come to play a major role in the treatment of cardiac diseases. Although this treatment was introduced empirically, its physiological basis is found in the fact, shown by Frank and Hirschfelder, that a strain upon the ventricles which does not exhaust them tends to act as a stimulus which gives rise to more forci- ble contractions, increases their tonicity, and causes the residual blood (and hence the dilatation) to decrease. The guiding principle is further given by the experimental evidence produced by these writers, that when the strain was excessive it had the opposite effect, and caused weakening of the contractions, diminished tonicity, and dilatation of the heart. (See Fig. 119, page 192.) In dealing with normal individuals it is observed that the strengthen- ing of every normal individual, the training of every athlete or laborer con- sists in the habituation of the body, and particularly of the heart, to gradu- ally increasing muscular effort and exercises. (See page 193.) To a great extent, as has been seen, page 191, this consists in securing a greater increase in output of blood at each beat without calling upon any of the accessory nervous mechanism to bring this about. Such exercises have also been used with great success in the treatment of patients with heart failure. It stands to reason that they should not be used at once when the patient is brought in with an acute heart failure; but after a sufficiently long period of rest, when the acute condition has passed off and he can sit up in bed without discomfort, a few of the mildest arm movements may be begun with great advantage. It is often better to train the patient by a few mild passive or resisted movements while he is still in bed than to subject him at once to the strain of getting up for an hour or so after his sojourn in bed. Moreover, many other muscles may be kept in tone, the blood- vessels in the muscles may be kept dilated, and the resistance to blood flow may thus be diminished. SYSTEMS OF EXERCISE. In accordance with these facts several systems of exercises have been developed for assisting in the training of the heart. In all of them the cru- cial point lies in the avoidance of the slightest fatigue, holding of the breath, or increased breathing. Hence the actual result obtained depends more upon the vigilance and intelligence of the physician, nurse, or attendant who supervises the exercises than upon the exercises themselves. 267 268 DISEASES OF THE HEART AND AORTA. In general the exercises may be divided into four classes: (1) Passive movements. (2) Contraction of antagonistic muscles. (3) Resisted movements. (4) Mechanical gymnastics. Passive Movements. These are the mildest possible forms of exercise. The attendant grasps the patient by the hands or feet and moves these members gently and slowly about, while the patient makes no effort at contraction whatever. Such movements have the effect of increasing the circulation of lymph, the absorption of oedema, and, to a certain extent also, of increasing the rapidity of blood flow. It is impor- tant to avoid all exercises in which the arms are raised high above the head, since this hydrostatically increases the pressure in the vena cava and may cause momentary dilatation of the heart. The following exercises or modifications of them may be carried out while the patient is still in bed, provided the greatest precaution is used in their execution. (1) Arms horizontal, to the front and back to the line of the shoulders. (2) Arms horizontal in line of shoulders, thence down to the sides of the body. (3) Arms horizontal, describe circles with hands. (4) Arms vertically dependent at sides, flex and extend elbows. (5) Arms dependent at sides, pronate and supinate alternately. (6) Clinch and open fists. (7) Legs straight, abduct; then adduct thighs. (S) Flex and extend knee at side of couch, never raising knee above level of body. (9) Flex and extend foot at ankle-joint. (10) Rotate thighs internally and externally. (11) Execute small circles with feet without raising them more than one foot; legs straight. Contraction of Antagonistic Muscles. Substantially the same exercises may be carried out by allowing the patient himself slowly and simultane- ously to contract both the muscles concerned in the movement and those which antagonize them, i.e., biceps and triceps, flexors and extensors of wrist, etc. In this way little movement is made, the pulse-rate is slowed rather than accelerated, and yet a good deal of energy may be expended. The blood-pressure is raised, however. If the patient can be trained to avoid all difficulty in breathing and all discomfort, a good deal of improve- ment in muscular strength and in cardiac tonicity may be obtained by this method. Its main drawback lies in the fact that the intensity of the exercise is controlled not by the attendant but by the patient, and that the latter is most likely to do more than is beneficial. RESISTED MOVEMENTS. (sCHOTT MOVEMENTS.) Probably the most widely used of all the cardiac gymnastics are the passive movements introduced by August Schott of Nauheim. These are generally used in connection with the Xauheim baths. This combination is particularly advantageous and permits at once of all the advantages of mild exercise, of baths, of rest and stimulation to sleep, of psychic sedative, and of the psychic suggestion to the patient that a great deal is being done and a great effort is being made for his welfare. GYMNASTICS AND HYDROTHERAPY. 269 The Schott movements consist of practically the exercises described above carried out by the patient himself, but with an attendant who makes a slight resistance to each movement. The resistance should be just enough to prevent the movement from being made rapidly, and at no time should it cause the patient any apparent effort or increase his respirations. Each day the resistance may be increased slightly, so that in a short time the patient may be doing a good deal of work without realizing it. In exe- cuting the resistance the attendant's mind is kept fixed upon the condition of the patient, and he is consequently more likely to notice over-exertion in the latter than if he were merely supposed to watch him without doing anything himself. In carrying out the Schott movements the following rules are prescribed. 1 Precautions for Schott Exercises. (1) Each movement is to be performed slowly and at uniform rate. (2) No movement is to be repeated twice in succession in the same limb or group of muscles. (3) Each single or combined movement is to be followed by an interval of rest. (4) The movements are not to be allowed to accelerate the patient's breathing, and the operator must watch the face for the slightest indications of (a) dilatation of the nostrils, (6) drawing of the corners of the mouth, (c) duskiness or pallor of the cheeks or lips, (d) yawning, (e) sweating, (/) palpitation. (5) The appearance of any one of the above signs of distress should be the signal for immediately interrupting the movement in process of execution, and for either sup- porting the limb which is being moved or allowing it to subside into a state of rest. (6) The patient must be directed to breathe regularly and uninterruptedly, and, should he find any difficulty in doing so, or for any reason show a tendency to hold his breath, he must be instructed to continue, counting in a whisper throughout the progress of each movement. (7) No limb or portion of the body of the patient is to be so constricted as to compress the vessels and check the flow of blood. Schott Exercises. The following is a list of Schott exercises in the order in which they are given. The resistance is moderate and steady, the operator's hand always being applied upon the surface of the extremity toward which the movement is made, even if that entails gliding around it gently during the movement. Usually the operator's hand is at one side of the patient's limb at one phase of the exercise and at the opposite when the movement is reversed. 1. Arms extended in front, palms facing each other. The operator's palms rest upon the backs of the patient's hands. Patient's arms carried backward to line of shoulders, the movement being gently resisted by operator (Fig. 135). The operator's palms are then rested against those of the patient, and the return of the arms in front of the chest is re- sisted. 2. One arm at side, elbow-joint flexed upward to shoulder, then extended to original position. 3. Arms at side, raised outward till thumbs meet over the head, then brought back to the original position. 4. Hands at level of pelvis in midline, fingers slightly flexed. Arms raised to the vertex of the head, then back. 5. Arms at sides, then raised forward in parallel planes until they are vertical, then moved back. The hand of the operator must glide around the wrist so that it is always applied to antagonize the movement. 1 Quoted from W. Bezly Tliorne. 270 DISEASES OF THE HEART AND AORTA. 6. Trunk flexed on hips, knees straight; trunk then extended. 7. Trunk rotated without movement of the feet. Operator exerts resistance against the shoulders. Fi... 13') cate . Srhottro liu black; tl isted movements. (Modified from W. Hezly Tliorne.) The attendant's hands are indi- le direction of the movement made l>y the patient Vindicated by the black arrows. S. Trunk flexed laterally, first to one side then (o the other, the movement being an- tagoni/.ed l>y resistance applied in the axilla, the operator's other hand resting on the hip. 0. Movement like No. 2; fists clinched. 10. Same, l>ut palmar surface of fist turned outward. 11. Arm extended from side, palm down, raised forwards and upwards describing a .--eniicircle until it is raised vertically along side of the ear. The movement is then reversed. GYMNASTICS AND HYDROTHERAPY. 271 12. Arms at sides, palms inward, moved upwards and backwards in parallel planes. 13. Patient rests one hand on chair or table, raises knee to horizontal, flexing at hip and knee. 14. With one hand resting on table, patient swings extended leg forward and back- ward from the hip-joint. 15. Resting with both hands on chair in front, raises foot by flexing knee without movement at hip. 16. Resting one hand on chair at side, patient swings opposite extended leg out- ward from hip-joint, then returns to normal. 17. Arms rotated outwards and inwards from shoulder-joint, operator grasping the metacarpal portion of the hand. 18. Wrist-joint flexed and extended. 19. Ankles dorsoflexed and extended alternately. In advising the patient either to resort to such gymnastic exercises at home or to pay a visit to one of the spas or sanitoria at which they are given the physician should bear in mind that the exercises are to be regarded as a form of training for hearts with reserve power rather than as a panacea for regenerating a diseased heart already working at its utmost. In such cases, notably in persons w r ith severe arteriosclerosis, hypertension, severe myo- carditis, and badly broken compensation, much harm may be done. It is unfortunate that certain spa physicians are liable to become over-enthusiastic in the use of one method and to employ it in all cases regardless of the con- traindications, and deaths under treatment sometimes result. MECHANOGYMNAST1CS. Movements may also be carried out by means of the elaborate and ingenious apparatus devised by Zander for regulating them in direction and intensity. In these exercises the movements are semi-passive, being determined to a great extent and carried on by the apparatus. Hence it becomes more difficult to control them accurately than is the case with the resistance movements. It is unquestionable that excellent results have been obtained by this method, especially in cases where there is mild dilatation but no serious heart lesion; but it is certain that the limits of the patient's strength are too readily overstepped; and equally certain that, in the large institutions where this is carried out, the superintendents usually pay so little attention to the individual patient that these exercises very frequently do distinct harm. Budingen has recently devised an apparatus for passive motion of the legs, which consists of a horizontally moving treadle run by a motor and can be brought to the patient's bed. He claims that it relieves oedema and strengthens the legs. Simple home-made modifications of (his apparatus can readily be made by mounting the treadle of an old sewing-machine (detached from the wheel) vertically upon the foot of the bed. The effort of keeping this moving with the feet is so slight that it can be run by the patient himself for short periods. WALKING AND CLIMBING. The question of walking involves not only an important form of exer- cise treatment but also the regulation of the convalescent's daily life. As has been stated above, walking up and down stairs frequently introduces 272 DISEASES OF THE HEART AND AORTA. the greatest strain upon the patient's heart. It is most important that this strain should be minimized. This may be done by causing him to rest upon each step long enough to count five, ten, or twenty, thus insuring him against hurry and breathlessness (J. O. Hirschfelder) . Another method which has been found useful was suggested by the writer's wife while climbing moun- tains in the Sierra Nevadas. She noticed that she could climb quite steadily up the steepest trails provided she took a deep or normal inspiration each time the same foot touched the ground. In this way a relation was estab- lished between speed and respiration, the former was regulated by the latter, and a certain balance maintained between the rate at which oxygen was used up and that at which it was supplied. As the pulse-rate is often some definite multiple of the respiratory rate, this procedure also tends to regulate the former. This rhythm is one which is very satisfactory for patients with heart disease. It is readily acquired, and, having once become habitual, does much, automatically, to keep the patient within his physiological limits, thus enhancing the beneficial effect of the exercise while establishing a safeguard against overstrain. OertePs Mountain Climbing. Long walks and mountain climb- ing were introduced as an after-treatment in cardiac disease by O e r t e 1 . Oertel found that patients convalescent from heart failure, and especially those suffering from fatty infiltration of the heart, were much benefited by long walks taken slowly, interrupted by frequent rests. Walks along gradually sloping paths in the mountains were most beneficial, and in fact became a feature of the method. This is designed, however, only to put the finishing touches upon the treatment, and to fit the patient whose heart is already in good working order for the more strenuous life to be pursued after his discharge. CHOICE OF EXERCISE. As regards the choice and use of exercise in treatment, the following general principles may be laid down: (1) No exercise should be begun until the patient has been under observation for a few days, so that his general condition is thoroughly understood. (2) If the patient is not improving under absolute rest, exercises would only increase the work imposed upon the heart and would do harm. (3) If the patient has improved under absolute rest, he may be given one or two passive movements (each carried out five or ten times) two or three times a day, and the exercises very carefully increased in number and intensity each day before allowing him to get out of bed. Even a few mild resisted arm exercises may be tried, bearing in mind the same princi- ples, for it must be remembered that the patient may obtain much more complete and immediate rest after these exercises while in bed than when out of it, and also that he is not at the same time subjected to the strain of standing. 1 1 The relative mildness of such exercises in patients still bed-ridden is seen in the fact that their pulse-rate and respiration return at once to normal on cessation of the exer- cise. Physiologically, to exercise in the horizontal posture increases the systolic output more and changes the pulse-rate less than in the erect posture (Erlanger and Plooker). GYMNASTICS AND HYDROTHERAPY. 273 Once out of bed the patient should at first be given a day or two of complete rest to accommodate himself to the new position. Then he may be allowed to begin gradually with a few of the resisted movements, if a competent attendant or physician can supervise them; if this is not avail- able, he may be allowed to practise a few exercises in contracting antago- nistic muscles (Selbsthemmungsbewegungen), at first under the direction of the physician, later under the observation of a skilled attendant, or of some reliable member of the family who has been carefully instructed in the pre- cautions given above. About this stage the bath treatment may be begun. (4) Mechanical gymnastics (with the Zander apparatus or modifica- tions thereof) can be recommended only when supervised by persons of great experience and excellent judgment. Training at End of Treatment. (5) When the patient has recovered somewhat, but not sufficiently to withstand the wear and tear of daily life, he should be encouraged to take short walks, gradually lengthening the space covered, at first about the hospital grounds, later about the city or country, keeping records of the distance traversed each day. He may then be allowed to walk up hill. Pari passu with this the resisted or antagonized movements and the baths should be given. Before dis- charging the patient, he should be compelled to take some regular gym- nastic exercises every day and made to do work at least as strenuous as that which will form the routine of his daily life after passing from under the physician's care. It is no more fair to the convalescent to put him directly back from the sedentary life of the bedroom or the hospital to the deadly struggle for existence outside than it would be to match the average citizen against a prize-fighter. He must be gradually trained for the effort. This principle was very well recognized by da Costa during the Civil War. Before sending his patients back to their regiments where they were subject to heavy field duty, forced marches, etc., he kept them at lighter duties about the hospital, upon local guard duty, etc., and from time to time during this period subjected them to tests of increasing severity (running races, etc.) until he was quite certain of their ability to stand the strain. The magnificent results which he reports from his large series of cases treated under otherwise unfavorable conditions constitute a fitting monu- ment to one of America's greatest clinicians, and merit the careful study of all who would learn how cures should be obtained in heart diseases. Treatment and Occupation. On the other hand, the training to which the patient need be subjected should be suited to the life that he leads. It would be unnecessary to train a clerk in a store up to the point of muscular strength that is necessary for the ordinary laborer. But it is necessary that he should not be exhausted by a few hours' standing lest the cardiac overstrain return. On the other hand, when restitutio ad intcgrum has not been possible, the patient's life must not be the same as it was before his illness. His work must be cut down. This may often be clone in the more well-to-do without changing the business by employing assistants to attend to all except the more essential affairs. Poorer persons must change their occupations. It is as much the duty of the physician to see that this is cl o n e after the recovery as it was his duty during the height of the illness to give correct treat- 18 274 DISEASES OF THE HEART AND AORTA. m e n t . Otherwise he has merely prepared the patient for another break- down. The difficulty in finding suitable occupation and the acumen neces- sary in meeting changed conditions increase rather than decrease the responsibility of the physician in this regard. He must see to it that, as stated by Professor Osier, "the patient must always live within his income of cardiac energy." His mode of life, and especially the speed of his move- ments and the intensity of his efforts, should be so regulated that he no longer feels at any time palpitation, shortness of breath, or precordial pain. HYDROTHERAPY IN THE TREATMENT OF HEART DISEASES. Although the healing power of mineral springs and baths was thought by the older physicians to be well-nigh universal, the scientific application of hydrotherapy to heart disease is due largely to the studies of a small group of men at Bad Nauheim, Germany. Benecke, in 1870, noted the favorable action of baths at this watering-place, but it is to August Schott that is due the real credit for introducing into cardiac therapy what is really a very valuable method of treatment. PHYSIOLOGICAL ACTION OF BATHS. Physiologically it has been found, especially by Erlanger and Hooker, and a little later by Jacob and Strasburger, that all baths given at about the temperature at which the body neither gives off nor loses heat (92 F., 33 C.) increase the pulse-pressure and slow the pulse-rate. Strasburger found this to be particularly true as regards baths of the same composition as those at Nauheim, or indeed any other baths in which CO, is effervescing; and ascribes this action to the dilatation of the vessels in the skin over the whole body, as well as to the cardiac reflexes from stimulation of the sensory nerves by the prickling sensation of the C0 2 . These effects in themselves would be sufficient upon a priori grounds to indicate a probable value of such baths in weakened hearts. Schott's treatment has, however, long antedated these explanations. Schott, Thorne, Schminke, and a host of other observers have demonstrated that the area of cardiac dulness and the X-ray shadow of the heart diminished after such a bath (cardiac tonicity increased). An excellent treatise of his results and those obtained by other ob- servers is given in extenso in English in the monograph of W. Bezly Thorne, to which the reader is referred for details of the method. Other excellent accounts are given by Satterthwaite, P. K. Brown, et al. PRECAUTIONS. The baths should not be given to patients who are in the extreme stages of cardiac break-down, nor indeed to any very weak patients, until they have been prepared for the slight strain which accompanies them by some course of mild exercises, preferably resistance exercises (see page 268). They should never be taken less than one or two hours after a light meal or four to five hours after a heavy one, and, on the other hand, should not be given upon an absolutely empty stomach. GYMNASTICS AND HYDROTHERAPY. 275 NATURAL AND ARTIFICIAL NAUHEIM BATHS. The Nauheim baths are obtained from several mineral springs of different com- position. A course of baths is begun in the Great Sprudel (composition H 2 O 1000, NaCl 2.18, KC1 0.5, CaCU 1.7, MgCl 2 0.4, calcium bicarbonate 2.3, CO, 3.17; temperature 31.6 C., 88.8 F.), most of the CO, being allowed to escape before immersion of the patient. The effect of the Nauheim baths can be imitated at home or in the hospital by add- ing the same salts to the water in the bath-tub. A great variety of such artifi- cial Nauheim salts are on the market, put up in packages ready for use. The most satisfactory known to the writer 1 contains: Grammes. Pounds. Per cent. Sodium chloride 3500 8 2.2 Calcium chloride (magnesium chloride) 900 2 0.53 Sodium bicarbonate 800 If 0.1 Sodium bisulphate yielding CO 2 1000 2\ 0. 29 In order to prevent the bisulphate from injuring the tub it is advisable to cover the walls and floor of the latter with a large sheet of rubber cloth about 6 x 8 ft. in size. The bath is filled with warm water, 90-95 F. (a good-sized bath requires 40 to 45 gal. 150 to 175 litres) and the salts added first the sodium chloride, then the calcium chloride, then the sodium bicarbonate, and lastly the acid sulphate (NaHCO 3 + NaHSO 1 = Na 2 SO 1 + CO 2 + H 2 O). The effervescence continues throughout the bath. CAUTIONS IN GIVING BATHS. In preparing the first bath it is better to begin with half strength of the salts or even less. The patient is allowed to remain in this bath not longer than fifteen minutes, being watched care- fully during this time and removed at once if there is the slightest increase in cyanosis or real discomfort of any kind flushing, excitement, or syncope. "The immediate effect of the first few baths is to produce a sense of oppression at the precordium, under the influence of which the patient breathes slowly and deeply for two or three minutes. Respiration then becomes easy and continues slower by from two to four breaths a minute," after which the symptoms subside. In general the effect should be similar to that in the following case quoted from Thorne: "A patient, aged 46, whose health had been declining for years, was found to have a pulse of 80 in the recumbent, and of 88 in the sitting, position. While he stood it varied from 100 to 104, and if he walked ten paces it rose from 120 to 130. The apex was found to beat an inch outside the nipple line. Within two minutes of immersion in his first thermal bath the pulse had fallen to 70, and judged by the finger appeared to have doubled its volume; 2 at the end of four minutes it was 68, in six minutes 66, in eight minutes 68, and while standing after the bath it was 90. Before he left the bath after an immersion of ten minutes, the apex beat was found to have receded half an inch in the direction of the mesial line, and nails and fingers, which had been snow-white up to the junction of the second with the first phalanx, had assumed a healthy flesh tint." This healthy reaction of the skin should be present within a few minutes after the bath. * Its absence indicates that the treatment has been too 1 Put up by R. R. Rogers Chemical Co., San Francisco. This preparation is partic- ularly useful, owing to the excellent grade of sodium bisulphate prepared and the perma- nent and convenient form in which it is put up. Moreover, the sodium bisulphate is put up in lumps the size of a hazel-nut, which allows the CO 2 to be generated uniformly through- out the bath. 2 Probably the pulse-pressure had actually doubled. 276 DISEASES OF THE HEART AND AORTA. violent, too prolonged, or in other ways unsatisfactory, and unless this can be obviated after the next bath or two the treatment should be dis- continued. After the bath the patient should be made to lie down and rest, if pos- sible to sleep, for at least an hour before leaving the building or doing any- thing else, and upon this rest as much as anything else depends the success of the treatment. MUD AND PEAT BATHS. A number of observers favor the use of mud (Schlammbader) and peat baths (Soolbader), especially those containing carbon dioxide, in cases of heart disease. Their effects are, in the main, similar to those of the Nauheim baths, but, owing to the after-cleaning, the procedure is somewhat more severe and the latter is to be preferred. Boehr is particularly careful to warn against their use in patients with anginal symptoms. ELECTRIC BATHS. Electric baths, in which the patient is immersed in water through which an electrical current is passing, are also used extensively in the treatment of cardiac disease. Either alternating or sinusoidal currents are employed, using large copper or zinc electrodes. The current should be strong enough to produce well- marked prickly sensations upon the skin, but not to cause suffering to the patient. Sinusoidal currents are, as a rule, more soothing than simple alter- nating currents and therefore have a somewhat wider application. In the main, the effects of electric baths are similar to the carbon diox- ide baths, the chief effects being the vigorous counterirritation of the skin, dilatation of the superficial blood-vessels, and reflex stimulation of the heart through the prickly cutaneous sensation. It cannot, however, be stated with certainty that their actions are the same in every particular, especially since Sir William Ewart and others have suggested that the action of the Nauheim baths is due largely to the excess of carbon dioxide escaping into the air and inhaled by the patient, a factor which is of course lacking in the electric baths. On the other hand, the electric currents produce a certain amount of stimulation of the muscles with a corresponding dilatation of their blood- vessels and thus, as Budingen and Geissler have claimed, exert an effect similar to mild gymnastics. Accurate comparisons of the effects of electrical and carbon dioxide baths in large series of cases are, unfortunately, lacking, and the effects depend so largely upon the watchfulness and discretion of the individual administrator that it is difficult to draw conclusions. As Budingen and Geissler have stated, the indications, contraindications, and precautions are about the same as for the Nauheim baths. Rumpf reports beneficial results in cases of cardiac overstrain, arteriosclerosis, and especially in the hearts of acute alcoholism; but, though this author has met with no ill effects in cases of coronary sclerosis, most observers will agree with Budingen that this treatment is contraindicated in such cases. GYMNASTICS AND HYDROTHERAPY. 277 CONSIDERATIONS REGARDING THE ADVISABILITY OF BATH AND SPA TREATMENTS. In spite of the undoubted excellent results which are obtained by hydro- therapeutic measures, it must always be borne in mind that the class of cases in which these effects can be expected is a limited one. From the earliest days of medicine to the present there has prevailed a tendency to look upon the mineral spring with a certain superstitious awe as some miracle of nature, some gift of the gods possessed of mysterious powers, rather than as a definite therapeutic measure exerting definite physiological effects. Accordingly, as has been stated above, there has resulted an indiscriminate flocking to the various spas, and particularly to Nauheim, of all classes of patients in all stages of disease; and many patients who could barely survive the effort of travel have hurried off to the spa as a last resort, hoping, with the fervor of a pilgrim to Lourdes, to obtain a cure which under such conditions would be indeed miraculous. To expect all but the most conscientious of the spa physicians to refuse or delay bath treatment to a patient who has made such a pilgrimage to obtain it would be expecting a great deal of human nature. These are, of course, the cases which result badly and reflect discredit upon the places which they frequent and upon spa treatments in general. The taking of all forms of bath, whether hot or cold, carbonated or non- carbonated, whether clear or muddy or charged with electricity, constitutes more or less of an effort to the patient. They are, therefore, of benefit chiefly to those patients who are capable of obtaining benefit from graded efforts, and are often harmful to those to whom such efforts are injurious. The patient with severe angina pectoris, coronary sclerosis, badly broken com- pensation, anasarca or severe dyspnoea when at rest is not the one for whom the bath treatment is desirable, unless perhaps under exceptional circum- stances. For these cases the bath treatment is not a mode of treatment, but an after-treatment; and whether one agree entirely with Mackenzie, that their effects are no different from those of a vacation spent elsewhere, or whether one accepts the results of the careful studies upon blood-pressure mentioned in the foregoing chapter, it is perhaps a safe rule not to recom- mend patients to a treatment at a spa until they are almost in a fit condition to take a vacation elsewhere. It is in the cases between the grade of actual cardiac failure and complete return to vigor, those suffering from lassitude, undue fatigue and slight dila- tation on exertion, that the good effects of bath and spa treatment are most pronounced. Exactly how much of this is due to the rest and change of scene, how much to the physiological effects upon the circulation, and how much to the stimulating effects of suggestion from the surroundings and the optimis- tic enthusiasm of fellow patients is extremely difficult to gauge; and on the other hand it must be borne in mind that recent observations have shown the presence of radio-active substances in the waters of just those springs to which popular tradition and clinical experience had ascribed the greatest medicinal powers. Radium and the radio-active substances are unquestion- ably possessed of tremendous physiological activity, giving rise to tissue changes which are often late and remote, effects difficult to study with accu- racy even in experiment. 278 DISEASES OF THE HEART AND AORTA. In cases of persistent high blood-pressure of arteriosclerotic or nephritic origin, the effect of baths in dilating the vessels of the cutaneous circulation is often of benefit; but here, again, the stage of the disease and the degree of cardiac compensation is of more importance than the exact nature of the condition. What is beneficial to the man who suffers from occasional head- aches, insomnia or nervousness but who remains free from oedema may prove distinctly harmful to the same individual when, a few years later, he has passed into the stages of dyspnoea and anasarca, in which every minimal effort must be undertaken with caution. Even in the early stages of high blood-pressure, however, too great caution cannot be urged in the prescribing of heavily carbonated baths or baths at high temperatures, and these should when ordered be carried out for some time under the personal supervision of a physician, lest some momentary weakening effect carry the heart past the limits of its tonicity and a dangerous or even fatal dilation set in. As regards the use of home modifications of the various baths versus a sojourn at a spa, each case must be considered on its own merits. After carefully weighing the question of whether in the individaul case hydrother- apy is advisable at all, the physician should balance the expense and efforts of the trip against the beneficial effects of the stimulating surroundings at a spa, which he cannot fail to realize are lacking in home treatment. In this regard the home conditions and the mental attitude of the patient himself toward his surroundings play quite as important a r61e as the mere physio- logical effects. BIBLIOGRAPHY. GYMNASTICS AND HYDROTHERAPT. Herz, M.: Lehrbuch der Heilgymnastik, Berl. and Vienna, 1903. Schott, Aug.: Zur Therapie der chronischen Herzkrankheiten, Berl. klin. Wchnschr., 1885. Thorne, W. B.: The Schott Methods in the Treatment of Chronic Diseases of the Heart. Biidingen : Ruhekuren fur Herzkranken im Verbindung mit passiven Bewegungen, Deutsches Arch. f. klin. Med., Leipz., 1911, cii, 54. Nebel: Bewegungskuren mittelst schwedischer Heilgymnastik und Massage mit besonderer Beriicksichtigung der mechanischen Behandlung des Dr. G. Zander, Wiesbaden, 1889, Oertel: Ueber Terrainkurorte, Leipz., 1S86. Ueber die chronischen Herzmuskelerkrank- ungen und ihre Behandlung, Verhandl. d. Kong. f. inn. Med., Wiesb., 1888, v, 13. Allgemeine Therapie der Kreislaufstorungen, 1891, 4th ed. Beneke, F. W.: Ueber Nauheim's Soolthermen, Marburg, 1859; Weitere Mittheilungen ueber die Wirkung der Soolthermen Nauheims, Marburg, 1861; Xauheim's Soolther- men gegon Gelenkrheumatismus mit oder ohne Herzaffection., Berl. klin. Wchnschr., 1870, 269. Schott, A.: Die Wirkung der Biider auf das Herz, ibid., 1880, xvii, 357, 372. Erlangor and Hooker, I.e., page 54. Strasburger, J.: Ueber Blutdruck, Gefiisstonus und Herzarbeit bei Wasserbadern ver- schieder Temperatur und bei Solbadern, Deutsches Arch. f. klin. Med., Leipz., Ixxxii, 459. Satterthwaite: Xauheim Methods in Chronic Heart Disease with American Adaptations, Internat. Clin., Phila., 1903, 13 ser., i, 52. Biidingen, Th., and Geissler, G.: Die Eimvirkung der Wechselstrombiider auf das Herz, Miinchen. med. Wchnschr., 1904, li, 7S9. Rumpf : Ueber die Eimvirkung oscillirender Strome bei Herzkrankheiten. Biidingen, Th.: Grundziige der Anstaltsbehandlung nervoser und organisch bcdingter Herzstorungen, Therap. Monatsh., Berl., 1907, xxi, 467. VII. HYPERTROPHY AND ATROPHY. HYPERTROPHY. To enable the heart to recover from an overstrain and the consequent dilatation, to maintain the circulation in the presence of a valvular lesion or dilatation, or to reestablish compensation once broken, it must put forth an increase in force. The stimulus for this seems to lie in the increase in residual blood in the ventricle, which acts as an increase in load upon the heart muscle, and thus tends to increase both irritability and force of con- traction, as shown by 0. Frank (see pag3 191), and particularly to bring HYPERTROPHIED 75O G. 24/iaz FIG. 130. Hypertrophic, normal, and atrophic hearts. (From specimens in the Army Medical Museum, Washington, D. C.J about an increase in tonicity. It seems probable that this increase in tonicity is of primary importance as a predisposing factor to hypertrophy, and Barcroft and Dixon have shown that increased tonicity is accompanied by an increased C0 2 metabolism in the heart. PATHOLOGICAL ANATOMY. Changes in the Fibres. The main visible change which the heart muscle undergoes is a swelling of the individual fibres (Tangl, Goldenberg, Dehio, R. M. Pearce) with little if any multiplication of the muscle-cells. Goldenberg finds that the muscle-cells in the wall of the hypertrophic heart have a diameter of 17. (55 ,", in the normal heart 12.85 ,", and in the atrophic heart 10.84 ,. The striation of the fibres also becomes less distinct, and vacuoles appear in the sarcoplasm, changes which are similar to what is observed in 279 280 DISEASES OF THE HEART AND AORTA. a striated muscle as the result of prolonged contraction. Ranke has shown that in skeletal muscle these changes are due to imbibition or endosmosis of water, which, according to the beautiful experiments of J. Loeb and his pupil, Miss Cooke, is brought about in the following way: During the muscular contraction the more complex molecules break down into several simpler ones, thereby increasing the number of molecules in solution in the muscle plasma, the osmotic pressure rises, and hence brings about an endosmosis of water into the fibres. 1 Having once entered, the water molecules remain and the muscle swells. There can be little doubt that the same process is going on in cardiac muscle, and H. A. Stewart (Proc. Soc. Exper. Biol. and Med., 1911, viii, 13) has found that the water content of heart muscle of animals with experimental aortic insufficiency is greater than normal. In cardiac hypertrophy three anatomical changes may be said to take place simultaneously: (1) an increase in size of the individual muscle- cells, but apparently no increase in their number; (2) a certain amount of FIG. 137. Photomicrographs of atrophic and hypertrophic heart muscle. A. Atrophic heart muscle, showing small cells. The specimen also shows some oedema and slight mononuclear infiltration between the muscle cells. B. Hypertrophic heart muscle showing large cells with swollen nuclei. degeneration is almost always present in some of the muscle-cells; (3) a proliferation of the strands of connective tissue between the bundles of muscle-fibres (interfascicular myofibrosis, see page 313). Dehio and Pearce have shown that each fibre may pass through the following stages: normal -* hypertrophy degeneration, the latter stage being associated with proliferation of interstitial connective tissue (myo- fibrosis). Accordingly, we may find the heart-cells in the following con- ditions: (1) Xormal + hypertrophied (heart somewhat enlarged; as in athletes, also in Kiilbs's dogs). (2) Hypertrophied + degenerated; some proliferation of connective tissue (heart much enlarged cor bovinum; still strong). (3) Degenerated. Marked proliferation of connective tissue. Marked weakness of the heart. Large failing heart. Hypertrophy 4- dilatation (digitalis often harmful). 1 Fleischer and Leo Loeb have advanced the same explanation. HYPERTROPHY AND ATROPHY. 281 Types of Hypertrophy. Hypertrophy was supposed by Cohnheim to assume three types: (1) General concentric hypertrophy, involving all the chambers of the heart about equally. (2) Local concentric hypertrophy, involving the walls of one or more chambers of the heart which is subjected to extra work. The fibres are not especially elongated. (3) Local (excentric) hypertrophy with elongation of the muscle-fibres, as in aortic insufficiency. The elongation of the fibres is somewhat out of proportion to the increase in size of the heart. The existence of these three types of hypertrophy as separate entities was already disputed by Cruveilhier in 1833. It is probable that the size of the cavities as found at autopsy bears no constant relation to that pres- ent during life. Moreover, the ventricular cavities in cases of chronic nephritis are often quite as large as those in hearts of aortic insufficiency, though the former typifies the so-called concentric, the latter the excentric hypertrophy. Occurrence and Sites of Hypertrophy. The relative frequency with which these factors occur in cases of hypertrophy is shown in the following statistics compiled by W. T. Howard from autopsies made in the Patho- logical Department of the Johns Hopkins Medical School upon 108 subjects showing hypertrophy of the heart. Cases. Per cent. Arteriosclerosis 65 59 Nephritis 14 13.4 Valvular lesions of the heart 13 12.4 Adherent pericardium 8 7.6 Hard work 4 3.8 Tumors 2 1.9 Aneurism of the heart wall 1 . 95 Haemic plethora 1 . 95 Total 108 100 The right ventricle showed hypertrophy in 70 cases (66 per cent.), of which there were Arteriosclerosis (often of pulmonary artery), 52; adhesive pericarditis, 6; valvular lesions, 8; chronic nephritis, 3; hydrsemic plethora, 1. Hypertrophy of the auricles (atria) was most marked in mitral stenosis and adhesive pericarditis. Strain, Exercise, and Hypertrophy. In normal individuals the weight of the heart is almost proportional to the weight, not of the entire body, but of the musculature (W. Miiller, Hirsch), being relatively low in fatty and relatively high in muscular individuals. The absolute weight of the heart is about yi-g- (.0059) of the body weight in men, yj-j (.00546) in women. The same general principle applies in animals, the most active animals having the largest hearts, especially race-horses, hares, etc., as compared to less active members of the same species. When, however, the heart is subjected to abnormal strain, especially as the result of valvular lesion, it hypertrophies and increases in size to dimensions which arc often enormous. It is not very uncommon to find 282 DISEASES OF THE HEART AND AORTA. hearts of twice or even three times the normal size (500 to 800 Gm.. 17 tcr 26 oz.). and in the Army Medical Museum in Washington there is a speci- men of one weighing 1000 Gm. (33 oz.). Another heart of 1400 Gm. (-MH oz.) has been reported. Such a heart is usually designated as a beefy heart or cor borinum, indicating the animal to which its size would be proportioned. Work Hypertrophy. Whether a true hypertrophy occurs in a per- fectly healthy heart has been much disputed, many writers taking the stand with Romberg that, ''though the possibility of a 'work hypertrophy' cannot be denied, more proofs of its existence are necessary/' FIG. 13s. Hear. A of r-ormal dog aud r B of dog wLii-b ha? run for tire* months on a tread-milL Recently. Low-ever, absolute proof of a work hypertrophy without myocardiaJ degen- eration La? been brought by the beautiful experiments of Kiilbs. This observer took two dogs of the s.ame litter and of equal size. kept them in neighboring cages upon the same die:, but compelled one of them to run upon a tread-mill daily for three to six months. w?;i:e * v .e o'her was kepi ouiet and us-ed as a control. At the end of this time both does were killed in tne s.ame m.anner. W.rt ~^r. COL-.-V]. Work 'i-jg C^--.."^. Total weight . lo.2>0 15. j 1^.2^>j 20.400 Heir 172 113 K^lbs s results n.ave veen cor.f.rme-u by Grober and by Joseph. T:.e ;:.creas-e ::. -.ze of th>e hear. v.'as not accompanied by any change in the skeletal .uiature. nor were a. r .'-' r-ratnoJOsrical cnanges present in the heart or arteries. The ie nere simply underwent an increase in size, tne purest form of hypertrophy. Kulbs s '._- re simpiy in train.ng to run on a tread-mill. Tne proc--es.- was exactly the same as 'training of an athlet.e. and.clinicaJly.it is often found that a::.le:es have mildly r.ropnie-'J! r.'-a 1 "-. ><:'.. - "':-.* nas f j*-monstrat- : "ions r*-', ,l:e nar-'j v.-o. r *i and decreased jn He h.as a -o -:.o^ :. Armv :ncr'-ase hoi or toUoco. ^ r.Ut U-or^- s^'-r-ici-rr. of r:.f-n ;:/;* K:-hl v. ork h .- :.< r* :^ ;. h y : m ^.s- f.-e :-:-ase in weight of the h'-^r; HYPERTROPHY AND ATROPHY. 283 amounted to only 52 per cent, as compared with changes of 100 to 300 per cent, often observed in man. It is doubtful whether a corresponding degree of hypertrophy would be noticeable clinically. ETIOLOGICAL FACTORS. Hypertrophy in Chronic Nephritis. The most remarkable and most important of all these forms of hypertrophy is that taking place in chronic nephritis. This was first noticed by Richard Bright in his classical descrip- tion of dropsy in nephritis. In 18.53, Wilkes thought that the lesions of the kidneys and arteries were part of the same morbid condition; while Gull and Sutton assumed that the general arteriocapillary fibrosis brought about an increased resistance through narrowing of the arterial bed, and, as a result of this, high blood-pressure and hypertrophy of the heart. Senator ascribed the hypertrophy to a "dyscrasic" property of the blood in nephritis, stimulating the heart to contractions of abnormal force. Passler and Heineke have recently subjected the matter to critical experiment. They found that if they cut out pieces of kidney from a dog bit by bit until renal substance equal to H kidneys had been removed, the heart then began to hypertrophy and the blood-pressure to rise. If considerably more tissue was removed, the animal became cachectic, the blood-pressure remained low, and the heart did not hypertrophy. They ascribed these cardiac changes, as George Johnson had done, to the presence in the blood of some substance having a digitalis-like action, being either retained in the circulation in abnormally large quantities as the result of disturbed excre- tion, or being a true internal secretion from the diseased kidney. 1 Numerous other theories of cardiac hypertrophy in renal disease have been advanced. Chief among these is the theory of J. Cohnheim and Traube that the sclerosis of renal vessels narrowed the arterial bed in the kidney, thereby introducing an increased resistance into the general circulation, and that these changes in the renal vessels were enough to raise the general blood-pressure. It would appear in the light of more modern research that this cutting off of the blood stream is in itself insufficient. Jores (Deutsches Arch. f. klin. Med.) claims to find hypertrophy only in patients with red granular kidneys (glorn- erular sclerosis) and not in those with small white kidneys (tubular nephritis) (see page 45). There is a true hypertrophy and not a mere growth of connective tissue as suggested by Buhl, Huchard, and Albrecht. Hypertrophy from Overdrinking. Closely allied to this condition is the tremendous heart hypertrophy which is universally found to result from drinking large quantities of beer, and, since it does not accompany excess in any other form of alcohol to the same extent, it is thought to be due to the large quantity of fluid ingested. That increase in the fluid in the blood at once results, not so much in a rise in arterial blood-pressure as in rise in venous blood-pressure, dilatation of the heart, and increases in the systolic output, even to the point of doubling or trebling it, can easily be shown with Henderson's cardiometer, and this no doubt illustrates the mechanism by which the change is brought about. Hypertrophy and Arteriosclerosis. The relation of hypertrophy of the heart to arteriosclerosis independent of any renal changes is also of funda- mental importance. The coincidence of the two conditions in the same individual has long been noted, and both have been Brought about experi- mentally by administration of certain poisons, notably adrenalin (Josue, Erb, Pearce, et al.). 1 Tigerstedt and Bergmann (Skand. Arch. f. Physiol., Loipz., 1S9S, viii. 224) found that injection of renal extract actually raised the h It >od- pressure, owing to the presence of a substance which thev named "renin." 284 DISEASES OF THE HEART AND AORTA. Cardiac and Adrenal Hypertrophy. A new light has been thrown upon the subject by the studies of Vaquez and Aubertin (1905), Aubertin and Clinet, Wiesel, and Gaillard. Aubertin was able to produce cardiac hypertrophy in rabbits by various means, and found in every case a simultaneous hyperplasia of the medullary substance in the adrenals. A similar finding had been made by Vaquez and Aubertin in cases of chronic nephritis associated with hypertrophy of the left ventricle, which was confirmed by Wiesel in 1907. In December, 1907, Aubertin and Clunet made a study of 120 unselected autopsy cases. Of these 18 showed very definite hypertrophy of the medulla of the adrenals, and 16 of these 18 showed marked hypertrophy of the heart. On the other hand, but 10 of these hypertrophied hearts were associated with renal disease: the others occurred in conjunction with valvular lesions, congenital defect in the septum ventriculorum, aortic sclerosis, etc. Aubertin, however, states very definitely that besides these groups they encountered cases of cardiac hypertrophy without the existence of adrenal hyperplasia, so that this association is not invariable; and they conclude that it is at present impossible to decide whether the cardiac hypertrophy occurs as a result of oversecretion of adrenalin, or whether the hyperplasia of the adrenals occurs as a result of slight venous stasis in those organs while the hypertrophy is going on. Arteriosclerosis was the rule but not invariably in these cases with adrenal hypertrophy. It must be noted that the action of adrenalin is just that which might be expected to bring about hypertrophy of the heart, for it causes, (1) a general vasoconstriction; (2) a marked increase in the tonicity of the heart; (3) an increase in the force of the beat and in the systolic output. However, the results of Cohn, under Aschoff's direction, are less favor- able to this theory. In 12 cases of hypertrophy of the left ventricle with chronic nephritis, he found hypertrophy of the adrenal cortex in only 3 (25 per cent.), while in 23 cases of chronic nephritis without hypertrophy of the heart he found hypertrophy of the adrenal cortex in 8 (34 per cent.). These findings tend to throw considerable doubt upon the theory of Vaquez and "Wiesel. Hypertrophy and Abdominal Arteriosclerosis. Hasenfeld has found that no hypertrophy sets in unless arteriosclerosis is present in the aorta above the level of the superior mesenteric artery. Practically all the substances which are known to bring on arteriosclerosis are vasoconstrictors, and beginning arteriosclero- sis in man seems usually to be accompanied by vasoconstriction. It is readily conceivable that any sclerotic obstruction below the mesenteric would be easily compensated for by dilatation of the abdominal vessels, and. consequently, would bring about no increased resistance to blood flow, while at the higher level the presence of sclerosis is more or less equivalent to clamping the abdominal aorta. 1 DIAGNOSIS. It would appear at first sight to be extremely easy to determine clini- cally whether in a given ca.se hypertrophy is present or not, and the older clinicians laid down very definite rules for its detection, most of which were fallacious. In general, we may agree with (iibson that the most important signs of hypertrophy of the left ventricle are increase in cardiac dulness to the loft, with a more or less steady, forceful, and "heaving" impulse, and a 1 An excellent discussion of the theoretical and experimental side of the question is given by K. M. Pearce. HYPERTROPHY AND ATROPHY. 285 booming first sound of low pitch, and an accentuated second sound at apex and aortic area. These signs are dependent largely upon the contact of the heart with the chest wall; and if, as is often the case in an emphysematous individual, the lung intervenes between the left border of the heart and the chest wall, all the signs may be diminished beyond recognition. The diag- nosis may, however, often be made from the history in spite of the clinical findings. Thus, if an aortic or mitral insufficiency has persisted for some time and the heart is in a condition of moderate vigor with a normal pulse-rate, it may be assumed that hypertrophy of the heart has had to take place in order to maintain the circula- tion, in spite of distant heart sounds and absence of the apex beat. Prolonged high blood- pressure is usually associated with some degree of hypertrophy of the left heart, but not invari- ably. In differentiating from dilatation it may be stated that, except under unusual conditions brought on by stimulation of the vagus, the factors bringing on dilatation quicken the pulse- rate, and an enlarged but slowly beating heart is almost always hypertrophied. The electrocar- diograms are, however, character- istic. In hypertrophy of the right ventricle the R wave is normal or inverted in the first derivation (Dl) and large in D2 and D3 (page 286). In hypertrophy of the left it is inverted in D2 and D3 (plate IX, Fig. F). Hypertrophy of the Left Ven= tricle. Palpation of the apex impulse, which many writers, even as late as Romberg, con- sider a most important sign of hypertrophy of the loft ventricle, need not be decisive, since, as Katzenstein has shown, the weakest hearts may often beat the most violently, especially when beating rapidly; the strongest, on the other hand, may be separated from the chest wall by a layer of lung. Dulncss is, however, increased to the left. Hypertrophy of the Right Ventricle. The hypertrophy of the right ventricle is not so easy to diagnose. Its presence may be inferred when the area of cardiac dulness is enlarged and a svstolic retraction is Fro. 139. Areas of pulsation and retraction hyper- trophy of the right and left ventricles. ^, retraction; '"', pulsation. The light line indicates the area of the cardiac dulness. A. Hypertrophy of the left ventricle. B. Hypertrophy of the right ventricle. 286 DISEASES OF THE HEART AND AORTA. PLATE IX. A B Elootrorardiofrrams showinp hypertrophy of the ventrioleg. A, B, C, Tracings from a case of hyper- trophy of the riirljt ventricle by the first, second and third le:ids (Dl, D'2, D3) respectively, showing inver- sion of the- K wave in the first lead, and an abnormally high R wave in the second and third. HYPERTROPHY AND ATROPHY. PLATE IX. D 287 B F Tracings from a patient with hypertrophy of the left ventricle by th e first, second and third leads (Dl, D2, D3) respectively, showing inversion of the 11 wave and T wave in the third lead (F). 288 DISEASES OF THE HEART AND AORTA. noted at the point of maximal impulse and over the interspaces between it and the sternum as well as in the epigastrium. The heart need not be enlarged toward the right, since the right ventricle rarely passes the sternal margin. Indeed it rather tends to lift the apex and shift it to the left. The area of cardiac flatness is increased to the right, reaching to the sternal margin. An increased area of dulness to the right of the ster- num is due to the right auricle. The second pulmonic sound is intensified and ringing, but this may also be the case in any condition in which there is sonic obstruction to the pulmonary circulation or some insufficiency of the left heart. Hypertrophy of the auricles cannot be diagnosed from objective signs except in mitral stenosis, in which an hypcrtrophied auricle gives rise to a loud presystolic murmur. This is not present when the auri- cle is weak. Hypertrophy of the right auricle is sometimes shown by a high presystolic wave upon the jugular venous pulse-curve and very rarely by a presystolic wave upon the liver pulse (Mackenzie); but, as a rule, it shows no signs. Prognosis. A certain amount of hypertrophy is necessary whenever a valvular lesion or any other abnormal factor tending to increase the work of maintaining the circulation is present. Hence failure of the heart to hypertrophy under these conditions would be regarded as an unfavor- able condition, and would probably soon be associated with cachexia. On the other hand, an extreme degree of hypertrophy is evidence that the heart is doing its maximal work, that the fibres ere long will begin to degenerate, and the heart must be spared as much as possible. Hypertrophy in itself does not demand treatment, but diminution of the causal factor as far as is possible is advisable. If this be nephritis or arteriosclerosis, a quiet life and diet poor in salt and purin bodies should be resorted to, with occasional courses of potassium iodide. If a valvular lesion be present and the hypertrophy is slight, little attention need be paid to it until the patient reaches the latter half of the fourth decade, when he should begin to spare his heart and arteries as much as possible, should abstain from alcohol, coffee, and tobacco, and should in every way avoid those influences leading to the production of high blood-pressure and arteriosclerosis. Reserve Force of the Hypertrophied Heart. One of the most impor- tant questions that arise in connection with hypertrophied hearts is whether or not a hypertrophied heart possesses as much reserve force as a normal one. This question is variously answered in the text-books, most of them agreeing with Krehl et al. that the reserve force is lessened; while the experimental work, especially that of Romberg and Hasenfcld, indi- cates that the strength of the hypertrophied heart muscle itself is actually increased. However, a great deal depends upon the stage of hypertrophy in which the individual heart happens to be. Thus a heart in the first stage, with fibres normal and hypertrophied, would show an increased strength (as in athletes' hearts, or in hearts of early hypertrophy after valvular lesion as compared to the same hearts at the very onset of the lesion): while a heart in the second stage, with fibres partly hypertrophic, {tartly atrophic, would in most cases show a marked diminution in HYPERTROPHY AND ATROPHY. 289 strength and still greater loss in reserve force, and an increased effort would hasten the degeneration. Another and really main factor in the apparent weakness of the hyper- trophied heart is that in practically all hearts the hypertrophy is brought on by some valvular lesion or by some persistent increase in peripheral resistance; so that such hearts are continually wasting much of their energy in overcoming these pathological conditions, besides bestowing the usual amount of it upon the maintenance of the circulation. In bodily exertion or other conditions calling upon the reserve force, not only the actual circulation must be increased, but the abnormal factor inducing wasting of energy, the valvular lesion, etc., z becomes more severe as well, and hence the extra call i 5 upon the diseased heart is double the extra call upon the normal and requires double the reserve force to meet it. Otherwise the reserve force, though actually more, may be apparently less than in the normal heart, as shown diagrammatically in Fig. 140. For practical purposes, however, it may be regarded as indisputable that, in every case where a cardiac lesion is present, the hyper- trophicd heart has less available reserve force than normally, and in some cases (stage 3) less than if it had not hypertrophied at all. UJ j INORMAL I DISLA5E.D HEART ATROPHY. Flo. 140. Diagram showing power of nor- mal and hypertrophied (athlete's) heart at rest and during exercise, also that of a diseased heart. The length of the arrow indicates the reserve force. The unshaded portion indicates the cardiac energy ex- pended, but wasted, owing to the lesion. Atrophy of the heart is more or less the reverse process of hypertrophy. Whenever the body diminishes in weight from cachexia, infectious disease, or starva- tion, the heart muscle diminishes with it, and according to Hirsch in about the same ratio. The epicardial fat, on the other hand, is but little diminished. When the atrophy is the result of starvation it may be of very high degree, but the size and condition of the heart may return to normal when an adequate diet is resumed (Schieffer). As in the case of hypertrophy, there seems to be little change in the number of the muscle-cells, but the latter diminish in size (10.84 t.t instead of 12. S5 /'., Goldenberg), and the removal of substance is marked by the deposition of brown granules of hcematoidin in fusiform arrangement about the nucleus. These granules are formed when part of the muscle-cell pro- teid is broken down during the atrophy, the ruematoidin portion being left. Macroscopic-ally they impart a tobacco-brown color to the heart, so that the condition is often designated as '"'brown atrophy of the heart." To a certain extent a diminution in size of any chamber of the heart may occur if its work is lessened by obstruction to the blood flowing into it; as, for example, the left ventricle in pure uncomplicated mitral stenosis. The atrophy is rarely so marked here as in starvation, phthisis, or cachexia, and is indeed the exception rather than the rule in mitral stenosis, for other factors, tachycardia, irregularity, or mitral insufficiency, usually contrib- ute to keep the left ventricle doing an at least normal amount of work. 19 290 DISEASES OF THE HEART AND AORTA. Like hypertrophy, cachexial atrophy of the fibres may lead on to growth of interstitial connective tissue and fibrous myocarditis, but true brown atrophy is not so common a forerunner of myocarditis as is hypertrophy of the heart. Functionally, the force of the heart is impaired about propor- tionally to its diminution in weight. The blood-pressure is usually low and the muscle easily fatigued. Overstrain readily occurs in such hearts; and sudden death is not uncommon. BIBLIOGRAPHY. HYPERTROPHY. Thorel, Ch.: Pathologie dor Kreislauforgane, Lubarsch-Ostertag's Ergebnisse cler Patho logie, Wiesb., 1903, ix, Abth. I, 559. Heinz, R.: Handbuch der experimentellen Pathologie und Pharmakologie, Jena, 1905, i, iite Hiilfte. Gibson, G. A.: Diseases of the Heart and Aorta, Edinb. and London, 1898. Barcroft, J. L., and Dixon, \V. E.: The Gaseous Metabolism of the Mammalian Heart, J. Physiol., Lond., 1906-7, xxxv, 182. Tangl: Arch. f. path. Anat., etc., Berl., 1S89, cxvi, 432. Goldenberg, B.: Ueber Atrophie und Hypertrophie der Muskelfasern des Herzens, Arch. f. path. Anat., etc., 1886, ciii. 88. Dehio: Ueber myofibrosis Cordis, Deutsches Arch. f. klin. Med., Leipz., Ixii, 1. Pearce, R. M.: Experimental Myocarditis; a Study of the Histological Changes following Intravenous Injections of Adrenalin, J. Exper. Med., X. York and Lancaster, 1906, viii, 400. Pearce, R. M.: The Theory of Chemical Correlation as Applied to the Pathology of the Kidney, Arch. Inter. Med., Chicago, 1908. ii, 77. Ranke, J.: Tetanus, Eine physiologische Studie, Leipz., 1865. Loeb, J.: Ueber die Entstehung der Activitatshypertrophie der Muskeln, Arch. f. d. ges. Physiol., Bonn, 1894, Ivi, 270. Cooke, E.: Experiments upon the Osmotic Properties of the Living Frog's Muscle, J. Physiol., Camb., 1898, xxiii, 137. Fleisher, M. S., and Loeb, L.: Experimental Myocarditis, Arch. Inter. Med., Chicago, 1908, ii, 78. Miiller, W.: Die Massenverhaltnisse des menschlichen Ilerzens, Berl., 1878. Hirsch, ('.: L'eber die Beziehungen zwischen dem Herzmuskel und der Korpermuskulatur und ueber sein Verhalten bei Herzhypertrophie, Deutsches Arch. f. klin. Med.. Leipz., ls<>9, Ixiv. 597. Romberg, E.: Lehrbuch der Krankheiten des Ilerzens und der Blutgefa'sse, Stuttgart, 1906. Krelil, L.: Erkrankungen des Herzmuskels, Xothnagel's IL-.ndbuch des speziellen Pathol. u. Therap., Wicn, 1*98. Lewy, B.: Die Arbeit des gesunden und des kranken Herzens, Zeitsclir. f. klin. Med., "Berl.. x\i, 321 and 521. Kulbs: Experimentelle ueber Herzmuskel und Arbeit, Arch. f. exper. Patliol. u. Pharma- kol., Leipz., 1906. Iv, 2s*. Groeber: Untersuchungen zur Arbeitshypertrophie des Ilerzens. Deutsches Arch. f. klin. Med., Lei])/.., 1907, xci, 502. Joseph. I). R.: The Ratio l)et\vi-en the Heart-weight and Body-weight in Various Animals, J. Exper. Med.. X. York and Lancaster, 190S, x, 521. Schief'fer: I'eber den Einfluss der Berufsarbeit auf die Herzgrosso, Deutsch. Arch. f. klin. Med., Leipz., 190S. xcii, 3N3; also, Ueber den Einfluss des Militardienstes auf die Herzirn.sse. ibid., 1908, xcii, 392. Howard, W. T.: An Analysis of 105 Cases of Heart Hypertrophy (from the Autopsy Records of the Johns Hopkins Hospital), Johns Hopkins Hosp. Rep., Bait., 1894, iii. 266. Wilks, S.: Cases of Bright '.s Disease, with Remarks, Guy's IIosp. Rep., Lond., 1853, ii Ser., viii, '2'.}'2. HYPERTROPHY AND ATROPHY. 291 Senator, H.: Ueber die Herzhypertrophie bei Xierenkranken, Deutsch. med. Wchnschr.. Leipz. u. Wien, 1903. Die Erkrankungen der Niere, Nothnagel's Handb. d. speziellen Pathol. u. Th., Wien. Passler, H. - Ueber Ursache und Beutung der Herzaffektion Nierenkranker, Volkmann's Sammlung klin. Vortriige, Leipz., 1906, Xo. 408. Johnson, G.: Lectures on Bright's Disease with Especial Reference to Pathology, Diag- nosis, and Treatment, Lond., 1873. Cohnheim, J.: Lectures on General Pathology, New Sydenham Society. Traube, L. : Gesammelte Beitrage zur Pathologie und Physiologic, Berl., 1871-1878. Buhl: Mitth. a. d. pathol. Inst. Munchen, 1878, 38. Huchard, H.: Maladies du Cceur, Paris, 1899-1905. Albreeht, E.:.Der Herzmuskel, Berl., 1903. Josue O.: Hypertrophie cardiaque causee per 1'adrenaline, Compt. rend. Soc. de Biol., Par., 1907, Ixiii, 285. Erb, W.: Experimentelle und histologische Studien iiber Arterienerkrankung nach Adre- nalininjoktiorien, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1905, liii, 173. Vaquez: Hypertension arterielle, Bull. soc. med. d. hop. de Paris, Feb. 5, 1904. Vaquez and Aubertin: Sur 1'hyperplasie surrenale des nephrites hypertensives, ibid., 1905, xxii, 705. Wiesel: Renale Herzhypertrophie und chromaffines System, Wien. med. Wchnschr., 1907, Ivii, 673. Schur, H., and Wiesel, J.: Beitrage zur Physiologic und Pathologie des chromaffinen Gewebes, Wien. klin. Wchnschr., 1907, xx, 1202. Also, Ueber eine der Adrenalin- wirkung analoge Wirkung des Blutserums von Nephritikern auf das Froschauge, Wien. klin. Wchnschr., 1901, xx, 699. Gaillard. Quoted from Aubertin. Hasenfeld, A.: Ueber die Entwicklung eincr Herzhypertrophie bei der Pyocyaneusendo- carditis und der dadurch verursachten Allgemeininfection, Deutsch. Arch. f. klin. Med., Lripz., 1899, Ixiv, 763. Hasenfeld und Romberg: Ueber die Reservekraft des hypertrophischen Herzmuskels, u. s. w., Arch. f. exper. Pathol. u. Pharmakol., 1S97, xxxix, 333. Katzenstein, J.: Dilatation und Hypertrophie des Herzens, Muenchen, 1903, Aschoff and Cohn: Bemerkungen zu der Schur- Wieselschen Lehre von der Hypertrophie des Xebernierenmarkes bei chronischen Erkrankungen der X T ieren und des Gefass- apparatus, Verhandl. d. deutsch. path. Gesellsch., Jena, 1908, xii 131 VIII. FATTY DEPOSITS IN AND ABOUT THE HEART. Fat may be deposited in the heart in two ways: (1) In solid masses of adipose tissue, especially in the pericardium in fat individuals, particu- larly in those addicted to alcohol, and very often associated with coronary sclerosis. This condition is designated as fatty infiltration or obese FIG. 141. Distribution of fat in and about the heart. A, normal; B, deposit in an obese heart; C, deposit in a fatty degenerated heart. heart (Mastfettherz, Kisch). (2) In fine droplets occurring diffusely within the heart muscle-cells, especially in anremia, infectious diseases, in persons poisoned by phosphorus, arsenic, and numerous other substances, and in association with other changes in the myocardium. This condition is called fatty degeneration. FATTY INFILTRATION OR OBESITY OF THE HEART. DEPOSITION OF THE FAT. Harvey, the discoverer of the circulation, describes the hearts of certain fat persons as covered with a layer of fat so extensive as almost to obscure the heart muscle from view, and this condition is one of not very infrequent occurrence. In normal hearts there is a considerable amount of fat (30 to 60 Gin.. 1 to 2 ounces) collected just beneath the endothelial layer of the pericardium, along the auriculoventricular and interventricular grooves (coronary and longitudinal sulci), at the base of the aorta, and scattered elsewhere over the heart. As the individual lays on more body fat, more fat is deposited in the pericardium, at first only at the usual sites along the sulci: but later it spreads over and into the myocardium, penetrating into it between the larger strands of muscle, and finally settling beneath the endocardium, especially about the bases of the papillary muscles. The weight of adipose tissue may actually exceed the weight of cardiac muscle (W. Mailer, Hirsch, Kisch), as shown by the following figures determined by W. M tiller (who dissects off the fat and weighs the heart muscle). 292 FATTY DEPOSITS IN AND ABOUT THE HEART. 293 Total weight Heart Fat removable by Per cent. of heart. muscle. dissection. of fat. 253.6 240.7 12.9 5.1 Normal male (thin). 363.5 326.2 37.3 10.3 Cardiac hypertrophy. 327.6 494.3 181.3 228.3 146.3 266 45.6 53.5 ST 1 "} fatty heart. Nature of the Fatty Deposit. Under these circumstances the fat is deposited in exactly the same manner as elsewhere in the body. The pathological character con- sists not in the process but in the amount of the deposit. The adipose tissue in this region does not differ macroscopically or microscopically from the fat elsewhere. Neither does it differ chemically. It is ordinary "translocation fat" (Rosenfeld, Leick and FIG. 142. Photomicrographs' of fat deposits in the heart. A. Heart muscle of an obese indi- vidual, showing fat cells. B. Heart muscle of a patient who died of pneumonia, showing fat droplets within the cells (fatty degeneration). (Photomicrograph by Dr. Chas; S. Bond.) Winckler), derived directly from the food ; for Leick and Winckler have shown that if dogs be overfed with mutton tallow, the fat deposited in the pericardium has an iodine absorption coefficient approaching more nearly to what is in the sheep than to that of the dog. The pericardial fat differs from the fat elsewhere in but one important respect, and one which is especially to be borne in mind in treating the condition, namely, that it is relatively poor in lipase, the enzyme which forms and splits fat, and he nee is relatively stable. According to Loevenhart it would appear that lipase is present in the cells in considerable amounts at the time the fat is deposited, but is then gradually destroyed; so that if subsequently the fat of the body is reduced from inanition or other cause, there is no more enzyme remaining in the pericardium to split up what is stored there and to return it to the general circulation. Accordingly, it is found that in starva- tion the pericardial and peri renal fat remain after all the rest has disappeared from the body (Loevenhart, Schieffer). This matter will be re- ferred to again in connection with treatment. 294 DISEASES OF THE HEART AND AORTA. CARDIAC CONDITION'S ASSOCIATED WITH OBESITY. . There are three definite conditions which, though in no way part of the general process of obesity, are often associated with it; and it is these, rather than the obesity itself, which give rise to the symptom complex referred to as "fatty heart," or, as Romberg more properly designates it, "cardiac insufficiency of fat per- sons " (Die Herzmuskelinsufficienz dcr Fettleibingen). These are (1) atrophy of the heart muscle, and (2) sclerosis of the coronary arte- ries, (3) a high diaphragm. 1. Atrophy and Cardiosclerosis. It is especially worthy of notice that the increase in size and weight of the heart may conceal an actual atrophy of the heart muscle (Hirsch) (see table above) and a correspond- ing weakness of the heart. Accord- ing to most writers, this lies mainly in the left ventricle, but Hirsch has shown that not only does the fatty infiltration penetrate chiefly the wall of the right ventricle, but that the symptoms most common among fat persons are those due to primary failure of the right side of the heart. A general cardio- sclerosis (see page 313) is often asso- ciated with the deposit of fat. It is a self-evident fact that such enormous deposits of fat increase the work done by the heart, first by increas- ing the weight to be moved at each FIG. 143 An excessive deposit of epicardial ^ v ^ T nlo ind secondlvbv inr-ren^irier fat. (From a specimen in the Army Medical Mu- *V ST 1C ' dnu >U )IHU } r) > ] rCESlDg >eum, Washington, D. c.) the total bed of the blood stream. It might be supposed that this would in itself bring about hypertrophy, but hypertrophy is rarely demonstrable. The tendency to obesity usually occurs either in persons whose lives are sedentary and whose skeletal and cardiac muscles are therefore under- developed, or else in those addicted to excesses of alcohol or overeating, factors which in themselves bring on myocardial changes and hypertrophy. J. Coronary Sclerosis. The pathological changes and symptoms due to sclerous of the coronary arteries do not differ from those arising without the presence of abnormal fat deposits and will be discussed in a separate chapter ('page 366). '>. High Diaphragm. V. Frey and Krehl have shown in animals that pushing up the diaphragm, and thus displacing the heart, greatly inter- FATTY DEPOSITS IN AND ABOUT THE HEART. 295 feres with the work of the latter. Myers and Schott found that soldiers whose diaphragms are pushed up by tight belts about the abdomen exhibit symptoms of cardiac overstrain much more readily than do normal indi- viduals. Myers found acute dilatations most common in the British regiments in which cuirasses and tight belts were worn. Wenckebach has called attention to the fact that a large amount of intra-abdominal fat pushes up the diaphragm and thus pushes the heart into a more transverse position (apex often in the fourth interspace), thereby hampering its action. This factor must be reckoned with in the genesis of the cardiac weakness of fat persons. ETIOLOGY. Clinically, the cardiac manifestations in fat persons are very variable. They occur most frequently in association with (1) general obesity, either hereditary or arising primarily from over-eating; (2) in childhood; (3) after castration or menopause; (4) overindulgence in alcohol, especially malt liquors, with or without the presence of gout; (5) diabetes mellitus with obesity (lipogenous diabetes) ; (6) they are most frequent and most intense after the age of fifty. PHYSICAL SIGNS. Upon physical examination the most striking features are the general obesity; the relative weakness of the skeletal muscles; the groups of dilated venules, especially the "Bardolphian" "butterfly" area of dilated venules about nose and cheeks, as well as similar areas along the attachment of the diaphragm and elsewhere. According to Hirsch, dilatation of the superficial veins in the subcutaneous fat is a premonitory sign of cardiac weakening; but this is certainly not the case always. Often there is no visible apex impulse; the relative cardiac dulness is increased to both left and right, owing to the transverse position; the cardiac flatness is dimin- ished. The heart sounds usually have a distant character and may be free from murmurs. Occasionally there may be slight oedema of the feet and a small amount of albumin in the urine. In advanced cases of cardiac insuf- ficiency the patient may become much thinner (owing to diminished absorp- tion of fat from the intestine, see page 215), but the pericardial fat may remain undiminished. TREATMENT. The treatment of cardiac weakness of fat persons depends entirely upon the stage at which the patient is seen. If oedema and persistent dyspnoea or palpitation upon slight exertion are already present, the case must be treated exactly like one of cardiac overstrain or heart failure from any other cause manifesting similar symptoms, except that, owing to the frequent atrophy and infiltration of the heart muscle, drugs of the digitalis group are often of little use and may even be harmful. The patient should be put upon rest, restricted diet, with liquids restricted to 1000 c.c., purged freely, and bled if symptoms of failure of the right heart set in. Amyl nitrite, nitro- glycerin, and erythrol tetranitrate may be used to relieve attacks of dysp- noea, and massage, passive movements, and finally resisted movements, and cold water or Nauheim baths when the patient is able to get out of bed. 296 DISEASES OF THE HEART AND AORTA. When, as is usually the case, the patient is seen before the stage of actual heart failure has set in and is suffering only from what may be con- sidered as the premonitory symptoms of cardiac affection, palpitation and shortness of breath on exertion, weakness, and giddiness, the treat- ment should then be directed toward the obesity rather than toward the heart. A main indication is then gradually to restrict the diet to a heat equivalent of about 1200 to 1700 calories, of which 500 calories (about 120 Gm., 4 oz.) should be proteid (v. Xoorden). (1) Restricted Diet. Numerous restricted diets have been laid down, especially by Banting, Oertel, Hirschfeld, Kisch, and Ebstein. The restric- tion should not take place suddenly, for fear of weakening the patient, but should take place in several stages, reducing 500 calories each week until the lower limit is reached. 1 (2) Liquids should be restricted to less than 1000 c.c. (1 quart) per day; this also should be done gradually. 2 Sample Diet. V. Xoorden gives the following outline diet, which is very satisfactory as a basis capable of modification: Prot. Fat. Carb. ' Cal. S A.M. Breakfast SO Gin. cold lean meat 30.5 1.4 ^ white roll (25 Gm.) 1.8 0.2 14 20* 10A.M. 1 eg* 6.5 6.1 85 12 M. 1 cup lean bouillon O.S 7 1 1 small plate clear soup S 2 4 ' 150 (im (5 oz ) lean meat or fi^h 57 3 2 S 1 P.M. ^ 100 Gm. potatoes. . . 1 9 ISO i Peas beans cauliflower aspara (r u* 3 10 15 1 100 Gm freh fruit 5 S 583 3 P M Black coffee 4 P M. 200 Gm fre>h fruit 6 16 90 6 P M 250 c c (1 r la <;i O kim-milk 6 S 2 12 97 8 P.M. Supper 15 Gm cold lean meat with pickle* . 3(3 3 Red beets, radishes, etc 2 5 30 Gm. graham bread 2 3 12 2-3 teaspoonfuls boiled fruit (no sugar). . . 0.5 S 299 Total 1556 2S.6 112 10S7 1 100 Gm. (3 oz.) raw meat (proteid 20 per cent., fat 1.7 per cent.) = 100 cal. 100 Gm. (3 oz.) cooked lean meat (proteid 37 per cent., fat 2.5 per cent. ) = 175 cal. (about 25 per cent, higher in well-done roasted meats). 100 Gm. (3 oz.) cooked meat of stall-fed animals (no visible fat) (proteid 36 per cent., fat 6 per cent.) = 200 cal. 1 egg (6.5 Gm. proteid 6.2 Gm. fat) = 85 cal. Cheese (proteid 28 per cent., fat 30 per cent., carbohydrate 2 per cent.) =400 cal. Milk (proteid 3.4 percent., fat 3.0 percent., sugar 4.5 per cent.) =60 cal. per 100 c.c. (20 cal. per ounce). Potatoes 100 Gm. (3 oz.)=>>0 cal. Bread (proteid 7-9- per cent., carbohydrate 35 to 80 per cent., the latter in zwieback and dry breads) 100 Gm. = 200-350 cal. Sugar 100 Gm. = 400 cal. Butter 100 Gm. = 930 cal. : Oertel and Schwenineer thought that drinking water is a factor producing fat. Ptraub and others have shown that this is by no means the case. The only influence of the water lies in the fact that when a meal is taken dry the appetite is less than when water is taken, and consequently less is eaten. However, considerable amounts of fluid increase the volume of blood and the work of the heart, and hence the limitation of fluid saves the heart in this wav. FATTY DEPOSITS IN AND ABOUT THE HEART. 297 (3) Increased Exercise. Increase exercise gradually as much as pos- sible, especially by walking, either on the level or on gentle gradual ascents, interrupted by frequent rests before either weariness or shortness of breath sets in. 1 In this way the energy used by the body, and hence also the fat burned up, can be materially increased. Weight of patient Walking on Level. Per mile. Per hour. 150 Ibs. 60 cal. 75 cal. 200 Ibs. 85 cal. 100 cal. 150 Ibs. 170 cal. (18 Gm 230 cal. (30 Gm fat) fat) 200 Ibs. 225 cal. (25 Gm. 310 cal. (40 Gm. fat) fat) Rate 2.7 miles per hour. . . Rate 3.4 miles per hour . . . In walking up grade the energy used up is equal to elevation X weight of patient plus the energy expended in traversing the distance; but this is theoretically equalled by the energy saved in the subsequent descent, and, on the other hand, both are increased by bringing into play a different group of muscles; these factors can scarcely even be approximately estimated in the individual case. However, Zuntz gives the fol- lowing empirical figures: a man, 150 Ibs., climbing 3 kilometres (1.8 miles) in one hour upon a 10 per cent, grade uses up about 28 Gm. (almost 1 ounce) of fat. (4) Resisted movements (Schott) carried out under the supervision of an attendant; or contraction of antagonistic muscles (Herz) (see page 268). (o) Xauheim baths (see page 274) or daily cold baths as cold as can be borne by the patient without shock. (G) Drug Treatment. Strychnine may be administered to increase muscular tone, provided this does not also increase the appetite too much. Thyroid extract and other " a n t i f a t " medication should be scrupulously avoided. Metabolism experiments have shown that the admin- istration of thyroid substance, though increasing the oxidative processes, causes a split- ting of proteid to a greater degree than of fat, and hence defeats its own end, namely, that of burning up the fat without affecting the muscle. It also brings about palpita- tion, tachycardia, and other distressing symptoms, and tends to increase rather than to diminish the cardiac features, even though it maybe diminishing the obesity itself. In the obesity of the menopause, tablets of ovarian extract are used to increase oxidation, as this effect has been demonstrated in animals, but clinicallv the results from its use are rather uncertain. FATTY DEGENERATION. PATHOLOGY. Pathological Anatomy. In the condition known as "fatty degenera- tion" the fat is deposited not by an increase of adipose tissue but in the form of fine droplets within the heart muscle-cells (Figs. 141 and 142). In some cases these droplets can be seen to almost fill the entire cell, in others they appear as a few diffusely scattered droplets in the sarcoplasm. 1 It must be borne in mind that sclerosis of the coronary arteries is a frequent con- comitant of heart weakness in fat people, and hence sudden overexertion or severe exer- cises are to be avoided, at least until the physician has thoroughly acquainted himself with the patient's condition and endurance. 298 DISEASES OF THE HEART AND AORTA. Not all the cells are invaded by the fat, but with the naked eye yellow areas of fatty degeneration may be seen mingled with normal areas of red-brown color, which appear normal in structure under the microscope. As regards distribution, Ribbert recognizes three types: (1) diffuse general fatty degeneration, in which all the cells are loaded with fat; (2) mottled de- generation, occurring in the areas which lie midway between or at points most distant from the larger arteries ; occurring especially in anaemic individuals and in persons whose blood-pressure is very low, so that the cells which are most distant from the arteries suffer from ischsemia; (3) mottled periarterial fatty de- generation produced by the action of poisonous substances in the circulating blood, such as phosphorus, arsenic, bacterial poisons, etc., in which those cells suffer most which are brought most closely into contact with the poison, i.e., the cells lying in the vicinity of the larger arteries, while the areas remote from these vessels are normal or involved to a lesser degree. Nature of Fatty Degeneration. The fatty degeneration may go on in hearts otherwise healthy in connection with infectious diseases, or in chronic myocarditis and in valvular heart diseases. The exact nature of the process is not clear. Virchow termed it a "degeneration," but this term, although in very general use, does not seem to designate accurately the process. It appears to be a disturbance of cellular metabolism rather than a degeneration of cell protoplasm, and it has been suggested that perhaps this is due to some interference with the oxidizing enzymes such that the fat cannot be oxidized, just as the sugar fails to be oxidized in diabetes. But this suggestion is not founded upon any experimental data. It is therefore most important from the stand-points of both pathology and prognosis to learn where this fat comes from and how it is formed. Virchow w.as the first to teach that there was a true fatty degeneration, that is that the fat was formed from non-fatty (probably proteid) substances of the sarcoplasm. It must be borne in mind that the fat might be present in combination as it is in lecithin without being visible, but that it may become visible when it is split off from the lecithin molecules and deposited as highly refractive droplets of true fat. However, the analyses of numerous observers (Bottcher, Krehl, Rosenfeld) show a definite increase in the fat present in the heart muscle in fatty degeneration. Indeed, according to Rosenfeld, the muscle shows " fatty degeneration " whenever it contains more than 1")-17 per cent, of fat within the muscle-cells (in marked fatty degeneration usually 20-21 per cent.). As he put it, ''there is no true fatty degeneration, but the cell becomes p o o r i n proteid and fat enters it. 1 ' That this fat is noi derived from the breaking down of cell substance, but is derived either from the fat of the food or from that transferred from the subcutaneous tissue else- where in the body, has been shown in many ways. In the first place, Krehl demonstrated that the lecithin content of the heart muscle was practically constant and quite indepen- dent of the degree of fatty degeneration, and hence that the fat was not derived from this source. Secondly, Rosenfeld showed that in a heart whose left ventricle appeared normal, but whose right ventricle was very yellow in appearance (and showed fatty degeneration on section), the nature of the fat was identical in both. Thirdly, it was shown also by Rosen- feld that if dogs were starved until their subcutaneous fat had disappeared and were then poisoned with phosphorus, the fatty degeneration did not then appear as it did in well- fed dogs. This fact was further demonstrated by Leick and Winckler, who poisoned their doirs with phosphorus and then fed them on mutton tallow (iodine absorption coefficient. 3S.2), and obtained a deposit within the heart muscle not of dog fat (I. A. ('. 5S.C>) but of mutton tallow. This seems to prove that the "fatty degeneration" of heart muscle is simply a deposit of fat within the muscle-cell, just as it occurs within the connective-tissue cell under normal circumstances. The deposition of this fat is not associated with any FATTY DEPOSITS IN AND ABOUT THE HEART. 299 change in the lipase of the heart muscle nor of the liver, in spite of the apparent increase in fat metabolism. The author also found that the amount of lipase in the lean areas of a human liver mottled with fatty degeneration was the same as in the neighboring yellow areas. It would appear, therefore, that, chemically, the primary change being absent, fatty degeneration lies not in the heart but elsewhere in the body. This is further borne out by the fact that in animals poisoned with phosphorus, oil of pulegon, etc., the total amount of fat in the body is diminished, while that in the heart and liver is increased. The latter organs seem merely to deposit the fat thrown into the general circulation. ETIOLOGY. Fatty degeneration in the human heart occurs most commonly in association with alcoholism, either acute or chronic, primary and secondary anaemias, after hemorrhages, in association with myocarditis, valvular and other cardiac lesions, in most infectious diseases, in miners, smelters, and many metal workers, as well as in numerous other industries where poisonous, substances are employed. In a number of cases of death from chloroform anaesthesia fatty degeneration has been found and is usually ascribed to the action of the chloroform, but Rosenfeld believes that in these cases the fatty degeneration is always present before the chloroform was given, and that this fact accounts for the death of the patient. Not infrequently, as in cases of phosphorus poisoning and of infectious diseases, the same agent which brings about the fatty degeneration also gives rise to diminished tone of the vasomotor centre. Failure of the cir- culation may result from the latter factor, but this need scarcely be ascribed to the fatty change in the heart. STRENGTH OF HEART WITH FATTY DEGENERATION. These results of chemical investigation also find their parallel in the effects upon muscle. Welch, in 1888, was able to show that the hearts of rabbits rendered fatty by prolonged exposure to high temperatures were quite normal as regards preservation of blood-pressure, reactions to vagus stimulation, etc.; while Hasenfeld and Fenyvessy ten years later showed that animals poisoned with phosphorus withstood the strain from clamping the abdominal aorta quite as well as did normal animals. On the other hand, de la Camp compelled his phosphorus dogs to run a tread-mill until fatigue set in, and found with the X-ray that their hearts had dilated, whereas those of normal dogs did not dilate under these circumstances. The tonicity of the c a r d i a c muscle was d i m i n i s h e d . De la Camp's experiments have not been repeated as yet, but they seem to have been very carefully carried out. It seems certain that, as Kraus claims, there is a considerable difference between the endurance of normal hearts and of those with fatty degeneration. Moreover, patients with fatty degeneration of the heart are very sen- sitive to digitalis and are frequently injured by it. Sudden death from overdose of digitalis or from acute cardiac overstrain is more common in patients with fatty degeneration of the heart than in almost any other condition. The relative frequency with which fatty degeneration is asso- ciated with spontaneous rupture of the heart is also evidence of weakness of the walls. 300 DISEASES OF THE HEART AND AORTA. SYMPTOMS AND SIGNS. The most characteristic symptoms associated with the condition are those of general debility and feebleness, more or less languor and somno- lence, as a rule without marked cardiorespiratory symptoms except short- ness of breath on exertion. The pulse is usually small, rather collapsing, and feeble; the blood-pressure is below normal, except when complicated by chronic myocarditis or valvular lesion (maximal pressure 90 to 115 mm. Hg) ; the pulse-rate is increased. On physical examination the heart may be either normal or dilated, the sounds either feeble and distant or short and sharp; the apex impulse may or may not be well marked. The liver and spleen are often enlarged as part of the general malady of which the cardiac condition also forms a part. There is sometimes cedema of the feet and ankles. However, it must be frankly admitted that none of these is either constant or characteristic; and the diagnosis may have to be made from inference only. DIAGNOSIS. The diagnosis of fatty degeneration may often be made with more or less probability from a knowledge of the etiological factors,, but not from any of the physical signs, so that, as Krehl puts it, the re are no clin- ical signs for the diagnosis of fatty degeneration of the heart. TREATMENT. "When the condition is recognized, or rather suspected, the treatment consists of absolute rest in bed for at least two weeks after the acute dis- turbance has passed off and until slowed respiration and increased tolerance to mild but gradually increasing arm exercises show that the heart muscle has regained its normal condition. Whether it is possible to overcome the fatty degeneration of a chronically diseased heart is questionable, but in that, as in other conditions, treatment must be guided by the general response of the patient, and over-exertion must constantly be shunned. It must be borne in mind that hearts which are in a state of fatty degeneration are particularly sensitive to digitalis; so that, when this con- dition is suspected, digitalis should be either avoided or given in smaller doses than usual. PROGNOSIS. Spontaneous recovery is the rule if too great a burden is not imposed on the heart; but in spite of the results of animal experiments, especially those of Welch and Hasenfeld and Fenyvessy, attention must be called to the fact that sudden death is far from a rare occurrence in hearts with fatty degeneration. It occurs most frequently after or during exertion. One can scarcely avoid the suspicion that perhaps the condition which brings about the change in the fat metabolism is also one which limits the total metabolism of the heart muscle-cells and consequently their contrac- tility; so that after a certain limit is passed they suddenly cease their func- tion, just as is the case in the cellular asphyxia of intermittent claudica- FATTY DEPOSITS IX AND ABOUT THE HEART. 301 tion and coronary sclerosis (see page 368, Fig. 166), or in toxic myocarditis from diphtheria. Spontaneous rupture of the heart is par- ticularly common in cases of fatty degeneration. The latter was present in 77 per cent, of the cases collected by Hamilton. BIBLIOGRAPHY. HEART OF OBESITY. Kisch, H.: Zur Lehre vom Mastfettherzen, Muenchen. med. Wchnschr., 1902, Hi, 546. Miiller, W. : Die Massenverhaltnisse des menschlichen Herzens, Hamb. u. Leipz., 1883. Hirsch, K.: Ueber den gegenwartigen Stand der Lehre vom sogenannten Fettherzen, Muenchen. med. Wchnschr., 1901, xlviii, 1867. Leick and Winckler: Herkunft des Fettes bei Fettmetamorphose des Herzfleisches, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1902, xlviii, 163. Loevenhart, A. S.: On the Relation of Lipase to Fat Metabolism Lipogenesis, Am. J. Physiol., Bost,, 1902, vi, 331. Schieffer: Ueber den Einfluss des Ernahrungszustandes auf die Herzgrosse, Deutsch. Arch. f. klin. Med., Leipz., 1908, xcii, 54. Romberg, E.: Lehrbuch der Krankheiten des Herzens und der Blutgefasse, Stuttgart, 1906. V. Noorden, K.: Die Fettsucht, Nothnagel's Spec. Pathol. u. Therap., Vienna, 1900, vol. vii, 1st half. Banting, W.: Letter on Corpulence; address to the public, 1863, 1864, 1865, 1868. Oertel: Kritisch-physiologische Besprechung der Ebstein'schen Behandlung der Fett- leibigkeit, Leipz., 1885. Obesity, Twentieth Century Practice of Med., N. Y., 1895. Hirschfeld: Die Behandlung der Fettleibigkeit, Ztschr. f. klin. Med., Berl., 1893, xxii, 142. Kisch: Das Mastfettherz, Prag, 1894. Zur Insufficienz des Mastfettherzens, Therap. d. Gegenwart, 1899, xl, 296. Ebstein, W.: Die Fettliebigkeit und ihre Behandlung, Wiesbaden. FATTY DEGENERATION OF THE HEART. Ribbert, H.: Beitriige zur pathologischen Anatomie des Herzens, Arch. f. path. Anat. etc., Berl., 1897, cxlvii, 193. Krehl, L.: Ueber fettige Degeneration des Herzens, Deutsch. Arch. f. klin. Med., Leipz., 1893, li, 1, 416. Rosenfeld, G.: Der Prozess der Verfettung, Berl. klin. Wchnschr., Berl., 1904, xli, 587. Ueber Herzverfettung beim Menschen., Zentralbl. f. innere Med., Leipz., 1901, xxii, 145. Leick and Winckler: Herkunft des Fettes bei Fellmetamorphose des Herzfleisches, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1902, xlviii, 163. Rubow: Ueber die Lecithingehalt des Herzens und der Nieren unter normalen Verhalt- nissen, Hungerzustande und bei der Fettigen Degeneration, Arch. f. exper. Path. u. Pharmakol, Leipz., 1904-5, lii, 173. Welch, W. H.: Cartwright Lectures on the Nature of Fever, Medical News, X. Y., 1SS8. Hasenfeld, A., and Fenyvessy, B.: Ueber die leistungsfahigkeit des fettig entarteten Her- zens, Berl. klin. Wchnschr., 1899, xxxvi, 80, 125, 150. De la Camp, O.: Quoted on page 201. Kraus, F.: Die klinische Bedeutung der fettigen Degeneration des Herzmuskels sclnver ansemischer Individuen, Berl. klin. Wchnschr., 1905, xlii, p. 44A. IX. AFFECTIONS OF THE MYOCARDIUM. A certain amount of degeneration in the fibres of the heart muscle occurs during the course of every acute febrile disease or intoxication. As has been seen in previous chapters, the heart under these conditions exhibits signs of overstrain, and the diagnosis of myocarditis, therefore, depends upon the degree rather than the mere existence of cardiac weakness. However, in certain cases the signs of cardiac weakness overshadow those of the original disease and it is in these that acute myocarditis is usually recognized. The chronic changes, however, which follow long after the original disease has subsided, present a less complicated picture and there- fore are more easily recognized. PATHOLOGICAL ANATOMY. The lesions of acute and chronic myocarditis are merely different stages in a process which is more or less continuous. The lesions of chronic myocarditis are always preceded by the acute lesions, but the degeneration may not be so severe at any of the earlier periods as to give rise to symp- toms of cardiac weakness. In the first stage of acute myocarditis there is injury and degeneration of the muscle-fibres, with oedema about them, and infiltration of polymorpho- nuclear or mononuclear cells into the cedematous spaces between the fibres. Degenerative Changes. The degenerative changes which take place in the heart muscle are : (1) parenchymatous degeneration, (2) fatty degeneration, (3) hyaline and amyloid degenera- tion, (4) calcareous degeneration, and (5) fragmentation. Parenchymatous degeneration of the heart muscle was first described by Virchow and Boettcher. The muscle-fibres swell, lose their striation, and the plasma contains numerous granules of an albuminous material, probably altered muscle proteid (myosin). They retain their contractile power to a certain extent, but its force at this stage is somewhat impaired, and the cell may subsequently return to normal without under- going complete necrosis. In the more severely injured cells the nucleus is destroyed, the sarcoplasm becomes filled with vacuoles, takes on a basic stain, and is gradually absorbed, leaving only the sarcolemma. Often, but not always, parenchymatous and fatty degeneration go on in the same fibre, the fat being deposited as the proteid is removed. In sonic cases fibres undergo hyaline or waxy degeneration (Zenker) and present an absolutely homogeneous appearance, taking up the acid stains (protoplasmic) with great avidity. In rarer cases there is a c a 1 c a re o u s de ge n e r a t i on with deposit of calcium salts in the muscle- cells. These cells then take up the basic (or nuclear) stains (description of 302 AFFECTIONS OF THE MYOCARDIUM. 303 a case and discussion of the literature is to be found in the article of E. K. Cullen). The degeneration is never uniformly distributed throughout the cells, not all the cells being affected at once or in the same degree. Occasionally the heart muscle-cells show peculiar splits extending transversely across the whole or part of the cell. This condition is known as "fragmentation." The fibres may show no other signs of degeneration, the transverse striations may be clear, and the longitudinal strias may be distinct up to the line of the fracture. Fragmentation has been found after death from a tremendous variety of causes, even in individuals dying from accident. It does not seem, therefore, to be a sign of specific degeneration. Dietrich's attempts to prove it an artefact, and either to exclude it when once present or to bring on fragmentation by allowing the heart to pass through various stages of decomposition, have been unsuccessful, and Buhlig in a very careful research seems to have shown that it is an artefact which is produced when the microtome knife cuts at right angles to the muscle-fibres. This observation still requires confirmation. Otherwise the consensus of opinion seems to be that fragmentation is the result of some change in the muscle-fibres occurring during the death agony, and that it is not to be regarded as a degeneration. As illustrating the frequency of the several types of myocardial degeneration Romberg finds the following frequency in 29 cases: Typhoid fever 11 cases: Parenchymatous (albuminous) degeneration, moderate or intense 10: fatty, present 6, absent 5; hyaline or waxy (slight) 2, absent 9. Scarlet fever 10 cases: Albuminous degeneration, present 8, absent 1, not noted 1; fatty, intense 1, moderate 1, absent 8; hyaline or waxy, moderate 3, absent 7. Diphtheria 8 cases: Albuminous, intense 1, moderate 4, absent 3; fatty, intense 5, absent 3; hyaline or waxy, present 2, absent 6. Distribution of Myocardial Changes. In man, according to Krehl, 1 acute myocardial 1 c s io n s a r e particularly com m on in the papillary muscles of the left ventricle 1 and in the m u s - 1 Examination of Specimens. In cases in which the state of the myocardium is of importance, the microscopic structure of the heart muscle should always be examined by the method of Krehl. Krehl cuts the heart into cubical blocks 1 cm. in si/c, numbering them in order so that the exact location of each block can be accurately determined. These blocks are fixed in Midler's solution and a section or two from each is examined. In this way a very thorough idea of the extended distribution of lesions may be gained, and a study of a very few hearts thus reveals more accurate knowledge than can otherwise be gained from a large number of organs examined less thoroughly. 304 DISEASES OF THE HEART AND AORTA. culature about the left auriculoventricular ring, lying within the lymph spaces about the small arteries, which they sur- round in sleeve, cuff, or signet-ring distribution. The osdema produced during experimental cardiac overstrain (Roy and Adami) and the myocardial lesions produced with adrenalin (Josue, Loeb and Fleisher, Pearce) and adrenalin and spartein (Loeb and Fleisher), all have this same distribution. Loeb and Fleisher have shown that two deleterious agents, such as adren- alin and spartein or caffein, given together produce myocarditic lesions in a much greater number of cases than either of them acting alone, and this rule is probably true for all diseases and intoxications. They found oedema of the connective tissue appearing within two days, fol- lowed by perivascular infiltration several days later and then by fibrosis in a few weeks. The muscle-fibres were at first swollen and vacuo- lated, and later either remained enlarged (hy- pertrophied) or underwent atrophic changes. Abscess. The form which the foci as- sume depends chiefly upon the nature and properties of the infective agent. If the virulence of the germ is great, abscesses may be produced in the heart muscle (suppurative myocarditis) as elsewhere in the body. These abscesses are usually produced by small septic thrombi which plug 'the minute branches of the arteries. Under the influence of the fibrin ferment secreted by the bacteria, the vessel soon becomes completely filled with a throm- bus, an area of ischsemia results in the heart muscle, which quickly becomes infected and breaks down to form an abscess. These ab- scesses vary in size from a submiliary nodule to a cavity separating the muscle layers in the entire interventricular septum. They are usually produced by the pyogenic cocci in septicaemia or following trauma to the heart (see page 617). The outcome is usually fatal. Occasionally there is rupture of the ventricle through the necrotic portions of the wall. "Rheumatic" Foci. In the less virulent infections, such as rheuma- tism, typhoid fever, influenza, the foci do not undergo suppuration, but the lymph spaces around the arteries and capillaries are filled with cellular infiltration, polymorphonuclear in most of the acute infectious diseases, while mononuclear cells predominate in myocarditis from typhoid fever and subacute rheumatism. Since rheumatic fever is perhaps the most common cause of myocar- ditis, the lesions which it produces are of particular interest. Romberg, Aschof'f, (leipel, and Coombs have called attention to the presence of small submiliary foci 0.1-0.2 nun. in diameter, which occur with great frequency in rheumatic patients, especially in the musculature about the mitral ring. Kach focus consists of a hyaline centre formed by agglutinative thrombosis within a capillary. About this there is a zone of giant cells each containing Fir,. 145. Septic myocarditis with multiple abscesses in the heart wall. The arrows point to the abscesses. AFFECTIONS OF THE MYOCARDIUM. 305 2-4 nuclei, and these in turn are surrounded by a wider zone of mononuclear cells interspersed with eosinophiles. The writers mentioned regard these foci as pathognomonic of rheumatism, although they may bear only the general features of a subacute inflammation about an area of hyaline throm- bosis. Indeed the most typical specimen of these found in the Johns Hopkins Pathological Museum was seen in a case of non-rheumatic myocar- ditis. On the other hand, Freund has reported a case of acute rheumatic myocarditis in which the infiltration was mainly polymorphonuclear. Bracht and Wachter have recently produced arthritis, endocarditis, and myocarditis with lymphocytic infiltrations in animals by injection of cultures of diplococci obtained from two cases of acute articular rheumatism. These infiltrations contrast sharply with the polymorphonuclear infiltrations usually produced by pyogenic streptococci. FIG. 146. Photomicrograph showing an abscess in the heart muscle. A. Low power. B. Same, higher power. Subsidence of Lesions. The changes which occur in the myocardium when the patient recovers from the acute infection or intoxication, which is the causal factor, vary both with duration and intensity of the disease and the rapidity and completeness of the recovery. If the causal factor completely disappears and its sojourn in the body has been a short one, no permanent changes may have taken place. The oedema of the fibres disap- pears, the cellular exudate may be absorbed in toto, and the myocardium may resume its normal appearance. If areas of fibres have been destroyed their place may be taken by scar tissue. But if the duration of the process has been so long that connective tissue has begun to be formed in the exudate, the traces are no longer obliterated and a chronic myocarditis has set in. PATHOLOGICAL PHYSIOLOGY. As has been seen in previous chapters, h e a r t s w hose muscle is injured become'dilated upon c o m p aratively s 1 i g h t exertion, while healthy hearts resist dilatation in spite of tremendous 20 306 DISEASES OF THE HEART AND AORTA. exertion. Moritz and Dietlen, whose X-ray studies have demonstrated that the normal heart becomes smaller in severe exercise, have shown that, on the contrary, the heart whose muscle is diseased undergoes tremendous dilatation. Fleisher and Loeb found that oedema of the lungs from NaCl infusion sets in much more readily in myocarditic than in normal rabbits. The blood-pressure is usually low in acute myocarditis, but this is due to the fact that the toxic substances which injure the heart muscle also depress the vasomotor centre. The low blood-pressure is due to the latter influence and not to the weakness of the heart. These facts were brought out by very interesting studies of the physiology of the heart muscle after injections of diphtheria toxin which were made by Roily and later by v. Stejskal. Roily used a dose of toxin which just killed his rabbits in twenty-four hours, and then began his experiments about twenty-two hours after the injection. He found that at this time the blood-pressure and pulse-rate of the animal were still quite. normal, and that the heart was still able to respond well to increased work thrown upon it by compressing the abdominal aorta, etc., and that the blood- pressure increased considerably. About half an hour before death, however, the blood- pressure began to fall, owing to loss of vasomotor tone, as had been shown by Romberg. Even at this time the heart was still strong enough to respond by a second rise of blood- pressure upon clamping the abdominal aorta. Very soon after this, however, within a few minutes, the rate became irregular and the heart weak- ened completely. V. Stejskal's results were similar. The action of the diphtheria toxin had not been immediate, but it had required several hours to combine with the heart muscle, after which its weakness was manifest. The conclusion reached by Roily and v. Stejskal is that the heart remains competent in spite of muscular weakness until a certain degree of strain is imposed upon it, when it suddenly crosses the threshold that leads to failure, dilatation, and even death. The threshold of cardiac overstrain in the healthy heart is at a much higher level. Arrhythmia in Acute Myocarditis. Irregularity of the pulse cannot be brought about by injuring the myocardium by injection of alcohol, iodine, or even KCX, but often occurs in man as a result of myocardial lesions, especially after exercise and overstrain. Gerhardt, Miiller, and Schonberg have called attention to the association of irregularity with structural changes in the right auricle and fibrillation. In mitral disease it is probable that irregularity arises in the left auricle rather than in the right, since the latter is then not the seat of pathological conditions. 1 Bradycardia is met with in the late forms of diphtheric, influenzal, and pneumonic myocarditis and occasionally during the febrile stage. It is often vagul in origin, but is sometimes due to depressed conductivity of the auriculoventricular bundle, the ventricle responding only to alter- nate contractions of the auricle (2 : 1 rhythm). It is probable that under these conditions toxic myocardial changes have taken place in the bun- dle (Mackenzie). It is not unlikely that some of the sudden deaths during convalescence from diphtheria may be due to this cause (Dunn, see page 566). 1 More fully discussed in chapter on Mitral Stenosis. AFFECTIONS OF THE MYOCARDIUM. 307 SIGNS AND SYMPTOMS. The most characteristic sign of myocardial weak- ness is dilatation of the heart (see page 199). The heart is usually, but by no means always, rapid, the sounds may be clear but tire usually short and sharp; they may be embryocardiac in rapid hearts; a gallop rhythm, especially of the presystolic type, may be present, or the sounds may be definitely split (reduplicated). It is also very com- mon to hear soft systolic murmurs over the apex or the tri- cuspid area, due to functional insufficiencies at the auriculoventricular orifices (see page 165), or to hear the "accidental" systolic murmur in the pulmonary area. The second pulmonic sound is usually a c - centuated from stasis in the pulmonary vessels. Clinically, uncomplicated myocarditis is met with in the course of the febrile diseases and the intoxications, especially alcohol- ism, phosphorus poisoning, and ptomaine poisoning. 1 1 is present also in a certain degree in almost every case of acute endocarditis or peri- carditis, where it is but part of the general "carditis." Its manifestations are simply those of acute heart failure or of cardiac overstrain occurring while at rest or upon very slight exertion. The symp- toms are, therefore, sometimes those of broken pulmonary compensation (failure of the left ventricle, page 195), sometimes those of broken systemic compensation (failure of the right ventricle), according as the left ventricle or the right is the one most affected. In many cases there are attacks of precordial pain amounting almost to angina pectoris, coming on when the heart is acutely dilated after excitement or exertion. ACUTE MYOCARDITIS IN RHEUMATIC FEVER. Although weakening of the heart is one of the most important factors in general asthenia that accompanies or follows tonsillitis or rheumatic fever, it does not often kill the patient and hence is not often a striking fea- ture at the autopsy table. The following history illustrates the course in fatal cases, showing (1) the gradual insidious onset, (2) shortness of breath, extreme weakness, and finally ascending oedema, (3) dilatation of the heart, with cedema and degenerative changes in the heart muscle, without either hypertrophy, fibrous changes, or valvular lesion. CASE OF ACUTE RHEUMATIC MYOCARDITIS. Annie Jones, female, colored, 48, admitted July 5. 1904, complaining of ' ' rheu- matism,'' of which she has had attacks for many years, especially marked during the last two years. The knees and shoulders have been the joints most frequently affected. She has had no other infectious diseases and the previous history is otherwise negative. No shortness of breath nor palpitation. During past four weeks lias been com- pelled to sleep upright in a Morris chair, and has had incontinence of forces. PHYSICAL EXAMINATION. Patient is a very stout colored woman, lying quietly on her back in bed. Pupils equal and react to light and accommodation. Chest clear. Heart. Impulse is not visible. Relative cardiac dulness extends 13 c m . to left of midline in fourth interspace, 30 cm. to the right. First sound at apex 308 DISEASES OF THE HEART AND AORTA. is very loud and not perfectly clear, though there is no definite murmur. Second sound resembles the first in quality but is clear. Pulse regular, of good volume, rather high tension, 100 per minute. Vessel wall somewhat thickened. Abdomen is extremely large and swollen; there is dulness in dependent portion. Liver is not enlarged. Legs are extremely swollen and indurated; do not even pit on pressure. Knee- and ankle-joints much swollen and stiff. A round perforating ulcer is present at left heel. No disturbance of sensation anywhere. Temperature 99; red blood-corpuscles 4,046,000; haemoglobin 55 per cent.; leuco- cytes 3SOO. Ordered rest in bed; soft diet; diuretin 1 Gm. (gr. xv) q. 4 h.; ulcer of foot to be irrigated with sol. potass, permang. 1:20000 b. d. On July 7, ordered tinctura dig- italis 1 c.c. (TTLxv) q. 4 h., ad dos. viii; this was then repeated and continued throughout the course of disease. Spts. glycerylis nitrat. gtt. ii, q. 4 h., alternating with sod. nitrit. 0.3 Gm. (gr. v) q. 4 h.; morphin. sulph. O.OOS Gm. ( gr.) p.r.n. July 12. Heart's action irregular; first sound reduplicated over tricuspid area; no murmurs. July 15. There is a large perforating ulcer just below coccyx. This was irri- gated with potass, permanganate 1 : 20000 and packed with iodoform gauze. July 16. Temperature 106; percussion note impaired at left base behind, where breath sounds are absent. A few rales have previously been heard in this area. Ordered strychnine sulph. 0.003 Gm. ( 3 'o gr-) and digitalin 0.003 Gm. (?V gr.) hypo. q. 4 h. At 7.30 P.M., respiration shallow with expiratory grunt. At 11.00 became unconscious, and died at 12.45. AUTOPSY showed about 1 litre of fluid in peritoneal cavity; congestion of lower lobe of lungs. Heart . Several opaque white patches over epicardium, one with a diameter of 3 cm. Coronary arteries soft and smooth. Heart muscle soft, flabby, and of yellowish -brown color, studded with numerous small opaque white areas. The muscle bundles are widely separated nuclei. Under the microscope the muscle-fibres are seen to be swollen; little new growth of interstitial connective tissue. Heart weighs 250 Gm. Slight sclerosis about base of aorta, none elsewhere. Kidneys normal in size, pale and cloudy. Liver shows some fatty degeneration. DIPHTHERIC AND IXFLUEXZAL MYOCARDITIS. Acute myocarditis is the chief cause of death in diphtheria and influenza. In these conditions it may manifest itself either, (1) as an early form during the course of the fever, or (2) as a late form which becomes manifest after the temperature has fallen. The cases of diphtheric myocarditis have been most carefully studied by Hibbard in 800 cases with 119 deaths (15 per cent.) at the Boston City Hospital. In spite of the high average mortality, the mortality was less than 5 per cent, in those cases in which the pulse- rate was below 130 per minute, increasing as the pulse-rate increased above that figure. Death was especially frequent in those cases in which a gallop rhythm was noted. Bradycardia (under GO per minute) was not a severe sign in adults (14 cases without a death; only 2 with cardiac symptoms), whereas in cases under 7 years it was a very grave sign (U cases, 5 deaths). In all Hibbard's fatal cases there were both acute myocardial change and degeneration of the fibres of the vagus. S u d d en d e a t h is not uncommon in cases of diphtheric myocar- ditis; in Dunn's case, from the onset, heart-block (Adams-Stokes syndrome) FIG. 147. Orthodiagraphic out- lines of the heart of a child during the course of a severe diphtheria. (After Dietlen, Miinchen med. Wc/tnschr.. 1905, lii.) + + + ++, outline on fiftli day (MR. = 3.0 cm.. ML. = ('..0 cm., L. = 9.1 cm.); , outline on seventh day (MR. = 3. 5 cm., ML. = 8.1 cm., I.. = 12.4 cm.); , outline on twenty-Mxth day (MR. = 2.0 cm., ML. = 0.5 cm.. L. =9.3 cm.). AFFECTIONS OF THE MYOCARDIUM. 309 was the result of myocardial change in the vicinity of the auriculoventricular bundle. The slow pulse also is often due to partial heart-block, 2 : 1 rhythm, though this may be due to overstimulation of the vagus as well as to injury of the bundle. Just as diphtheria affects the myocardium in the very young, influenza affects it in the aged. Indeed myocarditis constitutes one of the gravest effects of this disease, and is especially to be feared after the sixth decade. The following case serves as an example : CASE OP INFLUENZAL MYOCARDITIS. Patient, aged 75, of sedentary habits, rather stout, but free from all cardiac symp- toms. Pulse had always been of good volume and regular. Had a severe attack of influenza in March, 1903, confining her to bed for a month. No special car- diac features. After a short convalescence she was again able to be up and about. A few days later, just after retiring, she had a severe attack of cardiac asthma, breathlessness, orthopnoea, and slight precordial pain. Xo true angina. Moderate degree of cyanosis. Pulse small, rapid, irregular. Cardiac dulness slightly enlarged. Soft systolic murmur heard over the entire heart. The attack lasted half an hour, symptoms being much relieved by inhalations of amyl nitrite. Patient was given complete rest in bed for a few days, with fluidextract of digitalis NLV (0.3 c.c.) three times a day and soft diet, and was then kept at rest in a large arm-chair. Gradual convalescence. Soon became free from symptoms, but pulse remained 70 and irregular and she was compelled to refrain from every effort except one daily trip up and down stairs, during which she rested at each step long enough to count twenty. In June and July, 1904, she had several similar attacks, and though she improved somewhat her pulse remained permanently irregular. Died suddenly a year and a half later, death fol- lowing six weeks after a severe cellulitis of the leg. CASE OP SUBACUTE ALCOHOLIC MYOCARDITIS. B. C. S., reporter, married, aged 36, admitted to the service of Prof. J. O. Hirsch- felder, City and County Hospital of San Francisco, January 23, 190,5, complaining of shortness of breath and swelling of feet. Father and brother are subject to rheumatism, and patient himself had swelling of joints four years ago, about the time of a gonorrhoea! infection. He had measles, whooping-cough, and scarlet fever as a child, and typhoid fever seven years ago. Denies syphilis. Married, but has had no children. Uses tobacco in moderation, but drinks whiskey in excess, as a probable result of which he has fallen from the best to the lowest strata of society. PRESENT ILLNESS. Four weeks ago while in the midst of a series of debauches he noticed that his shoes became tight, and in a few days his legs became so swollen that he could not put on his drawers. He had pain in the legs on walking, owing to the oedema. He also felt very weak and became exhausted easily. Has had shortness of breath on exertion. PHYSICAL EXAMINATION. Well-nourished man of good color. Tongue and uvula deviate slightly to the right. General glandular enlargement. Epitrochlears palpable. Chest negative except for a few moist rales over right axilla and base. Heart. Cardiac impulse not visible. Relative cardiac dulness extends to 1 '2 . ."> cm. from mid line in fifth interspace (3 cm. outside mammillary line). 4 cm. to right of midline and above to the third rib. Sounds are very rapid, the first sound every- where replaced by a systolic murmur which is loudest at the apex; not transmitted to the axilla; pulmonic second accentuated. Pulse 10^, regular in force and rhythm, low tension, fairly good volume. Radial artery not palpable. Liver just palpable. Xo scar on genitalia. Lower extremities are covered with pediculi and raw scratch marks. Marked oedema of both legs. Trine nega- tive, sp gr. 1028. Ordered liquid diet; fluidextract digitalis 0.3 c.c. (n\,v) q. 4 h.: spir. glycerylis nitratis 1 gtt. q. 4 h.; sol. magnes. sulphat. sat. 30 c.c. (oi); ung. xinci oxid. to legs. 310 DISEASES OF THE HEART AND AORTA. Jan. 30. Pulse slow and somewhat irregular, venous tracing show- ing that some of the auricular impulses did not reach the ventricle (2 : 1 heart-block). Given at ropine 0.0015 Gm. (7 gr.) at 12.45 P.M. At 200 P.M., max. pr. 135, min. 75- 80. Pulse-pressure 60 X pulse-rate 60 = 3600. Pulse-rate absolutely regular, as shown in the brachial artery tracing taken at 1.45 P.M. Digitalis was now discontinued. Feb. 2. G'xlemagone. Soft systolic murmur still present at apex. Pulse-rate 72, abso- lutely regular, responding to all impulses from the auricle. It never again became irregular. Feb. 11. Feels quite strong. Up and about. Heart has been regular and all mur- murs gone. March 2. Has had slight swelling of feet. Was again put to bed. The swelling disappeared within 24 hours. In a few days the patient was again up and about, and in a week or ten days later was allowed to continue his work in the pantry. Was discharged apparently cured about May 15. DIAGNOSIS. As has been seen, the diagnosis of acute myocarditis in many cases is made more by inference than by definite signs. The presence of symptoms of cardiac weakness in an infectious disease, out of proportion to the severity of the latter or to the apparent seventy of the endocardia! lesion, is presumptive evidence of severe myocardial involvement. The symptom- complex of restlessness or marked clulness, constriction over the chest, and precordial pain, vomiting, cyanosis, and increase in the area of cardiac clulness, during or after an attack of an infectious disease or of delirium tremens, is practically pathognornonic. The presence of a systolic murmur at the apex and over the body of the heart, which may even be transmitted to the axilla but which disappears during convalescence, added to the other symptoms above mentioned, would indicate myocarditis rather than endo- carditis. It must be borne in mind, moreover, that the presence of true endocarditis or pericarditis is evidence in favor rather than against the presence of an additional myocarditis, and that in the acute form the symp- toms are quite as liable to be due to the insufficiency of the muscle as to the valves. On the other hand, just as a most acute nephritis may be pres- ent without the presence of albumin or casts in the urine, so acute myo- cardial changes may be present without definite signs of cardiac weakness other than a tendency to fatigue. In view of the observations of de la Camj), Moritz, Dietlen, and Hornung, myocardial changes may be diag- nosed in cases in which the heart undergoes transitory dilatation (with or without transitory valvular insufficiencies) upon comparatively slight exertion. The cardiac area under such conditions must be most carefully outlined, if possible with the orthodiagraph. In the absence of the latter careful percussion may often suffice. The changes must be 1 cm. or more before they should be considered as definite. TREATMENT. The management of a case of acute myocarditis differs essentially from that of the chronic form, owing to the fact that in the former the changes in the muscle may be of a temporary character, while in the latter the changes are permanent. Accordingly, in the acute form the aim is to allow t h e muscle to return to its no r m a 1 s t ate, AFFECTIONS OF THE MYOCARDIUM. 311 while in the chronic form this cannot be hoped for, and the treatment is directed toward obtaining the best functional result possible in the changed muscle that is left. The one aims at bringing about subsidence, the other at inducing hypertrophy. Accordingly, even in the mildest form of acute myocarditis rest is all- important c omplete rest in bed until the degenerative changes in the muscle have subsided. This is especially important, since cardiac overstrain sets in very easily in such hearts, and it is probable that this, in even the slightest degree, increases the injury to the muscle-fibres as well as the extent of the interstitial cedema and infiltration. The patient should be kept in bed at least two weeks after any indications of myocardial weakness have subsided, and if possible until the pulse-rate has again become slow. An easily digestible diet equiva- lent to about 1000-1500 calories should be enforced (see page 223), frequent feeding of small quantities being resorted to in the place of three compara- tively large meals. An ice-bag should frequently be applied to the precordium, since it tends to slow the heart-rate. Some writers, especially Caton, strongly favor the application of small blisters to the precordium and the administra- tion of small doses (0.3 Gm. or 5 gr.) of potassium iodide, but it is extremely doubtful w-hether this has any effect upon the course of the disease. If anaemia arises, iron should be ordered in some form, usually as Eland's pills, ferri carbonas saccharatus (0.25 Gm., 4 gr.), or Yallet's mass (same as Blaud's pills with honey instead of sugar but more perma- nent), or elixir ferri, quinina?et strychnina3 phosphatum (4 c.c., 1 fluidrachm). If constipation or other digestive disturbances result, ha>matin or some other "organic" iron preparation, that is, where the iron is combined with proteid. The patient's bowels should be kept freely moving without effort, best by means of Rochelle salts, sodium phosphate, Epsom salts, or Seidlitz powders. The effervescent citrate of magnesia usually causes greater abdominal distention than is desirable, owing to the upward displacement of the diaphragm. Hypersensibility to Digitalis. The usefulness of digitalis in acute myocarditis is a debatable question. Digitalis acts as a spur to the heart and raises the strength of the contraction until it enables the fibres to draw on their reserve force at each contraction, but it does not raise the limit strength. When that limit is already approached it spurs them too far, and drives them to overstrain and even to death. Whether, in any individual case, digitalis will do good or harm will depend, therefore, upon the degree to which degenerative changes have progressed and the amount of reserve force that is left. Thus, in the case of B. C. S., the myocardial degeneration was slight and the beneficial action of digitalis was marked. With A. J., however, the case was different. Degeneration had reached too advanced a stage and the drug was useless, perhaps even harmful. Even the heart of B. C. S., however, manifested the abnormal suscepti- bility of such hearts to digitalis, since it produced partial block and extra- systoles with doses which barely sufficed to slow the heart of the average patient. 312 DISEASES OF THE HEART AND AORTA. Moreover, in acute myocarditis the heart is hypersensitive to digitalis. For example, in the case of B. C. S., a normal dose produced an abnormally intense reaction with signs of the first stage of digitalis poisoning partial heart-block and extrasystoles. Fortunately in this case the good effects outweighed the bad, but it belonged to the group of cases which prove con- clusively that in acute myocarditis digitalis should always be given in smaller doses than would be used for a heart with a valvular lesion \vhich showed the same degree of heart failure. Strychnine. As regards strychnine, both its beneficial and its harmful effects are less marked than those of digitalis. It is therefore less liable to overstep the limit of tolerance. In ordinary doses it tends to increase the cardiac tonicity, as well as to stimulate the cardiac nerves, the respiratory and vasomotor centres, so that it becomes a valuable drug in such conditions. CHRONIC MYOCARDITIS. PATHOLOGICAL ANATOMY. Pathologically the chronic inflammatory changes in the myocardium may be divided into three groups: 1. Cicatricial patches or scars arising from the healing of isolated areas of inflam- mation (abscess or focal infiltrations) or from the organization of areas of infarction. 2. Thickening of the septa that separate the muscle strands (interfascicular myo- fibrosis, Dehio) occurring when the heart muscle hypertrophies. ;>. Diffuse degeneration of the muscle-fibres with invasion of the fibre bundles by strands of connective tissue (cardiosderosis, Huchard; interstitial myofibrosis, Dehio). FIG. 148. Specimen showing a rardinr aneurism coverts! with pericardia! adhc.-ions. FIG. 149. Chronic myocarditis Ccardiosclerosis). Cardiac Cicatrices. The areas of cardiac cicatrices are quite common in coronary sclerosis, in which they represent the site of healed infarcts in the area supplied by the affected artery. The fibrous tissue composing the scar, relatively poor in elastic fibres, is weaker than the rest of the heart wall, presenting the condition termed by Ziegler myomalacia cordis, and it may bulge out to form an aneurism of the heart (Fig. 148). AFFECTIONS OF THE MYOCARDIUM. 313 Spontaneous rupture occurs in such areas, and death occurs from hemor- rhage into the pericardium, though, according to Hamilton, this is not as frequent a cause of spontaneous rupture as is fatty degeneration. On the other hand, the smaller areas of cicatrization may represent complete obliteration. Interfascicular Connective-tissue Proliferation. Interfascicular myo- fibrosis or hyperplasia of the septa between the bundles is to be regarded as a concomitant of cardiac hypertrophy, and represents a strengthening rather than a weakening of the heart. FIG. 150. Specimens showing chronic myocarditis. (Photomicrographs by Dr. Chas. S. Bond.) A. Intrafascicular myofibrosis, penetrating into the bundles of muscle-fibres. Hypertrophy of some fibres; atrophy of others. B. Coarse strands of connective tissue penetrating between the bundles of muscle- fibres (interfascicular myofibrosis). Cardiosclerosis. The most important form of lesion in chronic myo- carditis is the interstitial myofibrosis or cardiosclerosis. This form is met with in senile hearts and in most cases of chronic heart failure. According to Dehio, it occurs only in those hearts which have been sub- jected to long-continued dilatation, frequently in hearts in which hyper- trophy has preceded the dilatation. The heart muscle is anlematous. The fibres are found in all stages of change normal fibres, large healthy hypertrophie fibres, large vacuolated degenerating fibres, and small ones in the various stages of atrophy in a single microscopic field. Many of them are undergoing fatty degeneration. In response to the well-known biological law that wherever the parenchyma of an organ is gradually destroyed hyperplasia of the interstitial tissue takes its place (Weigert, Dehio), fine strands of connective tissue are seen everywhere winding their way between the muscle-fibres and gradually taking their places. RELATION OF SITE OF MYOCARDIAL LKSIOX AND DISTTK I! A XC K OF Fr.NCTIOX. Lesions in the Ventricles. Attempts have been made by numerous investigators to demonstrate a definite connection between the exact site of the myocardial lesions and the disturbance of function met with. Krehl, who under Ludwig's inspiration was the pioneer in this field, inau- 314 DISEASES OF THE HEART AND AORTA. gurated the method of studying sections from every part of the heart, and found that the papillary muscles and the musculature about the mitral ring were affected with great frequency; but he was unable to establish more definite relations. Albrecht's attempt to do this for the various muscle layers discovered by Krehl and J. B. MacCallum has called forth a vigorous contradiction from Aschoff and Tawara, who have made a most careful study of 150 pathological hearts by Krehl's method. On the other hand, His, Erlanger, Stengel, Schmoll, and a host of others have demonstrated that lesions in the auriculoventricular bundle give rise to heart-block, while Aschoff, Tawara, Saigo, Barker, and Hirschfelder have shown that lesions affecting one branch of this bundle do not affect the contrac- tion of either ventricle. Very recently, however, H. E. Hering has revived interest in these questions by showing upon the excised heart that if the strand of Purkinje fibres (conduction system) to one papillary muscle is cut or injured, that papillary ceases to con- tract, although the rest of the heart continues to do so. Lesions in the Auricles. Studies of lesions in the auricles, though fewer, have been still more remunerative. Dehio and his pupil, Radasew r sky, demonstrated that in chronically dilated hearts the myocardial changes in the auricles were much more marked than those in the ventricles; and Schonberg, under D. Gerhardt's direction, has shown that per- manent arrhythmia with auricular paralysis is asso- ciated with infiltrations of the intervenous area which correspond to the embryonic sinus, the spot at which the cardiac impulse probably originates. FIG. 151. Hypertrophy of some muscle bundles in the auricle with atrophy (transparency) of o t h e r areas. (From a specimen in the Army Medical Mu- seum, Washington, D. C.) PATHOLOGICAL PHYSIOLOGY. The chief physiological features of chronic myocarditis are: (1) Chronic weakness of the heart, with tendency to undergo dilatation and overstrain. (2) Frequency of extrasystolic or absolute irregularities. Compensation in Myocarditis. The course and characteristics of myo- cardial weakness have been fully discussed under the pathological physiol- ogy of cardiac overstrain (page 190). Indeed, the persistence of a primary overstrain with the concomitant oedema of the heart muscle may be an important factor in instituting chronic myocardial changes or in rendering the heart especially susceptible to alcohol, toxins, tobacco, or other influ- ences that would otherwise not affect it. 1 The changes in the myocardium, the lowered tonicity, the persistent oedema, the reduction in the number of efficiently contracting muscle-fibres, all tend to lower the threshold of exertion at which overstrain is ushered in. Whether the overstrain manifests itself as a broken pulmonary or a broken systemic compensation, or as both together, 1 R. H. Habcock (J. Am. M. Ass., 1909, Hi, 1904) has found that chronic cholecystitis predisposes to myocardial insufficiency. AFFECTIONS OF THE MYOCARDIUM. 315 depends upon the relative and absolute strength of the two ventricles as well as the nature of the exertion. Blood=pressure. The occurrence of such overstrain is, however, quite consistent with the maintenance of a normal or, especially, a high blood- pressure. This high blood-pressure, strange to say, is in itself the result of the chronic cardiac insufficiency and the slowing of the circulation. With the slowing of the circulation there comes asphyxia of the medul- lary centres, which stimulates them and brings on an intense vaso- constriction. The vasoconstriction narrows the arterial bed so much the arterial pressure must be raised until the blood flows through the medullary centres at the proper rate. The weakened heart must thus rise to the occa- sion and sacrifice itself to save the medullary centres. The more it fails the more work these inexorable centres demand from it, the more they throttle the arteries in their struggle to get blood from the flagging heart. The more the arteries are throttled the greater the constriction, the smaller the arterial bed, and the less the systolic output necessary to overfill the arteries, the greater the force necessary to drive it. The heart may therefore empty itself incompletely but at high pressure against this high peripheral resistance, while the increase in residual blood within the ventricles leads to dilatation and stasis. This condition of stasis with high pressure, both resulting from chronic cardiac weakness, is usually termed "high pressure stasis" (Hochdruckstauung) . Its factors actually constituted vicious circle : Cardiac weakening t I Increased cardiac effort Slowed circulation High blood-pressure through medulla t _1 Vasoconstriction FIG. 152. Curve of blood -pressure in a case of chroni sisting until shortly before .wf, hardening. 327 328 DISEASES OF THE HEART AND AORTA. the high blood-pressure but independent of the lumen of the vessel, return- ing to a certain degree to the view of Virchow. These observers con- sidered the changes in the i n t i m a as primary, and tended rather to neglect the second important change which characterizes arteriosclerosis, namely inflammatory changes within the media. On the other hand, Koster and his pupils called attention to the im- portance of degenerative and calcareous changes in the media and adventitia as well as in the intima. Koster studied the inflammatory process very carefully by means of serial sections and injected specimens, and claimed that the arteriosclerotic lesion always took its origin in the adventitia as an infiltration surrounding the vasa vasorum like a sleeve. This infiltration followed the vasa vasorum into the media. Koster found that in the normal artery the vasa vasorum do not pass deeper than the outer third of the media, though in certain arteries (notably those of the brain and the lungs) there was a fine capillary network penetrating the deeper layers of the media as well and spreading along the medial surface of the elastica interna. Changes in Vasa Vasorum. This view is confirmed by v. Ebner (in Kolliker's Handbuch der Gewebelehre), who states that "the media of the larger arteries and veins, according to the consensus of opinion of many authors, contains blood-vessels, though in small numbers and only in the external layers; whereas the inner layers of the media and the intima seem to be always free from vessels (in the ox the wall of the vena cava is richly supplied with vessels even down to the intima). The infiltration about the vasa vasorum follows these paths, setting up areas of infiltration, necrosis, and calcification in the smooth muscle and elastic fibres of the media. When it penetrates to the elastica interna a small area of this is first injured, the inflamma- tion acts as a stimulus, and hyperplasia of the intima sets in. The intima becomes thick- ened until its cells undergo spontaneous fatty degeneration, after which they either calcify or the capillary network penetrates through the elastica interna and a true process of organ- ization and proliferation of connective tissue goes on. Koster admits that it is possible that the degenerative and hyperplastic changes in the intima may go on without the entrance of blood-vessels, as do those seen in inflamma- tions of the cornea; but he states that if the lesions are followed in serial sections there is almost always a demonstrable continuity between the patches of endarteritis, mesar- teritis, and periarteritis. The number and size of the vasa vasorum and the richness of the capil- lary network are always increased in arteriosclerosis and in phlebosclerosis. He states that endarteritis occurs only in arteries that have vasa vasorum,. that is. in the larger arteries and in the smaller arteries of the brain and the lung-s. These observations have been confirmed by March and, Ophiils, Klotz, and a host of other writers. Heller and his pupils, Dohle, Moll and Isenberg, as well as Marchand and Klotz, have shown that in syphilitic disease of the media the strands of infiltration along the vasa vasorum are much thicker than in arteritis (medial arteriosclerosis) due to other causes. As far as the media and adventitia are concerned, Koster's findings have been confirmed by Ophiils, whose careful study constitutes one of the most important and clearest of the recent contributions to the subject. Ophiils, however, was unable to demonstrate any constant relation between lesions in the media ARTERIOSCLEROSIS. 329 and those in the intima, and believes that they are produced independently though from the same general cause. He states that " anatomically arterio- sclerosis of the aorta is a unit. It is a chronic inflammatory process of the vessel wall which attacks all the coats simultaneously, which as a rule first produces changes in the intima and adventitia." He believes, therefore, that, as Koster suggested, the changes in the intima begin as parenchymatous changes without the presence of blood-vessels, like the inflammations within the cornea. Calcification. In degenerative lesions of the intima and media, calcare- ous deposition (atheroma) is very common, and is in fact a phenomenon which is normal for the eighth and ninth decades of life. These deposits always occur in areas of fatty degeneration; and it was thought, especially by the older German investigators, that certain acids within the tissues acted as lime-catchers (Kalkf anger) , combining with the calcium and precipitating it in situ. It was at first thought that phosphoric acid derived from autolysis of the cell nucleoproteids might be the main lime-catcher, but Gideon Wells and his collaborators have shown that when spleen or thymus which are rich in nucleoproteids are transplanted into another animal and allowed to degen- erate, no more deposition of lime occurs than in the degeneration of other tissues. It has also been assumed that the calcium first combines with the fatty acids produced in the process of fatty degeneration, a phenomenon which may actually take place in true adipose tissue. This theory was advo- cated by Klotz on the basis of the histological appearance when stained with Sudan III, but Baldauf and Aschoff have shown that exactly these appear- ances might be given by mixtures of oleic acid, triolein, and lecithin. The analyses of Baldauf, Selig, and Wells have failed to demonstrate the presence of calcium soaps; but, on the other hand, Baldauf and Wells have found that the calcium phosphate and carbonates which are the main constituents exist in the same proportions as are found in bone (about 85 to 90 per cent, of the former to 10 to 15 per cent, of the latter). However, Wells has shown that this proportion is also ex- actly the proportion in which the phosphates and carbonates exist in the serum, and his own observations, as well as those of Hofmeister and Tanaka, indicate that this is the composi- tion to which any calcium salts whatever are ultimately reduced by the mass action of the lymph and serum. Wells believes that the " calcium is carried in the blood in amounts not far from the saturation point, held in solution by the colloids and the carbon dioxide, and existing probably in the form of an unstable double salt of calcium bicarbonate and dicalcium phosphate. In normal ossification and in most instances of pathological calcification the deposition is probably initiated by a process of colloid adsorption, causing a concentration of this double salt in the hyaline matrix which is to be calcified and which has a strong affinity for calcium salts. Calcium deposition seems to depend more on physico-chemical processes than on chemical reactions. Ossification. Virchow and subsequent writers, notably Moenckeberg, Bunting, Oppenheimer, Poscharissky, Klotz, and Wells, have called atten- tion to the fact that not only plaques of calcification but even true bone may be deposited in the walls of diseased arteries, and even in calcified portions 330 DISEASES OF THE HEART AND AORTA. of the heart itself. Wells has shown that the calcium salts act as a stimulus, in the sense of Virchow's formative stimuli, in giving rise to the formation first of tissue resembling bone-marrow in structure and later to a growth of ANEURISM KRIARTtfilTONODOM FIG. 153. Various types of arteriosclerotic lesions. (Schematic.) true bone. Such arterial ossification is more common than is generally sup- posed, especially in calcareous mesarteritis. Classification of Arteriosclerotic Lesions. From the stand-point of structure, Ranvier has divided the arteries into two great groups : 1. Vessels of the elastic type, the aorta, pulmonary, carotid, and common A I', FIG. 154. Types of aortic lesions. A, fatty degeneration of the intima from a patient dying of typhoid fever; B, syphilitic aortitis, showing the sharp demarcation of the diseased area; C, generalized non-luetic arteriosclerosis (atherosclerosis). iliac arteries, whose media is made up of lamellae of elastic tissue interwoven with elastic fibrils. 2. Arteries of the muscular type, embracing all the other arteries of the body, whose media, though containing elastic fibres, is composed chiefly of strands of smooth muscle. ARTERIOSCLEROSIS. 331 Diseases of the arteries occur in a variety of forms, which affect these two types of vessels somewhat differently, so that for clinical convenience they may be divided into two groups, according as they affect the vessels of the elastic type, and especially the aorta, or the muscle-walled vessels of the periphery. I. Diseases of the aorta and vessels of the elastic type. 1. Changes in the intima: a. Acute aortitis, with fatty degeneration or gelatinous plaques in the intima. b. Atheroma, with formation of plaques of intimal thickening, fatty degen- eration, and calcification (endarteritis chronica deformans, Vircho\v; atherosklerose, Marchand), sometimes syphilitic associated with syph- ilitic mesaortitis. 2. Changes in the media (mesaortitis, mesarteritis): a. Syphilitic, showing large, thick strands of fibrous tissue with destruction of the elastic tissue. b. Acute and chronic inflammatory mesarteritis due to other germs, among them the tubercle bacillus, or perhaps to the results of clinical poisons (lead, alcohol, etc.). II. Diseases of the peripheral arteries (muscular type). 1. Acute endarteritis: a. Suppurative, with purulent infiltration of all the coats of the artery and the formation of small abscesses in its walls. This is usually attended with thrombosis within the lumen as well (thromboangitis) and final suppuration of the thrombus itself. b. Swelling and fatty degeneration of the intima, as the result of bacteria or toxic substances either directly from the blood strain or reaching it through the vasa vasorum. 2. Atheroma or endarteritis deformans resulting from calci- fication of degenerated patches. 3. Changes in the intima (endarteritis, product! v a or oblit- erans). Inflammatory changes in the intima, leading to fatty degeneration and swelling of the intima or to the proliferation of fibrous and also of elastic tissue within the lumen, so. that the latter may be either encroached on or completely obliterated. 4. Thromboangitis obliterans (to be discussed in a follow- ing chapter), in which spontaneous endo vascular clot- ting precedes demonstrable changes in the artery and the clot gradually becomes organized with solid fibrous tissue free from elastic fibres III. Diseases affecting the media (mesarteritis). 1. Hypertrophy of media. 2. Simple media! fatty degeneration with calcification or ossification (Marchand and Moenckeberg). 3. Infective mesarteritis with infiltration along the vasa vasorum. Syphilitic with very coarse strands of fibrosis. 4. Bacterial invasion of media : a. Acute septicamic, giving rise to necrosis of media and mycotic aneurisms. b. Chronic, as in typhoid fever, giving rise to chronic nu-sarteritis with strands finer than those of lues. c. Tuberculous arteritis (rare). IV. Diseases affecting the adventitia (periarteritis). a. Diffuse periarteritis part of process of all infection, luetir and tubercu- lous arteries. b. Periarteritis nodosa (Kussmaul and Mayer) (supra-arterial fibroid nod- ules) : (a) Acute. (b) Chronic. 332 DISEASES OF THE HEART AND AORTA. Fatty Degeneration of the Intima. The mildest form of disease of the intima is manifested by the formation of small, slightly raised, round or elon- gated patches, white or yellow in color, which are most frequently situated along the inner surface of the aorta above the valves or about the mouths of the intercostal arteries. The surface is smooth and lined with intact endothelium, but the subendothelial connective tissue is swollen and filled with granules of fatty degenerated material rich in lecithin and cholesterin, thus causing the surface of the plaque to be elevated above the surrounding structure (Fig. 154, A; Plate X, A). Such patches of fatty degeneration are common at all ages, especially in conditions of anemia, chlorosis, febrile disease, and acute intoxications; and they are also found accompanying the various types of arteriosclerosis and atheroma. Calcification of the Intima. Endarteritis chronica deformans (Virchow) (atheroma) is usually the result of a more chronic process, probably the gradual deposition of calcium phosphate and carbonate, in a preliminary focus of fatty degeneration in the intima. Frequently the endothelial surface becomes ulcerated over the calcification. A similar change often occurs upon the aortic and mitral valves (Fig. 155) and also in the heart muscle itself. And the mechanism by which the lesion is produced is probably the same in all. This form of arteriosclerosis is prob- ably the most common form of all, for it is the arterial disease of old age, but its importance in the causation of signs or symptoms depends upon the location of the plaques. Thus, a few FIG. 155. Syphilitic aortitis (atheroscle- plaqUCS along the COUrse of the rosis) with deposition of calcified plaques just flor fj, ^qv po^p n n above and upon the aortic valves. m & aorta may Cause whatever, not even a rise of blood-pres- sure; while a plaque upon the valvular surface of a sinus of Valsalva may cause active insufficiency, or a small area of calcification over the mouth of one of the coronary arteries may keep the heart from receiving a sufficient supply of blood and give rise to angina pectoris. Klotz has claimed that the degeneration of an area of intima is due to diminished circulation through the diseased vasa vasorum supplying nutri- ment to the corresponding part. Definite proof for this theory is, however, lacking; and the older theory, that the intimal cells are destroyed by toxic products in the circulating blood or in the lymph that bathes them, explains as many of the conditions. In the smaller vessels a small patch of calcification or even an area of intimal swelling from fatty degeneration has much more effect on blood flow than in the aorta, and may occlude a sufficiently large part of the lumen to cause more or less ischsemia and impairment of function of the organ sup- plied, which is permanent in the case of calcification but may be temporary if due to fatty degeneration. ARTERIOSCLEROSIS. 333 i Acute Aortitis and Acute Arteritis. In septicaemic conditions when large numbers of virulent cocci or bacteria are circulating in the blood, or in arteries in the vicinity of abscess-cavities or local infections, it is but natural that some of them should at times lodge and proliferate in the vasa vasorum, and thus give rise to acute inflammatory processes in and about them, following into the media and giving rise to lesions in all three coats of the artery. The elastic fibres degenerate exactly as in luetic arteritis, and mycotic aneurisms may result. The intima may undergo necrosis, the endothelium degenerate, fibrin fer- ment be liberated from it into the lumen, and thrombosis of the vessel may take place (thromboarteritis acuta, Ziegler). In less severe infections the lesions may heal, and the areas of degeneration be replaced by fibrous tissue. In other acute infectious diseases, especially those which are severe, the intima alone may undergo necrosis and be covered with elevated white gelatinous patches (acute gelatinous aortitis, described by Cornil and Ranvier and the subsequent French writers) . Vegetative Endarteritis. In some cases, especially in those in which there is a severe endocardial lesion involving several valves at once, the vegetative process may extend upward into the aorta and give rise to vegetations which arise out of the intima exactly as vegetations upon the valves arise out of the endocardium (endarteritis verrucosa). They may be produced during the course of severe infections, as in one case reported by Nauwerck and Eyrich; they may be found in cases of very chronic endocarditis without other signs to indicate their presence. The condition is homologous with endocarditis of the more severe grade, notably with chronic infectious endocarditis. Endarteritis Productiva seu Obliterans. Complete obliteration of the lumen of an artery by the proliferation of connective tissue which passes out from the intima is a normal process in certain arteries, notably the umbilical and hypogastric arteries and the ductus arteriosus; and it also represents the normal method of healing a wounded vessel. The studies of Thayer and Fabian quoted above show that a certain amount of thickening of the intima (endarteritis productiva) is also a normal process as age advances; and similar changes represent one of the most com- mon forms of pathological change in arteries all over the body, particularly in those of the muscular type, in which it is frequently accompanied by mesarteritis. The lesion consists of a gradual thickening of the intima by proliferation of both the fibrous and the elastic tissue until it encroaches upon the lumen of the artery (endarteritis productiva) or actually obliterates it (endarteritis obliterans). In some cases the lesion is secondary to a mesur- teritis, the infiltration and the vasa vasorum penetrate the entire media, destroy the elastica interna and penetrate into the intima, as Koster described, while in others the connective tissue is laid down layer by layer in response to some chemical stimulus which enters from either the lumen of the artery or the lymph spaces that bathe the intima. Thoma's theory, that this pro- liferation is a compensatory one in response to increased pressure, in order to retain the lumen of the artery, is disproved by the experiments of Jores, who showed that dilating the vessels of the leg by cutting the srhitic nerve is not followed by sclerotic changes. 334 DISEASES OF THE HEART AND AORTA. Endarteritis productiva occurs to a somewhat greater extent in the peripheral arteries than in the aorta, in the latter only in patches, while in the former it may be diffuse. Hypertrophy of the Media (Arterial Hypermyotrophy, Savill). While trying to explain the rise of blood-pressure in chronic interstitial nephritis upon the basis of diminished blood flow through the kidneys, George Johnston in 1873 called attention to the fact that there is a direct relation between hypertrophy of the heart and hypertrophy of the muscular walls (media) of the small arteries (the arteriocapillary fibrosis of Gull and Sutton), not only of the kidney but also throughout the entire body, and especially those of the skin and mucous membranes, the constriction of which causes the high blood-pressure. This observation has received ample confirmation, especially by writers of the British school, by Savill, Russell, and Sir Clifford Allbutt. F. Parkes Weber claims that it bears the same relation to arteriosclerosis that cardiac hypertrophy bears to cardiosclerosis. The clinical importance of this arterial hypertrophy is best shown by the fact that hypertrophy of the media was present in every one of the Savill's 257 autopsies on patients who had during life presented circulatory symptoms without valvular disease, though in many it was associated with other forms of arterial lesion. Savill states that in these cases without marked endarteritis " the vessel loses some of its pliability, remains unduly patent, and does not collapse as a normal artery should. . . . The increase in muscular tissue takes place in length as well as in thickness, so that the artery becomes tortuous." The hypertrophy of the media is w r ell marked in the radials, but best in the arteries of the lower extremity, which, owing to the influence of gravity, are under the highest pressure; and, on the other hand, it is relatively slight in the cerebral vessels, probably owing to their elevation when the body is erect. Savill believes that the absence of hypermyotrophy in these arteries is responsible for the relative frequency of cerebral hemorrhage. Savill dis- tinctly states that, though common in chronic nephritis, arterial hypermy- otrophy is by no means universal in that condition. Jores, on the basis of a relatively small series of carefully investigated cases, has claimed that hypertrophy of the heart and the presence of extremely high blood-pressures is confined to the cases of small red kidney in which an intracapsular fibrosis about the loops of the glomerular capillaries represents the predominant lesion, and the lesions of the tubules are less marked. In primary tubular nephritis, even when the glomeruli are greatly injured, he finds no hypertrophy of the heart nor elevation of blood-pressure. On the other hand, it has been shown by W. Russell, and later by Jane- way and Park, that changes in consistency of the arterial wall may be respon- sible for great changes in the compressibility of the artery and therefore for errors in the determination of blood-pressure; and it is most likely that this form of disease is largely concerned. It is, indeed, not impossible that the extremely high figures for blood-pressure in this condition may be due in part to those changes in the internal wall, and may be often apparent rather than real. Syphilitic Mesaortitis and Mesarteritis. While Lancisi and the writers of the early part of the nineteenth century noticed the association of aneurism ARTERIOSCLEROSIS. 335 and weakening of the arterial wall with syphilis, it remained for Francis Welch to point out the existence of a well-defined type of aortitis of syphilitic- origin. He noted that these lesions were usually confined to definite zones of the aorta, most commonly near the sinuses of Valsalva or encircling the first part of the aorta, but sometimes confined to the transverse arch or to the de- scending aorta just above the diaphragm. The areas of change in the aorta end abruptly, and the rest of the vessel is almost always clear (Fig. 154 B). These lesions are composed of patches over which opaque elevated nodules alternate with punched-out depressions, which, as Dohle puts it, are as uniform as if punched out with a stamp. The fibrous plaques are elevated above the areas in which the media is normal. Heller and his pupils Dohle, Moll, and Isenberg have shown that the histological picture of these lesions is quite as characteristic as their gross appearance. They represent the prototype of the form described by Koster, sleeve-like infiltrations about the vasa vasorum, along which, as the recent observations of Schmorl, Klotz, and Wright and Richardson have recently shown, the spirochaetes (treponema pallidum) lodge in the vessel wall. When this invasion is recent, the lesions consist chiefly of small areas of necrosis infiltrated with lymphocytes, plasma cells, and here and there a few giant cells and miliary gummata. According to the observations of Wright and Richardson, the spirochsetes (treponemata) are most numerous in the areas of necrotic tissue, and " their numbers and distribution in the lesions would suggest that they rapidly multiply at a given point, produce necrosis, and then degenerate and disappear." The necrosis is especially marked in the elastic tissue and muscle-fibre of the media, which fragment, degenerate and are then absorbed. As the spirochsetes disappear, the cellular infiltration is replaced by fibroblasts and these in turn by fibrous tissue, so that in the older lesions the media is seen to be broken up by coarse bands of fibrous tissue which pass along the vasa vasorum and may reach into the intima. Miliary or submiliary gummata are sometimes present in the areas of fibrosis. The elastic and muscle fibres are fragmented, entirely destroyed in the path of the invasion and are replaced by the above-mentioned fibrous tissue. The latter is entirely rigid; but the intervening areas of elastic or muscular tissues contract, and when the artery is opened " appear as areas of depres- sion between the elevated areas of fibrosis. This is the exact opposite of the conditions in inflammations of the intima, in which the diseased portions are the elevated ones; and moreover it applies only to pure mesarteritis, for in many cases the latter is accompanied by plaques of endarteritis as well as fibrosis. W^hen the blood is circulating through the artery, however, condi- tions are reversed, for then the strong elastic and muscular tissue resists the pressure better than the weaker and distensible elastic tissue; and the arras of the latter bulge outward or may even appear as definite aneurisms, tor it is this form of arteriosclerosis from which aneurisms arise. The process of fibrosis may also be accompanied by a gradual prolifera- tion or obliterating of the vasa vasorum, by which the nutrition of the corre- sponding areas of arterial wall is still further cut off. This, as Klolz has claimed, probably causes ischsemia and secondary changes in the corre- sponding areas of intima, so that necrosis, atheromu, and in the more slowly developing cases proliferation of connective tissue (endarteritis progressiva 336 DISEASES OF THE HEART AND AORTA. sea obliterans) results. There is thus an endarteritis of the vasa vasorum giving rise to endarteritis of the vessel itself. Clinically, as Welch, Heller, and a host of subsequent observers have shown, syphilitic mesaortitis is particularly likely to affect the first part of the aorta, especially in young men, and to be confined to this zone or at least to extend.no further than the transverse arch. The lesions are especially prone to extend downward into the sinuses of Valsalva and produce constric- tions about the mouths of the coronary arteries, thus giving rise to cardiac weakness and angina pectoris. Somewhat more commonly the same process extends over to involve the cusps of the aortic valves themselves, causing deformation and shrinkage of the latter with the development of the very common syphilitic form of aortic insufficiency. Syphilitic aortitis is therefore of great clinical importance, and, though less common than endarteritis, is more prone to give rise to striking clinical entities, and thus to attract the attention of the clinician. Another common form of the luetic lesion is the formation of a band or collar about the descending aorta just above the attachment of the diaphragm, leaving the rest of the aorta clear. This is the zone from which aneurisms of the descending aorta often arise. Moreover, common as are the luetic involvements of the aorta, it is still more common for the spirochsete to be filtered out in the smaller periph- eral, visceral, and cerebral arteries, where their distribution determines the various pleomorphic lesions of the disease. In these arteries the histological picture is quite similar to that in the aorta, except that, as the media is thinner, the necrotic and sclerotic processes extend more readily to the intima and a more severe grade of endarteritis results, often to the complete obliteration of the lumen. Non-syphilitic infective mesaortitis and mesarteritis also occur, but, as in the non-syphilitic cirrhosis of the liver, the strands of infiltration and fibrosis are much less coarse than in those of syphilitic origin, giving rise to less weak- ening of the arterial wall, and are less striking in the pictures which they present. In the arteries of rheumatic patients Klotz has found " small areas of medial fibrosis which in many respects simulate the sclerotic patches in the heart described by Aschoff. During the progressive stage of these lesions narrow lines of cellular infiltration are seen along the small capillaries in the adventitia and also in the media. The larger arteries and arterioles of the media do not share this infiltration. Moreover, the inflammatory process is limited to a narrow zone just along the vasa vasorum. Frequently this infiltration is only a few cells deep." As healing goes on this becomes replaced by a strand of fibrosis. Arterial changes affecting all throe coats have been described in typhoid fever by Landouzy and Siredey, Thayor, and numerous other observers. The cells of the intima become raised, swollen, and desquamated; the elastica interna is injured. The layers of the media are infiltrated with mononuclear cells; and the vasa vasorum of the adventitia are surrounded with dense infiltrations, .similar to those seen in myocardial lesions. Klotz has found that in this disease the mesarteritis is less extensive than in rheumatism, but a different light is thrown upon his findings by the over- ARTERIOSCLEROSIS. 337 whelming mass of clinical evidence brought forward by Landouzy and Siredey and by Thayer. The apparent discrepancy is probably due to the fact that, as Landouzy and Siredey have claimed, typhoid fever not only produces immediate lesions but exerts an especially marked effect in lowering the resistance of the arterial wall to subsequent infections and intoxications. In scarlet fever Klotz found small areas of necrosis of the media lying about the vasa vasorum which had been obstructed by agglutinative thrombi ; and these, on subsidence of the infection, are readily replaced by areas of fibrosis. Similar infiltrative and fibrous changes occur in other infectious diseases. Degeneration and Calcification of the Media. Marchand and, later, Moenckeberg have called attention to the fact that the ordinary rigid " pipe- stem," "beaded," or " goose-neck " arteries of old are produced by a special form of arteriosclerosis, which occurs only in arteries of the muscular type. This type is characterized by a pure medial sclerosis (mesarteritis) or, more accurately, a necrosis (arterionecrosis), most marked in the deeper layers of the media, accompanied by fatty changes, necrosis of the elastic and muscle fibres and especially by the deposition of calcifications in masses in the necrotic areas and in rows of fine granules between the elastic and muscle fibres. These calcifications often follow the transverse fibres around the artery in rings, which cause it to give to the palpating finger a sensation like that of a goose's trachea. Occasionally, especially when the calcification is of long duration, ossi- fication takes place in the calcified areas, with the formation of true bone in the walls of the arteries. Calcareous mesarteritis is very common in the femoral, radial, temporal, and dorsalis pedis arteries, and, owing to the striking changes in the walls of the arteries, it represents the most easily diagnosed of all the forms of arterio- sclerosis. On the other hand, since it attacks only the arteries of the muscular type, its presence furnishes no clue to the condition in the aorta. It is usually much more marked in some arteries than in others, and hence, although changes of this type may go on in the coronary arteries, these also cannot be prophesied from the condition of the radials. For the same reason, the most extreme changes of this type may be noticed in the radials of patients whose blood-pressure is absolutely normal, or even below normal, owing to the fact that the changes in the arteries are purely local ones. Periarteritis. The most striking form of inflammation of the adventitia is the so-called periarteritis nodosa (Kussmaul and Mayer, 1865), or supra- arterial fibroid nodules; small grayish nodules 1-2 mm. in diameter, located along the course of the vessels affected, most commonly the coronary, renal, or mesenteric arteries, though it also occurs along the arteries of the muscles, the stomach, the genitalia, diaphragm, peritoneum, and more rarely in the cervical arteries, bladder, adrenals, brain, lungs, and pleura (Moenckeberg). The lesions are frequently accompanied by the formation of small multiple aneurisms, owing to the weakness of the medial coat. Histologically the lesions consist of areas of fibrous tissue occurring along the course of the vasa vasorum and represent processes very similar to those which occur within the media in infective mesarteritis. ing difference is that, whereas the fibrosis of mesarteritis replaces a dense. 338 DISEASES OF THE HEART AND AORTA. PLATE X. A. INT. MED. Endarteritis with thickening of intima in a patient dying from typhoid fever without complications. Degeneration of the media of a cerebral artery, showing destruction of the elastic fibres, which are stained black. c. Radial artery showing great hypertrophy of tunica media. (After W. Russell.) ARTERIOSCLEROSIS. PLATE X. D. E. 339 INT MED ADV ADV MED Syphilitic aortitis showing destruction of the elastic fibres in the media and their Mononuclear infiltration along the course replacement by fibrous tissue: INT, intima; of the vasa vasorum of s-dventitia and media in MED, media; ADV, adventitia. syphilitic aortitis. F. G. **.-' >5 rv jr.. Endarteritis productiva ot obliterans in the vasa vasorum and periarteritis of the latter in a case of syphilitic aortitis. 340 DISEASES OF THE HEART AND AORTA. tissue already formed, the fibrosis of periarteritis represents a new formation which is located in a very scant amount of loose tissue and rises exuberantly above it. The inflammation usually extends further along the vasa vasorum into the media, whose elastic and muscle fibres it destroys, and passes into the intima to produce an area of proliferative endarteritis. As regards etiology, Kussmaul and Mayer, Chvostek and Weichselbaum, Miiller and Graf, regard syphilis as the most common cause, while Fletcher, v. Kahldan and a host of others, among them Moenckeberg, describe cases in which lues could not have played a role. Intes- tinal intoxication, congenital weakness of the vascu- lar tissues, polymyositis and polyneuritis, all seem to play roles in certain cases (Moenckeberg). Tuberculous Arteritis and Aortitis. In the ordinary forms of chronic tuberculosis the only change in blood-vessels outside the area of the lesion is, as a rule, the presence of small areas of fatty degeneration in the cells of the intima and media (Frothingham). It is only in the more severe forms of tuberculous infection when the germs are circulating freely in the blood that diffuse arteritis occurs. In localized tuberculous lesions the bacilli may gradually invade the walls of the smaller vessels per extensionem, and it is, as a rule, the rupture of tubercles in the intima of one of the smaller vessels that gives rise to generalized tuberculosis. In the latter condition the presence of miliary tubercles in the walls of the vessels is not infrequent, particu- larly in the small pulmonary vessels and in the small meningeal branches in tuberculous meningitis. Tubercles in the wall of the aorta, on the other hand, are rare, and Woolley, who has recently reviewed the subject, has found accounts of only ten cases besides his own. In most of these cases the tuberculosis arose by extension from tuberculous lymph-glands, but in several the lesions existed in the form of solitary tubercles of the intima, measuring from one to four centimetres and occasionally surmounted with polypoid growths. In all these cases the tubercles contained very large numbers of tubercle bacilli, so that their rupture might easily give rise to a wide-spread infection. FIG. 156. Arte sclero of the descending art:i, show- ing atheromatous plaque.-). ETIOLOGY. The most important etiological factors in the production of arterio- sclerosis in man are age, hard work, alcohol, syphilis, and the more acute infectious diseases, especially typhoid fever. The relative frequency of those causal factors, as indicated by the palpability of the radial artery in ARTERIOSCLEROSIS. 341 4000 consecutive cases admitted to the Johns Hopkins Hospital, has been made the subject of a careful study by Thayer and Brush. These observers found palpable arteries in the following percentage of the patients under fifty years who had been subject to various etiological factors: After scarlatina, radials palpable in 16.4 per cent. No causal factor, radials palpable in '. . 10.5 p er cent. Pneumonia, radials palpable in 17 p er cent. Diphtheria, radials palpable in 17 p er cent. Malaria, radials palpable in 20 per cent. Typhoid fever, radials palpable in 26 per cent. Rheumatism, radials palpable in 34 per cent. Alcohol, radials palpable in 46.8 per cent. Hard work, radials palpable in 57.5 per cent. Richard Cabot takes exception to these findings of the high frequency of arteriosclerosis after alcohol, basing his conclusions upon autopsies of dipsomaniacs under fifty, in whom he says arteriosclerosis was not present in more than twenty per cent. His exceptions to Thayer's findings are, however, somewhat against the general consensus of opinion, as well as against the experimental evidence of Aubertin, who produced arteriosclerosis and cardiac hypertrophy in rabbits by the injection of alcohol. On the other hand, Cabot is supported by Fahr, who performed 309 autopsies on habitual drunkards dying at the Harbor Hospital of Hamburg and found arteriosclerotic changes no more common than in abstemious indi- viduals, occurring in 95 cases, 82 of whom were over 40 years of age. Only 7 drunkards in his series died before 40 from causes referable to arteriosclerosis. Similar changes existed in only six other persons under 40. Unlike Aubertin, Fahr was unable to produce arterio- sclerosis in rabbits by administration of alcohol for over two years. From this it would appear that the evil effects of alcohol have been considerably exaggerated, at least as far as the arteries are concerned. It must be borne in mind that indulgence in a certain amount of alcohol i.s almost universal, especially in thosa persons who do hard work, hence it is extremely difficult to segregate these factors in any large number of cases. If, for example, a patient has had typhoid fever, has used alcohol, and has done hard work, it is not logical to enter his name into each of the three columns, for it is not possible to deter- mine which of the factors is the most important. Fortunately, however, for the decision of these doubtful points, the experiments of Pic and Bonnamour (1. c.) upon experimental adrenalin arteriosclerosis have shown that where two factors are acting together, arteriosclerosis may be pro- duced in conditions in which it could not be brought about by one of them alone. Thus, tuberculosis + adrenalin yielded arteriosclerosis in young rabbits which would not have shown arteriosclerosis after adrenalin alone, and there is no doubt that the same is true in man. Syphilis, as stated above, is an important factor, especially in persons under the age of thirty-five. Pearce (Arch. Int. Med., 1910, vi, 478) has tabulated the results of a large number of observers, showing the "\Yasser- mann reaction positive in 57 cases of mesaortitis, negative in 70; positive in 29 cases of endaortitis, negative in 214; in aortic insufficiency, positive in 85, negative in 122. Collins, Sachs, dough, Guthrie, Longcope, and others call attention to its great frequency in the sclerotic form. Worry and continued pain have long been regarded 1 clinicians as causes of arteriosclerosis, but a physiological basis for this belief was not found until Cannon and de la Pax (Am. J. Physiol., 1911, xxviii, (i-4) showed that the blood obtained by catheter from the adrenal vein of a cat excited by the presence of a dog contained more adrenalin than that obtained when the animal was quiet. 342 DISEASES OF THE HEART AND AORTA. Lead poisoning (especially chronic plumbism) and gout are important etiological factors, as is also chronic nephritis. Overeating is thought to play an important role, especially when the diet is rich in meats, sweetbreads, livers, kidneys, etc., in other words, in purin bodies and in kreatin. The exact role of these substances has not been carefully studied, although Croftan found that long-continued injection of 0.5 to 5.0 mg. xanthin into rabbits caused a rise of forty millimetres in blood- pressure, as well as sclerotic changes at least in the renal arteries. (He does not describe the condition of the other arteries.) From the stand-point of both blood-pressure and gaseous metabolism it has been shown that the digestion of large meals materially increased the work of the body, pro- ducing thereby an effect not dissimilar to that of hard physical exercise (increase in pulse-pressure, increase in pulse-rate, increase in CO 2 output) (effect of large meal, after Erlanger and Hooker). It is therefore quite nat- ural that overeating should rank with hard work as a main cause of arte- riosclerosis, but the exact extent of its occurrence is more difficult to deter- mine in a large series of cases than in an individual case in private practice. Lastly, and still more important in the etiology of arteriosclerosis, are age and heredity (Israel). Thus, Osier states that "entire families sometimes show this tendency to early arteriosclerosis, a tendency which cannot be explained in any other way than that in the make-up of the machine bad material was used for the tubing." This is especially true as regards alcoholism, as has been shown in a recent statistical study by Emerson, who found that this factor was of more importance than the drinking of alcohol by the individual himself in determining arteriosclerosis and longevity, and that an alcoholic ancestry was very frequently followed by a generation with a tendency to early arteriosclerosis. Experimental Arterionecrosis in Animals. A most interesting side light upon the genesis of arteriosclerosis has been thrown by attempts to produce it experimentally in animals, especially in rabbits and guinea- pigs. The lesions which have been produced cannot be termed true arterio- sclerosis like that seen in man, but are confined to the media and adventitia, the intima always remaining clear. The reason for this is not evident. Even the possibility that in these small animals the blood supply of the arterial wall is different from that in man, and that owing to this difference lesions occur most readily in the media, does not hold, since Ophiils has demonstrated the occurrence of spontaneous endarteritis in rabbits. The experimental and clinical conditions seem to be closely analogous, but it is not possible to draw an absolute parallelism between them. Gilbert and Lion have been able to produce arteriosclerosis experimentally in ani- mals by the injection of bacterial toxins, and this has been confirmed by Klotz. This fact is of great importance, not only from the stand-point of experimental arterio- sclerosis, but also because it establishes the importance of bacterial disease in the etiology of arteriosclerosis met with clinically. The earliest observation of arteriosclerosis brought about by toxic action of organic compounds, and one which establishes beyond doubt the deleterious action of tobacco upon the arteries, is that of Isaac Adler, demonstrating sclerosis in the smaller peripheral arteries of rabbits as a result of feeding them with infusions of tobacco. Boveri confirmed these results by giving infusion of tobacco by stomach-tube, and obtained atheromatous plaques or thickening at the base of the aorta in ten out of sixteen rabbits, while Baylac obtained sclerosis in each of eight rabbits into which tobacco infusion was injected either intravenously or subcutaneously. Jebrowsky and later W. E. Lee have produced it in rabbits made to inhale tobacco smoke. From Baylac's experiments it would appear that ARTERIOSCLEROSIS. 343 in general the liability to occurrence bears some relation to the channel by which it enters the body. This may explain the very marked action of tobacco inhaled and entering the heart directly from the pulmonary circulation in smokers, as compared with the somewhat milder effects of chewing tobacco, under which condition the nicotine passes through and is perhaps somewhat attenuated in the liver before entering the systemic circulation, and has still to pass through the vena? cava), right heart, and pulmonary circulation before reaching the coronary circulation. In smoking, however, the nicotine enters through the lungs and strikes its first blow at the coronary a/teries and base of the aorta, where the elastic fibres are under the greatest tension and hence most liable to degeneration. It is therefore, easy to understand why smoking of heavy cigars should be one of the most potent factors in the etiology of arteriosclerosis and coronary sclerosis. An almost new era in the study of arteriosclerosis was, however, introduced by the discovery of Josue that the repeated intravenous injection of adrenalin into rabbits brought about sclerosis and calcification in the aorta within a few weeks. This was very soon confirmed by W. Erb, Jr., who produced the lesions in a large number of animals, and demonstrated the considerable uniformity with which such lesions fol- lowed the injections. Similar results have been obtained in rabbits by Fischer by the intravenous injection of a very large number of substances, h ydrochloric acid, phosphoric acid, lactic acid, calcium phosphate, chloralamide, mercuric chloride, trypsin, diuretin, and physiological salt solu- tion, so that the effect can scarcely be considered as specific for adrenalin. 1 On the other hand, Pic and Bonnamour, as well as Adler and Hensel, have called attention to the fact that in none of the series of experiments published did more than a certain number of the animals injected show lesions, and in a very large series the latter showed that it was practically impossible to produce arteriosclerosis in rabbits by these poisons until they had attained a certain age. After that age arteriosclerosis occa- sionally occurred spontaneously, but could be brought on with considerable frequency by the injection of toxic substances. As stated above, Pic and Bonnamour have, however, been able to produce it in young animals whose vitality was diminished by tuberculosis, etc., indicating that disease may be an accessory factor in diminishing the resistance of the arteries to toxic influences which ordinarily leave no traces. This carries the clinical corollary that persons liable to arteriosclerotic changes should particularly avoid all con- tributing factors (alcohol, tobacco, hard work, etc.) for some time after infectious diseases. It is quite remarkable that Pearce and Baldauf, as well as other investigators, report that they have been able to produce arteriosclerosis, and that Josue" claims to have produced permanent elevation of blood-pressure in rabbits by a single injection of adren- alin, since Fleisher and Loeb failed to do so in a large series of experiments in which such injections did produce severe myocarditis. Mechanism Producing Experimental Arteriosclerosis. The mechanism by which arteriosclerosis is produced has been the object of considerable study. In the case of adrenalin at least, Erb believes that a spasm of the vasa vasorum takes place, bringing about an insufficient blood supply to the coats of the vessels, and thereby ischsemic degeneration of the latter, especially of the tunica media. This view was also shared by Pearce and Stanton and other observers, but Fleisher and Loeb have shown that considerable areas of aorta may be kept ischaemic by com- pression without producing arteriosclerosis. The factor must , therefore, be toxic. It is possible that in some cases with high blood-pressure actual rupture of the weakened elastic fibres takes place, which serves as a centre for areas of necrosis. \V. 1 1. Harvey has shown that if bits of excised aorta are filled with agar under various pressures and then transplanted into subcutaneous tissue, those under tension degen- erate more rapidly. The same is probably true of the fibres within the artery. Moreover, Josue has shown that repeated injections of adrenalin in the rabbit are followed by permanent rise in blood-pressure. An increase in blood-pressure is indeed the rule in arteriosclerosis, although, as Hasenfeld has pointed out, it occurs mainly in persons whose sclerosis involves the splanchnic arteries. Neither increase in blood-pressure nor hypertro- phy of the heart necessarily occurs in patients where these vessels are not involved. The J A summary of the recent literature upon this point will be found in the papers of Saltykow, Adler, and Benda. 344 DISEASES OF THE HEART AND AORTA. reason for this may be that the cutting down of the circulation of so large an area a the splanchnic region in itself increases the resistance to blood flow and thereby raises pressure. There is also no doubt that, besides the single artery involved in the sclerosis, the latter is often the result of prolonged vasomotor spasm in the femoral artery, etc. On the other hand, such spasm may be transitory and be accompanied by temporary rise of blood-pressure and sensory phenomena which cause the syndromes described by Pal as vasomotor crises (see page 356). Aubertin, Vaques, Wiesel, and others have found hyperplasia of the adrenals present in many experimental and clinical conditions in which hypertrophy of the heart and high blood-pressure are present. It therefore seems quite possible, in the light of these findings, that hypertrophy of the heart and arterio- sclerosis may often be the result of a hypersecretion of adrenalin, perhaps also of some other internal secretions. Why this should be associated with splanchnic arteriosclerosis is easy to see. The latter condition tends to diminish the circulation through the abdominal viscera, and more blood is thus shunted through the adrenal arteries which lie just above the mesenteries, thus bringing about an increase in adrenal secretion. It may be added that Bayer, in Krehl's clinic, has shown that some- times the high blood-pressure is, in part at least, dependent upon the amount of salt in the food, being low on salt-free and high on diet rich in salt, though this is by no means the rule. DISTRIBUTION OF ARTERIOSCLEROTIC LESIONS. As regards the distribution of arteriosclerotic lesions and its relations to etiology, Harlow Brooks has given the following statistical summary based upon notes of autopsies on 400 cases: Artery. Cases. Etiological factors. Aorta 400 301 Alcohol 149, among laborers 118, nephritis 51, syph- ilis 38, old age 38. Males 275, females 125. Visceral trunks 368 Coronary arteries 270 Alcohol 107, nephritis 35, svphilis 27, excessive Brain 132 tobacco 9. Alcohol 48, nephritis 21, svphilis 19. Renal 81 Alcohol 43, nephritis 10, svphilis 10. Pancreas 74 Alcohol 19, svphilis 9, senilitv 9. Hepatic 43 Alcohol 12, nephritis 8, syphilis 6 senility 3 Splenic 35 Alcohol 9, svphilis 7, nephritis 4, endocarditis 2 Lungs senility 2, tuberculosis 2. Svphilis 5, senility 5, alcohol 4, tuberculosis 4 Cooliac axis and branches. . Spinal vessels 19 20 nephritis 2. Most of them with alcoholism. Sclerosis of mesen- teric, all cases with adiposis. Alcoholic 4, svphilitic 4, most of the rest in primary spinal diseases. ARTERIOSCLEROSIS IN THE YOUNG. Arteriosclerosis in infants, children, and young persons while rare is not extremely so. According to Fremont Smith, who has given an excellent review of the subject, congenital syphilis is the cause in about forty per cent, of the cases, and diphtheria, scarlet fever, and typhoid fever, as well as infections in the mother during pregnancy, are impor- tant factors. The blood-pressure is not usually elevated, often being as low as 70 mm. Hg. The writer has seen one case of a boy aged six suffering from acute nephritis, com- ARTERIOSCLEROSIS. 345 plicated by lobar pneumonia, large bacillus coli abscess of the buttocks, cystitis caused by the same germ, who in spite of continuously low blood-pressure developed tortuous and apparently thickened temporal and thickened radial arteries. After a few months these arteries were no longer palpable. It is possible that these changes may have been merely mononuclear infiltration about the vessels of the adventitia. CLINICAL MANIFESTATIONS OF ARTERIOSCLEROSIS. Clinically, the symptoms due to arteriosclerosis usually express themselves in several groups dependent upon the arteries most affected. (1) Cardiac, associated with myocarditis and coronary sclerosis; often with renal symptoms (see Chapter IX). As shown by Fleisher and Loeb, the myocarditis may be produced by the same cause and may be more severe than the arteriosclerosis itself. (2) Simple coronary sclerosis, paroxysmal dyspnoea, angina pectoris, Adams-Stokes syndrome, paroxysmal tachycardia, sudden death. Cerebral symptoms. Aneurism. (5) Intermittent claudication. (6) Vasomotor crises (Pal) : (a) Abdominal pain from vasoconstriction; (6) Raynaud's disease; (c) Pain down arms and legs. The clinical characteristics of the cardiac and renal cases have been discussed in Chapter I X under the head of the myocarditis which invariably accompanies them. They may be briefly summarized as short- ness of breath, especially on exertion, often asthmatic or paroxysmal in character; palpitation; weakness ; occasionally a considerable degree of nervousness, loss of memory, and insomnia. In advanced cases with some sclerosis of cerebral arteries there may be more or less transient irrationality, especially at night or on awakening. There may be pains over the precordium, in the shoulders, or down the arms, or in the abdomen or legs, which may be definitely associated with periods of high blood-pressure (the vasomotor crises of Pal) ; there may be sudden p a i n and sudden paralysis of a leg, disappearing on rest, reappearing after a few steps are taken (intermittent claudication, Charcot, Erb) ; or there may be severe precordial pain with a feeling of weight and constriction over the sternum and an utterable fear of impending death (angina pectoris). On the other hand, the hand or foot may become cold or n u in b , the pulsation disappear from the arteries, intense pain set in (Raynaud's disease), or finally be followed by gangrene (thromboangitis obliterans). Still further the patient may suffer from all the signs and symptoms of aneurism. On physical examination the radial arteries may or may not be found to be thickened or beaded (atheromatous), 1 dependent partly upon the distribution of the sclerosis, since the radial artery may be spared. Some writers state, however, that in men who do hard manual labor the radial arteries are the first attacked, while in those who lead a sedentary life sclerosis may appear very early about the base ot the aorta, and the radial, nevertheless, may be perfectly normal. 1 Wertheim Salamonson (Arch, dos malad. du cu>ur, 1910, iii, OSS) recommends feel- ing the wall of the artery with the finger-nail instead of the linger. 346 DISEASES OF THE HEART AND AORTA. The artery in which the sclerosis is next most readily observed is the temporal, which usually stands out like a cord or is very tortuous, and when pressed against the bone feels thickened and leathery. This tortuosity may also be present in the brachials and even in the abdominal aorta, and is probably brought about by the stress of the arterial tension exerted upon the walls, which are in some places weaker and less elastic than in others; so that we have a force (blood-pressure) which is exerted equally on all sides against walls which interpose a greater resistance on one side than on the other, hence the curvature results. As might be expected, the tortu- ousness is therefore greater when the disturbing force is high (high blood-pressure) and less when it is low, as shown in the figure (Fig. 157). Other superficial arteries which may be felt are the brachials, axillaries, facials, popliteals, and dorsalis pedis. Changes in the Retinal Vessels. Hirschberg in 1882 called attention to the fact that changes in the retinal vessels constitute an early sign of arteriosclerosis, and later demonstrated that this change was normal in old persons and usually began in the fifth decade. Friedenwald and Preston exam- ined twenty-three persons suffering from general arteriosclerosis, and found only seven normal reti- nas among them. De Schweinitz gives the following criteria for sclerosis of the retinal vessels: (1) Suggestive Signs. Uneven caliber and undue tortu- ousness of the retinal arteries (corkscrew form), increased dis- tinctness of the central light streak, an unusually light color of the artery, and alterations in the course and caliber of trie veins. (2) Pathognomonic Signs. Changes in si/e and breadth of the arteries, loss of translucency, lesions in the arterial walls consisting of white stripes in the form of perivasculitis, inden- tation of the veins by the stiffened arteries, tortuousness of veins and white stripes or varicosities along their courses, oedema of the retina in the form of gray opacity around the disk or following the course of the vessels, hemorrhages as linear extravasations or roundish infiltrations. Sometimes very sudden changes in the caliber of the retinal arteries may be seen accompanying vasomotor crises. X-ray Examination. Absolute proof of arteriosclerosis is also given by the X-ray, by which calcified plaques along the course of deeply situated arteries (popliteals, femorals, abdominal aorta, etc.) may be discerned as distinct shadows ranged along the course of the artery. These may be brought out more distinctly by using two stereoscopic pictures instead of one. Unfortunately, it has not been possible to discern sclerosis of the coronary arteries in this way. Sclerosis of the Abdominal Aorta. Arteriosclerosis of the abdominal aorta and splanchnic vessels is very common, as has been shown by Hasen- fold, Bond, Brooks, Ortner, and Gilbride. In fact, it may almost be diagnosed with certainty when the blood-pressure is elevated. Occasionally the course of the abdominal aorta may be felt to be tortuous. Sclerosis of the abdom- FIG. 157. Tortuous radial artery. (After Pal.) Solid line, course of the radial artery at 200 mm. Hg blood-pressure. Broken line, course of the ar- tery at 95 mm. blood-pressure, after amyl nitrite. A a Fir,. 158. Retinal changes in arteriosclerosis. A, Normal fundns. 1? to F, successive changes occurring in arteriosclerosis, including pallid arteries (B), later assuming a silver-wire appearance (C); indented veins (B, C), afterward showing ampulliforrn enlargements (I), K); corkscrew capillaries (C, D); corkscrew arteries and veins (D, E); perivasculitis (C, D); sclerosis of vessels (F); irdema of disk (B, C, D, E). hemorrhages (C F). D. (After de Schweiiiitz.) ARTERIOSCLEROSIS. 347 inal vessels is not infrequently accompanied by great flatulence with pains not unlike those of tabes (abdominal vasomotor crises), but these may also be present from simple pulsation of the abdominal aorta when tugging upon loose peritoneal moorings. Sclerosis of the pancreatic artery is often accompanied by diabetes mellitus. BLOOD-PRESSURE AND PULSE. In arteriosclerosis the mechanical factors affecting blood-pressure tend to approach those in a system of rigid tubes, a high pressure through- out systole, a low pressure in diastole. In such a system we should have, as a rule, a greater difference between pressure in systole and in diastole than when the normal elasticity tends to keep up the diastolic pressure, so that the pulse-pressure is often more than 50 to 60 mm. rather than being nearer 30 or 40 mm. as in the normal individual. FIG. 159. Effect of arteriosclerosis upon the circulation. I, normal. II, arteriosclerosis, with high peripheral resistance and anacrotic form of pulse wave; the arrow points to a rise in maximal and minimal pressure and increased pulse-pressure. Ill, arteriosclerosis with low peripheral resistance, showing low blood -pressure and increased pulse-pressure and collapsing pulse. (Compare with Fig. 26.) Pulse. The pulse may assume any form whatever, from collapsing and almost water-hammer in character to an anacrotic plateau, or even in rare cases to a pulsus tardus. These depend upon the relation between strength and size of beat and outflow through the arterioles. Thus, if the peripheral arteries or any large areas of blood-channels are dilated and lacking in elasticity, there will be a momentary rise in pressure at the begin- ning until the pressure wave is transmitted from the aorta to the periphery. When it reaches this point there is a sudden outflow through those vessels and a sudden fall or collapse, which is greater than it would be in a more elastic system (see Fig. 159). On the other hand, if the peripheral outflow is small, the pressure in the non-elastic system quickly rises higher than in an elastic system and remains so throughout systole, forming a systolic plateau (anacrotic pulse) with a large rapid rise and plateau reaching to the end of systole, then a gradual fall during diastole. The pulse form accordingly gives us the information in arteriosclerosis as in other condi- tions (see page 65), namely, indicates low peripheral resistance when it is collapsing and high peripheral resistance when it is anacrotic or sus- 348 DISEASES OF THE HEART AND AORTA. tainecl. The pulse may either be quite large or very small, dependent upon the degree either of vasoconstriction or of endarteritis. Its character may be very variable ; it may be quite quick and collapsing, corresponding to a general rigidity of the whole vascular system, or the vessel may fill rapidly, remain well sustained with long systolic plateau, and may then decline either rapidly or slowly. However, the lumen of the radial artery may have decreased so much from an endarteritis that the filling of the artery is slow and the up-stroke on the pulse-tracing very oblique, just as would be typical of aortic stenosis. This is not extremely common, and the very quick up-stroke is the form most frequently seen. On the other hand, in rarer cases when, as Romberg and also Hasenfeld have pointed out, the splanchnic vessels are not involved, the maximal blood-pressure may be quite normal (110-120 mm.) and the minimal also (90 mm.). Blood=pressure. The blood-pressure is often high. Thayer found in his studies of post-typhoid arteriosclerosis that the maximal blood- pressure was usually 20-30 mm. higher than for normal individuals of corresponding age. Romberg and Sawada, on the other hand, found that this occurred in only 12.5 per cent, of all arteriosclerotics, while Groedel found hypertension in only 37 per cent, of 446 cases of arteriosclerosis free from chronic nephritis. Dunin found similar results. Israel, however, found hypertension over 140 mm. Hg or 180 cm. H 2 O (v. Recklinghausen apparatus) in 64.4 per cent, of 45 cases of arteriosclerosis. The minimal pressure was also increased, but less than the maximal. Israel gives the following average figures: Max. Min. Mean. Pulse-pressure (amplitude). Normal cm. H,O 170 110 140 GO mm. He 125 81 103 44 Arteriosclerosis cm. ILO 240 140 190 100 mm. Hg 177 103 140 74 Average increase mm. Hg 52 23 37 30 Israel's figures accord well with the writer's experience (using the Erlanger apparatus). The highest of these blood-pressures are seen in cases with chronic nephritis (Israel, Jane- way, Horner). The writer has often found a maximal pressure of 220 mm. Hg with a mini- mal of 160, though usually in association with nephritis. 1 As has been seen under cardiac overstrain, the presence of arterio- sclerosis has a marked effect in impairing the bodily strength and the ability to withstand strain. The diminution in arterial bed increases the total work of the heart, and the patches of arterial fibrosis prevent the arteries from dilating under functional activity. On the other hand, the loss of arterial elasticity removes a factor which tends to propel the blood during diastole and thus to maintain the blood flow at the least expenditure of energy by the heart. As a result of this factor, the heart is compelled to increase its systolic output (increased pulse-pressure) under normal condi- 1 Russell has shown that these determinations may be too high in thick-walled arte- ries (see page 2Sj. ARTERIOSCLEROSIS. 349 lions and hence has little ability for further increase in reserve. Muscular effort therefore gives rise to signs of greater strain than in normal individ- uals, greater increase in blood-pressure, and greater fatigue. The intensity of vasomotor reactions varies considerably in different cases of arteriosclerosis. In some cases, as Romberg has shown, the vaso- motor reaction of the arm vessels to cold may entirely disappear; while in others (vasomotor crises) the reactions are so intense as to produce ischiemia of the parts. The Second Aortic Sound. Corresponding to the high blood-pressure there is also accentuation of the second aortic sound, which on the one hand may be due to the heightened blood-pressure and the greater tension of the aortic valves, or, on the other, to the thickening and partial calcification of the valves themselves, which gives rise to a louder sound than usual when the valves strike together, even under the usual pressure. A marked accentuation of the aortic second sound therefore always leads to the suspicion of arteriosclerosis, even in the absence of thickening in the walls of the superficial vessels. However, it is not pathognomonic, since it may often be heard in cases where no special sclerosis is present, especially at times when the heart is acting strongly and probably giving forth a larger output into the aorta at each systole, as in typhoids with dicrotic pulse or in perfectly healthy young persons during attacks of palpitation. In such cases the accentuation of the second sound is transitory. BLOOD COUNT IX ARTERIOSCLEROSIS. The blood count may vary considerably, first on account of the great variety of diseases associated with arteriosclerosis, and secondly, because the latter is sometimes accompanied by polycythsemia or erythra>mia. There are no blood changes which in themselves can be said to be defi- nitely associated with arteriosclerosis. AORTIC SCLEROSIS. When the aortitis near the base of the aorta is marked, and especially if calcified plaques are present, the first sound as well as the second may be changed and may be accompanied by a loud murmur which is usually trans- mitted to the carotid and brachial arteries, resembling that heard in aortic stenosis but less intense. Since the condition is much more common than the latter, this murmur is also more commonly duo to this cause, but- in the absence of the characteristic pulse it is quite indistinguishable from that of aortic stenosis, for both arise at the same site at the same time and are transmitted in the same way. The murmur is often accompanied by a marked thrill having the same distribution and is followed by a distinct diastolic shock. As regards sclerosis of the aorta alone, Bittorf has found that it frequently occurs at an average age of fifty-five (forty-five in syphilitics) as a result of the usual factors: some- times a single trauma to the chest may seem to he the important moment in the etiology. It is especially common in syphilitics and fat persons, and is frequently associated with pale, ashy-gray color, very high blood-pressure (170 to 220 mm.), occasionally difference in size of the pupils, pains over the chest and down the arms, oedema over the sternum, 350 DISEASES OF THE HEART AND AORTA. unilateral dilatation of veins in second and third interspaces, ringing aortic second sound without diastolic murmur, hypertrophy of the heart, often pulsus celer, rarely pulsua tardus or pulsus paradoxus. Cardiac pain may be present, often felt just after percus- sion, and described as something boring through the sternum, sometimes with a feeling of constriction, sometimes radiating to the arms and neck. Occasionally spells of weakness in the arms may be felt not unlike intermittent claudication. The differential diagnosis from aortic stenosis is made by the gradual up-stroke on the pulse tracing in the latter case, as contrasted with the sudden up-stroke and plateau in the former; from aortic insufficiency by the diastolic murmur and high pulse-pressure; from aneurism by the percussion and fluoroscopic findings. R. Knox (Arch. Roentg. Ray, 1910, 147) has been able to recognize atheromatous plaques in the aorta with the X-ray. SCLEROSIS OF THE PULMONARY ARTERY. Sclerosis of the pulmonary artery may occur whenever there is increased work of the right heart, especially in mitral stenosis, emphysema, and phthisis. Giroux (Arch, des malad. du coeur, 1910, iii, 59o) finds that the lesion usually consists of opaque yellow ath- eromatous patches in the arteries near the hilus, rarely in the main trunks; but in the latter there may be a mesarteritis which may lead to pulmonary insufficiency. Clinically, the cases are characterized by headaches, giddiness, shortness of breath, a tendency to pulmo- nary hemorrhage, and a peculiar purplish cyanosis of hands and face. The pulmonic second sound is very loud; but a systolic murmur may be present over the pulmonary area or a diastolic (pulmonary insufficiency) be transmitted down the left sternal margin. CASE OF PRIMARY PULMONARY SCLEROSIS. Romberg reports the case of a man, aged 24, who had had no infectious diseases except measles as a child and a recent slight muscular rheumatism, three months after which he began to have gradually increasing shortness of breath, epigastric pressure, occasional headaches and giddiness, and his color became very blue. On exami- nation he showed marked cyanosis over the face, body, and limbs. There was a pulsation due to the right ventricle in the fourth interspace 4 cm. inside the mammillary line and thence inward to the sternum, also a smaller pulsation (left ventricle) in the fifth interspace mammillary line, cardiac dulness 7 cm. to right, 15 cm. to left. Both pulmonic sounds were louder than the aortic. Pulse small, regular, 116. Liver enlarged; spleen enlarged. No oedema; no swelling of vessels of neck. Probable diagnosis (Curschmann), congenital heart lesion. Patient gradually became worse; digitalis was without effect. Died one month after admission. Autopsy showed enlarged heart; right ventricle h y per trop hied and forms the entire apex, and the conus arteriosus and right auricle are especially hypertrophied. All the valves intact and normal; aorta free from sclero- sis, but unusually small. Duct us arteriosus closed. Tremendous sclerosis and a t h c r o m a of the pulmonary artery and all its branches. 1 Sanders has recently collected similar cases from the literature. TREATMENT. The general treatment of arteriosclerosis is mainly prophylactic, hygienic, and dietetic, and actual specific treatment is of far less value. Diet. Carefully selected diet is a most important factor, restriction being in both quality and q u a n t i t y . The general diet given in heart cases (see page 223) is of great benefit here, or equivalent diets with 1 Xotf-s of a case of pulmonary arteriosclerosis (O. A. K.) secondary to mitral stenosis are given on p. 440. ARTERIOSCLEROSIS. 351 this as a basis. However, in simple arteriosclerosis the quantity taken at a time need not be so greatly restricted ; but the total quantity in twenty- four hours should not exceed twenty-five hundred calories, and should always be near the lower level for proteids, and as free as possible of purin bodies (nitrogenous extractives such as are found in meat), creatinin, etc., and also of salt. The more recent studies quoted above seem to indicate that excess in salt is almost as injurious as are excesses in alcohol, and that the salt mackerel of Boston is as dangerous as the beer of Milwaukee. For the sclerotic danger probably lurks in the Smithfield ham or the cold smoked tongue as well as in the Baltimore rye or the Martini cocktail (Beyer, Barie, Hadfield). The patient's safety lies in milk, eggs, potatoes, bread, other carbohydrates, butter, and the simpler fruits. Restriction of Liquids. On the other hand, the liquid intake also should not be excessive, since drinking large amounts either of water or of beer seems to favor sclerosis (Krehl), but the amount ingested should remain in the vicinity of fifteen hundred cubic centimetres a day, some persons thriving best at five hundred cubic centimetres above, some at five hundred cubic centimetres below this level. Tobacco and alcohol should be dispensed with entirely if possible; if the patient insists on taking small quantities, one or two light dry cigars, as thin as possible (Lee), or "stogies," a day are perhaps the mildest that one may prescribe. Cigarette smoke is usually inhaled and pipes are very heavy. Thick Havana cigars should be entirely prohibited. As to alcohol, if the patient insists upon taking a small quantity, this should be limited to an occasional glass of claret or white wine, or perhaps a single glass of beer at rare intervals. The latter in large quan- tities is especially undesirable, both on account of the large amounts of liquid taken and because it contains both alcohol and proteid and purin substances extracted from the yeast. Gin is perhaps more dangerous than whiskey. Coffee and tea should be taken in only small quantities, since the vasoconstrictor action of the caffeine favors the onset of spasmodic vasoconstriction (vasomotor crises), and, on the other hand, the increase of blood-pressure itself brought on by caffeine is damaging to the arteries. However, it must be stated that, in contrast to nicotine, lead, adrenalin, etc., injections of caffeine into animals have thus far failed to bring on arteriosclerosis and that perhaps the deleterious effect of caffeine may be overestimated. Hydrotherapy. Systematic hydrotherapy is of considerable value in arteriosclerosis, especially the use of w a r m b a t h s , warm douches (Brieger), or alternating warm and cold douches (Riley) applied both locally and generally. They owe their efficacy to the vasodilatation which they bring about, and hence must be classed in effect with the drugs of the nitrite group. In most cases the effect of a good warm douche or warm bath is more marked and more lasting than that of any of these drugs, and it is further devoid of that certain residuum of deleterious effect which all drugs leave behind them. So that, while one cannot agree with Brieger that arteriosclerosis can be entirely cured symptomatic-ally by proper hydrotherapy, nevertheless w a r m b a t h s a n d w a r m s h o w e r ? 352 DISEASES OF THE HEART AND AORTA. once or twice a day should be an indispensable part of the treatment of every arteriosclerotic. Cold baths should be avoided, since they precipitate vasomotor reactions, which in the arteriosclerotic may amount to vasoconstrictor spasm. Drugs. Potassium Iodide. As to drugs, universal experience points to the efficacy of potassium iodide in doses ascending from 0.3 Gm. (gr. v) t.i.d., p.c., to as high as 4 Gm. (5i); some clinicians favor- ing the smaller, some the larger doses. In the writer's experience doses under 1 Gm. (gr. xv) seem to have some effect in alleviating symptoms; and when there is a suspicion of lues the dose should be increased still further. (The therapeutic action and its limitations are discussed in Chapter V.) It has been attempted to settle the question experimentally by deter- mining the effect of potassium iodide upon the course of adrenalin atheroma in rabbits. Koranyi, Boveri, and Cummins and Stout, who were the first to undertake these investigations, all reported that potassium iodide or iodipin, when injected during the time that adrenalin was being injected, inhibited the production of atheroma. However, it must be borne in mind that Biland, Loeb and Githens, Adler and Hensel found that large doses of potassium iodide seemed to increase rather than inhibit the atheromatous changes. For persons who cannot tolerate iodides in sufficient doses, sajodin, iodipin, or some other iodine derivative which has fewer unpleasant gastric ani cutanteous effects may be used, often with great satisfaction. Salvarsan. Salvarsan is as dangerous a remedy in most cases of arterio- sclerosis as in myocarditis, and the indications and contraindications are about the same (see pages 260 and 261). Nitrites. Next to the iodides in general use is the group of nitrites, - amyl nitrite, nitroglycerin, sodium nitrite, erythrol tetranitrate. These drugs are of value for symptomatic treatment, to relieve pain or discomfort for the time being, but they exercise no inhibitory influences upon the prog- ress of the arteriosclerosis, as has been shown for adrenalin arteriosclerosis. On the other hand, their effect upon the symptoms due to arteriosclerosis, the pain of intermittent claudication, of angina pectoris, of the abdominal and peripheral vascular crises, is most remarkable, and in this regard they are invaluable (Lander Brunton). However, in their administration it must be borne in mind that persons with arteriosclerosis seem to have considerable tolerance for nitrites (page 256), and to bring about vasodila- tation and fall in blood-pressure much larger doses must be given than is necessary to produce the effect in normal individuals. Accordingly, as indicated in Chapter V, the drug should be administered in increasing doses until the physiological effect (flushing, throbbing in head, ringing of the ears) is obtained, arid then continued in a dose just a little smaller than this. One need not be surprised, however, to find that this dose for a person with arteriosclerosis, particularly a colored person, may be ten or even twenty times the average dose for a normal individual. When such is the case the blood-pressure is probably a beneficial compensatory phenomenon, and the nitrites should bo discontinued. In the chronic hypertension of arteriosclerosis venesection is not onlv useless but often harmful. ARTERIOSCLEROSIS. 353 BIBLIOGRAPHY. ARTERIOSCLEROSIS. Thayer, W. S., and Fabyan, M.: Studies in Arteriosclerosis, with Special Reference to the Radial Artery, Trans. Ass. Am. Physicians, Phila., 1907, xxii, 694, and Arn. J. M. Sci., 1907, cxxxiv, 811. Wells, H. G.: Pathological Calcification, Jour. Med. Research, Bost., 1906, xiv, 491. Calcification and Ossification, Arch. Int. Med., Chicago, 1911, vii, 721, in which there is an excellent review of the literature. Klotz, O.: Studies upon Calcareous Degeneration, J. Exper. Med., X. Y., 1905, vii, 633. Baldauf, L. K.: The Chemistry of Atheroma and Calcification, J. M. Research Bost 1906, xv, 355. Aschoff, L.: Zur Morphologic der lipoiden Substanzen, Beitr. z. path. Anat. u. allg. Path., 1909, xlvii, 1. Selig, A.: Ueber den Kalkgehalt der Aorta, Verhandl. d. Kong. f. innere Med., 190S, xxv, 333; Chemische Untersuchung atheromatoser Aorten, Ztschr. f. physiol. Chem., Strassb., 1911, Ixx, 451. Hofmeister, F. : Ueber Ablagerung und Resorption von Kalksalzen in den Geweben, Ergebn. d. Physiol., 1910, x, 429. Ranvier: Traite technique d'histologie, Paris, 1875. Marchand: Die Arterien, Eulenburg's Realencyclop. d. ges. Heilk. Moenckeberg, J. G.: Ueberreine Verkalkung der Extremitatenarterien und ihre Verhalten zur Arteriosklerose, Arch. f. path. Anat., etc., Berl., 1903, clxxi, 141. Cornil and Ranvier: Manuel d'histologie pathologique, Par., 1884, 2d ed., ii. Mauwerck, C., and Eyrich, W.: Zur Kenntniss der verrucosen Arterien, Bcitr. z. path. Anat. u. allg. Path., Jena, 1889, v. Koster, \V. : Ueber die Entstehung der spontanen Aneurysmen und die chronische Mes- arteriitis, Berl. kl. Wchnschr., 1875, xii, 322; Endarteriitis und Mesarteriitis, ibid., 1876, xiii, 454. Thoma, R. : Ueber die Abhfingigkeit der Bindegewebsneubiklung in der Arterienintima von der mechanischen Bedingungen des Blutumlaufes, Arch. f. path. Anat., etc., Berl., 1893, xciii, 443; 1884, xcv, 294; 1886, cvi, 209; 1886, cvi, 421; Ueber einige senile Veranderungen des menschlichen Korpers, Lcipz., 1884. Jores, L.: Ueber das Verhalten der Blutgefasse im Gebiete durchschnittener axsomotor- ischer Nerven, Beitr. z. path. Anat. u. allg. Path., Jena, 1902, xxxii, 146. Savill, T. D.: On Arterial Sclerosis, especially in regard to Arterial Hypermyotrophy and other Morbid Changes which occur in the Muscular Tunic of the Arteries, Trans. Path. Soc., Lond., 1904, Iv, 375, and Discussions by T. C. Allbutt, G. Oliver, J. Broad- bent, and F. P. Weber. Russell, W.: Arterial Hypertonus, Sclerosis, and Blood-Pressure, Phila. and Edinb., 1908. Janeway, T. C., and Park, E. A. : An Experimental Study of the Resistance to Compression of the Arterial Wall, Arch. Int. Med., Chicago, 1910, vi, 58(5. Welch, F. H.: Aortic Aneurism in the Army and the Conditions Associated with it, Trans. Med. Chir. Soc., Lond., 1876, lix, 59. Dohle: Ueber Arterienerkrankungen bei Syphilitischen und deren Beziehung zur Aneurys- mabildung, Deutsches Arch. f. klin. Med., Leipz., 1895, Iv, 190. Heller, A.: Die Aortensyphilis als Ursache von Aneurysmen, Miinchen. mod. Wchnschr. , 1899, xlvi, 1669; Aortenaneurysma und Syphilis, Arch. f. path. Anat., etc., Berl., 1903, clxxi, 177. Moll, G. W.: Ueber einen Fall von Aortenaneurysma bei Tabes dorsalis, Thesis, Kiel, 1! Isenberg, D.: Ein Aneurysma Aortse mit Durchbruch in den Oesophagus, Thesis, Kiel, 1899. Schmorl: Miinchen. med. Wchnschr., 1905. Klotz, O.: Arteriosclerosis, Diseases of the Media and their Relation to Aneurysm, Pub. f. Univ. Pittsburgh Med. School, Lancaster, 1911. Wright, J. H., and Richardson, O.: Treponemata (Spirochaetse) in Syphilitic Aortitis, Five Cases, One with Aneurysm, Bost. M. and S. J., 1909, clx, 539. Landouzy, L., and Siredey, A.: Etude des localisations angiocardiques typhoidiquea leurs consequences immediate prochaines et eloignees, Rev. d. med., Par., 1887, vii, 804; 919. 354 DISEASES OF THE HEART AND AORTA. Thayer, W. S.: On the Late Effects of Typhoid Fever on the Heart and Blood-vessels, Am. J. M. Sc., N. Y. and Phila., 1904, cxxvii, 391. Kussmaul, A., and Mayer: Einige eigenthiimliche Arterienerkrankungen, Deutches Arch. f. klin. Med., Leipz., 1865, i, 184. Moenckeberg, J. G. : Ueber Periarteritis nodosa, Beitr. z. path. Anat. u. allg. Path., Jena, 1905, xxxviii, 101. Chvostek and Weichselbaum : Herdweise syphilitische Endarteriitis mit multipler An- eurysmenbildung, Allg. Wien. mod. Ztg., 1877. Miiller, P.: Ueber Periarteriitis nodosa, Festschr. z. Feier des 50 jahr Bestehens des Kran- kenh., Dresden-Friedrichstadt, 1899. Graf: Ueber einen Fall von Periarteriitis nodosa mit multiplen Aneurysmabildung, Beit. z. path. Anat. u. allg. Path., Jena, 1897, xix. Fletcher: Ueber die sogenannte Periarteriitis nodosa, ibid., 1892, xi. v. Kahlden: Ueber Periarteriitis nodosa, ibid., 1894, xv. Frothingham, C. H.: The Relation of Arteriosclerosis to Acute Infectious Diseases, J. Am. M. Ass., Chicago, 1911, Ivii, 149. Woolley, P. G.: Acute Tuberculous Endoaortitis, Johns Hopkins Hosp. Bull., Baltimore, 1911, xxii, 82. Thayer, W. S., and Brush, C. E. : The Relation of Acute Infectious Diseases to Arterio- sclerosis, J. Am. M. Assoc., Chicago, 1904, xliii, 726. Cabot, R. C.: The Relation of Alcohol to Arteriosclerosis, ibid., 1904, xliii, 774 Fahr: Zur Frage des chronischen Alcoholismus, Verhandl. d. deutsch. Path. Gesellsch., Jena, 1909, xiii, 162; abstracted in editorial: The Pathology of Chronic Alcoholism, J. Am. M. Assoc., Chicago, 1909, liii, 1824. Heiberg, Heller. Quoted from Ophiils. Croftan, A. C.: The Role of Alloxuric Bases in Nephritis, Am. J. M. Sci., Phila., 1900, cxx, 593. Israel: Ueber envorbene Storungen in den Elasticitatsverhaltnissen dor grossen Gefasse, Arch. f. path. Anat., etc., Berl., 1886, ciii, 461. Osier, W.: The Principles and Practice of Medicine, X. York and Lond., 5th ed., 1903. Emerson, C. P. : Personal communication. Brooks, H.: A Preliminary Study of Visceral Arteriosclerosis, Am. J. M. Sci., Phila. and N. York, 1906, cxxxi, 778. Gilbert, A., and Lion, G.: Arterites infectucuses experimentales, Compt. rend. Soe. de Biol., Par., 1889, 583; Arch, de med. exper., Par., 1904, xvi, 73. Adler, I.: Remarks on Arteriosclerosis, Med. Rec., N. York, 1902, Ixi, 721; J. M. Research, Bost., 1902, viii, 309. The Present Status of Experimental Arterial Disease, Am. J. M. Sc., Phila. and N. York, 1908, cxxxvi, 241. Benda, C.: Ergebn. d. Pathol., herausg. v. Lubarsch und Ostertag, Leipz., 1907-08, xi. Die Arteriosklerose (Atherosklerose), Therap. d. Gegenw., Berl., 1909, 1, 121. Saltykow: Experiment elle Forschung in der Lehre der Arteriosklerose, Zentralbl. f. d. ges. Physiol. u. Path. d. Stoffwechsels, Berl., 1908, iii, 654. Baylac: Atherome experimental de 1'aorte consecutif a 1'action du tabac, Compt. rend. Soc. de Biol., Paris, 1906, Ix, 935. Jebrowsky and Lee. See p. 717. Josue, O.: Atherome aortique experimental par injections repetees d'adrenaline dans les veinos, Compt. rend. Soc. de Biol., Par., 1903, Iv, 1374, and Presse med., 1903, ii, 798. Fischer, B.: Ueber Arterienerkrankungen nach Adrenulininjektionen, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1905, xxii, 235. Pic and Bonnamour: Contribution a 1'etude du determinisme de 1'atheroma aortique experimental, Compt. rend. Soc. de Biol., Par., 1905, Iviii, 219. Adler, I., and Hensel, O.: Studies on So-called Experimental Arteriosclerosis, Trans. Asso. Am. Physicians, Phila., 1907, xxii, 683. Erb, W., Jr.: Experimented und histologische Studien ueber Arterienerkrankung nach Adrenalininjektionen, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1905, liii, 173. Harvey, W. II.: Studies on the Influence of Tension in the Degeneration of Elastic Fibres of Buried Aorta, J. Exper. Med., X. York, 1906, viii, 388. Pearce, R. M., and Stanton, E. McD.: Experimental Arteriosclerosis, J. Exper. M., X. York, 1906, viii, 74. ARTERIOSCLEROSIS. 355 Hasenfeld, A.) Ueber die Herzhypertrophie bei Arteriosklerose, Deutsch. Arch. f. klin Med., Leipz., lix, 193. Bond, C. S.: Clinical Observations of Arteriosclerosis from Alimentary Toxins Trans Asso. Am. Phys., Phila., 1906, xxi, 73. Ortner, N.: Zur Klinik der Angiosklerose der Darmarterien, Volkmann's Samml. klin Vortr., Leipz., N. S. No. 347. Gilbride, J. J.: Gastrointestinal Disturbances due to Arteriosclerosis, J. Am. M Asso. Chicago, 1909, lii, 955. Hamburger, W.: Beitrage zur Atherosklerose der Magenarterie, Deutsch. Arch. f. klin. Med., Leipz., 1909, xcvii, 49 (with excellent bibliography). Hasenfeld. Quoted on p. 398. Pal, J. : Die Gefasskrisen, Leipz., 1905. Vaquez, Aubertin, Wiesel. See p. 291. Bayer, R.: Ueber den Einfluss des Kochsalzes auf die arteriosklerotisclie Hypertonie, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1907, Ivii, 162. Fremont-Smith, F.: Arteriosclerosis in the Young, Am. J. M. Sc., Phila. and X. Y., 1908, cxxxv, 199. Hirschberg: Centralbl. f. prakt, Augenheilk., 1882, vi, 329. Quoted from de Schweinitz. Raehlmann: Ueber ophthalmoskopisch sichtgare Erkrankung dea Netzhautgefasse bei allgemeiner Arteriosklerose, Ztschr. f. klin. Med., Berl., 1889, xvi, 606. Friedenwald, H.: Report on the Ophthalmoscopic Examination of Dr. Preston's Cases of Arteriosclerosis, J. Am. Asso., Chicago, 1891, xvi, 623. De Schweinitz, G.: Intra-ocular Angiosclerosis, and its Prognostic and Diagnostic Sig- nificance, Internat. Clinics, Phila., 1907, 17th Ser., vol. i, 177. Romberg and Hasenfeld. Quoted on p. 291. Romberg, E.: Ueber Arteriosklerose, Verh. d. Kong. f. innere Med., Wiesb., 1904, xxi, 60. Sawada: Blutdruckmessung bei Arteriosklerose, Deutsch. med. Wchnschr., 1904, xxx, 425. Groedel: L T eber den Wert der Blutdruckmessung fur die Behandlung der Arteriosklerose, Verhandl. d. Kong. f. inn. Med., Wiesb., 1904, xxi, 113. Israel, A : Klinische Beobachtungen ueber das Symptom der Hypertension, Samml. klin. Vertr., Leipz., 1907. Innere Med., Nos. 135-136. Janeway and Homer. Quoted on p. 54. Bittorf, A.: Zur Symptomatologie der Aortensklerose, Deutsch. Arch. f. klin. Med., Leipz., 1904, Ixxxi, 65. Romberg, E.: Ueber Sklerose der Lungenarterie, Deutsch. Arch. f. klin. Med., Leipz., 1891, xlviii, 197. Sanders, W. E.: Primary Pulmonary Arteriosclerosis with Hypertrophy of the Right Ventricle, Arch. Int. Med., Chicago, 1909, iii, 257. Rogers, L. : Extensive Atheroma and Dilatation of the Pulmonary Arteries, without Marked Valvular Lesions, as a not very Rare Cause of Cardiac Disease in Bengal, Quart. J. Med., Oxford, 1908-9, ii, 1. Brieger, L.: Clinical Lectures at the Hydrotherapeutische Anstalt der Kgl. Poliklinik, Berlin, 1906. Riley: Blatter f. klin. Hydrotherap., 1X98; cited from Buxbauin, B., Lehrbuch der Hydro- therapie, Leipz., 1903. Senator, II.: Ueber die Arteriosklerose urul ihre Behandlung, Therap. d. Begenw., Herl., 1907, xlviii, 97. Koranyi, V.: Ueber die Wirkung des lods auf die (lurch Adrenalin erzcugte Arterione- krosc, Deutsch. med. Wchnschr., Leipz., 1908, xx.xii, 679. Boveri, P.: Contributo allo studio degli ateromi aortici sprrimentali, Clin. med. ital., Milano, 1906, xlv, 41. Cummins, W. T., and Stout, P. S.: Experimental Arteriosclerosis by Adrenalin Inocula- tions and the Effect of Potassium Iodide, Univ. Penn. M. Bull.. Phila.. 1906-7. \i\. 101. Biland, J.: Ueber die durch Nebennicrenpraparate geset/ten Gef-iss- und Organverander- ungen, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxvii. 413. Loeb, L., and Githcns, T. C.: The Effect of Experimental Conditions on the Yascuhr Lesions Produced by Adrenalin, Am. J. M. Sc., Phila. and X'. York. 1905, cx> Loeb, L., and Fleisher, M. S.: Influence of Iodine Preparations on the Vascular Lesions Produced by Adrenalin, ibid., 1907. cxxxiii, 903. XI. VASOMOTOR CRISES AND THE ANGIONEUROTIC LESIONS. VASOMOTOR CRISES. GENERAL CONSIDERATIONS. The general clinical manifestations of arteriosclerosis bear a close relation to the condition described by Pal as "vasomotor crises," under which he includes all conditions which are associated with more or less sudden constriction or dilatation of the arteries, and whose symptoms and signs disappear or markedly diminish as soon as this paroxysmal change in the blood-vessels passes off. There are accordingly (1) Vasoconstrictor crises, usually associated with hypertension. (2) Vasodilator (hypotension) crises. The vasoconstrictor crises Pal divided into (1) Abdominal type. (2) Pectoral type. (3) Cerebral type. (4) Crises in the ex- tremities. (5) Crises in the large arteries. The vasodilator crises according to Pal include (1) Ordinary syncope. (2) Surgical shock. (3) Collapse after infectious disease or most poisonings. (4) Erythromelalgia and many other "trophic" skin disease. 1 (5) Occasional cases of tabes with lancinating pains and low blood-pressure. (6) Various attacks of weakness in Addison's disease. Probably no unit cause exists for the crises themselves; the visceral crises and lancinating pain in tabes, the painter's colic, the uraemic con- vulsion, the delirium of the cerebral sclerotic, the pain of angina pectoris, and the attack of cardiac asthma seem to have little etiology in common except their relation to the sympathetic nerves. 1 However, all manifest high blood-pressure, and, according to Pal, all are relieved by artificial depression of blood-pressure. It is, therefore, not unlikely that, however diverse the ultimate causes of the condition, the 'cause of the symptoms is high blood-pressure with localized vasoconstriction. The variation in the areas of constriction in regions whose arteries are already sclerotic accounts for the occurrence of the different symptom complexes. As to treatment, the statements of Pal would lead one to believe that they are all relieved by vasodilators, especially nitro- glycerin and the nitrites, occasionally by sodium thiocyanate, and that marked improvement results while the blood-pressure is lowered. The symptoms return if the blood-pressure again rises. (Pal, also Heitz, and Xorrero.) However, Prof. Barker's experience at the Johns Hopkins Hospital does not warrant such sweeping conclusions. 1 The cardinal signs of sympathicotonie should be carefully tested for (see page 19). 356 VASOMOTOR CRISES. 357 CASE OF ABDOMINAL VASOMOTOR CRISES. (QUOTED FROM PAL.) P. V., sausage maker, aged 57, had rheumatism 14 years ago, and for the past year pain and pressure in the epigastrium, especially on taking a deep breath. Has occa- sional paroxysms of extreme dyspnoea ami palpitation of the heart, but always has some shortness of breath. He was formerly a heavy drinker, now drinks two or three litres of beer a day as well as a half litre of wine and some whiskey! He also smokes in moderation. On admission, April 7, 1904, he was found to be a well-nourished man, slightly eyanotic. Lungs clear, respiration 34. Heart. Maximum impulse in sixth interspace two fingers' breadth beyond mammillary line. Dulness extends to third rib above and two fingers' breadth beyond the right margin of the sternum. Sounds quite clear at apex and base, second aortic sound not accentuated. Pulse 68; radial walls stiff; blood-pressure 225. Liver enlarged; spleen not palpable. Slight oedema of feet and legs. Urine 2600 c.c.; sp. gr. 1010; albumin 1.5 Gm. per litre. Patient was given 0.5 Gm. (gr. viii) so- dium thiocyanate t.i.d. to diminish his blood- pressure. April 21. Patient delirious; blood-pres- sure 110. Thiocyanate discontinued, where- upon delirium disappears. The chart in Fig. 160 shows the course of the blood-pressure, pulse-rate, and respiration. The patient was free from other exceptional symptoms from April 7 to May 1. May 1, 8.00-11.30 A. M. Feels hot and cold. 11.30. Sudden attack of severe pain and great feeling of pressure in epigastrium. 11.35. Pains in back and third to seventh vertebra?. Cries out with pain, and also cries "I am choking." Lungs clear. Cardiac dulness only to right sternal margin and to two fingers' breadth within left mammillary line. 11.40. Symptoms diminish but pressure in epigastrium still present. 11.41. Symptoms reappear. 11.42. Diminution of symptoms, pains less. BLOOD PRESSURE -PULSE RATE- RESPIRATION FIG. 160. Blood-pressure chart of P. V. Typical vasomotor crisis. A second severe attack as before. 11.55. After a few minutes patient has a third momentary attack with blood-pressure over 200 mm. Hg, which then subsides. 12.10. Feels better. 12.55. Still better. Free from attacks until May 3, during which time he receives 0.5 Gm. (gr. vii) diuretin t.i.d. On May 18, sodium thiocyanate was again given, which lowered blood-pressure but caused delirium. From that time until discharged frequent attacks of pain and hypertension. Pal reports similar hypertensive crises in association with the colic of lead poisoning and also with the visceral crises of tabes, 1 the pain being always relieved when the blood-pressure is brought down by ainyl nitrite or nitrogiycerin; as, for example, in the following case. CASE OF ABDOMINAL CRISIS IN LEAD POISONING. X. J., painter, aged 31, has had lead colic twice before. Was free from it on change of occupation, but it returned when he again worked in lead. Drinks little; denies lues. He has had abdominal pain for three weeks. During past few days has 1 The claim of Pal that a similar association of pain with high blood-pressure exists with the lancinating pains of limbs cannot be maintained, since the pains in his own cases are sometimes associated with hypotension, sometimes with hypertension. 358 DISEASES OF THE HEART AND AORTA. had continuous cramps, loss of appetite, and no stool. He is pale and has a marked lead line. Pupils react readily. Lungs clear. Heart normal; pulse rather hard. Abdominal walls tense, tender on both sides. Spleen just palpable. July 23. 8.30 P.M. 9.10 P.M. 9.13P.M. 9.15P.M. 9.17 P.M. 9.45 P.M. 9.48 P.M. 12 M. 4.20A.M. B. P. 130. Slight pain. P. 68. B. P. 170. Increased pain. Amyl nitrite inhalation. B. P. 105. No pain. B. P. 165. Pain again, lasting then over one-half hour with same B. P. B. P. 95. After amyl nitrite, which again gave relief. B. P. 140. Pains return. 160. Further increase of pain. B. P. 135. Pains diminish under amyl nitrite. They return again, but 6.30A.M. B. P. 85. Pains disappear under amyl nitrite. After July 25, blood-pressure was always under 130 (during last four days under 110), the patient was free from pain, and bowels were regular. CASE ILLUSTRATING THE CEREBRAL CRISES. The following case, illustrating what Pal terms the cerebral type of vascular crisis, was under the writer's care at the Johns Hopkins Hospital: J. M. C., grocer, aged 52, who had suffered repeatedly with myocarditis, hypertrophied heart, irregular pulse, and general anasarca, entered the Johns Hopkins Hospital in September, 1903. Oct. 24. Restless at night. Left pupil larger than right; both react normally. Nov. 2. Very weak. Pulse weak and irregu- lar. Liver enlarged. Nov. 5. At 12.30 P.M. began to complain of general discomfort with numbness in legs; complained of nervousness and restlessness. At 12.45 P.M. the restlessness became very marked; he began to strike out with his hands and to try to get out of bed. Was at this time conscious and able to understand questions. (Blood-pressure curve shown in Fig. 161.) No aphasia. Pupils equal and dilated. Head and eyes drawn to right and rigid. There was some twitching of muscles of both arms and hands. Reflexes of right arm slightly exaggerated. Soon became cya- notic and vessels of neck stood out. Be- came unconscious. Respiration stertorous. Blood-pressure 270 mm. Hg. After 600 c.c. of blood had been withdrawn from left arm, cyanosis slowly subsided, respira- tion becoming less stertorous and blood-pressure falling to ISO mm. Hg. Becomes conscious after catheterization at 7.30 P.M. Still picking at bedclothes, which continued until next morning. He was then mentally clear by 11 A.M. and pupils reacted to light. Nov. (i. 9 P.M. Remained clear and recalled hallucinations of previous night, realizing them as hallucinations. Blood-pressure 160. Had no further attacks of this kind and blood-pressure remained below 190. Died March 28, 1904. Autopsy showed chronic myocarditis (heart 1000 Gin.), chronic adhesive pericarditis, coronary sclerosis, hydronephrosis, and stone in right kidney. 1 1.50 FIG. 1G1. Blood-pressure chart showing a vascu- lar crisis of the cerebral type. 1 It is possible that this attack may have been duo to transitory cerebral oedema like that described by H. Cashing and James Bordley (Subtemporal Decompression in a Case of Chronic Nephritis with Uraemia; with Especial Consideration of the Neuroretinal Lesion, Am. J. M. Sc., 1908, cxxxvi, 484). VASOMOTOR CRISES. 359 INTERMITTENT CLAUDICATION. This condition is always associated with sclerosis of the. femoral, popliteal, or one of the other arteries of the leg which are usually pipe-stem in character. Often the atheromatous changes are readily demonstrable by the X-ray. Owing to the narrowed lumen of the artery, the amount of blood that can flow through it is limited, but this is sufficient to supply the muscle when at rest. During slow walking the C0 2 pro- duced by the muscle and the oxygen needed by it increase greatly. If the arterial flow is sufficient, no symptoms appear; but when rapid walking or running is begun, there is a sudden increase in the oxidation in the muscle, and, since the blood supply cannot keep pace FIG. 102. Diagram to illustrate with it, asphyxia of both the muscle and its ^e elimination of co 2 by the blood , J . . m normal and sclerotic arteries. nerve endings sets in, accompanied by paralysis solid line indicates co formation of the limb and often intense pain arising from Sn i^SL^th. ^S Stimulation Of the Sensory fibres by the CO,. of C 2 elimination. * indicates the rr,, ,. , . ,, , , , ,. -,,. degree of COz accumulation at which Ine patient is compelled to halt. During the pa in sensations .set in. rest the CO 2 production falls, and the slow cir- culation is able to carry off the excess and to supply fresh oxygen to the tissues. With the renewed aeration, function returns. The patient is able to walk again until local asphyxia sets in; and, since this will be brought about by the same amount of C0 2 as before, his walking will be limited to the same distance. He must travel in stages. (Fig. 162.) CASE OF INTERMITTENT CLAUDICATION. H. E., carpenter, aged 74, complains of pain in right foot, drinks beer and whiskey in moderation, smokes very little, and has always been healthy. In October toe was red and ached. For the past ten or fifteen years patient has been at- tacked by severe pains in both feet, causing him to stop in his walks. Knees never gave way. The attacks came on oftenest during exercise. On examination, thorax is emphysematous; heart slightly enlarged to left. Blowing systolic murmur heard over the tricuspid area, becoming musical over the apex, well heard in the axilla, but faint and blowing in the pulmonary area, where the second sound is accentuated. Pulse slightly irregular. Right radial more sclerotic than left. Blood-pressure 10") nun. General reddening from tarsometatarsal joints to the toes of right foot, where pulsa- tion of dorsalis pedis is not felt. Both tibials are palpable, but pulsation is well felt. Left foot normal, artery pulsating well. Both popliteals are very sclerotic. Given nitroglycerin mg. 1 (gr. -, 1 ,,) t.i.d., alternating with sodium nitrite 0.2 (!m. (gr. iii) t.i.d. He was somewhat improved by treatment, but left the hospital a few days later. Prognosis. Since the claudication is simply part of the general arterio- sclerosis, the prognosis is bad, for the coronary arteries, aorta, and cerebral arteries may be involved. Sometimes, however, the arterial change is confined to the limbs, occurring simply as degeneration of the media with atheroma, exactly as is found in experimental adrenalin arteriosclerosis. In that case the prognosis as to life is, of course, better. 360 DISEASES OF THE HEART AND AORTA. HYPOTENSIVE VASOMOTOR CRISES. The so-called " hypotensive " crises seem to bear no relation to arterio- sclerosis, but rather to trauma, action of toxic substances, and perhaps to cutaneous diseases. They are in the main associated with depression of the vasomotor system and have been discussed elsewhere. The one condition with paroxysmal depression of the blood-pressure which may owe its origin to arteriosclerosis is paroxysmal tachycardia (see page 669). ANGEIONEUROSES. Maurice Raynaud in 1862 described many cases of this group, espe- cially of the condition which bears his name. He showed that the three phenomena manifested in these conditions are: 1. Local syncope, i.e., blanching from absence or diminution of blood in the arteries of the part affected; Raynaud's disease a spas- modic vasoconstriction. This is usually symmetrical in its distribution, affecting the ends of the extremities, i.e., toes, hands or feet, arms or legs. The trouble in one extremity is frequently more intense than in the other. Often it leads to formation of bulla?, ulceration, and to symmetrical gangrene (Raynaud's disease). 2. Local asphyxia, i.e., presence of a venous blood, that is to say of a blood insufficiently oxygenated, causing blueness of the part (now designated as acrocyanosis) with a distribution corresponding to that of Raynaud's disease. 3. Local hyperaemia, giving rise to redness (as in the condi- tion termed erythromelalgia by Weir Mitchell). Later investigations have enabled Cassirer as well as Barker and Sladen to epitomize the symptoms of vasomotor disease as follows: The vasomotor symptoms include (1) hyperscmia, (2) syncope, and (3) asphyxia; the sensory, (1) pain, (2) hypersesthesia, (3) anaesthesia, (4) pargesthesia; the trophic, (1) ulceration, (2) gangrene, (3) dystrophies of the skin (Barker and Sladen). They affect the fingers and particularly the toes. The chief types of disease are acrocyanosis (Cassirer), erythro- melalgia (Weir Mitchell), and Raynaud's disease. The symptoms may be arranged as follows in ascending scale (Barker and Sladen) : 1. Acrocyanosis. Vasomotor symptoms venous stagnation and hyperaemia in fingers and toes with cyanosis; sensory and trophic disturbances absent. 2. Acroparaesthesia. Acrocyanosis sensory symptoms (paraesthesia), numbness, pain, and tingling. 3. Erythromelalgia. Vasomotor hyperamia (arterial). Sensory pain. 4. Raynaud's disease (all the symptoms). Vasomotor hyperaemia, syncope, and asphyxia. Sensory pain, anaesthesia, parcesthesia. Trophic gangrene and scleroderma. As might be expected, there are many cases with symptoms inter- mediate between these groups and many transitions from one to the other (Sachs). AXGEIOXEUROSES. 301 Pathology. Raynaud realized that the gangrene in the disease which bears his name differed from ordinary gangrene and directed his first inves- tigations to the state of the arteries. He found that, though the pulse became very small or impalpable d u r i n g t h e attacks of blanching, it returned to normal volume between attacks. He made very careful pathological studies of the extremities in a number of cases, and finding the arteries clear con- cluded that the trouble was of vasomotor origin, a view which he supported by demonstrating transitory changes of caliber in the radial, popliteal, and retinal arteries, associated with the attacks. In accordance with these studies of Raynaud the vasodilation of erythromelalgia corresponds to a period of paralysis of the vasoconstrictor nerves (sympathetic paralysis) quite similar to the active hyperrcmia which Claude Bernard produced in the rabbit's ear by cutting the cervical sympathetic. Just such a local paralysis of the vasomotors produced by the overheating of a hand or foot benumbed by cold gives rise to the condition of "chilblains." The latter condition is always associated with overheating after exposure to cold and often with formation of blebs, while attacks of erythromelalgia may occur spontaneously from slight emotional or nervous disturbances or from slight exposure to cold without overheating. There is rarely bleb forma- tion. An attack of chilblains induced by overheating may thus be con- tinued in spontaneous attacks of erythromelalgia. Rayiiaud's disease, on the other hand, c o r r e s p o n d s to an extreme vasoconstriction, like that produced in ergotism. Raynaud himself was so much impressed with this similarity that he made searching inquiries in all his cases regarding the character of rye bread taken, and conducted an extensive series of experi- ments upon ergotism in various animals. He w-as forced to discard the ergot hypothesis by the absence of any obtainable evidence of ergot ingest ion, but the parallelism between the two conditions remains. CASE OF MILD RAYXAUD'S DISEASE. A. S., a trained nurse, aged 30, was always healthy until the age of nineteen, when during her period of training she was compelled to have a small ovarian cyst and one ovary removed. For some years she suffered considerable pain from adhesions, so that three years ago these were broken up by a second operation. She bore the operation well, but during convalescence three weeks later had a fainting spell, since when she suffers from severe palpitation. For the past two years she has found that in cold weather both her hands and forearms become absolutely white, cold, and numb. This condition is soon relieved by rubbing or by laying them in a basin of warm water, but is sufficiently severe to prevent her from accepting a very desirable appointment in a colder climate. Between attacks the patient seems perfectly healthy, has a good color. All the arteries are soft. They appear to be of normal caliber and pulsate normally. The heart is normal in size but moves 7 cm. from left to right as the patient turns from one side to the other. The right kidney is also palpable and very movable. The rest of the abdomen and the lungs are clear. The blanching of the hands occurs less frequently and less intensely when the patient's health is good, but it occurs much more frequently when the patient is excited. Nitrites, belladonna, digitalis, bromides, and a large number of cardiac stimulant.s have been tried by the patient without marked effect. 362 DISEASES OF THE HEART AND AORTA. THROMBOANGITIS OBLITERANS. In recent years Weiss and v. Winiwarter, and especially L. Buerger, have discovered a group of cases in which symptoms at times simulating those of the vasomotor trophoneuroses are produced by complete occlu- sion of the arteries or veins with spontaneous thrombosis (thromboangitis or thrombophlebitis obliterans). In such cases the largest artery and sometimes both artery and vein become occluded by a thrombotic process of considerable extent. After a short time the fresh red thrombi within the vessels undergo organization, usually with permanent obliteration of the lumen by white fibrous tissue. There is no proliferation of new elastic fibres encroaching on the lumen as is the case in arteriosclerosis (Fig. 163), though a few elastic fibres are found in the newly formed blood- vessels. A B FIG. lf>3. Thromboangitis obliterans (A) and endarteritis obliterans (B). (After Buerger.) The elastic fibres (stained black) are absent from the organized thrombus in A but present in large numbers in the arterioscleriotic lesion B. This was the condition first sought for by Raynaud to explain the origin of symmetrical gangrene, and described by him under the head of senile gangrene. In Buerger's experience of over 70 cases, however, it is most frequent in Russian and Polish male Hebrews between twenty and thirty-five or forty, and hence is usually a "presenile" gangrene. In such cases the local syncope and ulceration are due to arterial occlusion. The red blush is due to compensatory capillary dilatation (termed eryth- romelia by Buerger, in contrast to erythromelalgia) . Cyanosis of the limb occurs when the venous circulation is slowed from any cause. The sensory disturbances found in the trophoneuroses are also found in thromboangitis obliterans. The clinical picture produced by thromboangitis obliterans is some- times so similar to that of Raynaud's disease (spasmodic vasoconstriction) that Buerger has found some undoubted cases of the former condition reported in the literature as cases of the latter. Differentiation between Thromboangitis Obliterans and Angeioneuroses. Dr. Buerger has informed the writer that he finds the following points useful for clinical differentiation: 1 . There is always at least one vessel which remains permanently p u 1 s e 1 e s s , while in Raynaud's disease the pulse soon returns to normal. THROMBOANGITIS OBLITERANS. 363 2. Intermittent claudication is present in most of the cases. 3. Usually one limb is affected a considerable time before the other, and the disease usually attacks the lower extremities. 4. There are exacerbations, but they come on and subside rather gradually and are not paroxysmal like Raynaud's disease. 5. Limbs which are red (erythromelia) or blue in the dependent position become blanched and ischaemic when elevated. 6. Migrating phlebitis is not infrequently associated with thromboangitis obliterans. 7. He has seen over 70 cases in Russian and Polish male Hebrews, but never in a female. Raynaud's disease occurs more often in females. 8. Onset is usually gradual, while it is sudden in Raynaud's disease. 9. The circulatory phenomena are for the most part not of " vasornotor " origin, but are due to occlusion of vessels. They therefore bear the stamp of permanency. Nevertheless, Dr. Buerger has found a number of cases in which the clinical differentiation from Raynaud's disease was very difficult. Dr. Bernard Sachs, on the other hand, believes that the vasomotor neuroses manifest themselves in diseased blood-vessels as well as in healthy ones, and that the pathological diagnosis of endarteritis or thromboangitis does not exclude the clinical diag- nosis of erythromelalgia or Raynaud's disease. Indeed it is readily conceivable that thrombosis should occur more readily in somewhat diseased arteries than in normal ones. Even Dr. Buerger has found some intimal changes in his cases. Vasoconstriction may also favor thrombosis. More- over vasoconstriction, arterial disease, and the formation of agglutinative thrombi may, as is seen in ergot poisoning, all be produced by the action of a single toxic agent. CASE OF THROMBOAXGITIS OBLITERAXS. The following is the history of a case which, though at the time diagnosed as Raynaud's disease and manifesting many symptoms of the latter, in the light of Buerger's in- vestigations appears to be one of thromboangitis obliterans. H. F., tailor, aged 32, admitted April 14, 1903, complaining of sore toes and sore fingers. Had rheumatism at 12 years; otherwise well. Smokes ten cigarettes daily. In December, 1899, cold began to cause a burning sensation in big toe of right foot. In March, 1900, pus collected under the base of nail. The nail was removed, and four months later the entire toe. Wound did not heal well. After this, tingling in other toes when out of doors, never when indoors. In April, 1902, the fingers and thumb of the right hand began to tingle and become painful, and a little later on those of the left hand. In January, 1903, the left big t o e began to become gangrenous. FIG. 164. Hands and feet of a patient with thrombo- angitis obliterans, showing gangrenous ulcers and the stumps of amputated toes. The arrows point to the gan- grenous ulcers. 364 DISEASES OF THE HEART AND AORTA. Physicial examination on entrance, negative except for the extremities. Both hands are flushed, not blue, not tender, but there is some deformation of the second phalanx of the middle fingers. Right big toe missing; sloughs between third and fourth digits. Left great toe nocrotic; tenderness and pain over both first metatarsals. Patient complains of paroxysms of intense pain during the night, lasting five to ten minutes. Elevation of the limb, warm dressings, massage, were ail without effect. Condition became worse in spite of hot HgC-l 2 compresses, etc., and the left great toe had to be removed. The stump did not heal for several months. There was never pulsation in either popliteal; very little in either femoral. Patient discharged in February, 1904, unimproved. During this time blood count: red blood-corpuscles 5,000,000-5,500,000. Haemo- globin 100 per cent. Urine normal. Blood-pressure 100 to 130 mm. Hg. Pulse 80. The following history represents a more typical case of thromboan- gitis obliterans (quoted from Buerger). M. K., 44 years, Russian Hebrew, father of three healthy children, was admitted to Mt. Sinai Hospital on December 8, 1908. His limbs never troubled him until about a year ago, when he felt the presence of tender spots on the inner side of the right foot. Soon other hard "lumps" and "cords" appeared; some of these in the neighborhood of the ankle, others higher up on the leg. After two months these disappeared, only to recur after a very short interval. Since then he has never been absolutely free from peculiar "painful spots," and now, on admission, he still has signs of some of them. About three months after the onset of these symptoms he experienced pain in the big toe, especially on walking. This has become gradually worse, so that he has been unable to get about properly for almost two months. Of late he has often had cramps in the calf and instep of the right leg after walking for a short distance. His chief complaint, however, is the painful condition of the inner side of his right leg. Physical examination showed evidences of circulatory disturbance in the right lower extremity. Both the dorsalis pedis artery and the anterior tibial were pulseless, although pulsation of both the femoral and posterior tibial artery could be easily detected. Over the inner border of the right foot there is a red streak about one-half inch in length. This corresponds to a tender indurated mass which thins out and is lost as it is traced upward. A short distance below the middle of the leg the upper end of a hard cord can be palpated. This extends down behind the border of the tibia for more than two inches, is adherent to the skin, somewhat nodulated, and marks the centre of an area of hypersensitive, swollen, turgid skin. There are no trophic disturbances. Diagnosis: thrombnangitis and thrombopfilebitis of the internal saphenous and some of its tributaries. On December 15, 1908, a portion of the thrombosed saphenous was removed for pathological examination. On December 26, 1908, the physical examination was recorded as follows: In the horizontal position, the right foot has a light shade of red; this is most marked over the big toe and fades off towards the ankle. In the web between the third and fourth toes there is a superficial ulcer. On the inner side of the foot almost two inches from the internal malleolus there is a hard, cord-like nodule which is adherent to the skin. Behind the tibia there is the scar left after removal of a portion of the saphenous vein. The saphenous can no longer be felt. On elevation of the foot blanching sets in rapidly and pain becomes intense. The pendent foot turns very red (marked erythromelia). FURTHER COURSE. February 15, 1909. the pain in the foot has been getting steadily worse, and the fourth toe is beginning to turn black. On the 23d of February amputation at the knee was done, at the request of the patient, for early gangrene of the fourth toe. TREATMEXT. In the light of Buerger's pathological studies, treatment should be directed toward keeping up a rapid circulation through the part and dimin- ishing the tendency to coagulate. To bring about the former the vasodilator drugs, especially the nitrites, should be freely used, but most of all the THROMBOANGITIS OBLITERANS. 365 mechanical methods of inducing arterial hypersemia, hot poultices, mustard foot or hand baths, or the Bier's hyperaemia by suction in vacuo (not Bier's stag- nation hypersemia). Exsanguination of the limb with the Esmarch bandage, administration of sodium citrate in the hope of reducing coagulation, etc., have proved of little avail. From the time of Raynaud to the present excellent results have been reported from the use of warm (but not too hot) poultices. Arteriovenous Anastomosis. The recent advances in vascular surgery, introduced by Carrel, have made it possible to anastomose the artery with the vein and to lead blood to the limb through the vein instead of the artery (reversal of the circulation). Bernheim, whose operative results are the best thus far obtained, has reported four operations upon cases of Raynaud's dis- ease, three done by himself and one by Quenu. In Quenu's case partial success was obtained, but the limb had to be amputated four months later. Two of Bernheim's operations were followed by complete success, but in the third no re- lief was afforded. Of fifty-two cases of gangrene from various causes collected by the same writer, fifteen were successful, while among his own cases the satis- factory result was obtained in five out of six. Bernheim insists upon the impor- tance of operating early, before all the vessels supplying the part have become so thrombosed as to render recovery impossible. The importance of perfect technique and of much practice in vascular surgery cannot be overestimated. All but one of Bernheim's anastomoses were end-to-end anastomoses ; the other was a lateral anastomosis done by the method of Bernheim and Stone. BIBLIOGRAPHY. VASOMOTOR CRISES AXD AXGIOXEUROSES. Pal, J.: Die Gefasskrisen, Leipz., 1905. Charcot, J. M.: Sur la claudication intermittente observee dans un cas d'obliteration com- plete de 1'une des arteres iliaques primitives, Compt. rend. Soc. de Biol., Paris. 1857, 2 serie, xii, 225. Sur la claudication intermittente par obliteration arterielle, Progres Med., Paris, 1887. Erb, W.: Ueber das "intermittirende Hinken" und andere nervose Storungon infolge von Gefasserkrankungen, Deutsch. Ztschr. f. Xervenheilk., xiii, 1. Ueber Dysbasia angio- sclerotica, Mlinchen. med. \Ychnschr., 1904, li, 905. Barker, L. F., and Sladen, F. J.: On Acrocyanosis Chronica Ansesthetica with Gangrene, etc., J. Xerv. and Ment. Dis., X. York, 1907, xxxiv, 745. Cassirer, II.: Die Yasomotorische Trophoneuroscn, Berl., 1901. Mitchell, S. \Yeir: Phila. M. Times. 1872; quoted from Sachs. Mitchell. S. "\Y., and Spiller, W. G.: A Case of Erythromelalgia with Microscopical Examination of the Tissue from an Amputated Toe, Am. J. M. Sc., Phila,. 1899, X. S. cxvii, 1. Raynaud, A. G. M.: De 1'asphyxie locale et de la gangrene symmetrique des extremitos, Par., 1862; also, On Local Asphyxia and Symmetrical Gangrene of the Extremities, Transl. by T. Barlow, Lond.. 1888. Buerger, L. : Thromboangiitis Obliterans; a Study of the Yascular Lesions loading to Pre- senile Gangrene. Am. J. M. Sc., Phila. and X. York, 190S, cxxxvi. 51)7. The Veins in Thromboangiitis Obliterans, with Particular Reference to Arteriovenous Anas- tomosis as a Cure for the Condition, J. Am. M. Assn.. Chicago. 1909. lii, 1319. Sachs, B.: Raynaud's Disease. Erythromelalgia, and the Allied Conditions, in their Relation to Yascular Disease of the Extremities. Am. J. M. Sc.. Phila. and X. Y.. 190S. cxxxvi, 5(50. Also, Strauss, H.: Ueber angiospastische Gangran (Raynaud'soho Krankheit). Arch. f. Psychiat., Berl., 1905, xxxix. 109. Bernheim, B. M.: Arteriovenous Anastomosis Reversal of the Circulation as a Preven- tive of Gangrene of the Extremities Ann. Surg.. Phila.. 1912. 195: Bernheim. B. M., and Stone, H. B.: Lateral Yascular Anastomosis, an Improved Method, ibid., 1911, 497. XII. SCLEROSIS OF THE CORONARY ARTERIES, AND ANGINA PECTORIS. PHYSIOLOGY OF THE CORONARY CIRCULATION. The coronary arteries have usually been considered to be terminal arteries in the sense of Cohnheim; that is, that their branches did not anastomose with one another suffi- ciently to maintain an adequate circulation, and infarction follows their occlusion. This is correct under most clinical conditions; and Porter has found experimentally that the infarction is proportional to the size of the ligated branch. In many cases ligation of a coro- nary gives rise to fibrillary contractions and sudden death (Porter, Magrath and Kennedy, Kronecker); in others death may follow within a few minutes (Cohnheim and v. Schulthess- Rechberg). within an hour (Panum), or the animal may live several weeks or more (Baumgarten) if the operation is done aseptically. Death even then often occurs suddenly. FIG. 165. Effect of ligation of a large coronary artery upon the blood-pressure. (After Cohnheim and v. Schulthess-ltecliberg.) Coronary artery ligated at a. Distribution of the Coronary Arteries. Walter Baumgarten in Porter's laboratory was able to ligate the various coronary branches of cats and dogs under aseptic precau- tions and produced infarcts in the corresponding areas of the myocardium. He found the following effects by ligating the various branches: R a m u s d e s c e n d e n s : Anterior wall of left ventricle, anterior papillary mus- cle, left half of the thickness of the interventricular septum. R a m u s e i r c u in f 1 e x u s : Posterior wall of left ventricle, apex, posterior papil- lary muscle, a certain extent of the right ventricle, posterior wall of left atrium, posterior third of the septum. R a m us s e p t i : This is given off in the dog near the origin of the ramus descen- dens or independently of it. Ligature produces a triangular infarction with the apex of the triangle towards the ligature. Right coronary: Greater part of right ventricle, posterior portion of the appendix atrii. (The smaller branches of the atria are not caught in the ligature.) Baumgarten also excised the aiurmic area and perfused it with defibrinated blood, and found this region was able to resume contractions when the cir- culation was renewed within six to eleven hours after the artery had been ligated. The region of the centre of the infarct lost its contractility before that near the periphery, indicating that a certain degree of collateral circulation, perhaps through the vessels of Thebesius, had taken place. This work explains why it is that a certain time elapsed between the obstruction of the artery and the sudden cessation of beat in the experi- 366 SCLEROSIS OF THE CORONARY ARTERIES. 367 ments of Panum and of Cohnheim and v. Schulthess-Rechberg. Many of Baumgarten's animals survived for long periods; and two of them died with sudden heart failure, one in the midst of violent exertion. Wassiliewski (Ztschr. f. exper. Path. u. Therap., 1911, ix, 146) injected lycopodium spores into the coronary arteries, producing dilatation and weakness of the heart, often with a rise of blood-pressure. Administration of nitroglycerin then caused fall of 'blood- pressure and dilatation diminished. Hirsch and Spalteholz found that, though infarcts were produced by ligation of the coronary artery, the infarcts were smaller than the area supplied anatomically by the artery, and there was a not inconsiderable amount of anastomosis, especially between the branches near the surface of the heart. In man Chiari has found complete occlusion of the right coronary artery without infarction, and Pagenstecher has ligated that artery in an operation without evil result. These are the main facts regarding the coronary circu- lation which throw light upon the clinical conditions observed. Pratt has shown that the excised mammalian heart can be nourished through the veins of Thebesius sufficiently to carry out forcible contrac- tions for a considerable time, though this probably is not the case in the living animal. It has long been a matter of debate whether the heart muscle was nourished with blood during the systolic or during the d i a s - t o 1 i c period; the earliest contention being that of Scaramucci (16X9) that the coro- nary vessels are squeezed empty by the contraction of the heart muscle-fibres during systole and fill from the larger and more superficial coronary vessels during diastole. After a long controversy, during which Rabatel showed that the curve of coronary blood-pressure and apparently also the curve of blood velocity were exactly similar to the curve in the aorta, the question was definitely settled upon the excised heart by Porter and his pupils in favor of the old view of Scaramucci. Martin and Sedgwick (Studies from Biol. Lab., Johns Hopkins Univ., 1882-3, ii, 322) observed sudden changes in calibre in the coronary arteries, and ascribed this to the action of vasomotor nerves. Tracings by Porter (Bost. M. and S. J., 1896) and Maass (1899) confirm this view. This was confirmed by O. Langeridorff and Wiggers, who found also that adrenalin exerted a vasodilator action upon the coronary arteries of the excised heart instead of its usual vasoconstrictor action. Both Wiggers and G. S. Bond have found that the outflow through the coronary veins of the dog's heart in situ is increased by the administration of adrenalin. Bond investigated the effects of a large number of other drugs as well, and found that the coronary outflow always followed the curve of general blood-pressure; so that, under the experimental conditions, he was unable to demonstrate any specific action upon the coronary vessels, even from doses far larger than would be administered in thera- peutics. However, the operation is so severe that the animals are always in profound shock. Ida Hyde in Porter's laboratory found that the coronary blood flow was diminished by distention of the heart, a fact which may account for the weaker contraction of over- dilated hearts. SCLEROSIS OF THE CORONARY ARTERIES. PATHOLOGICAL AXATOMV. While the sclerosis of the coronary arteries does not differ in its pathol- ogy from the sclerosis of arteries elsewhere, nevertheless the action upon the heart gives rise to clinical and to secondary pathological conditions which are quite different from those of general arteriosclerosis, and which therefore deserve special consideration. 368 DISEASES OF THE HEART AND AORTA. Another important condition which is very common is arterioscle- rotic or atheromatous change arising in the aorta with or without associated involvement of the coronaries themselves, but spreading so as to involve the mouths of the coronaries as they arise from the aorta, and strangu- lating these vessels as they pass through the aortic wall (see Fig. 166). This has the same effect as a metal band constricting an artery would have; namely, of diminishing the blood-pressure and the velocity of flow in the artery beyond it, of allowing the walls of the artery to contract down and hence of producing a further permanent secondary narrowing of the lumen, with progressive diminution in the blood supply to the part (Halsted). The course of the artery may show patches of hardening with indentations and widenings, collar-like constrictions, or uniform widenings; or, on the other hand, the arteries may be converted into uniform tubes whose walls may give the sensation of rubber tubes on the one hand (uniform fibrous sclerosis), or of absolute pipe-stems (complete calcification) on the other. This condition is, of course, particularly common in arteriosclerosis affecting the base of the aorta, i.e., luetic aortitis and Fir,. IfiO. Sclerosis of a coronary artery, producing an area of infarction near the apex. A. Show- ing the entire specimen. B. The sclerotic coronary artery, camera brought closer; a wire has been passed through the mouth of the coronary artery. luetic aortic insufficiency, and may account for many of the symptoms to be discussed later (see page 369). Since the heart muscle requires much more blood when it is beating forcibly and rapidly than when it is beating slowly and quietly, it is easily seen that this collateral circulation may be sometimes adequate and some- times not. Also, since in different individuals of the same species there are variations both in the structure and disposition of the minute arteries and in the needs of the muscle-fibres for nourishment, it is but natural that the results of coronary disease should vary greatly. CLINICAL MANIFESTATIONS. The clinical pictures associated with coronary sclerosis are character- ized by some or all of the following features: pain over the precordium or down the arms, feelings of suffocation or of impending death, SCLEROSIS OF THE CORONARY ARTERIES. 369 paroxysms of most intense dyspnoea with palpitation, enlargement and pulsation of the liver, general weakness, sudden death. A considerable grade of arteriosclerosis may be present in both young and old individuals without giving any symptoms whatever, as shown in the case of J. L. (page 561). Another example of this was a colored boy under the writer's care who after very vigorous life died at the age of nine- teen in the fifth week of typhoid fever. Neither before nor during the fever had he had any cardiac symptoms. However, his coronary arteries were found to be very sclerotic. Sudden Death. S u d d e n d e a t h is frequently the first manifesta- tion of the condition, and examples are almost daily in the newspapers of persons, usually men past middle life, who drop dead without warning and with no previous illness, due to sudden thrombosis of the sclerotic coro- nary arteries, or perhaps merely to the fact that, though the sclerotic process has been going on gradually, the instant has passed at which the cardiac nutrition becomes insufficient and ischsemia sets in with sudden functional insufficiency, just as occurs in the leg in intermittent claudica- tion. This must be the case in many hearts in which no actual thrombosis or embolism can be found post mortem. Paroxysms of dyspnoea such as those described on page 204, the so- called cardiac asthma, are also extremely common in coronary sclerosis, especially when combined with aortic insufficiency (vide page 456), in w r hich case they are no doubt due to the dilatation and weakening of the left heart and the consequent accumulation of CO, in the blood. It has been suggested by Drs. C. M. Cooper and E. O. Jellinek of San Francisco that this was always an accompaniment of sclerosis of the right coronary artery and dilatation of the right heart, but in autopsies of two cases under the writer's care who had suffered from such attacks the right coronary was absolutely free from sclerosis. Sensations of pain in the precordium, and especially behind the sternum, as well as pains and tenderness over various interspaces and radiating down the arms, are especially common in coronary sclerosis. Paroxysmal Tachycardia. Attacks of tachycardia beginning with sudden doubling of the pulse-rate and ending in sudden halving of the latter, just as is present in essential paroxysmal tachycardia, have been described by Romberg as manifestations of coronary sclerosis, and Krehl also cites similar findings. In Romberg's case the pulse-rate rose suddenly from 100 to 200, while the respira- tion remained at 20. The attack lasted t\vo days and then the pulse-rate dropped sud- denly to 100. Later an aortic stenosis developed gradually and the patient died of heart failure, the autopsy showing aortic stenosis and sclerosis and marked coronary sclerosis. Dr. Barker informs the writer that he also has seen a couple of cases in which such attacks were associated with coronary sclerosis. Quite recently similar attacks have been produced by T. Lewis upon ligating the coronary arteries in cats even after the cardiac nerves had been sectioned. Painful sensations about the heart are particularly common in asso- ciation with coronary sclerosis, but on the one hand they are by no moans confined to this condition, and on the other hand most extensive coronary sclerosis may be present without the occurrence of cardiac pain. The most marked form of cardiac pain, the .so-called "angina pecloris" (pronounced 24 370 DISEASES OF THE HEART AND AORTA. an'gina, not angl'na) to be discussed below, is in its most typical form usually associated with a certain degree of coronary sclerosis. ANGINA 1 PECTORIS. In 1768 both Heberden and Rougnon described attacks of pain in the chest. Tne former recognized the condition the more clearly and described it in the following words: "But there is a disorder of the breast marked with strong and peculiar symptoms, considerable for the kind of danger belonging to it, and not extremely rare, which deserves to be mentioned here at length. The seat of it, and sense of strangling and anxiety with which it is attended, may make it not improperly be called angina pectoris. " They who are afflicted with it are seized while they are walking (more espe- cially if it be up-hill and soon after eating) with a painful and most disagreeable sensation in the breast, which seems as if it would extinguish life if it were to increase or to continue; but the moment they stand still all this uneasiness vanishes. "In all other respects the patients are, at the beginning of the disorder, perfectly well, and in particular have no shortness of breath, from which it is totally different. The pain is sometimes situated in the upper part, some- times in the middle, sometimes at the bottom of the os sterni, and often more inclined to the left than to the right side. It like- wise very frequently extends from the breast to the middle of the arm. The pulse is, at least sometimes, not disturbed by this pain, as I have had opportunities of observing by feeling the pulse during the paroxysm. Males are most liable to this disease, especially such as have passed their fiftieth year. After it has con- tinued a year or more, it will not cease as instantaneously upon standing still, and it will come on not only when the persons are walking but when they are lying down, especially if they lie on the left side, and oblige them to rise out of their beds. In some inveterate cases it has been brought on by the motion of a horse or a carriage and even by swallowing, coughing, going to stool, speaking, or any disturbance of mind. "Such is the usual appearance of this disease, but some varieties may be met with. Some have been seized while they were standing still or sitting, also upon first waking out of sleep, and the pain sometimes reaches down the right arm as well as the left and even down to the hands, but this is uncommon ; in a very few persons the arm has at the same time been numbed and swelled. In one or two persons the pain has lasted some hours or even days, but this has happened when the com- plaint has been of long standing and thoroughly rooted in the constitution; once only the very first attack continued the whole night. " I have seen nearly a hundred people under this disorder, of which num- ber there have been three women and one boy two years old. All the rest were men near or past the fiftieth year of their age. "Persons who have persevered in walking till the pain has returned four or five times have then sometimes vomited The termination of angina pectoris is remarkable. For if no accident intervene but the disease go on to its height, the patients all s u d d e n 1 y fall d o w n a n d perish almost immediately. The angina pectoris, as far as I have been able to investigate, belongs to the class of spasmodics, not of inflammatory complaints. For. "In the first place, the access and the recess of the fit is sudden. "Secondly, there are long intervals of perfect health. "Thirdly, wine and spirituous liquors and opium afford considerable relief. "Fourthly, it is increased by disturbance of mind. "Fifthly, it continues many years without any other injury to the health. ''Sixthly, in the beginning it is not brought on by riding on horseback or in a car- riage, as is usual in diseases arising from scirrhus or inflammation. "Seventhly, during the fit the pulse is not quickened. "Lastly, its attacks are often after the first sleep, which is a circumstance common to many spasmodic disorders. 1 Pronounced ''angina"; e.g., " Insporato abiit quern una angina sustulit hora" (Lucilius). ANGINA PECTORIS. 371 "With respect to the treatment of this complaint, I have little or nothing to advance. . . . . Quiet, warmth, and spirituous liquors help to restore patients who are nearly exhausted and to dispel the effects of a fit which does. not soon go off. Opium taken at bedtime will prevent the attacks at night." Heberden's contemporary, the great John Hunter, suffered from this disease, and described his attacks most vividly. The modern aspects of the whole subject have been discussed in a masterly way by Sir W. Gairdner as well as in the more recent monographs of W. Osier and G. A. Gibson. CHARACTER OF THE PRECORDIAL PAIN AND CLINICAL SUMMARY. In Heberden's description we have epitomized almost all the clinical features. (1) The sudden attacks of oppression in the chest, with a feeling of strangling, and, as Hunter puts it, " as though the sternum was being drawn back to the spine," or, in the words of Matthew Arnold, as "though there were a mountain upon my chest." (2) The mental anguish (termed by Gairdner angor animi), with the fear of impending death, especially pro- nounced in John Hunter. (3) The intense pain, situated sometimes in the lower sometimes in upper part of the sternum, more frequently to the left than to the right (although occasionally to the latter), and very often radiating to the arm, especially the left. (4) Some of the disturbances of sensation; even Heberden speaks of numbness of the arm. (5) Changes in the pulse in some cases: intermissions; extrasystoles in some cases (Hunter) ; alternating pulse in others (Mackenzie). (6) The extreme pallor and constriction of peripheral arteries during the attack. (7) The sudden death. (8) The main factors in bringing on attacks, walking up-hill, flatulence and digestive disorders, bending down in undressing, mental excitement or anxiety, and especially anger; but none of the more gentle emotions, such as pity, sorrow, etc., even when felt intensely. (The effect of exposure to cold does not seem to be mentioned by these writers.) (9) The association of the condition with sclerosis of the coronary arteries. (10) Its frequent association with abnormal fatty deposits about the heart (cf. Jenner and also page 294). (11) The relief of symptoms by means of opium, warm applications, hot drinks (vasodilator mechanisms), and counter-irritation (Heberden). (12) Its incurability, owing to the seat of the trouble. To these points clinical observations since Jenner have added: (1) The existence of anginoid attacks with several conditions other than those of coronary sclerosis, particularly with over-indulgence in tobacco, with hysteria, with hyperthyroidism, and with other purely vasomotor phe- nomena, as well as with practically all the valvular diseases of the heart. (2) The frequent association of angina pectoris with certain definite areas of tenderness which represent spinal segments corresponding to the referred pain. (3) The occurrence of rise in blood-pressure with each attack The relief of the attacks by inhalations of amyl nitrite and other vasodilator drugs. (5) The ending of the attack in diaphoresis. Sir William Gairdner has called attention to the occurrence of certain cases resembling Heberden's angina pectoris in every way except in the absence of pain as a symptom (angina sine dolore). 372 DISEASES OF THE HEART AND AORTA. Paths Traversed by the Pain Sensations. The afferent impulses from the heart have been traced by Ludwig and Cyon through the depressor fibres of the vagus. It has been shown by Eyster and Hooker that the afferent impulses from the aorta and coronary arteries do not take this same path but pass upward in the main bundle of the vagus. There is no evidence from animal experiment that afferent impulses pass in any other way; but Henry Head, as a result of his most extensive studies upon pain in visceral disease, states that this "produces impulses which pass into the spinal cord by the white rami. The segment on which they infringe is excited and pain is produced. At the same time all potentially painful influences passing into this segment from the afferent nerves are exaggerated, and ultimately the body wall may become tender." These sensations of referred pain follow the same path as has been described by Bayliss for the vasodilator fibres with which protopathic sensation seems to be closely associated, as shown in herpes zoster, etc. Protopathic sensations are referred back to the distribution of the corresponding nerve segments without close reference to the points at which they arise. Insensibility of the Heart to Touch. The heart itself seems to be devoid of tactile sensation, for Harvey gives the following description of the condition in the nineteen-year- old son of Viscount Montgomery, who had a fistulous opening in the chest wall over the heart following fracture of the rib in early childhood. The youth never knew when we touched his heart except by the sight or the sen- sation he had through the external integument. The writer has found that tapping the skin over the heart of a patient whose chest wall had been removed for empyema caused no sensation, while gripping the ventricles caused a feeling of oppres- sion over the lower end of the sternum, but no extrasystoles or pain. 1 Palpitation and Anginal Sensations Compared. The sensations which may be felt from the heart itself may be either rhythmic and felt as a distinct sensation accompanying each systole of the heart, such as the feeling of palpitation, or the pain felt at each beat in some cases of pericarditis, especially those associated with pneumonia. The sensation in the latter condition may, however, arise in the parietal pericardium, and may have nothing to do with the heart itself. Sensations of palpitation may be very distressing, partly on account of the feelings of suffocation which accompany them, partly on account of the mechan- ical shock of the heart beating forcibly against the chest wall like a bird in a cage. But, however intense and distressing, the sensation of palpi- tation is always a pressure sensation and never one of pain. On the other hand, the real cardiac pain is never intermittent, never felt as a distinct sensation with each beat of the heart, but, whether dull and aching or 1 Sano (Arch. f. d. gos. Physiol., 1909, cxxix, 217) states that touching the exposed heart of an unana-sthctized rabbit does not even frighten the animal. FIG. 167. Distribution of pain in attacks of angina pectoris. (Schematic, after Head and Mackenzie.) ASCAO, area correspond- ing to the ascending aorta; TR.AO, area cor- responding to the transverse aorta; L.A,R.A, area corresponding to left and right auricles. ANGINA PECTORIS. 373 sharp and stabbing, it has no throbbing quality about it. It is, therefore, to a quite different category. Hirschfelder has added some evidence for this view by observing that in some cases of palpitation the sensation was referred definitely to the root of the aorta, and was exactly similar in character to other sensations of throbbing in the radial artery alone, which were sharply localized along its course and not spreading like a pro- topathic sensation. Referred Pains in Angina Pectoris. James Mackenzie and Henry Head have called attention to the commonness of referred pain and tender- ness in angina pectoris. Mackenzie showed that there is often tenderness in the areas supplied by the second and third cervical segments, whose fibres along with some from the spinal accessory run down to the heart through the vagus. This would account for the occipital headaches and tenderness of the sternocleido- mastoid and trapezius muscles which are frequently present. The muscu- lar tenderness is elicited by squeez- ing gently between the thumb and forefinger. The distribution of the pain and hypersesthesia, according to Head, bears a close relation to the chamber most affected, and particularly to the somatic segment of the embryo to which it corresponds. FIG. 168. Distribution of attacks of pain and sensory disturbances in a case of angina pectoris. (After Head, with permission of the publishers of Brain.) Correspond embryo- logically to Nerve supply Associated phenomena and pain referred to Auricles. . Ventricles. 5, 6, 7, 8 thoracic 2,3,4,5,6 thoracic Ascending aorta. . . 3 and 4 cervical. ments segments Transverse arch . . . C. IV C. IV.. . . Descending aorta. . Pulmonary arterv. Thoracic segments corresponding 2-12 C.V-VIII 2-12, esp. C. V 4-12 . . . 5, 6, 7, 8 segments , Lower axilla and shoulder- blades. 2-6 thoracic seg- \ Chest wall from 2d-7th rib, ulnar surface of forearm to wrist, and inner aspect of upper arm. 3 and 4 cervical [ These segments also to 3 and 4 c. and 1 thor. Tenderness in neckof sternomastoid and trapezius muscles. Tender- ness and pain at back of neck. (Dilatation of pupil?) Laryngeal areas of neck (1th branchial barV Back or front of chest, espe- cially below nipple; abdo- men. Outer two-thirds of arm and hand; arm muscles. Thus, the auricles (atria), which are the hindmost in the development of the cardiac tube, receive their innervation from and refer their pain to the fifth, sixth, seventh, and eighth thoracic segments. The ventricles, the next chambers headward, correspond to 374 DISEASES OF THE HEART AND AORTA. the second to the sixth thoracic; the ascending aorta from the semilunar valves to the origin of the ductus arteriosus corresponds to the primitive aorta with the third and fourth branchial artery, and the pain is referred to these segments (but an aneurism, etc., involv- ing this in adult life will also involve the neighboring nerves and the pain will be referred to the first, second, and third thoracic segments as well). The fifth to the eighth cervical segments, corresponding to the pulmonary artery, will not be involved, and pain may not be referred over these areas. 1 (There are many notable exceptions to this rule even among Head's cases; but there is usually overlapping of these areas.) Sudden Death and Motor Disturbances. The phenomena thus far considered are purely sensory; and the question arises, what are, if any, the motor disturbances connected with angina pectoris? It is evident that the cessation of the heart-beat in sudden death that occasionally occurs may be due either to the occlusion of the artery or to a sudden onset of complete heart-block as in the Adams-Stokes syndrome. The lat- ter condition is sometimes associ- ated with angina pectoris and in some cases due to coronary sclerosis (see page 561), though this is rare. Much more frequently the pulse be- comes regular after a short time, or sudden death from heart-failure sets in just as in the experiments of Cohn- heim and v. Schulthess-Rechberg. During the attacks of angina FIG. 169. Blood -pressure curve showing crises of hypertension during attacks of angina pectoris. pectoris the blood-pressure is often high, though Mackenzie states that in many cases there is no change whatever. This seems to be due to a true pectoral vasomotor crisis in the sense of Pal, rising sharply with and falling sharply after the attack, as shown in Fig. 169. ETIOLOGY AND VARIETIES OF ANGINA PECTORIS. The idea that sclerosis of the coronary arteries was the lesion which caused angina pectoris seems to have originated not with Heberden but with Edward Jenner, the discoverer of vaccination, who was so certain of its pathology that before doing an autopsy upon a case he made a bet with a friend that he would find thickening of the coronary arteries. He won the bet. This indeed seems to be correct for very many cases of fatal angina, since Hue-hard found coronary sclerosis present in 128 out of 145 autopsies recorded in the literature, and most of the others were in cases of adherent pericardium or valvular disease. Vernon (Brit. M. J., 1911, i, 613), on the other hand, finds but 50.1 per cent, of coronary disease in a series of 283 cases collected from various authors. Osier calls attention to occasional deaths from tobacco and other toxic anginas. 1 Hi.s own rases 50, 57, and 58, as well as cases of many other writers, show tenderness during and after attacks due to aneurism involving the ascending aorta. ANGINA PECTORIS. 375 Angina Pectoris without Coronary Sclerosis. However, in IS 12, J. Latham reported a number of cases which, in spite of the occurrence of intense anginal symptoms, did not run the usual course ending in sudden death, and to these he gave the name of "pseudo-angina" (angina notha). Bean, Stokes, and Graves also described reflex and toxic forms of angina, but a much clearer light was thrown upon the subject by Noth- nagel's article entitled "Angina pectoris vasomotoria." He says, "We must interpret this symptom-complex to indicate that we are not dealing with a disease which arises primarily in the heart, but that the symptoms of stenocardia are of secondary origin and are brought on by a very general spasm of the arteries." The term "pseudo-angina" has been severely criticised by Balfour and Gibson, since "angina" is a symptom, not a disease, and in all cases it is a very real one. NothnagePs term, "vasomotor angina," or Huchard's "reflex angina," seems to the writer to be preferable. Theories as to Causation of Anginal Pain. Many theories have been advanced to explain the causation of pain in anginal attacks. These may be classified as follows: (1) Ischemia from Coronary Stenosis. The original view of Jenner was later supple- mented by Allan Burns, that the attack may be brought on by asphyxia of the heart muscle when there was a disproportion between the amount of blood flowing to it and the amount of blood which it needed. Potain, in 1870, was the first to introduce the theory that angina pectoris is due to "the intermittent claudication of the heart"; but Allan Burns had already completely demonstrated this causal factor in 1809 and had described his observations in the following words: "If we call into vigorous action a limb round which we have with a moderate degree of tightness applied a ligature, we find that the member can only support its action for a very short time, for now its supply of energy and its expen- diture do not balance each other . . . we witness an induction of an extreme degree of debility and we have the patient complaining of an unusual painful feeling in the limb, but still all its muscles are in a state of inactivity. . . . If a person with the arteries of the heart diseased in such a way as to impede the progress of the blood along them attempt to do the same (ascend a steep or mount a pair of stairs), he finds that the heart is sooner fatigued than the other parts are," and the same pain results. (2) Ischaemia from vasoconstrictor spasm of the coronary arteries, which reduces the functional condition to the same state as described by Allan Burns for the coronary sclerosis. This seems to apply to the vasomotor and toxic anginas and often consti- tutes a factor superimposed upon the coronary sclerosis in the angina vera. Such an action of drugs upon the coronary vessels has been demonstrated on the excised heart by O. Loeb, Langendorff, and \\iggers (see page 367). (3) Acuie dilatation of the heart, producing a pain similar to that of in- testinal colic. This theory particularly has been adhered to by many writers. The similarity between the anginal pain and that of renal, biliary, pancreatic, and intestinal colic suggests that it belongs to the common form by \vliicli the visceral nerves give expression to overdistention. Some dilatation usually accompanies the attack, and seems to be a primary cause of the pain in cardiac overstrain and in many cases of val- vular lesion. (4) Neuritis. It may at times lie due to neuritis of the cardiac nerves, or, on the other hand, to a neuritis primary in the brachial nerves and referred to the heart. Lesions of the cardiac plexus have been described by Lnncereaux. (iroeco. and Benenati. Inn Herard and others have failed to find them. Nevertheless it is i|iiite possible that sub- stances like tobacco (nicotine), which stimulate sensory nerves in the heart and \\hich have a specially toxic action upon the ganglion cells, may produce toxic neuritis of these nerves. (.">) Neuralgia of the cardiac nerves. (6) Action of other constitutional diseases like gout, diabetes, and chronic nephritis. 376 DISEASES OF THE HEART AND AORTA. But it is most probable that the effects are due to the other above-mentioned factors which accompany these diseases, arteriosclerosis and the presence of vasoconstrictor substances; either as retention products or internal secretions. ASSOCIATED CLINICAL CONDITIONS. The various conditions with which angina is associated most commonly might be classified as follows: I. Organic Lesions. A. Sclerosis of coronary arteries. B. Aneurism, especially of first part of ascending aorta. C. Valvular lesions, especially aortic insufficiency. (This constitutes a very common group.) D. Aortic aneurism, especially of the sinuses of Valsalva and the ascending arch. E. Adherent pericardium. (The most frequent form which is seen in children.) II. Vasomotor anginas. A. Hysterical type, most common in women, associated with other vaso- motor disturbances and stigmata of hysteria. B. Toxic, due to the action of various poisons, especially (a) tobacco, (6) caffeine, taken both as tea and as coffee. C. Associated with hyperthyrodism and exophthalmic goitre. III. Attacks of more or less anginoid pain occur in the cases of acute dilatation of healthy hearts, due to primary cardiac overstrain. Angina Pectoris in Valvular Diseases. The attacks of angina pectoris associated with coronary sclerosis, which represent the original form de- scribed by Heberden, are usually designated as angina vera. These are very often associated with valvular lesions, especially with aortic insuffi- ciency in which the coronary lesions are usually continuous with those of the aorta, but they are also common in association with other valvular lesions, since it is rare to find a case of chronic valvular disease without some disease of the coronary arteries. The presence of valvular disease, therefore, rather favors than excludes the diagnosis of coronary sclerosis. In spite of the frequency with which these two conditions are asso- ciated, occasionally one encounters cases of angina with valvular disease, especially aortic insufficiency, without any disease of the coronary vessels whatever, as was well exemplified by a patient with a ruptured aortic valve who was for five years under observation at the Johns Hopkins Hospital. During this time he suffered from very frequent attacks of typical angina pectoris. He died suddenly while at stool. Autopsy showed rupture of aortic leaflet. The coronary arteries were soft and the walls were not thickened anywhere. Angina Pectoris in Acute Dilatation. It is possible: (1) that under these conditions acute dilatations of the heart, due to momentary diminu- tion in tone of the heart muscle, might be the immediate cause of the pain, which would thus be of primary cardiac rather than vascular origin. (2) That in such dilatation, etc., centripetal stimuli may arise in the heart which may cause a general vasoconstriction. (This is contrary to the usual depressor effect of stimuli arising in the heart, but it is not at all certain that in the presence of such a pathological condition as angina pectoris the paths of least resistance in the central nervous system may not be quite ANGINA PECTORIS. 377 different from what they are in the normal individual.) (3) Miss Hyde in Porter's laboratory has shown that dilatation of the heart in itself caused diminution in the flow through the coronary arteries, and it is possible that the circulation may thus be diminished to a point at which relative ischsemia of the heart may set in and cardiac pains result. Angina Pectoris in Aneurism. Attacks of angina pectoris are very common in cases of aneurism involving the ascending arch, and especially in early small aneurisms near the sinuses of Valsalva. This has long been known, but is the subject of an especially interesting article by Dr. Osier upon "Angina pectoris as an early symptom of aneurism." The anginoid pains in this condition are probably simply reflex, not the result of primary peripheral vasoconstriction, cardiac ischaemia, etc., but simply the occurrence of pain sensation arising in the aortic walls from overstretching of the aorta under pressure heightened from any cause whatever, or from increased excursion of the aortic wall as a result of increased systolic output, etc., as is so frequently seen in the abdomen in nervous women with epigastric pain due to a throbbing of the abdominal aorta. In the later stages of the aneurism, the symptoms may be less intense, due perhaps to the fact that by erosion, etc., pressure upon the aneurism has diminished, perhaps to the fact that after a time endings of the sensory nerves have been permanently injured or rendered less sensitive by the progressive change in the aortic wall. Anginal Attacks in Children. Angina pectoris also occurs in children, especially in association with mitral stenosis, as illustrated by the following case: The patient was a boy aged 8 who had had rheumatism in the right hip two years previously, and since then " had attacks of pain over the heart, especially after exercise. The pain was so severe that it compelled him to stand perfectly still until it passed off; his cheeks became blue and pale. He sometimes felt as though held in a vise, but never had any feeling of fear. He also had at times pain on the right side over about the sixth rib, which was sometimes present with that on the left side, but often present without it. Exercise seemed to bring on both. Examination showed a very slightly enlarged heart with systolic retrac- tion over the fourth left interspace, none about origin of diaphragm (Broadbent's sign absent). Area of cardiac flatness changes with respiration. The first sound at the apex was snapping in character and was preceded by a well-defined rumble. Second sound was clear, accentuated over the pulmonic area. Pulse 92 per minute, of good volume, regular in force and rhythm." Such attacks are quite definite angina vera in the sense of Heberden, and indeed the latter includes a similar case in his list. In children the association is, however, much more commonly with valvular lesions than with coronary sclerosis, and perhaps most frequently of all with Adherent Pericardium. This is an extremely common concomitant and cause of anginal attacks, especially in children and adolescents. The pains are, perhaps, simply reflex aches from the ordinary tugs upon the pericardium, perhaps brought about by the stretching of the pericardial fibres which occurs when the heart becomes dilated. VASOMOTOR ANGINA. The second great group of cases with anginal symptoms are those in which the anginal symptoms are of purely vasomotor origin (IJaynaud's disease of the heart) and are not associated with organic lesions,- angina pectoris vasomotoria of Nothnagel (angina pectoris spuria of Lat ham. angines de poitrine reflexes of Huchard). The characteristic phenomenon in this group is the occurrence of g e n e r a 1 o r 1 o c a 1 v a s o < o n - striction ushering in the att a c k; that is, there are usually coldness, numbness, often tingling, weakness, and heaviness in the left arm, pallor of the latter, with marked diminution in sixe ami caliber of the left radial, often also of the right radial artery, sometimes of the vessel.- 378 DISEASES OF THE HEART AND AORTA. of the leg, trunk, and head. The patient may become pale and blue or the lips ashen, and the course of the attacks may exactly simulate those of coronary sclerosis. Death in such attacks is, however, extremely rare. It has occurred in several cases in which no coronary sclerosis nor other lesion was present to account for the death. However, Dr. Osier suggests that in these cases there may have been myocardial changes demonstrable only by the method of Krehl. Hysterical Angina. The most common form of vasomotor angina is the neurotic or hysterical type, which is most common in young women and is associated with the other stigmata of hysteria. It may also occur in men. For example, a neurotic young physician recently under the writer's care developed anginal symptoms (fear, precordial constriction, pain down left arm) after seeing a relative die of angina pectoris. He recovered after being assured his trouble was trivial. Clinical Groups with Anginal Symptoms and their Characteristic Features (modified from Huchard) . Coronary Angina. Site of disturbance. Stenosis or obliteration of the coronary arteries. (In some cases valvular lesion or aneurism only). Age. Age of arteriosclerosis after 40. Factors bringing on attack. Effort of some sort, mental or physical. Rarely spontaneous, sometimes nocturnal. Not associated with any other form of neurosis. Nature of pain. Ag- onizing sensation of pressure. Usually felt most acutely behind sternum. Referred pain down arm, especially left arm, and over chest, neck, etc. Duration. 2 to 15 minutes, stopping soon after standing still. Attitude. Silent, immobile. Prognosis. Grave; almost always fatal. Treatment. Vasodilators. Hysterical Angina. Site of disturbance. Central nervous system acting through the vasomotor nerve and cardiac plexus. Age. At all ages, even childhood; sometimes at menopause. Most frequent in women. Factors bringing on attack. Usually spontaneous onset without effort, often recur- ring at fixed hours and associated with other neurotic symptoms. Nature of pain. Pain less agonizing, with feeling that the heart is distended felt, most intensely at the apex. Duration. 1 to 2 hours, not diminished by standing still, not increased by walking. Attitude. Agitated ; walking about. Prognosis. Mild ; never fatal. Treatment. Antineurotics and antineuralgics. Gastrointestinal. Site of disturbance. Distention or neuralgia due to gastric troubles. Age. At all ages, especially among women. Factors bringing on attack. Not brought on by effort. Nature of pain. Precordial, not substernal pain; with fulness of chest and distention of heart but less radiation. Signs of dilatation of right heart; increase of inverse diameter to right. Duration. 1 to 2 hours. Prognosis. Death rare. Treatment. Antidyspeptic remedies. Tobacco. Site of disturbance. Spasm of coronary arteries. Factors bringing on attack. Angina associated with toxic disturbances, vertigo, gastric and respiratory troubles. Onset spontaneous. Nature of pain. Attacks associated with bradycardia, intermittent pulse, arrhythmia, pal- pitations. Attacks longer than those of angina vera. Prognosis. Death ANGINA PECTORIS. 379 rare. Attacks often disappear rapidly on giving up tobacco. Treatment. Stopping tobacco, tea, and coffee. Rest and mental quiet. Light diet. (Anginas due to tea, coffee, etc., brought about by the same cause.) Acute Cardiac Overstrain (with or without Valvular). Site of disturbance. Sudden dilatation of the heart. Age. At any age, but most common in young athletes, soldiers, anaemic girls. Factors bringing on attack. Comes on in the midst of some unusual effort, such as a mountain climb, boat race, a charge, or a dance. Nature of pain. In the heart itself, usually retro- sternal. Associated with signs of dilatation to right and left, extreme dyspnoaa, often systolic murmur and arrhythmia. Duration. In maxi- mum intensity a few minutes, after cessation of attack, the pains often continuing or recurring as less intense pain, tachycardia or arrhythmia usually persisting some time after attack. Attitude. Immobile. May throw himself to the ground in the midst of the effort. Prognosis. Death rare. Permanent weakening of the heart if the over-exertion is soon and frequently repeated. Treatment. Prolonged rest and general cardiac therapy until cardiac dilatation has passed off; gradual resumption of active life. Angina Pectoris in Hyperthyroidism. Very closely resembling the neurotic group are the cases of angina associated with exophthalmic goitre, in which the attacks are sometimes more like those of neurotic, sometimes more like those of the coronary type. The crucial point in the diagnosis is the detection of hyperthyroidism by the application of the numerous tests for Graves's disease, etc. A case which has been for the past year and a half and still is under the writer's care will serve as type of this condition (see page 690). Treatment is the same as for the Graves's disease which is the primary condition (see Part IV, Chapter II). The attacks themselves may be treated symptomatically with amyl nitrite, etc., but the important factor is the treatment of the underlying disease. Tobacco Angina. Anginal attacks due to tobacco are not uncommon, both in young persons beginning their first excesses in tobacco and in older persons whose over-indulgence is adding itself to a beginning or advancing coronary sclerosis. In both the symptoms disappear soon after the tobacco is absolutely given up, persistence of the attacks more than a few clays after this being evidence that some damage to the coronaries has occurred. The attacks themselves may very closely resemble those of true angina, but very frequently precordial pains not of an anginal character may be felt by smokers between or for some time before such attacks. The main factor in the effect of tobacco smoke, as shown by Ratner and Lee, i.s the nicotine, although small amounts of HCX, CO, and pyridine liases are present in tlie smoke. Moreover, it is probable that the action of smoked tobacco is exerted especially upon the coronary arteries, because it enters the heart directly from the pulmonary vein without preliminary dilution in the peripheral circulation. Nicotine seems to have the effect of (1) stimulating the vagus, (2) producing vaso- constriction, (3) thereby of raising the blood-pressure. In most cases this leads gradually to hypertrophy of the heart, but in some, especially weaker individuals, it tends to facili- tate dilatation, thus facilitating angina. Moreover, Jackson and Matthews have recently shown for aconite, which in many ways is a similar drug, that much of its action is exerted through stimulation of the sensory endings of the depressor nerve. It is possible that nico- tine angina is due in part to similar sensory stimulation. 380 DISEASES OF THE HEART AND AORTA. Angina in Acute Dilatation. The attacks of pain and precordial dis- comfort during acute cardiac overstrain and dilatation may reach anginoid intensity, as was noted by da Costa among the soldiers of the Civil War. He not infrequently encountered patients who had suffered so intensely in the midst of a charge that they could endure it no longer and had thrown themselves to the ground, exposed to almost certain death from the point- blank fire of the enemy, rather than continue to bear the torment within (page 177). These pains are usually retrosternal, often with numbness of the arms and tingling in the fingers, and associated with feeling of compres- sion and with palpitation. These pains occur in otherwise healthy persons during the height of supreme effort, while in patients with myocardial weakness or coronary sclerosis only a slight effort or indeed even emotional excitement may suffice to bring them on. DIAGNOSIS. The actual differentiation of the various groups is not always easy in the individual cases, as one frequently has a coronary sclerosis with a tobacco angina superinduced upon it, a gastric etiology where there are already attacks of angina vera, etc., and since it is a safe rule never to diag- nose the milder conditions until the more serious can be ruled out with reasonable probability. These cases may cause the physician anxiety, since he remains uncertain whether to expect sudden death or whether he is dealing with a comparatively mild condition. CASE ILLUSTRATING DOUBTFUL DIAGNOSIS. E. W., widow, aged 65, has had, since her menopause at 54, occasional attacks of precordial p a i n , most intense just behind the sternum and especially about the level of the third costal cartilage. She feels as though some one were bor- ing through from sternum to spine with a sharp instrument. The pain is also felt over the left side of the chest and down the left arm, which sometimes becomes numb, cold, weak, and heavy. During the attack she feels as "though the end has come." These attacks come on apparently spontaneously without definite asso- ciation with either emotional disturbance, exposure to cold, or muscular effort. They last an hour or two and are relieved by amyl nitrite or nitroglycerin. She feels weak for a day or so after an attack, but at other times is extremely active for her age and rarely short of breath. The patient is not at all neurotic. She has used coffee and beer in moderation all her life. It must be added that near the end of the menopause and before the first cardiac attack, she had a severe spell of grippe which kept her in bed for four weeks and left her very much prostrated. On physical examination the patient is well nourished. Slightly emphysematous, but lungs otherwise normal. Heart not enlarged; action regular in force and rhythm; sounds clear, neither second sound especially accentuated. Pulse between attacks is of good large volume and quality, apparently about normal tension; vessel wall not specially thickened. Xo ascites. Liver not enlarged. Feet always swollen from varicose veins, not especially so during or after attacks. In this case the question of crucial importance is whether the angina is due to the occurrence of the menopause and is neurotic, or to the influenza which she contracted about the same t i m e a n d which may have brought on a coronary sclerosis. The attacks themselves resemble angina vera, although their duration is longer than usual. The age of the patient and the history of severe influenza also are in favor of coro- nary sclerosis. On the other hand, the fact that ordinary exertion does not seem to bring them on. but that they .occur when the patient is moderately quiet, is in favor of the neu- rotic. It must, however, be borne in mind that the patient's statements in this regard ANGINA PECTORIS. 381 may be inaccurate, and, further, that in occasional cases, where the diagnosis of functional angina seemed quite well established, autopsy has shown definite coronary sclerosis. It seems impossible to establish a definite diagnosis here, and the management of the case is therefore directed toward the severer form, ordering as quiet a life as the patient will carry out (since potassium iodide is not well borne), vigorous use of amyl nitrite and nitroglycerin at the time of the attacks, and erythrol tetranitrate thereafter. A diet of small quantities of food low in purin bodies and salt is insisted on. Since these measures have been instituted she has remained entirely free from anginal attacks for over two years, in spite of another attack of influenza. These facts are in favor of a reflex origin of the condition. Differentiation from Abdominal Diseases. Angina pectoris is, as a rule, easily differentiated from other diseases, though occasionally an attack of biliary, pancreatic, or left renal colic referred to the shoulders or even intestinal colic high in the epigastrium may closely simulate it. Careful physical examination and location of the areas of tenderness over the af- fected viscus should rule out this error. TREATMENT. General Therapeutic Measures. The old treatment of Heberden men- tioned above, "quiet, warmth," and hot drinks, even if spir- ituous, also ''opium," best in the form of morphine, 15 mg. Q gr.) hypo- dermically or by the mouth, during the attack, and repeated if necessary. As Heberden stated, it is well to bring on perspiration (and hence vasodila- tation) in any way possible. 1 Nitrites. The most important means for the relief of the attack is, however, the inhalation of a m y 1 nitrite. In 1867, Lauder Brunton tried the effect of inhalations of this substance upon patients suffering from an acute attack of angina pectoris, and demonstrated that it produced very marked, almost instantaneous relief. He was led to investigate this substance by the realization that the attack was accompanied by vasoconstriction and high blood-pressure, and by the knowledge that the newly investigated amyl nitrite had been found to have a vasodilator action. Lauder Brunton's observations have been generally confirmed, and this drug has become the classical remedy for relief of the attack. Its action should be supplemented at once by hypodermic or oral administration of one or two drops of spirits of nitroglycerin (or more if the patient has been found resistant to it), and this may be followed by erythrol tetranitrate by the mouth, since this drug exerts a slower action lasting over three to six hours. Erythrol tetranitrate should be continued for some time after the attack. Potassium Iodide. Between attacks potassium iodide in moderate doses 0.3 Gm. (gr. v) to 4 Gm. (3i) t.i.d. should be given, as it seems to diminish the frequency and severity of attacks. Dr. G. S. Bond in the writer's laboratory has found that practically all the drugs which he has investigated affected the outflow from the coronary veins in the dog's lie-art exactly as they affected the general blood-pressure. Amyl nitrite and nitroglycerin were no exceptions to this rule. They lowered the general blood-pressure and decreased the outflow through the coronaries. The effect was the same whether the heart was dilated or not. and seemed also to be independent of the strength of the heart. In view of these findings, it must be borne in mind that Hewlett has found that a rise in blood-pressure fol- lows quite uniformly within one minute after the inhalation of amyl nitrite is begun. Whether it is the fall of blood-pressure or the rise of blood-pressure which is accompanied bv increased flow through the coronarv vessels after the inhalation cannot be regarded as Perhaps this may bring with it a dilatation of the coronary arterie- 382 DISEASES OF THE HEART AND AORTA. certain. It must be admitted, however, that in Bond's experiments the coronary arteries were not in a state of vasomotor spasm, and therefore the analogy is not an absolute one. It is also probable that the mere lowering of the general blood-pressure, independently of any action upon the coronaries, tends in itself to relieve the cardiac dilatation by dimin- ishing the work of the heart. Caffeine, Theobromine, and Theophylline. Caffeine and especially theobromine and theophylline preparations especially acettheobromine sodium ("agurin") and acettheophylline have been highly recommended, from the clinical stand-point, by Askanasy, Kaufmann and Pauli, R. Breuer, Buch, Pineles, v. Leyden, and others, to relieve and to ward off the attacks of stenocardia. Oswald Loeb has given an experimental basis to these observations by demonstrat- ing on the excised heart that these drugs increase the blood flow through the coronary vessels as well as increase the systolic output and the force of the heart-beat. 1 Theobromine and theophylline are to be preferred to caffeine, since they do not increase peripheral resistance and have little action upon the higher nervous centres, but, on the other hand, a more marked action on the coronary arteries. On the other hand, they are not very certain in producing their effect. They may be helpful in some cases and may absolutely fail in others, and, while they are worthy of a trial in almost every case, they cannot as yet be expected to supplant the nitrites and iodides. Diet. Diet is all-important. It should be chiefly lactovege- t a r i a n in character. The meals should be small in amount, to prevent overloading and distention of the stomach and hence the pushing up of the diaphragm. Gastric fermentation should be prevented by removing from the diet any articles, such as soft hot breads, heavy and greasy pastry, etc., which may be found to produce flatulence, and by general treatment of the gastric condition. Air-swallowing should be carefully looked for and treated (see page 708). Meat and soups should be reduced to small quantities, since they contain considerable quantities of purin bodies which have a vasoconstrictor action and which also act injuriously upon the kidneys. The vegetable and cereal foods should make up the bulk of the diet. Salt should be reduced for the same reason. Liquids should be restricted to about 1500 c.c. a day. Milk may be a staple article in the diet, unless, as in many persons, it tends to flatulence. This is sometimes obviated by adding a very little weak tea or coffee, but very often it must be dispensed with altogether. T o 1) a c c o should be absolutely excluded in both organic and func- tional cases. Tea and coffee in small amounts (one cup a day, very weak) probably have very little effect upon the average individual who has been accustomed to them, but may be quite important factors in bringing on the attacks in persons whose sensitiveness is a little above normal and in whom there is a tendency to angina. It is best for them to be given up". Local Treatment of the Chest Wall. Vigorous counter-irritation to the chest wall, by blistering, etc., is also of value, and Hasselbach and Jacobaeus report very marked improvements, lasting a year or so, from 1 Dr. (1. S. Bond, in the writer's laboratory, has been unable to produce any appre- ciable chanse in the outflow from the coronary veins of the dog's heart in situ; and with the ainyl nitrite and nitroglycerin observed a marked decrease in the outflow, even when the animal's heart was dilated. ANGINA PECTORIS. 383 exposure of the precordium to the Finsen light for an hour a day until a marked cutaneous reaction or even blistering has set in. Electrical Treatment. J. 0. Hirschfelder states that in five cases he has obtained striking relief of the symptoms by treatment with the galvanic current, applying the anode (a pad 4 cm. in diameter) to the neck over the course of the vagus, and the cathode (G-12 cm. in diameter) to the precordium, and passing a current of 20 m i 1 1 i a m - p e r e s for five minutes to each side of the neck. One patient remained free from attacks until his death two years after the treatment; another has remained free for several years. In the other three the relief was less permanent, but still very gratifying. In other cases the use of electric baths, and especially with the sinusoidal current, may be of value (Rumpf), but the effect is readily overdone. Sir William Ewart recommends inhalations of CO 2 (see page 229). BIBLIOGRAPHY. Porter, W. T.: On the Results of Ligation of the Coronary Arteries, J. Physiol., Camb., 1893, xv, 121. Magrath, G. B., and Kennedy, H.: On the Relation of the Volume of the Coronary Circula- tion to the Frequency and Force of the Ventricular Contraction in the Isolated Heart of the Cat, J. Exp. Med., N. Y., 1897, ii, 13. Cohnheim, J., and v. Schulthess Rechberg, A.: Ueber die Folgen der Kranzarterienver- schliessung fiir das Herz., Arch. f. path. Anat., etc., Berl., 1881, Ixxxv, 503. Panum: Experimentelle Beitriige zur Lehre von der Emholie, ibid., 1862, xxv, 308 and 433. Baumgarten, W.: Infarction in the Heart, Am. J. Physiol., Bost., 1899, ii, 243. Hirsch, C., and Spalteholz, W.: Coronarterien und Herzmuskel, Deutsch. med. Wochen- schr., Berl., 1907, xxxiii, 790. Pratt, F. H.: The Nutrition of the Heart through the Vessels of Thebesius and the Coronary Veins, Am. J. Physiol., Bost., 1898, i, 86. Porter, W. T.: The Influence of the Heart-beat on the Flow of Blood through the Walls of the Heart, ibid., 1898, i, 145. Maass, P.: Experimentelle Untersuchungen iiber die Innervation der Kranzarterienge- fiisse des Saugethierherzeus, Arch. f. d. ges. Physiol., Bonn, 1899, Ixxiv, 281. Langendorff, O. : Ueber die Innervation der Koronargefasse, Zentralbl. f. Physiol., Leipz. u. Wien, 1907, xxi, 551. Hyde, I.: The Effect of Distention of the Ventricle on the Flow of Blood through the Walls of the Heart, Am. J. Physiol., Bost., 1898, i, 215. Halsted, W. S. : The Results of the Complete and Incomplete Occlusion of the Abdominal and Thoracic Aortas by Metal Bands, J. Am. M. Ass.. Chicago. 1906. xlvii, 2117. The Partial Occlusion of Blood-vessels, Especially of the Abdominal Aorta. Johns Hopkins Hosp. Bull., Baltimore, 1905, xvi, 346. Also Miller, J. L., and Matthews, S. A.: Effect on the Heart of Experimental Obstruction of the Left Coronary Artery, Arch. Int. Med., Chicago, 1909, iii, 476. Romberg, E.: Lehrbuch der Krankheiten des Herzens, Stuttgart, 1906, 115. Lewis, T.: Paroxysmal Tachycardia, Heart, Lond., 1909, 42; 98. Jellinek, E. O., and Cooper, C. M.: Cardiac Asthma and Sclerosis of the Right Coronary Artery, J. Am. M. Asso., Chicago, 190S, 1, 689. ANGINA PKCTOIUS. Heberden, Wm.: Commentaries on the History and Cures of Disease. Philadelphia, 1^1 Home, Everard: Life of Hunter, prefixed to the "Treatise on Inllammation." 1791. p. 45. Quoted from Sir W. T. Gairdner's article on "Angina IYrt<>ris and Allied States' in Reynolds's System of Medicine, Philadelphia, 1S77, iv. 531. Baron: Life of Jenner, London, 1827. Quoted from W. Osier's States," X. York, 1897. 384 DISEASES OF THE HEART AND AORTA. Gairdner, W. T.: Angina Pectoris and Allied States, in "A System of Medicine," edited by J. Russell Reynolds, Phila., 1877, iv, 534. Osier, W.: Lectures on Angina Pectoris and Allied States, N. York, 1897. Gibson, G. A.: The Nervous Affections of the Heart, Edinb. and Lond., 1905. Ludwig and Cyon: Ber. d. k. Sachs Gesellsch. d. Wissensch. math. phys. 01., Leipz., 1886. 307. Quoted from Shafer's Physiology. Eyster, J. A. E., and Hooker, D. R.: Vagushemmung bei des Blutdruckes, Zentralbl. f, Physiol., Leipz., 1908, xxi. Mackenzie, James: Heart Pain and Sensory Disorders associated with Heart Failure, Lancet, Lond., 1895, i, 16. Head, H.: Pain in Visceral Disease, Brain, Lond., 1893, xvi, 1; 1894, xvii, 339; 1896, xix, 153. Head, H., Rives, W., and Sherren, Jr.: The Afferent Nervous System from a New Aspect, ibid., 1905, xxviii, 99. Sherren, J. : Some Surgical Observations on Referred and Reflected Pain, Clin. J., Lond., 1905, xxxvi, 168. Abstracted in editorial, J. Am. M. Ass., Chicago, 1909, Hi. Head, H., and Thompson, Th. : The Grouping of Afferent Impulses within the Spinal Cord, ibid., 1906, xxix, 536. Harvey, Wm. : The Works of Wm. Harvey, trans, by R. Willis. Printed for the Sydenham Soc., Lond., 1847, 382. Hirschfelder, A. D.: Observations on a Case of Palpitation of the Heart, Bull. Johns Hopkins Hosp., Baltimore, 1906, xvii, 299. Huchard, H.: Traite clinique des maladies du cceur et de 1'aorte, 3d edit., Paris, 1899, ii, p. 1 et seq. Ratner, Lee. Quoted on p. 717. Jackson, D. E., and Matthews, S. A.: The Sensory Nerves of the Heart and Blood-vessels as a Factor in Determining the Action of Drugs, Am. J. Physiol., Bost., 1908, xxv, 255. Lancereaux: De 1'alteration de 1'aorte et du plexus cardiaque dans 1'angine de poitrine, Compt. rend. Soc. de biol., Par., 1864, 4 s., i, 15. Grocco, P.: Sull angina di petto, Settimana Med. di Sperimentale, Firenze, 1896, i, 1, 13, 109, 169, 181. Benenati, U.: Sull' origine nevritica dell' angina pectoris da aortite sifilitica, Riforma Med., Roma, 1902, xviii, 326, 339, 351. Mott, F. W. Quoted from Oliver, Th.: A Lecture on Angina Pectoris and Allied Con- ditions, Lancet, Lond., 1905, ii, 812. Herard: Angine de poitrine caracterisee anatomiquement par un retrecissement considera- ble des deux arteres coronaires a leur origine sans lesions des plexus cardiaques, Bull. Acad. de Med., Par., 1883, 2 ser., xii, 1522. Latham, J.: Med. Trans. Roy. Coll. Phys., Lond., 1812. Quoted from Gibson. Nothnagel, H.: Angina pectoris vasomotoria, Deutsch. Arch. f. klin. Med., Leipz., 1867, iii, 309. Osier, W.: Angina Pectoris as an Early Sign in Aneurism of the Aorta, Med. Chron., Man- chester, 1906, Ixiv, 69. Lauder-Brunton, T.: On the L'se of Nitrite of Amyl in Angina Pectoris, Lancet, Lond., 1S67, ii, 97. Askanazy: Klinisches ueber Diuretin, Deutsch. Arch. f. klin. Med., Leipz., Ivi, 209. Kaufmann and Pauli: Zur Symptomatologie des stenokardischen Anfalles, Wien. klin. Wchnschr., 1902, xv, 1160. Breuer, R.: Zur Therapie und Pathogenese der Stenokardie und verwandter Zustande, Munchen. med. Wchnschr., 1902. Pinelos, Fr. : Theocinbehandlung stenokardischer Anfalle, Mitth. d. Gesellsch. f. inn. Med., Wien, 1903-1904. (Quoted from Pal.) Leyden, K. v.: Fiinfzig Jahre innerer Therapie, Therap. d. Gegenw., Berl., 1909, 1, 1. Hasselbach, II. A., and Jacobaeus, H.: Ueber die Behandlung von Angina Pectoris mittelst starken Kohlbogenlichtbadern, Berl. klin. Wchnschr., Berl., 1907, xliv, 1247. Hirschfelder, J. O.: Personal communication. Rumpf: Zur Einwirkung oszillierender Strome auf das Herz, Zentralbl. f. innere Med., Leipz., 1907, xxviii, 441. PART III. i. ENDOCARDITIS. IN spite of the greater frequency of arteriosclerosis and myocarditis, the clinical pictures of valvular diseases are so much more definite as to render them the most striking of all diseases of the heart. They constitute indeed a large percentage of all diseases seen by the physician, numbering 1781 (7.6 per cent.) of the 23,200 cases admitted to the medical service of the Johns Hopkins Hospital from 1889 to 1908. HISTORICAL. Vieussens in 1715 described lesions of the valves occurring in the form of warty or cauliflower excrescences or vegetations, which prevented the closure of the valves. Vir- chow called attention to the fact that as a rule these vegetations were not situated at the margins of the cusps, but at a little distance from the margin, at the line of closure where the cusps struck together, at the point where injury to the endothelial cells was most likely to occur. That this injury was usually due to the action of bactei ia was shown when Winge and Heiberg and Virchow in 1869 demonstrated microscopically the presence of minute granules within the vegetations. In 1S83 Weichselbaum cultivated staphylococci and streptococci from endocardial vegetations, and his pupil Wyssokowitch, as well as Orth and Ribbert, produced them experimentally in animals by the injection of bacteria into the blood. PATHOLOGICAL ANATOMY. Development of the Lesions. Mechanical or toxic injury is an important factor in bringing about these lesions upon the valves. Indeed Wyssokowitch found that his experiments suc- ceeded only after he had punctured or injured the valves with probes: while Ribbcrt supplied the mechanical factor by injecting emulsions of potato cultures which contained small masses of potato that hurled themselves against the valves. E. C. Rosenow has shown that vege- tations are due to the lodging of bacterial einboli within the valves and are best produced when the valves are vascular. The fibrinous exudate is poured out rapidly after the injury, and is whipped into strands by the action of the current, so that within one hour after mechanical injury of the aortic valve a mass of fibrin having the cauliflower shape of a vegetation may be found filling the hole in the valve (Hirschfeldcr). 25 385 386 DISEASES OF THE HEART AND AORTA. Ulcerative Endocarditis. The fate of this fibrinous exudate and the type of the lesion varies with the virulence of the germ. If the virulence is high the lesion is often large and may involve the walls of the auricle or ventricle (mural endocarditis) as well as the cusps of the valve (valvu- litis) . The necrosis spreads into the deeper tissues of the valve or even penetrates through it, and the vegetation consists of a mass of degenerated fibrin, clumps of bacteria, and necrotic tissue (Fig. 174) rich in polymor- phonuclear leucocytes. Under the influence of the ferments which these secrete, the masses become partly liquefied, so that their attachment to the cusps is loosened and they may be readily swept off as emboli by the force of the blood stream only to cause infarction and abscesses in dis- tant tissues. Such emboli naturally vary in size from a small bit of fibrin barely capable of plugging a capillary to a mass almost the size of the Fir,. 171. Mitral endocarditis showing large vegetations. A, mural portion of the vegetations; B, vegetations along line of closure. FIG. 172. Injection of chronically inflamed valves. (After v. Langer.) valve itself. However, they rarely reach the tremendous size attained by the non-septic cmboli which arise from intra-vitam thrombi in the auricles. Chronic Endocarditis. When the bacteria upon the valves are less virulent or the immunity of the patient develops, a different process occurs. The areas of necrosis are smaller and are walled off with leucocytes. Later these give place to the fibroblasts and plasma cells of chronic inflammation, which in turn are replaced by strands of newly formed connective tissue, which push out into the exudate and finally replace it altogether, leaving a solid vegetation composed entirely of fibrous tissue. With the ingrowth of connective tissue blood-vessels penetrate into the vegetation, entering it from the subendocardial layers of myocardium just as they enter scle- rotic patches in arteriosclerosis (Koester, v. Langer, Darier, Ribbert), Fig. ll'l. As healing becomes complete the endothelial layer of the intima slowly grows in from the periphery and gradually covers the entire vegeta- ENDOCARDITIS. 387 tion. This relmmg of the vegetation with cndothelium is, from a pro'- nostic stand-point, a most important step in the healing, for, as Wyssoko- witch has shown, infection occurs most readily when the surface' of the valve is injured, and clinical experience shows that a valve once injured is particularly liable to rein- fection. Thus, it is common to find a fresh ulcerative endo- carditis occurring upon a valve ... e i- Muscular tissue which is already the subject of a chronic endocarditis, several different stages appearing upon F ^ a r ' ic the same specimen. tissue of valve- leaflet INFECTIVE AGENTS. The most important infec- Endo- tive agents in the causation of endocarditis are the micro- coccus of rheumatic fever, the pyogenic cocci, the pneumococcus. the gono- coccus, the bacillus influ- enza?, and the spirochaete p a 1 1 i d a (triponema pallidum) of syphilis. riu * T> f ,1 Chords Rheumatism. By far the tendinee most frequent cause of heart disease is rheumatism, which gave rise to 62.6 per cent, of Herder's cases of malignant endocarditis, and occurs in about the same percentage in the milder forms. However, the exact causal factor of rheu- matism itself is not yet settled. Sahli in 1893 isolated what he thought to be a staphylococcus from joints, endocardium, and the heart's blood of patients dying of acute non-suppurative arthritis, and then stated that he garded acute articular rheumatism as an infectious dis- ease due to the action of attenuated pyoge n i < cocci.'' Recently Menzer and Rufus Cole have revived this view, and the latter has |>n>dueed non-suppurative arthritis and endocarditis in rabbits by the injection of streptococci from various sources, showing also that in the joints these assume the diploeocnis arrangement. Triboulet, Wassermann, Westphal and Malkoff, and Poynton and Paine, however, regard the micrococcus (diplococcus) which they have obtained in cases of the rheumatic FIG. 173. Structure val ilar 1 " . . . Auffassung des Gelenk rhenmatismus als einer auf schwachter pyogcnen Kokkenberuhenden Infektionskrankheit." der \\ irkung abge- 388 DISEASES OF THE HEART AND AORTA. cycle as a specific organism or at least a specific strain, though Walker has shown that its cultural characteristics are by no means sharply defined. The micrococcus (rheumaticus) of Poynton and Paine assumes the diplococcus form in the joints but becomes a strep- tococcus in culture media, just as Cole found for many ordinary streptococci. Beattie and Longcope also have isolated what they believe to be the micrococcus of Poynton and Paine from cases of arthritis with endocarditis and have produced both conditions in animals. Poynton has obtained the same germ from the cerebral cortex in simple chorea and from the tonsils. Meakins, on the other hand, has found large foci of streptococci in the tonsils which have been removed from patients having rheumatism, but these germs do not show Fie;. 174. Photomicrograph of a specimen showing acute and suhacule endocarditic lesions upon the mitral valve. A. Entire specimen (low power). B. Outline sketch showing the portions from which I'. 1), and K are taken. ('. Margin of the area of acute endocarditis (high power). IX Ulcerating area, showing masses of necrotic tissue and exudate. K. Area where the process is more chronic, showing strands of newly-formed fibrous tissue entering the vegetation. any uniformity which would permit them to be identified with the strain of Poynton and Paine. These points tend to favor the original view of Sahli that rheumatism is not due to a single strain but to a variety of attenuated cocci, and is therefore to be regarded as a clinical group of diseases rather than as a single disease. The Pyogenic Cocci. The pyogonic cocci of puerperal fever, abscess, and septicaemia are also very common causes of endocarditis. They are identified with special frequency in the malignant forms, owing to the readi- ness with which they are then cultivated, but there seems little doubt that less virulent strains are responsible for cases of chronic endocarditis as well. ENDOCARDITIS. 389 Pneumococcus. Wells found that the pneumococcus caused endo- carditis in 4 per cent, of his 517 autopsies upon cases dying of pneumonia, and hence the latter disease is a relatively frequent cause of endocarditis. Lenhartz states that the endocarditis often arises as a recrudescence after the fever from the original pneumonia has subsided (13th to loth day), and that it is often malignant and accompanied by meningitis. Gonococcus. The importance of the gonococcus in producing endo- carditis as well as rheumatism is growing from year to year. The clinical association of endocarditis and urethritis was recognized by Ricord in 1847 and by Brandes in 1854. V. Leyden in 1893 demonstrated upon the valves cocci which decolorized by Gram's methods, but the first positive cultures of the B FIG. 175. Endocarditic lesions. A, uleerative endocarditis with perforation of one of the aortic cusps. B, healed chronic endocarditis of the mitral valve. gonococcus from the blood during life were made at the Johns Hopkins Hospital by Thuyor and Blumer in 1895. Since then the condition has boon found frequently, and should always be sought for in cases of gonorrhoeal rheumatism. Miscellaneous Infections. Occasionally endocarditis arises during or after diphtheria, scarlet fever, and smallpox, though in these cases, as in tuberculosis, the lesion is probably most frequently produced by streptococci which are present as a mixed infection. True tuberculous endocarditis is rare (Marshall), though it has been produced experimentally in animals (Michaelis and Blum). Cecil and Soper (Arch. Int. Med.. 1911, viii, 1 ) reported meningo- coccus endocarditis. The bacillus of influenza is also an important factor (Austin!, though it has been encountered far less frequently in endocarditis than in myocar- ditis; but this germ must always be reckoned with, especially on additional changes in valves which have been subject to previous infec- tion by other organisms. 1 The term micrococcus rheumaticus is used for convenience, but with all reservations as to possible specificity. 390 DISEASES OF THE HEART AND AORTA. Syphilis. Whether true valvular lesions are produced by the spiro- chaete pallida of syphilis has not been absolutely proved, but recently Collins and Sachs and Longcope have obtained a positive Wassermann reaction in a large percentage of cases of aortic insufficiency in which the valves were puckered, shrunken, and calcified. In these cases it is not the intima but the middle fibro-elastic layer of the valves in which the change goes on, exactly analogous and usually coincident with similar changes in the deeper layers of the intima and media of the aorta. Sclerotic and Atheromatous Lesions of the Endocardium. Besides these forms of endocarditis there seems to be a certain number of cases, especially of lesions about the aorta, in which sclerosis and calcification take place in the fibro-elastic layer of the valves exactly as in the luetic lesion, but in which the patient has never had a luetic infection (as in the case of J. L., page 561). The similarity here is exactly like that between luetic and non-luetic arteritis, as shown by Ophiils, and needs no further comment. PATHOLOGICAL PHYSIOLOGY. The disturbances in heart action due to endocarditis may depend upon three immediate causes: (1) The mechanical effects due to leaks or obstructions at any of the valvular orifices. (This will be discussed in detail in connection with each of the chronic valvular lesions.) (2) The weakening of the heart muscle due to the acute myocarditis and the fatty and parenchymatous changes in the muscle cells, resulting from the direct invasion of the muscle by the cocci, from effect of their toxins upon it, and from the anemia which fre- quently accompanies the infection. (3) The weakening of the heart which, as in other febrile and infectious diseases, results from lowering of vasomotor tone, and which is brought about by a relative empti- ness of the blood-vessels. This is accompanied by low blood-pressure and rapid pulse. In the chronic forms of carditis the first is the most important factor; while in the simple acute and the malignant forms the two latter frequently outweigh it, so that there may be few symptoms referable to the local mechanical effects upon the circulation. Effects on the Circulation. The physical signs will be discussed par- ticularly in the case of individual valvular lesions; but in general it may be said that a leak at an orifice necessitates an increase in the output of the c h a in b e r in order to compensate for the amount regurgitating or an increase in force of contraction of the cham- ber behind it. Thus, in mitral insufficiency, Ventricular systolic output = Output into aorta + Backflow into auricle; while in aortic insufficiency Ventricular systolic output = Output into aorta = Outflow through peripheral vessels + Backflow into ventricle. In either of these cases the circulation may be maintained either by increasing this output per beat or by increasing the heart-rate; and in neither of these cases is the pulse-pressure proportional to the systolic output of the ventricle. On the other hand, when a valvular orifice is narrowed it may have little or no effect until the narrowing reaches a certain point; for, though it slows the inflow or the outflow, as the case may be, yet the duration of systole or of diastole may be sufficiently great to ENDOCARDITIS. 391 permit of complete filhng or emptying during the time available; but beyond this greater driving power is needed and the chamber behind the stenosis must undergo hypertrophy Regurgitations usually cause dilatation of the c h a m b e r s into which t he leak occurs, unless a great increase in tonicity of the muscle has caused the cavity actually to decrease in size (Stewart, Cameron, Hirschfelder, Cloetta). CLINICAL GROUPING. Clinically, endocarditis (or carditis 1 ) has been divided by Osier into three groups: (1) The malignant type, in which septic and highly febrile symp- toms, with symptoms also due to septic embolism in various parts of the body, dominate the clinical picture, and in which the cardiac lesions may spread rapidly and involve almost all the valves. This' is usually fatal during the acute attack. 88 __i_U_L FIG. 176. Temperature curve from a case of malignant endocarditis. Fir,. 177. Temperature curve from :\ < i.-e <>f simple acute enmia. 2. The typhoidal type, which closely resembles severe typhoid fever or acute miliary tuberculosis, continuous high fever, enlarged spleen, and absence of other local- ized symptoms. 3. The cerebral type, dominated by embolism of the brain, coma, meningitis, paralyses. Septicaemic Type. The septicsemic type is the most common ami typical, usually following abscess, puerperal fever, operation, wounds, occasionally tonsillitis or quinsy, or some other definite infection, and is characterized by prostration, anorexia, malaise, frequently headaches, and shaking chills. In Herder's 150 cases the fever was continued in 12, irregular and intermittent in 37, quotidian in 40, absent in 5. The temperature sometimes fell for a period before death. The complexion has the sallow yellowish color of hacmatogenous jaundice, there is rapidly progressing increasing anaemia, and the eyes are dull. There is sometimes acute purulent conjunctivitis, sometimes disturbances of vision or even blindness due to the presence of minute emboli or hemorrhages upon the retina. The cheeks are sunken; the skin is usually dry except during the rigor (in contrast to the drenching sweats of rheumatic fever); the tongue is dry and furred; the lungs may be clear or septic bronchopneumonia may be present. Respiration is usually rapid. The signs over the heart are variable. In some cases there are no abnormalities in heart sounds, cardiac area, or in pulsations, except for a rapid pulse-rate, and then the diagnosis may long remain obscure; or, on the other hand, the loudest murmurs may be present both in systole and in diastole, and these have a distribution corresponding to almost any of the valvular lesions, or more usually to several lesions combined. These signs often change markedly from day to day, corresponding to the progression of the lesion from valve to valve, the growth of the individual vegetations, or the dis- appearance of the latter as they slough off into the blood stream. The pulse is small and collapsing, but usually too rapid for dicrotism. and the blood-pressure is low (maximal ">/ '*\ \ 1 / Ai ^ FIG. 178. Diagram showing relative frequency of the most im- portant valvular lesions at various ages. (Modified from Gillespie.) Solid line, mitral insufficiency; bro- ken line, mitral stenosis; dotted line, aortic insufficiency. The figures in- dicate the decades. Under 9 years, 9; 10-19, 19; 20-29, 29; etc. B CASES J.H.H. F=3 AUTOPSIES -BERL. Fir,. 179. Diagram showing the relative frequency of the various valvular lesions in 1781 cases of valvular heart disease admitted to the Medical Service of the Johns Hopkins Hospital from 1889 to 1908. as well as those found by Sperling in 300 autopsies in Berlin. Small space, 5 per cent.; Berl., Berlin; J. H. II., Johns Hopkins Hospital. Sex. Many authors, among them Osier, state that men are more fre- quently affected than women; though v. Jurgensen states that valvular disease occurs with practically the same frequency in both sexes. INVOLVEMENT OF INDIVIDUAL VALVES. The relative frequency with which the valves are involved is shown by the analysis of 17S1 cases of endocarditis admitted in the Johns Hopkins Hospital from 1SS9 to 190S, represented diagrammatically in Fig. 179. The figures show a general correspondence to those of v. Jurgensen in 2470 cases in the German clinics. ENDOCARDITIS. 399 PATHOLOGICAL PHYSIOLOGY. The pathological physiology of simple acute endocarditis presents the condition due to the individual valvular lesion (to be considered in detail in the appropriate chapters dealing with the chronic endocarditis), modi- fied or added to by an element of diminished vasomotor tone due to the acute febrile condition. As the result of this vasodilatation, especially in the abdominal area, the blood collects in the dilated veins and capillaries, the blood-pressure may be low, and the symptom complex of arterial ansemia or low blood-pressure sets in. Moreover, there is usually a certain degree of actual anaemia added to the lesion, and this often increases the difficulty in breathing; although it does not, as a rule, bring on the red and purple hue of chronic cyanosis. Still further the increase in the leakage causes clamming back and secondary dilatation of the chambers behind it, O3dema in the walls of the ventricles and in the valve cusps, and increased susceptibility to infection. PATHOLOGICAL ANATOMY. The endocarditis itself is less severe than in the malignant form. Fewer bacteria are deposited upon the valves, and these show less tendency to multiply, so that the process of organization, as a rule, outraces necrosis, and consequently the separation of emboli is rare. The valves thus show an injured surface covered by a more or less thick or exuberant layer of fibrin, with active organization proceeding upward from its base. This may be seen in any stage of advancement, from fresh fibrin in the early stage to completely organized firm young connective tissue, covered by intact endothelium, when healing has become complete. Pathologically, the difference between the malignant and the simple endocarditis is merely the usual difference between a mild and a virulent infection of any tissue. There may be no actual difference in etiology, and the malignant form may represent only a very virulent strain of the same organism which would ordinarily produce a milder infection; or, on the other hand, micro-organisms of the same virulence may produce different types of lesion in persons with different powers of resistance. SYMPTOMS. It is particularly noticeable that in these cases during the first attack the symptoms due to distinct heart failure are largely absent, and the m a i n s y m p t o m s a re t h o s e of a c c o m p a n y i n g r h e u - m a t i c disease, along with the weakness, pallor, and aiuemia (usually about GO per cent, haemoglobin), such as might bo clue to any mild fever, though occasionally, as in the case of J. A. (page 402), the onset of aortic insuffi- ciency is attended by pain and sudden collapse. The temperature rarely attains 101 unless an acute arthritis or acute pneumonia is present. The pulse is usually rapid and regular. Its quality depends upon the nature of the lesion- being large and collapsing in the presence of aortic insuffi- ciency, small in mitral stenosis, and of moderate size in mitral insufficiency. The blood-pressure is sometimes above, sometimes below normal. 400 DISEASES OF THE HEART AND AORTA. PHYSICAL SIGNS. As a rule, the patient does not seem very ill, he has sometimes an anxious expression, is usually pale and sallow, in contrast to the older cases of mitral disease, who usually show a flushed and cyanotic hue. Occasionally choreic movements are present. It is very common for the tonsils to be enlarged, since these are the usual portals of entry for the rheumatic infection, and there is frequently a yellow exudate in the crypts or a membrane over their surfaces. In almost all rheumatic cases there are foci of cocci (streptococcus or micrococcus rheumaticus?) in the deeper tissue of the tonsil. Along with this infection the so-called tonsillar lymph gland just below the angle of the jaw and often the submaxillary and anterior cervical lymph glands are enlarged. The chest shows no special peculiarity except that precordial bulging is often present, espe- cially marked in children (see page 140), even in the first attack of endo- carditis. The cardiac signs are the same as for the chronic valvular lesions, though usually less marked. They will be discussed in detail under the special chapters. The liver is usually not enlarged unless there is marked heart fail- ure. Occasionally the spleen is palpable and even hard, tender, and painful, as a result of a fresh or old infarct, and this condition may persist unchanged for years. A few months ago the writer saw in the Johns Hopkins Dispensary a young girl in whom a large, very hard spleen had been present for several years, first appearing during a rather severe attack of simple acute mitral endocarditis. There is often slight oedema of feet and ankles, though very many cases come to treatment before this has set in. The presence of cedema in an early acute endocarditis is a rather grave sign, since it indicates the failure of the heart to respond promptly to the added load. The u r i n e is usually of high specific gravity and contains a small amount of albumen and a few coarsely or finely granular casts, a typical febrile albuminuria. The blood examination usually shows a slight grade of secondary ana?miu. SUBSEQUENT COURSE. As in the cases cited on page 402, there is usually gradual improve- ment under any treatment in which the main factor is sufficient rest, during which the infection subsides (the bacteria dying, or more commonly becoming latent), the vegetations undergo gradual organization and more or loss thickening or .shrinkage, and fever passes off, as does the acute myo- cardial weakness. The patients almost always recover from the first attack. Recurrence is especially common, and is the danger against which especial precaution must be taken, the more so as the second attack often spreads to another valve or even to two more. It is the liability to repeated attacks which keeps the pathological process ever fresh and increasing. There is then usually a little area of incompletely organized fibrin always present to give soil to any stray micrococcus that may be carried by the blood stream, and thus produce a new outbreak of fresh endocarditis with exacer- bation and perpetuation of the old symptoms. After a single attack, ENDOCARDITIS. 401 especially when one only is involved, complete organization of the vegeta- tion may set in, the acute myocardial changes subside, and the heart muscle may soon regain its normal function. Compensation. A slight leak (see page 408) may remain at the site of the vegetation, just enough to produce a murmur and perhaps even bring about slight hypertrophy, but without really impairing the function of the heart; and the individual who suffers from no further acute endo- cardial changes may go on for thirty or forty years, until the age of sclerosis sets in and the leak is widened by sclerotic shrinkage, without the appear- ance of any further symptoms. On the other hand, as da Costa has shown, persons with old perfectly compensated valvular lesions are much more susceptible to cardiac overstrain and acute dilatation than are normal individuals. With the dilatation there comes a functional insufficiency of the valves, which adds its effect to that of the organic lesion; and finally, as Roy and Adami have shown, stasis brings about osdema and cellular infiltration in the cusps. This infiltration is followed by further valvular sclerosis and shrinking, and thus the cardiac overstrain in itself tends to increase permanently the original lesion. When hypertrophy and compensation are good and the individual either lives a quiet life or has developed his muscles gradually to meet the strain of his surroundings, he may escape overstrains entirely, and the lesion may either be stationary or may shrink by gradual sclerosis. It is a rather common occurrence to find perfectly healthy young adults or even active men in middle age who have had well-compensated mitral insuffi- ciency persistent since childhood. The same is also true of aortic insuffi- ciency except that this usually again makes itself felt about the age of arterio- sclerosis, i.e. about the age of forty. Even then, with good care, general hygiene, avoidance of muscular overstrain, nervous excitement, and over- eating, great moderation in the use of alcohol and tobacco, and especially personal prophylactic measures against infectious diseases, a long life may be attained by the patient. Reinfection. On the other hand, when the patient is still subject to recurrence of his rheumatism or tonsillitis, or to repeated attacks of pneu- monia, bronchitis, or influenza, the probability that the cardiac lesion will remain quiescent is a small one, and it becomes more likely that both valve and muscle will suffer further changes whose limit it is impossible to pre- dict. It is therefore most important not to give a definite prognosis to the family or friends of the patient until he has been under observation for about a year after the attack of endocarditis has subsided, so that all these factors may be carefully watched and taken into account, prophylactic measures be instituted, and the recuperative power of the heart muscle be gauged. Complications. Another factor even more important than the endo- cardial lesion is the involvement of the pericardium and especially the production of adherent pericardium, so common in the first and second decades. This condition perhaps more than any other leads to early heart failure, since it imposes the greatest strain of all upon the heart; and, as it develops insidiously and frequently reaches its maximum only after the first acute attack has passed off, it should be watched for with great care. 26 402 DISEASES OF THE HEART AND AORTA. SIMPLE ACUTE ENDOCARDITIS. J. A., male, cannery worker, aged 15, entered the hospital complaining of r h e u - m a t i s m . He has been a rather delicate boy, having had erysipelas, measles, whooping- cough, and chicken-pox when a child, and attacks of definite articular rheumatism at nine and ten years. He lias done soldering in a cannery for the past two years. About five weeks before admission he began to complain of p a i n in h i s ankles and knees, for which he was put to bed. At this time his physician found a temperature of 104, and he had chilly sensations, but no shaking chills. About two weeks later while lying down he felt an intense pain in his heart and be- gan to get w h i t e in the face and blue at the lips. Since then, though he has been losing weight and strength, he has had no more pain. He has had occasional headaches during the illness. Examination shows a well-nourished boy of sallow color, with injected pharynx, enlarged tonsils, and enlarged posterior cervical and axillary lymph-glands. Chest is well formed and lungs are negative but for a few moist rales over the left apex. Heart . There is marked precordial bulging. The apex beat is seen in the 4th left interspace 9 cm. from the midline. Dulness extends 4 cm. to the right of the midline and above to the second rib. There are no thrills. The first sound at the apex is preceded by a short rumble (Flint murmur) and replaced by a soft blowing systolic murmur. The second sound is clear at the apex, but at and near the sternum is followed by a blowing diastolic murmur, maximum over the insertion of the third right rib. The pulse is 124 per minute, small but definitely collapsing, and there are well-marked capillary- pulsation and throbbing of the carotids. Blood-pressure: maximal 115-125 mm. Hg. Joints. There are swelling of right elbow and left ankle and soreness of elbows, knees, and right hip; slight wasting of interossei of hands and feet. Genitalia and reflexes are normal. There is no oedema. Red blood-corpuscles 5,000,000; haemoglobin 75 per cent.,* leucocytes 11,000. Urine. Lemon yellow. Specific gravity 1015; alkaline; no sugar; a trace of albumen; a considerable number of coarsely granular casts. Oct. 31. Dulness extends 7.5 cm. to the left of the midline and 2.5 cm. to the right. Nov. 13. Red blood-corpuscles 5,000,000; ha-moglobin 80 per cent.; leuco- cytes 6,600. General condition is excellent. Pulse continues rapid. The joints are clear. Jan. 5. There has been gradual progressive improvement. Red blood-corpuscles 4,700,000; haemoglobin 90 per cent.; leucocytes 11,000. There has been a gradual rise in the maximal pressure to 150-160 mm. Hg, as the patient's improvement has continued in spite of the rapid pulse. The patient was discharged quite well on Jan. 17, but had a second more severe attack several years later. TREATMENT. The treatment of the acute attack of endocarditis partakes in general of the treatment of a mild febrile disease or a secondary amrmia on the one hand, and of the particular valvular disease on the other. Rest in bed until a couple of weeks after the subsidence of all febrile symptoms is therefore an absolute necessity, also light and easily digestible diet, at first of SOO-1000 calorics, later 2500. Digitalis and Strychnine. As a rule, digitalis is not absolutely necessary, and is dispensed with by most Anglo-American practitioners. However, Cloetta has shown that the hearts of animals in which aortic insufficiency has been produced experimentally recover much better, undergo much less dilatation, and acquire much greater strength if digitalis treatment is begun at once and is continued over long periods (about a year) than if this treatment is omitted. Cloetta claims equally good results in man, but. his cases are too few to warrant conclusions. Nevertheless, the results ;uv sufficiently definite to warrant the prolonged use of digitalis in small doses (0.3 to 0.6 c.c.: i\ v ;> x of tli) tri?'U".') i i oa; 1 ; of r>cu"' e~i l~>"".~'!i'i- vi*h cn^'linc dilatation. ENDOCARDITIS. 403 In cases in which digitalis is not used strychnine should be given in doses of 2 to 3 mg. ($ to ^o g r -) three or four times a day. The salicylate preparations, sodium salicylate, salol, salipy- rin, aspirin, etc., should be given for the rheumatism; but, although they certainly relieve the pain, and it has been shown that they are excreted into the joint cavity, the duration of the fever and arthritis does not seem to be much affected by them, and certainly the frequency of cardiac involvement is unchanged. On the other hand, the salicylates, especially in large doses, have a depressant effect upon the heart, and the use of these drugs should therefore be as restricted as is consistent with relief of arthritic pain. According to many authorities, the salicylates seem to be more effective when in- jected directly into the joint or into the tissues immediately surrounding it. The writer's experience with this method is limited and in the cases tried its results were not striking, but it is sometimes worthy of trial. Oil of wintergreen (Oleum gaultheriae, methyl sali- cylate) applied to the skin over the joint also seems to cause great relief of pain, but it is possible that the rubbing may also cause more of the micrococci to be thrown out in the blood stream than might otherwise be the case. Hot compresses of saturated aqueous solutions of oil of wintergreen to the joint may suffice to allay pain. Other Therapeutic Measures. It is most important to relieve ansBmia, which is usually present and which is always a contributing factor to the fatty degeneration and weakness of the myocardium. Rest, full diet especially rich in eggs, milk, and green vegetables, and administration of iron usually relieve this symptom. The iron may be administered as Pil. ferri carbonatis (Blaud's pills), 0.2 to 0.3 G. (gr. iii to gr. v) t.i.d., p.c.; or Massa ferri carbonatis (Vallet's mass, a more stable prepa- ration containing honey instead of sugar); Elixir ferri, quininse et strychninae, 8 c.c. (oii) t.i.d., a.c.; or as Syrup, ferri iodid., 1 c.c. (n\, xv) t.i.d., p.c. If the anaemia is severe or does not yield to iron alone, arsenic should be given as well, since it has been shown that iron and arsenic together accelerate formation of red corpuscles and haemoglobin more than does either drug alone. Arsenic is usually given in the form of Liquor potassii arsenitis (Fowler's solution), beginning in doses of 0.2 c.c. (rc\,iii) t.i.d., p.c., and increasing one drop at each dose until 1 c.c. (tr^xv) is reached or puffy eyelids and albuminous urine show that the physiological limit has been reached. Prophylactic Treatment. One of the most important factors in hasten- ing the healing of a fresh vegetation is to keep it from being reinfected by bacteria floating in the blood stream. Every focus of infection is a store- house from which a few bacteria are given off from time to time, and hence is a source of danger. Accordingly in a number of clinics, and particularly in the medical clinic of the Johns Hopkins Hospital, under Prof. Barker's direction, an effort is being made to stamp out every focus of infection to be found anywhere in the body. Carious teeth, paronychias, and ischiorectal abscesses are removed. Particular attention is given to the tonsils. These organs are the main portals of entry for the- rheumatic infection. In persons who are subject to recurrent tonsillitis there are almost always small ab- scesses containing cocci persisting in the depths of the tonsillar tissue, even when there is no inflammation visible upon the surface. These are perma- 404 DISEASES OF THE HEART AND AORTA. nent portals of infection. Dr. Barker therefore insists upon the removal of enlarged tonsils in most cases of rheumatic heart disease. This should be done between but not during the attacks, since there is danger of throwing more cocci into the blood. The improvement which follows removal is sometimes immediate and striking. The patient's color improves within a few days. He feels better. His expression is brighter,, and he appears more robust. Improvement is more rapid and, since reinfection is less frequent, it is more permanent. It is naturally of great importance that all the tonsillar tissue should be removed, since a small amount left in place may again undergo hypertrophy and become reinfected. Such complete removal is impossible with the guillotine, the snare, and the electro-cautery, and is extremely difficult by even the ordinary intracapsular dissection. The most satis- factory method known to the writer is the extracapsular dissection. Palliative Treatment of the Tonsils. By way of palliative or prophylactic treatment various antiseptic gargles may be used. Gargles which contain hydrogen peroxide are to be preferred, because the pus-cells contain a catalase which sets free the oxygen. The nascent oxygen is a powerful antiseptic, and the excess collects in bubbles which mechanically loosen and sweep off the exudate. The hydrogen peroxide should not be stronger than 2 volume per cent, (one part commercial hydrogen peroxide to four parts of water). Other gargles that may be used are Dobell's solution, dilute Lugol's solution, and dilute potassium chlorate solution (especially with equal parts of dilute hydrogen peroxide). Prym's suction cups may also be applied to the tonsils. BIBLIOGRAPHY. ENDOCARDITIS. Bouillaud: Trait e des maladies du cocur, Paris, 1835, ii. Quoted from Xothnagel's System, "Diseases of the Heart," tran.sl. by G. Dock, Philu., 190S. Lenhartz, II.: Die septischen Erkrankungen, Xothnagel's Handb. d. spec. Pathol. u. Therap., iii, 2te Theil, Wien, 1904. Vieussens. Quoted from C. Hilton Fagge, "Diseases of the Valves of the Heart," Rey- nolds'* System of Medicine, vol. iv, Phila., 1877; from which the subsequent references are quoted. Hunter, John: Catalogue of Pathological Specimens, iii, 197. Meckel: Mem. de 1'Acad. Roy. des Sciences, Berl., 1756. Quoted from Friedreich, " Krank- heiten des Herzens," Virchow's Handb. d. spez. Pathol. u. Therap., 18(i7. De Senac. J.: Traite de la structure du cunir, de son action et de ses maladies, Par., 1749. Corvisart : Essai sur les maladies et les lesions organique du cceur et des Gros Vaisseaux, Paris. l^Oli. Burns, Allan: Observations on some of the Most Frequent and Important Diseases of the Heart, Edinb., 1809. Kreysig: Die Krankheiten des Iler/ons, Berlin, 1815. Virchow, R.: Ueber die Chlorose und die damit zusamrnenhangenden Anomalien im Gefiiss-Apparate insbesondere ueber Endocarditis puerperalis, Berl., 1872. Luschka: Sitzungsber. d. k. Akad. d. Wissensch., Wien, 1859. Quoted from Ribbert. A'. Lunger. L.: Ueber die Blutgefasse in den Herzklappen bei Endocarditis valvularis, Arch. f. path. Anat.. etc., Berl., 1887, cix, 405. Darier. J.: Les vaisseaux des valvules du cmic" (accidental) and "functional" murmurs so common in clinical notes seems therefore to be both unnecessary and misleading, and should be carefully avoided. 420 DISEASES OF THE HEART AND AORTA. level, and at times even exceed it. For example, a prominent medical educator who has a mild leak at the mitral valve but suffers no symptoms, has a maximal pressure of 140, a minimal of 95, and a large full pulse. The compensation in this case has more than balanced the disturbance in the circulation. This increase of pulse- and blood-pressure is not always indica- tive of improvement, but may occur also as terminal events under the stimulation of medullary asphyxia (see page 38). On the other hand, the presence of a rather small pulse and rather low blood-pressure and pulse- pressure may merely represent the natural effect of the lesion unaltered by compensatory changes on the one hand, or on the other may represent the failure of the left ventricle to maintain the circulation. The presence of arteriosclerosis may in itself tend to modify the blood-pressure, and to increase a blood-pressure and pulse-pressure that would otherwise be small. In any case the blood-pressure shows no characteristic features in mitral insufficiency, and the figures obtained are to be viewed as the algebraic sum of various circulatory factors, rather than as absolute measures of cardiac vigor. It must be remembered further that the cardiac symptoms are due mainly to changes in the pulmonary circulation, while the blood- pressure changes are concerned only with the systemic. Arrhythmia. The action of the heart is often irregular in mitral dis- ease, so that the arrhythmia in these conditions is frequently described as ''the mitralized pulse,' 1 though the latter is more frequently present in mitral stenosis than in mitral insufficiency. In the latter case, owing to the overdistention of the left auricle, extrasystoles arising in this chamber are sometimes met with. Such extrasystoles may persist for a long time and give rise to a form of pulse easily confounded with the typical pulse of auricular fibrillation, though the pulsation in the neck will be seen to be "double and not single" (see page 123). In most very advanced cases, however, the irregularity is due to auricular fibrillation with absolutely irregular pulse and a positive single venous pulse with distended veins (20). The absolute diagnosis is, however, made with the electro-cardiograph. The origin of the irregularity is probably in the distended left auricle (cf. also page 116). It is sometimes, but by no means always, accompanied by paralysis of the auricle, as shown by the venous tracings, but the exact mechanism by which this form of irregularity is produced requires further investigation in order that its diagnostic and prognostic significance may be thoroughly understood. The condition of the radial, temporal, and other arteries may vary considerably, but, especially in patients above 40, may show considerable grades of arteriosclerosis. This is more common and somewhat more exten- sive in patients suffering from any cardiac disease than in persons with normal hearts (Wild). Lungs. Examination of the thorax and lungs in mitral insufficiency reveals the usual signs corresponding to the pulmonary changes described above small, moist, and piping rales corresponding to the bronchitis often associated with hyper-resonance on percussion. Over areas of hydrothorax there are absolute flatness on percussion, absence of vocal fremitus and breath sounds, Koranyi's flatness over the lower thoracic spines, and Grocco's triangle, paravertebral dulness to the left of the midline. MITRAL INSUFFICIENCY. 421 Abdomen. The abdomen rarely shows any special change during the milder stages of the disease. Occasionally one finds, as in a young girl recently under the writer's observation in the Johns Hopkins Dispensary, the remains of an old splenic infarction, characterized by enlargement, hardness, and tenderness of the organ. This may persist for some months. Enlargement and pulsation of the liver and ascites (portal stasis) belong to the stage of broken systemic compensation (see page 414). The same also applies to cedema of the feet, ankles, and legs, which occurs in the mildest form of broken compensation. These phenomena, though of serious import, are by no means harbingers of death, for with proper treatment many cases outlive one or even several breaks in compensation for many years. The following represent the course of typical cases of mitral insuf- ficiency. CASE OF MITRAL INSUFFICIENCY. C. H., ship carpenter, aged 63, first admitted to the Johns Hopkins Hospital in No- vember, 1899, complaining of shortness of breath. Family history negative. The patient has always been a robust man. He gives a doubtful history of rheumatism, but a definite history of pneumonia five years before admission. No venereal his- tory. He has always been a hard eater, hard drinker, and a hard worker. The present illness began with attacks of paroxysmal dyspnoea upon exertion eight or nine months before admission. Two months before admission an attack came on spontaneously while in a warm room. During the past month he has not been able to lie down in bed owing to dyspnoea and the onset of a smothering feeling. He has had no cough, no haemoptysis. Examination on this admis- sion showed a stout, well-nourished man with mucous membranes a trifle purple and dilated venules over the face. His chest was barrel shaped and there was a little fluid (flatness and impaired breath sounds) at the bases behind. Heart. Apex was situated in the 6th interspace 16.5 cm. from the midline. The area of cardiac dulness reached upward to the second costal cartilage and 5 cm. to the right of the sternum. There is a well-marked systolic murmur heard over the body of the heart and over the anterior part of the axilla. The second sound is every- where clear; the second aortic booming. The liver is slightly enlarged, being just palpable; the spleen is not. The abdomen is full, the flanks bulge, and there is slight movable dulness in the flanks. Genitalia normal. There is slight oedema of the ankles. Blood count normal. Urine is dark sherry colored, specific giavity 1024, acid, contains a small amount of albumin and some hyaline and granular casts. The patient was put to bed on soft diet, given daily purgation with magnesium sulphate (30 Gm., i), also 8 doses of tincture of digitalis (1 c.c., n^xv) at intervals of four hours, followed up by strychnine 1.5 mg. He was also given potassium iodide 1 Gm. (gr. xv) after meals. CEdema disappeared and orthopnosa also, so that within ten days the patient could sleep with his head low and could walk without dyspnoea. He then left the hospital. He was next seen three years later, having been perfectly well until he took cold one month before, since when he had shortness of breath on exertion and on lying down. He had some c o u g h and slight swelling of the feet. The physical condition was about as on the first admission, except that the systolic m u r m'u r entirely replaced the first sound and was well heard in the axilla. Maximal blood-pressure 182 mm. Hg. He again improved rapidly and left the hospital in two weeks. He entered the hospital again one year later with the same signs, the liver being now 2 cm. below the costal margin. Once more he improved rapidly under treatment; the liver receded, and he was discharged, only to be readmitted in the same condition five weeks later, when symptoms dated from exposure to the wet. He then had some tenacious sputum streaked with blood and numerous moist rales were heard everywhere over his chest. Re- covery was once more uneventful. 422 DISEASES OF THE HEART AND AORTA. COMPLICATIONS AND SEQUELS. There are few complications and sequelae which are more character- istic of mitral insufficiency than of other valvular diseases. Those symp- toms due to pulmonary engorgement, bronchitis, haemoptysis, and pulmonary oedema have already been discussed. Embolism from loosening of vegetations upon the mitral valve or of clots which have formed in the left auricle during periods of stasis is an occasional occurrence, especially in severe cases, but less common than in mitral stenosis. As the result of this there may be the production of infarcts in the various organs spleen, kidneys, and brain and of ecchymoses in the skin. In contrast to mitral stenosis, pulmonary tuberculosis occurs in mitral insufficiency with the same frequency as in otherwise normal individuals (Meisenburg) . As may be seen in Fig. 166, mitral insufficiency is very frequently asso- ciated with other valvular diseases, 29 per cent, of all the cases of valvular disease at the Johns Hopkins Hospital being accompanied by aortic insuffi- ciency, 21 per cent, by mitral stenosis. In these cases the mitral insuffi- ciency is sometimes the original lesion, the other lesion resulting from a metastatic infection or subsequent organization. On the other hand, the mitral insufficiency associated with aortic insufficiency may also be a func- tional one due to overfilling of the ventricles. The mitral insufficiency which appears late in the course of mitral stenosis is due to the inability of the thickened valves to close. Coronary sclerosis, as shown by Wild, is more than usually common in chronic valvular disease, and hence should be borne in mind in establishing the prognosis. Pericarditis is one of the common complications, especially in children, in whom adhesive pericarditis is to be feared. Since the majority of cases of mitral disease are of rheumatic origin, diseases of the rheumatic cycle, tonsillitis, articular rheumatism, chorea in children, and affections of the urticarial group, are particularly common. Of these arthritis is the most frequent as well as the most stubborn and dangerous. TREATMENT. The management of cases of mitral disease does not depart in any essential particular from the general type of treatment of cardiac disease. It should be directed to three ends: 1. Removing the overstrain; 2. Increasing the strength of the heart; 3. Avoidance of infection, and removal of the foci. In the mildest cases, the insufficiency shown by signs but not by symp- toms, due especially to the formation of a new vegetation, it is most impor- tant that the cardiac t on i city should be maintained, that the amount of leakage should thus be kept down to its minimum, and that cardiac hyper- trophy should be induced before symptoms have set in. It is therefore most important to spare the heart every effort. If the patient is seen jat the onset of the disease he should be kept at absolute rest in bed for at lea-t a couple of weeks after temperature has returned to normal and all MITRAL INSUFFICIENCY. 423 signs of acute disease have passed. Too much care cannot be exercised at this time, since this is the crucial epoch in determining the severity of the case. It is important not only to maintain the tonicity of the heart muscle but to preserve the valves from all further injury until the vegeta- tions have become thoroughly organized and lined with endothelium, and the germs have disappeared from the original focus of infection. When the tonsil is the source of infection, it should be completely dissected out as soon as acute infection has passed off, in order to prevent reinfec- tion of the valves from this source. The results obtained in the Medical Clinic of the Johns Hopkins Hospital, where this practice has been carried out at Prof. Barker's suggestion, have been very gratifying. In many cases the recovery from the first attack has been more rapid than had been usual before this treatment had been resorted to (see page 403), and it seems probable that reinfection of the valve is of less frequent occurrence thereafter. Similar results are seen in gonorrhoeal endocarditis after treat- ment of the urethritis. In these mild cases drug treatment may not be absolutely necessary. In how far Cloetta's suggestion as to the early use of digitalis should be carried out is still unsettled, but at least the administration of strychnine in doses of from 1 to 3 mg. (-$ to -jV gr.) is advisable in order to increase the tonicity of the heart muscle. However, the blood-pressure and hence the strain upon the valves should not be materially increased (not more than 10 mm. Hg), and the dose of strychnine should be reduced if it rise above this level. Digitalis is not necessary in cases of this type. The bronchitis which frequently accompanies cases of this type does not differ greatly from the ordinary forms of chronic bronchitis, and is associated with the usual pulmonary bacteria found in these conditions the streptococcus, pneumococcus, influenza bacillus, Friedlander's bacillus, etc. Treatment is therefore the same as for ordinary bronchitis, a soothing steam inhalation being very useful. The following are to be recommended : Oleum pini sylvestris, or Creosoti, oiss; 5 Tr. benzoin, co., Tr. opii camphorat., aa oiiss 75 A teaspoonful inhaled with steam from an atomizer, or from a funnel above a glass jar into which a teaspoonful of the remedy and a pint of boiling water have been placed. Codein .015 to .030 Gm. (gr. \ to It) or heroin 2.5 mg. (gr. ^V to yV) may be given by mouth to relieve the cough by reducing bronchial secretion and irritability. Physical Re=education. When the stage of acute symptoms has passed the stage of re-education begins. The heart though injured must be trained to perform the day's work without strain. To do this the heart muscle must be stronger than normal; it must have hypcrtrophied. The process of hypertrophy after valvular lesion, like the heart hypertrophy of an athlete in training, requires time. However, the amount of hypertrophy setting in after a valvular lesion is greater than that after a prolonged period of muscular exercise, and hence may be expected to take a longer time. At this stage Nauheim baths and resisted movements may be dispensed with 424 DISEASES OF THE HEART AND AORTA. as long as a reasonable supervision is kept over the patient. He should never be allowed to become either very tired or short of breath, and six months or a year should elapse before he is allowed to run, participate in games, severe exercise, or manual labor. The current statement that the prognosis is doubtful during the first year after the occurrence of a' valvular lesion is due largely to the intercurrence of acute overstrain of the heart muscle before hypertrophy is complete. The condition is quite different, however, when the mitral insufficiency is of long standing before it is encountered by the physician, as is frequently the case in routine examinations for life insurance, civil service, etc. The disease may then be said to have cured itself already, and beyond gently admonishing the patient against over-exertion no further precautions are necessary. It is often unwise to inform a man or woman of nervous tem- perament that a heart lesion is present, since worry may in itself contribute to the cardiac overstrain. Cases of functional mitral insufficiency are rarely devoid of cardiac symptoms, and hence will be considered under the second group. Treatment of the Second Stage. The second stage of mitral insuffi- ciency, in which dyspnoea and other symptoms of cardiac origin are present, represents a condition of chronic cardiac overstrain. Indeed it is the abnormal severity of these symptoms following some slight exertion which usually calls attention to the existence of the lesion. The treatment does not depart in any essential particular from that which has already been discussed in the case of chronic overstrain of the myocardium. Just as in the milder cases the most important element in the treatment is absolute rest in bed, continued until long after symptoms have subsided. The diet should at first be very light (see page 224), and should be very gradually increased after symptoms have subsided. As in the milder cases, vigorous doses of strychnine (2 to 3 mg. [gr. -jV to -oVl every four hours) should be begun at once. The bowels should be kept moving freely by means of Seidlitz powders, Epsom salts, Hunyadi water, Mistura ferri aperiens, or some other mild laxative. It is important that the patient should sleep well at night, and trional (1 Gm.=gr. xv) or some other soporific may be given, if necessary with the addition of codcin (15 mg. =gr. ss). If symp- toms have not diminished after a couple of days of this treatment, digi- talis should be resorted to (see page 236), for it is important not only to reduce the strain but also to strengthen the heart muscle as rapidly as pos- sible in order to prevent the overstrain from becoming permanent. Indeed it may be said that this is the all-important stage in the course of mitral insufficiency and of all other valvular lesions, the stage which determines whether the patient may hope to return to a life of activity or must look forward to one of permanent invalidism, and this question is often decided by the promptness or tardiness with which the symptoms dis- appear when the patient is at rest. In this stage the primary source of infection or reinfection should be treated just as in the milder ones, but the period of rest should be longer and the period of physical re-edu- c a t i o n and g y in nasties should be very carefully undertaken. The more systematic methods, such as those of Schott, Herz and Oertel, are especially valuable, as are also the Xauheim baths. The important factor, MITRAL INSUFFICIENCY. 425 however, is that, whatever the method of treatment, the patient should never be allowed to become fatigued or short of breath, he should be gradually trained up to his optimum strength, and he should never be allowed to attempt to exceed his limit. Treatment of the Third Stage. In the third stage of mitral insuffi- ciency, that of broken compensation, the burden of the cardiac fail- ure has been shifted from the left ventricle to the right. The treatment therefore follows the rules laid down for broken compensation due to any cause whatever: absolute rest, immediate use of digitalis (especially along with nitroglycerin, sodium nitrite, or erythrol tetranitrate), free purgation, and very light diet being the essential features. Hypodermic injections of morphine (8 to 15 nig., gr. to |) may be necessary, but they should be used with caution, since they decrease the irritability of the respiratory centre and thus lead to accumulation of C0 2 and cardiac asthma. Since many of the symptoms are due to a high pressure in the vena cava and consequent dilatation of the right auricle and ventricle, venesection is often followed by great improvement, and should be regarded as an important therapeutic measure during the acute stage of the overstrain. But in the presence of anaemia it should not be resorted to. Intravenous strophanthin (0.5 to 1 mg.) is of the greatest value when the symp- toms have become alarming, and should be followed by the usual course of digitalis, or by daily intramuscular injections of strophanthin. As symptoms subside, the condition and its treatment pass into those of the second stage, and a gradual return to normal may occur. On the other hand the symptoms may increase, hydrothorax and ascites may become extensive and may require tapping, and the oedema may become extreme. To diminish these it may be advisable to use diuretics, such as theobromin acetate (agurin), theocin, or acettheocin sodium, or else potassium acetate and citrate. PROGNOSIS. Exactly how much benefit can be effected by treatment varies with each individual case, and depends upon factors which are difficult to fore- tell. It is especially true of mitral insufficiency that while there is life there is hope, for the patient may almost completely recover from one or more attacks of broken compensation and yet remain comparatively free from symptoms for a number of years. As regards the prognosis for the individual attack no absolute rule can be laid down, but much importance may be attached to the rapidity of change for the better or for the worse. A rapid improvement during the first two days may be construed as favorable for the ultimate outcome; a slow recovery usually indicates a severe residuum of trouble; an increase of symptoms in spite of treatment is of grave significance. Between attacks the patient's ability to hold his own or even to im- prove his condition depends entirely upon his ability to keep himself free from overstrain and reinfection. In all cases the physician should be some- what guarded in his statements regarding the future. 426 DISEASES OF THE HEART AND AORTA. BIBLIOGRAPHY. MITRAL INSUFFICIENCY. Krehl, Geipel. Quoted on page 324. Roy and Adami: The Failure of the Heart from Overstrain, Brit. M. J., Lond., 1888, i, 1321 and 1395. Kiilbs. Quoted on p. 290. Weber and Deguy: Du role des hsemorrhagies intracardiaques dans les retrecissement mitral, Presse med., Par., 1898. La region mitro-aortique; 6tude anatomique et pathologique, Arch, de med. exper. et d'anat. path., Par., 1897, ix, 235. Meigs, V. A.: A New Method of making a Hydrostatic Test of the Mitral and Tricuspid Valves, Med. News, Phila., 1884, xlv, 533. Bleichroeder: Die Funktionspriifung der Mitralklappe, Arch. f. path. Anat., etc., Berl., 1902, clxix, 159. Gibson, G. A.: Diseases of the Heart and Aorta, Edinb. and Lond., 1898. Weiss, O., and Joachim, G.: Registrierung und Reproduktion der menschlichen Herz- tone und Herzgeriiusche, Arch. f. d. ges. Physiol., Bonn, 1908, cxxiii, 341. Marey, E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Paris, 1881. Gerhardt, D.: Ueber die Compensation von Mitralfehlern, Arch. f. exper. Pathol. u. Pharm., Leipz., 1901, xlv, 186. King, T. W.: An Essay on the Safety-valve Function in the Right Ventricle of the Human Heart, etc., Guy's Hosp. Rep., Lond., 1837, ii, 104. Osier, W., and Gibson, A. G.: Modern Medicine, Phila. and N. Y., 1908, iv, 205. Moritz, F.: Einige Bemerkungen zur Frage der percutorischen Darstellung der gesammten Vorderflache des Herzens, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxviii, 276. Cf. also article by Dietlen and Simon in the same volume. Harris, Th.: Some Clinical and Post-mortem Observations on the Cardiac Dulnes^; in Cases of Mitral Disease, etc., Med. Chron., Manchester, 1892, xvii, 287. Groedel, F. M.: The Examination of the Heart by the Roentgen Rays, Arch. Roentg. Ray and Allied Phenom., Lond., 1908. Hofmann, Aug. Quoted on p. 173. Gerhartz, IL: Zur Frage des Stethoskops, Deutsch. Arch. f. klin. Med., Leipz., 1907, xc, 501. Naunyn, B.: V eber den Grund weshalb hin und wieder das systolische Gerausch bei der Mitralinsufficienz am lautesten in der Gegend der Pulmonalklapp zu vernehmen ist, Berl. klin. Wchnschr., 1868, v, 189. Boy-Teissier: L'auscultation retrosternale, Rev. de Med. Paris, 1892, xii, 169. Wild, R.: A Contribution to the Pathology of the Coronary Arteries, Med. Chron., Man- chester, 1892, xvi, 223. Meisenburg: Ueber das gleichzeitige Vorkommen von Herzklappenfehlern und Tuber- kulose, Ztschr. f. Tuberk., etc., 1902, iii, 378. III. MITRAL STENOSIS. HISTORICAL. After mitral insufficiency the most common affection of the mitral valve is that which leads to mitral stenosis. This condition was first de- scribed by John Mayow in 1669 in the case of a young man who died after several years of dyspnoea, palpitation, and attacks of syncope. " At autopsy he found dilatation and hypertrophy of the right ventricle and almost complete closure of the left auriculoventricular orifice by a 'cartilaginous product, ' so that the blood could scarcely traverse the left ventricle and was compelled to flow backward to the pulmonary vessels, hence the disten- tion of the right ventricle." Vieussens (1715) described similar findings, noting also that the papillary muscles were changed to small short tendons, and that the right ventricle was so dilated as to allow reflux of blood past the tricuspid valve. He further noted weakness and irregularity of the pulse, and ascribed it to "too small quantity of blood which the left ven- tricle furnished to the aorta . . . and the irregularity of its contrac- tions." Senac (1749) and others described cases, so that the lesion became quite familiar to pathologists in the early part of the nineteenth century. PATHOLOGICAL ANATOMY AND PATHOGENESIS. Pathologically, it is brought about by a chronic inflammatory process taking place in the tissue of the valve which leads to thickening and fusion of the cusps. By this fusion the valve comes to form a sort of funnel, some- times elongated, sometimes short and shallow. The walls are much thicker than those of the normal valve, owing to a chronic infiltra- tion and proliferation of the con- nective tissue within them. They are usually more or less rigid, some- times smooth, sometimes rough from remains of old vegetations and calci- fications, and the auricular surface is often puckered or thrown into folds. The lower margin of the valve is attached to the chordae tendinese, which become shortened and thickened very early in the process. The orifice thus formed is sometimes circular, sometimes oval or button-holed, sometimes irregular (Fig. 189). According to Sansom, the funnel shape is more common in 427 FIG. 189. Human heart, showing mitral (^f) and tricuspid (Tl stenoM.s. Viewed from above. The auricles have been cut through. 428 DISEASES OF THE HEART AND AORTA. children, while the buttonhole is more common in adults and represents a lesion of longer duration. The orifice may often become very small before death ensues, sometimes barely large enough to admit a goose-quill (Sansom). In some long-standing lesions the margin of the valve may become so thick and stiff (sometimes calcified, cartilaginous, or ossified) that it does not close during ventricular systole; in others the edges become retracted so that they no longer cover the orifice. In either case secondary mitral insufficiency may result. Occurrence. According to the studies of Lockhart Gillespie, mitral stenosis is most common in women, increasing in frequency up to the age of 29. In men it is scarcely more than half as common, but reaches its maximum frequency a decade later. The males affected die earlier than the females, however; the average period of death being from 30 to 39 with the former, while with the latter it is 40 to 49. The presence of the double mitral lesion does not shorten the average period of life. Etiology. As regards etiology, Cheadle, Samways, Duroziez, and Dyce Duckworth agree that rheumatism is the etiological factor in at least 60 per cent, to 78 per cent, of the cases, other acute infections, chlo- rosis (Goodhart), chronic nephritis, gout, arteriosclerosis, and puerperal infections representing the other etiological factors. Potain also believes that pulmonary tuberculosis is an important factor, but this is disputed by many writers; most of whom agree with Traube that tuberculosis is far less frequent (5 per cent.) in the presence of mitral stenosis than in normal individuals (12 per cent.) or in those with other heart lesions (Meisenburg, Tileston). Pathogenesis. As regards pathogenesis, Huchard (1. c.) 'divides the cases of mitral stenosis into three groups: 1. The congenital form, resulting from fetal endocarditis, w r hich, as Sansom has shown, is very rare. 2. The endocarditic form of infectious origin (due especially to rheumatism, scarlet fever, measles, typhoid fever, smallpox, etc.), resulting from the organization and fusion of old vegetations. This is the most com- mon form, since rheumatism alone can be demonstrated as an etiological factor in about 70 per cent, of the cases. 3. The sclerotic form, which is associated with general arterio- sclerosis, gout, and plumbism. In this group no traces of endocarditic vege- tations occur upon the valve, and the process is more closely allied to that within the vessel walls in arteriosclerosis. Under this group should also fall the Large group of cases associated with chlorosis and other anaemias in which no other causal factor is present to explain the presence of the lesion. Goodhart, who lays especial stress upon this group, believes that the o h r o ii i c overstrain of the anaemic heart muscle is followed by cedema and petechise in the substance of the mitral valve, as has been demonstrated experimentally by Roy and Adami. He thinks that this oedema is followed by cellular infiltration and finally by proliferation of fibrous tissue resulting in the mitral stenosis. While this view is suggestive, no careful histological or experimental studies have been made to bear it out. On the other hand, it must be remembered that most anaemic and gouty persons are subject to repeated slight infections which might suffice to produce chronic changes in MITRAL STENOSIS. 429 the heart during the lapse of years. Weber and Deguy have shown that hemorrhage occurs often in the valves after labor, etc. This is followed by infiltration and organization and finally by sclerosis of the valve. PATHOLOGICAL PHYSIOLOGY. The nature of the disturbance to the circulation in mitral stenosis was already discerned by Vieussens in 1715, who noted that owing to the inabil- ity of the blood to pass through the mitral orifice with sufficient rapidity, it had become dammed back in the pulmonary veins and pulmonary arte- ries, increasing the work of the right ventricle and leading to insufficiency of the tricuspid valve. At the same time the force of the pulse (blood-pressure) and amplitude of the pulse were diminished, owing to the diminution of the blood which entered or was forced out of the left ventricle. Vieussens noted further that the force and rhythm of contraction were irregular. NORMAL n BROKEN PULMONARY COMPENSATION III BEGINNING FAILURE OF LEFT VENTRICLE FIG. 190. Diagram showing the changes in the circulation due to mitral stenosis. The stage of perfect compensation is not shown, since there are practically no pressure changes. II represents the stage at which pulmonary compensation is broken but systemic circulation has not yet become affected. Ill represents the stage in which there is broken pulmonary compensation, and the left ventricle has failed to maintain the arterial pressure. The last pressure changes in the last stage, with broken systemic com- pensation as well, correspond exactly to those in the last stage of mitral insufficiency. (Compare with Fig. 26.) The changes of pressure corresponding to these phenomena have been studied experi- mentally by Bettelheim and Kauders, D. Gerhardt, and MacCallum and McClure, who have found that the production of a mild grade of experimental stenosis causes distinct rise in the mean pressure within the left auricle, the pulmonary veins and the pulmonary artery. Filling of the Ventricles. The effect of the stenosis upon the filling of the ventricles as shown in the volume curve has recently been investi- gated by the writer, aided by Mr. J. M. Wolfsohn. As shown in Fig. 191, the first effect of the mitral stenosis is to slow the inflow into the left ven- tricle. As a result of this the left auricle is more than usually full at the time of its systole, and forces an unusually large quantity of blood into the ventricle (Fig. 192, AS). This increase in auricular output at first suffices to complete the filling of the ventricle, but as the lesion progresses a little further even this fails to do so and the amount of blood entering the ven- tricle falls below normal. As a consequence of this, the ventricle forces 430 DISEASES OF THE HEART AND AORTA. less blood into the aorta, the arterial blood-pressure falls and the pulse- pressure diminishes. This is the condition as observed in the experiment. In man, however, where the pathological change is a gradual one, the arteries gradually accommodate themselves by constriction of their chan- nels until the blood-pressure has returned to about its normal level. The pressure in the systemic veins is diminished, as has been shown by Kornfeld. LIGATURE TIGHTENED VOL OAK. FIG. 191. Volume of the ventricles in experimental mitral stenosis. (Kindness of the Johns Hopkins Hospital Bulletin.) Tracings obtained from a dog's heart in experimental mitral stenosis. VOL., volume curve ; CAR., carotid pressure. The arrow indicates the moment at which the stenosis was produced. The filling of the ventricles (downstroke) was slowed, diastasis (horizontal part of curve) sets in prematurely, and the part of the curve due to auricular systole (second downstroke) becomes more pronounced. The heart rate is practically unchanged. S D NORMAL S D II S D III S D IV FIG. 192. Diagram illustrating the variations in the volume curve of the ventricles in increasing degrees (I, II, III, IV) of mitral stenosis. . 5 cm. from the midline. The presystolic rumble and sys- tolic murmur are well heard, as at the last discharge. Red blood-corpuscles 5,000,000; haemoglobin 105 per cent.; leucocytes 5500. MITRAL STENOSIS. 441 On the night of admission the patient felt bad and had attacks during which he felt faint and " saw stars." Venesection caused much r e 1 e i f in the symptoms and the blood-pressure rose from 120 mm. Hg to 140mm. The patient's condition then gradually improved, but on January 24 he had a definite attack of precordial pain and constriction lasting 1-3 minutes. Feb. 23. Has had pain in head and the left side of the face due to a beginning otitis media. During the next few weeks he had several attacks of angina pee- to ris , the pain being usually most marked behind the lower part of the sternum. In one attack it radiated to the left shoulder and down the left arm to the hand (left ventric- ular pain). On April 20 he complained of pain in the left axilla and back, com- ing in paroxys ms lasting for 15-20 minutes (left auricular pain). May 6. Sputum bloody. From this time on he gradually improved, cyanosis and dyspnoea almost disappeared, and he was discharged in August in fair condition. From that time until his readmission in November he suffered from numerous attacks of angina pectoris. beginning in the left hand and passing up the arm to the shoulder and heart. He also had an attack of rheu- matism and severe tonsillitis. His physical condition was like that on pre- vious admission, but the anginal attacks were more frequent. He was given hypodermic injections, sometimes of morphine, sometimes of distilled water, to relieve them. His condition gradually improved, most markedly after venesec- tion. Toward the end of his stay, while up and about, he became subject to sudden paroxysms of acute dyspnoea (respirations 130 per minute), with small moist rales filling the lungs (acute pulmonary cedema). These persisted in spite of repeated rest and digitalis treatments. He was discharged on July 11, 1905, seven months after admission. (Edema and dyspnoea returned within ten days, and he was soon back in the hospital again. Dur- ing this admission he never thoroughly rallied. His blood -pressure remained low, 105 mm. maximal pressure (as compared with 120-130 mm. on previous' ad- missions). The pulse was irregular. Rales were constantly present in his chest. The liver was palpable. A slight pleurisy developed on October 13 and he died on Octo- ber 20. At autopsy the mitral orifice was found to have the form of a small button -hole barely admitting the tip of the little finger (about 5 mm. in diameter). The left auricle was dilated and hypertrophied. The left ventricle was not dilated, but was much hypertrophied, its walls being 15 mm. thick. The right auricle and ventricle were much dilated, the tricuspid orifice admitting four fingers (13-14 cm. in circumference). The coronary arteries were patent but showed scattered areas of sclerosis. There were old fibrous patches upon the pericardium. The pulmonary arteries were markedly sclerotic; the sclerosis extended into their smaller branches. The aorta and peripheral arteries showed less sclerosis. There were also chronic passive congestion of the other viscera, anaemic infarctions of the spleen, hemorrhagic infarction of the lungs, acute bronchitis, bronchopneumonia, acute ulcerative follicular colitis, old tuberculous foci in the lymph-glands and lungs, chronic adhesive pleuritis, and adhesive peritonitis. COMPLICATIONS. As seen by the table in Fig. 179 mitral stenosis is frequently associated with other valvular lesions. Mitral insufficiency, present in one-half of the Johns Hopkins cases and in 75 per cent, of Steell's cases, may be regarded as an essential part of the disease rather than a special complication, and its presence does not shorten the average length of life. The association of aortic disease, and indeed of any additional burden upon the circulation, increases the gravity of the condition. Tricuspid stenosis is an occasional concomitant, though rarely as often found as by Sarmvays, who encountered it in severe grade in 24 out of 196 442 DISEASES OF THE HEART AND AORTA. autopsies upon cases of mitral stenosis, and in mild grade in 8 additional cases. In the Johns Hopkins Hospital it was found clinically 7 times among 298 cases of mitral stenosis. A certain degree of myocarditis is the rule, especially in cases in the third and fourth decades. Acute pericarditis is quite common in the youthful rheumatic cases, frequently leaving a residual adherent pericardium, a lesion which aggra- vates the condition considerably and greatly shortens the life of the patient. One of the most important and dangerous complications arising with mitral stenosis is pregnancy (see Chapter I X) . Thrombosis in the Left Auricle. Another not uncommon complication of mitral stenosis, more than any other valvular lesion, is thrombosis within the left auricle. This may occur even while the auricle is still contracting vigorously, as shown by the presystolic thrill and rumble. The thrombus may remain quiescent in the tip of the auricle or it may obstruct the pul- monary veins. Sometimes it is so large as to stop up the narrow mitral orifice and kill the patient. More frequently it is small enough to pass through, and if carried on by the blood current gives rise to a small area of embolism. Embolism. Embolism of the middle cerebral artery may give rise to paralysis or aphasia. Embolism in other organs gives rise to corresponding signs and symptoms. Pulmonary embolism and infarction are caused by thrombi from the right auricle and ventricle; and hence are due to secondary stasis in the latter and not primarily to the mitral stenosis. However, as failure of the right ventricle is particularly common in mitral stenosis, pulmonary embolism is especially frequent in this disease. A few months ago a patient was admitted to the medical service of the Johns Hopkins Hospital with gangrene and anaesthesia of both lower ex- tremities, due to plugging of the abdominal aorta by such an embolus. He has a well marked mitral stenosis, with purring presystolic thrill and loud presystolic rumble, showing that his left auricle was contracting vigorously. Needless to say, nothing could be done to relieve him, and he died within a few days. TREATMENT OF MITRAL STENOSIS. As regards indications for treatment, cases of mitral stenosis fall into several groups. I. 1. Compensated cases with regular pulse-rate. 2. Occasional extrasystoles with some cardiac weakness or occasional attacks of paroxysmal tachycardia. II. Paroxysmal or permanent arrhythmia with or without broken compensation. III. Broken compensation. In the mildest and most chronic forms the treatment is mainly prophy- lactic and the patients may often be kept free from .symptoms for years by MITRAL STENOSIS. 443 maintaining a carefully regulated life, by taking special precautions against overstrain, anaemia, and infectious diseases. All foci of infection should be carefully looked for and eradicated. Diseased tonsils and abscessed teeth should be removed, furuncles and foci of pyorrhosa alveolaris vigorously treated, suppurations of the various sinuses and of the sexual organs treated or drained. When bronchitis is present it may bring on a vicious circle: Bronchial congestion and infection / \ Pulmonary f Reinfection of and increase stasis of cardiac lesion, and therefore it should be treated carefully. The patient should be protected as far as possible from draughts and severe weather, and the bronchial condition relieved with inhalations. The writer has found the following mixture especially soothing: K Menthol 2 G. 333 Eucalyptol 5 3 iss Camphor 5 3 iss Tr. benzoin co 30 3 i Alcohol 45 3 iss Sig. One teaspoonful in boiling water for inhalation. Pulmonary tuberculosis, though not extremely uncommon, must not be overlooked ; and must be vigorously treated by the usual methods. Anaemia is such a potent factor in keeping up the oedema infiltrations of the valves that when present it deserves special attention. Anaemic patients should be given complete rest and diet rich in eggs and milk, some form of iron, especially Vallet's mass (0.3 G., gr. v), Blaud's pills, or the saccharated oxide of iron (Ferrum oxidatum saccharatum, one teaspoonful in water). When the haemoglobin is low, arsenic (Fowler's or Donovan's solution) may be given. The patients whose compensation in itself remains good but who suffer occasionally from the palpitation and discomforts attending extrasystoles and paroxysmal tachycardia which owe their origin to the distended left auricle present a condition which, though as a rule not dangerous, is difficult to relieve, for it bears a closer relation to the heightened irritability than to lessened contractibility of the heart muscle (see pages 108 and 694). Drugs of the digitalis series affect this condition only occasionally, and no remedy has thus far proved of great use. The cheerful side, however, is found in the fact that in man}', though by no means the majority of instances, the patient's actual strength and his outlook may not be seriously impaired by the occurrence of these disturbances. Extrasystoles, when not associated with signs of cardiac failure or weakness, 444 DISEASES OF THE HEART AND AORTA. may be disregarded, even though when accompanied by cardiac weakness they may have a serious import. The same is true of paroxysmal tachycardia, although in the latter the cardiac failure due to the paroxysm itself (see page 695) may be entirely out of proportion to the slight disturbance of the cir- culation from the mitral stenosis. The management of this condition is discussed on page 703. Mitral Stenosis with Absolute Arrhythmia and Auricular Fibrilla= tion. It is in the cases of mitral stenosis with transitory or permanent arrhythmia resulting from fibrillation of the auricle that, as Mackenzie and Lewis have shown, the most brilliant improvements are to be obtained (page 244). In these cases the symptoms are to a great extent due in part to stasis in the left auricle, pressure upon the bronchi and the recurrent laryngeal nerve, congestion of the pulmonary circulation, and at times cedema of the lungs, and in part to diminished filling of the arterial blood- vessels. This, as the experiments of Hirschfelder and Wolfsohn have shown, is due largely to the fact that in mitral stenosis the ventricles fill more slowly than normally during diastole, and moreover that in this condition the pump- ing action of the auricles assumes a role of importance about equal to that of the passive filling; so that, when the latter factor is eliminated by fibrillation and the diastoles are shortened by a rapid heart-rate, the filling of the ven- tricle is greatly impeded, the pulmonary circulation becomes overfilled, and the outflow into the arteries becomes diminished. The physiological requirements for this condition are therefore exactly met by the action of digitalis, for digitalis causes the heart-rate to become slow and allows the ventricle time to fill. In some cases, especially those in which the arrhythmia has been of short duration, digitalis may cause the auricles to cease fibrillation and to resume coordinate contractions so that the heart-rate again becomes regular. In these cases, and especially in the cases of combined mitral stenosis and insufficiency, the effect of digitalis in increasing the force of ventricular contraction and the tonus of the heart walls is beneficial, but the chief benefit from the drug is derived from its action on heart-rate and rhythm rather than on force. This fact is, unfortunately, brought home only too plainly by its frequent failure to give decided relief in those cases in which the heart-rate remains regular in spite of a breaking compensation, either because the auricles con- tinue their coordinate contractions or because they undergo a complete atrophy, and it is this group of cases in which all forms of treatment seem doomed to disappointment. In order to secure the full benefit in these cases, as stated on page 244, the drug must be administered in sufficient doses over a sufficient period of time and must be kept up as long as the arrhythmia lasts. In general, three or four doses of 30 minims of the (physiologically standardized) tincture of digitalis at four hourly intervals, followed by fifteen-minim (1 c.c.) doses until the pulse-rate falls below 70, will suffice to bring about improvement without danger of cumulative action. If the larger doses are continued too MITRAL STENOSIS, PLATE XI. 445 R R S Typical electrocardiogram from a case of mitral stenosis showing large P wave. EXSYS Electrocardiogram from a case of mitral stenosis with permanent arrhythmia due to auricular fibrillation, showing one extrasystolc (EX. SYS.) arising m the right ventricle. 446 DISEASES OF THE HEART AND AORTA. long, the period of full benefit may be only transitory, and may be replaced by several weeks during which the patient may be troubled by palpitation (" uncomfortable thumping " of the heart), weakness, and peculiar sensa- tions in the extremities, which one patient of the writer's described as " feeling as though her limbs were empty." The two extremes, therefore, of too much and too little digitalis must be carefully avoided in each case, if the best results are to be attained, but the amount of digitalis and the time necessary to bring this about vary with each individual, and indeed with each attack. To slow the pulse and keep it slow must be the aim in those patients. In unfortunate contrast to these cases of mitral stenosis with absolute arrhythmia are the patients whose pulse, in spite of failing compensation, remains regular, either because the muscle of the auricle becomes atrophied or because it remains strong enough to carry out its share of coordinate con- tractions throughout. In these patients the effect of digitalis is confined to its action on force and on tonicity. In the milder cases of cardiac failure, and especially those in which the latter has been of short duration, this treatment alone may suffice; but in patients whose heart has been weak and rapid for some time it no longer has much effect in slowing the heart. This may be on account of exhaustion of the vagi, or else be due to the simultaneous stimulation of the accelerators. Accordingly, in cases of this type, digitalis, and other drugs as well, cannot be relied upon, and treatment must be directed along the lines of rest, grad- uated exercise, and careful regulation of life. In the acute heart failure of mitral stenosis with pulmonary oedema, various methods for tiding over the crisis must be resorted to. Atropine (0.5 to 1 mg., gr. y^u to -$-$) may be given to diminish the secretion into the bronchi and alveoli, inhalations of amyl nitrite and hypodermic injections of nitroglycerin (0.5 to 1.5 mg., gr. YTJT to ^V) to lessen the peripheral resist- ance; and as quickly as possible an attempt should be made to increase the force of the heart with an intravenous injection of strophanthin (0.5 to 1 mg., gr. -i-J-jj to !/o). If the patient is not anaemic, a prompt venesection with removal of 300 to 500 c.c. of blood will do more than anything else to relieve the circulation, and should bo resorted to promptly, but never before the hsemoglobin has been taken. If the latter is in the vicinity of 70 per cent., venesection should bo used only under exceptional circumstances, for there is danger of impoverishing the blood too greatly and bringing on cardiac weakness from ano?mia. In such cases a gradual cutting off of the venous return by bandages upon both arms and both legs, as recom- mended by v. Tabora and Tornai (page 225), has been found to have a similar action without removing the blood-corpuscles from the body and thus without bringing on the symptoms of anaemia. Care must be taken that the bandages, which for this purpose may well be composed of ordi- nary clastic tape, must compress the arm at a pressure well below the diastolic pressure, so as to impede the backflow through the veins but not the flow through the arteries. MITRAL STENOSIS. 447 W. Arbuthnot Lane and later (1902) Sir Lauder Brunton suggested that in the light of modern surgical technic it might be possi- ble to slit the narrowed valve with a fine knife and thus remove the stenosis. The experiment of slitting the mitral valve has been performed by Gushing and Branch in hearts of normal dogs. It does not present extreme difficulties, but the recoveries were few, in spite of the fact that the heart muscle of these dogs was in good condition. Bernheim in the same laboratory arrived at similar results. Lauder Brunton had advocated the operation only for cases which were otherwise doomed; and it is evident that here the danger from a weakened myocar- dium would be far greater. Moreover, even if successful, the mechanical effect of suddenly converting a severe mitral stenosis into a severe mitral insufficiency would impose an intense strain upon the heart, and might, even in that way, do more harm that good. PROGNOSIS. In spite of the numerous complications and the progressive character of the lesion, the average duration of life in mitral stenosis is not extremely short, being 33 years for males, 38 for females. This is due to the large number of cases in which the process is dormant or progresses very slowly, and indicates in the individual case the importance of avoiding everything which may start it afresh, particularly infections and overstrain. In many cases the condition then remains dormant for many years, the patient con- tinuing to live a normal if somewhat careful life without further trouble. Lenhartz has seen cases pass through seven pregnancies without manifesting signs of cardiac distress, and endurance of equal magnitude may be met with in men. On the other hand, the lesion may progress rapidly and death may occur within a few years. In the more severe cases it may come on without warning, often due to the loosening of an embolus from the left auricle. BIBLIOGRAPHY. MITRAL STENOSIS. Mayow, John, and Vieussens. Quoted from Huchard, Maladies du coeur, vol. iii, 3d ed., Paris, 1905. Sansom, A. E.: The Pathological Anatomy and the Mode of Development of Mitral Stenosis in Children, Am. J. M. Sci., Phila., 1908, xcix, 229. Gillespio, A. Lockhart: An Analysis of 2368 Cases Admitted with Cardiac Lesions into the Royal Infirmary, Edinburgh, Edinb. Hosp. Rep., 1898, v, 31. Cheadle. Quoted from Sansom. Samways, D. W.: Mitral Stenosis, a Statistical Inquiry, Brit. M. J., 1898, i, 364. Duroziez. Quoted from Petit. Duckworth, Dyce: On the Etiology of Mitral Stenosis, St. Barth. Hosp. Rep., Lond., 1877, xiii, 263. Goodhart, J. IL: On Anaemia as a Cause of Heart Disease, Lancet, Lond., 1880. i, 479. Meisenburg: L T eber das gleichzeitige Vorkommen von Herzklappenfehlern und Lungen- schwindsucht, Ztschr. f. Tuberkl. u. Heilstattenwesen, 1902, iii, 378. Tileston, W.: Passive Hypersemia of the Lungs and Tuberculosis, J. Am. M. Asso., Chicago, 1908, 1, 1179. 448 DISEASES OF THE HEART AND AORTA. Bettelheim, K., and Kauders, F.: Experimentelle Untersuchungen ueber die kiinstlich erzeugte Mitralinsufficienz und ihren Einfluss auf Kreislauf und Lunge, Klin, exper. Unters. a. d. Lab. S. v. Basch, Berl., 1891, i, 144. Kornfeld, S.: Experimentelle Beitrag zur Lehre vom Venendruck bei Fehlern des linken Herzen, ibid., 1892, ii, 126. Gerhardt, D.: Ueber die Compensation von Mitralfehlern, Arch. f. exper. Pathol. u. Phar- makol., Leipz, 1901, xlv, 186. MacCallum, \V. G., and McClure, R.: On the Mechanical Effects of Mitral Stenosis and Insufficiency, Tr. Ass. Am. Phys., Phila., 1906, xxi, 5; also Bull. Johns Hopkins Hosp., Baltimore, 1906, xvii, 260. Hirschf elder, A. D.: The Volume Curve of the Ventricles in Experimental Mitral Stenosis and its Relation to Physical Signs, Bull. Johns Hopkins Hospital, Baltimore, 1908, xix. Miiller, G.: Ungewohnliche Dilatation des Herzens und Ausfall der Vorhofsfunction, Ztschsr. f. klin. Med., Berl., 1905, Ivi, 520. Harris, Th. Quoted on p. 426. Petit, A.: Retrccissement mitrale, Traite de Mod. (Charcot, Bouchard, Brissand), Paris, 1893, v, 247. Corvisart, J. N.: An Essay on the Organic Diseases of the Heart, etc., translated by Jacob Gates, Phila., 1812. Gendrin and Fauvel: Arch, de Med., Paris, 1843, Scr. iv, i, 1. Quoted from Gairdner. Gairdner, W. T.: A Short Account of Cardiac Murmurs, Edinb. M. J., 1861, vii, 428; also Clinical Medicine, 1862. Mackenzie, James: The Study of the Pulse and Movements of the Heart, Lond., 1903. The Extrasystole, etc., I, Quart. J. M., Lond., 1907, i, 131, 481. Minkowski, O.: Demonstration eines Herzens mit ungewohnlich starker Dilatation der Vorhofe, Miinchen. mod. Wchnschr., 1904, li, 182. Hofbauer: Rekurrenslahmung bei Mitralstenose, Wien. klin. Wchnschr., 1902. Also Alexander: Berl. klin. Wchnschr., 1904; and Frischauer: Wien. klin. Wchnschr., 1905. Quoted from Thorel, C.: Pathologic der Kreislauforgane, Lubarsch-Ostertag's Ergebnisse der Path., Wiesb., 1907, ii, iite Abth., 386. Osier, W.: De la paralysie du nerf recurrent gauche dans les affections mitrales, Arch, des malad. d. coeur, Par., 1909, ii, 73. Reviewed in an editorial, J. Am. M. Ass., Chicago, 1909, liii, 35. Einthoven, W., with the assistance of Flohil and Battaerd: Die Registrirung der mensch- lichen Herztone mittelst des Saitengalvanometers, Arch. f. d. ges. Physiol., Bonn, 1907, cxvii, 461. Brockbank, E. M.: The Murmurs of Mitral Disease, Edinb. and Lond., 1899. Fenwick, W. S., and Overend, W.: The Production of the First Cardiac Sound in Mitral Stenosis, Am. J. M. Sci., Phila., 1893, ex, 123. Haycraft, J. B. : The Cause of the First Sound of the Heart, J. Physiol., Camb., 1890, xi, 486. Broadbent, W. II., and J. F. II.: Heart Disease and Aneurism, N. Y., 1906. Acland. Quoted from Fenwick and Overend. Steell, G. : The Auscultatory Signs of Mitral Obstruction and Rogurgitation, Med Chron., Manchester, 1888, viii, 89. The Diagnosis of Mitral Regurgitation through a Con- stricted Orifice, ibid., 1891-2, xv, 361. The Conduction of the Murmur of Mitral Regurgitation, ibid., 1892, xvi, 116. The Distinction between Mitral Stenosis and Muscle-failure in Cartain Heart Cases, ibid., 1892-3, xvii, 24. The Auscultatory Signs of Mitral Stenosis; a Statistical Inquiry, ibid., 1895, X. S. iii, 409. Case of Mitral Stenosis Presenting a Widely Distributed Tc-and-fro Murmur Resembling that of Aortic Incompetence, ibid., 1896-7, X. S. vi, 174. Mitral Stenosis, Internat. Clin., Phila., 1898, s. viii, iii, 1411. Huchard: 1. c., p. 673. Cabot, R. C., and Locke, E. A.: On the Occurrence of Diastolic Murmurs without Lesions of the Aortic or Pulmonary Valves, Bull. Johns Hopkins Hosp., Baltimore, 1903, xiv, 115. Bard, L.: Die Physikalische Zeichen der Mitralstenose, Samml. klin. Vort., Leipz., Xo. 45. Inn. Med. Xo. 137, 1907. MITRAL STENOSIS. 449 Flint, A.: The Mitral Cardiac Murmurs, Am. J. M. Sc., 1886, xci, 27. Phear, A. G.: On Presystolic Apex Murmur without Mitral Stenosis, Lancet, Lond., 1895, ii, 718. Weber and Deguy: Du role des hsemorrhagies intracardiaques dans le retrecissement mitral, Arch, de Med. Exper., Par., 1897, and Presse med., Par., 1898. Sewall, H.: A Common Modification of the First Heart Sound, etc., Trans. Ass. Am. Phys., Phila., 1909, and Am. J. M. Sc., 1909. Brunton, T. Lauder: Preliminary Note on the Possibility of Treating Mitral Stenosis by Surgical Methods, Lancet, Lond., 1902, i, 352. Discussed by Shaw, L. E., ibid., 1902, i, 619. Cushing, H. W., and Branch, J. R. B.: Experimental and Clinical Notes on Chronic Val- vular Lesions in the Dog and their Possible Relation to a Future Surgery of the Cardiac Valves, J. Med. Research, 1908, xii. Bernheim, B. M.: Experimental Surgery of the Mitral Valve, Johns Hopkins Hospital Bull., Baltimore, 1909, xx, 107. IV. AORTIC INSUFFICIENCY. HISTORICAL. Our knowledge concerning lesions of the aortic valves producing leak- age at that orifice (aortic insufficiency, aortic regurgitation, aortic incom- pctency) dates from 1705, when the English anatomist Cowper first de- scribed the occurrence of stiffening and thickening of the valves so that they "did not apply adequately to each other, whence it happened some- times that the blood in the great artery would recoil and interrupt the heart in its systole." Shortly after this, and quite independently of Cow- per, Yieussens (1715) described two similar cases, noting also the presence of a very full quick pulse, like the rebound of a tightly-stretched cord, associated with palpitation of the heart so severe that it prevented lying- down. Morgagni also described sev- eral cases, in one of which he recog- nized both aortic insufficiency and aortic stenosis. Hodgkin in 1S29 de- scribed a number of cases, and also noted for the first time the diastolic murmur, but did not recognize any diagnostic features; so that the clear clinical picture of aortic insufficiency may be said to date from the publication of Dominic Corrigan in 1S32. Fin. 201. Speci upon the aortic valves. vegetation. iving vegetations The arrow points to the PATHOLOGICAL ANATOMY. Modern classifications of aortic insufficiency differ little from that of Corrigan, and we distinguish, as he did 1. Organic forms of aortic insufficiency due to pathological changes in the valves. 2. Functional or relative aortic insufficiency due to dilatation of the mouth of the aorta (Fig. '202, I)). The organic forms of aortic insufficiency may be of three types: 1. Emlocarditic, due to the occurrence of inflammatory changes upon the valves, usually vegetations, occasionally to calcified atheromatous plaques (Fig. 202, A). 450 AORTIC INSUFFICIENCY. 451 2. Rupture of the valves, sometimes from mechanical strain, sometimes from ulcera- tion (Fig. 202, B). 3. Sclerotic shrivelling of the cusps, usually associated with arteriosclerosis (Fig. 202, C), especially the syphilitic form. 1. The pathology of the endocarditic lesions has been sufficiently dis- cussed in a preceding chapter (page 385), since they represent quite typi- cal vegetations. This form of lesion results from the usual causes of endocarditis, especially rheumatism, scarlet fever, pneumonia, as well as gonorrhoeal, puerperal, septicsemic, and other acute infections (see page 388). It is the most common form in persons below thirty-five, whereas the sclerotic is more common in later life. 2. Rupture of the valves is one of the less frequent but by no means rare occurrences, and usually takes place suddenly during a period of great muscular strain, such as wrestling, lifting a heavy weight, drawing a heavy burden, or even during a bicycle race (Huchard), or else after severe blows upon the chest (Osier). Under these circumstances, as has been seen, the blood-pressure may suddenly rise to a tremendous height (see page 188), FIG. 202. Schematic, .showing the various forms of lesion producing aortic insufficiency. A. Vegetation. B. Perforation. C. Arteriosclerotic shrinking. D. Dilatation of the aorta. and the blood stream tears its way through the valve at the weakest point- usually near the base of the sinus of Valsalva. The ruptured valve may have an apparently normal structure, but probably contains minute areas of degeneration, since it is impossible to rupture a normal valve experi- mentally by subjecting it to the highest pressures that are ever reached in the animal body. In many cases the ruptured valves show arteriosclerotic changes which have tended to weaken the tissue. Where endocarditic changes are already present, rupture or perforation of the valve takes place spontaneously and at ordinary or even lowered blood-pressures. 3. The sclerotic form is the most common type of the lesion, and is brought about by a progressive fibrosis of the valve tissue in which contraction, thicken- ing, calcification, aneurismal dilatation or perforation of the valve may be pres- ent. The process is in all the essentials similar to that in mesarteritis and is usually associated with the latter. Here also extensive vascularization accom- panies the fibrosis (Fig. 172). In any individual case the symptoms depend upon the size of the leak as well as upon the state of the peripheral vessels and heart. Although the usual etiological factors, old age, hard work, tobacco, lead poisoning, nephritis, etc., are responsible for aortic insufficiency, one of the most frequent and most striking single factors is syphilis (Osier). Citron, Collins and Sachs, Longcope, and others have found positive Wassermann reactions in about half their cases, and Pearce (Arch. Int. Med., 1910, vi, 478), who has tabulated the cases reported by a number of authors, has found 452 DISEASES OF THE HEART AND AORTA. it positive in 85 out of 207 cases (41 per cent.), while in other valvular diseases it was a little more than half as frequent (23 per cent.). When the cases of aortic insufficiency arising in childhood and those directly traceable to rheumatic infection are excluded, the proportion due to syphilis looms a great deal larger. A certain number of cases, however, are due to the other causes of arteriosclerosis, infectious diseases, hard work, worry, heredity, tobacco, alcohol, lead poisoning. Sex. In women aortic insufficiency is far less frequent than in men, constituting 8.4 per cent, of all heart lesions in the former as compared with 28.5 per cent, in the latter ((iillespie). Moreover, as shown by Rombcrg and Hasenfeld, the presence of aortic insufficiency from causes other than sclerosis in itself leads to the produc- tion of general arteriosclerosis, and hence the presence of any other form of the lesion predisposes to the superposition of sclerosis. Functional Aortic Insufficiency. The existence of leaks at a dilated aortic orifice was already suspected by Corrigan, especially when there was an aneurism near the base of the ascending arch. This has been verified by subsequent observers and a diffusely dilated aorta with insufficiency of the valves is not a rare finding. As regards the presence of tran- sitory leaks from dilatation Gibson has also shown experimentally that such a dilata- tion may occur as a result of too high pressure in the excised heart, and Stewart claims to have produced it by cutting the aortic ring muscle. But since transitory aortic insufficiency does not often accompany the high blood-pressures of uraemia, meningitis, and brain tumor, it is probable that this factor plays little role clinically. The cases of supposed functional aortic insufficiency are rare, but Anders has reported a considerable number. In some at least it is possible that the phenomena (diastolic murmur, collapsing pulse, etc.) are due to other causes, especially functional pulmonary insufficiency. Cardio pulmonary murmurs, like those described by Potain, must also be excluded. However, the possi- bility of functional aortic insufficiency must be borne in mind by the clinician; but it can rarely be verified, and the clinical diagnosis is, at best, hazardous. Yic,. 203. Effect of aortic insufficiency in the mechanical model. (After Marey.) The horizontal line shows the point of production of aortic insufficiency. P.\'., intraventricular pressure; PR, arterial pressure; O, auricular systole. The diastolic pressure in the ventricle after aortic insufficiency is consid- erably higher than in the normal condition and approximates the diastolic pressure in the aorta. Tiie wavelet Medullary asphyxia j f Increased regurgitation 1 J Vasoconstriction j ( Weakening of ventricle j ( Increased peripheral resistance j Venesection is not indicated except when there are a considerable grade of venous stasis, high venous pressure, and dilatation of the right auricle: but in the writer's experience its results are then excellent, AORTIC INSUFFICIENCY. 469 In the anginal attacks and the spells of dyspnoea or for insomnia, codein, .03 Gm. (gr. ), or morphine, .0075 Gm. to .03 Gm. (gr. % to gr. ), hypo- dermically, may be necessary, but should always be used as sparingly as possible, since the habit is readily formed and the patient injures himself by feigning dyspnoea in order to get the drug. They depress the respiratory centre and thus predispose to Cheyne-Stokes breathing and to cardiac asthma. Strychnine 3 mg. (gr. -^Q) should be given to stimulate the respiratory centre. Sir William Ewart recommends CO 2 inhalations (see page 229). BIBLIOGRAPHY. AORTIC INSUFFICIENCY. Cowper: Phil. Trans., 1705, No. 299. Quoted from Osier and Gibson, Diseases of the Valves of the Heart, Modern Med., Phila. and N. Y., 1908, iv, 205. Vieussens: Nouvelles decouvertes sur le co3ur, 1706. Traite nouveau de la structure et des causes du mouvement naturel du cceur, Toulouse, 1705. Quoted from Huchard, Mai. du cceur, 3d ed., Paris, 1905, iii. Morgagni: also quoted from Huchard. Hodgkin, T.: On Retroversion of the Valves of the Aorta, Lond. M. Gaz., 1829, iii, 433. Corrigan, D. J.: On Permanent Patency of the Mouth of the Aorta or Inadequacy of the Aortic Valves, Edinb. M. and S. J., 1832, xxxvii, 225. Gillespie, A. L. : An Analysis of 2368 Cases Admitted with Cardiac Lesions into the Royal Infirmary, Edinburgh, Edinb. Hosp. Rep., 1898, v, 31. Hasenfeld, A., and Romberg, E.: Ueber die Reservekraft des hypertrophischen Herz- muskels, u.s.w., Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1897, xxxix, 333. Gibson, G. A.: Jugular and Triscupid Reflux, Edinb. M. J., 1880. Marey, E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Paris, 1881. Cohnheim, J. : Vorlesungen ueber allgemeine Pathologic, Berl., 1882, i. Jaager: Arch. f. d. ges. Physiol., Bonn, xxxi. Rosenbach, O.: Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1878, ix, 1. Kornfeld, S.: Ueber den Mechanismus der Aorteninsufficienz, Ztschr. f. klin. Med., Berl., 1896, xxix, 91, 344. Moritz, F. : Ueber ein Kreislaufsmodell als Hilfsmittel flir Studium und Unterricht, Deutsch. Arch. f. klin. Med., Leipz., 1899, Ixvi, 349. Stewart, H. A. : Experimental and Clinical Investigation of the Pulse and Blood-pressure Changes in Aortic Insufficiency, Arch. Int. M., Chicago, 1908, i, 102. Head, H. : On Disturbances of Sensation, with Especial Reference to the Pain of Visceral Disease, Brain, Lond., 1896, xix, 153. Certain Mental Changes that Accompany Visceral Disease, ibid, 1901, xxiv, 345. Frankel: Des secousses rhythmiques de la tote chex les aortiques, Rev. de Med., Paris, 1902, 664. Miiller, Fr.: Pulsation des Gaumens bei Aorten insufficienz, Charite Annalen, Berl., 1889, 251. Becker: Ueber Rctinalarterienpuls bei Insuffizienz der Aortenklappen, Monatsschr. f. Augenheilk., 1870. Quincke, H.: Beobachtungen ueber Kapillar- und Venenpuls, Berl. klin. Wchnschr., 1868. Lennhoff : Ueber Pseudoaorteninsuffizienz, Diss., Berl., 1893. V. Weissmayer, W.: Insuffizienz der Aortenklappen ohne Geriiusch und Pseudoaortenin- suffizienz, Ztschr. f. klin. Med., Berl., 1897, xxxii, 29. Huber: Ueber Pseudoaorteninsuffizienz, Berl. klin. Wchnschr., 1898. Flint, A.: On Cardiac Murmurs, Am. J. M. Sc., Phila., 1862, xliv, 29. Thayer, W. S.: Observations on the Frequency and Diagnosis of the Flint Murmur in Aortic Insufficiency, Am. J. Med. Sci., Phila., 1901, cxxii, 538. V. Jurgensen, Th. : Valvular Disease of the Heart, Nothnagel's Encyclopedia of Practical Medicine, Amer. edition, trans, by G. Dock, Phila., 1908. Gerhardt. Quoted from v. Jurgensen. 470 DISEASES OF THE HEART AND AORTA. Romberg, E. : Lehrbuch der Krankheiten des Herzens und der Blutgefasse, Stuttgart, 1906. Huchard, 1. c., Sibson, quoted from Huchard. Broadbont, W. H.: Heart Disease and Aneurism of the Aorta, 4th ed., N. Y., 1906. Osier, W.: The Principles and Practice of Medicine, 4th ed., N. Y., 1901. Cole, R. I., and Cecil, A.: The Axillary Diastolic Murmur in Aortic Insufficiency, Johns Hopkins Hosp. Bull., Baltimore, 1908, xix, 353. Foster, B.: Essays on Clinical Medicine, Lond., 1874. Balfour, G.: Diseases of the Heart, Lond., 1898. Grocco: Arch. ital. riv. clin., 1888. Also Borgherini, A.: Ueber das Verhalten des riick- laufigen Blutstroms bei Insuffizienz der Semilunarklappen der Aorta, Deutsch. Arch, f. klin. Med., Leipz., 1898, Ix, 139. Eastman, T. J. E.: The Diagnosis of Circulatory Conditions by Temperature Measure- ments, Bost, M. and S. J., 1908, clviii, 639. Holzknecht, G. : Die roentgenologische Diagnostik der Erkrankungen der Brusteinge- weide, Hamb., 1901. Cloetta, M.: Ueber den Einfluss der chronischen Digitalisbehandlung auf das normale und pathologische Herz, Arch. f. exper. Path. u. Pharmakol., Leipz., 1908, lix, 209. V. AORTIC STEXOSIS. PATHOLOGICAL ANATOMY. In a certain percentage of cases (10 per cent.) in which the aortic valves are diseased, the cusps become fused into a ring by which the orifice into the aorta is narrowed (aortic stenosis) . Owing to the force within the ven- tricle, this ring is usually pushed upward into the lumen of the aorta until the orifice has a sort of dome- shaped appearance (Figs. 216 and 217, A). The inflammatory or atheroma- tous changes most commonly begin in the cusps separately, and the process extends until their edges be- come fused with an organization or atheroma at the line of union. Oc- casionally there is a progressive uniform diffuse sclerosis like that which often occurs in mitral lesions. The condition almost always arises from the same conditions as aortic insufficiency, but in rare cases may also be of congenital origin. Naturally many of the manifestations depend upon the degree of stenosis, which is sometimes so extreme that a quill can barely be passed B c A FIG. 210. Specimen showing aortic Viewed from above. stenosis. Forms of stenotic aortic orifices-. A. Lateral view of the specini is, with edges of cusps flexibly fixed at ring shown bv broken lin C, c. Aortic stenosis with rigid cusps through the orifice. On the other hand, the orifice may be, relatively speak- ing, wide, and the valves retain sufficient flexibility to close it during dias- tole, so that a pure aortic stenosis occurs without any insufficiency 471 472 DISEASES OF THE HEART AND AORTA. whatever (a condition present in about 60 per cent, of the cases). In the other 40 per cent, the orifice is not only narrowed but the cusps are so fused and rigid that they do not close the aortic orifice during diastole, and an aortic insufficiency is present along with the ste- nosis (double aortic lesion). OCCURRENCE AND ETIOLOGY. Aortic stenosis is by far the rarest of left-sided valvular lesions, occur- ring in only 5 per cent, of the 1781 Johns Hopkins cases and in 2.73 per cent, of Romberg's cases. This is in accordance with the experience of most waiters. Gillespie's statistics, in which it was supposed to occur in 18 per cent, of all the heart cases in the Edinburgh Royal Infirmary, are unique and arouse the suspicion that the fault lay in the diagnosis. The etiological factors are practically the same as in aortic insuffi- ciency. Syphilis and arteriosclerosis play a relatively important role. Con- genital stenosis also occurs occasionally. In rare cases there is a double stenosis, one at the aortic orifice, and one occurring within the ventricle by the formation of a fibrous ring from the septum to the anterior cusp of the mitral valve. The disease is rare among women. PATHOLOGICAL PHYSIOLOGY. The changes in the circulation due to stenosis of the aortic orifice were very completely shown by Liideritz under the guidance of Prof. Gad. Liid- eritz found that if the aortic orifice w r ere narrowed by the tightening of a clamp, the aortic blood-pressure might or might not fall, but the form of the CAR. INT. FIG. 218. Carotid pulse and intraventricular pressure in experimental aortic stenosis. (After Liideritz, Ztschr. f. klin. Med., xx.) | St marks the point at which aortic stenosis was produced. The carotid pulse !<".-lft.) shows the gradual development of the pulsus tardus, with a fall in blood-pressure, while the intraventricular pressure (INT.) increases tremendously. pulse-curve changed. The upstroke changed from sudden to gradual and slanting, ending with a broad rounded top whose sum- mit was reached near the end of systole (pulsus tardus). This form of pulse, as will be seen, is perfectly typical of aortic stenosis, and furnishes the basis for the diagnosis. AORTIC STENOSIS. 473 AORTIC STENOSIS LV Rise of Intraventricular Pressure. The pressure within the ventricle, on the other hand, rises greatly, often as much at 100 per cent., without affecting the aortic pres- sure; for the greater part of the contraction is unable to force much blood into the aorta. The excess of intraventricular over aortic pressure is therefore much greater than in any other condition. The conditions under which the contraction takes place conform more or less to those for the execution of an isometric contraction, and the curve of intra- ventricular pressure comes to resemble that of an isometric contraction, the summit changing from flat to the dome-shaped, as is typical for the latter (as shown by Frank and by Huerthle). That is, the pres- sure does not at once reach its maxi- NORMAL mum, but rises gradually, coinciding quite well with the rise of the curve in the aorta. It is the direct com- munication of this progressive rise of pressure to the aorta which gives rise to the pulsus tardus, as well as the fact that the volume of blood flows into the aorta more slowly than usual. The duration of systole is prolonged considerably, seven to ten per cent, in mild grades of stenosis, ten to fifty per cent, when stenosis is extreme. FIG. 219. Diagram of the circulation showing the effect of aortic stenosis. The broken line indicates the intraventricular pressure. The vertical black line indicates the volume of the heart, the shaded portion representing, the amount of residual blood. (Compare with Fig. 26.) When the ventricle is not able to expel its quota even by the end of systole, extrasystoles are likely to occur, and this fre- quently assumes the form of a continuous bigeminal pulse. Such overfilling of the left ventricle naturally leads to stasis in the auricle and pulmonary veins, with rise of pressure in these parts, pulmonary con- gestion, cardiac dyspncea (v. Basch), oedema of the lungs (Welch), and secondarily also of the right ventricle. These in turn lead to dilatation and hypertrophy of the left ventricle and left auricle and hypertrophy of the right ventricle, which are usually found to be present at autopsy. SYMPTOMS AND CLINICAL COURSE. Aortic stenosis is probably the most chronic of all valvular lesions, and persists for years without affecting the duration of life. However, as soon as the stenosis becomes marked, so that the left ventricle has difficulty in emptying itself completely, slight exertion, excitement, or emotion brings on disagreeable symptoms, palpitation, constriction, substernal pain or anginal attacks, and shortness of breath. These sensory stimuli probably arise in the depressor nerve as the result of distention of the ventricle, for experiments of Sewall and Steiner have demonstrated that distention has this effect in animals. The symptoms at first pass off when the patient rests or leads a quiet and hygienic life, but as the disease persists they become more frequent and persistent. Sudden death is relatively common, and is probably due to acute dilatation. Compensation. As in mitral stenosis, compensation is dif- ficult. The left ventricle may by increasing its power continue to drive enough blood into the aorta to maintain the blood-pressure, and even to cause the pulse to resume the normal form (Fig. 223), but this is done at 474 DISEASES OF THE HEART AND AORTA. an enormous waste of energy, which sooner or later brings on heart failure. Moreover, the lesion itself is slowly progressive, and this constantly increases the difficulty of maintaining the circulation. In the final stage broken compensation sets in exactly as in other advanced valvular lesions. When aortic insufficiency coexists the circulatory difficulty is naturally increased, since the ventricle must drive an even excessive amount of blood into the aorta in order to maintain the circulation, in spite of the difficulty under which it already labors. Moreover, these are often the cases with the most advanced pathological lesions, so that the coexistence of aortic insuffi- ciency renders the prognosis less favorable than that of pure aortic stenosis. PHYSICAL EXAMINATION. The most striking feature upon general physical examination in aortic stenosis is the presence of a well-marked systolic thrill and bruit over the larger arteries. Over the chest there is usually a certain amount of pre- cordial bulging. The apex impulse is sometimes well marked and heaving, situated quite outside the mammillary line in the fifth or sixth interspace ; frequently, however, it is not visible nor palpable. Between the apex and ^^^^^^^^^_ the sternum there is often some systolic retraction of the inter- spaces from the contraction of the hypertrophied right ventri- Icle. The left ventricle hypertro- _^_ liLs-TTTrrrffm. u ' i liK pines, increasing in size along its \ long axis (obliquely downward). V I I Palpation. Palpation re- veals a systolic thrill which is usually very marked and felt over the whole heart, especially over the aortic area. It is pres- I ent in the carotid and brachial Fio. 220. Diagram showing the cardiac outline and distribution of the murmur in aortic stenosis. The par- allel shading indicates the distribution of the systolic murmur and thrill; the dot indicates the point at which thev are most intense. arteries, and is transmitted in the direction of the blood stream (see page 144). The intensity of this thrill is often the most striking feature of all the phys- ical signs, and may far exceed that which is found in any other condition. The shock of the first sound is usually felt, while that of the second is often, though not always, absent. Percussion and X=ray examination reveal no peculiarities other than an area of cardiac dulness enlarged along its longitudinal axis, as in aortic insufficiency; but, owing to the presence of functional mitral insufficiency and dilatation of the conus arteriosus. the area of dulness may be higher and broader than in aortic insufficiency and resemble that found in organic mitral insufficiency. Auscultation. On auscultation one is immediately struck by the pres- ence of a loud systolic murmur most intense over the aortic area, and transmitted thence to the first right inter- AORTIC STENOSIS. 475 space and along the course of the arteries, where it is, as a rule, still loud and distinct. It is also heard over the pulmonic area, body of the heart, and over the apex, but far less loudly than in the aortic area and the arteries. This murmur is usually the loudest that is heard in any form of valvular disease, and is often heard several feet away from the patient. The mechan- ism of its production exemplifies perfectly the simple experiment for the production of thrills and murmurs described on page 144. Since it cannot be produced until the blood begins to flow into the aorta, c ^ RQTID ^^^^^^^^^^^l this murmur does not begin until an appreciable in- terval after the begin- ning of systole (Boy- SOUNDS Teissier, Romberg, Weiss and Joachim) and follows the first sound in that region " s SEC as well as at the apex (Fig. x MUR 2 i 221). Weiss and Joachim have , FIG. 221. Murmur of aortic stenosis. . (After Weiss recorded this murmur with their and Joachim.) Upper curve, carotid pulse; middle curve, i i c- i ,i , heart sounds; lower curve, time; one vibration equal phonoscope, and find that it to ^ second . The gecond 80Und is practically absent . Sets in with a Crescendo Char- The murmur is composed of a crescendo followed by a , , , , decrescendo character loudest with the upstroke on acter at the very end of the first the pulse-wave. sound. The crescendo continues until the crest of the carotid pulse, after which it changes to decrescendo throughout the rest of systole. The form of the carotid wave portrays the amplitude of the vibrations and the variations in loudness of the murmur. When mitral insufficiency (organic or functional) is present, the mitral murmur may enter into or replace the first sound. The second sound may vary considerably in aortic insufficiency. If the valves are fused throughout their whole extent, it will be entirely absent , but if portions of the cusps remain freely movable" their closure may give rise to a sound. Owing to the small excursion, this sound may not be as loud as it would be if no stenosis were present, but this factor may be more than balanced by the presence of sclerotic plaques and calcifi- cations whose concussions may actually render the second sound louder than normal. PULSE. Aortic stenosis may be said to be the only disease in which the absolute diagnosis is determined by the pulse-tracing. The pulse is small, hard (high diastolic pressure), and in typical cases rises and falls very slowly (pulsus tardus). Like the curves in experimental aortic stenosis (Fig. 21!)), 'the typical radial pulse-curve (Fig. 222) shows a very oblique ascent which lasts throughout systole, the summit of the curve appearing just be- fore the dicrotic notch. This is produced by the slow, gradual, and progres- sive filling of the arteries from the gradually increasing intra ventricular pressure. It may be recalled that during the period of the up-stroke upon the pulse-wave blood is flowing into the aorta more 1 rapidly than onward 476 DISEASES OF THE HEART AND AORTA. to the periphery; that during the period of the plateau the inflow and out- flow are equal; and during the period of fall blood is flowing onward to the periphery more rapidly than it flows into the aorta. The pulse of aortic stenosis, there- fore, reflects the true condition, that blood is flowing into the aorta less rapidly than usual and out of it also less rapidly. However, it must be admitted that this typical form of pulse is rather rare. Most commonly, either the aortic stenosis does not reach this stage without being complicated by an insufficiency which changes the pulse form or death intervenes before these signs of inability of the heart to empty itself have set in. Indeed, many practitioners may pass through long lives of busy practice without encountering a single example of aortic insufficiency with pulsus tardus. The anacrotic pulse is so much more FIG. 222. Diagram showing the pulsus tar- dus and the anacrotic type. Solid line, pulsus tardus, showing the slow gradual rise; broken line showing the anacrotic form with sudden almost vertical rise surmounted by a plateau which takes up the greater part of systole. VI VII ;. 223. Pulse tracings from cases of aortic stenosis. The heavily sha led curve represents the sys- tolic portion nf the tracing. I. Anacrotic pulse from a case of tricuspid insuffi showing quick upstroke with only the sun nosis I L. S.). IV. Tracing from a case of ; another case of aortic stenosis and insulHcipnc of cardiac weakness well marked; maximal hi ing. VI. From same patient on March 24 af it sloping. II, III. Pulsus tare ortic stenosis and insufficiency. V. Taken on February 28 so< 1-pressurr Kid mm. llg. The er recovery from cardiac sympt iency but no aortic stenosis, js from a case of aortic ste- V, VI, VII. Tracings from i after admission; symptoms ipstroke is gradual and slop- ms. Maximal pressure 100. The strong heart forces blood rapidly through the stenosed orifice and causes a sudden upstroke. VII. Pulse tracing taken immediately after VI, witli other arm raised. The increased resistance changes the tracing to a puNus bisferiens. common in aortic stenosis that examples of it are given in many text-books erroneously labelled pulsus tardus. A p u 1 s e - c u r v c w i t h a s u d - d e n ]) e r p e n d i c u 1 a r u p - s t r o k e , h o w e v e r , i s n o t a pulsus tardus, but an anacrotic pulse, whatever may be the form of its summit. AORTIC STENOSIS. 477 It indicates that blood is flowing into the aorta from the heart more rapidly than it is flowing out of the aorta toward the periphery, a condition which occurs in aortic stenosis only (1) when the orifice is so slightly narrowed that the hypertrophied left ventricle is able to drive blood through it with great rapidity, and (2) when the peripheral vasoconstriction is so great that, in spite of a slow inflow into the aorta, the blood still enters the latter much more rapidly than it can leave it. The former is the more common condi- tion; and it would appear that the hypertrophy of the ventricle can usually keep pace with the advancing stenosis until a very late stage is reached. The pressure within the ventricle produced under these conditions is prob- ably tremendous. These facts are well illustrated in Curves V, VI, VII (Fig. 223). The first (V) was taken when the patient's heart was weak, and the blood-pressure shows a gradual up-stroke and is fairly typical of aortic stenosis. The other curves (VI and VII), taken after his heart had improved, have taken on the characters of aortic insufficiency and have lost those of aortic stenosis. Arrhythmia. The rhythm of the heart in man, as in animal experi- ments, is frequently irregular; small beats and dropped beats being frequent, due to the occurrence of a pulsus alternans or to extrasys- toles arising in the left ventricle when that chamber is unable to empty itself sufficiently. Exercise, emotion, or any other form of cardiac over- strain, on the one hand, or of cardiac weakening, on the other, precipitates this irregularity. Blood=pressure. The blood-pressure in aortic stenosis is usually slightly elevated (maximal pressure 130 to 160 mm.), due in part to the accompanying arteriosclerosis, in part to the increase in the intraventricular pressure, especially when the heart hypertrophies. DIAGNOSIS. In typical cases the diagnosis of aortic stenosis is extremely simple. The presence of slow, gradual pulse, the pulse-tracings, the enlarged heart, the very intense systolic thrill, the thrill and murmur over the aortic area and arteries, and the absence or marked diminution of the aortic second sound, present a perfectly characteristic picture. In certain cases, however, and especially when there is arteriosclerosis or aortic insufficiency, it may become extremely difficult to decide whether a mild grade of stenosis is present. CASE OP AOIITIC STENOSIS. Mrs. L. S., housewife, aged 58, entered the Johns Hopkins Hospital, April 29, 1904, complaining of heart trouble. She has always been healthy; has had no infectious diseases and never had rheumatism, but occasionally has had sore throat. She has occasionally had fainting spells and palpitation after mental excitement, and during the past year has had to void three or four times a night. Except for these symptoms she was quite well until a year before admission, when one night after a heavy meal she awoke with extreme dyspnoea, palpitation, and a feeling of extreme weakness. She had no pain, but felt considerably alarmed. Immediately after this her feet became swollen and in spite of a sojourn in bed she became subject to attacks of extreme dyspnoea. The cedema of the feet subsided, however, but reappeared after exertion. At the time of examination the patient was propped up in bed. with slight dyspnoea. She was fairly nourished, pale, sallow, lips very cyanotic. Lungs 478 DISEASES OF THE HEART AND AORTA. clear on percussion and auscultation, except at both bases, where the note is impaired and the breath sounds are accompanied by crackling rales. Heart. The apex impulse is barely visible in the sixth left interspace 13 c in . from the midline, from wliich point dulness extends upward to the third rib, as well as 3 cm. to the right of the midline. There is slight impairment of the percussion note over the sternum. A soft systolic murmur is heard at the apex and in the axilla, becoming louder, however, as the sternum is approached, and maximal over the second right interspace, where it becomes rough in character. It is transmitted to the carotids but not to the subclavians. The second p u 1 - ni o n i c sound is louder than the second aortic. There is a well-marked thrill over the base and manubrium, most marked in the second right interspace. Slight pulsation over the manubrium. No tracheal tug. The pulse is small, regular, 100 per minute. The left radial pulse is a trifle larger than the right. Tracing shows a well-marked pulsus tardus (Fig. I and II). Blood- pressure 150 m m . Hg. The abdomen is distended but does not contain fluid. The legs are very oedematous. Urine is reddish; specific gravity 1030; acid, and contains a large number of hyaline casts. Red blood-corpuscles 5,300,000; haemoglobin 85 per cent.; leucocytes 10,000. During the first week she improved under rest, purgation, and digi- talis; but on May 8 had a severe spell of dyspnoea not controlled by morphine or nitroglycerin, but somewhat relieved by strychnine, 3 mg. ( 2 V gr. hypo.). During the attack the aortic murmur was much less marked than it had been before. The cardiac outlines were unchanged. There was very slight development of fresh rales, indicative of pulmonary oedema. After the attack and the nitroglyc- erin there was unequal dilatation of the peripheral venules. Cheyne-Stokes respiration developed during the night. A few purpuric areas were seen over the extremi- ties and the sacrum. On the next day she had another attack of dyspnoaa, after which cyanosis deepened, respiration became labored, the pulse weakened, and the blood-pressure fell gradually until the patient died in the early evening. At autopsy the three aortic cusps were found to be fuse d together by a calcareous cement, leaving an orifice not more than 3 mm. in diameter. The left ventricle was markedly hypertrophic, the right less so. Both were dilated. The heart weighed 600 Gm. There were slight atheroma of the aorta below the transverse arch, infarction and oedema of the lungs, left hydrothorax, left pleural adhesions, chronic passive congestion of the liver (nutmeg), spleen, and kid- neys; general anasarca. TREATMENT. As regards treatment there is little to be said. Fortunately, the disease is very chronic in its course, especially when it begins after the period of adolescence has passed. A quiet life under the best possible hygienic con- ditions, with avoidance of infections, excitement, and all forms of stimulants and overstrain, usually serves to stave off the onset of symptoms for many years. When these once appear in spite of quiet, the case is practically hopeless. Absolute rest, light diet, moderate purgation, and lessening of the peripheral resistance by means of the nitrites and the Xauheim baths Constitute the most important means of treatment. Digitalis is of value until the heart reaches its limit of hypertrophy, after which it merely precipitates overwork and irregularity of the heart. In the acute attacks of acute heart failure, venesection should be resorted to promptly, in order to lessen the residual blood in the left ven- tricle bv diminishing the inflow into it. AORTIC STENOSIS. 479 BIBLIOGRAPHY. AORTIC STENOSIS. Romberg, E.: Lehrbuch der Krankheiten des Herzens und der Blutgefasse, Stuttgart, 1906. Gillespie, A. L.: An Analysis of 2368 Cases Admitted with Cardiac Lesions into the Royal Infirmary, Edinburgh, during the Five Years 1891-1896, Edinb. Hosp. Rep., 1898, V, 31. Liideritz, C.: Versuche ueber den Ablauf des Blutdrucks bei Aortenstenose, Ztschr. f. klin. Med., Berl., 1892, xx, 373. Welch, W. H.: Zur Pathologic des Lungenoedems, Arch. f. path. Anat., etc., Berl., 1878, Ixxii, 375. Sewall, H., and Steiner, D. W.: A Study of the Action of the Depressor Nerve, etc., J. Physiol., Camb., 1885, vi, 162. Boy-Teissier: L'auscultation retrosternale, Rev. de Med., Par., 1892, xii, 169. VI. PULMONARY INSUFFICIENCY. Insufficiency of the pulmonary orifice usually occurs either as a con- genital lesion or as a result of a severe endocarditis in which other valves are involved. Even as such it is a very rare disease, only 3 cases having been seen among 24,000 admitted to the medical service of the Johns Hop- kins Hospital. Lesions of the pulmonary valves had been described by Morgagni, but the first clinical cases of pulmonary insufficiency were described by Norman Chevers in 1846, and after him by Frerichs, Benedikt, Walshe, and Stokes. Bane in 1891 was able to collect detailed records of 58 cases with 24 autopsies. PATHOLOGICAL ANATOMY. The conditions leading to regurgitation at the pulmonary orifice may be divided into six groups: I. Congenital malformations of the valve resulting in atrophy and deformity. The presence of only two, or, on the other hand, of four cusps does not usually bring about any leakage. In this category may also be mentioned stenosis of the orifice. II. Endocarditic vegetations upon the valves, especially arising in very acute attacks of endocarditis with lesions of other valves. III. Arterioscl erotic changes in the cusps, often associated with dilatation and arteriosclerosis of the pulmonary artery. IV. Aneurisms of the cusps. V. Ruptures of the cusps during coughing or strain, especially of cusps already diseased. VI. Dilatation of the pulmonary artery and conus arteriosus lead- ing to a functional insufficienc y of the valves. According to many writers, especially Gibson, a functional insuffi- ciency of the pulmonary valve of more or less transitory duration takes place as a result of dilatation of the artery and of the right ventricle. This would naturally occur most frequently in cases of mitral stenosis with broken pulmonary compensation, and would account for the blow- ing diastolic murmur which is sometimes heard to the left of the sternum in these cases. The experimental data upon this subject are more or less uncertain. G. A. Gibson has shown upon the dead heart that the pulmonary valves become insufficient under much lower pressures than are necessaay to cause leaks at the aortic. He has also shown that these leaks can be prevented from occurring in the dead heart if the pulmonary orifice be pre- vented from dilating (as by surrounding it with a string). His studies would therefore lead one to believe that such regurgitations would occur readily in hearts whose tonicity was diminished and in which the fibres about the pulmonary orifice stretched accordingly. 480 PULMONARY INSUFFICIENCY. 481 On the other hand Sollman has shown in the living excised cat's heart perfused with Ringer's solution and other salt mixtures that the pulmonary orifice can withstand tremendous pressure without leaking. However, Stokes, Kolisko, Bristowe, Coupland, Litten, Chauffard, Gouget and Preble, have reported cases of relative pulmonary insufficiency, supported by autopsy. In all these cases there was dilatation of the right ventricle, and in three of them a mitral lesion with pulmonary stasis. It seems quite likely, moreover, that such a pulmonary insufficiency was present in cases W. H. (page 492) and B. I. (page 507), though the water test was not applied to the valves at autopsy. PULMONARY INSUFFICIENCY ETIOLOGICAL FACTORS. Barie's statistics collected from 50 cases of organic pulmonary insuf- ficiency show that the two sexes are affected with equal frequency. It was found in patients of all ages from birth to 75 years, but 37 out of 46 cases (80 per cent.) occurred between the ages of 18 and 34 years. In 40 per cent, the disease was congenital, but in these it never occurred as the sole lesion, being usually associated with stenosis. Rheumatism was the etiological factor in 16 per cent, of the cases. Puerperal infection, gonorrhoea, and the other infectious diseases rank next in frequency. There is also an arteriosclerotic group due to syphilis, alcohol, and other affections especially associated with mitral stenosis and scle- rosis of the pulmonary artery. PATHOLOGICAL PHYSIOLOGY. Pulmonary insufficiency bears the same relation to the lesser circulation that aortic insufficiency bears to the sys- temic circulation. The effect of the leak is to bring about a lowered diastolic pressure and an increased pulse-pres- sure in the pulmonary a r t cry, accompanied by a somewhat greater systolic out- put from the right ventricle to compensate for the leak. The increased intraventricular pressure in the right ventricle during diastole gives rise to hypertrophy when the strain is compensated, and dilatation when the strain becomes too great. As a result of this dilatation, functional insufficiency of the tri cuspid valve very readily sets in. The results of these secondary changes are, therefore: 1. To slow the circulation through the lungs. 2. To cause a marked rise of pressure and stasis in the systemic veins. 3. When this occurs less blood enters the left ventricle than before. This would naturally lead to a fall in blood-pressure; but, just as in mitral stenosis, it is compensated 31 FIG. 224. Diagram of the circulation in pulmonary insufficiency. I. Normal. II. Moderate grade of pul- monic insufficiency, showing a rise of pressure in the sys- temic veins and a large pulse amplitude in the pulmonary artery. (Compare with Fig. 25.) 482 DISEASES OF THE HEART AND AORTA. by constriction of the peripheral vessels and the blood-pressure maintained. The vaso- constriction, however, manifests itself in the smallness of the arteries and of the pulse, which thus presents a striking contrast to the pulse of aortic insufficiency. The pulse-pressure also is never increased, as is the rule in the latter condition. SYMPTOMS. The symptoms and complications are chiefly respiratory in origin: dyspnoea, especially in intense paroxysms which are brought about by slight exertion; cough and bronchitis, resulting from the poor circulation through the lungs. The intense pulsation of the pulmonary vessels weakens their walls and predisposes to haemoptysis and the expectoration of blood-tinged sputum. Phthisis is a common complication. Palpitation is sometimes noted. An gi no id attacks and pressure at the base of the sternum are frequently met with; also pain, which, in contrast to that aris- ing in aortic insufficiency, is more commonly referred to the right shoulder and down the right arm. Sudden death is rela- tively common, sometimes re- sulting from over-distention of the right ventricle, sometimes from embolism in the pulmo- nary artery. FIG. 225. Distribution of the murmur in pulmo- nary insufficiency. The parallel shading indicates the area over which the murmur is heard. The dot indicates the point at which it is loudest; the diagram at the right indicates its position in the cardiac cycle. The diagrams over the shaded area represent the pulsations, i. e. the systolic impulse over the pulmonary area and the systolic retraction over the right ventricle. PHYSICAL SIGN'S. Cyanosis, as a result of the slowed circulation in the lungs, is one of the earliest signs. It is usually very marked and is liable to occur in paroxysms. Signs of bronchitis or often of bronchopneumonia are found in the chest. Examination of the heart shows, as a rule, some precordial bulging, with well-marked pulsation of the conus arteriosus in the second left interspace, and a systolic retraction in the third, fourth, and fifth left interspaces and epigastrium, due to the vigorous beating of the right ven- tricle. The area of cardiac dulness is increased to the right in the trans- verse diameter, owing to dilatation of the right auricle. Very often it extends upwards in the second left interspace as well (dilated conus arterio- sus), where it extends ">-() cm. to the left of the midlino. The area of cardiac flatness is increased to both left and right, and forms a scalene triangle extending to the right border of the sternum. On palpation the vigorous beating of the conus arteriosus may be felt in the second left interspace, also a diastolic or systolic and diastolic thrill in this region and over the right ventricle. On auscultation the sounds at the apex may be clear. The characteristic feature is the presence of a very superficial dias- PULMONARY INSUFFICIENCY. 483 tolic murmur maximal over the pulmonary area, varying from short and soft to loud, rough and hissing in character and not infrequently musical, It is also heard along the left sternal margin, but less distinctly over the aorta. The difference is accentuated on coughing. Owing to the presence of other lesions in the pulmonary artery, there may also be a loud systolic murmur at the base, while over the base of the sternum a systolic mur- mur, due to the secondary tricuspid insufficiency, may also be present. The pulse, in contrast to aortic insufficiency, with which this con- dition may be confounded, is small and weak; the blood-pressure is prob- ably but little affected. Marked systolic pulsation of the veins and liver (positive venous pulse) is frequently present, due to the secondary tricus- pid insufficiency. In the extremities oedema sets in readily, and there is often clubbing of the fingers and toes even in cases which are not congenital. The following notes are taken from the records of the medical service of the Johns Hopkins Hospital: CASE OF PULMONAKY INSUFFICIENCY. R. R., a colored laborer, aged 48, was admitted on Feb. 8, 1900, complaining of pain in the stomach and chest. He had measles and whooping-cough as a child, several attacks of tertian malaria, syphilis in 1897, rheumatism in 1899, and several attacks of gonorrhoea. He uses alcohol and tobacco in moderation. Present illness began two years ago, coincident with the onset of urethra! discharge and an attack of rheumatism (gonorrhceal ?) . This caused him to stop work. Since then the rheumatism has become better, but he has been troubled with shortness of breath and palpitation, though these are not very severe. Xote by Dr. Henry Harris states that the patient is a well-nourished man, not dys- pnoeic nor cyanotic. Lungs clear except for a few moist rales over the upper fronts. The note on the heart by Dr. Osier on Feb. 10, 1900, is as follows: "Chief impulse is in the fourth left interspace just at the nipple, also a little impulse above. The impulse in the second left interspace extends 5-6 cm. outside of the left sternal border. Xo impulse in the aortic area; no dilated veins; no visible pulsation of the arteries. On palpation there is no thrill. There is not a very large area of cardiac dulness. The pulse is easily com- pressed and not collapsing. In the fifth interspace, at the apex, and over the aortic area the sounds are practically normal. In the fourth left interspace and at the nipple itself both sounds are loud. There is a short, distant, slightly rumbling murmur before the first sound, becoming distinct on moving towards the sternum. "At the third interspace 5 cm. from the left sternal border a short, loud d i a s t o 1 i c murmur is heard, much louder as the left sternal border is approached, maximal at the left sternal border. There is also a roughness of the first sound. The diastolic murmur disappears in the sternum, being very circumscribed. At the second left interspace 5 cm. from the left sternal border the diastolic is louder. At the left sternal border it has a maximal intensity. There is a short systolic, and a loud somewhat booming dia- stolic, with a rough somewhat vibratory quality. In the first interspace the murmur diminishes, being just feebly heard. In the second interspace the murmur practically abolishes the second sound, which is clearly heard at the aortic area. " Xo thrill after walking about. X' o evidence of congenital heart disease. 'The condition is most likely pulmonary insufficiency. There is a possibility of aneurism, but firm pressure with the stethoscope far out in the second left interspace gives no sense of lifting and no diastolic shock. There is no trachea! tugging and no diastolic shock." 484 DISEASES OF THE HEART AND AORTA. DIAGNOSIS. The diagnosis of pulmonary insufficiency is rarely made during life. The history of very severe endocarditis or evidence of affection of several valves or of a lesion dating from birth leads to the suspicion of right-sided valvular disease. It is always difficult to exclude aortic insufficiency or the presence of the two lesions at once. The small size of the pulse, the absence of visible pulsation of the large arteries, the small pulse-pres- sure, the marked pulsation of the conus arteriosus (both against the chest wall and as shown by the fluoroscope) , the retraction of the interspaces over the right ventricle, the increase in the horizontal diameter of dulness to the right and not to the left, and especially the dulness in the second left interspace furnish the basis for the diagnosis. This is also confirmed when there is pain down the right arm instead of the left. On the other hand, the congenital heart lesions open ductus Botalli, open septum auriculorum or ventriculorum, etc. are very difficult to exclude, and will be dealt with in connection with congenital heart diseases. The diagnosis of functional pulmonary insufficiency is based upon the presence of a transitory diastolic murmur along the left sternal border during periods of pulmonary stasis, in the absence of other signs of aortic insufficiency. No doubt this diagnosis may sometimes be made correctly especially in cases of mitral stenosis, but it is one of which even Gibson cannot feel certain in any individual case. TREATMENT. Treatment is the usual procedure for cardiac overstrain of any sort, rest, light diet, purgation, and digitalis. Venesection, by relieving the distention of the right auricle and ventricle, is particularly useful, arrd, as stated by Alexander Morison, yields remarkably good results in this condition. The main hope, however, lies in bringing about the hypertrophy of the right ventricle and in preserving the balance between the strength of the right ventricle and the strain put upon it. Symptomatic treatment of the bronchitis and pulmonary complications may do much to relieve the patient. THE PROGNOSIS is bad when pulmonary stenosis is present, but in the presence of a pure insufficiency depends greatly upon the condition of the right ventricles and the amount of cardiac embarrassment caused by the lesion. As seen from Barie's cases, patients may reach the age of seventy-five in spite of the lesion. These cases are, however, rare. BIBLIOGRAPHY. PULMONARY INSUFFICIENCY. Chevers, X.: A Collection of Facts Illustrating the Morbid Conditions of the Pulmonary Artery, Lond. M. Gaz., 1846. Frerichs: Insufficientia valvularum arteriae pulmonae, Wien. med. Wchnschr., 1S53, iii, S17 and 833. PULMONARY INSUFFICIENCY. 485 Benedikt, J.: Ein Fall von insufficientia valvularum semilunararum arteriae pulmonae, ibid., 1854, iv, 547. Walshe: A Practical Treatise on Diseases of the Lungs, Heart, and Aorta, Lond., 1854. Barie, E.: Recherches sur 1'insuffisance des valvules de 1'artere pulmonaire, Arch, de med. gen., Paris, 1891, i (vol. xxvii), 650, and 1891, ii (vol. xxviii), 30 and 183. Gibson, G. A.: Jugular Reflux and Tricuspid Regurgitation, Edinb. M. J., 1880, xxv, 978. Preble, R. B.: Relative Insufficiency of the Pulmonary Valves, J. Am. M. Asso., Chicago, 1897, xxviii, 1012. Morison, A.: On Dextral Valvular Disease of the Heart, Edinb. M. J., 1880, xxv, 102, 439, 515, 619, 748. VII. TRICUSPID INSUFFICIENCY. ORGANIC AND FUNCTIONAL TRICUSPID INSUFFICIENCY. Insufficiency of the tricuspid valve occupies a unique position among the valvular lesions. In the functional form, due to dilatation of the right ventricle, it is extremely common, and indeed probably occurs at some stage in every dying or failing heart. In the organic form, on the other hand, it is rare, occurring only 16 times in 1781 cases of valvular disease at the Johns Hopkins Hospital (0.85 per cent.) and in less than 0.7 per cent, of Gillespie's cases at Edinburgh. The organic forms occur more frequently in severe or malignant endo- carditis, as is indicated by the fact that in none of the Johns Hopkins cases was it the only valve affected, mitral stenosis being present in 10, aortic insufficiency in 7 of the cases. Three valves, the aortic, mitral, and tricuspid, were involved in 7 of these cases, the pulmonary orifice once. Although severe rheumatic fever is perhaps the most frequent cause, streptococcus and gonococcus infections are relatively common etiological factors (see Chapter I), more so than in the milder valvular affections. Occasionally it occurs as a congenital lesion, the result of endocarditis during fetal life. Anatomically the lesions of the tricuspid valve exactly resemble those of the mitral, with which they are so frequently associated, being due to vegetations, thickenings, ulcerations, hemorrhages, and occasionally tumors or malformations upon the valves. Functional Tricuspid Insufficiency. Our knowledge of functional tri- cuspid insufficiency dates from the remarkable anatomical and physiolog- ical studies of T. W. King in 1837. King stated that " the right ventricle is liable to dilatation and that the dilatation deranges its valves. "The last proposition is thus explained. The cavity is formed by the solid septum of the heart for its inner wall, and by a thinner, more extensive and yielding layer of muscle for its outer or right wall; whilst each of these walls affords points of attachment to the cords of the valves. ... In the progress of post-mortem examinations, I have found in hearts thus dilated, or only greatly distended by the final congestion, that upon injecting the ventricle by the pulmonary artery the tricuspid curtains when stretched out were under all circumstances a great deal too small to close the opening, .... and it appears from careful examination that the united areas of these valvular portions are scarcely more than equal to the mean extent of the oval opening I have shown that upon injecting fluids into the ventricles by their respective arteries (the semilunar valves destroyed) the left or bicuspid valve (human heart) was always seen to close completely and firmly, the curtains being so extensive as to fold together in the form of a cone or wedge within the ventricle, whilst the tricuspid valve w r as constantly found in its ordinary state incapable of preventing a considerable reflux. With every attempt to induce an accurate closure of this valve, its scanty and divided curtains united imperfectly or scarcely met, and were only sufficient at the best to form a plane 486 TRICUSPID INSUFFICIENCY. 487 equal to the area of the opening No position in or out of water, no degree of gentleness or force, no state in anywise natural to the organ that I was able to induce, would prevent a considerable riband-like stream of regurgitation between the ill-apposed edges of the valve... The only possible means of obtaining a nice, though weak, adjustment of the tricuspid curtains was to compress the ventricle, and by the same means to lessen the extent of the valvular aperture. ... I have twice had an opportunity of experimenting on the human heart at the earliest period that propriety could admit of. In one of the cases (of which I have not hitherto spoken), after performing the experiment and eliciting results similar to those related, the heart was set aside, with the expectation that its t on i city would gradually contract the ventricles and fleshy pillars, which accord- ingly occurred. The first trial of this heart FIG. 226. The outline of a normal heart super- , .,, , ,, ,, . , posed upon that of a dilated heart, showing the was made With warm water, and the fluid enlargement of the tricuspid orifice. Normal heart was thrown in at first gently, and after- shown in light shading, dilated heart shown in wards pretty forcibly; but the regurgitation black, the diameter of the orifices in white and at this time was always considerable. Now black bars ' respectively, upon repeating this experiment on the same heart when contracted after the lapse of a few hours, the tricuspid valve was still found to be much less incomplete; still in this case there was some refluent stream. In the second case, however, under precisely similar circumstances, I obtained at least an almost perfect valvular action." King also confirmed these observations by extended experiments upon the hearts of a great variety of mammals and birds during life as well as after death. His experiments were repeated and substantiated by G. A. Gibson in 1880, who showed that merely narrowing the orifices by constricting them with a cord was sufficient to prevent the reflux. Fran- cois-Franck in 1882 was able to demonstrate the production of tricuspid insufficiency in the living animal under conditions which led to cardiac dilatation, and to demonstrate its disappearance under digitalis. The frequency with which such functional insufficiencies occur in heart failure during life was shown by Friedreich, Mahot, Riegel, Mackenzie, Hirsch- f elder, and a host of other writers. In hearts which have been dilated for a long period there is a considerable stretching of the valvular orifice, as w r as already noted by King. This has lately been very clearly shown by Keith's figures of the hearts of Mackenzie's patients, in which the stretching was so great that the usual narrowing at the auriculoventricular opening had completely disappeared (Fig. 226). PATHOLOGICAL PHYSIOLOGY. As Rosenbach has shown, the production of tricuspid insufficiency has in itself little effect upon the systemic circulation. Blood-pressure in the arteries remains unchanged, and there is no characteristic change in the pulse. In the pulmonary circulation there may be a slight fall of pressure as a result of the regurgitation. On the other hand, this may be compensated by a slight increase in the systolic output of the right ventricle and no change may occur. 488 DISEASES OF THE HEART AND AORTA. The principal effect of tricuspid regurgitation is exerted upon the circulation in the systemic veins. The blood thrown back into them at each systole causes the pressure to rise, so that in such cases the pressure may reach as high as 26 cm. H 2 O (20 mm. Hg) (Hooker and Eyster). The stasis thus occurring also affects the peripheral circulation of the limbs and body, giving rise to oedema and ascites; stasis in the kidneys causing diminished excretion of a concen- trated urine rich in albumen and casts, also stasis in the medulla oblongata where the accumulation of C0 2 causes a general reflex vasoconstriction. The secondary effect of this vasoconstriction is rise of general blood-pres- sure, further increase of the work of the heart, and increased heart failure the vicious circle of asphyxia (see page 38). NORMAL TRICUSPID INSUFFICIENCY FIG. 227. Diagram showing the changes in the circulation in tricuspid insufficiency. The arrows show the rise in pressure in the right auricle (RA) and vena cava, and the fall of pressure in the pulmonary artery (PA). The white curves represent the pulse-waves, that above RA showing the ventricular type of the venous pulse. (Compare with Fig. 26.) Venous Pulse in Tricuspid Insufficiency. In contrast to the normal (negative, presystoiic, diastolic, "double") venous pulse, the typical pulsa- tion in tricuspid insufficiency is synchronous with and of the same frequency as ventricular systole (single venous pulse) (Friedreich, Riegel, Mackenzie, Hirschfelder). Since there is a free communication between auricle and vent ride, the jugular pulse- w a v e (Fig. 22S) closely resem- bles the curve of intraventricular pressure, with its up-stroke and plateau during systole and its fall during diastole. In the advanced stages the wave (a) due to auricular systole is absent, since the auricles are paralyzed (Mackenzie). Mackenzie states, however, that, contrary to preconceived notions, all cases with tricuspid insufficiency do not necessarily show a positive venous pulse, and in a number of his cases which at autopsy showed both organic and functional insufficiencies the positive venous pulse was absent. Mackenzie finds in these cases that the up-stroke of the wave (r), which is due to stagnation in the ventricle, begins earlier than usual. As the lesion increases, this wave (reflux) begins sooner and sooner after the beginning of systole, until finally it takes up the entire systolic period, and the posi- TRICUSPID INSUFFICIENCY. 489 tive or ventricular type is assumed. These observations have been con- firmed in man by Gibson and Sewall, and in animals with tricuspid lesions by J. Rihl, who found that as long as the regurgitation was slight the auricular type of venous pulse persisted, but when it became severe this gave way to the ventricular type. As Sewall states, " among patients pre- senting themselves for examination on account of a wide range of func- tional disorders, I have been struck with the uniformity with which evidences of cardiac insufficiency could be distin- guished, based upon the nature of the symptoms and the char- acter of the venous pulse . . . The v wave has a double crest; or rather, the wave v, which begins just at the moment of closure of the aortic valves, as determined by the dicrotic notch in the lower tracing, is immediately preceded by a wave 5HSSSHHSSSES55S i SEC. which is completed during the last moments Of Ventricular FIG. 228. Venous pulse of patients with tricuspid outflow " HP hplipvp<3 that insufficiency (positive venous pulse). JUG., pulsation Gnat over the j u g u i ar V ein; BRACH., pulse in the brachial this last-mentioned Wave (the artery; c, moment of onset of the pulse-wave in the JUG. BRACK. 4 t t Wave OI ' 1 1 u carotid artery. The tracing shows an elevation through- IS produced by out systole, with a very slight depression (perhaps due to a slight regurgitation due to nm S) immediately following the upstroke. The curve corresponds almost exactly to the curve of pressure in weakness of the papillary mus- the right ventricle. cles, and is indicative of such regurgitation, but he does not take into account the fact that it may be present without any other signs of tricuspid insufficiency. On the other hand, as shown by Theopold, Hewlett, and others (page 118), the positive venous pulse may be present without any regurgitation at the cricuspid. Fir,. 229. Venous pulse of another patient. VJD, right jugular pulse; Af'X,Mt carotid artery. The slow slanting upstroke indicates a slightly less smaller leak than in the preceding case. There is no fling, and hence no midsystolic depression. SYMPTOMS. The condition of patients with tricuspid insufficiency well illustrates the fact that this is one lesion which is not often compensated, though com- pensation can take place through increased suction-pump action of the right ventricle. They are usually markedly dyspnceic or orthopnocic, w r eak and readily exhausted by the slightest effort, often drowsy and somnolent. 490 DISEASES OF THE HEART AND AORTA. Palpitation may be extreme. One of the early symptoms is pain in the region of the liver, from the stretching of the capsule. This is often accom- panied by slight jaundice; and the appearance of an icteroid hue is one of the unfavorable signs in tricuspid insufficiency, since it marks an intense hepatic stasis. Gastric disturbances, loss of appetite, and indigestion are the rule and vomiting is frequent. PHYSICAL EXAMINATION. The patients are usually quite pale and deeply cyanotic. When secondary renal changes have set in, the face may be puffy. Emaciation and slight jaundice, the result of catarrhal cholangitis from stasis in the portal system, are among the most suggestive signs that tell the onset of tricuspid insufficiency. The veins are full and show well-marked pulsation, systolic in time and synchronous with the carotid pulse. There is often oedema of the extremities, genitalia, and back, and large ecchymoses are not uncommon. Ascites and right-sided hydrothorax are seen in the last stages of almost every case. Examination of the eye-grounds usually shows distention of the retinal veins (Black). The urine is usually scant and concentrated, and contains a large amount of albumen and casts in large numbers. Heart. The precordium often bulges, and the very vigorous beating of the hypertrophied right ventricle is seen in the retraction of the inter- spaces between the parasternal line and sternal margin. In the epigastrium and over the liver a systol'c pulsation is seen and felt. Percussion shows a marked extension of the cardiac dulness to the right of the sternum, due to dilatation of the right auricle. It often reaches 5-6 cm. from the mid- line, but the cardiohepatic angle remains acute. If the left ventricle also weakens, dulness may extend to the left of the mammillary line. Character- istic of tricuspid insufficiency is a murmur lasting throughout systole, usually loudest over the right ventricle, in the fourth and fifth left interspaces between the parasternal and the midline, and over the ensi- form cartilage. To these areas it is probably conducted along the papillary muscle. To the right of the sternum the murmur is of different character, caused by the direct impact of the regurgitant stream. Occasionally, as in Case J. D., this murmur cannot be heard when the patient is lying on his back or even standing, but can be elicited by causing him to bend for- ward to an angle of 45. This does not increase the accidental murmur which is often heard over the entire right ventricle, nor does it augment cardiopulmonary murmurs over this area. The murmur is often accompanied by a systolic thrill over the lower sternum and neighboring portions of the chest wall. The distribution to the right of and behind the sternum corresponds to the wall of the right auricle, the chamber into which the regurgitant stream is conducted (see Figs. 230 and 231). The area to the left of the sternum over which the murmur is loudly heard corresponds to the wall of the right ventricle. As in mitral insufficiency, it is difficult to explain the loud transmission of this murmur iu a direction opposite to that of the leakage, but it seems possible that the vibrations of the valve may be communicated to the ventricular wall along the tense chorda: 1 tendinea 1 . The murmur is rarely transmitted TRICUSPID INSUFFICIENCY. 491 FIG. 230. Distribution of the murmur and cardiac outline in tricuspid insufficiency. The shaded area indi- cates the region over which the systolic murmur is heard, cycle. The heart is seen to be enlarged to the right. The systolic pulsation of the liver is indicated by the small diagram and the arrows. as far as the pulmonary area, though a systolic murmur of different origin (accidental murmur) is often heard in the latter area in cases with tricuspid insufficiency as well as in others. The tricuspid murmur is, as a rule, not transmitted to the apex. Most frequently in dilated hearts there is also a functional mitral insufficiency coexisting, and it is this which gives rise to a systolic murmur at the apex and in the axilla, but this is usually less superficial than the tricuspid murmur and it can usually be differentiated from the latter. Moreover, there is, between the two areas at which each murmur has its maximum, a zone, correspond- ing to the interventricular sep- tum, at which both murmurs diminish in intensity. As Hering and others have shown, a systolic murmur is not heard in all cases of tricus- pid insufficiency, especially in the diagram at the left indicates its relation to the cardiac those in which the heart is too weak to give rise to a loud sound or in which the aperture of leakage is too large to produce one (large leaks) . Sometimes the murmur has a musical character. Occasionally, as in Case W. H., in which the pres- ence of tricuspid insufficiency was demonstrated conclusively by venous and liver tracings during life and by autopsy, peculiar diastolic murmurs are heard over the right ventricle, especially along the left sternal mar- gin. They are sometimes blowing and sometimes rumbling (mid-diastolic in character), and may perhaps be caused by functional insufficiency of the pul- monic valves due to the dilatation of the right ventricle. Organic murmurs are frequently rough, while those due to functional insufficiency are usually soft and 1)1 ow- ing, and sometimes barely audible. Hering states, as the result of pro- longed experimental investigation, that functional insufficiency which gives rise to distinct murmurs is usually of slight grade, but when the orifice is much diluted and the leak is a large one no murmur is heard. This aphony of the valves corre- sponds to the condition described on page 164. Except for the accompanying murmur which often replaces the first sound, the cardiac sounds are not greatly modified. The sounds at the FIG. 231. Cross section of the body, show- ing the paths of propagation of the murmur of tricuspid insufficiency. 492 DISEASES OF THE HEART AND AORTA. base are very considerably dependent upon the pulmonary and aortic pres- sures and on the degree of arteriosclerosis, and hence their relative loudness varies considerably. Pulse. The radial pulse in tricuspid insufficiency is usually small and weak and often irregular. The arrhythmia usually assumes the character of permanent absolute irregularity (pulsus irregularis perpetuus) (see page 118) and is accompanied by paralysis of the auricles. Blood=pressure. The blood-pressure is usually normal or a little below normal; but there are no characteristic features, and secondary rises of blood-pressure from medullary asphyxia are common. The liver is usually enlarged and may extend far below the costal margin or even below the umbilicus. It is usually hard and its edge smooth, and often shows a distinct systolic pulsation (Fig. 232). i ii SYSTOLIC PULSATION SYSTOLIC RETRACTION FIG. 232. Tracings of liver pulsation. I. Systolic pulsation of the liver in tricuspid insufficiency. LIV, tracing from the liver; BRACH, tracing from the brachial artery; b, pulse-wave in the brachial ar- tery; c and d have their usual significance. The upstroke of the arrow indicates a protrusion, the downstroke a retraction. II. Systolic retraction over the liver from a case of marked hypertrophy of the right heart. CAR, tracing from the carotid artery. A s c i t e s and oedema of varying grades may be but are not always present, dependent upon the patient's condition. "Broken com- pensation" does not always indicate "tricuspid insufficiency/' nor rice versa. CASES OF TRICUSPID INSUFFICIENCY. MYOCARDITIS WITH TRICUSPID INSUFFICIENCY AND PROBABLY ALSO PULMONARY INSUFFICIENCY. W. II., colored driver, aged 48, first admitted to the Johns Hopkins Hospital on May 12, 1S90, complaining of swelling of the feet and shortness of breath. He had always been healthy except for measles and chicken-pox in childhood and malaria in ISljl. Gonorrhoea at 33 but no lues. Drinks and smokes in moderation. Present illness began during the past winter, with gradually developing shortness of breath, especially on exertion. After such attacks the extremities would swell very much. A few days before admission his testicle also began to swell. On examination by Dr. Thayer at this time he was found to be a well-formed colored man, mucous membranes of good color. Lungs clear except for moist rales over the right front. The apex was then in the sixth interspace at the mammillary line. The first sound was feeble, but no murmurs were heard. The abdomen was full; liver and spleen not palpable. Slight oedema of the extremities. The oedema dis- appeared under rest and digitalis. The patient gained in strength and was discharged in three weeks. He returned again three years later, with similar symptoms, and again made a rapid recovery. On this admission the liver was felt by Dr. McCrae. He was treated in the hospital repeatedly during the next few years, always presenting TRICUSPID INSUFFICIENCY. 493 about the same clinical picture. On Dec. 9, 1903, the apex was 14.5 cm. to the left of the midline, and Dr. Thayer noted that the sounds were clear in the tricuspid area. There was, however, a soft diastolic and a rumbling presystolic murmur heard over the heart between the left parasternal line and the sternal margin (pulmonary insufficiency). When he first came under the writer's care in July, 1904, during a similar attack of cardiac failure, this diastolic murmur, and indeed all the other murmurs, had disappeared, the heart sounds were very feeble and the heart action irregular. As his condition improved under treatment, the former murmur reappeared and increased to about the previous intensity, though heard only with the larger beats. During the next admission a few months later the rumble was definitely mid-dias- tolic and very rough. Blood-pressure during these admissions ranged from 130 to 160 mm. Hg. He was readmitted for the last time in October, 1905, the sounds being about as before, the oedema somewhat greater. There was severe FlG 233 ._ Systolic pulsation of the liver right-sided hydrothorax. Venous O f patient W. H. Car., carotid arterial tracings showed a positive venous pulse of pulse; s, onset of ventricular systole, the ventricular type, and there was systolic pulsation of the liver (tricuspid insufficiency) (Fig. 233). The blood-pressure during this admission was 110 mm., but rose to 130 mm. on the day before death. Autopsy showed dilatation of the right auricle and ventricle, dilatation of the pulmonary artery, marked sclerosis of the cor- onary arteries, very marked chronic fibrous myocarditis (cardiosclerosis), and relative tricuspid insufficiency. There was marked cardiac hyper- trophy, the heart weighing 620 Gm. There were also chronic passive congestion of the viscera, cirrhosis of the liver, chronic interstitial nephritis, chronic fibrous pleurisy, and acute gastritis. There were no valvular lesions and there was no tricuspid steno- sis to account for the middiastolic rumble. It is quite probable that there was during life a functional pulmonary insufficiency. CASE OF MITRAL AND TRICUSPID INSUFFICIENCY. J. D., painter, aged 69, came to Johns Hopkins Dispensary complaining of swell- ing of the limbs. He has always been healthy except for inflammatory rheu- matism off and on during the last twenty years. Denies venereal disease. Has not worked during the past twenty years. He has had swelling of the feet and legs after exertion during the past four years, some shortness of breath, but can always sleep without a pillow. His legs and penis have been swollen for the past month. The patient is a well-nourished man, looking much younger than he acutally is. His color is a trifle sallow but not icteroid. Pupils equal. No glandular enlargement. No lead line on the gums, in spite of his occupation. The chest is clear on percussion and auscultation except for a few wheezing rales at the bases. The heart is markedly enlarged, d u 1 n e s s extending to the anterior ax- il 1 ar y line in the fifth left interspace, above to the middle of the second left interspace and 5 cm. to the right of the midline. At the apex the first sound i? replaced by a blowing systolic murmur heard distinctly throughout the entire left axilla, this diminishes in intensity to the right of the mammillary line. \V hen t h e patient is standing and bending forward at an angle of 45, a loud blowing systolic murmur of different character is heard over the entire tri- cuspid area, but this is not evident in any other position. In the pulmonic area there is a loud blowing mesosystolic murmur, also heard in the second right interspace, but not transmitted to the carotid arteries. The heart's action is somewhat irregular; the jugular veins are distended but do not pulsate; the venous pressure, as shown by Gaertner's method, is high. (The veins of the back of the hand and wrist do not empty until the hand is about 20 cm. above the level of the heart.) 494 DISEASES OF THE HEART AND AORTA. The liver is not palpable. There is little if any fluid in the abdominal cavity. The scrotum and penis are markedly cedematous, as are also the legs and thighs. The patient entered the hospital, where he died of heart failure a few days later. DIAGNOSIS. The absolute diagnosis of tricuspid insufficiency depends upon the presence of a dilatation of the right auricle (increased dulness to the right), a systolic murmur loudest at and about the base of the sternum, a positive venous pulse of the ventricular type, and an enlarged liver with systolic pulsation. As has been seen above, these features are not always present. Hering has summed up the whole question in the following conclusions: 1. A large tricuspid insufficiency may give no murmur, but small regurgitations usually give distinct murmurs. 2. A small tricuspid regurgitation may cause no change in the venous pulse, but a large leakage gives rise to a positive venous pulse of the ventricular type. Hence, I. Loud murmur + auricular (presystolic, diastolic, double, physiological) venous pulse = slight tricuspid regurgitation. II. No murmur + positive ventricular venous pulse + systolic pulsation of liver = severe tricuspid regurgitation. TREATMENT. Frangois-Franck showed, in his experiments upon functional tricuspid insufficiency, that the administration of digitalis caused the signs of insuffi- ciency to disappear. This is in perfect harmony with the clinical experience that "broken compensation" (and tricuspid insufficiency) is in general the signal for digitalis, and the administration of this drug furnishes the main therapeutic measure. Absolute rest is necessary for prolonged periods; but after the tricuspid insufficiency has persisted for months in spite of it, it is useless to reduce the patient to a permanently bedridden condition in the hope of final recovery. It is better to render his life as pleasant as possible under the conditions, to let him sit up and move quietly about the house, go driving, or indulge in other pleasant diversions which do not entail exercise, effort, or excitement. It must not be forgotten that worry and nervousness bring on palpitation and cardiac overstrain almost as readily as does exercise; and, conversely, mental diversion and cheerfulness assist in re-establishing conditions favorable for cardiac recovery. The important feature in this phase in the management of the case is the avoid- ance of dyspnoea. The simple methods of counting between steps on a staircase or of taking for one's gait one step for each inspiration may give the patient considerable latitude for accomplishment without strain or injury. Diet should always be light, partly to avoid the strain on the heart, partly on account of the disordered digestion, gastritis, and catarrhal jaundice, which are entailed by portal stasis. The b o we 1 s should be kept open with saline purgatives and several movements a day should be secured. In stages of acute heart failure when the venous pressure is high and the right auricle much distended, venesection should be resorted to promptly and continued until the right border of the heart has receded. TRICUSPID INSUFFICIENCY. 495 The best results are obtained when venesection is accompanied by intra- venous injection of strophanthin (\ mg.) (see page 241) and this followed by free purgation and digitalis. BIBLIOGRAPHY. TRICUSPID INSUFFICIENCY. Gillespie, A. L.: An Analysis of 2368 Cases admitted with Cardiac Lesions into the Royal Infirmary, Edinburgh, Edinb. Hosp. Rep., 1897, v, 31. King, T. W. : An Essay on the Safety-valve Function in the Right Ventricle of the Human Heart, Guy's Hosp. Rep., Lond., 1837, ii, 104. Part II. On the Safety-valve Action in the Mammalia, ibid., 142. Part III. Of the Safety-valve in Birds, ibid. Gibson, G. A.: Jugular Reflux and Tricuspid Regurgitation, Edinb. M. J., 1880, xxv, 979. Frangois-Franck: Sur la part importante qui revient a 1'etat du muscle cardiaque dans la production des insuffisances tricuspidiennes transitoires, Compt.-rend. Soc. Biol., Paris, 1882, xxxiv, 88. Friedreich, X.: Ueber den Venenpuls, Deutsch. Arch. f. klin. Med., Leipz., 1866, i, 241. Mahot: Des battements du foie dans I'insufnsance tricuspide, These, Paris, 1869. Riegel, F.: Ueber den normalen und pathologischen Venenpuls, Deutsch. Arch. f. klin. Med., 1882, xxxi, 26. Mackenzie, J. : The Venous and Liver Pulses, and Arrhythmic Contractions of the Cardiac Cavities, J. Path, and Bacteriol., Edinb. and Lond., 1894, ii, 84, 273. The Study of the Pulse and Movements of the Heart, Lond., 1903. The Interpretation of Pulsa- tions in the Jugular Veins, Am. J. M. Sci., Phila., 1907, cxxxiv, 12. Hirschfelder, A. D.: Graphic Methods in the Study of Cardiac Diseases, ibid., 1906, cxxxii, 378. Inspection of the Jugular Vein; its Value and its Limitations in Functional Diagnosis, J. Am. M. Asso., Chicago, 1907, xlviii, 1105. Keith, A.: An Account of the Structures concerned in the Production of the Jugular Pulse, J. Anat. and Physiol., Lond., 1907, xliii, 1. Rosenbach, O.: L T eber artifizielle Herzklappenfehlern, Arch. f. exper. Path. u. Pharmakol., Leipz., 1878, ix, 1. Hooker, D. R., and Eyster, J. A. E.: An Instrument for the Determination of Venous Blood-pressure in Man, Bull. J. Hopkins Hosp., Balto., 1908, xix, 274. Gibson, G. A.: Our Debt to Ireland in the Studv of the Circulation, Reprint from the Dublin J. M. Sci., 1907. Rihl, J.: L'eber den Venenpuls nach experimenteller Lasion der Trikuspidalklappe, Ver- handl. d. Kong. f. innere Med., Wiesbaden, 1907, xxiv. Sewall, H.: Safeguards of the Heart-beat, Am. J. M. Sci., Phila., 1908, cxxxvi, 32. Hering, H. E.: L'eber pulsus irregularis perpetuus, Deutsch. Arch. f. klin. Med., Leipz., 1908, xciv, 18o. VIII. TRICUSPID STENOSIS. OCCURRENCE AND ETIOLOGY. Stenosis of the tricuspid orifice belongs to the rarer valvular lesions, and also to the group which rarely occurs alone. In the 24,000 cases which have been admitted to the Medical Service of the Johns Hopkins Hospital tricuspid stenosis has been found in only seven cases, in all of which other lesions w r ere present. W. W. Herrick has recently given the following statistics from 187 cases collected from the literature: SUMMAKY OF REPORTED CASES. Sex. Male 38 Female 133 Sex not known . . 16 Age. 10 to 20 years 16 20 to 30 years 59 30 to 40 years 38 40 to 50 years 28 50 to 60 years 10 60 to 70 years 6 Not known . . 30 ^87 Previous History. Rheumatism 61 Doubtful rheumatism or chorea 11 No rheumatism 33 Not known . . 82 Association of Valvular Lesions. Tricuspid alone . 14 Tricuspid and mitral 102 Tricuspid and aortic 64 Tricuspid and aortic and pulmonary 1 Tricuspid and endocardium of left auricle 1 Tricuspid, mitral, and pulmonary 2 Total cases 184 Cases showing adherent pericardium 12 In Leudet's series rheumatism was an etiological factor in over 50 per cent., puerperal fever in 5 per cent. Syphilis has also been assigned as a causal factor. 496 TRICUSPID STENOSIS. 497 In the cases in which the tricuspid stenosis follows the mitral stenosis the same etiological factors are concerned as for the single lesion. In view of the work of Goodhart, Roy and Adami, and Weber and Deguy quoted above (page 429), it is not unlikely that the overstrain of the right ventricle, brought about by the latter conditions, leads to oedema and hemorrhage into the tricuspid valve, and that these processes usher in the fibrosis. In other words, the mitral stenosis itself becomes an etiological factor in the tricuspid lesion, and the pathological process completed in the mitral is now transferred back one step in the circulation and repeats itself in the tricuspid. Occasionally, as in a case reported by Gairdner, a fibrinous ball, a tumor, or a hemorrhage into the valve may assist in producing the stenosis. A certain percentage of the cases are congenital in origin. PATHOLOGICAL ANATOMY. The anatomical changes in the valve are exactly similar to those which occur upon the mitral in stenosis of that orifice : a progressive fibro- sis accompanied by fusion of the cusps along their line of closure, and gradual web-like extension of the valvular membrane, which grows down- ward between the shrunken chorda tendinese forming an elongated funnel with narrow outlet. The liver is usually enlarged, though in some cases it may be smaller than usual, owing to the cirrhotic changes and perihepatitis which result from the prolonged stasis. PATHOLOGICAL PHYSIOLOGY. The changes which tricuspid stenosis produces are exactly similar to those already seen in mitral stenosis, except that they affect the systemic veins instead of the pulmonic. The filling of the right ventricle is retarded. The amount of blood which enters it passively in early diastole is diminished, and the amount driven in by the .auricle is increased. The auricle thus begins to hypertrophy. 1 Its strength increases, and the presystolic wave which it produces in the venous pulse increases in size. In well-marked cases the force of auricular contraction may be great enough to produce a definite presystolic pulsation in the liver with a wave exactly similar to that found in the vein (Mackenzie) . When the tricuspid orifice is narrowed to such an extent that the increased force of the auricle no longer empties the latter, the auricular contraction begins to drive the blood back into the veins and to increase the already high venous pressure, thus still further impeding the circula- tion through the heart and lungs, so that the aeration of the blood is greatly interfered with and marked cyanosis produced. This in turn gradually predisposes to polycythsemia (red blood count 8,000,000 to 9,000,000). The latter condition causes increased viscosity of the blood, and still further increases the burden upon the heart. On the other hand, the 1 The right ventricle is almost always hypertrophied in tricuspid stenosis, owing to the presence of mitral stenosis and tricuspid insufficiency. 32 498 DISEASES OF THE HEART AND AORTA. NORMAL TRICUSPID STENOSIS hypertrophy of the right auricle gradually reaches its limit, and when the venous pressure becomes too high from exercise or' other cause, this chamber becomes dilated and paralyzed, and the pre- systolic wave disappears from the jugular and liver pulse (Mackenzie). Unlike lesions of other valves, no further compensation is now possible, and only rest of the heart can prevent the over-distention of the veins. Consequently slight, overstrain results at once in venous stasis, oedema, etc., which may pass off readily when the patient is at rest. The liver is often, though not always, enlarged; and a pulsation presystolic in time may be felt in it as long as the right auricle is beating strongly (Mackenzie). (Edema, ascites, and hydrothorax may be present as in other cardiac diseases. The pulse is usually small because the peripheral arteries are constricted in or- der to maintain the blood- pressure, which may be per- fectly normal. The rhythm may continue regular or may become irregular as the disease advances. Still more common are attacks of heart failure and dropsy. In many cases, notably those of Shattuck and Mackenzie, such attacks may recur at intervals during a decade or more. At first the condition yields readily to rest and treatment, but later the attacks become more and more frequent and persistent. FIG. 234. Diagram showing the changes in the circu- lation in trieuspid stenosis. The arrows indicate the rise in venous pressure in the right auricle (RA) and the vena cava, and the fall in pressure in the pulmonary artery (PA). The pressure in the left auricle and ventricle may remain unchanged or may fall. (Compare with Fig. 26.) SYMPTOMS. Fortunately for the patients, the course of tricuspid stenosis is usually a chronic one, the development of the lesion generally lagging behind the concomitant stenosis of the mitral or the other lesions that may be present. As a consequence, the lesion may be present for a number of years without manifesting any signs other than cyanosis, and no symptoms whatever. Osier quotes a case reported by Ilirtz and Lemaire who was known as "I'homme bleu" for two years before lie developed any symptoms. On the other hand, in the case mentioned by Shattuck there was said to be "no cyanosis." There is nothing pathognomonic about the symptoms. Dyspnoea on the slightest exertion sets in and becomes progressively worse. Pain clown either arm is relatively common, occasionally pain about the right side and abdomen due to distention of the auricle or of the liver. Sudden death is quite common. TRICUSPID STENOSIS. 499 PHYSICAL SIGNS. On inspection the extreme cyanosis is striking, and there may be dila- tation and accentuated pulsation of the veins. When carefully timed this pulsation is seen to be presystolic, and is often a "double" pulse of the physiological type. Those characteristics are brought out more clearly by a venous tracing. In long-standing cases the fingers may be clubbed. The lungs usually show signs of bronchitis, oedema, or often of tuber- culosis. Pulmonary infarction, with the presence of areas of consolidation and the expectoration of dark red or "prune-juice" sputum, is relatively common. In the physical exam- ination of the heart the real lesion is often overlooked. Ex- cept for the systolic retraction over the right ventricle, there may be nothing abnormal on inspection. The area of cardiac dulness is increased to the right, corresponding to the dilated right auricle; occasionally also to the left, as a result of con- comitant lesions other than the tricuspid stenosis. Palpation sometimes re- veals a presystolic thrill over the lower part of the sternum and just to the left of the latter, but it is rarely as distinct in the former situation as in the latter (due to concomitant mitral stenosis). The shock accompanying the first sound over the right ventricle may be tapping. The second pul- monic shock is usually less marked than might be expected to result from the lesions present. The characteristic sign on auscultation is the pres- ence of a short presystolic rumble, which is maximum over the base of the sternum and different in character from the presystolic rumble heard at the apex. There is also a snapping character to the first sound m this area, and it may be accompanied by a tricuspid systolic murmur. This murmur is, however, often absent, indistinct, or merges so gradually into the mitral murmur that its existence is not noted. Except when other lesions are present the second aortic and pulmonic sounds are not as loud as might be expected. DIAGNOSIS. So indistinct are the murmurs due to the tricuspid lesion and so com- pletely are they overshadowed by those of the mitral or other orifices that the diagnosis before death was made in only six of Leudet's 114 cases. The correct diagnosis has been almost equally rare since then. It may be made with certainty in the presence of marked cyanosis, dilatation of the right FIG. 235. Cardiac outline and distribution of the presystolic rumble and snapping first sound in tricuspid stenosis. 500 DISEASES OF THE HEART AND AORTA. auricle (increase of dulness to the right), presystolic thrill and rumble, and presystolic liver pulsation. But these signs disappear as the auricle begins to weaken, and in very many cases the existence of the lesion is one that lan be suspected rather than proved. CASE OF TRICUSPID STENOSIS. The following notes are from one of the rare cases in which the diagnosis was made during life. This diagnosis was made by Professor T. B. Futcher, who has kindly permitted the writer to make use of the notes. Mrs. A. J., aged 37, entered the private wards of the Johns Hopkins Hospital on April 30, 1909. The family history was negative. She was not a blue baby; has been healthy since childhood, but subject to occasional sore throat. She has never had acute articular rheumatism. At the age of nineteen she had an obscure fever lasting several weeks. She has been somewhat short of breath for the past nineteen years, and since an attack of grippe about twelve years ago has complained of palpitation on exertion or after eating. These symptoms became much more marked four years ago, when oedema of the feet and ankles and cyanosis appeared for the first time. This condition passed off under treatment, but returned again two years later, again pass- ing off, only to return with increased severity eight weeks before admission. During this attack she has been blue and has had severe orthopnoea. Note by Dr. Futcher, May 1, 1909: "Patient is of short stature, a little overstout; very marked cyanosis of ears, lips, cheeks, and finger-nails, although this is nothing as compared with the day she reached Baltimore. There is a distinct jaun- diced tint to the face and sclerotics. Propped up in bed; considerable dyspnoea. Tongue moist, only a trifle coated; pupils normal size and equal, react to light and accommodation. " Still impossible to count pulse at wrist, although very faint beats are occa- sionally appreciable. Thorax well formed, expansion good and equal on both sides. Lower left axillary region expands slightly less than right. Lungs : Right side clear throughout front and axilla on percussion. There is an occasional crackling rale heard at the base. Fairly numerous fine moist rales audible throughout whole back. Left lung (in semi-recumbent posture) flatness reaches to level of fourth interspace in anterior axil- lary line. In midaxillary line it reaches nearly to apex of axilla, and in posterior scapular line to a point about 3 cm. above left scapula. Slight m o v a b 1 e dulness in front with change of position. On auscultation, breath sounds are harsh above and below clavicle, as in compensatory breathing. Below level of flatness there is absence of vocal fremitus and distant tubular breathing and distant nasal quality of the voice sound. '* Heart. Point of maximal impulse seen and felt in fifth interspace 11 cm. to the left of the midsternal line and just in the mammillary line. There is very slight pre- cordial bulging, but practically no pulsation or heaving. Systolic shock distinctly tap- ping at apex; no definite thrill. Relative cardiac dulness commences at the upper border of the third rib, in fourth right interspace, extends 8.5 cm. from midsternal line, and merges into the fluid flatness to left, but apparently dulness extends considerably outside of midline. There is no apparent Rotch's sign to the right. The absolute cardiac dulness begins at the upper border of the fourth rib at the left sternal margin, extends to right sternal margin at level of fourth rib and to point of maximal impulse in fifth left interspace. On auscultation, the first sound is very snap- ping at apex. There is as yet no definite presystolic murmur, but there is a slight echo- ing rumble in diastole. There is no systolic bruit at the apex. The second sound is not audible here. In the fourth and fifth interspace at the left ster- nal border the snapping quality of the first sound is even more marked than at the apex and the tapping systolic shock is very striking here. The second sound is audible and there is definitely reduplicated. There i s n o rumbling presystolic murmur here. In diastole, however, there is, on very careful auscultation, a faint, soft, prolonged, blowing diastolic murmur. At the aortic area yesterday there was a faint systolic thrill. It is just perceptible this morning. The first sound is audible and is accompanied by a very rough systolic bruit transmitted upwards to stenoclavicu- TRICUSPID STENOSIS. 501 1 a r articulation. The second aortic is quite loud and, if anything, accentuated. There is no aortic diastolic bruit heard here. Pulmonic sounds clear, second pulmonic accentuated. The external jugulars are only slightly distended. ''Liver. Absolute flatness extends from sixth rib to a point apparently on a level with the costal margin in right mammillary line. In median line it reaches only to tip of ensiform. Owing to oedematons abdominal walls, it is not possible to palpate for liver edge. No visible or palpable liver pulsation. "Abdomen moderately distended, walls cedematous, tympanitic in elevated and flat in dependent portions. Undoubtedly some ascites. There is very marked oedema of dependent portions of trunk, moderate of arms and hands, very marked of thighs and legs. " Over dorsal surfaces of both wrists there are quite numerous pin-head sized petechise." The urine was very scant (300 c.c.), of orange color, specific gravity 1015, acid, con- tains a trace of albumin and many hyaline and finely granular casts. Her chest was aspirated by Dr. Henry on May 1, and 500 c.c. of dark straw- colored clear fluid removed. She became worse, however, and her kidneys refused to act. On May 3 her pulse became irregular, cyanosis increased, and the petechial eruption on the dorsum of wrists became more extensive. She died at 3.15 P.M. Intra vitam diagnosis by Dr. Futcher: Aortic stenosis and insuffi- ciency, mitral stenosis, probable tricuspid stenosis. Autopsy showed tricuspid, mitral, and aortic stenosis, dila- tation and hypertrophy of the auricles, contraction and atrophy of the ventricles, chronic passive congestion of all the tissues except the lungs, generalized oedema, pleural and pericardial effusion, compression and atelectasis and oedema of the lungs, hemorrhagic infarctions of lungs, acute diphtheritic hemorrhagic colitis, generalized narrowing of arteries and thickening of veins. TREATMENT. Except for rest, purgation, and palliative treatment, little can be said in this condition. Digitalis is sometimes of value to restore tone to the auricle and increase the force of the ventricular contraction, but it very frequently fails. In the spells of acute heart failure a free venesection may ward off impending death by lowering the venous pressure, relieving the heart failure ; and by diminishing the viscosity of the blood may afford more lasting relief. Free purgation is often also of great benefit, because it may lower the pressure in the veins. PROGNOSIS. The prognosis depends entirely upon the degree of stenosis and the rapidity of its progress. As has been said, this is frequently very chronic. Mackenzie's famous case, which is typical, was a woman whose lesion probably dated from an attack of rheumatism in 1880, at the age of twenty- nine. In 1892 she complained of weakness and shortness of breath, and at that time the liver showed a presystolic pulsation. She w r as subject to numerous temporary attacks of extreme heart failure and died in 1899. However, this woman was under excellent care during the last seven years of her life, and lived a tolerably discreet and hygienic existence. Had she been compelled to do heavy work her life would probably have been much shorter. 502 DISEASES OF THE HEART AND AORTA. BIBLIOGRAPHY. TRICUSPID STENOSIS. Herrick, W. W.: Tricuspid Stenosis, with Report of a Cure, 1 Arch. Int. Med., Chicago, 1908, ii, 295. Huchard, H.: Maladies du coeur, tome iii, Paris, 1905; based upon statistics of Leudet, R.: Essai sur le retrecissement tricuspidien, Paris, 1888. Herrick, J. B.: Tricuspid Stenosis, with Report of Three Cases with Autopsies, etc., Bost. M. and S. J., 1897, cxxxvi, 245. Goodhart, Roy and Adami, Weber and Deguy. See page 449. Gairdner. Quoted from Herrick. Mackenzie, J.: Notes on a Case Presenting some Novel Features in Cardiac Symptoma- tology, Edinb. Hosp. Rep., 1897, v, 22. Studies on the Pulse and Movements of the Heart, N. Y., Edinb., and Lond., 1902. 1 Probably intended to be, " with Report of a Case." IX. MARRIAGE, PREGNANCY AND LABOR IN CASES OF HEART DISEASE. PULSE-RATE AND BLOOD-PRESSURE. The effect of pregnancy upon the heart is influenced by several factors. The gradual pushing of the diaphragm as the uterus grows causes the heart to assume a more transverse position (raising the apex to the fourth inter- space in 28 out of 35 cases observed by Stengel and Stanton), and thus plac- ing it in a position which embarrasses its action. Moreover, a reflex vagus inhibition is often present, which causes the pulse-rate to become slowed. Blot has reported a pulse-rate as low as 36; 40 per cent, of Vegas's cases were slow, but only 26 per cent, of Skabo's cases were below 75 per minute. There is also an increase in the width of the blood channel through the uterine vessels, which is manifested by the presence of a dicrotic pulse. In order to overcome these factors and to keep up the equilibrium of the circulation, the heart is compelled to put forth increased efforts. Siemens and Goldsborough in a most careful series of observations have found the following figures, which accord well with the previous findings of O. Fellner, Stengel and Stanton, and Vogeler. They found the following figures : l BLOOD-PRESSURES. Pulse- Cardiac Work of heart. Max. Min. Pulse- pressure. Mean pressure rate - (min. + 4 P.P.) output P.P. x P.R. Mean pi. x pulse- rate. Normal . 110 65 45 80 72 3240 259,000 (Erlanger) Pregnancy . . . 127 74 53 91.6 80.5 3325 49 _ (primig.) Primis;. in primig. 5332 195,000 to 429,000 60 (multip.) Multip. in multip. 421, OOOto 1,065,000 Puerperium . . 115 72.5 42.5 86.5 70.5 3000 Primig. 290,000 to 327,000 Multip. 156,000 to 337,000 HYPERTROPHY. This prolonged increase in work was supposed by Larcher to bring about hypertrophy of the heart, a fact which has found some support in the weighings of certain observers; but the more careful work of W. Miiller and of later observers (average weight of heart during pregnancy 227 Gm.) 1 While this method of calculation is not intended to be regarded as quantitatively accurate (see p. 36), it shows the qualitative changes fairly well. 503 504 DISEASES OF THE HEART AND AORTA. fails to substantiate this view. The increase in size supposed to represent hypertrophy is probably due in part to dilatation of the heart, and in part to the apparent increase in cardiac area which occurs when the heart lies in a more transverse position. However, a very slight hypertrophy, like that of the athlete's heart, arising from the slightly increased work of the heart during nine months, would not be surprising. During labor an additional strain is thrown on the heart, but this is of comparatively short duration. FUNCTIONAL TRICUSPID INSUFFICIENCY AND OVERSTRAIN DURING LABOR. James Mackenzie has shown, moreover, that the dilatation during pregnancy affects the right heart particularly, and that in very many cases even of otherwise normal women a definite insufficiency of the tricuspid valve may appear, disappear, and reappear accord- ing to the condition of the patient. The presence of this insufficiency is shown by both the positive venous pulse and the systolic murmur in the tricuspid area. The effects during the labor pains are exactly comparable to those of heavy lifting, defecation, etc. (exercises of strain of maximal intensity), and are accompanied by forced expiration with glottis closed (Valsalva's experiment) as well as by very general muscular contractions. Dr. Slemons informs the writer that during the labor pains there is often a rise of fifty millimetres of mercury in the maximal pressure, though these elevations are of short duration. It is therefore not surprising that some hearts should fail and that pulmonary oedema should be an occasional com- plication, especially in mitral stenosis where the pulmonary circulation is already engorged. It is perhaps surprising, however, that so few cases actu- ally succumb during the strains of labor. Schlayer's results typify the gen- eral experience in this regard. He lost eight out of twenty-five cases (32 per cent.) of severe heart disease, but only two of these (8 per cent.) died during labor. From this, as well as from the work of Slemons and Goldsborough and the metabolism experiments of Williams and Slemons, it would appear that the act of labor itself does not impose a much more severe strain upon the organism than that arising during the course of pregnancy. CAUSE AND FREQUENCY OF DEATH FROM LABOR. The immediate cause of death during labor is usually pulmonary oedema from failure of the left ventricle. However, as above stated, only about one-fourth of the fatal cases die during labor, the greater number surviving some days, weeks, or months. In the cases of mitral stenosis, apoplexy or cerebral embolism is not uncommon, owing to loosening of thrombi which form in the left auricle during the periods of stasis. As regards the results obtained by different writers in cases with heart lesions the greatest divergence is found. The following represent the mortality reported by various writers: Macdonald 61 per cent., v. Guerard 34 per cent., Lublinsky 60 per cent., v. Leyden 55 per cent., Schlayer 48 per cent., Wessner 49.3 per cent., Lwoff 12 per cent., Gusserow 6 per cent., Joss 31.5 per cent., Wiesenthal 12.5 per cent., Schneider 7.1 per cent., M tiller 3 per cent. PREGNANCY AND LABOR IN HEART DISEASE. 505 A very careful study of these conditions has been made by O. Fellner in Schauta's clinic in Vienna. Fellner noted that the percentage of heart cases reported in obstetrical clinics was far too low for the general prevalence of cardiac disease, and upon careful routine examination found that about six cases out of seven of compensated heart diseases were actu- ally escaping detection in the clinics. So little effect had heart disease made upon the course of pregnancy and labor! Of the cases that had been recognized in the obstetrical clinic in ten years he found the following: 1 Cases. Mother died. Child died. Mitral insufficiency, Compensated 26 3 Uncompensated ... 14 1 2 Mitral stenosis, Compensated Uncompensated 4 3 Mitral stenosis plus insufficiency, Compensated .... . . . . 10 2 Uncompensated . ... 17 1 10 Aortic insufficiency, Uncompensated 2 1 1 Aortic insufficiency plus mitral insufficiency, Compensated 3 1 Uncompensated 5 4 Total . 81 3 26 In the 900 cases occurring since his own routine examinations of the heart were instituted, he found: Cases. Mother died. Child died. Mitral insufficiency, Compensated 14 4 Uncompensated 1 o o Mitral stenosis plus insufficiency, Compensated 3 1 Uncompensated 1 o Aortic insufficiency plus mitral insufficiency, Compensated . 1 o FACTORS INFLUENCING PROGNOSIS. These statistics from unselected cases are much more favorable than the previous reports would indicate, and are in accordance with the con- clusions of Hicks and French that few women with heart disease are sterile, that they are not particularly liable to abort, and that most of them bear 1 Jaschke (Arch. f. Gynaekol., xcii, 466) reports similar findings in 546 heart cases among 37,014 women. 506 DISEASES OF THE HEART AND AORTA. children well. Blacker, in a most excellent resume of the subject, coin- cides with these opinions, but finds 53 deaths (12 per cent.) in 453 cases of heart disease taken from the literature. Most writers believe that the variety in the results is due to the severity of the cases which happen to be encountered, or at least recognized; but the excellent statistics from Schauta's clinic \vould indicate that skill in the management of the case plays a considerable role. It must not be forgotten that the recognition of an organic valvular lesion in a pregnant woman may be by no means easy, for the functional or accidental systolic murmurs at the apex, occurring during pregnancy, may closely simulate those from an organic mitral insufficiency; and, unless their disappearance is noted by the end of the puerperium, this discrepancy may not be noted. The constancy of the murmur, its roughness, its transmission to the axilla and the increase rather than decrease in intensity at times when the condi- tion of the heart improves favor the diagnosis of an organic mitral insuffi- ciency; while in the presence of a soft murmur occurring with a dilated heart, a rapid pulse, and a break in compensation the presumption is temporarily in favor of the more common functional insufficiency. The diagnoses of mitral stenosis and of aortic insufficiency are probably more uniformly correct and present less difficulty. Broken Compensation in Pregnancy. On the other hand, it may be difficult to judge \vhen compensation should be considered broken. The pushing up of the diaphragm by the pregnant uterus causes some short- ness of breath; anaemia is also a factor. The pressure upon the pelvic veins may give rise to oedema of the feet and legs and even of the genitalia. And, moreover, a relative tricuspid insufficiency of muscular origin may be present as ? result of the pregnancy without organic lesion, but may never- theless give rise to the same signs and practical effects as the latter. The diagnosis of broken compensation in pregnancy therefore depends upon signs which are relative rather than absolute, since, as Mackenzie shows, a certain degree of broken compensation is an almost normal phe- nomenon in the later months of pregnancy. This again is relative, for some women are almost as active throughout pregnancy as at other times, while other quite normal women may be almost invalids throughout the entire period. It is upon degree rather than upon actual symptoms that the diagnosis of a pathologically broken compensation should be made. Dyspnoea and cyanosis on very slight exertion, such as quietly walking a distance of a few hundred yards or less, walking up a few stairs, etc., and the presence of a small rapid pulse, persistent cough, enlargement of the liver, and oedema of the feet and legs may be regarded as the most impor- tant symptoms. The earlier in pregnancy they occur the more alarming they are. Persistent dyspnoea or orthopnoea and cyanosis alone, especially in the presence of a valvular lesion, are in themselves most significant and should warrant immediate attention. MANAGEMENT OF CASES OF HEART LESIONS IN PREGNANCY. The correct management of a case of heart lesion complicated by pregnancy is, as stated by Blacker, to treat the heart disease w i t h o u t regard to the p r e g n a n c y until the break in PREGNANCY AND LABOR IN HEART DISEASE. 507 compensation is seen to persist, and then to termi- nate the pregnancy. In other words, as long as compensation is good the patient should merely be carefully watched but no medication need be resorted to. At the first signs of cardiac weakening and dilatation (dyspnoea and cyanosis, etc., on slight exertion) absolute rest should be insisted on and digitalis or strophanthus should be given. This procedure should be insisted on even if the diagnosis of organic valvular lesion is not definite, for these procedures will afford quite as much relief in cases of functional tricuspid insufficiency. Moreover, they should be repeated at the slightest indication (see page 241). especially toward the end of pregnancy. It is advisable in such cases to give a few prophylactic doses of digitalis when labor seems imminent, or a few doses of strophanthus at the begin- ning of labor pains, so as to have the tonus of the heart muscle at its opti- mum by the time the strain of the second stage is imposed upon it. At periods of acute dilatation, and especially when pulmonary cedema sets in, venesection affords the greatest relief. If cardiac symptoms disappear the patient may be gradually allowed up and around, but she must be more careful than before, and if signs of a second break in compensation occur, terminating the pregnancy should be seriously considered. This is especially true in cases of mitral stenosis, in which the cardiac accidents of pregnancy are particularly fre- quent. Women with compensated mitral stenosis may pass through five, six, or seven pregnancies without appearing to be injured by them (Len- hartz) , but when cardiac symptoms appear in a case of this disease during the course of a pregnancy it is nearing the danger line, and if these persist in spite of rest and treatment or when compensation is once broken, the danger becomes great. Fellner's low mortality (21 cases with 1 death) is probably due to the careful practice of Schauta's clinic, which he summarizes in the advice to "terminate pregnancy in cases of mitral stenosis as soon as the slightest signs of broken compensation appear/' or in cases in which signs of danger had been present in previous pregnancies. CASE OF MITRAL STENOSIS WITH PREGNANCY AND LABOR. The danger of disregarding this advice was well illustrated by a patient under the writer's care during the past year. She was a young married woman of twenty-six, and was seen in November, 1907, in the sixth month of pregnancy, complaining of shortness of breath and was quite c y a n o t i c . Her trouble dated from the birth of her first child nine months before, at which time she had evidently received a mild puerperal infection. The veins were rather full; her heart was not enlarged, and at the apex the first sound was snapping and preceded by a slight presystolic rumble. This varied in intensity from time to time. Occasionally a blowing d i a s t o 1 i c murmur was heard along the left border of cardiac dulness, but not over the aortic area. The p u 1 s e was s m a 1 1 and w e a k , not collapsing, usually regular. There was slight o e d e m a of the shins and ankles. The patient was placed in the hospital, and her condition improved at once, so that within two weeks she was allowed to enter the waiting ward of the obstet- rical department. It was then proposed that labor should be induced, but the obstetrical house staff did not regard the case as imperative. She left the hospital contrary to advice, and on January 1, 190S, in the seventh month of pregnancy, she was delivered of a healthy premature child. The labor was easy. She insisted upon giv- ing the infant the breast for a couple of weeks, but remained in bed and quiet, suffering 508 DISEASES OF THE HEART AND AORTA. from orthopnoea. This continued in spite of digitalis. Her liver was enlarged, and oedema of the legs gradually set in. She finally returned to the hospital, but never recu- perated, and died in June, 1908. The child, which had always been under the care of a district nurse and later in the Thomas Wilson Hospital, also died dur- ing the same month. Termination of Pregnancy. In an almost exactly similar case Hellendal performed an abortion as soon as the sjgns of broken compensation were definite, and eight days later resected both tubes to prevent subsequent pregnancy. The patient made a perfect recovery and her life is no longer endangered. In deciding the question of terminating pregnancy, it must be borne in mind that in from 25 to 40 per cent, of patients with severe heart lesions the pregnancy does not reach term, but premature labor occurs spontaneously owing to partial asphyxia of the fcetus. The placental circulation is slowed, the aeration is poor, and, as Fellner has shown, there is often a large necrotic border about the pla- centa. This probably results from thrombosis. Moreover, the statistics of the obstetrical clinics, even of Schauta's, are far more favorable than the end results would show. Our own case above mentioned would be classed in such statistics as "improved" at the end of the puerperium and the child as "living"; while, as a matter of fact, both died within six months after the labor. Since most statistics are compiled from the histories of hospitals, where the cases are subsequently lost sight of, it is probable that this represents a very large class of cases. The children are especially deli- cate, and, even if they survive, succumb more easily to pulmonary and gastro- intestinal infections during the first or second year than do other children. The inevitably high child mortality and the danger to the mother, especially in mitral stenosis, somewhat lessen the moral responsibility of terminating pregnancy. Moreover, as Weber and Deguy have shown, pregnancy and labor are in themselves causal factors in valvular disease, and especially mitral stenosis, through the occurrence of hemorrhages into the substance of the valves (see Chapter III), or, as in the case of our patient, bring about the recurrence of a slumbering endocarditis, and thus leave the patient w T orse than before, often with a progressive lesion. When it has been decided to terminate pregnancy, this should be done as soon as possible. The procedure of choice depends upon the severity of the symp- toms and the necessity for immediate emptying of the uterus. They have been summed up by Fellner in the following scale: (1) Induction of labor with de Ribes bag or packing the cervix; (2) craniotomy; (3) forceps; (4) version and extraction; (5) Csosarean section. In general it must be said that the less the operative interference with the physiological course of each stage, the less shock to the patient and the better the end result. On the other hand, each stage of labor is likely to be prolonged in such cases and this must be avoided. When the condition is alarming, the relief should be rapid. Pulmonary oedema is often at once relieved by tapping the fetal membranes, removing the amniotic fluid, and allowing the diaphragm to descend; although the labor then becomes much harder. The patients usually stand the operative interference well. As in other conditions, ether is preferable to chloroform where the heart is diseased. PREGNANCY AND LABOR IN HEART DISEASE. 509 AORTIC DISEASE IN PREGNANCY. As aortic disease is comparatively rare in women, it usually receives little mention. It is significant, however, that in Fellner's series there was a very high mortality (60 per cent.) in the foetus. Newell reports a case in which there was little cardiac discomfort throughout pregnancy, but a hard labor set in. Forceps were used. Collapse and pulmonary oedema ensued, and the mother died four hours after labor. The child died also. This is simply an example of the acute heart failure (probably acute dila- tation of the left ventricle with sudden onset of functional mitral insuffi- ciency) so characteristic of aortic insufficiency. Mitral lesions are usually more dangerous than aortic, but they usually give signs of gradual progres- sion. The danger in aortic insufficiency may, as in Newell's case, come on very rapidly and result in the death of the patient. SUBSEQUENT PRECAUTIONS. In cases in which dangerous breaks in compensation occur during the course of pregnancy and termination of the latter becomes necessary, as well as in those which reach a natural termination under conditions in which the life of the mother is endangered, measures must be taken to prevent subsequent conception. As Feis points out, the physician's advice to a married woman to absolutely avoid coitus is so rarely followed that for practical purposes it is scarcely worth giving. To rely entirely upon it therefore savors of hypocrisy. Feis believes that in these cases prophylactic measures against conception should be advised. Fellner and Hellendal go one step further. They both advise and practise sterilization of the mother by resection of the tubes, an operation which is not fraught with much danger, and which then relieves her from the sword of Damocles that otherwise hangs over her head. MATRIMONY AND HEART DISEASE. The question also arises under what condition may women with heart disease be permitted to marry. As Fellner's statistics show, the danger is not very great. Blacker sums up the facts in the statement that all women with heart lesions will suffer from them sooner or later, and that this period need not be much accelerated by pregnancies. Some writers even go so far as to state that pregnancies do not alter the duration of life at all, but this view is much too optimistic. The best proof, however, that the compensated heart lesion should not be a bar to matrimony is shown by Fellner's statistical proof that six out of every seven heart lesions are not even suspected in the average obstetrical clinic. On the other hand, if compensation is poor, marriage, like any other strain, should of course be forbidden. This again, as Fellner points out, depends as much on socio- logical as on physical factors, for a woman in poor circumstances may be able to live more quietly and avoid cardiac strain more readily in married life than when supporting herself by her own work. Under such circum- stances the patient should be made fully aware of the dangers of conception and coitus. All things being considered, compensated mitral stenosis cannot 510 DISEASES OF THE HEART AND AORTA. be made an exception to these rules, although its presence warrants a cer- tain foreboding in the physician consulted, and should direct his advice toward the side of caution. If compensation has once been broken in a case of mitral stenosis, conception should be forbidden and marriage strongly advised against. The same applies to well-marked chronic myocarditis or nephritic cardiopathy when these can be diagnosed with probability, since they run a more unfavorable course for both mother and fcetus than do the cases of valvular lesions. MARRIAGE IN MEN SUFFERING FROM HEART DISEASE. In men with cardiac disease the problem of marriage is, as a rule, less serious than in women, owing to the less severe physical strain imposed upon the patient; but, nevertheless, it entails certain dangers. These may be divided into two groups, the purely physical strain of coitus and the mental strains incident to providing for a family, as well as those of domestic arguments and disagreements. Whether the effects of coitus will be deleterious depends upon many factors. As long as compensation is good and sexual indulgence is moderate no ill effects need be feared, but in patients whose compensation is poor or uncertain, the effect will depend largely upon the frequency and the intensity of the sexual excitement. It is by no means rare to find heart failure begin- ning shortly after marriage in men whose compensation, though otherwise maintained, was never very good. This is especially true of old men married to young and passionate wives. Coitus raises the blood-pressure more in men than in women, and also increases the force of the heart-beat, apparently in proportion to the degree of sexual excitement, and therefore differently with different people and under different conditions. When repeated several times during the same night it is especially deleterious, since the fatigue is far greater and the after- effects are of longer duration than from a single coitus, and sudden death during coitus is far from rare, especially in patients with aortic insufficiency or diseased coronary arteries. On the other hand, the worries and psychic excitements entailed by marriage are equally important. In all but the most well-to-do it becomes necessary for the man to earn more money than would suffice him if unmar- ried, and as his whole life becomes more strenuous the wear and tear on the body, and especially upon the heart, increases. He may, for the sake of his family, take greater chances, endure greater exposure, which in itself may bring on rheumatism and bronchopneumonial infections, and these in turn react unfavorably on the heart. Among the individual valvular lesions the greatest danger is encountered in aortic insufficiency, for the act of coitus imposes a sudden strain which, in the weaker hearts, may lead to an increase in the amount of blood regurgitat- ing and bring on acute dilatation immediately. It is not surprising, therefore, that in this form of disease particularly death during the act of coitus is not infrequent; though severe heart failure resulting in death subsequently is, of course, much more common. Such failures naturally occur in persons whose hearts are in a much weakened condition before the coitus. In hearts whose tonicity is low this balance is readily overthrown and dilatation sets in on PREGNANCY AND LABOR IN HEART DISEASE. 511 relatively slight provocation; so that all influences which tend to lower cardiac tonicity such as recent febrile or gastrointestinal diseases or even severe fatigue constitute definite contraindications to sexual intercourse in this class of cases. On the other hand, the greater number of patients with aortic insuffi- ciency which is well compensated may, with perfect safety, marry without misgivings; but the necessity of heeding the above-mentioned danger signals must be impressed upon them. One point worthy of consideration in all cases of aortic insufficiency, except those upon a definitely rheumatic basis, is the frequency with which this lesion is the result of syphilitic aortitis, and this question ought to be carefully investigated before the patient is permitted to marry. In all cases of possible doubt a Wassermann reaction should be resorted to; and if this is positive antisyphilitic treatment should be instituted promptly. In cases of mitral disease the contraindications to matrimony are a little less urgent, since, from the nature of the lesion, sudden heart failure results in oedema and congestion of the lungs rather than in extreme dilatation of the ventricles, and the patient's chances of recovery from an acute heart strain are therefore greater than in the aortic cases. The same general principles and precautions, however, in the management of the patient should be followed. In cases of arrhythmia, the advisability of matrimony depends upon the severity of the condition. The sinus arrhythmias and paroxysmal tachy- cardia, when the attacks are not severe and are unaccompanied by valvular lesions or signs of coronary sclerosis, are in themselves no bar to marriage. Occasional extrasystoles also fall into this category, particularly those asso- ciated with flatulence and gastrointestinal disturbance, but not with muscular effort. If their frequency is increased on exertion or they are associated with the presence of severe valvular lesion or chronic hypertension, however, they should be regarded much more seriously and the question of marriage be- comes a much more dubious one. Heart-block is in most cases, of course, a definite bar to marriage. This is particularly the case in persons with partial heart-block, and especially those who are subject to attacks of weakness, giddiness or syncope, or in persons with complete block, unless the latter condition has shown a tendency to remain complete and the ventricle has demonstrated its ability to main- tain an adequate circulation over a long period of time. However, one occa- sionally encounters persons who, in spite of long-continued complete heart- block, retain their cardiac compensation, reserve force and bodily vigor; and in these persons the case is different. This was strikingly exemplified by a gentleman (cited on page 571) whose pulse-rate had remained at about half the normal (about 32 per minute) since some time before his marriage, which had occurred 35 years previous to his examination. During this time he had enjoyed perfect health and had led an extremely active life, and not until old age was upon him had any symptoms referable to the circulatory system set in. During this period he had led a normal married life and had been the father of several healthy children. Such cases are unfortunately extremely rare; and before marriage is permitted in heart-block the greatest precaution should be exercised, and the patient should be subjected to a variety of ex- ercise and exertion tests to demonstrate that he is thoroughly able to accom- modate himself to new taxes upon his system. 512 DISEASES OF THE HEART AXD AORTA. The same restrictions apply also to absolute arrhythmia with auricular fibrillation. Here, also, occasional cases are met with in which the arrhythmia exists for years without signs of cardiac weakness or any symptoms referable to the circulation. In these cases the heart has accommodated itself to the abnormal rhythm and may be fairly expected to do so for some time to come. In the great majority of cases auricular fibrillation entails not only persistent arrhythmia but persistent inability to withstand exertion, and for most of these marriage is out of the question. Should the patient insist upon marry- ing against the physician's advice, the prospective bride should be cautioned that she must assume more or less the role of nurse toward her husband and she must be informed that his chances of life rest largely in her hands. In chronic hypertension the same general rules apply, though this con- dition is perhaps a little more likely to be insidiously progressing and the patient may pass into the danger zone without realizing the transition. The degree of renal function and the presence or absence of dyspnoea or presence of extrasystoles en mild exertion constitute the main criteria. In cases in which the condition is progressive, the prospective bride should be informed that her husband's life is probably of limited duration. BIBLIOGRAPHY. Stengel. A., and Stamen: Heart and Circulation in Pregnancy and the Puerperium. Trans. Asso. Am. Phys.. Phila.. 1904. xLx. 520. Ye;as: Mittheilungen ueber den Puls und die vitale Lungencapacitat . etc.. Samml. klin. Vor*r.. Leipz.. 1SS-6. No. 269. Szabo: Veber die Bradykardie im Wochenbette. Frommel's Jahresb.. 1910. 700. Slemon-. J. M.. and Goldsborough. F. C.: The Obstetrical Significance of the Blood-pres- sures and their Relation to the Work of the Heart. Johns Hopkins Hosp. Bull.. Bah., 190S. xix. 194. FeLlner. 0.: H~rz und Schwangerschan. Monatschr. f. Geburtsh. u. Gynakol., Berl.. 1901, xvi. 370. Vogeler. W.: The Blood-pressure during Pregnancy and the Puerperium. Am. J. Obstetr., 1907. }-.-. 490. Macdonali. A.: The Bearing? of Chronic Diseases of the Heart upon Pregnancy. Parturi- tion, an:: Childbed. Lond.. 1S7S. L-rvi-n: T her die Complication der Schwangerschaft mit chronischer Herzkrankheit, Ztsc-hr. :. klin. Me-i..' B~rl.. 1S93. xxiii. 1. S-vhliver. Schneider, and Vinay. Quoted from Fei-. M^i".-r. W.: F>ie Ma.s.^-nverha:*.ni"nakol. No. 7*-. -. R -;.". ani by L-vnhar-z. H. Die Beziehungen der weiblichen Ge- r^anezu inn-re E:-:ran-:un2en. Verhandl. d. Kong. f. inn. Med.. Wiesb., -': Tu-zkii. r-^ r >. Gravidi'a- una H-rz. ibid.. 190S. xxv. US, and the X. COXGEXITAL HEART DISEASE. DEVELOPMENT OF THE HEART. In the human heart, as in all other complex anatomical structures. there are many portions whose form and function are obscure and difficult of comprehension when considered only in the light of conditions pres- ent in the adult, but which become quite clear when seen in the various stages of their development. A brief consideration of the embryol- ogy of the heart will therefore greatly simplify the study of the anatomy. Moreover, it must be borne in mind that occasionally some portion of the adult heart fails to develop beyond the embryonic stage, giving rise to the signs and symptoms of congenital heart disease: and there- fore a knowledge of the ernbryologi- cal development is necessary for pur- a mode! of a hurr.an er.;: r> 2.5 rr.r.. . .:'.;. a ::;.;: two 1 the bioxi to the eb.orior.ic v:II;. an : :':_? "w M::.r:^.;a. hear: H. The ave bra=.cr.:a: or aortic arc:-.es .= -= -* also. A. IV'r?al a^pec:. B. Lateral i-p-e;-- : t'r.e b.ea-i poses ot practical ciiaffnosis an>.i prognosis as we.: as The earliest staire of the circulatorv svstem in the mammr iar. embrvo consists in the formation of a number of small blood-vessels and c-aril'arv 514 DISEASES OF THE HEART AND AORTA. plexuses, which arise from the mesoblast over the surface of the yolk-sac. These soon unite to form a definite symmetrical vascular system. Eternod has carefully described the earliest development of the circu- latory system in a human embryo 1.2 mm. long, estimated at about eleven days after fertilization. Another embryo of almost the same age (Fig. 236) has recently been discovered by Dr. Mall and modelled by Mr. "NV. E. Dandy. In this embryo the venous system is represented almost entirely by the umbilical veins (Umb T^, which carry the blood that has been aerated in the placenta back to the heart. They follow the border between the embry- onic area and the yolk-sac and pass forward to the head end of the embryo. Here (FT) the two veins unite, and at the union there are given off a second set of vessels consisting of a group of four upon each side, the aortic arches (A A), which pass backward more or less parallel to the midline and soon reunite to form a single vessel on each side, the primitive aortse (AO). These two aortae earn' the blood from the embryo proper back on each side of the midline to the numer- ous ramifications in the placenta, whence, as we have seen, it is returned through the umbil- ical veins. At this stage the heart is simply a small dilatation of the venous tube, and the blood is propelled by the pulsations of the ves- sels throughout their entire lengths. There is scarcely a widening of the lumen to mark the site at which the heart will develop, namely, at the point of union of the two umbilical veins just behind the place where the aortic arches are given off. At a little later stage (Fig. 237) we find the heart the form of an S-shaped tube just ventral to the pharynx of the embryo to which it is fixed, and already two dilatations have taken place in the lumen, forming the primitive sacs of the ventricle (T) and the auricle (atrium) (A). The point of union of the veins (sinus reuniens, X /?) has been pushed further backward. The umbilical veins have received veins entering from the yolk-sac (vitelline veins) as well as a branch (duct of Cuvier. D Cur) from the body wall on each side. The duct of Cuvier is in turn formed by the union of a branch to the head (jugular vein. Jug] and a branch (cardinal vein. Card) extending downward along each side of the body wall and giving off branches to the muscle segments. The veins to the intestine arise from the vitelline vein, while the umbilical or omphalomesaraic veins continue as before to carry the blood back to the placenta and yolk-sac. Anteriorly the arterial portion of the circulatory system may now be observed to be composed of the truncus arteriosus (Tr A), a continuation of the ventricle, and four aortic arches each now corresponding to a definite FIG. 237. Human embryo 4 mm. long (about the fourth week after fertilization ), showing the further development of the heart and of the branchial or aortic arches (M.41. (Modified from Hi*.) The heart has assumed an S shape, and is divided into a truncus arteriosus (TR A\ a single ventricle (T"\ and a single auricle (AL'R'). The inner en- dothelial cardiac tube (shaded light) is much narrower than the outer muscular tube (Mi'S'i. On each side the jugular veins (JL'G from the head unite with the cardinal veins (CARD* from the trunk to form the duct of Cuvier (D Cl'V'i which empties into the sinus reuniens (5 /?). CONGENITAL HEART DISEASE. 515 visceral (or gill) arch of the embryo (V A}. These branches of the aorta are of great importance, for from them the carotid, axillary, innominate, and pulmonary vessels will develop. As the embryo grows older (Fig. 240) the heart is still more S-shapecl, / . ?{ Ao. SEPT.V. OAV. CA. AUR 5.R. FIG. 239. A diagram showing the interior of this heart; AO., aorta or truncus arteriosus; SEPT. V ., septum of the ventricles; OA V., auriculoventric- ular orifice; CA., canalis auricularis, or auricular- ventricular channel; AUR., auricles; S.R., sinus reuniens, or common chamber into which the two vena? cava3 empty, which corresponds to the sinus venosus of the lower vertebrates. FIG. 238. Heart of an embryo slightly older than that shown in Fig. 237, showing the earliest stages in the formation of two auricular and two ventricular pouches. (Drawn from a His model.) FIG. 240. Schema to show the development of the arterial system from out of the primitive aortic arches. A. Schema of the circulatory system at about the same stage as Fig. 237. I-VI, aortic or bran- chial arches (the fifth branchial arch described by Tandler arises from and anastomoses with the fourth, which is the largest of the branchial arches). AO, AO, primitive aorta;; PA, PA, rudimentary pulmonary arteries; V, primitive common ventricle; RA, LA, auricular pouches. B. Schema of the adult arterial system derived from the aortic arches. EXT CAR, external carotid artery (3d arch); INT CAR, in- ternal carotid artery (connecting bars of first three arches); COM CAR, common carotid artery connect- ing bar between third and fourth arches. A. The aorta is seen to be derived from the fourth branchial aich, the pulmonary arteries arise along the course of the sixth. The ductus arteriosus (Botalli) represents the distal end of the sixth branchial arch. The dotted lines indicate the outline of embryonic arteries which have atrophied. and at the junction of the two halves of the S a small crescentic infolding of the muscular and endothelial wall has begun to protrude into the cavity of the ventricle (interventricular septum, Sept. V.), while the ascending limb of the lower half of the S represents a stenosis in the lumen, the canalis auricularis (CA.}, whose narrowest part forms a small slit, the ostium aurieuloventriculare (atrioventriculare) (O.I V.). DISEASES OF THE HEART AND AORTA. The development of the interventricular septum continues rapidly (Fig. 241), and also a similar ridge appears running longitudinally along the truncus arteriosus, changing the lumen from circular to U-shaped, each arm of the U being a channel leading to the corresponding half of the ventricle. The auricular (or atrial) cavity is now also widened into two symmet- rical pouches, the right and left auricles, the cavity of which is continuous with the junction of the veins. OAV VE SEPT V. FIG. 241. A. Heart of slightly older embryo viewed from the dorsal aspect, showing the separation of the aortic and the pulmonary channels in the truncus arteriosus. (Drawn from a His model.) B. Diagram of the auricular portion of the same heart. Lettering as in Fig. 239. VE, Eustachian valve, separating the sinus from the auricular portion of the heart. The arrows indicate the course of the blood-currents. C. Diagram of the ventricular portion of the same heart, showing the course of the cur- rents through the separate channels of the truncus arteriosus. The trunks of the veins have already undergone considerable changes, such that the left duct of Cuvier is now atrophied, and most of the blood from the head and upper limb returns to the heart through the right duct of Cuvier, foreshadowing the superior vena cava, while the blood from the placenta returns through the two omphalomesaraic (or omphalomesen- teric) veins, which along with anastomoses from the body wall, intestinal tract, and liver will form the inferior vena cava. The junction of the two vena:' cavte forms the sinus reuniens which opens into the auricular cavity. In the wall of the sinus reuniens at this stage there is a longi- tudinal valve-like fold of endothelium (VE, Fig. 241, B), so arranged that blood from the superior vena cava flows over it into the right auricle (atrium), while the blood arriving from the placenta is directed under it into the left auricle. CONGENITAL HEART DISEASE. 517 \ FIG. 242. Still later stage, showing com- plete division of the truncus arteriosus into pulmonary artery and aorta. (Drawn from a Born model of a rabbit's embryo 10 mm. long.) The arrows show the course of the blood-stream. DA, ductus arteriosus. Very shortly after this stage the most important changes take place in the heart (Fig. 242). The two channels of the truncus arteriosus are now completely separated off from one another, and exist as distinct vessels, the aorta (AO) and the pulmonary ar- tery (PA), connected with each other at only one point through the ductus arteriosus (DA). The interventricular septum (septum ventriculorum, Sept V., Fig. 241, C) is now found to be almost completely closed, and the originally single auriculoventricular opening is now divided into two portions (mitral and tricuspid, Mil. and Trie.) separated by the ingrowth of the septal ridge. In the auricles also great changes have occurred. The greater portion of the sinus reuniens has been drawn into the cavity of the auricle, and exists there as a separate chamber, whose right margin opening into the right auricle is formed by the longitudinal valve (VE) (described in connection with the previous stage of development, now known as the valvula venosa dextra, or Eustachian valve). The left wall of the right auricle is formed by the septum auricu- lorum, which has grown considerably, partly through the gradual ingrowth of the septal ridge and partly by the pushing in of a mass of connective tissue arising from the latter and from the left wall of the sinus reuniens and known as the septum inter- po si turn. The left wall formed in part by the wall of the vein is imper- fect, and on the left the cavity extends over to the auricular septum (sep- t u m a t r i o r u m) . This sept um has also not completely closed, and the reconstruction (Fig. 243) from a model by Born at this stage shows a reuniens uSA' .which is separated from the right J ou bl e Opening between the two ailll- auricle (R.ALK.) by the Eustachian valve (I E), which at this stage forms a large partition between C'leS. At il later Stage (Fig. 245, B) the two cavities. The foramen ovale (FOR. O\~.) .1 V, U,,^ 1-^- 1^, connects the sinus reuniens with the right ventri- theS6 Openings haVC broken down cle; it is ^divided into two parts by a thin lamina into One, the foramen OVale, and it is the opinion of Born, in opposi- tion to His, Sr., that the latter struc- ture is of secondary formation and does not arise directly from the primitive interauricular openings, although it performs the same function, namely, of allowing the blood to pass from the right into the left auricle. FIG. 243. Auricular end of the same heart. The blood enters through the superior and inferior vena cava (SVP.V.C., INF.V.C.) into the sinus formed from the interauricular septum. TRIC, tricuspid orifice; P.V., pulmonary veins. 518 DISEASES OF THE HEART AND AORTA. In the later stages a valve-like flap of connective tissue projects over the foramen, allowing the blood to flow only from right to left. DEVELOPMENT OF THE PERICARDIUM. The pericardial cavity develops as a part of the original body cavity or ccelom, from which it is separated at a later stage. In the earliest em- bryos (Fig. 236) the pericardial cavity arises as a small space lined with endothelium, surrounding the blood-vessels on each side of the embryo (Fig. 244, A). These two spaces or cavities unite at the head end of the embryo to form a single pericardial cavity which surrounds the primitive heart. At a slightly later stage the heart and the pericardial MEDIAST. FIG. 244. Development of the pericardial cavity. A. Earliest stage in the development of the pericardial cavity. (After Robinson.) Embryo corresponding roughly to the stage shown in Fig. 230. E, ectoderm; C, co?lom; En, entoderm; PB, primitive blood-vessel. The pericardial cavity is represented by the part of the coelom present at this level. B. Later stage showing the division of ccclom into pleural arid pericardial cavity. (Schematic.) The arrow points to the channel connecting the two cavities. C. Relations of the pericardium in the adult. (Schematic). ANTER. MEDIANT., anterior mediastinum. cavity lie upon the ventral aspect of the pharynx and the pericardial and pleural cavities together form the anterior or cephalic portion of the coelom. At a later stage (Fig. 244, B) the heart has grown to fill almost all the ventral portion of the codom in its vicinity, and about its contour the connective tissue of the body wall is closing in, as shown by the arrow, beginning to divide the original coclomic cavity into a pleural and a pericardial portion. CONGENITAL HEART DISEASE. 519 In Fig. 244, C this closure has become complete, and we have, represented in rough diagram, the conditions present in the adult chest. The pericardial cavity is completely separated from the pleural cavity, and is lined throughout by a single layer of flat endothelial cells, the portion growing directly upon the heart called the epicardium, and the portion forming the opposite wall of the pericardial cavity, the pericardium proper. The pleural cavity has now grown more extensive than before, owing to the growth of the lungs, which have pushed forward along the sides to well in front of the heart and almost to the midline, leaving a narrow pleural cavity between them and the chest wall. Like the pericardial cavity the pleural cavity is lined with endothelium which extends partly over the lung (visceral pleura) and partly along the thoracic wall (parietal pleura). The anterior portion of the visceral pleura passes over the pericardium, from which it is separated only by a very thin mass of connective tissue, occasionally containing fat-cells. The three layers pleural endothelium, connective tissue, and pericardial endothelium are so closely fused that together they are generally designated as the pericardium, of which one speaks of the pleural and pericardial surface. The pericardium does not extend quite to the chest wall, while the pleura does so, and ventral to the heart we find a small space filled by connective tissue and known as the anterior mediastinum. PHYSIOLOGY OF THE FETAL CIRCULATION. The blood of the foetus is aerated in the placenta and passes back through the umbilical veins and through the ductus venosus (D.V.) to the inferior vena (V.C.I.}, without passing through the liver. The sinus reuniens has now become part of the main cavity of the auricle, and the inferior vena cava (V.C.I.) empties into the latter near the septum ventric- ulorum. Over its mouth pass the remains of the Eustachian valve (val- vula venosa dextra) which directs the blood not into the right auricle but away from it across the right auricle to the limbus fossse ovalis. According to the views of Galen and Harvey, the blood from the superior vena cava and that from the inferior are mixed in the right auricle before any of the stream passes to the left auricle. Haller and Sabatier, however, believed that no such mixing took place, but that all the blood from the inferior vena cava (aerated blood) passed across to the left auricle, while the blood from the superior vena cava passed down into the right ventricle. Pohlman has recently given an excellent review of the subject. He has investigated it experimentally on the fetal pig's heart by injecting starch granules into the superior vena cava in some living fetal pigs and into the inferior vena cava in others. The hearts were then removed, and the bloods in the two ventricles and auricles were shown to contain the starch granules in equal amounts, confirming the theory of Galen and Harvey. Pohlman introduced capillary glass tubes into the two ventricles and demonstrated that the pressures within them were equal. The blood from the left ventricle passes at first to the innominate and carotid and subclavian arteries, below which the aorta is joined by the ductus arteriosus Botalli. The blood from the 520 DISEASES OF THE HEART AND AORTA. right ventricle passes into the main trunk of the pulmonary artery, from which about one-fifth enters the rami passing to the lungs and about four- fifths passes onward through the ductus arteriosus and enters the descend- ing aorta. As the ductus arteriosus carries a little more blood than the descending aorta, the volume of blood in the aorta is more than doubled and the lumen considerably widened below its entry. The blood below this point goes to the kidneys, the alimentary tract, the bladder, and the lower limbs, and the rest goes on through the umbilical arteries (Umb. A.), to be aerated in the placenta and returned as described above. FORAMEN OVALE EUSTACHIAN VALVE FIG. 245. A. The circulation in the foetus just before birth. Course of the blood to and from the placenta. (Semi-schematic.) UMB A, UMB V, umbilical artery and umbilical vein; DV, ductus venosus. B. The heart just before birth. The course of the blood-stream is indicated by the arrows. VCS, VCI, superior and inferior vena cava. These are the conditions present up to the time of birth. After the first respiration the expansion of the lungs greatly reduces the resistance in the pulmonary circuit, so that it becomes less than that in the aorta, and most of the blood is diverted from the ductus arteriosus into this new channel of low resistance. Hence it persists only a year or so after birth and soon becomes changed into a simple strand of connective tissue. On the other hand, the pressure in the left auricle becomes greater than that in the right, and the valve of the foramen ovale is therefore kept closed against the septum, and soon becomes organized as a part of the latter. With the cessation of placental circulation, the ductus venosus loses its physiological importance and soon undergoes atrophy and closure. CONGENITAL HEART DISEASE, 521 CLASSIFICATION OF CONGENITAL HEART LESIONS. Classifications of congenital heart lesions are difficult, and from a clinical stand-point not always satisfactory. From the anatomical stand- point they may be classified as follows: I. Malformations about the heart. 1. Malformations of the chest wall (ectopia cordis). 2. Malformations of the pericardium. II. Abnormalities in the position of the heart. 1. Heart on the right side (dextrocardia or dexiocardia) . 2. Position of all the organs inverted (situs transversus). 3. Heart situated in the neck (cervical heart). 4. Heart situated within the peritoneal cavity (abdominal heart). III. Abnormalities of the valvular orifices. 1. Pulmonary stenosis or atresia. 2. Supernumerary or defective cusps of pulmonary valves. 3. Tricuspid stenosis or insufficiency; malformation of the valve. 4. Aortic stenosis; atresia of the aorta; malformations of the aortic valve. 5. Mitral stenosis; malformation of the mitral valve. IV. Defects in the septa. 1. Interventricular septum. a. In the septum membranaceum. b. In the muscular part of septum (below). 2. Interauricular septum. a. Defect or absence of valve of the foramen ovale. b. Valve normal but not closed. c. Defect between the muscle strands in the lower portion of interauricular septum. V. Abnormalities in the cavities. 1. Supernumerary septa. 2. Cor biatriatum triloculare. 3. Cor biloculare. 4. Cor biventriculatum triloculare. 5. Bifid apex. 6. Double heart. VI. Deviations of the septum cordis with transposition of vessels. VII. Persistence of ductus Botalli. VIII. Abnormalities of the aorta. 1. Coarctation of the aorta. a. Above the ductus arteriosus. b. Below the ductus arteriosus. 2. Hypoplasia of the aorta. 3. Malformations of the aortic arch. IX. Abnormalities in the arrangement and formation of the veins. GENERAL CHARACTERISTICS. Such a purely anatomical classification, though sufficiently complete, does not furnish a good basis for the study of the cardiac malforma- tions, because it does not take into account the relation of the indi- vidual lesions to one another. For, since these lesions are usually produced in groups rather than singly, it is quite as important from a clinical stand-point to recognize these groups and understand their effect upon the circulation as to recognize the individual lesions. Moreover, as will be seen, the mere clinical manifestations show great similarity in the various lesions, and may be summed up in what may be 522 DISEASES OF THE HEART AND AORTA. termed the ''syndrome of congenital heart lesions;" or, in the words of Peacock (1866), ''the characteristic symptoms of malformations of the heart cyanosis (especially from birth), palpitation, dyspnoea, faintings, occa- sional convulsive attacks and 1 i v i d i t y . ' Moreover, the most common physical sign of many congenital lesions is a loud superficial rnurrnur. most intense in the second and third left interspaces at the sternal margin in both systole and diastole and often heard over the entire pre- cordiurn arid the arteries as well. ETIOLOGY. As Lancereaux has well said, '"'cardiac teratology repre- s e n t s the pathology of i n t r a - u t e r i ri e life." The chief pathological conditions which affect the development of the fret us may be classed as 1. Inflammation (fetal endocarditis or myocarditis, the formation of adhesions about the heart or vessels, etc.). 2. Abnormal torsions of the cardiac tube. j. L'nderdevelopment of heart or branchial arches. These processes lead directly to the production of malformations which may be designated as primary congenital lesions, such as stenosis and atresia of the pulmonary artery, transposition of the great vessels, stenosis at the isthmus of the aorta, etc. The presence of these lesions in the fa-tus in turn exercises its effect upon the circulation, which alters the course of development arid brings about s e c o n d a r y congenital lesions. The developmental mechanics which results in the formation of such groups of lesions is well illustrated in pulmonary stenosis arid atresia. the commonest of congenital heart lesions which may be considered as the prototype. KV HTKXO.-aS ANU ATRK.SIA. 1 The commonest of all the primary congenital lesions is pulmonary stenosis, occurring in 2-">i COS per cent.; of the .'iOO cases of congenital heart disease reported by Peacock and by Keith. Two causes have been ad- vanc<-'i to explain its occurrence: 0> endocarditis in fetal life; (2; defec- tive- dev-lopment of the pulmonary artery. 1 . HouiHaud ( ] NJ.~;; ascribed it to endocarditis in fetal life. This theory s'-ems certainly to be- applicable to those cases in which the semi- lunar valves have already forrn'-d. but just as in the adult have fused along th<- lin f -s of <-losun-. This is w-11 shown in l-'ig. 2 J and in a case figured by }'<',-,.(! ,1-V.. Moreover, a number of cases have been reported in which rhf-u- ma*i-.m or iMe'-tious disease in the pr'-?rnant mother has led to the ocr-ur- renee of '-rj'iofar'iit.i- in the fortus. On the othf-r hand, it must be borne in mind that in ">2^ ( *'2.~> \><-r '-erjt./ of -I'.)'.) cases of pulmonary stenosis col- \(-f\<-r\ fr'ii:. T}J<- n-r>orts of liauchfuss. \'ie-rordt. and Abbott the- interven- l( ,:':'-\: ',-:,i-',>. ':i\r'~i.rf-, , riot fX:rforaU:'J;, from a = not, an'J -i>'/^". = a l^or- /r <:x' . r ':.'/j<: f:o;i-.trJ':tJo. r j of any natural pa-raL"; or op'.-ninjr of tfjf; oody. COXGEXITAL HEART DISEASE. 523 tricular septum remained incomplete, indicating that the primary lesion had taken place before the time at which the septum had closed (eighth week of embryonic life). As Osier has pointed out, "It is not easy to imagine a fetal endocarditis localized to so small an area as the pulmonary valves must be before the eighth week of fetal life." To this very objec- FIG. 240. Pulmonary stenosis due to fusion of the cusps. (.Drawn from a specimen in the Army Medical Museum. Washington. 1). C.} There is also a patent interventricular septum. INF. FIG. 247. Pulmonary stenosis due to a lesion of the infuiuiibulum. ^ Drawn from a specimen in the Army Medical Museum. Washington. D. f.) I\F, infundibular portion of the right ventricle. tion, however, the advocates of this theory might reply that in very many cases the lesion is by no means confined to the cusps of the valves, but in- volves the entire infundibulum, over which the endocardium may be thick- ened and shrivelled (Fig. 247). Xor does it necessarily follow that even though the interventricular septum has once closed it must remain so, PATENT INTKRVKNTRIOUl.AR SEPTUM PULMONARY ARTFRY PULMONARY ORIFICE since it may rupture under increased pressure or ulceration may result from the fetal endocarditis. Such phenomena have occasionally been observed (Abbott). '2. The malformation may also arise by " irregular evolution o f t h e b r a n c h i a 1 a r c he s ." Panuni has shown that malformations can be produced experimentally in birds by raising the temperature of incubation (fever in the mother); and His believes that at least a consider- 524 DISEASES OF THE HEART AND AORTA. able portion of malformations result from "disturbances of developmental conditions caused by insufficient nourishment, insufficient aeration of the blood, and mechanical causes resulting from malpositions of the uterus, dis- turbed placental circulation, etc." It must be recalled that, as shown by Rathke in 1843, the pulmonary artery separates from the rest of the truncus arteriosus about the eighth week of embryonic life, along with the remains of the sixth 1 left branchial arch which forms the ductus arteriosus and the left pulmonary artery which springs directly from this arch (Figs. 240 and 249) . The right pulmonary artery, according to Bremer, has sprung in a similar manner from the right fifth branchial arch, but the latter has atrophied and is now represented only by the small segment con- necting the right pulmonary artery with the truncus pul- monalis. In the twisting of the cardiac tube and separation of the ventricles the part of the truncus arteriosus corresponding to the pulmonary artery pro- trudes ventrally while the aortic portion protrudes dorsally. The truncus pulmonalis thus repre- sents the ventral half of the truncus or bulbus arteriosus and springs directly from the in- f undibulum of the right ventricle (Fig. 249). Stenosis or atresia may therefore take place from arrest of development in three C ^^^ places: 1. In the trunk of the pulmonary artery between the semilunar valve and the point of branching, i.e., where the pulmonary artery is in close contact with (and perhaps pressed upon by) the main trunk of the aorta. (This condition is represented in a case of Peacock's series.) 2. At the orifice itself (as in Fig. 246), from fusion or stenosis of the valves. 3. Below the valves and within the infundibulum of the right ventricle, as in Fig. 247. In some cases a supernumerary septum may separate the infundibulum from the main cavity of the right ventricle, thus producing the so-called third ventricle. Peacock regarded this structure as representing the condition present in the turtle, but states that "such separation" (into two cavities) Fie;. 249. Schema illustrating the genesis of pul- monary stenosi>. A. Fusion of the cusps. B. Fetal endocarditis affecting the infundibulum. C. Normal nuxle of development of the aortic branchial arches. 1). Maldevelopment of the sixth branchial arch, leading to pulmonary atresia. 1 Rathke, His, and the older writers speak of the last branchial arch from \vhich (lie pulmonary artery arises as the fifth branchial arch; but Tandler (Zur Entwicklungsges- chichte der Kopfarterien bei den Mammalia. Morphol. Jahrb., Leipz., 1902, xxx, 275) has recently shown that a small rudimentary arch is present upon the same stem with the fourth. He terms this small arch (which plays no important role in development) the fifth, and the pulmonary arch accordingly becomes the sixth. CONGENITAL HEART DISEASE. 525 "may be produced in different ways. It may depend simply on undue development of the ordinary muscular bands, or on this in conjunction with thickening of the endocardium or subjacent fibrous tissue." Re- cently Arthur Keith, of London, has revived Peacock's idea that this is the portion of the heart which is homologous with the bulbus cordis of the lower animals, and which, as Greil has shown, becomes incorporated into the substance of the ventricle (infundibulum) just as the sinus is swallowed up by the auricle. Keith believes that the period during which this is taking place represents the crucial epoch in the production of malformations. 1 Certain it is that most fetal lesions arise about the time when the pulmonary artery and the aorta and the remnants of the branchial arches are taking their final form, the interventricular septum is becoming com- plete, and the original portions of the branchial arches are disappearing, i.e., between the fourth and the eighth week of fetal life. SECONDARY MALFORMATIONS. As has been stated above, stenosis of the pulmonary orifice results in stasis within the right ventricle, and the blood is forced to take a new r channel. Patent Interventricular Septum with Pulmonary Stenosis. In 80 per cent, of the cases of pulmonary stenosis the interven- tricular septum is still open, and the blood is forced through the open septum and passes up through the aorta. As the condition is a permanent one, the current through the septum continues and its closure is prevented (stasis theory of William Hunter and Kussmaul). In rare cases, and especially those in which the stasis appears at a very early stage, the blood current eddies through and keeps open a passage between the muscle strands at the base, in contrast to the usual defect at the septum mem- branaceum. This opening at the base of the septum is often accompanied by defects in the mitral or tricuspid valves. Dextroversion (Rechtslage) of the Aorta. Moreover, the pressure upon the septum tends to deflect it toward the left and still further enlarge the septal opening (Figs. 248 and 250). In most cases the deflection of the septum to the left is so great that the aorta comes to lie in the axis of the right ventricle. The cavities thus come to form an inverted Y whose arms arc formed by the ventricles and whose shaft is the aorta. Since the shaft is inclined to the right, this gives the appearance as though the aorta arose directly from the right ventricle (Rechtslage dextroversion of the aorta). This condition is present in the majority of the cases reported by Abbott, especially in those in which there is complete atresia of the pulmonary artery (Fig. 248). 1 It is possible th.it in some cases, like those figured by Keith, the rudimentary septa represent endocardia! pockets upon Hie wall of the ventricle. Schminke (Endokardiale Taschenbildung bei Aorteninsuffizienz, Arch. f. path. Anat., etc., Berl., 1908, cxcii, 50) has shown that similar pockets may be formed in the left ventricle by the impact of a re- gtirgitant blood stream. 526 DISEASES OF THE HEART AND AORTA. Open Ductus Botalli. When the stenosis reaches a considerable grade, much of the blood that reaches the lungs must pass to them from the aorta back through the ductus arteriosus (Botalli) (Fig. 256), which is therefore forced to remain open after birth. Open Foramen Ovale. If the intraventricular septum has closed before the pulmonary stenosis has occurred, the resulting stasis causes a rise of pressure in the right auricle, and the path of least resistance to blood flow is through the foramen ovale to the left auricle. The stream in this direction is therefore larger than usual and prevents the initial sclerosis about the foramen, or even preserves a channel in the lower part of the septum, so that sometimes (as in Fig. 250) the valve of the foramen may close and a breach through this por- tion of the septum still remain patent. Three=chambered Heart (Cor bia= triatum triloculare) . When the atresia is complete and the intraven- tricular septum is closed, the right ventricle becomes converted into a blind sac into which no more blood can enter. The tricuspid orifice thus falls into disuse, and the valve under- goes stenosis and atresia until it is completely closed. The cavity of the right ventricle remains only as a small blind sac in the wall of the left, from which the aorta arises, cor biatriatum triloculare (Fig. 25]). Lesions of the Peripheral Vessels. The abnormalities in structure sec- ondary to congenital heart diseases are by no means confined to the heart, but especially involve the finer ramifica- tions of the vessels. Recent experimen- tal investigations throw much light upon the distribution and formation of these abnormalities in a manner which is of great practical importance. .1. I/>t-b in 1^3 was the first to demonstrate experimentally the effect of injury to the heart upon development. He poisoned the hearts of fish (Fundulus) embryos by tem- porary immersion in 1..5 per cent. KC1 solution, and found that, though the hearts of such embryos did not beat at all. nevertheless these embryos reached adult stage, and differed from normal fish chiefly in the irregular structure of their blood-vessels. Knower, working with froir tadpoles, ha- recently confirmed Loeb's observations, but studied the changes FIG. 250. Currents and lines of force in the embryonic heart which result from pulmonary stenosis and tend to produce patency of the septa and of the ductus arteriosus. A. Ventricular end of the fetal heart (before the eighth week of embryonic life). B. Auricular end of the fetal heart at the same stage. P A. pulmonary artery; I) A, ductus arteriosus fBotallij; R A, right auri- cle; R V, right ventricle; L .1, left auricle; L V, left ventricle; F O, foramen ovale. The large arrows indicate blood currents, the black within the ventricles, the white those within the auricles. The small arrow* indicate the forces tending to dilate the heart and to deflect the septa. In ca-e- of extreme grades of pulmonary atresia the current in the ductus arterio.-u- flows from aorta to pulmonary artery, in-tead of in the rever.-e direction. CONGENITAL HEART DISEASE. 527 in more detail, and has found that after mechanical or chemical (acetone-chloroform) injury to the heart the embryos usually become very oedematous and are less advanced than the controls. These embryos, according to Mall, are very similar to the oedematous moles frequently met with in gynaecological practice. Knower also found that the devel- opment of the brain, intestines, liver, and pancreas is retarded, '' both arteries and veins are very much distended, and follow very irregular courses. ... Inmost cases the first precapillary loops are represented by large sinuses, . . . . but there is a notable absence of capillaries in the fin. The smaller vessels do not push out nor form characteristic plexuses. Their development is inhibited. The weaker the heart-beat in fact the less does the blood flow outward from the larger vessels and precapillary loops." Similar changes had already been described by Panum and Dareste in chick embryos, by Stockard upon fish embryos poisoned with lithium, and by Bardeen upon toads which had been fertilized with sperm previously exposed to the action of X-rays. Knower also notes that similar malformations are com- mon in frogs at the end of the breeding season (when the sperm may well be weakened). The secondary changes in man, outside of the heart, are quite homologous with those in animals. These are especially underdevel- opment in stature and in intelligence and the occurrence of malformations of the arterioles and venules. Just as in Knower' s frogs, there is a dilatation and irregularity of venules often in the skin, viscera, and retina (Fig. 253), .from which hemorrhages frequently take place. Thickening and clubbing of the ends of the fingers (clubbed fingers, Fig. 254) also take place, from proliferation of the connective tissue as a result of the venous stasis. RUD. PATHOLOGICAL PHYSIOLOGY. The effect of pulmonary stenosis upon the mechanics of the circulation in the adult is FIG. 251. Three-chambered heart (cor biatriatum triloculare) produced by complete atresia of the pulmonary and tricuspid orifices. (From a speci- men in the Army Medical Museum, Washington, D. C.) Rl'D. rudimen- tary cavity corresponding to the right Very marked. In the first place it brings ventricle; F O. foramen ovale. The r n ! i i ,1 i ! arrow* indicate the course of the about a fall in blood-pressure (both arterial blood stream. and venous) in the pulmonary artery and in the lungs (Fig. 252), and consequently a corresponding .secondary lowering of pressure in the aorta. The extent to which other areas of the circulatory system are affected depends as much upon the correlated defects as upon the stenosis itself. If the stenosis is the only lesion, it produces a fall of pressure in the pulmonary artery, a rise of pressure (from stasis) in the pulmonary veins, and a marked increase in pressure within the right ventricle, like that which Liideritz found in the left in aortic stenosis (Fig. 252, light broken line). This always leads to hypertrophy of the right ventricle and right auricle, and usually to the signs of congenital venous congestion to be described later. Between these two grades of severity there exist all stages of cardiac insufficiency, the most important being the overloading or weakening of the right ventricle, which leads to transitory venous stasis, tricuspid insuf- ficiency, and cyanosis. The pressure in the pulmonary vein and left auricle 528 DISEASES OF THE HEART AND AORTA. is b)' virtue of the pulmonary stenosis lower than usual, while that in the right auricle is for the same reason higher. Accordingly the tendency is for venous blood to pass into the left auricle and ventricle in diastole to a much greater degree than when the pulmonary orifice is normal, and hence to cause a greater tendency to cyanosis and dyspnoea than in the uncompli- cated patent foramen ovale. When the foramen ovale is patent but the septum ventriculorum closed (12 per cent, of Abbott's cases), the effect upon the circulation varies. Owing to the pulmonary stenosis, the path of least resistance is through the open foramen ovale into the left auricle without passing through the lungs, and much blood may circulate in this way. Whether or not this gives rise to cyanosis depends upon the actual amount entering the lungs through the pulmonary artery. Under ordinary circumstances this may NORMAL PULMONARY STENOSIS AND ATRESIA Fio. 252. Diagram of the circulation in pulmonary stenosis and atresia. Simple pulmonary stenosis. The arrows show the fall of pressure in the aorta and pulmonary artery and the rise of pressure in the vena cava and right auricle. The broken line indicates the high intraventricular pressure in the right ventricle. Pulmonary atresia, with patent interventricular septum (l. Radiograph of a thirteen-year-old boy with patent ductus arteriosus (Botalli) and aneu- rismal dilatation of the ductus and pulmonary artery. (After Hochsinger, in Pfaundler and Schlossmann'a 'Diseases of Children.") A A, arch of the aorta; DB, ductus Botalli and pulmonary artery dilated like an aneurism, giving a cap-shaped top to the shadow of the heart; MI, internal mammary artery, consider- ably dilated, denoting an internal collateral circulation. A diastolic murmur is often heard along with the systolic, sometimes replacing the second sound but more often accompanying or following an accentuated pulmonic sound. The inequality in pressure between aorta and pulmonary artery persists during diastole, and the abnormal blood flow therefore continues and produces the murmur in diastole. When the difference of pressure is slight, especially with low peripheral resistance, the diastolic murmur may be absent. 544 DISEASES OF THE HEART AND AORTA. DIAGNOSIS. From the above discussion the points upon which the diagnosis of the open ductus arteriosus may rest are sufficiently clear, pulsation over the right ventricle, Gerhardt's dulness, a systolic or double murmur loudest at second left interspace and heard at the left upper back, expiratory accent- uation and pulsus paradoxus, and the pulsating mass in Gerhardt's area seen on X-ray examination. In addition, the history may show that the patient was blue at birth (before the pulmonary channels have opened up) but that cyanosis soon passed off. J. Plesch in Kraus's clinic (Berl. klin. Wchnschr., 1909, xlvi, 391) has attempted to make the diagnosis by analyses of the expired air. By a very simple device he deter- mines the percentage to which the blood flowing through the pulmonary artery is satu- rated with oxygen. Under normal conditions the saturation is 38-70 per cent, of its oxygen capacity. In patent ductus arteriosus the blood in the pulmonary artery is mixed blood and hence its oxygen content is higher (80-90 per cent.). The aerated blood could enter only through a patent ductus arteriosus. TREATMENT. Treatment for the persistence of the ductus consists mainly in those methods which improve pulmonary circulation, breathing exercises, careful hygiene, avoidance of exposure to pulmonary infections, and avoid- ance of fatigue, general muscular and cardiac overstrain. Since the per- sistence of the ductus is in itself a compensatory process, it calls for no special remedy. To ligate it, as might readily be done after opening up the thorax under positive pressure, would be harmful rather than bene- ficial. Otherwise general hygienic measures and cardiac stimulants are of value, as in other diseases. But in many cases open ductus Botalli has no effect upon the duration of life and requires no treatment. STENOSIS OF THE AORTA. Stenosis of the lumen of the aorta may occur in three places: I. At the aortic valve. II. Stenosis of the arch of the aorta. 1. Above the entrance of the ductus arteriosus Botalli. 2. Just below the entrance of the ductus arteriosus Botalli. I. Stenosis at the aortic orifice is one of the rarer con- genital lesions (2 per cent, of Abbott's series), though probably many of the milder cases escape detection. It is usually due to endocarditis late in fetal life. Those which develop earlier in fetal existence, in which true aortic atresia occurs, are quite analogous to the cases of pulmonary atresia, except that the posterior instead of the anterior channel of the common truncus arteriosus fails to develop. The changes in the fetal circulation are similar to those in pulmonary atresia, but affect the opposite sides of the heart. The septa remain open, and occasionally one ventricle (the left) fails to develop. Practically the entire systemic circulation is carried on by the pulmonary artery through the ductus arteriosus. The consequences of the lesion are very severe and few cases survive birth, in striking contrast to pulmonary stenosis and atresia. Xo doubt CONGENITAL HEART DISEASE. 545 this is due to the fact that, since the right ventricle is the stronger in fetal life, it succeeds in establishing a better compensatory circulation after atresia of its orifice than does the left. Moreover, when the first breath is taken after stenosis of the aorta, it is venous instead of arterial blood which is thrown into the organs. II. Stenosis in the vicinity of the ductus Botalli is one of the most common congenital heart lesions, occurring in 198 of Abbott's 412 cases. Like most abnormalities it arises as an exaggeration of a condition which is normally present in the fostus. As stated above, Klotz finds that there is a distinct narrowing of the aortic arch just above the entrance of the ductus into it. This is no doubt due to the fall of pres- sure in the aorta which occurs below the left carotid artery and the rise further on when the blood enters from the ductus. Hamernik in 1844 divided the cases into: (1) stenosis above the ductus, (2) those at the entrance of the ductus, and (3) those below the ductus. Bonnet, who made an exhaustive study of the subject in 1903, discards Hamernik's second group, and distinguishes two types: 1. The type in the new-born, in which the stenosis occurs above the ductus and the latter remains open. 2. The type found in adults, in w r hich the stenosis occurs below the ductus. The latter is closed and collateral circulation develops. Bonnet's studies were based upon 160 cases, of which 55 (34.3 per cent.) were of the new-born type and 105 (65.7 per cent.) were of the adult type. Type of the New=born. The cases of the new-born type represent an exaggeration of the slight narrowing in the aorta which, as Klotz states, is present above the left subclavian artery and the ductus Botalli. Em- bryologically, as Longa points out, this represents the branch joining the fourth and sixth branchial arteries (Fig. 240) and might correspond to a failure of development of this branch. On the other hand, the amount of blood in the aorta is very much depleted by the flow into the innominate, left carotid, and subclavian, so that its lumen is naturally smaller until replenished by the inflow from the ductus. There is consequently a region of functional stenosis between these two points which may be exaggerated by con- traction of the muscle-fibres in the wall of the aorta. The weaker the action of the left ventricle the more marked will be this functional steno- sis. The ductus Botalli therefore takes on more and more of the circu- lation in the lower parts of the body, and fetal life may be undisturbed as long as the right ventricle is pumping aerated blood; but when this con- dition ceases and the pulmonary channels widen and pressure in the ductus falls, the aortic circulation may become insufficient and the syndrome of 35 202. Stenosis of the isthmu aorta above the ductus arteriosus (Botalli). - type of the new-born. (From a specimen in the Army Medical Museum, Washington, D. C.) 546 DISEASES OF THE HEART AND AORTA. congenital heart disease may result. It is rare for these children to live more than a few weeks, or at most a few months, and many die at birth. Physical signs are indefinite, confined to double murmurs over the chest and back and in most cases cyanosis. There are very often asso- ciated malformations, such as pulmonary stenosis, open septum ventric- ulorum, etc. In this form there is very little attempt at establishment of a c o 1 1 a t- e r a 1 circulation, since the greater part of the systemic circulation is maintained by the right ventricle through the open ductus arteriosus, just as it is before birth. Owing to the completeness of this compensation, there may be little difference between the pulses in the upper and in the lower extremities, and the clinical diagnosis is scarcely ever made. Adult Type. In the second or adult type, which is more common, the stenosis occurs just below the entrance of the ductus Botalli, and this vessel is found to be closed. Indeed, the very stasis at this point assists in its closure. The mode of origin of the stenosis at this point is not clear. Bonnet calls attention to the fact that the lumen of the aorta at the stenosis (usually 2-4 mm.) is about that of the normal aorta at the time of birth, and thinks that the whole anomaly may be of post- natal development. It is possible, as he suggests, that, when the ductus Botalli is particularly long, the fibro- sis of the latter brings about a kink- ing of the aorta at this point, and with a dilatation above and stenosis at the point of kinking. Fir,. 263. Stenosis below the ductus arteri- Skoda. On the Other hand, has osus (Bolalli). adult tvpe. (After Bonnet, Rev. 1,1 ,1 de Mod., Par., 1903, xxiii.) suggested that the stenosis may result from a band of fibrosis passing around the aorta at this point; but, though this theory is alluring, there is no definite histological evidence in its support. The stenosis cuts off the circulation from all parts of the body below the stenosis, but the high pressure due to the stagnation above it causes a progressive dilatation of other arterial channels, such as the mammaries, thoracic and scapular arteries, which are always found to be much dilated. Indeed, the collateral circulation may be so good that the lumen of the aorta below the stenosis may be as great as above it (hour-glass constriction), though usually it is somewhat narrow and it may even be funnel-shaped. Clinically the presence of this type of stenosis does not necessarily shorten life, though this depends largely upon the completeness of the collateral circulation. The symptoms are chiefly those of cerebral conges- tion, headache, vertigo, buzzing in the ears. Occasionally there are pains in the chest. Bonnet calls attention to the fact that in his 105 cases there was never intermittent claudication, showing that the circulation in the lower limbs is alwavs sufficient. CONGENITAL HEART DISEASE. 547 PHYSICAL SIGNS AND DIAGNOSIS. Cyanosis is not common and not a sign of the disease. The most definite indication is the difference in the size and quality of the pulse in the upper and lower extremities, the carotid and radial pulses being large and throbbing, the femoral, popliteal, and dorsalis pedis as well as the abdominal aorta small or impalpable. Though the diagnosis intra vitam is rare, Lepine was able to make it from these data in two cases. Dr. \V. S. Morrow calls attention to the possibility of diagnosis from marked differ- ence in the brachial and tibial blood-pressures, but just as in aneurisms the difference in size and quality of the pulse on palpation would usually be more marked than that of the blood-pressures. Moreover, Halsted has found little difference between brachial and femoral pressures in man after the abdominal aorta has been occluded with metal bands for the treat- ment of aneurism. The presence of large tortuous mammary, thoracic, and scapular arteries aids in the diagnosis. There are usually low murmurs over the arteries, especially at the angle of the left scapula, as was present in a case diagnosed by Mercier in 1839. Valvular disease of the heart frequently results from the increased work thrown upon the heart and dilatation of aortic and mitral orifices, and their signs complicate the picture. Before making the diagnosis, it is always necessary to exclude aneurism and mediastinal tumor by the absence of dulness on percussion and of abnormal shadows on X-ray examination. TREATMENT. Treatment depends purely upon symptoms, occasional venesection being of value to relieve the headaches. It is most important for the patient who suffers from these symptoms to avoid over-exertion or excite- ment, which cause too vigorous action of the heart. DIFFUSE NARROWING OF THE AORTA. Virchow has also called attention to another form of abnormality in the lumen of the aorta, a diffuse narrowing of its entire lumen throughout its whole extent (hypoplasia of the aorta). This condition is associated with under-development of the elastic and muscular elements in the arterial walls. As Virchow and other observers have found, it is often associated with chlorosis of intense grades and occasionally accompanies other con- genital malformations of the heart. About the objective finding there is little dispute. The only point in question is whether the condition is to be regarded as a true congenital malformation or as a postnatal development, which, like the changes in rickets, is determined by conditions of growth and nutrition during child- hood and may be corrected by cure of these conditions. It is possible that it may be secondary to the conditions which bring on ana>min, and clue to the fact that the aortic walls have never been subjected to the stimulating influence of an adequately high blood-pressure. That this may be a factor in the development of and strengthening of blood-vessel walls has been shown especially by the results of arterio venous anastomosis and trans- 548 DISEASES OF THE HEART AND AORTA. plantation, in which the walls of the transplanted vein become thicker and richer in elastic and muscular elements (Carrel). It is of course extremely difficult to determine what would have occurred if such cases had recovered from their anamiia or primary debility and blood-pressure had reached a normal level. It is equally difficult to determine that any such cases have recovered under these conditions, though the fact that the lumen of the radial artery increases (pulse becomes larger) with the recovery from chlorosis is of course definite. For the present, therefore, one must hesitate somewhat in classing hypoplasia of the aorta among the definite congenital malformations. Fn,. L'114. Transposition of the viscera in embryo and adult. (Schematic.) .-I, B, C, position of organs in the embryo; a, b, c, position of organs in the adult. A, a, normal; B, b, transposition of the heart and arteries simple dextrocardia; C, c, complete situs transversus. COMPLETE AND PARTIAL SITUS TRAXSVERSUS. It is not extremely rare to meet with a case of complete transposition of the viscera, so that the heart and stomach are found to lie on the right side (dextrocardia, dexiocardia) and the liver upon the left. This condition is probably brought about by a change in position of the cardiac tube in early embryonic development, so that it lies in the position of nary artery with four cusps. 'From a Washington. ]). (.'. Medical Museum, of Abbott's 412 cases) it is due to alteration in development. Under these circumstances the pulmonary artery is given off from the left ventricle, the aorta from the right. (Ireat variations may be seen in the arrangement of vena 1 cava 1 , which sometimes enter the left, sometimes the right auricle. The results, as in other cases in which the blood is mixed, vary greatly. The syndrome of congenital heart disease may be present, owing to the mixing of blood, but the exact transposition of vessels can rarely be diagnosed intra vitam. CONGENITAL HEART DISEASE. 551 ABNORMALITY OF THE VALVES. The number and formation of the cardiac valves may also undergo alteration in fetal life. In the aortic and pulmonic this is usually due to inflammatory fusion of two cusps forming a bicuspid valve (Fig. 265), or to the fact that one of the leaflets is divided into two parts by a slit and finally under the influence of the blood-pressure grows to form symmetrical cusps (Fig. 266). In the mitral and tricuspid valves, especially in association with open septum ventriculorum, there may be a split in the middle of one leaflet, practically converting it into two separate cusps. Except for the forma- tion of valvular insufficiencies which result, multiplicity or paucity of the cusps has no pathological effects. A large number of other malformations, such as partial separation of the two ventricles to form a " bifid apex," defective formation of the chest wall with exposure of the heart (ectopia cordis), malposition of the heart causing it to lie in the abdomen or the neck, transposition and malformation of the great arteries and veins, are encountered. Space does not permit of a complete discussion of these conditions, for which the reader is referred to the magnificent article by Dr. Maude Abbott in Volume IV of Osier's Modern Medicine. BIBLIOGRAPHY. DEVELOPMENT OF THE NORMAL HEART. The development of the normal heart is well discussed in Piersol's, Morris's, and Quain's anatomies and in the various text-books of embryology. The following articles may be consulted also: Eternod: Premiers stades de la circulacion sanguine dans 1'ouef et 1'embryon humains, Anat, Anzeig, 1899, xv, 181. His, W.: Anatomic menschlicher Embryonen, Leipzig, 1880. For an excellent series of figures see also Kollman, J.: Handatlas der Entwicklungsgeschichte des Menschen, Jena, 1907. Born, G.: Beitriige zur Entwicklungsgeschichte des Saugethierherzens, Arch. f. inik. Anat., Bonn, 1889, xxxiii, p. 284. Robinson, A.: Early Stages of Development of the Pericardium, J. Anat. and Physiol., Loml., 1903, xxxvii, 1. Pohlman, A. G.: The Course of the Blood through the Heart of the Fetal Mammal, etc., Anat. Rec., Phila., 1909, iii, 75. CONGENITAL HEART DISEASES. Lancereaux: Das anomalies cardiaques, Gaz. d. hop., Paris, 1880, liii, 850, 875, 883, 890, 906, 930, 981. Morgagni: De sedibus et causes morborum, Venet., 1761. Peacock, T. B.: Malformations of the Human Heart, Lond., 1866. Keith, A.: Malformations of the Bulbus Cordis, Studies in Pathol., Quatercent. Pub. Aberdeen Univ., 1906, 55. Bouillaud: Traite clinique des maladies du coeur, Paris, 1835. Rauchfuss: Missbildungen des Herzen's, Gerhardt's Handb. d. Kinderkrankh., 1878, iv, 1 part. Vierordt, H.: Die angeborene Herzkrankheiten, Nothnagel's Handb. d. spe/. Pathol. u. Therap., Wien, 1901, xv, II part 1. Abbott, M. E.: Congenital Cardiac Disease, Mod. Med., ed. by Wm. Osier and Thos. Mc- Crae. Phila., 1908, iv, 323. 552 DISEASES OF THE HEART AND AORTA. Osier, Wm. Quoted from Abbott. Panum, P. L.: Ueber die Entstehung von Missbildungen, Berl., 1860. His, Wm., Sr. : Anatomic menschlicher Embryonen, Leipz., 1S80. Rathke, H.: Die Entwickelung der Arterien, welche beim Saugethier von den Bogen der Aorta ausgehen, Arch. f. Anat., Physiol. u. wissench. Med., Berl., 1843, 276. Bremer, J. L.: On the Origin of the Pulmonary Arteries in Mammals, Am. J. Anat., Balto., 1901-1902, i, 137. Greil, A.: Beitrag zur vergleichende Anatomic und Entwickelungsgeschichte des Herzens und des Truncus arteriosus der Wirbeltiere, Morph. Jahrb., Leipz., 1903, xxxi, 123. Hunter, Wm.: Medical Observations and Enquiries, 1784, vi, 300. (Quoted from Peacock.) Kussmaul, A. Quoted from Vierordt. Loeb, J.: Ueber die Entwicklung von Fisch-embryonen ohne Kreislauf, Arch. f. d. ges. Physiol., Bonn, 1893, liv, 528. Knower, H. McE.: Effects of Early Removal of the Heart and Arrest of the Circulation on the Development of Frog Embryos, Anat. Rec. (Am. J. Anat.), Balto., 1907. Mall, F. P.: A Study of the Causes underlying the Origin of Human Monsters, J. Morphol., Phila., 1908, xix, 3. Dareste: Ilecherches sur les monstrosites, Paris, 1891. Quoted from Mall. Stockard, C. R.: The Development of the Fundulus Heteroclitus in Solution of Lithium Chloride, with Appendix on its Development in Fresh Water, J. Exper. Zool., Balto., 1906, iii, 99. Bardeen, C. R.: Abnormal Development of Toad Ova fertilized by Spermatozoa exposed to the Rontgen Rays, ibid., 1907, iv, 1. Senac, quoted from Bard, L., and Curtillet, J.: Contribution a 1 'etude de la physiologie pathologique de la maladie blue. Forme tardier de cette affection. Rev. cle med., Paris, 1889, ix, 993, from whom Grancher et al. are quoted. Stille, Moreton: On Cyanosis or Morbus Coeruleus, Am. J. M. Sci., Phila., 1844, N. S. viii, 25. Osier, Wm.: Chronic Cyanosis, with Polycythaemia and Enlarged Spleen: a new Clinical Entity, Am. J. Med. Sci., 1903. Knapp, quoted from Posey, W. C.: Cyanosis Retina 1 , Am. J. Med. Sci., Phila., 1905, cxxx, 415. Tate, W. W. H.: Case of Malformation of the Heart, Trans. Path. Soc., Lond., 1892, xliii, 36. Hebb, R. G.: Hearts with Congenital Defects and Inflammatory Disease, ibid., 1897, xlviii, 41. McOscar, J., and Voelcker, A.: On a Case of Traumatic Rupture of the Ventricular Septum, ibid., 1897, xlviii, 47. Reiss, P.: Contribution a 1'etude des malformations congenitales du coeur, Maladie de Roger, These, Par., 1893. Roger, II.: Recherches cliniques sur la communication des co?urs par inocclusion du septum interventriculaire, Bull, de 1'Acad. de Med., Paris, 1879, ser. viii, t. ii, 1074 and 11S9. Cadet de Gassicourt, Potain. Quoted from Reiss, I.e. Klotz, ().: The Closure of the Ductus Arteriosus and its Bearing on Arteriosclerosis, Trans. Asso. Am. Pliys., 1907, xxii, 213. Gerhardt, C.: Persistenz des Ductus arteriosvis Botalli, Jenaische Ztschr. f. Med. u. Xatur- wissench., 1867, iii, 105. (Quoted from Vierordt.) Zinn, W.: Zur Diagnose der Persistenz des Ductus arteriosus Botalli, Berl. klin. Wchn- schr., 1S98, xxxv, 433. De la Camp, ().: Familiares Vorkommen angeborener Herzfehler; zugleich ein Beitrag zur Diagnose der Persistenz des Ductus arteriosus Botalli, Berl. klin. Wchnschr., 1903. xl, 48. Francois-Franck, A.: Sur le diagnostic de la perseverance du canal arteriel, Cong, de I'avancement des sciences, Paris, 1878. Bonnet: Sur la lesion de la stenose de 1'isthmus cnngenitale de 1'aorte dans la region, Rev. de Med., Paris, 1903, xxiii, 108, 255, 335, 419, 481. XI. HEART-BLOCK AND THE ADAMS-STOKES SYNDROME. HISTORICAL. In 1827 Robert Adams, of Dublin, reported the case of a revenue officer, aged 68, whose pulse-rate was 30 per minute and who suffered from dyspnoea, cough, and attacks of fainting ("apoplectic attacks"), ''during which his pulse would become even slower than usual. He recovered from them without paralysis." In the same year an exactly similar case was reported in great detail by Wm. Burnett. Burnett's observations were reported even more carefully and in greater detail than those of Adams and ill deserve to have fallen into oblivion. Burnett further called attention to the fact that Morgagni had described two cases of "epilepsy with slow pulse" in 1761. Holberton described another case in 1841, but general attention was not attracted to the condition until Wm. Stokes published four cases in 1846. Since then the condition of persistent extreme brady- cardia with syncopal or convulsive seizures has been known as the Adams-Stokes syndrome, though it may more accurately be designated by the names of Morgagni-Adams-Stokes, as Pletnew has done, or by that of Morgagni-Adams-Burnett or Adams-Bur- nett syndrome. As but little can be added to the clinical descriptions of these cases, one of Stokes's histories may be reported in some detail: "Edmund Butler, aged 68, stated that his health had been robust until three years before admission, at which time he was suddenly seized with a fainting fit. This occurred several times during the day and always left him without any unpleasant effects. Since that time he has never been free from attacks for any considerable length of time, and has had at least fifty such seizures. The fits are very uncertain as to their period of invasion and very irregular as to their intensity, some being much milder and of shorter duration than others. They are induced by any circumstance tending to impede or oppress the heart's action, such as sudden exertion, distended stomach, or constipated bowels. There is little warning giA-en of the approaching attack. He feels, he says, a lump first in the stomach, which passes up through the right side of the neck, where it seems to explode and pass away with a noise like thunder by which he is stupefied. This is often accompanied by a fluttering sensation about the heart At first he found that spirits were the best restorative or prophylactic, but latterly he has not used them, being 'afraid to die with spirits in his belly.' " On admission he was haggard and emaciated On percussion the chest is universally resonant. The respiratory murmur is louder and combined, especially pos- teriorly, with large mucous rales. The impulse of the heart is slow and of a dull heaving character The first sound is accompanied by a soft bruit de soufflet. The second sound is also imperfect We remarked to-day that on listening attentively to the heart's action we perceived that there were occasional semi-beats between the regular con- tractions, very weak, unattended with impulse, and corresponding to a similar state of the pulse, which thus amounts to about 28 in the minute, the evident beats being only 28. . . . 553 554 DISEASES OF THE HEART AND AORTA. " (June.) The cardiac phenomena remain as before, but a new symptom has appeared, namely, a very remarkable pulsation in the right jugular vein. This is most evident when the patient is lying down. The number of reflex pulsations is difficult to be established, but there are more than double the number manifest contractions. About every third pulsation is very strong and sudden and may be seen at a distance; the remaining waves are much less distinct. " He has scarcely had any of the cardiac attack since he was discharged." THE CONCEPTION OF HEART-BLOCK. Stokes did not appear to have any definite understanding of the nature of these " semi-beats " nor of the functional disturbance associated with them. A similar, more accurate observation was made by A. Chauveau. Chauveau in 1882 made observations upon a case whose usual pulse-rate was 24 per minute, and who suffered from occasional attacks of vertigo and loss of consciousness. Tracings made from the apex showed a series of large beats at regular intervals corresponding to the loud heart sounds and to the radial pulse, and also a second series of very small notches occur- ring at equally regular inter- vals but bearing no relation RESP whatever to the beats of the ventricle. As in Stokes's case, RADIAL these small pulsations were ac- companied by " small sounds APEX which may give the illusion of reduplication of either heart SECONDS sound." The usual presystolic notch due to the auricular beat was absent, and Chauveau cor- FIG. 2G7 Tracing of the apex beat in a case of Adams- rppt ] v ponHnHpH thlt thp<;p Stokes disease. (After Chauveau.) reCtiy Concluded tnat small notches were due to the contractions of the auricles, which were beating at a rate of 66 per minute while the rate of the ventricles was 24. Chauveau investigated the matter experimentally, and was able to demonstrate that in horses upon stimulation of the vagus the auricles could be observed to beat more frequently than the ventricles. He therefore naturally considered the dissociation of auricular and ventricular rhythm as due to over-stimulation of the vagus. Chauveau's conclusions that heart -block may result from stimulation of the vagus have been confirmed recently by Rothberger and Winterberg, Garrey, and Robinson and Draper, who have shown that it is chiefly the left vagus which acts upon the auriculoventricular bundle; and the latter have even been able to produce partial heart-block in man by pressure upon the left vagus. While Chauveau was experimenting in Franco, Wooldridge under Ludwig's direc- tion wa.s investigating the course of the nerves in the cardiac septum. Wooldridge found that when lie tightened a ligature which embraced only the septum, the auricles and ven- tricles beat independently and the ventricles no longer responded to vagus inhibition. When the ligature was loosened the rhythm returned to normal. Tigerstedt in 1884 also obtained dissociation of auricles and ventricles by cutting the septum. These observations under Ludwig's direction were made with the view only of cutting the intracardiac nerves. As a matter of fact, the muscular connections were severed as well, but the importance of these was disregarded. HEART-BLOCK AND ADAMS-STOKES SYNDROME. 555 The myogenic conduction from auricle to ventricle was, however, at this very period being demonstrated by Gaskell in Cambridge upon the heart of the tortoise and frog, in which the auriculoventricular function is repre- sented by a wide band of muscle whose properties differ somewhat from those of either the auricle or the ventricle. Gaskell demonstrated that " if this auriculoventricular ring were clamped, the auricle continued to beat at unaltered rhythm, but as the clamp was tightened the period between auricular and ventricular contractions (A S -V S interval, on conduction time) was gradually lengthened; then the ventricle failed to respond to some of the impulses from the s auricle, and, according to the tightness of the clamp, the ventricle could be made to .... respond to every second contraction of the auricles (partial heart-block), to respond to every third, fourth, or SEC. JUGULAR APEX BRACII. c c c c FIG. 2G8. Partial heart-block (3 : 1 rhythm) produced by pressure upon the vagus in a patient with disturbed conductivity who was also subject to attacks of the Adams-Stokes syndrome. (Tracing made by Dr. F. W. Peabody and the writer.; A, A, A, A, auricular contractions to which the ventricles do not respond. other contraction, or to remain quiescent. When the clamp was closed very tightly the ventricle remained still for a variable time, then, in accordance to its inherent rhythmical power, developed a rhythm of its own (rhythm of development), the rate of that rhythm when fully developed and the length of time that the standstill lasted being correlated with the rhythmicity of the tissues." The condition in which the contractions of the ventricle no longer follow any of the impulses from the auricles is termed complete heart- block, in contrast to the partial heart-blocks in which the ventricle is respond- ing to some, but not all, of the impulses arising in the auricles. Gaskell showed that heart-block also set in when the bridge of tissue connecting the auricles and ventricles was cut down to a sufficiently narrow strip. He was able to produce similar blocks between portions of the auricle or ventricle by clamping or cutting, just as Romanes had done for the muscle in the bell of the medusa. Gaskell demonstrate*! also that the block between auricles and ventricles remained complete when the only connection between the auricles and the ventricles was formed by the coronary nerve. 556 DISEASES OF THE HEART AND AORTA. THE AURICULO(ATRIO) VENTRICULAR MUSCLE BUNDLE. Anatomy. The existence of muscular connections between the auricles and ventricles in man and mammals was, however, denied until G. Paladino (1876) and A. F. Stanley Kent (1893) described certain fibres in the septum membranaceum which they thought bridged this gap. Paladino was some- what indefinite, and Kent's figures showing connections between the left auricle and left ventricle are apparently erroneous, so that the real discovery dates from the same year, when Wm. His, Jr., described the presence in the mouse, dog, and man of a bundle of muscle-fibres which " arises from the posterior wall of the right auricle near the interauricular septum, in the atrio- ventricular groove, lies upon the upper edge of the muscular interventricular septum, passes forwards and to the vicin- ity of the aorta, where it divides into a right and a left branch. The latter passes down to the base of the anterior mitral cusp." These anatomical findings of His have been confirmed by Braeunig, Hum- blet, Retzer, and Tawara. The latter found that the fusiform cells described by Kent were really Purkinje fibres, and that the muscles bundle of His is in reality continuous with the entire net- work system of Purkinje fibres which permeates both ventricles. Saigo has found that these fibres are much richer in glycogen granules than are the ordi- nary cardiac muscle fibres. Tawara also demonstrated the presence of nerve- fibres within the His bundle, and Gordon Wilson has recently demonstrated ganglion cells as well. In a later research Retzer has stated that this conducting system is continuous above with the septal portions of the right auricle (Fig. 269), and that its cells are of the same histological structure as those about the sinus region. He believes that it is a true sinoventricular bundle, but the recent work of Lydia de Witt seems to confirm the claims of Tawara. The idea that the cardiac impulse must pass from sinus to auricle before reaching the auriculoventricular bundle is borne out also by the observation of Dr. G. S. Bond that in the frog the auriculoventricular muscle can be seen to contract considerably later than the auricle but before the ventricle. Experimental Physiology of the Auriculoventricular Bundle. The first experiments upon the physiology of heart-block in mammals were performed by Stanley Kent, the discoverer of the auriculoventricular bundle, in 1893, and were recorded by him in his original publication in the following words: " By the use of a suitably constructed clamp ... I have been able to verify for the mammal (i.e., in the excised heart of the rat) almost all Fir,. 209. The right branch of the aurieulo- ventricular bundle in the dog's heart. (After Barkerand Hir^clifelder, Arch. Int. Med., 1909.) HEART-BLOCK AND ADAMS-STOKES SYNDROME. 557 the effects described by Gaskell as obtained in the frog." Kent thus seems to have forestalled all the later experiments upon the subject, but the brevity of his physiological note left much to be investigated. In 1895 His repeated the experiments of Wooldridge and Tigerstedt, and demonstrated that in order to bring about dissociation of the auricles and ventricles it was not necessary to injure the entire septum but merely this auriculoventricular muscle bundle. In 1899 he applied his anatomical and physiological studies to a case of Adams-Stokes disease, in which he confirmed Chauveau by finding inde- pendent action of the auricles and ventricles, and designated this by Gas- kell's term " heart-block." His also gave an excellent tracing, taken during a syncopal attack, demonstrating that the auricles continued at their usual RESP. FIG. 270. Tracings from the carotid artery and jugular vein of a patient with Adams-Stokes disease, showing stoppage of the ventricles and continuance of the auricular contractions during the attack. (After His, Deutsches Arch. f. klin. Med., 1899, Ixiv.) 1, 2, 3, 4, 5, G represent the onset of independent ventricular contractions. rate while the ventricles ceased to beat for several seconds and then re- sumed their beat at a gradually increasing rate (corresponding to Gaskell's " rhythm of development "). The experiments of Kent and His and their predecessors were con- firmed by Humblet, Hering, and Tawara, and led to the conclusion: 1. That the slow pulse of Adams-Stokes disease was due to dissocia- tion between the auricles and ventricles (heart-block) and the slow inde- pendent rhythm of the ventricles. 2. That the syncopal attacks (Adams-Stokes syndrome) were due to cessation of ventricular beat but not of the auricular beat. Experimentally they had produced the former but not the latter in mammals, while Gaskell had produced it in the frog and tortoise. Nor had pathological changes in the auricular ventricular bundle been shown in cases dying from the Adams-Stokes syndrome. The missing link was supplied by American scientists. Factors Affecting Degree of Heart=block. In 1904 E r 1 a n g e r began a series of experimental and clinical investigations upon this condi- tion. He first confirmed all of His's findings in man, and refuted Chauveau's claim, that the heart-block was due to the vagi, by showing that when in his cases the latter were paralyzed with atropine the heart-block did not pass off. 1 Then he devised a modification of Gaskell's clamp, an L-shaped hook of steel wire whose arm could be pressed against a brass block by means of a bolt and screw. The hook was introduced into the right wall of the aorta just above its origin (the pericardial fat having been dissected off), the point passed backwards and downwards into the left ventricle, and then pushed through the ventricular septum till it entered the 1 Kdes had previously shown that belladonna had no effect in his cases of Adams- Stokes disease. 558 DISEASES OF THE HEART AND AORTA. right ventricle (Fig. 271). The brass block was then pushed down over the long arm of the L and the nut gradually screwed taut. The first effect observed was lengthening of the conduction time (A S -V S or A-V interval); then alternate ventricular beats disappeared (2 : 1 rhythm), at first occasionally, then regularly. With further tightening of the clamp a 3 : 1 rhythm occurred, and finally complete heart-block. "After the ventricles have emptied themselves it may be seen that each contraction of the auricles sends into the former a distinct wave, upon the subsidence of which the volume of the ventricles is seen to have been considerably increased." In many but not in all of his experiments the com- plete block began with a complete stoppage of the ventricles, exactly like that in the Adams-Stokes syndrome, in which "the ventricles stop beating without warning. The auricles continue to beat with an apparently unaltered rate. .... The ventricles enlarge with each contraction until their distention becomes really huge Respiratory convulsions may begin. Witnesses are almost convinced that the experiment has come to a close when it may be that after more than twenty seconds the ventricles suddenly empty themselves with one great effort." This is sooner or later followed by another and another until the slow ven- tricular rate is gradually assumed. Factors Affecting Stoppage of the Ventricles. It is this " stoppage " of the ventricles which brings on the cerebral anaemia, syncopes, convul- sions, and death in man; but as long as the pulse remains regular, though slow, the circulation is maintained and the patients may remain quite free from symptoms. Erlanger and Hirschfelder found that stoppage of the ventricles was produced most frequently when the clamp was tightened suddenly, so that the stimuli from the auricles were cut off at once, especially when a certain degree of asphyxia was present. When partial block had once set in, tightening the clamp further usually produced complete block without stoppage; and when complete block had once been established stoppage of the ventricles during complete block was very rare, although in man it is relatively common. FIG. 271. The Erlanger heart-block clamp compressing the auriculoventricular bundle (.1 \~ B). S^f, septum mem- branaceum; MV, mitral valve. 1 : 1 damping Stoppage Undamped FIG. 272. Effect of gradually tightening the clamp. (After Erlanger and Tlirschfelder.) Shows 2 : 1 rhythm, finally stoppage of the ventricles with complete block. After this the ventricles can be seen to contract at an independent rhythm. The duration of stoppage of the ventricle seemed to depend largely upon the irritability and spontaneous rhythmicity of the ventricle, and varied greatly in different hearts; in some cases it was entirely absent or extremely short, whereas in one animal it lasted 55 seconds and death would then have resulted had not the heart been revived by mechanical stimulation. In HEART-BLOCK AND ADAMS-STOKES SYNDROME. 559 general, the tendency to stoppage seems to depend largely upon the condi- tion of the heart, and especially upon the degree of asphyxia. Whenever the rate of the auricles was increased from any cause (stimu- lation of the right accelerator, application of heat, or rhythmic induction shocks) the degree of block was also increased, a normal rhythm passing to a 2 : 1 rhythm, a 2 : 1 to a 4 : 1 or even complete block ; conversely, slowing the auricles by application of cold, etc., improved conductivity and caused the block to pass off. In this respect the experimental heart-block differs greatly from the clinical, since in a number of cases (Gibson, Thayer) it has been found that stimulation of the vagus increases the degree of block while atropine removes a partial but not a complete block. In other cases (Edes, Erlanger, Schmoll) it has no such effect. The duration of the period of " stoppage " (during which the ventricles remained quiescent) varied greatly, and was greatest in those hearts which could be inhibited longest by stimulation of the vagus. As in Gaskell's tortoise, it seemed to be definitely " correlated to the rhythmicity " of the ventricles, which is greater in some hearts and at some stages of the experi- ment than at others. In general it has appeared to the writer that the poorer the condition of the ventricular muscle the longer the period of stoppage. Slight asphyxia, though it did not in itself bring about stoppage of the ven- tricles, seemed to lengthen the period of stoppage from clamping. In some experiments the ventricle remained quiescent for so long (more than 55 seconds) that the animal would have died at once had not the heart been revived by mechanical stimulation. In a subsequent paper Erlanger has shown that the condition of block on clamping or injury depends upon the condition of the cells in the His bundle. Each cardiac impulse leaves them in a condition of lowered irrita- bility from which they recover gradually. When the injury is slight they recover just too late for the next impulse from the auricle and are only ready to receive the second stimulus (a 2 : 1 rhythm resulting). When they are injured a little more they recover in time for every third or every fourth impulse, and finally the stimulus always remains below the threshold of irritability and complete block sets in. Similarly, the more rapid the rhythm the less time the cells have had to recover and the less the intensity of impulse from the auricles, hence the greater the block. As regards the ventricle, the greater its irritability and rhythmicity the sooner it will respond to its own internal stimuli with a contraction and the shorter the stoppage and the more rapid the rhythm. A low ven- tricular rhythm (under 25 per minute) is therefore often a sign of poor con- dition of the ventricle and of a tendency to stoppage during the period of complete block in spontaneous attacks. The experiments of Erlanger and Hirschfelder have been confirmed by v. Tabora under Hering's direction. The latter has found that stimula- tion of the vagus may under certain circumstances increase the degree of heart-block and facilitate the onset of stoppage, especially when digi- talis has been administered. The apparent discrepancy between their findings is probably due to the presence of the different nerve-fibres in the vagus, so that sometimes conductivity, sometimes irritability is most affected. DISEASES OF THE HEART AND AORTA. Other Factors Affecting Heart=block. Mere cooling of the heart-muscle, as was shown by v. Kries upon the hearts of cold-blooded animals, is suffi- cient to bring on the various grades of heart-block. Florence Buchanan has found an example of this (2 : 1 rhythm) in hibernating dormice whose 'body temperature is much reduced. Asphyxial Heart=block. Heart-block very frequently comes on in dying animals, and may be brought on by the action of many poisons (digitalis, strophanthus, aconite, etc.), as well as by asphyxia alone. As Lewis, Oppen- heimer and Matthison have shown, heart-block from asphyxia is as inde- pendent of the central nervous system as is the block produced by clamping the bundle, and it is probable that this may be a factor to be reckoned with in many clinical conditions. Heart=block from Diminished Irritability of the Ventricular Muscle without Injury to the Auriculoventricular Bundle. When the auriculoven- tricular bundle is injured or its activity depressed by vagus stimulation, the conduction of the impulse from auricle to ventricle usually becomes slower and the conduction time (a c interval in the venous pulse, P-R interval upon the electrocardiogram) is prolonged. Occasionally, however, as in a case recently reported by A. M. Gossage, partial heart-block may be present without prolongation of the conduction time, and in such cases it is assumed that the auriculoventricular bundle is uninjured and conducts the impulse in the usual manner, but the irritability of the ventricular muscle is so much depressed that it fails to respond to all the impulses that reach it. Hirschfelder has shown that if the auricle of the dog is stimulated with weak rhythmic induction shocks at increasing rates they soon fail to respond to each stimulus and then respond to only alternate stimuli. Increasing the intensity of the stimulus or increasing the irritability of the heart muscle by pouring on warm salt solution, without changing the rate of stimulation, causes the auricles to respond to every stimulus. This condition simulates a " block " from loss of irritability, without loss of conductivity, and represents the condition of the ventricular muscle in the case reported by Gossage. Interaction of the Muscular and Nervous Elements in Heart=block. As can be seen from the studies of Chauveau on the one hand and His and Erlanger on the other, heart-block may be brought about either by over- action of the vagi, by injury to the muscle of the auriculoventricular bundle, or most probably by diminished irritability of the ventricular muscle. It is therefore not surprising to find that in most cases there is a summation of the effects of all three actions, though in very many of them the effect of one of them, either the vagus, the lesion of -the bundle, or the diminished irri- tability of the ventricular muscle, predominates. This is true for heart- block which results from the action of drugs or bacterial poisons, as well as from mechanical lesions. Thus, as in the case shown in Fig. 268, and in those reported by G. A. Gibson, Thayer and Peabody, and a number of other writers, it is common to find patients with lesions of the auriculoventricular bundle sufficient to impair its function a little, in whom direct or reflex stimulation of the vagus i- sufficient to bring on a partial heart-block which may be of a severe grade (3 : 1 or 4 : 1) but which is entirely removed by the administration of atropine. HEART-BLOCK AND ADAMS-STOKES SYNDROME. 561 Complete heart-block, as in the cases of Edes and Erlanger, is usually unaffected by the administration of atropine, because it is usually entirely organic in origin. Irregular Rhythm in Complete Block. Occasionally, as in two of the nineteen animals of Erlanger and Hirschfelder, the ventricular rate is irreg- ular, owing to the occurrence of ventricular extrasystoles which arise spon- taneously during the long diastoles. They are of no special significance, except in so far as they affect the rate of blood-flow. RELATION OF HEART-BLOCK TO ADAMS-STOKES SYNDROME. It cannot be too strongly emphasized that: (1) heart-block (complete) and Adams-Stokes syndrome are by no means synonymous; the former represents merely the dissociation of rhythms, while the Adams-Stokes syndrome brought on by cerebral anemia during ventricular stoppage is a totally different matter; (2) heart-block may persist for months or years without the occurrence of the syndrome, as in the case about to be described. FIG. 273. Tracing from jugular vein and carotid artery, in a case (J. L.) of complete heart-block after the syncopal attacks had subsided. Attacks of the Adams-Stokes syndrome may occur in three ways: (1) at the transition from normal rhythm to complete block; (2) in the midst of complete block; (3) probably also from stimulation of the vagus in certain cases where conductivity is already diminished. In the cases where the Adams-Stokes syndrome (ventricular stoppage) appears at the transition from normal rhythm to complete block, the attacks are usually preceded by quickening of the pulse; and the block passes off and reappears suddenly. When the complete block becomes permanently established, the Adams-Stokes syndrome may disappear, as is well shown by the following case, 1 seen by the writer in consultation with Dr. H. G. Beck. The Adams-Stokes syndrome may be present only in the initial and not the later stages of the heart-block. CASE OF HEART-BLOCK, WITH ADAMS-STOKES SYNDROME ONLY AT ONSET OF BLOCK. J. L., aged 72, had been perfectly healthy all his life except for attacks of malaria when between 14 and 40 years of age, and pneumonia about ten years ago. Denies syphilis and gonorrhoea; drinks little, but smokes considerably. Had been a blacksmith until July, 1907. At this time he was struck on the head by a railroad gate, became unconscious for one or two minutes, after which he recovered at once except for a slight transitory weakness of the right arm and slight transitory aphasia. He remained well until Novem- ber, 1907, pulse being 60 to 64. In the latter part of November he began to 1 A study of this case has been reported by Drs. H. G. Beck and W. R. Stokes, Arch. Int. Med., Chicago, 1908. 36 562 DISEASES OF THE HEART AND AORTA. have weak spells in which he fell but did not lose consciousness. He was seen by the writer on January 12, when he had been having numerous attacks for about a week. Patient was fairly nourished man of good rosy color, pupils reacting normally; no signs of intracranial disturbance or of lues. Chest clear. Heart not enlarged; action regular ; pulse-rate 33 per minute. Sounds accompanying the beats are loud and the first sound is accompanied by a flowing systolic murmur not transmitted to axilla. Second sound clear. Between these in the long pause there can be heard two or three very soft distant sounds like the ticking of a watch, accompanying which small undulations may be seen over the jugular vein, and on most delicate pal- pation of the radial a slight impulse can be felt there as well, due to the beating of the auricles against the root of the aorta. The venous tracing (Fig. 273) showed complete heart-block. At this time he had no attacks. On January 17, however, he was again seen. His attacks had been very numerous, the pulse-rate rising and falling with great rapidity. Tracings from the jugular vein and carotid arteries, taken as an attack came on, show the following sequence events: At first a period of com- plete heart-block lasting a few minutes. This then passed off and was succeeded by a few moments of2:lrhythm. The 2 : 1 rhythm passed suddenly into a 1 : 1 rhythm FIG. 274. Diagram representing the conditions found in the tracing Fig. 273. A, auricular contractions ; 1', ventricular contractions ; 1, 2, first and second heart sounds ; a, a, sounds due to contractions of the auricles. at a rate of about 90 per minute and began to quicken. It was then prophesied that an attack was imminent, and in an instant the ventricles suddenly ceased to beat. The patient cried out, became ashy pale, and a convulsion set in, during which the auricles continued to beat at the old rate. In about 11 seconds the ventricles began to beat, and soon resumed their regular independent rate of 28 to 30 per minute in complete block. After a few more seizures an hour or so passed without further change in rate or further symptoms. When seen in the afternoon and again on the next day the pulse-rate had not varied. It was then prophesied by the writer that no more attacks were imminent, but the patient was kept in bed for several weeks afterwards. A few weeks later he had a sinking spell with weakness of the pulse, but no change in rate and regularity and no unconsciousness or convulsions. This he also recovered from and remained free from symptoms and attacks until his death two months later. He died rather suddenly but was conscious to the last; his pulse- rate had not changed, and he died not from the Adams-Stokes syndrome but from his coronary sclerosis. The lesion found in the His bundle will be discussed below. In this patient the A d a in s - S t o k e s syndrome passed off as the complete block became established. Variations in Pulse=rate. This case is no isolated example of such a condition. Even Burnett's case (1824) furnishes an example, for he says, ' The pulse beats at the rate of 74 in the minute for the space of about a minute, then intermits for 7, 8, or 10 seconds In the evening I found that he had been attacked many times but was then much better He complained, however, of more pain about the precordia and his pulse beat only 20 in the minute." A similar tendency to improvement after heart-block set in has been noted in Stokes's first case (1846), in that of Alfred Webster (1900), in one of the cases reported by Edes (1901), and in one of Erlanger's cases (1905). HEART-BLOCK AND ADAMS-STOKES SYNDROME. 563 1 2 FIG. 275. Heart of a patient (J. L.) showing calcifications which produced Adams-Stokes disease. (Drawn from the specimen.) A, B, C, D, E. Sections through the: interventricular septum, showing the calcification pressing upon the auriculovcntricular bundle. (After Beck and Stokes.) F. Section through a. (Photomicrograph by Dr. C. S. Bond.) 564 DISEASES OF THE HEART AND AORTA. Stoppage of the Ventricles during Complete Heart=block. Unfortu- nately, the Adams-Stokes syndrome does not always end with the estab- lishment of permanent complete block. Just as in the two experiments of Erlanger and Hirschfelder mentioned above, stoppage of the ventricles sometimes occurs in the midst of a complete block when the pulse-rate is ii Fio. 276. Diagram showing the two types of ventricular stoppage producing the Adams-Stokes syndrome. 1. Ventricular stoppage only at the moment when conduction ceases. 2. Stoppage of the ventricles setting in during the periods of complete block. .4, auricular contractions; }', ventricular contractions; AV, conduction of impulses from auricles to ventricles. slow and without preliminary variations in rate. This took place in the case reported by His and in Erlanger's first case. The influences producing this stoppage act directly upon the ventricles, the auricular rate being unchanged or quickened, but the nature of these influences is not well understood. Erlanger has shown that the plugging of a coronary artery in animals does not bring stoppage from com- plete block. On the other hand, slight asphyxia, such as holding the breath after slight exercise, brought them on regularly. How- ever, it cannot be said that the prognosis is much if any more un- favorable in these than in the other group of cases, since Erlanger's case at least lived several years after observation, and this point has not been noted in most of the reported cases. Prof. Thayer has recently reported a case in which the block has passed off. INF. FIG. 277. Section of a luetic infiltration of the auriculoventricular bundle. (After Ashton Norris and Lavenson.) IXl 1 '., area of round-cell infiltration. LESIONS OF THE AURICULOVEN- TRICULAR BUNDLE. These two groups represent cases in which the block appears to be myogenic; and pathological evidence indicates that such is the case. Although Adams (1872) mentions fatty degeneration of the ventricular septum in his case, and many other autopsies had been performed, the first case in which a lesion of the auriculoventricular (or atrioventricular) muscle bundle was demonstrated was that of Luce in 1902 in which a sarcoma was found in- volving the auriculoventricular bundle. Luce, however, did not regard this as a causal factor for the Adams-Stokes syndrome, and the first case in which this connection was definitely established was reported by Stengel, of Philadelphia, HEART-BLOCK AND ADAMS-STOKES SYNDROME. 565 PLATE XIII. Electrocardiogram from a case of complete heart-block. The P waves, which correspond to the auricular contractions, bear no relation to the R waves of the ventricular systoles. There is also splitting of the P waves and fine tremor of the galvanometer string due to extraneous causes. Electrocardiogram from a case of auricular fibrillation with complete heart-block. (.Kindne.- Proi. Thayer.) 566 DISEASES OF THE HEART AND AORTA. in 1905, with excellent figures showing fibrosis of the bundle. Soon after this Schmoll reported a case in which no lesion could be discovered macroscopi- cally, but fibrosis of the His bundle was demonstrated with the microscope. In the case of J. L. reported above, autopsy showed extensive atheroma of the aorta; the coronary arteries were converted into pipes of bony hard- ness. Large calcifications were present upon the mitral valve and in the upper part of the interventricular septum, in which a long tongue of calci- fication can be seen to intercept the auriculoventricular bundle. This was beautifully shown in the sections which were made by Stokes under Retzer's direction, and thoroughly explain the clinical features observed. In the past two years a considerable number of cases have been studied both histologically and physiologically, lesions in the His bundle being uni- formly found. The following represent some of the lesions reported: Gumma, 7: Handford (1904), Keith and Miller (1906), Grunbaum (1906), Ashton, Norris, and Lavenson (1907), Heineke (1907), Fahr (1907), Rendu (1895). Calcined patches involving the bundle, 4: Stengel (1905), Hay and Moore (1906), Beck and Stokes (1908), Heineke, Muller, and Hoesslin (1908). Fibrosis of the bundle, 6: Schmoll (1906), Gibson, G. A. (1906), Fahr (1907), Gibson, A. G. (1908), Dock, G., Vaquez and Esmein. Tumors in the septum: Fibroma: Sendler (1892). Round-celled sarcoma: Luce. Anaemic infarction of the auriculo(atrio)ventricular bundle: Jellinek, Cooper, Ophiils (1906), MacCallum (1908). Simple round-celled infiltration of the auriculoventricular bundle, 1 : Heineke, Muller, and Hoesslin (1908). Mural ulceration involving the auriculoventricular bundle (ulcerative endocarditis): James (1908). Fatty degeneration: Butler (1907). Arteriosclerosis of artery supplying auriculoventricular bundle: D. Gerhardt (1908). Heart=block in Acute Infections and Intoxications. As can be seen from the above list, a considerable number of cases occur during the course of acute febrile diseases. Dunn, Fleming and Kennedy, F. W. Peabody and Tanaka have collected these cases and report the occurrence of heart-block and the Adams-Stokes syndrome in rheumatic fever, ulcerative endo= carditis, typhoid fever, pneumonia, diphtheria, as well as in the gonorrhoea! infection described by Jellinek, Cooper, and Ophiils. In all these cases the lesions were either ulcerative anaemic necrosis or fibrous degeneration of the His bundle. Tanaka finds that the lesions of the conducting system do not correspond to those in the rest of the heart muscle. In a few cases like that reported on page 569, heart-block and the Adams-Stokes syndrome occur during the course of some form of acute gastro-intestinal disturbance; and may then be transitory (Taylor) or subject to recurrences (case on page 569, also reported by Thayer and Peabody). Heart=block without Demonstrable Lesion in the Auriculoventricular Bun= die. In spite of the anatomical and physiological demonstrations showing the connection between lesions of the auriculoventricular bundle and heart-block, Heineke, Muller and Hosslin, and Krumbhaar have reported cases in whom ab- solute heart-block was present during life and yet no macroscopic or microscopic lesions could be found at autopsy in spite of the most careful examination. This absence of even microscopic lesion, however, does not prove that the function of the auriculoventricular bundle was undisturbed. In Krumb- haar's case there was very marked atherosclerosis of the coronary arteries, HEART-BLOCK AND ADAMS-STOKES SYNDROME. 567 and it seems not unlikely that there may have been some ischaemia of the auriculoventricular bundle which just sufficed to diminish conductivity. Experiments showing the ready production of heart=block by the action of various drugs and poisons and by asphyxia without the production of demon- strable lesions show how readily heart-block may be set up. And since it is not unusual to find death setting in from failure of the whole heart without the presence of demonstrable anatomical lesions, it need not be surprising if such lesions are sometimes absent during functional insufficiency of one part of the heart, the auriculoventricular bundle. CASES OF ADAMS-STOKES SYNDROME NOT DUE TO LESION OF THE AURICULOVENTRICULAR BUNDLE. Although the overwhelming majority of cases of the Adams-Stokes syndrome (persistent bradycardia, complete heart-block, and syncopal attacks) have been proved to be due to lesions of the auriculoventricular bundle, a few cases in the literature remain which must be regarded as due to over-stimulation of the vagus. The most typical of these attacks is described by Thanhoffer (1875). A colleague was compressing his own vagi in the neck, when suddenly he "stared at me with glassy eyes, without releasing his grip and without answering. I could remove his fingers from his throat only with the greatest force and they still remained clenched. Consciousness did not immediately return even after removing his fingers." Another case was reported by Neuberger and Edinger in 1898: The patient was a neurasthenic man, aged 46, who had been repeatedly examined by various physicians but no signs of organic nervous disease discovered. He suffered from severe constipation. From Xov., 1896, to January, 1897, he occasionally fainted when at stool. His pulse dur- ing that period was usually 60 between attacks. On January 1, 1897, he fell in a faint while having a desire to go to stool; his head and eyes were drawn to the left and the eyes twitched. During that day he had several similar attacks, before each of which the pulse disappeared, returning during the attack to a rate of 16 to 18 per minute. By evening the rate had returned to 60. He died in one of these attacks on January 8. Autopsy, per- formed by Carl Weigert, showed almost complete atrophy of the right half of the cere- bellum and a varicose dilatation of the ependymal vessels in the medulla. It is probable that at stool or during effort the pressure in these varices rose and caused them to compress the medulla near the vagus nucleus. In spite of a very careful search by Weigert, no myo- cardial lesion could be found. It is, therefore, fair to assume that in this case the attacks and the probably existing heart -block were vagal in origin. Dr. Walter James also reported a case in which recurrent groups of ineffectual extra- systoles caused the circulation to become so slow at times as to produce syncopal attacks. A somewhat similar case was that of Holberton (1. c.) (1841), in which the attacks dated from a fall from a horse, and no myocardial lesion was found. On the other hand, our case (page 589) illustrates the need of caution in reaching this conclusion, since there the attacks dated from a blow upon the head, and yet autopsy proved the presence of a most typical lesion of the auriculoventricular bundle. Since these lesions may be micro- scopic (Schmoll, Gerhardt), it is evident that a neurogenic origin of the syndrome can be diagnosed only when the bundle has been examined by serial sections. The writer has also seen in consultation a case of complete heart-block associated with a tumor along the course of the vagus. Since it requires a very considerable lesion to produce the neurogenic syndrome, and since death occurs from the latter cause as well as from the syndrome, the prognosis is no better in these cases than in the myogenic, except in cases where the causal factor (tumor, etc.) may be removed by operation or by treatment. However, it must be added that even with 568 DISEASES OF THE HEART AND AORTA. the most liberal interpretation neurogenic cases are relatively rare, and the presence of the Adams-Stokes syndrome may in most cases be regarded as prima facie evidence of a lesion of the auriculoventricular bundle. Atropine Test. The origin of the block in these cases can be readily demonstrated by paralyzing the vagi by the administration of atropine, 1 mg. ( V gr.), which causes the block to pass off in the neurogenic cases and the pulse-rate to become rapid, but does not affect it in the myogenic. In most cases of the typical Adams-Stokes disease (Edes, Erlanger, Schmoll), atropine does not affect the rate, and the organic nature is further proved. In our own two rather exceptional cases the atropine test was, unfortunately, not permitted. Gibson and Ritchie have reported a most interesting case in which both neurogenic and myogenic factors seemed to be at work, since the complete block disappeared promptly upon giving atropine and reappeared an hour later when the effect had worn off. However, conductivity was always diminished (conduction time, a-c interval, being 0.6 second instead of 0.2) even when the vagi were paralyzed, so that the auriculo(atrio) ventricular bundle was probably injured as well. Professor Thayer and Dr. F. W. Peabody have found that atropine caused the partial block (4 : 1 rhythm) to pass off, but had no effect when the block was complete. This observation harmonizes well with the other experimental and clinical evidence regarding complete and partial blocks. CONTRIBUTING FACTORS. The Adams-Stokes syndrome is more common in men (84 per cent, of Ecles's cases), of which 48 per cent, occurred between the ages of 50 and 70. This, as well as the autopsy series mentioned above, establishes the importance of coronary sclerosis as an etiological factor. It is quite striking that in two cases of this small series (that of Cooper, Jellinek, and Ophiils and one of those mentioned by Dietrich Gerhardt) gonorrhceal infection was the etiological factor. Mackenzie describes cases of partial heart-block (2 : 1 rhythm) as a result of influenza and pneumonia, and the writer has seen a similar depression of conductivity during the course of the latter. Powers has reported a case with partial halving of the rate after pneumonia. Saigo has found extensive vacuolization, fatty and parenchymatous degen- eration, and cellular infiltration in the Purkinje fibres of the conduction system following acute rheumatism and other diseases. These were especially marked in the left branch of the auriculoventricular bundle. The importance of infectious diseases as directly causal factors is further shown by the case of Butler, in which the bradycardia dated from an attack of typhoid fever, and also in Dunn's case, in which a radial pulse (18 per minute) and typical Adams-Stokes syndrome occurred in a boy of 1 1 on the ninth day of diphtheria. There can be no doubt that many of the sudden deaths from pneumonia and diphtheria are due to heart-block. Cardiac overstrain may also be a factor, as in the case of a boy of 15 reported by Striibing, who when otherwise healthy ran a considerable dis- tance, fainted, then walked home, and had several other syncopal attacks with convulsions. His heart was enlarged, and the pulse 16 to 18 per minute. Rest and proper treatment brought some improvement, and his pulse finally rose to 44, but he died soon afterwards. HEART-BLOCK AND ADAMS-STOKES SYNDROME. 569 It is possible that ptomaine poisoning or autointoxication due to severe gastro-intestinal upset may give rise to the syndrome. CASE OF ADAMS-STOKES DISEASE WITH SUBSIDENCE AND RECURRENCE OF SYMPTOMS, AND WITH ATTACKS DURING COMPLETE BLOCK. Recently the writer, with Professor Thayer and Dr. H. M. Thomas, examined a gentleman who had lately suffered from a severe acute gastro-enteritis with vomiting and severe diarrhrea lasting several days. During this time he had fainted several times while at stool, and his physician found him with a pulse-rate of 20 per minute. With the improvement in digestion this bradycardia passed off within a few days, and he had no further syncopal attacks. When examined ten days later his pulse-rate was 60, increasing normally upon slight exercise. There was no sign of heart-block, and conduction time (a-c interval) was normal (0.2 second). No signs of nervous disturb- ance were present. After a few weeks of good health the fainting spells and bradycardia returned, and lasted for several months. Prof. Thayer informs the writer that during this period the rhythm varied from 1:1 to 2:1, and 4:1, returning to normal rate when atropine was administered. Syncopal attacks also occurred frequently in the midst of complete heart-block, and during the periods of complete heart-block the rate was very slow and irregular. In complete block the rate was unaffected by atropine. After some months conductivity gradually returned, and at the time of writing the patient has remained quite well and has had a normal pulse- rate for several months. The presence of a hemorrhage in the auriculoventricular bundle or its vicinity (apoplexy of the bundle) would ac- count for the occurrence and the subsidence of these symp- toms. An infiltration or fatty degeneration of the bundle might account for the occur- rence and subsidence of the first attack, but scarcely for the sudden recurrence during a period in which the patient had been in excellent health. Prentiss also mentions a case brought on by heavy lifting, in which either hemorrhage or myocardial degeneration may have been the cause. Partial heart-block has been reported from overdoses of digitalis (Mackenzie, Hewlett, A. G. Gibson) (page 237), but these have never given rise to complete block or Adams-Stokes syndrome. Heart=block with Auricular Fibrillation (Essential Bradycardia). A certain number of cases have been reported in which the ventricular rate is as slow as in the ordinary form of Adams-Stokes disease. The venous pulse is of the " single " ventricular or " positive " type and no regular " A " wave can be discerned upon it. Mackenzie formerly believed that in these cases the auricles and ventricles were beating simultaneously, but studies with the electrocardiograph, by Thomas Lewis and by Thayer, have shown that, on the contrary, the auricles were fibrillating, but their impulses were prevented from reaching the ventricles by an auriculoventricular block. As very many of the impulses from the fibrillating auricle are smaller than normal, a relatively slight injury to the bundle will prevent them from passing, especially if the effect of this is enhanced by the effect of digitalis. Indeed, the bradycardia which is produced intentionally in the thera- peutic administration of digitalis for auricular fibrillation represents a partial blocking of the impulses between the auricles and the ventricles. This therapeutic bradycardia differs from the essential bradycardia not only in the fact that the latter is spontaneous, but particularly because in the latter the auriculoventricular block remains complete, and the ventricular impulses arise in the ventricle or the Purkinje fi'bres below the auriculoventricular 570 DISEASES OF THE HEART AND AORTA. bundle. In these cases, as in the ordinary cases of heart-block, the important consideration is the maintenance of a sufficient blood flow through the walls of the heart and brain; this, in the last analysis, depends upon keeping up the pulse-rate and the blood-pressure. The indications for treatment in this condition are exactly the same as in the ordinary forms of Adams-Stokes disease and will be discussed as such. Heart=block with a Very Rapid Ventricular Rate. Hewlett and Bar- ringer and J. D. Windle have reported cases in which, in spite of complete block, the rate of the ventricle was beating with an extremely rapid inde- pendent rhythm. Hewlett and Barringer have shown that this may be brought on in certain cases by the administration of digitalis, although in other cases it probably arises spontaneously. In their case in which the ventricular rate reached 120 per minute in spite of complete block the rapid rate may have represented the toxic stage of digitalis action ; while in Windle's case of idiopathic heart-block the ventricular rate ranged between 50 and 60 per minute, about double the usual ventricular rate in complete block. PHYSICAL SIGNS AND DIAGNOSIS. As the Adams-Stokes syndrome may occur in cases having valvular lesions, the physical signs over the heart may vary, and all forms of mur- murs and of cardiac insufficiency may occur. Those which are character- istic of the condition, as observed by Stokes and Chauveau, are the very slow pulse disappearing entirely before the onset of the attack; the presence of small visible pulsations in the jugulars, of more than double the number of the pulse in the carotids, with the small jugular pulsations and occurring at a regular rhythm which is more rapid than that of the ventricles; a faint sound like the ticking of a watch may often be heard near the left sternal margin, i.e., the right auricle; and a slight pulsation or shock may at the same time be seen or felt over the apex. On. barely touching the radial a faint shock of the same rhythm may also be felt in the radial pulse. This corresponds to the small auricular wavelets upon the pulse, which, as Frangois-Franck has shown, are due to the beating of the auricles against the root of the aorta. All these signs may usually be made out in cases of heart -block, and the diagnosis should therefore be made by any clinician in the ordinary physical examination, though to tell partial from complete block is rarely possible. In X-ray examination the independent contraction of the auricles may be readily seen (Deneke), and this of course settles the diagnosis. Similarly G. A. Gibson and Einthoven, as well as Pick and Barker, Bond, and the writer, have demonstrated heart-block by the electrocardiogram. The usual and the most satisfactory method of diagnosis is by comparison of the venous pulse tracing with that from the carotid artery or the apex, by which means the exact relation of auricular to ventricular contraction, the degree of block, and the variations of conductivity arc readily shown. Difficulties in diagnosis may occur from the following causes: 1. The pulse-rate may be so slow that heart-block may be suspected. This occurs especially in old persons, in athletes when at rest, and in con- valescents from infectious diseases. For the absolute exclusion of heart- block a venous tracing may be necessary, in which the absence of a wave midway between the normal a waves excludes the presence of a heart-block. HEART-BLOCK AND ADAMS-STOKES SYNDROME. 571 The writer has seen a number of cases whose pulse-rate was 44 to 48 per minute with no sign of heart-block on the venous tracing. (Figs. 48 and 106.) 2. The early diastolic wave (h wave of Hirschfelder, b wave of Gibson) may sometimes occur midway between auricular waves, and may thus simu- late a 2 : 1 rhythm. Moreover, the "third heart sound" is usually present in these cases, and may easily be taken for the sound of auricular contraction. The presence of the h wave may be differentiated from that of partial block by increasing the heart-rate, by rapid respiration, mild exercise, etc., upon which the h wave is no longer found midway between a waves, but maintains its old interval from the v wave and approaches the second a, whereas in partial heart-block it would maintain the mid-position. This point is of great im- portance, since the presence of heart-block is a grave sign, and it should not be diagnosed without due care. The writer has seen a number of cases in w r hich heart-block might have been diagnosed had this precaution not been exercised, as for example the patient whose phlebogram is shown in Fig. 106. Slow pulse of vagal origin may also occur in brain tumor, fracture of the skull, meningitis, etc., and, especially in the first, may be accompanied by syncopal attacks. In these cases there is rarely any degree of heart-block between attacks, and the site of the cardiac disturbance can readily be deter- mined by its disappearance after the administration of atropine. A slow pulse with occasional attacks of vertigo may also occur as the result of extrasystoles too weak to open the aortic valves, and thus give rise to a rhythm which is too slow to nourish the brain (W. James and Norris), and a true Adams-Stokes syndrome arises without heart-block. The diag- nosis is, however, readily made on auscultation, from the fact that between effective beats a single loud sound is heard (whole rhythm being lub club 1 121 lub, pause, lub dub lub) and not the feeble tickling auricular sound of auricular contractions. The venous pulse and electrocardiogram char- acteristic of extrasystoles (see page 109) establish the diagnosis. In occasional cases, paroxysms of tachycardia are accompanied by fainting spells, the pulse between attacks being quite normal or even very slow. CASE OF PAROXYSMAL TACHYCARDIA SUGGESTING ADAMS-STOKES DISEASE. A few years ago the writer examined such a case in consultation with Professor Barker and Dr. I. P. Lyon of Buffalo. The patient was a man past middle age, had a pulse-rate of GO, and had been subject to attacks of palpitation with fainting spells. The case had been seen by several specialists in various cities, who had diagnosed it Adams-Stokes syndrome. Physical examination was negative except for a slight grade of arteriosclerosis. Tracings of the venous pulse, however, showed conductivity to be normal (a-c interval 0.2 second), and this continued to be the case even when, upon exercise, the pulse-rate rose to 120 per minute without dropping a beat. The Adams-Stokes syndrome was thus excluded. From the sudden onset and the fainting spells during the attacks, it was con- cluded that the condition was most probably paroxysmal tachycardia. The patient was subsequently seen in a typical attack, with sudden approximate doubling and sudden halving of the rate, and the diagnosis was thus verified. Dr. Lyon informs the writer that the patient is much improved and has now only mild attacks of tachycardia. CASE or HEART-BLOCK OF LONG DTHATIOX. In 1910 the writer, in consultation with Prof. L. F. Barker, examined a gentleman over sixty years of age, whose pulse-rate was from 30 to 35 per minute, in whom venous pulse and electrocardiogram showed a complete heart -block. From the accounts of his 572 DISEASES OF THE HEART AND AORTA. family his pulse had maintained this rate for at least thirty-five years, during which, to the great alarm of his physicians, he had led an active life free from symptoms of cardiac weakness, and devoid of cardiac symptoms until a few extrasystoles with palpitation appeared a few years ago. These extrasystoles produced no ill effects on the circulation, and at last accounts he was maintaining perfect health. Extrasystoles Simulating Heart=block. Walter James and also Norris have reported cases of typical syncope with a slow pulse at the wrist, due to the occurrence of ineffectual extrasystoles (see page 114). When early extrasystoles occurred which were often too feeble even to open the aortic valves (ineffectual extrasystoles), these did not play any role in driving on the blood. The circulation of the blood through the body in such cases is accordingly maintained entirely by the regular forcible heart-beats, and in a person with an already slow circulation these beats become separated by such long compensatory pauses that cerebral anaemia and Adams-Stokes syndrome set in, although the venous pulse or the cardiogram shows that the ventricle is beating during the whole period. There may occasionally be difficulty in differentiating the Adams- Stokes syndrome from epilepsy and brain tumor. Heart-block is, however, never present in the former, very rarely in the latter; so that the diagnosis can usually be made from simple inspection of the jugular vein. If necessary, venous tracings, supplemented by the atropine test, may be resorted to. PROGNOSIS. The course of cases suffering from the Adams=Stokes syndrome is very variable. It is probable that many cases die in the first attack, but the condition remains undiagnosed or is ascribed to coronary sclerosis. It is not unlikely that histological examinations of many cases of sudden death would reveal lesions in the bundle of His or its artery. In some cases death occurs within a few weeks or months after the first attack, but in very many the heart-block may last for many years, with or without disappearance of the syncopal attacks. Many cases of Edes's series lived seven or eight years after the first attack. Osier's case lived thirty, our patient has lived thirty-six years after the onset of bradycardia. It is stated that the pulse-rate of Julius Caesar and of Napoleon were abnormally slow (Napoleon's being sometimes 40, but at Elba 50 to 55), and that the epilepsy of the latter was a sign of the Adams-Stokes syndrome, but this is not proved. However, it is certain that the presence of com- plete heart-block is compatible with ability to do a considerable amount of work. Vigouroux had under observation a laborer with complete heart- block who during five years did hard work, driving a cart with six oxen in the hottest weather. His heart always beat at a rate of 20. Dr. Archibald Hewan was able to climb a mountain several thousand feet high when his pulse ranged from 32 to 40 and never rose above the latter. Most of the cases die in the attacks (Etles), but death from coronary sclerosis without Adams-Stokes syndrome, as in our case, is not uncommon. Gerhardt has recently reported three cases in which not only the syncopal attacks but also the heart-block completely disappeared, owing to subsidence of the pathological process in the auriculoventricular bundle which was not totally destroyed. Prof. Thayer's case, quoted above, probably belongs to this group. HEART-BLOCK AND ADAMS-STOKES SYNDROME. 573 TREATMENT OF HEART-BLOCK AND THE ADAMS-STOKES DISEASE. The problem of the treatment of Adams-Stokes disease presents several distinct phases and aims. 1. To bring about retrogression of the lesion to the bundle. 2. To remove as many factors as possible which tend to increase the block. 3. To increase the irritability and rhythmicity of the ventricular muscle, so as to shorten the periods of stoppage and to increase the rate of the ventricles. Retrogression of the lesion in the bundle can be brought about by medi- cation only in the cases of syphilitic origin, in which the gummata and luetic infiltrations may sometimes be made to subside under vigorous treatment with iodides and inunctions of mercury. Sodium or potassium iodide should be given in doses gradually increasing up to 4 Gm. (3i) or more three times a day, and these along with mercury should be kept for long periods and re- sumed at frequent intervals. In a considerable number of cases, as in those reported by Schmaltz and by Erlanger, subsidence of the lesion may be accomplished and the heart-rate restored to normal. In these cases Ehrlich's salvarsan (" 606 ") would be very desirable if it could be administered, but in its present mode of administration it is too dangerous to use. In non-luetic lesions, medication is of little use, but it is important to put the patient at complete rest for as long a period as practicable, in the hope that by reducing the strain upon the heart as far as possible cedema, infiltration, and hemorrhages may be gradually absorbed or at least may suffer no further increase. In the cases in which the lesion itself cannot be caused to subside, espe- cially in cases in which the block is a partial one, it may be possible to bring about an improvement which is sometimes temporary and which may some- times last for several weeks or even months by the administration of atropine (Gibson and Ritchie, Thayer and Peabody). This removes the effect of tonic action of the vagus. In patients in whom the heart-block is due to a combination of a vagal and a muscular element, a double vicious circle is operating: Vagal block / / Muscular / block / / \ Asphyxia of Slowing the heart < of the muscle circulation The administration of atropine, by removing the vagal block and increas- ing the velocity of the circulation, also improves the nutrition of the auric- uloventricular bundle and may do so to an extent that permits it to regain its function. In patients in which the block is due entirely to the muscular lesion, however, as Erlanger and Hirschfelder have shown, the degree of block is entirely unaffected by atropine or may even be increased somewhat by the increase in the pulse-rate. In the cases of partial heart-block digitalis is usually either without effect or positively harmful, since, as v. Tabora has shown, it diminishes the 574 DISEASES OF THE HEART AND AORTA. conductivity of the auriculoventricular bundle, although this effect is some- what lessened by the administration of atropine. On the other hand, the duration of ventricular stoppage brought on by clamping the bundle with an Erlanger clamp is greatly diminished by digi- talis, as v. Tabora has shown. Other drugs seem to have little effect in influ- encing the duration of stoppage and the onset of syncope. August Hoffmann reports a case in which inhalations of oxygen afforded distinct relief, and this measure is worthy of trial in every case. In most cases little benefit need be expected, for during the cessation of the pulse the blood does not circulate from the lungs to the brain. Peculiar postures sometimes help in warding off syncopal attacks by improving the blood through the brain until the ventricular rhythm has become established. Stokes (1846) writes that his patient " had two threaten- ings of fits since his admission, and warded both off by a peculiar manoeuvre: as soon as he perceives symptoms of the approaching attack he directly turns on his hands and knees, keeping his head low, and by this means he says he often averts what otherwise would end in an attack." This was the patient's physiological therapy to prevent cerebral anaemia. Another patient has been reported who made use of a similar procedure by lying on the floor and rais- ing his legs upon the arms of a chair, by which he obtained still better filling of the cerebral vessels. After the complete block has once been established, the patient is still beset with three dangers: 1. The circulation under the regular ventricular rhythm may be too slow to nourish the brain and the tissues, including the heart itself, and the patient may thus be kept a bedridden invalid or may even die as the result. 2. The ventricular rate may become irregular, through the appearance of ventricular extrasystoles and even of periods of stoppage during complete heart-Mock, exactly similar to those occurring at the onset of the block, and syncope or death may occur, as in the latter. 3. The block may pass off spontaneously, the rate and rhythm become normal, but the condition become so unstable that the patient's life becomes constantly endangered by the possible onset of heart-block, stoppage, and the Adams-Stokes syndrome. Though no drug is specific for these conditions, v. Tabora and also Erlanger have shown that digitalis increases the ventricular rate in experi- mental complete block, and Bachmann found that the rate of a ventricle of a patient with the Adams-Stokes syndrome was accelerated during com- plete heart -block and the patient's condition somewhat improved. Hewlett and Barringer and others have confirmed these observations, and it appears certain that more or less acceleration of the independently beating ventricles may he obtained with drugs of the digitalis series. (See page 570.) This acceleration of rate, as long as it is not accompanied by weakening of the heart-heat . is a thing to he desired, hut it must not be forgotten that acceleration of the ventricles may appear during the last stages of digitalis poisoning, and therefore the mere acceleration of the ventricular rate does not necessarily indicate an improvement in the circulation. Similarly, the maximal blood-pressure may fall either from better nutrition of the vaso- motor centre in. the medulla or from the fact that with the increasing pulse- HEART-BLOCK AND ADAMS-STOKES SYNDROME. 575 rate the pulse-pressure for each beat is diminished. The best index is, there- fore, the general condition of the patient, his ease of respiration, clearness of mind, and bodily activity. Drugs of the digitalis series, therefore, are contraindicated in partial heart-block, but should be used as soon as the block has become complete. Other drugs seem to be entirely without effect: caffeine, theobromine, strychnine, and amyl nitrite have all been used by certain writers, but with- out special benefit to the patient, and the writer has been unable to find any effect from them upon the ventricular rate in complete heart-block in dogs. Ammonium carbonate has not been extensively employed, although Burnett claimed to have been able to abort attacks hi his patients by its use. BIBLIOGRAPHY. HEART-BLOCK AND THE ADAMS-STOKES SYNDROME. Adams, Robert: Cases of Disease of the Heart, Dubl. Hosp. Rep., 1827, iv, 448. Burnett, Wm.: Case of Epilepsy Attended with Remarkable Slowness of the Pulse, Trans. Med. Chir. Soc., Lond., 1827, xiii, 202. Morgagni: De sedibus et causis morborum, Venet.. 1761. Holberton, T. H.: A Case of Slow Pulse with Fainting Fits, Trans. Med. Chir. Soc., Lond., 1841, xxiv, 76. Pletnew, D.: Das Morgagni-Adams-Stokes'sche Symptomenkomplex, Ergebn. d. innere Med. u. Kinderhk., Berl., 1908, i. Stokes, Wm.: Observations on some Cases of Permanently Slow Pulse, Dublin Quart. J. M. Sci.. 1846. ii. 73. Diseases of the Heart and Aorta, Philad., 18-54, p. 305. Chauveau. A.: De la dissociation du rhythme auriculaire et du rhythme ventriculaire, Rev. de Med.. Par., 1885. v, 161. whose observations on the same case appeared earlier in the thesis of Figuet, Etude du rhythme couple du co3ur, Lyon. 1882. Wooldridge. L.: Ueber die Funktion der Kammernerven cles Saugethierherzens, Arch. f. Physiol., Leipz., 1883, 522. Tigerstedt, R.: ibid., 1884. Gaskell. \V. H.: On the Rhythm of the Heart of the Frog and the Nature of the Action of the Vagus Xerve, Phil. Trans.. Lond.. 1882. 993. On the Innervation of the Heart, with Especial Reference to the Heart of the Tortoise, J. Physiol., Camb. and Lond., 1883, iv, 43. The Meaning of the Heart-beat, Schaefer's Text-book of Physiol., Edinb. and Lond.. 1900. ii. 169. Paladino, G.: Contribuzione all'anatomia istologia e fisiologia del cuore. II rnovimento medico-chirurgico. Naples. 1876: Une question de priorite sur les rapport.- innmes entre la musculature des oreillettes et celle des ventricules du ca-ur. Arch. ital. de biol., Pisa. 1910. liii. 47. Kent, A. F. Stanley: Researches on the Structure and Functions of the Mammalian Heart. J. Physiol.. Camb. and Lonipz. 1904. 1. Some Results of Recent Investigations on the Mammalian H-ar. Ar.at. Rec.. Phila., 1908. ii. 149. Humblet. M.: Allorhythmie cardiaque par section du faiiceau de His. Arch, in: -.-mat. de Physiol.. Liege et Par.. 1905-0. iii. 330. Herinc. H. E.: His'sche Ueberangsbundel, imniiuelbare Wirkunii der Ac'^-Ic-rans und Vagus. Arch. l. d. ges. Physiol.. Bonn. 1905. cviii. 207. Tawara. S.: Das reizleitende System des Saueethk-r-hvrzvns. Jena. 1900. Erlantrer. J.: Zcntralbl. f. Physiol.. Lv:;.z. u. Wien. 1905, six. A Report . vat ions on Heart-block in Mammals. Bull. Johns Hopkins H-sp.. Bui-., xvi. Cn the Physiology of Heart -block in Mammals, with Especial R-ferenot Adams-Stokes Disease. J. Exp. Mod.. N. Y-. 1905. vi:: 19CK3. viii. F^rth-r S:udies 576 DISEASES OF THE HEART AND AORTA. on the Physiology of Heart-block. Effect of Extrasystoles upon the Dog's Heart and upon Strips of Terrapin's Ventricle in the Different Stages of Block, Am. J. Physiol., Bost., 1906, xvi, 161. Recent Contributions to the Physiology of the Circulation, J. Am. M. Asso., Chicago, 1906. Irregularities of the Heart Resulting from Dis- turbed Conductivity, Am. J. M. Sc., Phila. and N. Y., 1908. Erlanger, J., and Hirschfelder, A. D.: Eine vorlaufige Mittheilung ueber weitere Studien in bezug auf den Herzblock in Saugetieren, Zentralbl. f. Physiol., Leipz. u. Wien, 1905, xix, 270. Further Studies on the Physiology of Heart-block in Mammals, Am. J. Physiol., Bost., 1906, xv, 153. Erlanger, J., Blackman, J. R., and Cullen, E. K.: Further Studies on the Physiology of Heart-block in Mammals, ibid., 1908, xxi, p. xviii. v. Kries, J. : Ueber eine Art polyrhythmischer Herzthatigkeit, Arch. f. Physiol., Leipz., 1902, 477. Buchanan, F.: The Frequency of the Heart-beat in the Sleeping and Waking Dormouse, J. Physiol., Camb., 1910, xl, Proc. Physiol. Soc., p. xlii. Lewis, T., and Oppenheimer, B. S.: The Influence of Certain Factors upon Asphyxial Heart-block, Quart. J. M., Oxford, 1911, iv, 145. Lewis, T., and Mathison, G. C. : Auriculoventricular Heart-block as a Result of Asphyxia, Heart, Lond., 1911, ii, 47. Gossage, A. M.: Independent Ventricular Rhythm, Heart-block and the Adams-Stokes Syndrome without Affection of the Conductivity, Heart, Lond., 1909-1910, i, 283. Gibson, G. A.: Certain Clinical Features of Heart Disease, Johns Hopkins Hosp. Bull., Bait., 1908, xix, 361. Dunn, A. L. : Atrioventricular Dissociation following Diphtheria, J. Am. M. Asso., Chicago, 1908, 1, 1985. Luce, H.: Zur Klinik und Pathologische Anatomic des Adams-Stokes'schen Symptomen- complexus, Deutsch. Arch. f. klin. Med., Leipz., 1902, Ixxiv, 370. Stengel, A.: Fatal Case of Stokes-Adams Disease, with Autopsy, Am. J. M. Sc., Phila., 1905, cxxx, 1083. Schmoll, E.: Adams-Stokes Disease, J. Am. M. Asso., Chicago, xlvi, 361. Zwei Fiille von Adams-Stokes'scher Krankheit mit Dissoziation von Vorhof und Kammerrhyth- mus und Lasion des His'schen Biindels, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxvii, 554. Handford: Brit. M. J., Lond., 1904, ii, 1745. Keith, A., and Miller, C.: Lancet, Lond., 1906, ii, 1429. Griinbaum, also reported by Keith and Flack (1. c.). Ashton, T. G., Xorris, G. W., and Lavenson, R. S.: Adams-Stokes Disease (Heart-block) due to a Gumma in the Interventricular Septum, Am. J. M. Sci., Phila. and N. Y., 1907, cxxxii, 28. Heineke : Drei Falle von Adams-Stokes'scher Krankheit, Berl. klin. Wchnschr., 1907, xliv, 1 125. Fahr: Ueber die muskularc Verbindung zwischen Vorhof und Ventrikel (das His'sche Biindel) im normalen Herzen und beim Adams-Stokes'schen Symptomenkomplex, Arch. f. path. Anat., etc., Ber., 1907, clxxxviii, 562. Rendu: Soc. med. d. hop., 1895. Quoted from James, W. B.: Am. J. M. Sci., Phila. and N. Y., 1908, cxxxvi, 469. Hay, J., and Moore, S. A.: Stokes-Adams Disease and Cardiac Arrhythmia, Lancet, Lond., 1906, ii, 1271. Gibson, G. A.: Heart-block, Brit. M. J., Lond., 1906, ii, 1113. Gibson, A. G.: The Heart in a Case of Stokes-Adams Disease, Quart. J. M. Sci., Oxford, 1908, i, 183. Vaquez and Esmein: Presse med., 1907, xv, 57. Sendler: Beitrag zur Frage ueber Bradycardie, Centralbl. f. innere Med., Leipz., 1892, xiii, 042. Jcllinck, Cooper, Ophiils: The Adams-Stokes Syndrome and the Bundle of His, J. Am. M. Asso., Chicago, 1906, xlviii, 955. MacCallum, W. G.: Stokes-Adams Disease with Infarction. Read before the Johns Hop- kins Medical Society, Nov. 4, 1907. Heineke, A., Miiller, A., and v. Hoesslin, A.: Zur Kasuistik des Adams-Stokes'schen Symp- tomenkomplexes und der Ueberleitungsstorungcn, Deutsch. Arch. f. klin. Med., Leipz., 1008, xciii, 459. HEART-BLOCK AND ADAMS-STOKES SYNDROME. 577 James, W. B.: A Clinical Study of some Arrhythmias of the Heart, Am. J. M. Sci., Phila. and N. Y., 1908, cxxxvi, 469. Norris, G. W.: Extrasystolic Arrhythmia Simulating Heart-block, Univ. Penn. M. Bull., Phila., 1910, xxii, 342. Butler, G. R.: Heart-block (Adams-Stokes Disease), Am. J. M. Sci., Phila. and N. Y., 1907, cxxxiii, 715. Gerhardt, D.: Ueber Ruckbildung des Adams-Stokes'schen Symptomenkomplexes, Deutsch. Arch. f. klin. Med., Leipz., 1908, xliii, 485. Edes, R. T. : Slow Pulse, with Especial Reference to Stokes- Adams Disease, Trans. Asso. Am. Phys., Phila., 1901, xvi, 521. Thanhoffer: Centralbl. f. d. med. Wissensch., 1875, 405. Quoted from His. Fleming, G. B., and Kennedy, A. M.: A Case of Complete Heart-block, with an Account of Post-mortem Findings, Heart, Lond., 1910-11, ii, 77. Peabody, F. W.: Heart-block Associated with Infectious Diseases, Arch. Int. Med., Chicago, 1910, v, 252. Taylor, F. L. : A Case of Transient Heart-block due to Intestinal Toxaemia, J. Am. M. Assoc., 1708, i, 1246. Thayer, W. S., and Peabody, F. W.: A Study of Two Cases of Adams-Stokes Syndrome with Heart-block, Arch. Int. Med., Chicago, 1911, vii, 289. Tanaka, T.: Ueber die Veranderungen der Herzmuskulatur vor allem des Atrioventricu- larbiindel bei Diphtheric, Arch. f. path. Anat., etc., Berl., 1912, ccvii, 115. Krumbhaar, E. B.: Adams-Stokes Syndrome with Complete Heart-block without Destruc- tion of the Bundle of His, Arch. Int. Med., Chicago, 1910, v, 583. Neuburger, Th., and Edinger, L.: Einseitiger fast totaler Mangel des Cerebellums, Varix oblongatse Herztod durch Accessoriusreizung, Berl. klin. Wchnschr., 1898, xxxv, 69. Gibson, G. A., and Ritchie, W. T.: Further Observations on Heart-block, Practitioner, Lond., 1907, i, 587. Mackenzie, James: Xew Methods of Studying the Affections of the Heart, Brit. M. J., 1905, i, 519, 587, 702, 759, 812. Saigo, Y.: Die Purkinjeschen Muskel fasern bei Erkrankungen des Myokards, Verh. d. Deutsch. path. Ges., Jena, 1908, xii, 165. Dunn, A. D. : Atrioventricular Dissociation following Diphtheria, J. Am. M. Asso., Chicago, 1908, 1, 1985. Strubing: Deutsch. med. Wochnsch., Leipz., 1893. Quoted from Edes. Hewlett, A. W.: Digitalis Heart-block, J. Am. M. Asso., Chicago, 1907, xlviii, 47. Gibson, A. G.: The Action of Digitalis on the Human Heart, Quart. J. M. Sc., Oxford, 1907, i, 173. Lewis, T., and Mack, E. G.: Complete Heart -block and Auricular Fibrillation, Quart. J. M., Oxford, 1909-10, iii, 273. Deneke: Zur Rontgendiagnostik seltener Herzleiden, Deutsches Arch. f. klin. Med., Leipz., 1906, Ixxxix, 39. Einthoven, W. Quoted on page 96. Pick, F.: Zur Klinik des Elektrocardiogramms (Discussion), Verhandl. d. Kong. f. innere Med., Wiesbaden, 1909, xxiv, 653. Barker, L. F., Hirschfelder, A. D., and Bond, G. S.: The Electrocardiogram in Clinical Diagnosis, J. Am. M. Ass., Chicago, 1910, lv, 1350. Schreiber, E.: Ueber Herzblock beim Mcnschen, Deutsches Arch. f. klin. Med., Leipz., 1906, Ixxxix, 277. Vigouroux: Gaz. d. hop., Par., 1876. Hewan, A. Quoted from Edes. Schmaltz: Zur Kenntniss der Adams-Stokes'scher Krankheit, Miinchen. med. Wchnschr., 1905, Iii, 1120. Erlanger, J.: Ueber die Mode der Vaguswirkung auf die Kammern des Hundeherzens, Arch. f. d. ges. Physiol., Bonn, 1909, cxxvi, 77. Bachmann, G.: Sphygmographic Study of a Ca.se of Complete Heart-block; A Contribu- tion to the Study of the Action of Strophanthus in the Human Heart, Arch. Int. Med., Chicago, 1909, iv, 238. Hewlett, A. W., and Barringer, T. B.: The Effect of Digitalis on the Ventricular Rate in Man, Arch. Int. Med., Chicago, 1910, v, 93. Windle, J. D. : Permanent Complete Heart-block, A Case with an Exceptionally Frequent Ventricular Rate, Heart, Lond., 1910-11, ii, 102. 37 XII. PERICARDITIS. Historical. The presence of changes in the pericardium in animals was known to Galen, and Senac in 1749 described the condition in man. Auenbrugger and later Corvisart were able to make out changes in dul- ness due to pericardial effusions. Laennec detected the murmur of fibrin- ous pleurisy, and described it as resembling the creaking of a new saddle, but its diagnostic significance was positively established by Colliri and by Devilliers in 1824. ETIOLOGY. The frequency with which pericarditis occurs varies greatly according to various observers, and particularly according to the age of their patients. It seems to be considerably more common in children than in adults with cardiac disease, as stated by Poynton, as it accompanied endocarditis and myocarditis in 94 per cent, of Sturges's cases of heart disease (carditis) from the Great Ormond Street Children's Hospital. This is in accordance with the somewhat exaggerated statement of Cadet de Gassicourt that all children who are killed by rheumatism die from pericarditis; but it applies more to children of the second decade than of the first, since death from rheumatic affections is most common in the second decade. Pericarditis was found in 19 of Osier's 73 autopsies upon cases of chorea. Pericar- ditis occurred in 230 (1 per cent.) of the cases admitted to the medical service of the Johns Hopkins Hospital. Of these 53 were associated with endocarditis; 8 with myocarditis. Other factors were pneumonia 39; rheumatism 31; nephritis 33; tuberculosis 25; pleurisy 17; gonorrhoea 3; aneurism 2; leukaemia 2; syphilis 1. Rheumatism occurred in 51 per cent, of the 100 cases reported by Sears from the Boston City Hospital. This relationship between pericarditis and rheumatism has been proved experi- mentally by Wasserman, Triboulet, Poynton and Paine, Walker, Cole and Beattie (page 387). Pneumonia is also one of the common causes of pericarditis (18 per cent, of Sears's series), and usually ranks next to the rheumatic cycle as an etiological factor. Pericarditis was present in 4. 60 per cent, of the cases of pneumonia at the Johns Hopkins Hospital (Chatard), and in 2-3 per cent, of Preble's series in Chicago. According to the latter observer its relative frequency is about proportional to the extent and severity of the disease. This claim is also borne out by Chatard's statistics (frequency of 15.7 per cent, in the cases coming to autopsy). Moreover, the appearance of an acute pericarditis in the course of the disease is a very grave sign, for only two cases (6.5 per cent.) of Chatard's series recovered. 578 PERICARDITIS. 579 Pericarditis is also common in scarlatina (especially with strepto- coccus infection), in severe measles, and in smallpox. In the latter it is frequently purulent. Tuberculous pericarditis is quite common (8 per cent, of Breitung's autopsies), and in contrast to the rheumatic form rarely subsides. It often ends in effusion. The pericarditis of chronic nephritis and uraemia constitutes a frequent termination of this disease, though it is by no means always fatal. It is usually due to an intercurrent infection, and the pyogenic cocci can often be cultivated from the exudate. Pericarditis may also result as a secondary infection in septicaemia and in puerperal infections as well as in gonorrhoea, especially when there is accompanying arthritis. It is rare in typhoid fever (3 times in McCrae's 1500 cases) ; occurs occasionally in influenza; and sometimes results from septicaemias due to B. coli, B. aerogenes capsulatus, B. pyocyaneus, etc. Trauma without direct injury of the pericardium or viscera was the cause of pericarditis in Blancard's case in 1688, and a large number of cases due to this cause were collected by Bernstein in 1896. Blows upon the chest, wagon running over the body, etc., are the common causes. FORMS OF PERICARDIAL EXUDATION. The exudate into the pericardial cavity may assume various forms. In simple venous stasis and asphyxia of the endothelial cells (hydro- pericardium) a clear thin fluid of low specific gravity, relatively poor in proteid and especially in fibrinogen, is secreted. When there is true inflam- mation of the pericardium, the exuded fluid is rich in fibrinogen and of rela- tively high specific gravity (over 1015) and contains nucleo-albumen (clouding with acetic acid). Samuel has shown that when the exudate is poor in fibrin ferment it remains fluid (pericarditis with effusion) , whereas when this is present the fibrinogen coagulates (fibrinous pericar- ditis). According to Opie, the enzymes are derived chiefly from the leucocytes, especially the polymorphonuclears, and hence the amount of fibrin deposited depends largely upon the number of these cells present. Moreover, since these cells pass out from the blood-vessels, the fibrin is first and most thickly deposited in the vicinity of the latter, i.e., along the epicardium above the circumflex and descending rami of the large coronary arteries, where it begins in the form of strands passing out from about the leucocytes, and hence gives the heart a shaggy appearance (cor villosuni, Fig. 279). This layer of fibrin usually has the appearance and consistency of a yellow batter. When fresh it is not very adherent to the heart, ami may reach a thickness of an inch or more. There may be no fluid in the pericardial cavity, but, as a rule, both fibrin and fluid are present, the latter often in large quantities. The fluid is usually thick, containing uncoagulated fibrinogen as well as small flaky masses of fibrin, which may render it too thick to be removed by aspiration. When the exudate is extremely rich in bacteria and leucocytes, the proteolytic enzymes are given off, which digest the fibrin, and the fluid becomes purulent. When the fibrinous exudate of a simple pericarditis is absorbed rapidly, it leaves no traces and the pericardium again becomes clear. But when it 580 DISEASES OF THE HEART AND AORTA. lasts for some time and the resolution is slow, organization takes place, and white patches of pericarclial thickening ("milky spots") are found over the surface of the heart. These may, however, result from small perivascular foci like those of chronic myocarditis, without ever giving rise to the clinical picture of pericarditis. FIG. 278. Acute fibrinous pericarditis. FIG. 279. Tuberculous pericarditis (cor villosum). Organization and Adhesion. The strands of newly formed connective tissue may penetrate the fibrin between the two layers of pericardium and completely bridge the cavity with fibrous strands (Fig. 286). In many cases the tug of the heart in systole stretches these out into fibrous cords an inch or more in length; in other cases, or over other parts of the same heart, the adhesions are denser, the two surfaces may be completely glued together and the cavity obliterated (adherent pericardium). The division into these forms of pericarditis is, therefore, an arbitrary one, but, as will be seen, is made necessary by the absolute difference in both diagnostic signs and mechanical effects upon the circulation, and thus as regards indications for treatment. Their relative frequency is shown in the following table, which Gibson quotes from Breitung's autop- sies at the Berlin Charite Hospital (Yirchow's Department). Cases. Serofibrinous 10S Hemorrhagic 30 Purulent 24 Tuberculous (secondary) 24 Tuberculous (primary) 2 Partially adherent Ill Totally adherent , 23 Ossified 2 0. 34. PERICARDITIS. 581 Although the pathogenesis is the same, the clinical manifestations of fibrinous pericarditis, pericardial effusion, and adherent pericardium are different; hence they are discussed separately. SIMPLE FIBRIXOUS PERICARDITIS. PATHOLOGICAL PHYSIOLOGY. The friction due to the presence of the fibrinous exudate imposes a slight increase in the resistance to both contraction and filling of the heart. The exudate itself takes up a certain amount of space in the pericardial cavity and may thus somewhat diminish the filling of the heart; but these factors rarely suffice to embarrass the circulation. Either as a result of the accompanying injury to the heart muscle or from irritation of the depressor nerve, the peripheral vessels are dilated and the blood-pressure is low. The pulse also becomes small and rapid, but is usually regular. SYMPTOMS. Precordial pain, palpitation, shortness of breath, and weakness are the common complaints, as well as occasional chilly feelings. Fever, with which these are associated, is generally, but not always, present. The onset is very often insidious, and the disease may not be recog- nized at all by the patient. Precordial pain is the most striking symptom. Sibson estimates that it occurs in 70 per cent, of the cases. Henry Head calls attention to the fact that the pain of pericarditis is not a referred pain, but a true local pain, often limited to the area over which the friction is audible and associated with tenderness on pressure and on percussion. It does not radiate from this site, and differs in this respect from the anginal pain. The other symptoms, shortness of breath and palpi- tation, manifest no special peculiarity. Occasionally, especially when the pericarditis affects the posterior wall of the pericardium, there is p a i n on swallowing. This pain is in every way similar to the tenderness of the interspaces in front, and occurs when the bolus of food presses upon the pericardium as it passes down the oesophagus. When the recurrent laryngeal nerve is affected by the inflammation, aphonia or change in the voice results. Involvement of the phrenic often produces hiccough. PHYSICAL SIGNS. The patients are usually quite pale, occasionally cyanotic. Except for accompanying joint involvement, fibrinous pleurisy, or pulmonary consolidation, there are few signs outside the heart. (Kdenia of the extremi- ties is rare unless there are accompanying valvular lesions. Over the heart there may be some precordial bulging, especially in children, but the cardiac impulse may be less marked than usual, weak, diffuse, and wavy. On palpation there is sometimes a slight superficial scratching felt, especially between the left parasternal line and the sternum; but this is by no means as marked, as frequent, or as regular as in valvular lesions. 582 DISEASES OF THE HEART AND AORTA. The area of cardiac dulness and flatness may or may not be increased in one or both directions, dependent upon the amount of the exudate as well as upon the degree of dilatation of the heart, but the outlines char- acteristic of pericardial effusion are not present when the exudate is plastic. The pathognomonic sign of fibrinous pericarditis is the superfi- cial scratching or churning murmur or friction sound described by Laennec as resembling the rubbing of a new saddle. It can be imitated more or less closely by placing the palm of the hand over the ear and then scratching to and fro upon the back of the hand with the finger-nail. The pericardial friction is exactly similar in character to the friction heard in pleurisy, but its time is coincident with the cardiac cycle. It does not, however, coincide sharply with either systole or diastole, but is usually heard during portions of both. It is usually louder during systole than during diastole, probably because the two surfaces are moved across one another with greater force. A short pause usually occurs between the systolic and the diastolic portion of the friction. The diastolic friction is softer than the systolic, occurs rather early, and ceases during the latter half of this period, or in other words as ven- A Ji lt\ i-JMV JNTs .4Nir* A-)flliv tricular filling diminishes. It FIG. 2so.-Diagram showing the relations of the may also be heard again at the pericardial and pleural frictions to the cardiac and time of auricular SVStole oivi respiratory movements. The pericardial friction is . , , '.,*? . indicated by narrow zigzag line, the pleural friction a triple SOUnCl tO tile IriCtlOn by black triangles, the heart sounds by the usual (BrOadbent) . Sometimes, 6Sp6- black bands. \ ' . ,. . . . dally when the pericarditis is just beginning and the friction very soft, it is not heard at all during diastole. The friction, us a rule, does not replace the normal heart sounds, but these, as well as loud endocardial murmurs, may be heard simultaneously with it. Their more distant quality tends to accentuate the superficiality of the friction sound. Moreover, the latter is considerably accentuated by moderate pressure of the stethoscope in the interspaces. As Emerson has shown, this is also true of certain endocardial sounds, but the latter' are quite different in quality from a fresh pericarditis. As the exudate is absorbed, the friction softens gradually into a barely distinguishable roughening of the first sound, and, finally, disappears altogether. When portions of the exudate become organized and remain as thick- enings of the endocardium, they may still give rise to some roughening of the first sound, which may be very difficult to interpret, and this is especially true when they remain in the form of fibrous strands and loose adhesions (see page 598). The friction is usually first heard over the third and fourth left inter- space near the sternum, over the area at which the exudate first appears. In the cases which are secondary to pneumonia and pleurisy there is often a " pie u roperi cardial' ' friction, with respiratory accentuation heard over a considerable strip along the left margin of the heart where PERICARDITIS. 583 the pleura overlies the pericardium. The pleurisy exists in the layers of pleura in front of the pericardium. The two processes exist simultaneously in separate cavities whose walls are in contact. Sears has pointed out that in recurrent attacks of pericarditis the friction may be heard only at the back in the left interscapular region. This occurred in a case in which the anterior portion of the pericardium was adherent. The pulse in acute pericarditis is usually small and rapid, the blood-pressure low (100 mm. or under) , and the pulse-pressure small (10-25 mm.), but this is, at least in part, due to the loss of vasodilator tone, and in part to the myo- cardial weakening brought about by the same process. DIAGNOSIS. Diagnosis is usually simple, and the murmurs are rarely mistaken for endocardial, although Osier mentions one case in which a to-and-fro aortic murmur was mistaken for a pericardial rub. When a certain amount of fluid is present in the pericardium the friction may disappear if the heart is pushed backward; and, as a small peri- carditial effusion is often overlooked, the whole condition may escape diagnosis. CASE OF SIMPLE FIBRIXOUS PERICARDITIS. F. G., a colored hod-carrier, aged 50, entered the Johns Hopkins Hospital on July 22, 1904, complaining of pain around the heart. Except for the fact that one son died of gal- loping consumption, the family history is negative. The patient has been a healthy man, but had measles, chicken-pox, whooping-cough, mumps, scarlet fever as a boy, and rheumatic fever at 38. He is not subject to sore throat. He had a cough with pain in the chest twenty years before admission, but has had no recurrence. He has had several attacks of gonorrhoea. He has always done hard work. He was perfectly well until six weeks before admission, when he had severe pain in the right thigh and hip which lasted five weeks, but he kept at work in spite of the pain. Four days before admission he began to cough, and two days later felt a cutting pain around the heart, which was especially severe on drawing a deep breath. This has persisted. He did not notice any special shortness of breath, and kept at work for three days after the precordial pain had set in. The examination note by Dr. Cole states that the patient is a well-nourished colored man, mucous membranes of fair color, no glandular enlargement. Lungs clear throughout on auscultation and percussion. Over the heart a feeble impulse is seen in the fifth left interspace 8.5 cm. from the midline. The impulse is localized. There is no bulging of the interspaces. On percussion the area of cardiac dulness is found to extend 11.5 cm. to the left of the midline in the fifth interspace, 3.0 cm. to the right opposite the fourth rib. The eardiohepatic angle is 90. The heart sounds are distinctly heard at the apex, but there is also a loud rough pericardial friction which is not exactly synchronous witli the heart sounds and is increased by pressure with the stethoscope. There are no endocardial mur- murs. The friction increases in intensity toward the base of the heart, where the heart sounds are distant and the second pulmonic is louder than the second aortic. The pulse is of fair volume, moderate tension, regular, 8S per minute. The sputum is mucopurulent, but contains no tubercle bacilli and no elastic fibres. Urine, 450 c.c., amber colored, acid, containing a considerable amount of albumin and numerous hyaline casts. Blood count shows: red blood-corpuscles 3,500.000; haemo- globin 50 per cent.; leucocytes 7100. Temperature ranges from 101 to 102.5 F. An ice-bag was kept continuously over the precordium, and he was given strychnine, 1.5 mg. ( T '. To avoid puncturing the heart. 4. To avoid injuring the internal mammary artery. 1 "Si non passis exhaurire istud serum per hydragoga, licet ne terebra sternum aperire, intervallo pallicis a cartilagine xiphoide." 2 It is interesting that this method has recently been advocated by J. H. Bacon (A Procedure for Opening the Pericardium, Am. J. M. Sc., Phila. and N. York, 1905, cxxx, 652) as a result of a series of experiments upon the cadaver. Bacon does not mention the work of these pioneer surgeons. 3 Dr. Chas. S. Bond has found a curved aspirating needle with lumen about 1 mm. in diameter very useful in tapping the pericardium when the fluid lies back or is encapsulated. The needle which he uses has a radius of about 10 cm. following the curve of the heart and enabling him to pass around the latter without injuring it. The danger of entering the ventricle by a straight push is also much less with an instrument of this form. 38 594 DISEASES OF THE HEART AND AORTA. Sites for Paracentesis. Trousseau (1854) recommended introducing the needle in the fourth interspace just below the mammilla; Dieulafoy (1873) in the fifth about six centi- metres from the sternal margin. Puncture at these sites or at the outer border of absolute dulness (flatness) has the disadvantage of always traversing and often infecting the pleural cavity, so that occasionally the patient may be caused gratuitous empyema or even a fatal pneumonia. In order to avoid entering the pleural cavity, Baizeau (1868) and Delorme and Mignon advocate puncturing the pericardium as near as possible to the sternal margin in the fifth, or if possible the sixth, left inter- space. In order to render the procedure more certain, the latter investigators advise making an incision through the skin with a bistoury. The needle (of medium diameter) is then introduced into the sixth interspace if possible, and otherwise into the fifth along the edge of the sternum, pushed in for a centimetre or two, and then the point directed downward and inward by a slow con- tinuous movement until the liquid emerges. In order to empty the peri- cardial cavity the needle should be connected with an aspirator bottle and the fluid collected by gentle aspira- tion. 1 When the instrument is inserted slowly in the manner described, the risk of injuring the heart (right ven- tricle) is minimal, for the beating of the latter against the point can be felt as soon as it is touched and long before it can be penetrated. Even i if through lack of care the right ventricle be penetrated, i harm rarely results. For / example. Hulke mentions a case in which he penetrated the right ventricle and a few jets of blood spurted out, but the patient's condition improved! and he cites several other similar cases. Only one case of death (from laceration FIG. 285. Sites for paracentesis pericardii and peri- carditomy. Ki, Riolan (1640), trephining the sternum; D A- M, Delorme and Mignon (1895), paracentesis; R, Romero (1819), perieardiotomy; E, v. Eiselsberg's pericardiotomy; Tr, Trousseau (1854); Di, Dieulafoy (1873), paracentesis; W, West, pericardiotomy (1883). of the right ventricle) due to para- centesis is on record (West). Unques- tionably when all goes well the technic of Delorme and Mignon is the most satisfactory, since the danger of injuring both heart and pleura is minimal. On the other hand, the chance of a "dry puncture" is great. At the place selected the point of the needle may penetrate a great deal of dense fibrous tissue and even periosteum and the lumen may thus become plugged. Should the fluid not appear, this source of error may be obviated by carefully inserting a wire through the whole length of the needle after it has been pushed into the cavity and then withdrawing the wire. Another difficulty may lie in the position of the heart itself, as occurred in the above-mentioned case of the writer's, in which the heart instead of lying behind the fluid lay directly against the chest wall in the position described by Schaposchnikoff. When the needle was introduced by Dr. Cole, it.encountered the heart at once, and the rubbing of the latter against the point could be readily felt. This might have been prophesied from the fact that the heart sounds were well heard over the precordium. With the exception of a few cubic centimetres of clear fluid the puncture was a dry one, in spite of several successive insertions of the needle both at this point and in the costoxiphoid angle. The patient's condition became very bad, and he died before a second paracentesis could be undertaken. Autopsy showed the heart lying directly against the chest wall with 1200 c.c. of fluid above and to the left. In this case, as in all those in which the heart sounds and pericardial friction are well heard at the time of paracentesis, 1 Sewall, J. Am. M. Asso.. Chicago, 1909. advises aspirating the fluid into the aspirator bottle by sucking out the air with the mouth instead of with a mechanical aspirator. The procedure is simpler and mistakes and failures of the pump are impossible. PERICARDITIS. 595 it would have been better to have introduced the needle at the outer border of cardiac flat- ness in spite of puncturing the pleura, and to have risked empyema to save the patient. Drainage of the Pericardium. Prof. Pearson, of Cork, punctures the pericardium, with a large trocar, withdraws, and then introduces a fine rubber catheter into the pericardial cavity through the canula. The rubber catheter fol- lows the curves of the pericardium without danger of rupturing it, and thus enables him to reach exudates which, as in the case of R. C. W. B. cited above, are located behind the heart. He also withdraws the metal tube and leaves the rubber tube in place as a permanent drain for several days at a time, and states that in this way he has been able to cure a number of stubborn cases of chronic pericarditis with effusion which had resisted all other methods of treatment. The fact cannot be too greatly emphasized that cases with pericardial effusion are usually desperate cases, and the fluid should be gotten out at all hazards. It is true that all the fluid need not be removed to effect recovery, since the removal of a small amount, just as in Starling's experiment, allows the circulation, to re-establish itself and often per- mits the rest to be absorbed. Resection. As has been seen, paracentesis pericardii, even in cases of simple serous pericarditis, may be far from satisfactory. In purulent pericarditis and haemo- and pneumopericardium it is still less so. In such cases paracentesis is inadequate and the pericardium must be opened freely. Radical as this procedure may seem, its satisfactory performance by Romero antedates paracentesis. Romero made an incision in the fifth intercostal space at the level of the costochondral articulation, introduced his finger into the wound, palpated the pericardium with his finger, and then seized it with forceps and opened it with curved scissors. The opera- tion is best performed under light chloroform anaesthesia. Though this must be carefully administered on account of the cardiac weakness, it is a significant fact that most of the patients have stood the anaesthetic well. The site for free incision has varied with different operators. Rosen- stein made a free incision in the fourth left interspace close to the sternum and then inserted a rubber-tube drain. West operated in the fifth left interspace in the nipple line, having previously introduced an aspirating needle, which he used as director for a long narrow-bladed sharp-pointed bistoury, subsequently enlarging the opening with a probe-pointed bistoury. V. Eiselberg resected the fourth costal cartilage and then opened the peri- cardium. Delorme and Mignon perform what is probably the least danger- ous and most satisfactory operation. They disarticulate the fifth and sixth costal cartilages from the sternum with a pointed bistoury, draw them forward one by one, and fracture them about 4 cm. from the sternum. They then dissect down to the pericardium, which they pull forward with forceps, and then slit it up with scissors for several centimetres. Many observers, from Aran to the present, supplement the simple drainage with irrigation of the p e r i c a r d i u in . Aran injected a dilute tincture of iodine at 100, a procedure which in his case (though not in all others) did not cause pain; West used warm 1 per cent, carbolic acid; others used simple salt solution. The importance of irrigation can- not be too freely emphasized, since the treatment should aim not only at recovery but also at reducing the exudate and the resulting adhesions to a minimum. Delorme and Mignon operated upon all forms of pericardial effusions. Their conclusions are summed up in the following: " 100 observations 596 DISEASES OF THE HEART AND AORTA. 82 paracentesis, 18 incision: 82 paracentesis mortality 65 per cent.; IS incisions mortality 38 per cent. Let us do for the pericardium what we have done for the peritoneum." The relative merits of palliative therapy, paracentesis, and free incision are well shown in West's case of purulent pericarditis: A van boy, aged 16, was struck in the back by a truck and knocked down. No symp- toms for two months, then shivering and pain in the left side and precordium. Pain sub- sided in a few days. Three weeks later he went out for a short walk; became very faint and almost fell down. Pain seized him in the pit of the stomach. Became cyanotic, dys- pnceic, and nauseated. Admitted Sept. 7. Pulse 78; paradoxic, losing 2-3 beats at each inspiration. Precordial bulging and oedema. Dulness from right nipple line to three inches outside left nipple line. Cardiac sounds almost inaudible. Liver pushed down and felt in epigastrium. Slight oedema of feet. Twelve leeches applied to the precordium followed by poul- tices. Palliative treatment for a week. Pulse and general condition feebler. Sept. 14. Paracentesis pericardii fourth left interspace below nipple; 90 c.c. 1 per cent, carbolic acid at 100 then introduced through the needle and used to wash out pericardial cavity. No pain. Patient much relieved. Sept. 17. Patient's condition again bad. Paracentesis fails to remove fluid. Free incision under chloroform, as above described, in fifth left interspace; at least two quarts of pus removed. Immediate improvement. Uneventful recovery. Left hospital Feb. 23, and the following September was perfectly well and had been following his usual work for the past six months as well as ever. Rosenstein's case and those of Delorme and Mignon show similar results. West gives the following statistics for paracentesis : Number. Recovery. Phthisis 13 4 9 Rheumatic fever 11 7 4 Scurvy 9 6 3 Pleurisy 6 5 1 Injury ". 3 2 1 Pneumonia 2 . 2 General dropsy: Morbus cordis 2 . . 2 Nephritis 2 2 Chronic bronchitis 1 1 Mediastinal tumor 1 . . 1 Unassigned 17 7 10 67 34 33 In spite of the comparative harmlessness and brilliant results obtained by the radical operation in purulent pericarditis, it is not probable that this procedure can be extended to the milder exudates, since, just as in joints, free prolonged drainage is followed by complete obliteration of the cavity. Irrigation of the cavity through an aspirating needle or trocar, after tapping, is possible only when the diameter is large and the outflow is a free one. PERICARDITIS. 597 BIBLIOGRAPHY. PERICARDITIS. Historical data are taken from G. A. Gibson, Diseases of the Heart and Aorta, Edinb. and Lond., 1898. Poynton, F. J.: Heart Disease and Thoracic Aneurism, Lond., 1907. Sturges. Quoted from McPhedran, A.: Pericarditis, Osier's Mod. Med., Phila., 1908, iv. Cadet de Gassicourt. Quoted from Hochsingers in Pfaundler and Schlossmann's "Diseases of Children," translated by Shaw and La Fetra, Phila., Lippincott, 1908. Sears. Quoted from Osier, Principles and Practice of Medicine, 4th edition, N. Y., 1901. Chatard, J. A.: Acute Pericarditis complicating Acute Lobar Pneumonia, Johns Hopkins Hosp. Bull., Balto., 1905, xvi, 334. Breitung: Ueber pericarditis tuberculosa, Berl., 1877. Head, Henry: On Disturbances of Sensation, with Especial Reference to the Pain of Visceral Disease, Brain, Lond., 1896, xix, 153. Emerson. C. P.: Bull. Johns Hopkins Hosp. Silva. Quoted from Buxbaum, B.: Lehrbuch der Hydrotherapie, Leipz., 1903. Rubino, A.: Les pericarditis experimentales et bacteriques, Arch. Ital. de Biol., 1892, xvii, 298, and Rif. Med., 1892, viii. Romberg, E.: Lehrbuch der Krankheiten des Herzens und der Blutgefiisse, Stuttgart, 1906. Verney: Gaz. hebd. de med., Par., 1856, iii, 793. Quoted from Thayer, W. S.: Observa- tions on Two Cases of Pericarditis with Effusion, Bull. Johns Hopkins Hosp., Balto., 1904, xv, 149. Franr'ois-Franck, A.: Recherches sur la mode de production des troubles circulataires dans les epanchements abandons du pericard, Gaz. hebd. de med., Par., 1877. Lagrolet: De la compression du coeur dans les epanchements du pericard, These, Paris, 1878. Cohnheim. J.: Vorlesungen ueber allgemeine Pathologic, Berlin, 1882. Starling, E. H.: Some Points in the Pathology of Heart Disease, Lancet, Lond., 1S97, i, 569, 652, 723. Bolton, C 1 .: The Experimental Production of Uncomplicated Heart Disease, with Especial Reference to the Pathology of Dropsy, J. Path, and Bacteriol., Edinb. and Lond., 1904, ix, 67. Auenbrugger, L., and Corvisart. Quoted from Ebstein. Rotch, T. M.: Absence of Resonance in the Fifth Right Interspace diagnostic of Pericardial Effusion, Bost, M. and S. J., 1878, xcix, 389, 421. Ebstein, W. : Zur Diagnose der Flussigkeitsansammlung im Perikardium, Virchow's Arch., 1893, cxxx, 418. Aporti, F., and Figaroli, P.: Zur Lage der akutentstandenen Ergiisse im Herzbeutel, Zentralb. f. inn. Med., 1900, xxi, 737; from whom Concato, Riv. clin. di Bologna, Anno vii, Fasc. 4, is quoted. Sibson: Article on Pericarditis in Reynolds's System of Medicine, Lond., 1877. Koranyi, F.: Ueber den Perkussionsschall der Wirbelsaule und (lessen diagnostische Ver- wentung, Ztschr. f. klin. Med., Berl., 1906, Ix, 295. Thayer, W. S.: Observations on Two Cases of Tuberculous Pericarditis with Effusion, 'Johns Hopkins Hosp. Bull., Baltimore, 1904, xv, 149. Pirogoff . Quoted from Schaposchnikoff . Schaposchnikoff, B.: Zur Frage ueber Perikarditis, Mittheil. a. d. Grenzgeb. d. Med. u. d. Chir.. Jena, 1897, ii, 86. Riolan and Romero. Quoted from Schaposchnikoff, Delome and Mignon. Jowett. Quoted from S. West. Dieulafoy: Traite de 1'aspiration des liquides morbides, Par., 1873. Delorme, E., and Mignon: Sur la ponction et incision du pericarde. Rev. de Chir., Par., 1895, xv, 797, 987, and 1896, xvi, 56. West, S.: A Case of Purulent Pericarditis treated by Paracentesis and by Free Incision, with Recovery, Statistics of Paracentesis pericardii, Med. Chir. Trans., Lond., 1883, Ixvi, 235. 598 DISEASES OF THE HEART AND AORTA. ADHERENT PERICARDIUM. (Adherent pericardium, adhesive pericarditis, synechise pericardii, concretio pericardii cum corde, chronic mediastinopericarditis.) Whenever a pericardial exudate, fibrinous or fluid, is absorbed slowly a certain amount of organization takes place in it and adhesions form just as after pleurisy or peritonitis. The form of these adhesions varies consid- erably, from long thin strands stretching like cords across the pericardial cavity to short bands of dense fibrous tissue, or even to a firm tissue which LONG DENSE Fir,. 280. Specimen showing the two layers of pericardium united in some parts by long strands and in others by short bands of dense adhesions. (From a specimen in the Army Medical Museum, Washington, D. C.) knits the two surfaces together and completely obliterates the cavity. All these forms may be present in different areas of the same pericardium, so that the process need not be considered as perfectly homogeneous. Moreover, not only the adhesions within the pericardium but particu- larly the extrapericardial adhesions which are formed simultaneously on the outer surface, arc of clinical importance, since it is the latter which form the tightest lines in the harness and determine the strain upon the heart. As shown by Manges' case cited below, complete obliter- ation of the pericardial cavity may cause no symptoms as long as the extrapericardial adhesions remain unimportant. PERICARDITIS. 599 The main adhesions do not always occupy the same position, but may be divided into the following groups (Fig. 288) : 1. Chondropericardial fixing the heart to the costal cartilages and chest wall in front. 2. Pleuropericardial gluing it to the pleura; and fixing the edges of the lungs. 3. Mediastinopericardial fixing its posterior surface and especially harnessing the auricles. 4. Phrenopericardial fixing it to the diaphragm. g < < ~'v T* *- "/^vi FIG. 287. Sections showing adherent pericardium. (Photomicrographs by Dr. C. S. Bond.) A. Seen with low power. B. Same specimen under high power. C. Another specimen, showing the extreme vascularity of pericardial adhesions. Each of these gives rise to a distinct group of physical signs; and, since these may occur separately, it is important that they should be consid- ered so. PATHOLOGICAL PHYSIOLOGY. The mechanical effects upon the circulation due to pericardial adhesions may be twofold: 1, the work of the ventricle is increased by the tug upon the adhesions; 2, the filling of the heart may be hindered by strangulation of the vena cava. At each contraction the heart must not only drive out the blood, but must pull on its harness of adhesions. The additional work which it thus has to perform depends both upon the tightness of the 600 DISEASES OF THE HEART AND AORTA. adhesions and upon the weight or rigidity of the structures pulled. The latter factor depends upon the position of the adhesions, whether it is the ribs, pleura, mediastinum, or the diaphragm and liver that are tugged upon, being greatest for adhesions to the ribs and diaphragm. 3. The emptying of the heart and the flow through the aorta may, as claimed by Kussmaul, be hindered by the tugging of the adhesions upon the arch of the aorta. This can readily be shown experimentally if such traction be made in a dog whose chest has been opened. The pulse may be made to disappear absolutely in spite of the fact that the heart rate remains unchanged and the heart dilates from overfilling; enough blood flows in from the venae cavso to dilate the heart. FIG. 288. Anterior and posterior pericardial adhesions. (Semi-schematic.) A. Anterior adhe- sions showing the stumps of adhesions to the ribs. B. Mediastinal adhesions, showing a side view of the heart. PLE. P., pleuro-pericardial adhesions; C. P., costo- (or cliondro)-pericardial, P. P., phreno-peri- cardial, Af. P., mediastirio-pericardial adhesions. When this additional work is imposed upon a heart already weak, it may succumb to the strain, and death may occur with all the manifesta- tions of broken compensation. The importance of adherent pericardium in causing death from heart disease is shown by the fact that it was present in almost all the cases of Sturges' series. Usually, however, the ventricles gradually recover from the strain and simply undergo a gradual work hypertrophy proportional to the additional strain, and an additional amount of work may be done at each systole sufficient to balance the amount required. During exercise, emotion, dis- ease, or other strains, however, not only the work of the heart in the circu- lation is increased, but with the increased systolic output and systolic excursion of the walls the tug upon. the adhesions is increased enormously, and the heart is thus readily overstrained. The heavy beating of the heart under emotional excitement is especially likely to bring this about. Moreover, the process of hypertrophy is not a pure one. With the fibrosis of the pericardial adhesions outward, the process of fibrosis also PERICARDITIS. 601 extends inward into the somewhat injured myocardium, and this process goes on progressively with each moment of overstrain until the myofibrosis cordis is advanced and the heart failure complete. The site of the adhesions determines not only the degree but the char- acter of the heart failure. If the densest adhesions are over the left ven- tricle, the effect is to inhibit the action of the latter alone. Nature performs the experiment of Welch, and gives rise to the clinical picture of broken pulmonary compensation with dyspnoea, cardiac asthma, or pulmonary redema. If the chief adhesions are over the right ventricle, on the other hand, broken systemic compensation sets in with venous stasis, tricuspid insuf- ficiency, enlargement of the liver, and collection of fluid at various sites, but particularly in the peritoneal cavity (cf. Pseudocirrhosis, page 607). On the other hand, the tugs of the adhesions on auricles and ventricles may act as mechanical extrastimuli and produce an extrasystolic arrhyth- mia, which in itself hinders the circulation. SYMPTOMS. Since the actual formation of the adhesions really represents the sub- sidence of the acute pericardial process, it is not surprising that the onset of the pathological lesion is insidious, and indeed may coincide with the sub- sidence rather than the onset of symptoms. This is well illustrated by cases of purulent pericarditis like that reported by Manges, in which obliteration of the pericardial cavity accompanied the curve of the healing of the incision. The patient was free from symptoms, and a year later was working as a messenger boy. In most cases the process continues insidiously during months or years before cardiac symptoms and heart failure set in, during which the patient may be apparently well or may suffer only upon over- exertion, over-indulgence in venere et potu, or emotional excitement. Sooner or later the pump wears out and symptoms become marked. The symptoms of adherent pericardium are mainly those of chronic heart failure palpitation, weakness, etc. Precordial pain localized about the apex or the base of the sternum is common (65 per cent.-70 per cent, of cases). As stated above, the other symptoms may fall into the category of cardiac dyspnoea or that of venous stasis and dropsy, dependent upon whether the failure of compensation is in the pulmonary or systemic circu- lation. In the former case there are attacks of coughing and acute dyspnoea, sometimes with smothering sensations. The latter often begins insidiously with weakness, enlargement of the liver and spleen, swelling of the abdomen (Pick's pericarditic pseudocirrhosis of the liver, or pericarditic polyse- rositis), and swelling of the feet. These symptoms may also set in more acutely as in the form of simple heart failure. Delirium occasionally occurs with adherent pericardium, perhaps due to disturbed cerebral circulation. In one case under the writer's care the patient was subject to hallucinations of vision during the periods when his cardiac condition was bad. These were probably clue to congestion of the retinal capillaries, so that he saw lions and tigers jumping over one another at the foot of his bed, even though lie realized it was a physiological hallu- cination. 602 DISEASES OF THE HEART AND AORTA. PHYSICAL SIGNS. Corresponding to the variations in the site of adhesions, the physical signs of adherent pericardium are both multifarious and interesting. The patients are often pale and pasty, the haemoglobin being low and the ca- pillaries rather empty of blood. Sometimes the opposite holds true, and plethoric cyanosis prevails. Inspection of the veins of the neck may show filling of the latter during inspiration (Kussmaul's sign), accompanied by inspiratory diminution in the size of the pulse or even omission of some beats during inspiration (pulsus paradoxus, Kussmaul) (see page 604). The sounds over the heart during this period may become weaker, but usually still continue. The so-called Friedreich's sign (diastolic collapse of the vein), now known to represent merely a weak positive venous pulse (see page 80), is common to many weak hearts and has no diagnostic or prognostic value. C. M. Cooper has recently added what seems to be a valuable accessory sign of ad- herent pericardium. He determines how long the patient can hold the breath in inspira- tion, and, five minutes later, the same for holding the breath in expiration. In normal insp.= 40-70 25 individuals orToV > m cardiac lesion ---; in persons with mediastmal and peri- exp. A() .*-o lo cardial adhesions - --- (paradoxical ratio). Patients with bronchial asthma also exp. = 25 J insp. = 15-20 showed - _ (paradoxical ratio); so that its chief value is as confirmatory exp. ~o GO evidence. The presence of a paradoxical ratio may prove very useful in confirming, and a normol ratio in excluding, mediastinopericarditis. Broadbent's Sign. The chest usually shows marked precordial bulging, especially in children. Walter Broadbent in 1895 called attention to a ''visible retraction, synchronous with the cardiac systole, of the left back in the region of the eleventh and twelfth ribs,' ' and "in less degree of the same region of the right back " (Broadbent's sign) . Such retractions of the interspaces have also been recognized in many cases of cardiac hypertrophy by the Broadbents as well as by other observers (Tallant). J. H. F. Broadbent has lately (Heart Diseases, 4th edition) stated the facts more definitely and more accurately in the following words: "The systolic recession of spaces alone is, however, not a trustworthy indication, as it may be due to atmospheric pressure, especially when the heart is much hypertrophied. When the costal cartilages or lower end of the sternum are dragged in, there can be little doubt as to the diagnosis, as this could not be effected by atmospheric pressure." This sign is often most marked in deep inspiration when the diaphragm is tense. Broadbent also states that systolic retraction over the apex is a valuable sign, but only when the impulse is forcible on palpation, as it may otherwise be due to atmospheric pressure (over the right ventricle; cf. page 143). This is certainly true in many cases, but in the writer's experience there are frequent exceptions to this rule, and it is of value chiefly as a cor- roborating sign. Percussion. The area of cardiac dulness is usually but by no means always enlarged, owing to the hypertrophy which usually takes place, PERICARDITIS. 603 though fixation of the lung borders may cause the area of flatness and area of dulness on the left to almost coincide. The characteristic features on percussion are: Absence of the usual change in the left border of flatness between deep inspiration and deep expiration. This movement of the border of the lungs, which is normally 2-3 cm., may be reduced to less than 1 cm. or may absolutely disappear. The position of the apex, as determined by palpation, auscultation, and percussion, also becomes fixed, and may not change at all when the patient turns from lying on his right side to lying on his left. However, both these fixations may be present with simple pleural adhesions and no actual involvement of the peri- cardial cavity. This was well exemplified in the case of a little girl who had been a pa- tient in the Johns Hopkins Hospital several times during the last couple of years, and who presented signs interpreted as adherent pericardium. At autopsy the pericardial cavity was free from inflammatory processes, but the pleura) were everywhere bound do\vn tightly around it. Practically the effects were nearly the same as if the pericardial cavity had been in- volved, Broadbent's sign and pulsus paradoxus being present to a slight degree. Such cases are, however, extremely rare, and difficult to diagnose when they yccur. Palpation. Sir William Broadbent has called attention to the im- portance of an exaggeration of the diastolic shock or rebound (accompanying the second sound) over the greater part of the pericardium as characteristic of adherent pericardium. This is certainly a useful aid especially in corroboration of other signs, but, unless the distinctness of the shock is far greater than would be warranted by the loudness of the sound at the base, it is of little value. Nevertheless, the writer recalls a case in which the diagnosis of adherent pericardium (accompanying a well- defined aneurism) was based upon this sign alone and was verified at autopsy. Professor Thayer has found that there is often in addition a protodiastolic shock accompanying the third heart sound, which may be the most intense shock in the whole cardiac cycle. Apparently this is distinctive of adherent pericardium. Thrills, especially presystolic in time, are occasionally felt, probably owing to tugs upon strands of adhesions, but these alone are not typical. Auscultation. Since pericarditis is frequently (34 per cent, of Sears's cases) accompanied by various forms of valvular disease, the presence of FIG. 289. Cardiac outline in adherent pericardium. The broken line indicates the fixation of the left border of the heart (apex) and of the left border of cardiac flatness (anterior margin of the left lung). The small diagram at the left shows the relation of the heart sounds to the cardiac cycle, indicating the unusually loud third heart sound. BK BK indicate areas of systolic retrac- tion of the ribs, xiphoid, and interspaces; R 1, 2, Kiess' gastric sounds in adherent pericardium. 604 DISEASES OF THE HEART AND AORTA. all varieties of valvular murmurs, especially of mitral origin, is not sur- prising. A presystolic rumble, probably due to the stretching of strands of adhesions by the contraction of the auricle, is occasionally heard in cases of adherent pericardium in which aortic, mitral, and tricuspid valves are normal. Sewall also reports several cases with reduplication of the first sound, which was s-hown at autopsy to be due to old peripheral adhe- sions. Professor Thayer finds the third heart sound and the corresponding protodiastolic shock and wave very distinct in adherent pericardium. This may be due to the fact that they are more easily transmitted to the chest wall, or perhaps because the filling of the heart causes sudden stretch- ing of the adhesions. COSTOPERIC RESP. RIEGELS P PHENOMENON VEN. CAROT. PULSUS PARADOXUS FIG. 290. Inspiratory and expiratory dropping of beats (Riegel's pulse and the pulsus paradoxus) in adherent pericardium, showing the position of the adhesions which bring the condition about. VEN., jugular pulse; CAROT., carotid pulse; RESP., respiration (downstrokes represent inspiration; upstrokes represent expiration). In cases with Riegel's phenomenon (anterior costo-pericardial adhesions) the conditions are as shown in the diagram (upper respiratory tracing, venous pulse, carotid pulse); those with pulsus paradoxus correspond to the conditions shown by venous pulse, carotid pulse, and lower respiratory tracing. Riess' Gastric Sounds. A very interesting sign was described by Riess in 1879, and, since it has been verified by so excellent an observer as Fran- c,ois-Franck, merits attention. On listening over the stomach in some cases of adherent pericardium, observers have been able to hear the heart sounds loud and metallic in quality. These sounds are not much influenced by changes of position, by respiration, nor by inflation or filling of the stomach. They are probably due to adhesions to the diaphragm only, and hence, as originally stated by Riess, are not present in all cases of adherent pericardium. Variations in the Pulse. The pulse in adherent pericardium is usually small and rapid, generally regular, but often showing an extrasystolic irregularity which is probably due to tugs upon the strands of adhesions. The striking and characteristic feature is the marked diminution of the pulse-wave dining inspiration, amounting sometimes to the dropping of a beat during that phase. This was first noticed by Griesinger in 1854 iti a case in which autopsy showed strands of adhesions about the arch of the aorta, causing kinks and stenosis in its lumen when pulled upon by the descent of the diaphragm. The vena) cavie were also caught in dense PERICARDITIS. 605 adhesions which strangulated them in similar manner during inspiration. Both inflow and outflow of blood were therefore hindered in that phase, hence the diminution of the pulse. The same condition was studied by Hoppe and later by Kussmaul (1873), since whose report it is known as the p u 1 s u s p a r a d o x u s . It is not entirely pathognomonic of adhe- rent pericardium or even of pericarditis in general, occurring with open ductus arteriosus Botalli ~(Franc.ois-Franck, see page 543) and in many normal or neurasthenic individuals (Reichmann), though in these the dimi- nution does not amount to complete dropping of beats during inspiration. ADHES FIG. 291. A. Radiograph of a case of adherent pericardium. (Kindness of I'rof. C. M. Cooper.) B. Diagram illustrating the condition seen in A, showing the pericardium pulled outward to the right and a portion of the diaphragm pulled upward by the adhesions (ADHES). The occurrence of exactly the opposite condition of the pulse, namely diminution of the wave and impulse during expiration, has been described by Riegel in cases in which autopsy showed pleuropericardial adhesions upon the anterior surface of the heart. Riegel believes that the relaxation of the lung during expiration pulls the heart upward and produces a fall of pressure from displacement of the latter. Rosenbach has been able to show experimentally that when the heart was displaced by an inflated rubber bulb the vena? cavae became kinked and the pulse became smaller and blood-pressure fell. When this displacement occurs during inspiration from downward traction, a pulsus paradoxus results; when it occurs during expiration, Riegel's phenom- enon occurs. Apart from these respiratory variations the blood-pressure shows no special features, being usually low in uncomplicated cases; but it is fre- quently normal from compensatory vasoconstriction and increased cardiac effort, and occasionally high in the nephritic and unemic cases. X=ray Examination. The demonstration of pericardial adhesions by means of the Rontgen rays was first made by Moritz Benedikt in 1S97. Some question was thrown upon his methods by the criticism of V. Moritz (1900), showing that normal shadows along the edge of the cardiac and liver shadows may simulate adhesions. These objections were obviated by Stuertz, who reported five cases in which the presence of adhesions was demonstrated not only by suspicious shadows through the lungs and along the edge of the pericardium, but also by the fact that the margin of the pericardium at these points was pulled downward or outward when the structures were rendered tense in inspiration. Some areas were also sho\Mi 606 DISEASES OF THE HEART AND AORTA. to be quite fixed during respiration. Stuertz's observations have been confirmed by Lehmann and Schmoll and by Dr. C. M. Cooper, to whom the writer is indebted for the X-ray shown in Fig. 291. The special value of the X-ray examination lies in the fact that it reveals the mediastinal and diaphragmatic adhesions with accuracy, and, by demonstrating the points at which the fixation and tension are greatest, points out the path for operative interference. Abdomen. The abdomen is often negative, but enlargement of the liver and spleen and ascites are frequent, as has been shown by Weiss in 1876. CASE OF ADHERENT PERICARDIUM. The following very typical case was under the writer's care in the City and County Hospital of San Francisco. (As the original history was lost, these notes are taken from the article of Lehmann and Schmoll, who have previously published the case.) L. A., engineer, 23 years old, entered the hospital complaining of headache, nausea, and shortness of breath. He had had rheumatism six years before admission, and then had pain over the heart. Since then he had had two attacks. During the past few years he has been subject to periods of heart failure with dyspnoea, during which he is frequently depressed and sometimes even maniacal. The patient's lips, ears, and extremities are deeply cyanotic. The pulse is irregular, with numerous extrasystoles, many of them ineffectual. The apex impulse (systolic pro- trusion) is visible in the sixth interspace 3 cm. outside the mammillary line, beyond which there is a well-marked systolic retraction of the interspaces in front and back. There is also systolic retraction of the ribs and costal margin (Broadbent's sign). The apex is fixed and does not move with change of position, but the area of flatness changes during respiration (movement of the lung border). There is well-marked pulsation over the right ventricle. Dulness extends above to the third rib and 3 cm. to the right of the right para- sternal line. A loud presystolic rumble and a loud systolic murmur are heard over the apex. The second pulmonic is markedly accentuated. Both sounds are heard with the extra- systoles. The lungs are clear except for dulness and bronchovesicular breathing at the left base behind. The liver is greatly enlarged and readily palpable, but there is no pulsation. There is some oedema of the feet. Clinical diagnosis: Left -sided pleurisy, adhesion of the pericardium with the pos- terior surface of the heart, mediastinum, and diaphragm, mitral stenosis and insufficiency. Examination with the fluoroscope showed the heart to be dilated to right and left. There was a marked angular protrusion along the right border of the cardiac shadow. In this region the outlines of the shadow are less sharply defined than usual, merging into the liver and vertebral shadows. The diaphragm is equally high on left and right, moving less on the latter. The patient's condition did not improve under rest and digitalis. He often had in- tense precordial pains. On one occasion he was subject to definite hallucinations, imagin- ing that he saw lions, tigers, and other brightly colored wild animals springing to and fro upon the floor of the ward and over his bed, though he was at the time otherwise rational, and even realized that it was an hallucination. He was placed in a solitary cell for twenty- four hours at his own request, for fear of doing personal violence to the persons about him. His condition became so much worse that cardiolysis was decided upon as a last resort and was performed by Professor Stillman. The ribs were resected over the pre- cordium and the pericardium opened in exploration. The heart was everywhere covered with adhesions, which over the anterior surface of the heart consisted of strands about an inch long. There was no fibrinous exudate and no fluid. The patient took the ether badly and became extremely cyanotic. The shock of the operation did him evident harm, for during his entire sojourn after that he felt even worse than before. The wound itself caused him no trouble and healed per primum. The patient left the hospital three weeks after the operation, in spite of advice. PERICARDITIS. 607 FIG. 292. Case of pericarditic pseuclocir- rhosis. (After Cabot, Host. M. and S. J., 1898, cxxxviii.) Pericarditic Pseudocirrhosis of the Liver (Pick), and Polyserositis from Adherent Pericardium (Cabot). Hutinal in 1895 described a form of liver cirrhosis of cardiac origin (cirrhose cardiaque). Friedel Pick (1896) in Pribram's clinic called attention to a very interesting clinical condition which is not infrequently encountered, but whose nature is often over- looked. This is seen in certain cases which run the course of a primary hepatic cirrhosis, beginning with asci- tes, enlargement of the liver, slight jaundice, general weakness and dyspnoea, but devoid of any special cardiac features. Occasionally there were also enlargement of the super- ficial veins of the abdomen and cedema of the feet. The first and second cases were considered clinically to be primary cirrhosis of the liver, and the discovery of adherent pericardium at autopsy came as a surprise. In his third case adherent pericardium was carefully sought for and found, and the diagnosis was correctly made. Death occurred in two to four years after onset of symptoms. The peri- cardia in these cases were found to be completely or almost completely adherent, the rest of the heart normal. The livers showed both interlobular cirrhosis and chronic perihepatitis (iced liver, Curschmann), the peritoneum was thickened, and chronic perisplenitis was present. An example of this condition is found in the case of J. M. C. cited on page 358, in whom the presence of adherent pericar- dium was not suspected during life. In 1898 R. C. Cabot described a similar case. Flesch and Schossberger find the con- dition not infrequent in children, presenting the superficial manifestations of a primary cirrhosis without the presence of alcohol and syphilis as etiological factors. On careful examination the presence of adherent pericardium is readily detected by its usual signs. Flesch and Schossberger were able to reproduce the condition experimentally in dogs. They produced pericarditis by injections of tincture of iodine into the pericardial cavity and allowed the animals to recover, during which period adherent pericardium occurred. After a few months ascites and oedema set in and the animals died. Their results have been confirmed by O. Hess, who has also produced cyanosis and cirrhosis of the liver by suturing the inferior vena cava to the diaphragm. Another point in the differential diagnosis from true primary cirrhosis is the fact that the veins of the arms and neck are usually enlarged to almost the same extent as those of the portal system, showing that the stasis is not confined to the latter. There is no caput medusae. TREATMENT. The treatment of adherent pericardium may be both palliative and operative. The palliative treatment is simply the general treatment for cardiac weakness: rest, diet, and cardiac stimulants, strychnine and digi- talis, during the onset and acute stages; careful graduated exercises and training during the period of relative freedom from symptoms. 608 DISEASES OF THE HEART AND AORTA. It is impossible to remove the condition, and the therapy must be simply so directed that that which cannot be cured may best be endured. Anaemia should be treated with iron, exposure to infection avoided, and general hygienic conditions maintained. For reasons mentioned above, these precuations should be carried out even more carefully than for simple valvular disease. Surgical Treatment (Cardiolysis) . In 1902 Brauer, of Heidelberg, introduced a simple method of treatment which promises to revolutionize the therapy of adherent pericardium. Brauer proposed ''to relieve the heart functionally by breaking the strong bony ring of ribs, not by a severe operation with the breaking up of exten- sive adhesions but only by substituting a soft covering for the natural bony covering of the heart On account of the tremendous strain upon the heart, due to traction on the chest wall, we foresaw a danger in opera- tion under narcosis The operation was tried upon a patient with adherent pericardium, broken compensation, ascites, and oedema. Seg- ments of the third, fourth, and fifth ribs 7 to 9 cm. in length were resected under light narcosis, the periosteum being carefully removed. The patient made an uninterrupted recovery. His pulse soon became stronger and more regular, the ascites and cedema disappeared, and he was able to do heavy work without symptoms. The pulse still remained irregular." Brauer reported two other cases with equally good results, and these have been confirmed by Beck, Umber, Meyer, Westfeld, Wenckebach, and others. Brauer particularly states that he does not attempt to break up the adhesions, as Delorme and Carl Beck have proposed, since he believes that this operation is too severe and that the adhesions would form again too rapidly, although he states that, in individual cases, this might be done besides his operation. As regards the indications for cardiolysis, it would appear that, since the adherent pericardium cannot otherwise be relieved, this operation is worthy of trial whenever symptoms of cardiac weakness occur and recur in a patient with well-marked adhesions to the chest wall (tugging in of the lower ribs, fixation of the left border of flatness on inspiration, immo- bility of the apex) and recur in spite of general cardiac hygiene. It is not necessary to wait for the complete cardiac break-down to prophesy that this must sooner or later occur in such a case, and to see that the sooner the work of the heart is relieved the longer will be the life of the patient. Moreover, it is evident that if the operation is performed between attacks of cardiac overstrain, the patient is in better condition to withstand the shock of the operation and the danger of the latter is diminished. If the cardiolysis is not performed until the patient's heart has almost completely given way. as in the case of the patient with the visual hallucinations referred to above, he can scarcely fail to suffer from the shock of the opera- tion: but even in such cases Brauer's results have been striking, and, since there is no other mode of relief, operation is warranted. It must be confessed that in such cases the manner in which the anaes- thesia is administered determines a large part of the shock from the opera- tion, and may prove a decisive factor in the outcome. The selection of the aiut-sthetist constitutes no small part in the management of the case. PERICARDITIS. 609 The question also arises whether operation should be advised in chil- dren or adolescents whose pericardia are adherent to the chest wall, but in whom, owing to the flexibility of the latter, the symptoms do not as yet demand operative interference. In this regard each case must of course be decided upon its own merits, but it is evident that as age advances the rigidity of the ribs is bound to increase and the strain upon the heart pro- portionately. If the case remains relatively free from symptoms as age advances, it should be left alone; but if the progress of the second or third decade brings with it increasing cardiac symptoms or the signs of pericardi- tic pseudocirrhosis, the question of early cardiolysis should be seriously considered. Since there is no hope that children will "outgrow" an adhe- rent pericardium, it should be relieved as much as possible before the strain has ruined the heart muscle. When valvular lesions are present, especially mitral stenosis, the danger from operation is of course greater, but in the hands of a skilful surgeon this is much less than might be expected and is probably less than that in pericardiotomy for purulent pericarditis. BIBLIOGRAPHY. ADHERENT PERICARDIUM. Manges, M.: Adherent Pericardium, Internal. Clin., Phila., 1905, 15 ser., i, 1. Hoppe, F.: Ueber einen Fall von Aussetzen des Radialpulses wahrend der Inspiration und die Ursachen des Phanomens, Deutsche Klinik, 1854, Xo. 3. Kussmaul: Ueber schwielige Mediastino-pericarditis und paradoxen Puls, Berl. klin. Wchnschr., 1873, x, 433, 445, 461. Friedreich, N.: Ueber den Venenpuls, Deutsches Arch. f. klin. Med., Leipz., 1865-6, i, -241. Cooper, C. M.: The Respiratory Ratio; a Preliminary Note, J. Am. M. Assoc., Chicago, 1909, lii, 1182. Broadbent, Walter: An Unpublished Physical Sign, Lancet, Lond., 1895, ii, 200. Broadbent, Wm. H.: Adherent Pericardium, Trans. M. Soc., Lond., 1897-8, xxi, 109. Broadbent, Wm. H. and J. H. F.: Heart Disease and Aneurism of the Aorta, New York, 4th ed., 1906. Camac, C. N. B.: Broadbent's Sign, Johns Hopkins Hosp. Bull., Balto., 1898, ix, 271. Tallant, A. W.: Some Observations on the Occurrence of Broadbent's Sign, Boston M. and S. J., 1904, cli, 457. Sewall, H.: On a Common Form of Reduplication of the First Heart Sound due to Extra- cardiac Causes, Contrib. Sci. Med., Vaughan, Ann Arbor, 1903, 29. Riess, L.: Ueber ein neues Symptom der Herzbutelvenvachsung, Berl. klin. Wchnschr., 1878, xv, 751. Weitere Beobachtungen ueber einer die Herztone begleitende Magen- consonanz bei Herzbeutelverwachsungen, ibid., 1878, xvi, 333. Francois-Franck, A.: Des bruits extracardiaques in general, en particulier des bruits gastrique rhythmes avec le coaur: contribution au diagnostic de 1'adherence au peri- carde, Gaz. hebd de Med., Par., 1885, 2 ser., xxii, 757. Griesinger's observation (18541, reported by A. \Yidenmann, Beitrag zur Diagnose der Mediastinitis, Diss., Tubingen, 1856. Hoppe, F.: Ueber einen Fall von Aussetzen des Radialpul&es wahrend der Inspiration, u.s.w., Deutsche Klinik, 1854, Xo. 3. Reichmann, E.: Die inspiratorische Yerkleinerung des Pulses (sogen Pulsus Paradoxus), Ztschr. f. klin. Med.. Berl.. 1904, liii, 112. Riegel, F.: L'eber extrapericardiale Yerwachsungen, Berl. klin. Wchnschr., 1877, xiv, 657. Rosenbach, O.: Experimentelle Untersuchungen L'eber die Einwirkung von Raumbesch- riinkungen in der Pleurahohle auf den Kreislauf apparat. Arch. f. path. Anat., etc., Berl., cv. 215. Benedikt, M.: Wien. med. Wchnschr.. 1897. Moritz, F.: Munchen med. Wchnschr., 1900. Quoted from Lehmann and Schmoll. 39 610 DISEASES OF THE HEART AND AORTA. Stuertz: Zur Diagnose der Pleuraadhasionen aus Pericard und Zwerchfell, Fortschr. a. d. Geb. d. Rontgenstr., Hamb., 1904, vii, 215. Lehmann and Schmoll: Pericarditis adhesiva im Rontgenogramm, ibid., 1905, ix, 196. Cooper, Charles Miner: Personal communication. Pick, F.: Ueber chronische unter dem Bilde der Lebercirrhose verlaufende Pericarditis (pericarditische Pseudolebercirrhose), Ztschr. f. klin. Med., Berl., 1896, xxix, 385. Cabot: Bost, M. and S. J., 1898. Flesch and Schossberger: Diagnose und Pathogenese der in Kindesalter, haufigsten Form der Conc r etio Pericardii cum Corde, Ztschr. f. klin. Med., Berl., 1906, lix, 1. Con- firmed also by Hess, O.: Diagnose und Pathogenese der im Kindesalter haufigsten Form der Concretio Pericardii cum Corde, Ztschr. f. klin. Med., Berl., 1906, Ix, 174. Brauer, L.: Cardialyse, Mimchen. med. Wchnschr., 1902, xlix, 982. Untersuchungen an Herzen Cardiolysis und ihre Indikationen, Arch. f. klin. Chir., Berl., 1903, Ixxi, 258. Beck. Quoted from Brauer. Umber: Perkiarditis und mediastinale Verwachsungen und Cardiolysis, Therap. d. Gegen- wart., 1905. Wenckebach, K. F.: Remarks on Some Points in the Pathology and Treatment of Adherent Pericardium, Brit. M. J., Lond., 1907, i, 63. Ueber pathologische Beziehungen zwi- schen Atmung und Kreislauf, Samml. klin. Vortr , Leipz., 1907, No. 465, 466. For a review of the subject see also Delatour, H. B.: Surgery of the Pericardium and Heart, Am. J. Surg., N. York, 1909. XIII. WOUNDS OF THE HEART AND CARDIAC TRAUMA. Hippocrates and Celsus, Paul of ^Egina, Roland, Lanfranc, and other writers of antiquity taught that wounds of the heart were followed immedi- ately by death; but Ambroise Pare (1552) saw a gentleman of Turin "who, although wounded in the heart during a duel, was able to pursue his antag- onist 700 feet before he dropped to the ground and died." Muler (1641) treated a soldier who lived for fifteen days after sustaining a wound of the heart, an observation so unheard of at the time that he had the autopsy protocols signed by the commander of the garrison! Aprilis (1680) de- scribes a wound of the right auricle, after receiving which the man had lived for five days. The results of modern times were summed up by G. Fischer in 1867 (351 cases) and Loison (1899) (277 cases). Fischer found the wounds occurring with the following frequency: Death within a few minutes. Recovery. Right ventricle 10721 . 9 per cent. 6 Left ventricle 95 25. per cent. 6 Both ventricles 24 34 . per cent. 2 Right auricle 28 25 . per cent. Left auricle 13 38 . per cent. Apex 12 4 Base 1 1 Septum ventriculorum 6 1 Whole heart 15 62 . per cent. 1 Left heart 5 Right heart 3 11 Coronary artery 1 1 Pulmonary artery 1 Not specified 40 17 351 50 (11.2%) In 452 cases there were 50 (12 per cent.) of spontaneous recovery. EXPERIMENTAL SURGERY. Elsberg in 1899 made a very careful study of wounds experimentally produced in the rabbit's heart. He found that those produced during systole, when the heart fibres are shortened, become enlarged during dias- tole and hence bleed more than wounds of corresponding size produced during the latter phase. Wounds that completely penetrate the heart wall bleed more than those which do so partially. Those which enter perpen- dicularly bleed more than those which penetrate obliquely, for in the latter case the walls form a valve-like approximation during systole. Indeed Prof. Barker and the writer have produced oblique wounds penetrating the entire wall of the dog's ventricle, which scarcely bled at all. 611 612 DISEASES OF THE HEART AND AORTA. Even the smallest incised wounds made by Elsberg in the rabbit's auricle were always fatal unless sutured, while those of the right ventricle were more fatal than those of the left. Wounds of 2 mm. or less in the left ventricle frequently healed spontaneously. However, when suture was employed a large part of the ventricles could be cut through and the ani- mal's life saved. The size of the instrument producing the injury plays little role, for, although in general large wounds bleed more and are more uniformly fatal than small ones, nevertheless large and fatal wounds have been produced by even ordinary needles. For example, Thiemann describes the case of a man who in pressing against a heavy beam accidentally drove a sewing needle through his chest wall, where it became imbedded and stuck into the Fio. 293. Wounds of the left ventricle. (From specimens in the Army Medical Museum, Wash- ington, 1). (.'.) A. Bullet wound in the heart of a soldier who lived for two days after. B. Stab wound in the left ventricle ; death within two hours. heart wall, ripping one hole 1.5 cm. long in the wall of the right auricle and another smaller hole in the wall of the right ventricle. His life was saved by operation four and one-half hours later. A single small puncture of the heart wall with a needle with prompt withdrawal of the needle and no laceration, as is occasionally done in para- ccntesis pericardii, as a rule causes no marked disturbance and does not require operative interference. Death from penetrating wounds of the heart results either from bleed- ing, or, as was already shown by Morgagni and by Cohnhcim, from accumu- lation of blood within the pericardium (see page 586), compressing the auricles and preventing the entry of blood into the heart. It is possible that in the rare cases of instantaneous death the Irauma may cause the ventricles to pass into a state of fibrillation and the circulation abruptly cease. There is no proof that this is frequent, however, and the cases of instantaneous death from wounding the heart are less common than might be expected. WOUNDS OF HEART AND CARDIAC TRAUMA. 613 SYMPTOMS. The symptoms accompanying a wound in the thorax which suggest a wound of the heart (intrapericardial pressure) are those of angina pec- tor is pain down the left arm, a feeling of precordial oppression and precordial pain, especially marked on expiration. Pressure upon the pre- cordium increases these pains. There is shortness of breath. Occasionally there are abdominal pain and spasm of the abdominal muscles (Rehn). As Fischer pointed out, pain is also felt about the external wound, but as a rule not in the heart itself. Even probing of the heart wound, while it may give rise to weakness and syncope, is not accompanied by pain. Thus, one patient whose, left ventricle had been wounded thought that the knife had only gone through his clothes. Blood is often found spurting from the wound with a well-defined pulsa- tion. Sometimes it is foamy and mixed with air, indicating that the lung has been penetrated. PHYSICAL SIGNS. The area of cardiac dulness is increased or is replaced by tympany (pneumo-hsemopericardium) . The heart sounds are replaced by loud churning or water-wheel murmurs. The blowing murmur caused by the jet of blood passing out of the heart may also be distinguished. The pulse becomes small, weak, rapid, and finally imperceptible. Whenever time warrants, an X-ray examination should be done at once, and the bullet or foreign body located. This may sometimes be very exactly done by means of stereoscopic pictures and greatly simplifies the operation. TREATMENT. Operative interference in the treatment of wounds of the heart was first proposed by Rose, who confined himself to opening the pericardium and removing the blood that compressed the auricles. This procedure was often of benefit and even effected cure in cases where bleeding ceased spontane- ously, but when the heart continued to bleed it was of no avail. Up to this time it had been thought, in spite of the experiments of physiologists, that suture of the heart wall itself would be accompanied by instant death. But in 1895 Salomoni and Del Vecchio demonstrated that wounds in the heart of the dog could be successfully treated in this manner; and in 1896 Cappelen, Farina, and Rehn sutured the heart wall in man. The passing of the sutures had no ill effects. Cappelen's and Farina's patients died a few days later from secondary causes, but Rehn's patient, who had received a stab wound in the right ventricle, operated on forty- eight hours after the injury, recovered, and thus a revolution in cardiac surgery was made. Rehn had demonstrated that wounds of the heart could and should be successfully explored and sutured like wounds of other viscera. If the patient is in severe collapse from loss of blood, an intravenous infusion of warm salt solution (37 C.) should be begun at once while the operators are hastily cleaning and disinfecting the field of operation. As a last resort a direct arteriovenous transfusion into the veins of the arm 614 DISEASES OF THE HEART AND AORTA. may be made from another individual by the method of Crile, Buerger, or Hart well while the operation on the heart is going on, and some exsan- guinated patients may thus be saved. Operative Procedure. The incision should be sufficiently large to admit of a satisfactory exposure. A flap is made in the chest wall over the point of penetration, usually including two ribs and three interspaces. The flap adopted by most operators is horizontal U shaped with bifurca- tions pointing to either left or right, the connecting bar passing through either sternochondral or costochondral articulations. Occasionally the FIG. 294. Exposure of the heart for suturing a wound. (After G. T. Vaughan, J. Am. M. Assoc., 1909, lii.) 1, heart; 2, deep sutures; 3, superficial sutures; 4 and 5, retractors on the pericardium; 0, left pleural line; 7, flap of chest wall including the fourth, fifth, and sixth ribs; 8, heart, outlined by broken outline. form is that of an upright or an inverted U, a H , or an H. If the wound is near the sternum and has not already penetrated the pleura, that cavity should not be opened, and the c| or E-i shaped flap is the best; but if the wound has pierced the pleura, any convenient exposure may be adopted. The incision through the pectoralis major should be parallel to its fibres which may be retracted. The sternochondral or costochondral articula- tions are cut through, the ends of the incision prolonged along parallel to the ribs, and the flap forcibly reflected back, fracturing the costal cartilages to permit a wide opening. If the pleura has not been penetrated, it should be pulled toward the outer edge of the wound with retractors. A free incision should be made into the pericardium, the pericardial cavity emptied of clots, the wound in the heart located, and sutured with a fine curved needle and silk thread. In passing the sutures the heart wall may WOUNDS OF HEART AND CARDIAC TRAUMA. 615 be grasped with forceps without danger, the irregularity which accom- panies the passing of the needle representing merely a few extrasystoles resulting from the irritation, and passing off rapidly. Elsberg never ob- served sudden stoppage of the heart and fibrillation following the inser- tion of sutures. The writer, after several hundred experiments upon ex- posed dogs' hearts, is able to confirm these statements of Elsberg. Elsberg states that the interrupted suture is preferable to the continuous, for, though it takes longer to apply, it injures fewer muscle fibres and is more certain to hold. The sutures should be tied during diastole; these do not tear out as readily as sutures tied during systole. In tightening the sutures the two serous surfaces of the wound should be pushed in so as to be brought into apposition. The surfaces unite by the usual growth of fibrous tissue. The nuclei of the muscle cells near the wound seem to be increased in number, and there is some amitotic and mitotic division but no definite regeneration of muscle. Control of Hemorrhage. When the bleeding was so profuse that death seemed imminent, Elsberg found it necessary to adopt provisional means for stopping bleeding while putting in the sutures. For this he used a hastily placed tobacco-pouch suture, or even a ligature about the whole heart just above the wound. (This does not apply, of course, to wounds in the upper half of the ventricles.) He was then able to place the sutures bloodlessly, after which the provisional ligature was removed. In this way he was able to suture tremendous wounds (2 cm. in a rabbit's heart, corresponding to about 10 cm. in the human heart), with 66 per cent, of recoveries. Large wounds of the auricle may be more difficult to control. Sauer- bruch recommends stopping the bleeding by gently compressing the auricle between the middle and ring fingers while grasping the point to be sutured between the index finger and thumb. Rehn finds that with some care a ligature may be placed about the auricle to still the bleeding while the sutures are rapidly put in, but there is danger of death from fibrillation if the circulation is completely cut off. The writer has been able to control the hemorrhage from quite large wounds in the dog's heart for over ten minutes by holding his finger gently against the wound. The heart's action was not weakened by this procedure, nor did it become irregular; and suffi- cient time was gained to lay the sutures carefully. This was found to be more bloodless, and for large wounds more convenient, than Elsberg's method of laying temporary sutures. If possible the bullet should be removed unless it is too deeply imbedded in the cavity of the heart. Under these circumstances it may be left at least for a subsequent operation, as it often becomes encapsulated and may do no further harm. All operators agree that operation in the Sauerbruch negative pressure chamber or with Brauer's positive pressure lessens the danger of pneumothorax, and is therefore advisable when it requires no delay. It is particularly useful when the wound is about to be closed, to prevent the continuance of the pneumothorax. As regards the question of drainage, each individual case must be de- cided on its own merits. It is, of course, important to prevent sepsis, purulent pericarditis., and pyopneumothorax. When the pleura has not 616 DISEASES OF THE HEART AND AORTA. been pierced, the pericardium may be closed in a large number of cases without drainage (Rehn's statistics show 4 cases 3 cures, 1 death with- out drainage of pericardium; with drainage, 5 cases 5 deaths; perhaps, however, drainage was used in only the more severe cases). When the pleura has been pierced, it should usually be drained. Whenever bits of cloth, dirt, etc., have entered the wound, it should always be drained. Before closing the wound the pericardial cavity should again be explored to see that no other wounds in the heart wall or vessels have been overlooked. Occasionally large branches of the coronary arteries are found to be pierced and must be ligatured. This is necessary, and, as shown by Porter and Baumgarten (see page 366), is not always fatal, as there is a certain amount of collateral circulation, but sudden death may result during subsequent excitement, so that in such cases more prolonged rest is advisa- ble than in cases of simple suture. It is worthy of note, however, that this complication is not mentioned in the twelve cases of late results com- piled by Rehn. After closure of the wound, with or without drainage, administration of urotropin is probably advisable, since Crowe has found that it is excreted in the pleural and pericardial fluids in a concentration sufficient to inhibit the growth of bacteria; and Bernheim believes that its use increases the resistance of these membranes (in dogs at least) to infection. It has, moreover, no harmful effects. Results of Operation. Since Rehn's first operation a large number of cases have been reported. In 1907 he was able to collect statistics of 124 cases 49 recoveries (39.5 per cent.), 75 deaths (60.5 per cent.). In this- series there were only 15 cases of gunshot wound, but in a series of 30 cases of the latter compiled from the series of Ricketts, Borchardt, and Rehn, there were 14 recoveries (46.6 per cent.) and 16 deaths (53.4 per cent.). Of the 75 deaths in Rehn's series 16 died on the operating table, 17 died of loss of blood and collapse within two days, 30 died of infection (purulent pericarditis and empyema). In many cases the haste of operation prevented disinfection of the field. One patient (Gerzen's) died of sudden hemorrhage on the fifty-third day. Rehn also collected reports of 1 2 cases from nine months to ten and one-half years after operation. In nine exam- ination of the heart was negative; in three there was slight dilatation. There were costopericardial adhesions in 5; 9 were absolutely free from symptoms; 2 had pains down left arm; 1 precordial pain. Only one had symptoms of definite cardiac weakness. G. T. Vaughan has recently summarized and tabulated 150 cases operated on between 1896 and 1909, of which 51 (34 per cent.) recovered, a striking contrast to the 12 per cent, of recoveries in the earlier years from which Fischer's series was taken. XOX-PERFORATIXG INJURIES. Injuries of the chest wall which do not enter the pericardium, such as blows upon the chest, frequently produce secondary lesions of the heart and pericardium, which have been mentioned in previous chapters. WOUNDS OF HEART AND CARDIAC TRAUMA. 617 The first case of cardiac disease from contusion was recorded by Blan- card in 1688 and is very typical. The patient was a peasant 45 years of age, previously healthy, who was run over by a hay-cart. He did not sustain any fracture, but suffered from pain in the chest, dyspnoea, then fever, delirium, and died 11 clays later of purulent pericarditis and myo- carditis. Similar cases were recorded by Bonetus (1700), Akonside (1766), and numerous other writers both ancient and modern. Bernstein in 1896 was able to collect 126 cases from the literature. In autopsies upon 42 of these cases there was found Endocarditis alone 16 times Myocarditis " " Pericarditis " 10 " Endo- and myocarditis 4 " Peri- and myocarditis 5 " Endo- and pericarditis 5 " The signs and symptoms appeared: Immediately after the trauma , 67.6 per cent. Within one month 17.5 " " Within one year 4.7 " " Later than one year 7.1 " " Time not given 3.1 " " G. Fischer gives a list of the causes of traumatic rupture of the heart in his series: Run over by or crushed between wheels of wagon 21 Crushed by machinery 4 Falls from considerable heights 13 Falls from heights of 10 feet or less 7 Struck by falling objects 6 Kicked in chest 4 Hurled against wall 2 Kiilbs has recently investigated the subject experimentally. The results in 23 animals within 12 days of the injury were: Hemorrhages into the heart valves 17 times (1 rupture of an aortic valve) Subendocardial or subpericardial hemorrhages 10 times extensive hemorrhage into the septum 3 times Pericardial hemorrhages 10 times Hemorrhages from lungs 6 times There was polymorphonuclear infiltration and disintegration of muscle fibres in the vicinity of the hemorrhages. The symptoms and signs of these conditions following trauma do not differ from those in similar lesions due to other causes, and have been considered under those heads. 618 DISEASES OF THE HEART AND AORTA. BIBLIOGRAPHY. WOUNDS OF THE HEART AND CARDIAC TRAUMA. For historical data see Ricketts, B. M.: The Surgery of the Heart and Lungs, New York, 1904. Borchardt, M.: Ueber Herzwunden und ihre Behandlung. Pfahlungs verletzungen von Herz und Lunge, Saniml. klin. Vortrage, No. 411-412; Chir. No. 113-114, Ser. xiv, Heft 21-22, Leipz., 1906. Elsberg, C. A.: An Experimental Investigation of the Treatment of Wounds of the Heart by Means of Suture of the Heart Muscle, J. Exp. Med., N. Y., 1899, iv, 479. Fischer, G.: Die Wunden des Herzens und des Herzbeutels, Arch. f. klin. Chir., Berl., 1868, ix, 571. Loison, E.: Des blessures du pe>icarde et du creur et de leur traitement, Rev. de Chir., Paris, 1899, xix, 49, 205, 774; 1899, xx, 37. Rehn, L.: Zur Chirurgie des Herzens und des Herzbeutels, Arch. f. klin. Chir., Berl., 1907, Ixxxiii, 723. Rose: Deutsch. Ztschr. f. Chir., xx. Rosenthal: Deutsch. med. Wchnschr., 1895. Del Vecchio: Rif. Med., 1895; Zentralbl. f. Chir., 1895, 574. Salomoni: ibid., 1896. Farina: ibid., 1896, 1224. Quoted from Rehn. Rehn, L.: Ueber penetrirende Herzwunden und Herznaht, Arch. f. klin. Chir., Berl., 1897, Iv, 315. Buerger, L. A: Modified Crile Transfusion Cannula, J. Am. M. Asso., Chicago, 1908, li, 1233. Hartwell, J. A. : A Simple Method of Blood Transfusion without Cannula, ibid., 1909, lii, 297. Thiemann: Nadelstichverletzung des rechten Herzventrikels und Vorhofs, Arch. f. klin. Chir., Berl., 1907, Ixxxiii, 565. Sauerbruch, E. F.: Die Verwendbarkeit des Unterdruckverfahrens bei der Herzchirurgie, ibid., 1907, Ixxxiii, 537; also The Present Status of Surgery of the Thorax and the Value of the Sauerbruch Negative Pressure Procedure in the Prevention of Pneumo- thorax, J. Am. M. Asso., Chicago, 1908, li, 808. For discussion of the positive pressure methods see Robinson, S.: Artificial Intrapul- monary Positive Pressure; Experimental Applications in the Surgery of the Lungs, ibid., 1908, li, 803; and Green, N. W., and Maury, J. W. D.: The Positive Pressure Method of Artificial Respiration, with its Experimental Application to the Surgery of the Thoracic (Esophagus, ibid., 1908, li, 805. Vaughan, G. T.: Surgery of Wounds of the Heart, J. Am. M. Asso., Chicago, 1909, lii, 429. Bernstein: Ueber die durch Kontusion und Erschiitterung entstandenen krankheiten des Herzens, Ztschr. f. klin. Med., Berl., 1896, xxix, 519. Kulbs: Experimentelle Untersuchungen ueber Herz und Trauma, Verhandl. d. deutsch. path. Gesellsch., Jena, 1908, xii, 172. XIV. ANEURISM. Aneurism (aneurysm) (Greek avevpvafia a widening out) = a dilatation of artery or veins (Galen). An aneurism is a blood-containing tumor whose walls are formed by the walls of a blood-vessel and whose cavity is in direct connection with the blood-vessel from which it arises (Osier). Historical. Hippocrates (430 B. C.) and the early Greek writers do not seem to have been familiar with aneurism, but its occurrence and nature were well known to Rufus and Galen (A.D. 131-201), who recognized two forms: "one from dilatation, the other from wounding of a vessel," usually from venesection followed by sepsis. FIG. 295. Specimen of a large aneurism. (After Hough.) "Vesalius (1543) was the first to recognize aneurisms within the thorax and abdomen and was even able to make the diagnosis of thoracic aneurism during life. Arabroise Pare (sixteenth century) recognized the existence of ''aneurism by anastomosis, rupture, erosion, and wound, along with the frequency of thrombosis within the sack." He was also the first to suggest that venereal disease was a factor in the genesis of aneurism. The role of syphilis was demonstrated definitely by Lancisi (1728). The next great stop was made by Scarpa (1805), who demonstrated that the most important mechanical factor was weakening of the middle layer of the arterial wall, a fact which has furnished a basis for the more modern pathology of aneurism. CLASSIFICATION OF ANEURISM. It is extremely difficult to make a satisfactory classification of aneu- risms, but the following, which is based upon that of Osier, may suffice for most purposes: 619 620 DISEASES OF THE HEART AND AORTA. 1. True aneurism (aneurysma verum, aneurysma spontaneum), in which one or more of the coats of the artery form the walls of the tumor. A. Dilatation aneurism. (a) S a c c u 1 a t e d , in which the bulging or out-pocketing of the walls does not embrace the whole circumference of the artery and is sharply localized. (6) Fusiform (or cylindroid) aneurism, in which the dilatation occurs over a larger area of artery whose entire circumference is involved in the dilatation. 2. Dissecting aneurism, in which the coats of the artery are separated and a new cavity (sometimes lined with endothelium) is formed between these layers (usually between media and adventitia). 3. False aneurism, following wound or rupture of an artery, consisting of a peri- arterial ha;matoma, all the coats of the artery having been penetrated. 4. C i r s o i d aneurism or telangioma, a tumor consisting of a large number of tortuous arteries which are continuous with the artery from which they arise. 5. Arteriovenous aneurism, a communication between artery and vein, either direct, aneurismal varix, or with the intervention of a sac, varicose aneurism. ARTERIES AFFECTED. By far the most common forms are the true aneurisms, fusiform and sacculated. The relative frequency in the various arteries is shown in the following statistics of 530 cases (Crisp) : Thoracic aorta 175 Popliteal artery 137 Femoral artery 66 Abdominal aorta 59 Carotid artery 25 Subclavian artery 23 Axillary artery 18 External iliac artery 9 Cerebral artery 7 Common iliac artery 2 Posterior tibial artery 2 Gluteal artery 2 Pulmonary artery 2 Brachial artery 1 Subscapular artery 1 Ophthalmic artery 1 OCCURRENCE. According to a large set of statistics compiled by Richter and by Arn- sperger, aneurism of the aorta represents one of the not infrequent causes of death, 0.6 per cent, of total mortality (Emmerich), Brodier 1.2 per cent., Miiller 1.49 per cent.; in American cities 0.6 per cent., Philadelphia 0.6 per cent., St. Louis 0.2 per cent. According to Gibbons and Richter the percentage of deaths from aneurism in San Francisco from 1866 to 1870 (1.35 per cent.) was much greater than elsewhere in the United States. Dr. Gibbons has informed the writer that aneurism at that time was par- ticularly common among stevedores, who formed a considerable percentage of the popula- tion, and in whom syphilis, alcohol, and hard work were ever-present factors. With the passing of the adventurer and the stevedore as important elements in the population, the percentage of aneurism in San Francisco has diminished, being 0.90 per cent, in 1880-1884, 0.42 per cent, in 1890-1894, 0.33 per cent, in 1900-1904 (Gibbons). On the other hand, in communities where syphilis is common the fre- quency of aneurism increases. Thus, it is eleven times more common in the British Army in India than in the civilians at home, and much more common ANEURISM. 621 in the British than in the Austrian and German armies, where venereal dis- ease is five times less prevalent. Aortic aneurism is much more common in men than in women. Crisp 67 women out of 551 cases Agnew 26 women out of 269 cases Lisfranc 13 women out of 154 cases Richter 58 women out of 736 cases 164 women out of 1810 cases 9.05 per cent., or 1 in 11. On the other hand, 48 per cent, of cases of carotid aneurism and 66 per cent, of dissecting aneurisms occurred in women. As regards age Crisp's cases were distributed as follows: 1 to 10 1 50 to 60 65 10 to 20 71 60 to 70 25 20 to 30 51 70 to 80 8 30 to 40 198 80 to 90 2 40 to 50 129 90 to 101 1 59 per cent, between the ages of thirty and fifty. As regards site Lawson gives the following figures: Ascending aorta 34 . per cent. Arch of aorta 34 . 8 per cent. Descending aorta 17.4 per cent. Abdominal aorta 13.8 per cent. Hare and Holder find in 953 cases collected indiscriminately : Ascending 570 = 60 . per cent. Transverse arch 104 = 10.6 per cent. Descending 110=11.5 per cent. Unclassified 169 = 17.5 per cent. figures which are certainly unusually high for the ascending portion. Aneurisms are by no means always single, but may sometimes be mul- tiple. Two, three, " or even a score " may appear along the course of the aorta, or numerous aneurisms may be present in the peripheral arteries. The condition is simply the manifestation of the generalized action of the factors of sclerosis and blood-pressure on the arterial walls, and multiple aneurism formation is one of the features of experimental adrenalin aortitis (Erb, Jr.). The symptoms, signs, and diagnosis present no specific features, except the ease with which the other aneurisms may be overlooked after one is diagnosed. Careful examination and especially fluoroscopic examination will prevent this error. PATHOLOGICAL ANATOMY AND PATHOGEXESIS. No change of pressure that can occur during life is sufficient to dilate an artery to the proportions of even the smallest aneurism. According to the elasticity curve of Hoy, the dilatation occurring between the blood- pressure of 120 and 170 mm. Hg is about 20 per cent, of the diameter of the artery, and the results of Grehant and Quinquaud show that very little fur- ther dilatation occurs if pressure is raised until the artery ruptures (at a pres- sure of 1680 to 4630 mm. Hg; 10 to 20 times the blood-pressure during life). 622 DISEASES OF THE HEART AND AORTA. FIG. 296. Aneurism arising just above a sinus of Valsalva. (From a specimen in the Army Medi- cal Museum, Washington, D. C.) OR., orifice through which the aneurism is connected with the aorta; AN., aneurismal sac. FIG. 297. Aneurism of the ascending arch and innominate artery. (From a specimen in the Army Medical Museum.) D. AOR. Fir,. 298. Aneurism of the transverse portion of the aortic arch penetrating through the sternum. (From a specimen in the Army Medical Museum.) I \.\O^f., innominate artery; L. CAR,, left carotid artery; L.Xl'B., left sublavian artery; D. AOR., descending aorta. FIG. 299. Aneurism of the descending aorta eroding the vertebra;. The sac contains a laminated clot. ANEURISM. 623 Changes in Arterial Wall in Aneurism. On the other hand, as was first shown by Scarpa (1805), aneurismal dilatation is always preceded by changes in the arterial coats and especially by weakening of the media. In 1875 Koester showed that this was due to localized degeneration of the elastic fibres as the result of certain inflammatory changes in the vasa vasorum of the media. "The inflammatory process begins in the vasa vasorum on the exterior of the blood-vessel, follows them perpendicularly into the muscularis (media) , and distributes itself within this layer, being most intense at the places where the vasa vasorum break up into capillaries. As a result of this chronic multilocular mesarteritis, the media (muscle fibres and elastic fibres) degenerate. The intima (which may be thickened) and the adventitia unite to form a thick and very vascular membrane which forms the wall of the aneurism." Since these studies of Koester, writers are practically agreed that the degeneration of elastic tissue result- ing from mesarteritis is the underlying cause of aneurism formation. WALL FIG. 300. Sections through the wall of an aneurism. (Photomicrographs made by Dr. C. S. Bond.) A. Section through the wall of an aneurism showing the clot unorganized. B. Orcein stain showing the destruction of elastic tissue in the aneurism wall. Elastic tissue (ELAS) stained dark. Simple arteriosclerosis in which thickening of the intima is the essential feature does not weaken the wall of the artery and plays no role unless the media be destroyed. This fact is further borne out by the experimental changes in the artery produced by injection of adrenalin (see page 343). The resulting lesion is a mesarteritis without changes in the intima, quite dissimilar to the ordinary arteriosclerosis of man; but aneurisms, and even multiple aneurisms, are present in a large percentage of the animals. Other toxic substances, bacterial toxins, lead, alcohol, nicotin, lactic and other acids, etc., produce these changes. Fabris has also produced aneurisms by external cauterization of the arterial wall with silver nitrate. A local inflammation was thus set up in the adventitia and media, which resulted in degeneration of the fibres of the latter and their replacement with young fibrous tissue devoid of elastic 624 DISEASES OF THE HEART AND AORTA. fibres. In a few cases there was slight intimal thickening. The resistance of such a fibrous tube is less than that of an elastic tube, and aneurismaJ dilatation, sometimes localized, sometimes fusiform, took place in from 20 to 25 days. Etiological Factors. In man the etiological factors of aneurism are those that produce mesarteritis. Chief among these is syphilis, which, as first noted by Ambroise Pare and Lancisi, is concerned in a very large per- centage of the cases (Klemperer 25 per cent., Fraenkel 36 per cent., Puppe 36 per cent., Trier 40.5 per cent., Heiberg 41.87 per cent., Bramwell 50 per cent., Thieberge 50 per cent., v. Xoorden 54 per cent., Gerhardt 56 per cent., Schutz 64.7 per cent., Welch 66 per cent., Etienne 69 per cent., Malmsen 80 per cent., Hanpeln 82 per cent., Backhaus 85 per cent., Heller 85 per cent., Rasch 92 per cent.). This is especially true of aneurisms occurring in young men and women, when the other factors of arteritis play a rela- tively less marked role than in later life; so that, as stated by Professor Osier, the presence of an aneurism in a man or woman under thirty is almost to be regarded as presumptive evidence of syphilis. Moreover, syphilitic aortitis is often most intense in the first part of the ascending aorta, hence the commonness of the lesion at this site (Heller). It must be added, however, that, though the careful researches of Ophiils have failed to substantiate this general belief, a positive Wassermann reaction is usually obtained in such cases. Other factors are alcohol, hard work, lead poisoning, tobacco, gout, nephritis, and especially the infectious diseases. Trauma (blows, gunshot and knife wounds, etc.) furnishes a frequent cause for aneurisms of the peripheral arteries and abdominal aorta, but is much rarer in thoracic aneurisms. Cases like that described by Hirsh and Robins show, however, that it is a factor to be reckoned with. The relative importance of these factors is shown by the figures of Etienne, who found syphilis as a cause of 166 out of 230 aneurisms, while alcoholism was present in only 28. More- over, according to Hamilton, aneurisms are extremely rare in sanitaria for alcoholics. They are, however, most important contributory causes, not only increasing the arteriosclerosis but, by raising the blood-pressure, increasing the liability to dilatation. Thus, aneurisms, according to most writers, are particularly common in syphilitics who perform hard work. This is exquisitely shown in the colored patients at the Johns Hopkins Hospital, in whom syphilis is very common and who, as a rule, perform hard work. Among these persons aneurisms are between five and ten times as common as in the patients in the white wards of the same hospital. The .sudden rise of blood-pressure which occurs during lifting and heavy strains (cf. page 188) is a particularly important predisposing factor, and the patient often notices that his first symptoms occurred at the time of a heavy muscular strain or began just afterwards. EMBOLIC AND MYCOTIC ANEURISMS. A somewhat rarer form of aneurism, described by Tufnell (1853), Ogle ;icSG6), Church (1S70), Smith (1870), Ponfick (1873), and Weinberger <1907). is the so-called embolic or mycotic aneurism, which arises especially ANEURISM. 625 during the course of acute septicaemias, of puerperal, arthritic, and influen- zal origin. Septic emboli become lodged astride of the bifurcation of the smaller arteries, causing necrosis of the neighboring portions of the arterial wall, which may protrude or form a true aneurism, or may rupture into the surrounding tissues, forming a false aneurism. These arise acutely during the course of the febrile diseases. They are usually multiple and are confined to the smaller arteries, while the sclerotic aneurisms are more common in the larger arteries. DEVELOPMENT OF THE ANEURISM. Once formed, the aneurismal sac expands progressively, usually pushed outward from the artery along the lines of the least resistance until it meets with some obstruction. The higher the blood-pressure the more rapid is the dilatation. When pointing freely into the thoracic cavity, it may expand until it fills almost the entire half of the cavity before ruptur- ing. On the other hand, if the proliferation of connective tissue in the wall of the aneurism does not keep pace with its growth, or if local necrosis from infection, pressure, or irritation takes place, a secondary bulging will take place at this point, and it finally ruptures there. A rupture is especially precipitated by high blood-pressure, such as occurs on exertion, and sud- den deaths from this cause are quite common in aneurism. When the wall of the sac presses upon neighboring tissues it begins to erode them. The pressure acts in the following way: First, it cuts off the blood supply to the neighborhood because the pressure within it (aortic pressure) is greater than that in the smaller blood-vessels. Secondly, necrosis of these tissues results from this compression. Thirdly, the products of necrosis are absorbed by the cells in the tissues of the very vascular wall of the aneurism as fast as they are produced. Bone tissue too is absorbed by the activity of the osteoclasts, and the wall of the sac thus advances gradually through the chest wall very much as a tumor might do, though without the intervention of abnormal cells. Thus, the aneurism eats its way through muscle, cartilage, bone, nerves, and skin, and also through the walls of the other vessels (pulmonary artery, vena cava, etc.), bronchi, and oesophagus, always forced onward in a straight line by the arterial pressure in the aorta. Hence, aneurisms usually point in the direction given them by the impact of the blood stream; those of the ascending aorta pointing to the right, those of the arch pointing upward, those of the descending arch pointing backward and to the left (Fig. 301). However, resistance of surrounding tissues, and especially local thinning of the aneu- rismal wall, may cause its course to be deflected somewhat from these typical directions. Rupture. The excessive thinning which results in perforation fre- quently occurs when the sac has just penetrated the wall of one of the sur- rounding structures, bronchus, oesophagus, etc., no doubt from the pres- ence of local infections within their lumina, and sudden death may result from hemorrhage. Or, on the other hand, small hemorrhages may occur from the erosion of smaller bronchial or rcsophageal arteries (see page 627) or through the wall of the aneurism without any such immediate results. 40 626 DISEASES OF THE HEART AND AORTA. The growth of an aneurism after penetrating the chest wall is well shown by the outlines in Fig. 302. The sac becomes larger and larger, secondary sacculations appear upon its surface (Fig. 302), and over these the thinned skin becomes smooth, tense, glossy, and finally of a reddish Fir,. 301. Composite figure showing the relations of various aneurisms to surrounding structures. (Schematic.) OEK, oesophagus; AN SUBCL, aneurism of the subclavian artery; SUP. V. C., superior vena cava; AN INNO^t, aneurism of the innominate artery, pointing through the skin; AN TR, aneu- rism of the transverse portion of the arch; PIIREN, phrenic nerve; REC LAR, recurrent laryngeal; L. VAff, left vagus; DA, ductus arteriosus (Botalli); AN. P. A., aneurism of the pulmonary artery; LBR, left bronchus; AN. KIN VALK, aneurism arising from a sinus of Valsalva; AN. R. COR and AN. L. COR., aneurism of right and left coronary arteries; AN RA, aneurism of right auricle; AN. L.V., aneurism of left ventricle. The arrows show the directions in which the aneurisms usually point. or brawny hue. The whole process usually requires a few months, but it may occur more rapidly. On the other hand, in a case described by Hirsh and Robins the pulsating' tumor upon the chest remained practically unaltered in size for twenty-five years, during which the patient continued to do heavy work. Finally, however, a stage is reached at which a small perforation appears, oozing blood, and soon after, with a rush of blood like ANEURISM. 627 the bursting of a dam, the aneurism ruptures and the patient bleeds to death within a few minutes. The rupture into the bronchus, trachea, or oesoph- agus proceeds in the same way. There is usually a slight premonitory haemoptysis. This generally occurs a few days before death, but may not occur until a few hours before the final rupture; or, as in the case reported by Clarke, it may be present for months. At the final rupture the blood spurts out of the patient's mouth and nose and may even be projected several feet away from the bed. On the other hand, when the aneurism ruptures inter- nally into one of the cavities of the body, the symptoms are quite differ- ent. The patient feels something giving way within. Sudden collapse, asthmatic attack, and gradual exsanguination mark rupture into the pleura. Rupture into the pericardium is attended with intense pain, breathlessness, collapse, an anginal attack, and occasionally a con- vulsion. In rupture into the pericardium death is accelerated by cutting off the venous inflow, just as in simple pericar- dial effusion, only within a minute or two. Of course, under these circumstances no blood appears externally. Rupture of the aneurism into the pulmonary artery, vena cava, . . , -i -i FIG. 302. Tracings of the outlines Or right auricle Or right Ventricle SOme- of an aneurism of the innominate artery, times occurs. The symptoms are usually showing the progress of its growth and J J tlie formation of secondary prominences Sudden Onset Of dyspnoea, Weakness, Often upon its surface. (Tracings made on collapse, and extreme cyanosis, which ends JJ r v d ^ViST'siX ^ ' in death after a period varying from sev- eral hours to several months, the heart being unable to accommodate itself to the sudden changes in the distribution of blood. However, in a large percentage of cases (863 cases 47 per cent. of Arnold's 1829 cases) death from aneurism is not due to rupture of the sac but " from pressure of the sac upon important nerves and blood- vessels, or from secondary changes which take place in these tissues and in other vital organs, as a direct or indirect result of such pressure." In 154 cases without rupture the causes of death were: Obstruction to air-passages 66 Exhaustion ">0 Affections of lungs and pleura 28 Pericardial affections 8 Pressure on the vena cava superior 1 Collapse Clotting within an Aneurism. The healing of an aneurism occurs by clotting within the sac. Since the latter is lined by arterial intima, there is under ordinary circumstances no more reason for clotting to take place there than elsewhere in the artery. As shown by Mall and Welch, arterial thrombosis occurs quite suddenly when the circulation is slowed and pulsa- tion disappears, especially if there is some injury to the wall of the artery, and this is a most important factor in bringing about thrombosis within 628 DISEASES OF THE HEART AND AORTA. an aneurism, though some fibrin ferment must be present. As a rule, in fusiform aneurisms the circulation is too strong and rapid for coagulation to set in, but in sacculated aneurisms a certain amount of fibrin collects along the wall. Each layer of fibrin serves as a filter for leucocytes, from which more fibrin ferment is generated and a second layer laid down, and so on until occasionally the entire aneurism may be filled spontaneously by a laminated clot. Owing to the large area and great thickness of the fibrin deposited, and to the fact that the intimal endothelium is in most places still intact, there is little entrance of fibroblasts into the clot and little organization goes on. The aneurismal clot is, therefore, not converted into a solid mass of connective tissue as in enclarteritis or thrombo-angeitis obliterans, but remains simply laminated fibrin. Deposits of calcium salts sometimes occur upon them, however, and tend to convert the obliterated aneurism into a solid tumor. SYMPTOMS. The signs and symptoms produced by aneurisms vary greatly, and depend upon the site at which they occur along the aorta, so that Broad- bent has been "led to divide thoracic aneurisms into two classes, namely, aneurisms of physical signs and aneurisms of symp- toms, from the predominance of physical signs and symptoms respec- tively, the former term applying to aneurisms of the ascending aorta and first part of the arch, the latter to aneurisms of the transverse and descending portions of the arch." The symptoms produced by aneurisms arise secondarily as the result of pressure upon surrounding structures. Shortness of breath is frequent, resulting both from pressure on the trachea and bronchi and from concomitant disturbances in the circulation (embarrass- ment of heart action, stasis from pressure on veins). Cough is a common symptom, from pressure upon the recurrent laryngeal nerves as well as from bronchitis as a result of pressure (occasionally from tuberculosis). The pressure on the laryngeal nerve causes paralysis of the corresponding vocal cord and gives the cough a peculiar metallic quality known as "the goose cough, brassy cough, stenotic cough, paretic cough," etc. It is really the cough characteristic of paralysis of one vocal cord, and it is characteristic of aneurism only in so far as that the latter is the com- monest circulatory disturbance in which laryngeal paralysis is a symptom. Paroxysmal dyspnoea may occur, and especially in certain postures in which the trachea and bronchi are pressed upon by the aneurism. This ''asthma'' is the most common symptom of patients presenting themselves for treatment, and careless physicians often accept its presence as the final verdict, remaining oblivious to the true nature of the disease. Attacks of dyspnoea or suffocation very commonly come on during sleep when the laryngeal muscles relax and narrow the laryngeal slit. They occur especially when the patient falls into an unpropitious position, so that he soon finds it most convenient to sleep bolstered upright and leaning slightly forward with chin depressed. This position affords the maximum space about the air-passages with the minimum of tension upon them. ANEURISM. 629 Not infrequently a small aneurism of the arch pointing backward and pressing upon the trachea or bronchi may cause actual suffoca- tion, for which tracheotomy may be necessary. In some cases, however, the aneurism may be situated so low that it may be impossible to do the tracheotomy below the area compressed. The only possible means of relief is then to dissect or pull the aneurism away from the trachea, or to intro- duce a metal tube into the latter and thus hold the trachea open at the point compressed. This procedure is, of course, extremely difficult, and under all circumstances great dyspnoea from pressure on the trachea is in itself a dangerous symptom. P ai n is a common symptom in aneurism, and may be of three kinds: 1. Angina pectoris reflex referred pain over the heart or down the arm. This is especially common in early aneurism at the beginning of the ascending aorta and from the sinus of Valsalva, and is probably due to changes in or pressure upon the aortic plexus. After these changes have been long established this pain may disappear (Osier). 2. Sharply localized pain may arise in or about the aneurism itself when its walls are pressed upon, or even spontaneously, and especially when it begins to erode the chest wall. 3. A second form of referred pain arises without reflex mechanism directly from pressure upon the intercostal nerves and those of the brachial plexus, especially in aneurisms of the transverse and descending aorta. The latter may give rise to pain in the back, shoulder-blades, and sides and also down the arm, and may for a while be mistaken for intercostal neuralgia or for the pain of pleurisy. Pain down the arm is especially com- mon when the aneurism involves the innominate or subclavian arteries, particularly when the return of venous blood is interfered with by pressure on the veins. Difficulty in swallowing and the feeling of a lump in the throat may result from pressure upon the oesophagus, especially when the aneurism is adherent to it or is infiltrating its walls. This is, of course, characteristic of aneurisms of the descending portions of the arch and to a less degree of the descending aorta. It is not at all a rare symptom, and yet is by no means as common as might be expected even when the aneurism is large. PHYSICAL SIGNS. 1. The presence of a visible mass upon the chest wall or elsewhere showing a pulsation of an elevation w r hich begins about 0.05-0.10 second later than the ventricular systole (or the first heart sound), and which on palpation is felt to be forcible and expansile in character (i.e., presses out\vard in all directions). The shock with the first sound is usually well felt and often accompanied by a thrill; and a diastolic shock accompanying the second sound is, when present, almost characteristic. 1 On auscultation there is usually a systolic murmur heard over the aneurism, and occasionally a diastolic murmur when the blood flows back into the aorta during diastole, especially through a narrow opening. This is, of course, most common and most marked when aortic insufficiency is present, either organic or relative, resulting from the general dilatation of the aorta. Long before an aneurism perforates, and in many cases when it is not pointing outward but upward toward the episternal notch or clavicles, 1 The writer lias seen one case of hypernephroma of the thigh in which a diastolic shock was palpable, but this is rare even in the most vascular tumors, such as the vascular mediastinal sarcomata. 630 DISEASES OF THE HEART AND AORTA. there may be seen a diffuse systolic lifting of the whole chest wall or of the parts above the tumor. The localized heaving is, of course, most marked when the aneurism is in the vicinity of cartilages or articu- lations in the chest wall and in younger individuals; while the most diffuse heaving occurs in the portions and persons where the ribs and sternum are most rigid. The impulse thrill and shocks, systolic and diastolic, are also frequently present when no heave or pulsation can be seen. For discerning and timing slight pulsations the writer has fre- quently found it convenient to hold the index finger a few millimetres away from the chest wall, and watch for either a periodic narrowing of the slit between the finger and the chest or for a visible movement of the shadow cast by the finger upon the chest. For the latter purpose the light should strike as nearly as possible paral- lel to the chest so as to magnify the movement of the shadow (Fig. 303). When aneurism is suspected, it is particularly important to ex- amine the patient's back as well as to inspect carefully the front of the chest. This precaution was always particularly emphasized by one of the great teachers of medicine who also un- intentionally illustrated its importance. On one occasion he and another pro- fessor, who was visiting the clinic, dem- onstrated to the junior students a case of suspected aneurism, but sent him to the wards for X-ray examination with- out having examined the back. The absolute diagnosis was at once made by the house officer, who in the routine examination discovered a well- marked pulsation at the back at the level of the third thoracic vertebra. Dulness on percussion is of course present over an aneurism as over other tumors, the note being flat when the tumor is near the surface, slightly improved when it is deep. This improvement is often very slight in deeply situated aneurisms of the arch, and percussion, especially in the first right and left interspaces and over the manubrium, should be very carefully carried out when aneurism is suspected. The exact outlining of an aneurism by percussion may be very difficult. The area of dulness on even the lightest percussion may be considerably greater than that of the aneurism itself (just as is true of the cardiac dulness, see page 147). The uniform dilatation of the aortic arch (to about twice its normal diame- ter) which is so frequent in aortic insufficiency may give an area of dulness over and on both sides of the sternum which may lead to a diagnosis of aneurism (Fig. 311). The true nature of the condition can be shown only by the X-ray (Fig. 308). In large and in deeply situated aneurisms direct percussion of the ver- tebral spines by Koranyi's method may show an unusual dulness over the corre- sponding area (especially between the third and the sixth thoracic spines) and may prove of assistance in establishing the diagnosis. It is, of course, of no value in those aneurisms FIG. 303. Method of inspecting for pulsa- tions. E, eye of observer looking down from above; E', eye of observer upon level with pulsating area; finger above pulsating area; K and .S v , shadows thrown by the finger upon the pulsating mass. Solid and dotted lines represent the outlines of the pulsating mass; arrows indicate the extent of movement seen. ANEURISM. 631 of the arch in which the trachea is interposed between vertebrae and the tumor. The heart is occasionally very much displaced by an aneurism which may itself come to occupy the usual site of the heart, so that on casual examination it may be mistaken for the latter. With careful auscultation, however, this error may be excluded. Pressure upon the sympathetic on either side may give rise to inequality of the pupils, usually with a dilatation upon the affected side. In late stages, however, the sympathetic on that side may be completely destroyed and the pupil then becomes smaller on the affected side. The dilatation is best seen when there is moderate illumination, for in strong lights the reflex pupillar constriction may overcome the dilator action of the sympathetic. Tracheal Tug. W. S. Oliver, who described the sign in 1878, gave the following directions:' "Place the patient in the erect position and direct him to close his mouth and elevate his chin to the fullest extent; then grasp the cricoid cartilage between the finger and thumb and use gentle upward pressure upon it; when if dilatation or aneurism exist the pulsation of the aorta will be distinctly felt transmitted through the trachea to the hand." This tracheal tug is no absolute sign of aortic dilatation. It is as readily produced when solid mediastinal tumors or enlarged bron- chial glands adhere to both aorta and air-passages as from aneurism. Sewall finds that in a large percentage of tuberculous individuals (91 out of 212 43 per cent.) a slight twitch of the trachea may be felt during inspiration, due to contraction of the accessory muscles, but this is not continuous, not synchronous with the pulse-beat, and should not be mistaken for the true tracheal tug. Moreover, in his large series of obser- vations this tracheal twitch of non-aneurismal origin was always confined to inspiration, Sewall found it particularly common in cases of tuberculo- sis or old pleurisies in which there was adhesion to the left pleura. Medias- tinal adhesions anchoring the aorta to the air-passages can produce it. Wenckebach has also called attention to the fact that it may occur in cases of enteroptosis, in which the heart is pulled downward with the liver, and the arch of the aorta thus made to pull upon the bronchi. (This is well illustrated by the patient mentioned on page 706.) The tracheal tug is most marked in inspiration. Tracheal Percussion Shock (Smith). H. L. Smith has found that if one lightly taps the chest wall (direct percussion) over an aneurismal area one feels a sudden increase in the impulse as soon as the aneurismal area is reached, a shock resembling "the sensation experienced by one when a rubber bag filled with water is simultaneously palpated and percussed " (semi- fluctuation). The fact that he has been able to elicit it in 62 per cent, of his cases of which only 46 per cent, gave a tracheal tug indicates the usefulness of the sign. In certain cases it is undoubtedly of considerable assistance. THE PULSATION' AND ARTERIAL PULSE IN T ANEURISM. The pulsation over the aneurism resembles the form of the arterial pulse except that owing to the elasticity of the sac the rise and fall are usually more gradual. It is sometimes of importance to determine whether the pulsation corresponds to an aortic aneurism or an aneurism of the ventricle. This requires the most carefully timed tracings simultaneously 632 DISEASES OF THE HEART AND AORTA. from apex and tumor. If the pulsation in the aneurism begins .07-.09 second later than the apex beat, the aneurism may be assumed to arise from the aorta. If it arises from the ventricle, the two will, of course, be synchronous. On the other hand, as occurred in a case still under the writer's observation, the two pulsations may be absolutely synchronous and yet X-ray and other signs may show that the aneurism arises from the aorta. Delay and Inequality of the Pulse. Inequality of the pulse in cases of thoracic aneurism was recognized by Harvey, who stated very correctly that " the pulse in the corresponding arm was small in consequence of the greater portion of the blood being diverted into the tumor and so inter- cepted." The nature of this inequality was made the subject of a careful clinical and experimental study by Marey and Frangois-Franck, who found that when an aneurism with elastic walls occurred along the aorta it served to damp the oscillations of pressure in the arteries nearest to it and thus to make the pulse smaller in these arteries. The pulse-wave thus became smaller and its onset less sud- clen ' the u P stroke becoming very oblique (pulsus tardus). Certain aneurisms, however, have no effect on the pulse, and it may be even larger upon the side of the aneu- FIG. 304. Effect upon the circulation of in- . , , ,. i i terposing (A) an inelastic, and (B) an elastic bulb HSm than Upon the Unattected Side. along the course of an artery in a model of the Marey and Francois- Franck showed circulation. (Modified from Francois-Franck.) * . * . 1, 2 3 represent successive time markings. upon their models that if the Sac VE.VT, pressure curve within the model of the inplastip thp nill^P-wavp ventricle; ART, pressure curve within the mod el ^ d -Wave artery. A, normal artery. The elastic sac dimin- W a S increased On the a f - ishes the size of the pulse, delays the upstroke, f 1 l i -j. and delays the transmission of the pulse-wave. I C C t 6 U Side, and its Character became collapsing. Owing to this damping of the pulse-wave, the maximal and minimal blood-pressures in the arteries nearest the aneurism tend to approach the mean pressure, so that the maxi- mal pressure may be from 5 to 30 mm. lower than the maximal pressure in the opposite arm, though there may be a considerable difference in the size of the pulses without any marked difference in maximal or minimal pressures. The minimal pressure, being already nearer to the mean, is less affected than is the maximal, and often no difference can be noted. Changes in the size and in the quality of the pulse in the two radial arteries are much more marked to the palpating finger than to the instrument, for the slowed circulation may be compensated by a local vasoconstriction which causes a smaller pulse without appreciable change in the pulse-wave. The pulse is usually smaller and less sudden on t h e side nearest the aneurism, and hence often appears to be retarded when this is not actually the case, though in actual fact the onset of the pulse-wave is synchronous and only the summit of the pulse-wave is belated (Francois-Franck, Marey, v. Ziemmsen) (Fig. 283). Francois-Franck and Marey showed, however, that, both in man and in the model, the presence of an elastic anetirismal sac along the aorta caused a general slowing in the transmission of the pulse-wave (apex beat radial pulse interval = 0.2-0.22 second instead of 0.12-0.14 second) 1 in all the arteries, so that the pulse-wave in both radial arteries begins at exactly the same time. When the aneurism arises not from the aorta hut upon the innominate or the subclavian artery, the result is different. The pulse-wave in the aorta now advances at the usual rate (apex radial = 0.12-0.14 second), while the 1 In cases in which aortic insufficiency is present, especially with aneurisms of tha ascending arch, this delay of the pulse-wave is not present. ANEURISM. BSB IHBBS! FIG. 305. Effect of aneurisms at various sites upon the blood-pressure, rate of transmission, and the form of the pulse-wave. (Schematic.) Bp, blood-pressure in mm. Ilg ; lift, pulse in right radial artery; LR, pulse in left radial artery. I. Aneurism upon innominate artery. II. Aneurism upon the ascending aorta. III. Aneurism upon the transverse portion of the arch of the aorta. IV. Aneurism upon the left subclavian artery. The first column of figures indicates blood-pressure in mm. Ilg; the second column indicates the transmission time of the pulse wave in seconds. The figures given are typical, though the differences are larger than are usually encountered. transmission in the artery from which the aneurism arises is slowed. The pulse-wave is, therefore, definitely retarded (0.05 to 0.07 second later than in the other radial), in some cases even when there is no difference in the suddenness of the upstrokes. This dif- ference in the time of the pulse-waves when pr e s e n t furnishes a means of differentiating between aneurism of the innominate or subclavian artery, and de- monstrates that the aorta itself is not involved (Francois -Franck). This fact may be of great practical importance in determining the oper- ative treatment, especially where the shadowcast by the aneurism lies close to that of the aorta. How- ever, this delay in the pulse does not occur in all aneurisms, but only in those whose walls are elastic, the FIG. 30f>. TJadial pulse tracings from the right and left greater number. It mav also disap- r f dial f te f ri f s of a pa ' u ; i!t with an of V' e first p : irt ," f . . , , the arch of (lie aorta. Hie upstroke of the pulse-wave in the pear as clotting occurs along the right radial artery, which is nearer to the aneurism than the Walls of the aneurism, and the elas- left, is more gradual than that in the hitter. ticity of the sac is thus lessened. In view of these facts, it is evident that the form of the pulse tracing is of no more value than the simple palpation of the pulse in the diagnosis of aneurism, and the only graphic method of practical importance is that of taking simultaneous tracings from both radial or both carotid arteries 634 DISEASES OF THE HEART AND AORTA. in cases where it is necessary to determine whether an aneurism is confined to the innominate, subclavian, or carotid artery, or whether it also involves the aorta. These relations often cannot be shown by the X-ray and rest upon this differentiation alone. X-RAY EXAMINATION. Most of the things which are inferred from physical examination can be actually seen \vith the fluoroscope, and an exactness of diagnosis can be reached which is utterly impossible with the ordinary methods. In 104 cases of aneurism thus examined by Baetjer, the clinical diagnosis had been correctly made in 70 per cent. ; there had been tentative diagnosis of aneurism in 20 per cent. ; and an unsuspected aneurism had been discovered with the X-ray in 10 per cent. These findings are particularly important, since it is just in these early cases when the physical signs are still indefinite that treatment may be profitably instituted. However, unless certain precau- tions are taken in the examination an aortic shadow may be seen which may be diagnosed an aneurism even though none be present. This rounded shadow is cast by the arch of the aorta just to the left of the sternum, and it may be specially marked if the aorta is somewhat tilteel, as sometimes takes place in enteroptosis (Wenckebach). Holz- knecht has shown, however, that this error will not be made if the patient is also turned so that the rays pass from left back to right front (Fig. 81). The normal aorta thus lies in a plane parallel to the rays and is seen as a narrow nearly vertical band, with the light spaces of anterior and posterior mediastinum in front and behind it. The uniformly dilated aorta appears as a wide but uni- form band. The aneurism of the ascending aorta appears as a battledore or tennis racket with handle up, the aneurism of the arch as a racket with handle down. Aneurisms of the innominate are separated from the aortic shadow by a clear space which is bridged by the narrow shadow of the artery. As Baetjer states, it is most important to examine the chest for mal- formations and for misplacement of the aorta which might be mistaken for aneurism. Persistence of the ductus arteriosus (Botalli) must also be considered in shadows near that of the descending arch. The shadow of enlarged mediastinal glands is usually speckled or blotchy with occasional lighter areas, rather than uniformly dark, while the edges of sarcomata and other. solid tumors are often irregular and may fade away gradually Fir,. 307. Radiograph of a patient with a large aneurism of ascending aorta and the arch, viewed from behind. (Kindness of Prof. 0. M. Cooper.) ANEURISM. 635 into the surrounding tissues. Moreover, unless there is a considerable degree of intrasaccular clotting, an aneurism will be seen to expand during systole and to contract in diastole, 1 whereas a solid tumor will at most rotate upon its axis. CHARACTERISTIC FEATURES OF ANEURISMS AT DIFFERENT SITES. Characteristic features of thoracic aneurisms are given in the table below. It must be borne in mind, however, that these represent the con- ditions only while the aneurisms remain relatively small, for with their fur- ther gro\vth they may press upon other structures and so present the picture of an aneurism affecting a different part of the aorta. Large aneurisms also displace the heart, and may even occupy the usual position of the latter. FIG. 308. Radiograph of a patient with dif- FIG. 309. Diagram of the radiograph shown fuse dilatation of the arch of the aorta. (Kind- in Fig. 308. The broken lines indicate the nor- ness of Prof. C. M. Cooper.) The figure also shows mal outlines. AO, aorta; OES, oesophagus; LV , dilatation of the left ventricle and slight dilatation left ventricle. of the left auricle. Aneurism of the Heart. Symptoms. Indefinite signs of cardiac weak- ness. Physical signs. Two points of maximal impulse over which tracings show exactly synchronous pulsations (this point is far from pathogno- monic). Irregular outline of cardiac dulness (encapsulated pericarditis, pleurisy, and tumors must be excluded). Sometimes systolic and diastolic murmurs over heart and aneurism not present over aorta. Pulse. Feeble but equal and not delayed. X-ray. Bulging of shadow of ventricle or auricle with enlargement of shadow synchronous with systole of correspond- ing chamber. Rupture. Into pericardium. Death often from cardiac weakness or coronary sclerosis. Aneurism of Coronary Arteries. Symptoms. Xo characteristic symp- toms. Occasional cardiac pain. Physical signs. Arteriosclerosis. Xo characteristic signs or even signs of illness. (Aneurism usually size of pigeon's egg.) X-ray. Xo abnormal shadows. Rupture. Into peri- cardium in 19 out of 21 cases. In one case into pulmonary artery. Ascending Aorta; Intrapericardial (Aneurism of Symptoms). St/mp- toms. Angina pectoris. Attacks of cardiac asthma. Precordial pains. 1 Ilolzknecht particularly emphasizes the importance of using the lead diaphragm in examining the edges of the shadow for pulsation. 636 DISEASES OF THE HEART AND AORTA. Pain down right or left arm. Shortness of breath. Symptoms of cardiac failure predominate. Physical signs. Distention of veins of head, neck r upper chest, arms; O2dema of these parts. Tracheal tug absent while aneurism is small. Pupils equal if aneurism is small. Aneurism usually small, situated in second and third right interspaces. Pulsation in second and third right interspaces. Often signs of aortic insufficiency. General oedema from aortic insufficiency. Pulse. Delay of pulse-wave uniform. Pulses may be equal in both radials or may be smaller in either. X-ray. Inverted racket-shaped shadow in left post, to right ant. illumination. Arch of aorta clear. Rupture. Into pericardial cavity. Pulmonary artery. Right auricle. Superior vena cava. (Esophagus. Left auricle. Right ventricle. Left lung. Right lung. Other causes of death. Dyspncea. Exhaustion. Hydrothorax. Hydropericardium. Bronchitis and pneu- monia. Pulmonary infarction. Suffocation. Aneurism of the Ascending Aorta between Pericardium and Innominate Artery (Aneurism of Physical Signs). Symptoms. Slight dyspnea. Pain when aneurism presses on or erodes chest wall. Often an accidental finding. Physical signs. Flushed face with dilated veins; sometimes oedema. Di- lated veins of arms. Pulsation in second, third, and fourth right interspaces (occasionally shifting). Dulness to the right of the sternum, not over the manubrium. Systolic, sometimes diastolic murmur, thrill and diastolic shock over aneurism. Tracheal tug, if aneurism is large. Pulse. Uni- form delay of pulse, both sides synchronous. Right radial usually smaller than left. X-ray. To right of sternum in second to fourth interspaces; best made out in post. -ant. or right post, to left ant. illumination. In left post, to right ant. illumination inverted racket-shaped shadow. Compli- cations. Often aortic insufficiency. Bronchitis. Tuberculosis of right lung. Hemorrhage. Right hydrothorax. Rupture. Into pericardium. Right pleural cavity. Right bronchus. Right auricle. Superior vena cava. Aneurism of the Innominate Artery. Symptoms. Like those of an- eurism of arch except that there is no dysphagia in small aneurisms. Pain and numbness down right arm and to right shoulder. Physical signs. Dilated veins and swelling over right arm and right side of face. Dulness extends out under right clavicle. Pulsating tumor may be felt under the right clavicle. Paralysis of right vocal cord. Right pupil in early stages larger than left. Pulse. Right radial pulse smaller and definitely later than left. X-ray. A f-shaped shadow is seen upon the left arm of the V which the shadow of the innominate artery makes with that of the aorta on left post, to right ant. illumination. Complications. Right- sided bronchitis. Bronchopneumonia. Tuberculosis. Hydrothorax. Rupture. Usually points upward and outward toward the clavicle, but may point downward to pleura or bronhci. Aneurism of the Arch of the Aorta (Aneurism of Symptoms). Symp- toms. Change in voice, especially high notes. Brassy cough. Difficulty in swallowing. Pain in throat. Dyspncea, sometimes amounting to suffo- cation. Physical signs. Inequality of pupils. Usually dilatation of left pupil. Dilated veins, flush, and sometimes swelling over left side of face, chest, and left arm, or changes bilateral. Tracheal tug early. Pulsation palpable in suprasternal notch. Pulsation in suprasternal and supraclavic- ANEURISM. 637 ular fossae. Lifting of manubrium; later perforation of manubrium or sternoclavicular articulation. Palpable heaving, systolic, and diastolic shocks, and often thrill over manubrium. Heart sounds: usually systolic murmur and sometimes diastolic murmur over the tumor. In aneurism beyond the innominate, the systolic murmur may be heard in the left car- otid and brachial but not in the right. Bronchoscopy may show tumor per- forating bronchus. X-ray. Shadow racket shaped, especially seen in left post, to right ant. illumination. Post. -ant. or ant. -post, illumination seen as massive shadow above that of the heart. Complications. Bronchitis. Tuberculosis. Suffocation (asphyxia). Inanition. Rupture. Externally (anteriorly through manubrium or above clavicle). Into left bronchus. Trachea. (Esophagus. Lungs and pleural cavity, pericardium, mediasti- num. Pulmonary artery. Other causes of death. Exhaustion. Pericarditis. Collapse. Suffocation. (Edema of larynx. Pneumonia. Tuberculosis. Aneurism of the Descending Aorta. 1 Symptoms. Lancinating and bor- ing pains in back, left shoulder, left side, and left side of abdomen. Stiffness of back. Shortness of breath. When the aneurism is near the diaphragm, abdominal pains may be present and the condition may be considered to be abdominal. Physical signs. Visible pulsation just to left of spinal column. Dulness on percussion. Heart sounds and corresponding shocks over aneurism and tenderness over corresponding spines. Areas of hyper- sesthesia or analgesia in corresponding spinal segments. Pulse. Pulses synchronous; smaller and more gradual in left than right. X-ray. ^-shaped shadow to left of sternum, especially in right posterior to left anterior illumination. Complications. Left-sided bronchitis, broncho- pneumonia, tuberculosis, hydrothorax, paraplegia from erosion of vertebrae. Rupture. Backward and externally; into oesophagus, left pleural cavity, right pleural cavity, bronchi and lungs, pulmonary artery. Other caucec of death. Pressure on trachea and bronchi, exhaustion, pneumonia, and tuberculosis. The following histories illustrate typical cases of aneurism: ASCENDING AHCH ABOVE PERICARDIUM (ANEURISM OF PHYSICAL SIGNS). D. N. L., aged 45, married. Except for a well-compensated aortic insufficiency for the past eight years, with slight shortness of breath, he has been quite healthy. In November, 1903, his aneurism was discovered accidentally by his brother, who is a physician. Examination by Dr. Osier revealed a well-nourished man who does not appear ill. Face a little congested, veins of neck and arms full; pulse 48 per minute, both apparently synchronous, a little larger on left than on right (maximal pressure: left arm 140; right arm 125). There is no tracheal tug. Over the thorax a wavy impulse is seen in all the right interspaces above the liver, and an area of dulness as outlined in Fig. 310, A. Rela- tive cardiac dulness in fourth interspace extends 16.5 cm. to left and 15 cm. to right of midline. Over the aneurismal area there is a marked systolic thrill and murmur; over the heart a svstolic and diastolic murmur. 1 In 120 cases of aneurism of the descending aorta collected from the literature Milanoff found pain in 72, dysphagia in 20, luematemesis 13, haemoptysis 21, left -sided pleural effu- sion in a fe\v cases. Andreef found only 8 cases of paraplegia from aneurism in the litera- ture. The duration is often from 10 to 15 years; longer than that of aneurisms elsewhere. The condition is very well discussed in English by Osier and more recently by Hewlett and Clark, who give excellent radiographs and a very useful summary of the literature. 638 DISEASES OF THE HEART AND AORTA. X-ray examination by Dr. Baetjer showed the pulsating shadow of an aneurism of size corresponding to the area obtained on percussion, arising from the ascending arch of the aorta. Patient left the hospital, and one month later died without warning while asleep. The only signs of the approaching end were fifteen minutes of stertorous breathing. Autopsy revealed a large aneurism corresponding to that diagnosed clinically, as well as arteriosclerosis and aortic insufficiency. There is no note of rupture of the aneurism. FIG. 310. Cardiac dulness in cases of aneurism. A. Ascending aorta (D. N. L.1. B. Suhclavian artery (J. B.): the shaded area indicates the tumor, the curve indicates the pulsation. C. Second part of the transverse portion of the arcli (K). ANEURISM OF INNOMINATE ARTERY. J. R., aged 44. Had syphilis 13 years ago, otherwise healthy. Two years ago complained of aching in right shoulder and right side of neck down arm to hand. No [join in chest. There were swelling of feet and ankles and shortness of breath. About this time he began to have troublesome paroxysms of coughing. In May, 1903, noticed that his voice was ''cracked.'' In August. 1903, he noticed a pulsating .swelling above the right clavicle. This was diagnosed as aneurism of the innominate, and the right carotid was li gated above the tumor. The subclavian could not be ligated, as the patient took chloroform ANEURISM. 639 badly. After the ligation the tumor rapidly increased in size. When he entered the Johns Hopkins Hospital two months later, his voice was husky, the right pupil was larger than the left (irritation of the right sympathetic ganglia), and a large rounded pulsating tumor was seen occupying the position of the manubrium and extending out along the right clavicle (Fig. 310, A, B). The prominence of this tumor is shown in Fig. 302. Over the tumor a well-marked systolic and diastolic shock may be felt. The two heart sounds are heard over the tumor. There is some resonance on percussion between the tumor and the heart. The area of cardiac dulness is not enlarged, but a soft diastolic murmur is heard at apex and base. The right radial pulse is smaller than the left and a little delayed. The blood-pressure varied, at first being 160 in left arm, 140 in the right brachial, later reach- ing 150 in right and 130 in left. Patient was seen by Dr. Finney, but wiring and other operative procedures were considered impracticable. He was kept at rest in bed on restricted diet, but nevertheless the aneurism grew rapidly, as shown by the successive elevations in Fig. 302. On Dec. 2, at 4.00 A.M., he felt a severe throbbing in the aneurism, and a couple of smaller bulgings (Fig. 302) appeared upon its surface, which had not been present the day before, and the whole aneurism appeared to be definitely larger. The patient insisted upon leaving the hospital at once to return to his home in South Carolina. ANEURISM OF THE FIRST PART OF THE TRANSVERSE ARCH OF THE AORTA. J. D., an unmarried sailor, aged 37, entered the Johns Hopkins Hospital on Jan. 5, 1909, complaining of pain in the chest and inability to sleep. He had had no infectious diseases except gonorrhoea, denied spyhilis, and gave no history of secondaries. Except for occasional sprees, he uses alcohol in moderation. As a sailor he has always done heavy work. He was well until about four months before admission, when he had an attack of "heavy pressure" and tightness across his chest at night, and some weeks later stinging pains in his chest 3-4 cm. above the xiphoid process, which seemed to radiate to both sides of the chest and to pass through to the back. The pressure kept him from sleeping. Upon examination the veins upon the left side of the neck were found to be dilated, and the veins were much more prominent than on the right. There was no tracheal tug. There was an area of dulness behind the medial end of the right clavicle, the manubrium, and the medial half of the left clavicle, which was continuous with the upper border of cardiac dulness. The left radial pulse was somewhat smaller than the right and seemed to be a trifle retarded. Maximal pressure in the right radial ranged from 115 to 130 mm. Hg, in the left from 85 to 110 mm. Hg. . Fluoroscopic examination by Dr. Baetjer showed a pulsating tumor about the size of a hen's egg projecting almost entirely to the left of the sternum opposite the first and second interspaces (transverse portion of the arch of the aorta). The patient was discharged somewhat improved after a short sojourn in the hospital. AXEUKISM OF THE LEFT SIDE OF THE TRANSVERSE ARCH. H. D. K., brush-maker, aged 49, admitted to the surgical service of the Johns Hopkins Hospital on March 14, 1908, complaining of aneurism. Family history was negative. He had been perfectly healthy all his life except for an attack of pleurisy six years before admis- sion, an attack of gonorrhoea at 19, and a chancroid, not followed by secondaries, at 25. Two weeks before admission he felt a burning pain in the left chest and had some shortness of breath, both of which have become worse since then. He sometimes is awakened with shortness of breath and precordial pain. For the past year his voice has been husky, a condition which set in suddenly after violent exertion while splitting wood. He is a well-nourished man of rather anxious expression. The pupils are equal and react to light and accommodation. There is a well-marked tracheal tug. Chest expansion is slight on respiration. There is a definite pulsation over the first left interspace and sternoclavicular junction, in which area the shocks accompanying the two sounds are readily palpable. Note by Dr. Boggs. H e a r t : Maximal impulse in fifth left interspace 11 cm. from midsternal line; dulness extends to this point on left, reaches above to middle of third rib, and on right 2.5 cm. in third left interspace. Cardiohepatic angle is normal. There is d u 1 n e s s behind the man u b r i u m , extending to left, as per diagram, S.5 cm. 640 DISEASES OF THE HEART AND AORTA. in first interspace and below to second interspace, on the right to just beyond the sternal margin. On palpation over the dull area there is a strong lifting pulsation, maximal at a point 5.5 cm. to left and definitely expansile. No thrill felt. Diastolic shock well marked. At apex and inward toward the base there is a very short systolic murmur, which is not transmitted beyond the border of the heart. First sound is rather tapping at apex. Along the left sternal border this murmur increases in intensity and is maximal over the mass above the heart at the point of greatest pulsation, where there is a well- marked systolic bruit followed by a ringing second sound. A very faint systolic murmur is heard at the aortic ring, and the second sound is clear. No diastolic murmur. The second pulmonic is louder than the second aortic. The pulse is of good volume, regular, rather high tension, and not collapsing. Vessel wall definitely thickened. Some cyanosis of finger-tips and lips. The volume of the pulse on the right side is decidedly larger than on the left. There is a circumscribed area of dulness in the left interscapular region in which percussion note has a peculiar wooden tympany like that over consolidated lung. Over this area the breath sounds are rather more intense than over the rest of the lung but they are not tubular in character. On January 20 the aneurism was wired, under Schleich solution anaesthesia, by Dr. Finney, with twelve feet of silver-copper wire, through which a 10-MA current was passed {Moore Corradi method). Clotting took place promptly. The patient stood the opera- tion well. The patient was considerably relieved as regards pain, but the pulsation soon returned, ANEURISM OF THE DESCENDING AORTA. Notes of the following case are taken from the records of the Johns Hopkins Hospital: C'h. L., colored laborer, aged 48, was first admitted to the Johns Hopkins Hospital on October 14, 1898, complaining of pain in the back, left side, and abdomen. His family history was negative. He had always been healthy, but had measles, whooping-cough, tertian malaria, and at 17 had syphilis which was not adequately treated. He has done a great deal of hard work on a farm, has drunk a great deal of whiskey, and smoked heavily. His present trouble began suddenly about four years ago, when he was seized with a severe pain in the lower left abdomen. This lasted a couple of weeks. It was always relieved when his thighs were flexed upon the abdomen, and was always increased after exposure to bad weather. Four years after this a pain in the left side of the back appeared, which has gradually increased. This also is relieved by flexing the thighs. For the past, six years he has passed blood in the stools during periods when the pain in the left flank was worse. A note by Dr. Futcher at that time states, that " the patient was found lying in bed on the left side with the knees flexed. Pupils are of normal size, equal, and react to light and accommodation. The lung expansion and vocal fremitus are diminished over the entire left lung, and the breath sounds were exaggerated in front and in the axilla. There were a few moist rales in the third and fourth left interspaces. Behind, the breath sounds are very indistinct below the angle of the scapula. The percussion note was found to be i m p a i r e d over the entire left front as far down as the fifth rib and over the entire left back, being flat below the angle of the scapula. Heart. The maximal impulse was seen in the fifth interspace 7.5 cm. from the mid- line, but dulness extended 3 cm. to the left of this point. Both the first and second sounds were reduplicated. The liver was slightly enlarged; the spleen just palpable. There were no masses nor areas of tenderness in the left flank to account for the pain. On Oct. 21 Dr. Futcher noted a definite heaving of the entire body of the sternum and a well-marked systolic retraction in the eighth, ninth, and tenth left interspaces be- hind. A tracheal tug was present, but the vocal cords were not paralyzed. The pulse was equal on the two sides. In spite of rest, restricted diet, and potassium iodide and repeated gelatin injections, his pain in the back gradually became worse, compelling him to seek relief by lean- ing over tbe back of the chair. It became so severe that it was not relieved by 30 mg. (gr. ss) of morphine. However, later in his stay his condition gradually became better and the pain became a little less frequent and less intense. ANEURISM. 641 There was very little change in his condition between that time and March, 1902, when for the first time there was noted a definite systolic pulsation in the left interscapular region which gradually increased until it involved three ribs and interspaces. His condition gradually became worse. Respiratory movement almost entirely disappeared upon the left side and a scoliosis developed with concavity toward the right. The area of cardiac dulness increased to the right, where pulsation was particularly well marked and a superficial scratchy systolic murmur was heard over the precordium. His pain became so intense that he could but rarely lie down. An area of absolute analgesia devel- oped in the sixth and seventh left interspaces, impaired sensibility to heat, cold, and pain being found in the fifth interspace as well. About this time he began to feel pain on swal- lowing, referred to the middle of the sternum. During the night of Oct. 25 he complained of pain and intense shortness of breath, and suddenly vomited about 50 c.c. of bright red blood. Ten minutes later he vomited 25 c.c. more blood. He was quieted with morphine during the night, but in the early afternoon of the twenty-fifth he vomited about 500 c.c. of blood within three minutes, became pulseless, and died. At autopsy the heart was found to be displaced to the right (extending 8 cm. to the right of the midline) by a tremendous aneurismal sac 18X14X9 cm. This sac was fusiform with sacculations at its upper and lower ends. It arose from the descending part of the arch and the descending aorta itself and pointed backward, eroding the bodies of all the thoracic vertebrae from the fifth to the tenth as well as the seventh, eighth, and ninth ribs. The erosion of the intervertebral disks was much less marked. The aneurismal sac also compressed the oesophagus at the level of the bronchial bifurcation, where it eroded through the oesophageal wall, making an opening 2.5 cm. in diameter. "The edges of this aperture were ragged and necrotic; the tissue about it dark gray-green in color." The aneurismal sac was partly filled by a large lamellated clot. The ascending aorta was dilated and atheromatous; the descending aorta below the aneurism likewise. The heart was much enlarged; the walls hypertrophic; the valves normal. There were many pericardial adhesions, especially firm over the left auricle and the coronary veins, and there were tortuous patches over both ventricles. The stomach contained a litre of clotted blood. Other organs normal. SIMPLE DILATATION OF THE ARCH. L. D., gardener, aged 55. native of Ireland, came to the Johns Hopkins Hospital Dispensary on July 13, 1909, complaining of pain on swallowing and trouble in passing water. The family history was negative. The patient had smallpox at is, gon- orrhea at 35 and again at 4S. and a chancre at 35 followed by definite secondary manifestations, for which he had been given medicine by mouth. He has drunk whiskey in excess and has done a good deal of heavy work. He was perfectly healthy until the past ten days, since when he feels food passing down his oesophagus and has a little pain which is referred to the level of the cardia. He vomits immediately after eating, but can swallow liquids without difficulty. Examination 'reveals a fairly nourished man of ruddy complexion witli some dilated venules. The left pupil is somewhat larger than the right, though both react to light and accommodation. There is a slight but dennite tracheal tug; no tracheal percussion shock. There is no glandular enlargement. The lungs are clear except for a few widely scattered piping rales. 41 Fie. 311. Area of cardiac dulness in a patient 'I.. D.) with dilated arch of the aorta. 642 DISEASES OF THE HEART AND AORTA. The heart is not enlarged; apex in fifth left interspace 10 cm. from the midline. Dul- ness extends 4.5 cm. to the right. The relative dulness is continuous above with a strip 3.5 cm. upon either side of the sternum, over which the percussion note is very slightly impaired. This area extends up as far as the upper border of the second rib, and is shown by the fluoroscope to correspond with a uniform shadow of the dilated aortic arch. The heart sounds are clear; the second aortic distinct; no diastolic murmur present. Pulse is of good volume, not collapsing. Abdomen shows no masses; no visible peristalsis. There are no tenderness and no ab- normalities palpable. The stomach tube is passed into the stomach without difficulty, and a very small amount of clear fluid, free from HC1, obtained; lavage fluid clear. Des- inoid test negative. He was given alkaline gentian tincture + strychnine (1 mg. = $ gr.) before meals, under which treatment his symptoms rapidly diminished. Diagnosis : Chronic alcoholic gastritis, anacidity, dilatation of the aortic arch. ANEURISM OF THE ABDOMINAL AORTA. M. P., machine agent, aged 30, was first admitted to the Johns Hopkins Hospital on Oct. 31, 1899, complaining of kidney and stomach trouble. The family his- tory was negative. The patient had had measles, chicken-pox, mumps, and whooping-cough, typhoid fever at 23, followed by pain in the ankles and knees. He had gonorrhrea two years before admission (about one year before the onset of the present trouble), but denies lues. He worked on a farm until his attack of typhoid fever, since when he has not been strong. He does not drink nor smoke and is a hearty eater. The present illness began six months before admission, with some soreness and pain in the abdomen, which had no relation to the taking of food except that it was more intense after a large meal. He vomited occasionally but rarely. The pain was at first a sharp throbbing pain in the left side. It was so severe as to cause him to remain in bed for a period of three months, during which he had to be given morphine. After the three months' sojourn in bed the pain became less, and he was almost free from symptoms for about six weeks, when he was taken with a sudden sharp cutting pain in the right side just under the ribs, running around toward the right and down toward the testicle. On examination he was found to be a well-nourished man of rather sallow color. There was no glandular enlargement. The lungs were clear on auscultation and percussion. The heart was not enlarged; the heart sounds clear. In the abdomen there was a very well-marked pulsation visible in the epi- gastrium. There was dull tympany over this area, and inflation of the stomach showed that the pulsating mass was covered by the latter. There was considerable tenderness over the pulsating area; Dr. Osier was able to make out a definite soft systolic mur- mur, and on Nov. 5 with the deepest possible palpation could make out a definite mass with expansile pulsation. The case was diagnosed as abdominal aneurism and wiring was advised. This was performed by Dr. Finney two months later. Note by Dr. Finney. An incision was made 2.5 cm. befow the xiphoid. The stomach was retracted downward; the lesser peritoneum was opened. The pancreas covered the lower surface of the tumor. Attempt was made to <1 i s s e c t the pan- creas. This was abandoned on account of profuse and persistent hemorrhage. The incision was then enlarged upward, the edge of the liver elevated, and the tumor exposed above and to the right of the pancreas. A needle was inserted at this point to a depth of 3-4 cm. and 8-9 feet of silver and copper alloy wire introduced. Ten milliamperes of current were passed for one hour. The needle was withdrawn, the wire cut close to the aneurismal sac and turned in with a clamp. Xo bleeding:. One or two bleeding points about the pancreas were tied with fine silk. The incision was closed. The patient made an uneventful recovery and experienced considerable relief from pain, so that nine months later it gave him little trouble, though the aneurismal pulsation was still expansile. There was now a loud systolic murmur over the mass. The pain, however, gradually returned and never left him. It was so severe that he was a frequent visitor at the hospital and was compelled to use a good deal of morphine. He was admitted to the writer's ward in Jan., 1904, somewhat worse than at any time previously. The aneurismal mass now extended from the ensiform to within 3 ANEURISM. 643 centimetres of the umbilicus. Its surface was smooth and no areas of bulg- ing could be made out. On Jan. 7 the leucocytes were 5000; the hsemogolobin 90 per cent. He was quite well (when given morphine) until the night of Jan. 21, when he had a s u d d e n a 1 1 a c k of most intense pain in the lower back and abdomen, "causing him to cry out and toss about, arching his back and stiffening all his muscles in his attempts to bear the pain in silence." There was no objective change in the abdomen, but the tenderness over the aneurism was more marked than before. The next day he had several attacks of pain and vomiting. At 4.00 P.M. the vomit- ing was very severe and was accompanied by intense pain and sudden collapse. His color became a ghastly pallor. He became almost pulseless before any one could reach him. He was still conscious and complained of great pain in the back and right side of the abdomen, to relieve which .15 Gm. (gr. iiss) of morphine were necessary, given within an hour. At 5.45 P. M. a small saline infusion was given and caused the pulse to improve slightly. Strychnine, 2 mg. (sV g r -)> + digitalin (German), .15mg. (TO gr-)> had no effect. The maximal blood-pressure before the collapse was 130 mm. Hg, after it was 70 mm. Hg. The next day there was dulness throughout the right flank extending up to liver dulness (due to outpouring of blood into the peritoneal cavity). The systolic murmur over the tumor disappeared, but the aneurismal mass still pulsated. The haemoglobin was found to have fallen to 55 per cent.; the leucocytes rose to 17,500. During the next few days the patient's condition seemed to improve. The pulse became stronger; the maxi- mal blood-pressure rose to 120 mm. Hg. However, his kidneys absolutely ceased secreting. He did not void at all spon- taneously, and 50 c.c. of clear reddish liquid, of neutral reaction and with a specific gravity of 1030, was all that could be obtained on catheterization on the evening of Jan. 24. It contained a large amount of albumen, no sugar, no casts, a few red blood- corpuscles, and a large number of pus-cells. This was the last urine obtainable, even by catheter. From this time on the patient's condition became worse. He complained of sudden shocks like electric shocks through his nervous system, to which he responded; by s u d d e n single twitches. lie had no general convulsions. His mind remained! perfectly clear, his pulse good until the morning of Jan. 26 (five days after the rupture), when his pulse gradually became weaker, he lapsed into unconsciousness, and died at 10.30 P. M. Autopsy confirmed the clinical diagnosis, showing a large s a c c u 1 ar aneurism of the abdominal aorta which had ruptured into the retropori- toneal tissue and lesser peritoneal cavity, causing infarction of the left kidney and oblitera- tion of the vessels to the right. There was thrombosis of all renal vessels and a tremendous hemorrhage into the greater peritoneal cavity as well. This rupture had evidently occurred at the time of the collapse on Jan. 22. There was an island of clot within the coil of silver wire within the sac, but a w i d e free blood channel between this clot and the aneurismal wall, so that the clot had not strengthened t h e I a 1 1 e r in the least. It is probable that during the months following the wiring, while he was free from pain, the clot filled the entire aneurismal sac, and that the eddy currents dissected it free from the aneurismal wall about the time that the pains returned. Fig. 312. Tumor and pulsation in a case of patient (M. P.) with aneurism of the abdominal aorta. 644 DISEASES OF THE HEART AND AORTA. FIG. 313. Tortuous subclavian artery, simu- lating a small aneurism. The tumor which it formed above the clavicle is indicated by the shading. DIAGNOSIS. The diagnosis of thoracic aneurism is, as a rule, easy, especially with the aid of the X-ray. Most of the conditions with which it can be confused have been mentioned above. The most important of these are simple dilatation of the aorta, mediastinal tumors, pulsating empyema or encapsu- lated pericarditis, and enlarged mediastinal or branchial glands. Any of these may cause the dulness, the tracheal tug, the inequality of pupils and pulse. The systolic thrill and murmur may also be communicated by a very solid tumor or may arise in a very vascular sarcoma, aberrant thy- roid with stroma, or metastasis from a medullary carcinoma or hyperne- phroma. A diastolic shock is scarcely ever felt over even the most vascu- lar tumors, but is, of course, well marked over a dilated aorta. The presence of a forcible expansile pulsation in the interspaces is suffi- cient to exclude tumors; but in the first and second interspaces when there is no actual bulging it may be due to a simple dilatation of the aorta. The tracheal tug may further be due simply to displacement of the heart or aortic arch or to enterop- tosis, while the inequality of the pulse may arise from the presence of adhe- sions or arteriosclerotic plaques about the origin of the subclavian arteries. The absolute diagnosis can almost always be made by X-ray exam- ination, but even then a tumor may be encountered whose shadow shows 110 expansile pulsation and whose nature remains in doubt. The homogene- ous shadow, with its regular spherical or oval form and its connection with the aorta, is usually evidence of aneurismal nature. In doubtful cases the greatest care is necessary, for the physician should always bear in mind that the earlier the aneurism can be treated the greater the chance of cure, and this stage of hope is usually the stage in which the physical signs are still far from definite. Occasionally a tortuous carotid or subclavian artery presenting its convexity in the supraclavicular fossa may simulate an aneurism, so that, as in the case seen in Fig. 313, it is necessary to outline the supposed aneu- rism with the tip of the little finger. In this case, which had once been diagnosed aneurism, it was possible to reach below the convexity and to feel the outline of a narrow but tortuous subclavian artery. Of course, the X-ray examination in such a case would at once clear up the diagnosis, even if the outline of the artery could not be felt. Another condition which may simulate aneurism of the subclavian artery is a dilated jugular bulb, which appears as a pulsating sac above the clavicle. This is especially marked when tricuspid insufficiency is present. In such cases the arterial blood-pressure may be low and the arterial pulses weak; nevertheless, the pulsation is so feeble and the connection with the dilated veins so evident that it should never be mistaken for an aneurism. ANEURISM. 645 DISSECTING ANEURISM. Shakelton in 1822 gave the first descriptions of dissecting aneurisms, which were soon confirmed by Hope (1833) and Henderson (1843). In this condition the coats of the aorta are split longitudinally into two sleeves, an outer, originally formed by the adventitia, and later lined by new- formed intimal endothelium; and an inner sleeve representing the original tube of the aorta, composed of the original intima and media, and later also covered with new-formed endothelium. PATHOLOGY. The condition is not an extremely rare one, so that Bostroem in 1887 was able to collect reports of 177 cases. It usually arises in the aorta, especially at the beginning of the descending arch, and not infrequently is formed as the continuation of a simple aneurism of the arch. From this region it commonly extends along the whole length of the aorta to FIG. 314. Dissecting aneurisms. A. Specimen of a dissecting aneurism (partial clot formation) in a man with only two aortic cusps. (From the Army Medical Museum, Washington, I). C.1 B. Dis- secting aneurism of I.. K., involving the arch and the descending aorta. (After MacCallum; kindness of the Johns Hopkins Hospital Bulletin.) the bifurcation, the arteries sometimes arising from the inner, sometimes from the outer tube. Occasionally the split occurs between the layers of the media, so that both sleeves have a wall of media. Very infrequently the outer tube ruptures into the inner tube near its lower end, so that the blood passes back into the latter. The most satisfactory explanation for this remarkable lesion seems to be the following (v. Moller, Flockemann, Schecle) : As long as the lumen of the artery is uniform, the blood exerts only a lateral pressure upon the 646 DISEASES OF THE HEART AND AORTA. arterial walls, which acts "across the grain" of the arterial coats. However, when calcined plaques project into the lumen, these tend to impede the blood-current so that the longitudinal pressure of the latter acts as well. As Bostroem has shown, the resultant force acts in a parabola pointing outward and downward. When this is acting upon an area where the media is thinned or absent, it tends not only to split the coats "with the grain" but also to push the adventitia outward. The wall gives way, the split lengthens, and the outer sleeve is formed. Whether or not the aorta then ruptures depends upon the ability of the adventitia alone to withstand the blood-pressure. The coagulation of the blood within the sac depends upon the formation of fibrin ferment in the tissues of the adventitia and the rapidity of the blood-flow within the new-formed sac. It is quite frequent for extensive and even total coagulation of the contents to take palce. SYMPTOMS AND SIGNS. A considerable proportion of the cases of dissecting aneurisms give no outward manifestation during life and are accidental findings at autopsy. A large number give the usual signs of ordinary aneurism, especially when they arise as a continuation of the latter. This is well exemplified by the following case, which was under the writer's observation during his last admission to the hospital. (The pathological findings and clinical notes are taken from the report of Professor MacCallum.) L. R., negro, aged 30, had been treated in the Johns Hopkins Hospital one year previous to his final admission, at which time the diagnosis of aneurism of the aorta had been made. At the final admission the patient was found to be suffering from an arthritis with symptoms of general fever, sweating, etc. The heart was enlarged, dulness extending 13.5 cm. to left and 3 cm. to right of midline. There was visible impulse and heaving in second, third, fourth, fifth, and sixth interspaces, far out in first and second left interspaces. Heart sounds were clear, dull, and ringing; second sound followed by soft diastolic murmur in third left interspace, not heard in neck. Patient died in delirium with high fever. Autopsy showed general streptococcus septicaemia, hemorrhagic nephritis, acute purulent arthritis, obliterative pericarditis, aneurism of ascending aorta, dissecting aneu- rism of the descending aorta. The aortic orifice is not dilated (8 cm. in circumference). A large aneurismal sac (7 cm. in diameter) lies behind the pulmonary artery; it extends upward in the aorta to the arch, beyond which the tube becomes double, the inner tube (the original lumen of the aorta) having for its walls the original intirna plus media, the outer tube media plus new-formed endothelium. Numerous trabecuhc jut out transversely into its lumen. Some of the intercostal vessels arise from the new, some from the old lumen. The left renal artery arises from the old lumen; the right has been torn and arises from the outer. At the lower end above the bifurcation the outer tube has ruptured back into the original lumen. Another type is exemplified by a case under the care of Professor Halsted; also reported by MacCallum. Patient, aged GO, subject to mental disturbance and epileptiform attacks, complained on May 2S of intense pain over the whole body, which he could not locate. On May 28 his abdomen was much distended and he was jaundiced. There was pain in the region of the appendix. His temperature was 100. Leucocytes 20,000. Exploratory laparotomy showed an extremely distended colon which was relieved by colostomy. Patient died the next day. ANEURISM. 647 Autopsy showed a dissecting aneurism along the whole aorta, splitting the media. The outer sleeve of the descending arch perforated into the posterior mediasti- num, giving rise to a tremenduous hsematoma which distended that space down to the diaphragm. The rupture had evidently given rise to the pain; the disintegration of red corpuscles in the clot had caused the haematogenous jaundice. Both these phenomena are common in cases of this type. ANEURISM OF THE PULMONARY ARTERY. Aneurisms of the pulmonary artery are very rare as compared with those of the aorta. Henschen (1906) has recently summed up the reported cases. In contrast to aortic aneurism, he finds that there is no close rela- tionship to hard work; 18 out of 34 cases (50 per cent.) were in men, 16 (47 per cent.) in women; 39 per cent, occurred under the age of 30 (as com- pared with 18 per cent, of aortic aneurisms). Acute infectious diseases and lues seem to be the main etiological factors. The ductus arteriosus Botalli was frequently found open (17.5 per cent.), which would indicate that some disturbance during fetal life or soon after birth had been a pre- disposing factor. Frequently there is a certain degree of narrowing of the pulmonary artery (32 per cent.). In 8 cases (20 per cent.) there were also marked arteriosclerotic changes in the pulmonary artery. Among 40 cases there were the following complications: pulmonary stenosis 2; relative pulmonary insufficiency 5; organic pulmonary insuffi- ciency; other valvular lesions 3. ' The subjective symptoms are not pathognomonic and are very similar to those of congenital heart disease; palpitation, dyspnoea and cardiac asthma, constriction of the chest, cough, often cedema of the lungs and blood-tinged expectoration, intense cyanosis, cedema, anasarca, ascites, hydrothorax. Death sometimes results suddenly from rupture, sometimes from intercurrent pericarditis and endocarditis, sometimes from diseases of the respiratory tract. DIAGNOSIS. According to Henschen, the diagnosis is justified when the following signs are all present simultaneously: 1. Intense cyanosis and other signs of stasis, constriction, and bloody expectoration, sometimes sternal pain. 2. Prominence of second and third left costal cartilages or second left interspace and well-defined dulness or X-ray shadow in this area. 3. Pulsation and well-defined thrill and murmur in second left inter- space. 4. Loud superficial rasping systolic murmur. 5. Hypertrophy of the light heart. 6. Absence of dilatation or hypertrophy of left heart (apex dulness not outside the mammillary line). 7. Absence of other signs of aortic aneurism. The X-ray shadow furnishes the most important aid in diagnosis. However, the correct diagnosis was made intra vita in only once or twice in his 40 cases. 648 DISEASES OF THE HEART AND AORTA. ANEURISM OF THE ABDOMINAL AORTA. Owing to its frequency (10-14 per cent, of aneurisms) and its surgical accessibility, aneurism of the abdominal aorta is of great importance. Owing to its exposed situation, trauma is a more frequent cause than in thoracic aneurism. As Sibson has shown, it is usually (133 out of 171 cases) situated just below the diaphragm and above the coeliac axis, in the place where it gives the greatest number of symptoms and is most inaccessible to operation. The most important symptom of aneurism of the abdominal aorta is abdominal pain, epigastric or in the regions of kidney and gall- bladder, sometimes in the flanks, sides, and back'. The pain is usually more marked on one side than the other, but may be bilateral. Until the appearance of a palpable tumor the condition may be readily mistaken for renal calculus, gastric ulcer, or other abdominal disease, or for psoas abscess. The pain may be so intense as to require morphine, even in large doses, though acetanilid, antipyrin, aspirin, etc., may be of use at first. Palpitation is also commonly felt in the aneurism. All these symptoms are common in neurasthenic women who have vigorously pulsating abdominal aortas, especially associated with enterop- tosis. It is probable that in this condition .the peritoneal moorings of the aorta are rather loose. When the arterial pressure rises at systole, the angle curves of the abdomnal aorta and common iliac arteries tend to straighten themselves and thus throw the aorta forward toward the abdominal wall, at the same time giving a painful tug upon the abdominal nerves as they emerge from the vertebral column. The looser the moorings of the aorta the greater its excursion and the greater the pull upon structures other than those which normally hold it. Arteriosclerosis of the abdominal vessels may also give rise to similar symptoms. Mere pulsation of the aorta in the epigastrium and else\vhere, even when associated with quite intense pain, is therefore not necessarily a sign of abdominal aneurism. In doubtful cases it is most important to outline the whole course of the aorta by pressing the ringers of the two hands down on either side of the vessel so as to include the abdominal aorta between them. The expansile nature of the pulsation can be felt by pressing downward and inward. Any irregularity or bulging along its course may be felt readily in this way. For the diagnosis of an aneurism it is necessary to outline a tumor with expansile pulsation arising from the abdominal aorta, limited in extent above and below, and spherical or oval in shape. There is usually a well-marked thrill over an aneurism. The pulse-wave in the femorals is- usually much retarded in aneurism (apex beat femoral pulse interval = 0.24+ sec.) but not in simple aortic pulsation. The early diagnosis may sometimes be made with the fluoroscope, care being taken to empty the bowels by a day or two free purgation and preliminary milk diet, and then to examine the abdomen with a "compression diaphragm" (Kompres- sionsblende) so as to push the other structures aside. Oblique illumina- tions and inflation of stomach and colon with air may be helpful. As the aneurism grows it may press upon the renal arteries and veins- and may cause a 1 b u in i n u r i a , cylindruria, ha-maturia, or even anuria. ANEURISM. 649 and death from this cause. It may press upon the intestines and cause intestinal paralysis, with death from obstruction, or may give rise to many symptoms from pressure. Erosion of the vertebrae and pressure on the cord or cauda equina may lead to paraplegia (flaccid) and may cause most intense pain. Abdominal aneurisms may rupture the retroperitoneal tissue into the peritoneum, especially the lesser peritoneal sac into the stomach, intestines, or vena cava. They rupture externally in the epigastrium. The rupture is attended with excruciating pain and often collapse, but death may not ensue for some time thereafter, as the clotting of blood in a small space may prevent further outflow from the vessels. Thus, in the case cited below, the aneurism ruptured into the retroperitoneal tissue, com- pressing the renal vessels. The pain accompanying and following rupture was excruciating, probably owing to stretching of the solar plexus. PROGNOSIS AND TREATMENT OF ANEURISM. In spite of the fact that aneurisms occasionally cease to develop or even undergo spontaneous cure by thrombosis, this procedure is to be re- garded as a rarity, and it is not, under any circumstances, to be expected. By far the greater number of aneurisms cause the death of the patient within from one to five years, though occasionally they remain stationary for twenty-five or thirty. It is, therefore, necessary to attempt to modify the course by treatment. As the intrathoracic aneurisms were not well known to the ancients, their therapy for aneurism was confined to ligature of the peripheral arteries. Valsalva (1666-1723) recommended lessening the force of the heart- beat by absolute rest in the recumbent posture, "starvation diet." arid frequent removal of small quantities of blood by venesection. The two former procedures were revived by Tufnell in 1874. Tufriell reported a number of cases, especially of aneurism of the abdominal aorta, cured by restriction of the daily intake to ten ounces of solids and ten ounces of liquids for several weeks. ( Bread and butter. . . .60 Gm. (oii) Breakfast < Ar . n /i / I Milk 00 c.c. (511) f Meat. . . .00-100 Gm. (oii-iii) Dmner I Milk 75-125 c.c. (3iii-iv) f Bread 00 Gm. (3ii) Sl 'PP er \Milk 00c.c.(5ii) The patient is given no water, and is not allowed to rise from the horizontal position even for an instant. As a result of this the blood-pressure falls and the pulse-rate also. In his first case the pulse-rate fell from 104 to 09 per minute, equalling a diminution of 50,400 beats in twenty-four hours. The wall of the aneurism is spared just this amount of strain, the volume of blood diminishes, and the aneurismal sac may gradually contract down, facilitating clotting. Tufnell's results (cure of two abdominal and one popliteal aneurism) are rather striking, but the treatment imposes the greatest hardship on the patient and few have the hardihood to give it an adequate trial. That the restriction of fluid to ten ounces daily may be harmful is suggested by 650 DISEASES OF THE HEART AND AORTA. the fact that his first case developed uraemia at the end of the treatment and died from that about as soon as he would probably have died from the natural progress of the aneurism. Alonzo Taylor has made very careful studies of the blood in three patients under Tufnell treatment, who were also receiving potassium iodide 1 Gm. (gr. xv) and calcium chloride 2 Gm. (gr. xxx) daily, and who were being bled (250 c.c.) every eighteen days. He found no change in the concentration of the blood or in calcium in the blood, and only slight fall of red corpuscles. The coagulation time was unchanged in one patient, slightly shortened in another. The aneurisms became somewhat smaller, but no cures resulted. At the Johns Hopkins Hospital the method was tried very assiduously for many years, supplemented by subcutaneous gelatin injections as suggested by Lancereaux. Later cal- cium lactate has been used. There have been but few satisfactory results (Futcher), though Professor Osier stated that he had seen several cases of cure in his extensive experience. Potassium iodide was used in aneurism by Bouillaud (1859) and Chuckerbutty (1862), and especially by Balfour, who found that it caused great relief from the pain, and claimed that the aneurism also dimin- ished considerably in size. Subsequent experience demonstrates the cor- rectness of the claim that aneurismal pains are often relieved by potassium iodide, but few, if any, cures of well-defined thoracic aneurisms can be ob- tained by its use. Its modus operand! is still obscure, probably acts pri- marily upon the spirochaetes and causes healing of the luetic arteritis. Gibson thinks that " we may admit it to be extremely probable that under the influence of iodide of potassium the nutrition of the walls of the sac, as well as of the whole of the arterial system, undergoes improvement." Wiring. The reason that an increased coagulability of the blood and a slowed circulation do not of themselves produce intrasaccular clotting is that the latter, like the vessels, is lined with endothelium and does not furnish fibrin ferment. As stated by Moore in 1864, " the first indispensable condition for the cure of a thoracic aneurism is to provide means of eliciting fibrin from the blood " (producing fibrin ferment in situ}, and the " second .... to extend the surface within it on which the fibrin may coagulate." In order to supplement these deficiencies, Moore suggested the introduction of fine wire into the aneurismal sac. Murchison submitted to him a case of aneurism of the ascending aorta which pointed on the surface oT the chest. Moore slowly introduced twenty-six yards of fine iron wire through a fine needle. The pulse fell from 116 to 92, the pulsation of the tumor almost ceased, but the patient died in collapse two days later. Previously to Moore, Guerad (1821), Petrequin (1845), and Ciniselli (1847) induced clotting by passing weak electric currents between the tips of two needles introduced into the sac (galvanopuncture). Corradi com- bined the two methods by using the wire as one pole of the battery. The writer is indebted to Prof. J. M. T. Finney for the following descrip- tion of his procedure in wiring aneurisms: The wire used in this operation is an alloy of 80 parts copper to 1000 silver, of about 0.33 mm. thickness (old English gauge No. 27), drawn so a> to be very springy. 1 Previous to the operation it should be wrapped upon 1 Gescheider Bros., Cor. Monument and Gay Sts., Baltimore, prepared this wire according to Dr. Finney's directions. ANEURISM. 651 an ordinary spool so that it will preserve the curve even after insertion into the aneurismal sac and curl around and around within the latter. Wire and spool are sterilized by boiling. The wire is introduced into the aneurismal sac through an ordinary infusion needle, which should be just large enough to allow the wire to enter. This needle must be carefully insulated by dip- ping in black enamel, after which it is dry sterilized by heating in a test-tube at 160 (Centigrade) for one hour. (Heating with water or steam might loosen the enamel.) Before proceeding with the operation a cathode pad electrode, at least 8 x 10 cm. in size, is placed over the patient's back, while a sterile anode wire of the medical battery is connected with the distal end of the sterile silver wire. The proximal end of the wire is inserted into the needle before the operation is begun. Just before the operation the patient may be given a hypodermic injec- tion of morphine 15 to 30 mg. (gr. J to i), the skin over the aneurism care- ^*f Fin. 315. Diagram showing the various methods for the operative treatment of aneurism. Arrows indicate direction of the blood stream. A. Ligature above and below the sac (Antyllus). B. Ligature above and below the sac; removal of the sac (Hueter). C. Ligature above and at some distance from the sac (Hunter). V. V. represent vasa vasorum. D. Ligature below the sac (Brasdor, Wardrop). fully sterilized, and a little sterile 1 per cent, cocaine or novocaine solution injected. In inserting the needle the skin should be drawn aside a little, so that the opening in the sac may not remain exactly beneath the skin puncture, after the needle is removed; the danger of infection of any ensuing hsematoma may thus be lessened. The entrance of the needle into the sac is marked by the egress of a small amount of blood. The wire is then pushed in slowly, while an assistant holds and rotates the spool in order to avoid kinking and to allow the wire to coil up well within the sac. After about 10 feet of wire has been inserted, the wire is cut off about 1 foot from the 652 DISEASES OF THE HEART AND AORTA. skin and connected by a clamp with the anode wire of the battery. The galvanic current is now very gradually turned on until a strength of 10 milli- amperes is reached, and this is allowed to run for 30 minutes, after which it is gradually raised to 20 milliamperes for 10 minutes unless this should cause great discomfort to the patient. The current is then turned off, the needle removed, and the excess of wire cut off. In cutting off the wire the skin should be held taut between two fingers, to prevent the formation of a haematoma, and the stump of wire then cut off with a curved scissors, ex- erting as much pressure as possible so that when pressure is removed the stump of wire shall be buried well below the level of the skin and the skin shall slide smoothly over it. If necessary, pressure over the tumor may be continued in order to avoid the formation of a haematoma, for the latter becomes infected easily and the presence of an area of inflammation may vitiate the result of the wiring. Even when the clotting within the sac is complete, the end result of the wiring is still in doubt. Thus, in 14 cases cited by Hunner which had been treated by wiring alone, two cases of abdominal aneurism (Morse and Langton) had been cured; in twenty-three cases (seventeen thoracic) there were three cures (17.7 per cent.). Prof. Finney has recently reported a series of 24 cases, all treated by himself by the Moore-Corradi method, with three recov- eries, though in many of the cases life was undoubtedly prolonged and the patient's comfort greatly increased. Rosenstirn's case of thoracic aneurism was still living and well twenty years after the operation. It is evident that there is great variation in the results obtained in dif- ferent cases, and the factors which determine this merit some considera- tion. In fusiform and partially sacculated aneurisms the clot held in the meshes of wire rarely resists the impact of the blood stream and may be carried away in large emboli. and death from such embolism is by no means rare, so that the treatment may sometimes actually hasten the patient's death. In aneurisms of this form there is little to be hoped from the operation. In well-sacculated and especially in bottle-shaped aneurisms with nar- row necks, better results may be obtained, for here the clot may completely fill the sac (Fig. 315) so that the blood stream may glide over its surface instead of gradually shattering the clot by striking full upon it. In wide- mouthed sacs, however, though the clot may at first fill the sac completely, it often happens that the blood stream gradually pushes in between the clot and the aneurismal wall, so that the area of expansile pulsation can be felt day by day encroaching upon the central solid area whose pulsa- tion is only transmitted, until finally the entire clot has been dissected free by the blood stream and remains in mid-channel as an island of clot held in the meshes of wire but no longer giving support to the aneurismal wall (Fig. 316). This loosening of the clot is facilitated not only by the general stretch- ing of the aorta walls under the influence of a high maximal blood-pressure, but still more so by the large expansions and retractions which occur at approximately normal pressures where the elasticity of the aorta is greatest. Such large pulsations are particularly common under nervous excitement. ANEURISM. 653 It is evident, therefore, that in order to secure the best results the aneu- rismal sac should be as small and its neck as narrow as possible before the wiring is undertaken. This is best secured by a long period of preliminary treatment with the modified Tufnell method, absolute rest in bed in the horizontal position, with diet and, especially, fluids very much restricted. In aneurisms of the aorta, which is an artery of the elastic type, the blood- pressure may be still further reduced by sodium nitrite, erythrol tetranitrate or vasotonin, though in aneurisms of arteries with muscular walls a relax- ation of the latter may not be desirable. Mental quiet should be insured in every way possible, but it must be remembered that isolating the patient from the visits of his friends and prohibiting him from reading in most cases merely leaves him a prey to the soul-racking worry from the contempla- tion of his condition, and, as Cannon and de la Paz have shown, this worry in itself keeps up the blood-pressure. Sedatives should be freely used, bromides, veronal, or trional, as much as conditions allow, and should be sup- plemented by codeine in 15 or 30 mg. (gr. % to Yz) doses, or even morphine where pain or unrest demands. Quiet of long duration should be secured at any cost. In order to bring the coagulability of the blood up to its maximum, calcium lactate should be administered in doses of 1 to 2 grams (grs. xv to xxx), best given in syrup of sarsaparilla, four times a day for a consider- able period both before and after the operation, and milk should form a large part of the diet. This preliminary treatment should be kept up for several weeks or a month, so as to bring the patient into the most favorable possible condition for the operation; for the outlook is much better in such a case than in an aneurism whose walls and mouth are stretched by a high blood- pressure. The treatment after the wiring is no less important than the preliminary treatment, but should be of even longer duration. It is all-important that the clot must be given a chance to harden and it should have an opportunity to become as firm and as adherent as possible to the walls of the sac. As is shown in Fig. 300, adhesions between sac and thrombus are relatively slight and form but slowly, but nevertheless they are of the greatest importance. Too much stress cannot be laid upon the harmful role of mental excite- ment mentioned above, for the large pulse-throbs tear the wall away from the clotted mass that cannot move with it, and thus prepare a channel into which the blood stream pushes its way. The entrance of such a channel between the wall and the margin of the clot (Fig. 315) is indeed an unfavorable sign, a sign for redoubled precautions, but one which is by no means hopeless. The clot itself is loaded with fibrin ferment, and if quiet is resumed secondary clotting may set in. The writer saw this strikingly illustrated in the case of a physician with an aneurism of the descending part of the arch wired by Prof. Finney, who was recently under his observation at the Johns Hop- kins Hospital. At the operation, on Nov. 17, 1910, per- fect clotting was secured, the aneurismal protrusion flattened somewhat, and the expansile character of the pulsation disappeared. Eight days later he had several extremely anginal attacks, so severe that he writhed in pain, and then he "had a distinct 654 DISEASES OF THE HEART AND AORTA. feeling of something giving way inside the aneu- rism.' After that the expansile pulsation returned about the margin of the tumor. The patient was kept at absolute rest in bed, but for several weeks afterwards he was very restless, had many disagreements with the attendants and nurses, and gave vent to frequent outbursts of temper. During this period there was no im- provement and the expansile pulsation became worse. At this stage he was first seen by the writer, who was able to bring him into a calmer frame of mind, and, as a result of frequent visits, much persuasion, and vigorous doses of potassium bromide, this mental calm was tolerably well maintained until he left the hospital. During this period the pulsation gradually diminished. On January 10, 1911, he " felt a sudden cooling of the left arm and then a lessened pulsation in the aneurism." There was, however, still some expansile pulsation in the upper left axilla, and a systolic murmur over the entire aneurismal sac longest in duration over the expansile portion. With continued rest, mental quiet, and bromide, pulsation gradually diminished, and by January 29, 1911, the mass had become about 1 cm. smaller and had receded entirely out of the axilla. Though the pulsation was more marked, it had entirely lost its expansile character; and it seemed probable that the apparent increase in pulsation was due to greater freedom in the movement of the sac after receding from the axilla. There was no longer any murmur audible over the tumor. All these signs seemed to indicate a complete clotting throughout the aneurismal sac, a result which, but a few weeks before, had been quite unhoped for. The patient remained in the hospital and at rest for another month, making a period of three months after the operation, and left the hospital in excellent condition with no sign of expansile pulsation. At time of writing a year later, he is still in excellent condition and there have been no signs of return of the pulsation. In striking contrast to this favorable result was another patient whose aneurism was in about the same part of the aorta as that of the patient mentioned above, but considerably smaller and apparently better saccu- lated. He was wired by Dr. Finney a few months later than this patient, and, as in the preceding case, the expansile pulsation completely disappeared. The patient was a very restless man, and in spite of advice left the hospital within a couple of weeks after the wiring, promising to keep quiet at home. The quiet was only relative. A few weeks later he went to a baseball game, at which he was carried away by his enthusiasm and became much excited. At this time he felt something giving way, the pulsation came back, and he returned to the hospital within forty-eight hours. He was wired again, with complete cessation of expansile pulsation, but again remained restless and fretful. The pulsation returned once more, and a third wiring was done at his request, though with little hope of recovery. As was to be expected, this failed to quell the tide, and he died within two months. This second patient had a lesion which seemed much more favorable for wiring than the first, the primary result was better, and his outlook then seemed far more favorable. The decisive difference lay in the after-treatment. ANEURISM. 655 The first patient submitted gracefully to a long stay in the hospital, allowed secondary clotting to set in and to regain the ground lost, and then remained long enough to permit the clot to become solidly fixed. The second patient obtained a better primary result, but left the hospital before the clot was solidly fixed, submitted it to a strain before it was able to withstand one, and paid the penalty with his life. The excellent results which can sometimes be obtained by a careful combination of both preliminary and after-treatment are well illustrated by a patient treated by Drs. C. L. Jones, of Jamestown, and C. S. Hamilton, of Columbus, Ohio, to whom the writer is indebted for the following data: The patient was a chef 48 years old, free from venereal disease, whose aneurism appeared within a few days after he had been thrown from a street-car. The tumor was most marked in the second right interspace about five centimetres to the right of the midline. The patient was put upon absolute rest and Bal- four's modification of Tufnell's diet (250 c.c. fluids and 300 Gm. solids in twenty-four hours), and, after forty-three days' preliminary treatment, the aneurism w-as wired in the usual manner by Dr. Hamilton. Recovery was uneventful except for occasional pains relieved by morphine. The patient remained in the hospital for three weeks, and was keep at rest and under continual observation for four months, with potassium iodide, light diet, and morphine to relieve the pains w r hich he occasionally felt. After this period he led an active life and died from some unknown cause about six years later. The excellent result obtained in this case seems to be due largely to the careful treatment, especially the preliminary treatment. The after-treatment, though adequate in this case, might well prove too short in many others. As can be seen from the foregoing, the treatment is quite as important as the operation itself. In justice to both himself and the patient, the sur- geon should before undertaking the case insist that the patient consent to remain under treatment and absolute rest for from three to five months, at least a month of w r hich should precede the operation, and at least another month should elapse after the last trace of expansile pulsation has been felt in the tumor. Only threatened rupture of the aneurism or intolerable symp- toms justify an operation without prolonged preliminary treatment. In the syphilitic cases potassium iodide and inunctions of mercury- should be given freely to bring about as far as possible the death of the spiro- chsetes in the arterial wall as well as the resolution of the syphilitic infiltra- tions about the vasa vasortim and to bring the walls of the aneurism and the aorta in its vicinity into the best possible condition. Since one of the main difficulties encountered in the operative treatment of aneurism consists of the lack of organization of the thrombus after it has once formed, it is possible that in certain cases a combination of MacEwan's method with the Moore-Corradi might be of benefit; that is to say, the inner wall of the aneurism might be lightly scratched with a roughened wire before introducing the mass of wire through which the current is to be passed. The removal of considerable areas of intimal endothelium without injuring the other layers of the aneurismal wall would enable the organization of the clot to go on at a much greater rate than is possible if the intima remains intact. 656 DISEASES OF THE HEART AND AORTA. WIRE CLOT On the other hand, it must be borne in mind that the walls of many aneurisms are much thinner than one would anticipate from external examination of the tumor, and unless the greatest care were taken in the manipulation great damage to the sac and even perforation or rupture might result. Under no circumstances should this procedure be attempted over areas where second- ary bulgings are present such as are shown in contour in Fig. 302, since these indicate a weakening of the wall over the corresponding area. Compression. Aneurisms of the peripheral arteries, and especially of the abdominal aorta, are sometimes cured by compressing that vessel above the aneurism. This was done successfully by Murray in 1864, who obliterated the aneurism and the femoral pulse by means of a tourniquet wound around the body above the tumor. A number of similar successful cases have been reported since Murray's, especially when the aorta is compressed with the fingers. The operator cannot continue digital compression longer than five or ten min- utes at a time, so that it is often the custom to obtain the assistance of a whole class of medical students working in relays. In this way Shepherd and others have been able to keep the aorta occluded for twenty-four hours, and have brought about recovery. On the other hand, the prolonged pressure may bring about necrosis of the abdominal wall, intestine and pancreas, or secondary peritonitis, and intestinal obstruction may result (Bryant, Lunn and Benham, Moxon and Durham). The method is therefore still a daring one, and is probably more severe and less certain than Halsted's metal band method. Moreover, Sibson found 133 out of 177 abdominal aneurisms (75 per cent.) above the level of the coeliac axis where they could not be reached by pressure. Ligature and Partial Occlusion. Double Ligature. The oldest method of treating aneurisms of the peripheral arteries is to ligate them above and below the sac (Antyllus) (Fig. 315, A), after opening the latter to remove the blood. A more modern modification of this method is that of Hueter, who dissected out the entire sac after ligating, thus removing a large mass of tissue which would otherwise become gangrenous. Proximal Ligature. Ambroise Pare (sixteenth century) departed from the procedure of Antyllus by merely ligating the artery close above the aneurism (proximal ligature close to the aneurism). This cut off the blood supply to the walls of the latter and to its vicinity, inducing necrosis and suppuration, so that Anel (1710), Desault (1785), and John Hunter (1785) were led to adopt the proximal ligature at a considerable distance above the aneurism (ligature of brachial for aneurism of the radial artery; FIG. 316. Specimen of wired abdominal aneurism, showing an island of clot within the coils of wire sur- rounded by a free blood-channel. ANEURISM. 657 ligation of femoral below the adductors for popliteal aneurism; ligation of femoral above the adductors in Scarpa's triangle for popliteal aneurism). Distal Ligature. In the eighteenth century Brasdor and later Wardrop practised ligation of the artery below the aneurism (distal ligature) in cases like aneurism of the innominate in which the proximal ligature was impossible. As a result of the procedure, a fusiform aneurism of the innomi- nate becomes practically a sacculated or flask-shaped aneurism of the aorta, the innominate artery being converted into a blind sac with narrowed neck, and coagulation is thus facilitated. This operation is still the one most commonly performed for aneurisms of the innominate, carotid, and first part of the subclavian artery. Sheen has collected statistics of 36 cases of innominate and subclavian aneurism, 22 before 1880 with 1 recov- ery, 14 after 1880 with 8 recoveries, 7 after 1890 with 5 recoveries and 5 cures. To this list might be added 2 cases of Haltsed and 1 of Finney with recovery and cure. The deaths before 1880 were usually due to sepsis and hemorrhage. In operating upon the innominate artery it is most im- portant that both the carotid and subclavian arteries should be ligated, for if one of these arteries be left open (as in the case of J. B.) the pressure in the sac is increased without stopping the blood-flow through it, and the gro\vth of the aneurism is actually favored. Moore in his first paper suggested the combination of this form of ligation with wiring for aneurisms of the innominate. This double proced- ure has not attracted much attention, as in the absence of sepsis the simple ligature is often satisfactory, but it is no doubt applicable in a certain number of cases where ligation is not quite adequate. The chief objection to the simple ligation of arteries lies in the fact that the permanent results are often unsatisfactory, for either the ligature may be so tight as to produce necrosis of the tissues under it and thus bring on rupture of the artery, or, as Halsted has shown, the arterial lumen may be re-established in spite of the ligature. In many of Halsted's experiments upon ligating the larger arteries, the lumen of the artery gradual!}' dilated above and below the ligature, so that the latter was left surrounded by a thin membrane or septum of scar tissue. This septum then perforated in one or two places. Occlusion with Metal Bands.- To obviate this and for other reasons Halsted has devised a very ingenious procedure, which consists in the occlu- sion of the vessel by surrounding it with wide metal bands. These metal bands take the place of the ligature; but when properly applied, do not occlude the vasa vasorum, and hence permit the proper nourishment of the arterial wall. Their effect is more certain than that of ligatures, since they do not allow the lumen to be re-established. The chief advantage, how- ever, lies in the ability of the operator to obtain a partial occlusion of the vessel sufficient to reduce pulsation in the aneurism to any desired degree, without obliterating the circulation below before a collateral circulation has been established. This renders it the operation par excellence in ab- dominal aneurisms and aneurisms of the iliac and femoral arteries, in which the other procedures are likely to be dangerous. The bands are made of Xo. 33 sheet aluminum of a width varying from 5 to 15 milli- metres according to diameter of the artery which is to be occluded. The strip is cut a little 42 658 DISEASES OF THE HEART AND AORTA. longer than the circumference of the artery (as shown by a tape passed around the artery). All the sharp edges must be carefully filed off until they are smooth and round, lest they cut into the walls of the artery. The strip is then inserted into a specially devised holder (Fig. 315, E), where it is held in a slot; from this it may be extruded by pressing upon the rammer above; and as it is extruded below it is curled by the curve at the foot of the slot. The faster the strip is extruded the more tightly it is curled. The curved foot of the holder is placed beneath the artery, which is held just tightly enough against the instep of this foot to almost occlude the lumen. The strip is extruded by pushing the rammer just fast enough to give the desired curl. Tension on the artery is then relaxed. The pulse can be felt in the artery below the band, accompanied by a well-defined thrill. The band is then tightened by rolling it gently under the fingers of one hand while palpating the artery below it with the other. The degree to which the band is tightened depends upon the artery affected. In the case of the abdominal or descending thoracic aorta it should be rolled until the thrill has greatly diminished but not disappeared; in the larger branches of the aorta the pulse may be made to disappear absolutely. In a few minutes a regurgitant pulse may mark the appearance of a collateral circulation. When this operation is performed successfully, the artery becomes gradually occluded at the point of constriction, and a rich collateral circulation formed, so good in fact that in one case in which Professor Halsted had occluded the descending thoracic aorta Erlanger found the blood-pressure in the femoral (eight months afterward) only thirty millimetres below that in the brachial. For practical purposes this exactly duplicates the conditions in the adult type of stenosis of the isthmus of the aorta (see page 546). except that the anastomoses take place later and hence are not quite as extensive. Professor Halsted has now operated upon a number of cases with very promising results, and the operation gives promise that in the hands of a surgeon who has practised the technic, it may completely supersede the methods of ligature and compression. Arteriorrhaphy (Matas Operation). R. Matas in 1905 introduced an entirely new technic in treating the aneurism of peripheral arteries exactly in accordance with the principles of treating inguinal hernia by obliteration of the sac. The opera- tion is performed bloocllessly. The limb is elevated, an Esmarch rubber bandage put on, or bleeding from the main artery prevented by compression with a traction loop, adjustable clamps (Crile's), padded forceps, or digital compression. A free incision parallel to the long axis of the sac is then made down to the sac to expose its whole length. Any important nerves or veins should be dissected away from it. The sac is then freely opened and emptied. It is then ready for closure. In most cases it will be decided to obliterate the sac completely, but in some cases of fusiform aneurism it may be preferable to leave a lumen the size of the original artery. When the sac is to be .completely obliterated, the lining of the sac is thoroughly scrubbed over its whole extent with sterile gauze soaked with salt solution to remove the endothelial layer of the intima, and thus accelerate union. The sutures (chromicized gut) are then applied very much like Lembert's intestinal sutures. The most important point is to approximate carefully intima to intima. The sutures are laid in three layers in such a way that the cross-section of the sac after suture is made to form a Y; the first and deepest layer of sutures shutting off the sac from the artery at the Y, and the third layer obliterating the cavities in each arm of the Y (Fig. 315, F). In suturing a fusiform aneurism the lumen of the artery is preserved by placing the first layer of sutures over a rubber tube which is inserted into the artery. After the new lumen is thus provided for, the rest of the sac is scrubbed and the sutures laid in the usual way. Care must be taken to preserve the blood supply and nutrition of the sac, and all portions of it which have been dissected away from their vascular surroundings should be excised. In 1908 Matas reported the results of 86 such operations, including aiHMirisms of the femoral, the iliofemoral, tibial, gluteal, external carotid, ANEURISM. 659 axillary, brachial, and subclavian arteries, as well as the abdominal aorta (the latter both fatal): 78 recoveries; 8 deaths; 4 cases of gangrene; 4 re- lapses, all in operations where the lumen was restored. In view of the fact that these 86 operations were performed by fifty-two different operators the excellent results obtained are a striking argument in favor of the feasi- bility of the operation. Experimental Surgery of the Aorta. Although not yet available for practical surgery, the experiments of Alexis Carrel (Jour. Exper. Med., 1912, xv, 389; 1912, xvi, 17) upon the permanent intubation of the aorta are extremely promising for the surgery of the future. Carrel has been able actually to open the dog's aorta, insert a tube of glass 4.5 centimetres long, suture it in place and then close up the thorax without impairing the circulation of the animal. Meltzer's method of intratracheal insufflation was used upon opening the thorax and the greatest care was employed to prevent bleeding into the pleural cavities, which were walled off from the surrounding structures by pads of silk soaked in petrolatum. An ordinary glass tube with slightly everted edges was used, and tied into the aorta with heavy silk ligatures. The nine animals upon which he has performed this operation lived for periods varying from several days to more than three months; death occurring from ulceration of the tube through the wall of the aorta or from the formation of a thrombus at the site pressed upon by the end of the tube. As Carrel states, however, "It is probable that the use of a tube of the proper calibre, form and composition would be followed by better results,'' and it is far from impossible that with such improvements in technique, after extensive trials upon animals with diseased as well as with healthy aortas, the pro- cedure may come to be applicable to the treatment of aneurisms in human beings. BIBLIOGRAPHY. ANEURISM. More complete historical accounts are given by Lobker: "Aneurysma," Eulenburg's Realencyclopaedie der ges. Heilk, Wien u. Leipz., 1S94, i, 560; and Osier, W.: Aneurism. Mod. Med.. Phila. and X. Y., 190S, iv, 448; also Gibson, G. A.: Diseases of the Heart and Aorta, Edinb. and Lond., 1S98; to which the writer acknowledges his indebtedness. Arnsperger, H.: Die Aetiologie und Pathologic der Aortenaneurysmen, Deutsch. Arch. f. klin. Med.. Leipz., 1903. Ixxviii, 3S7. Crisp: On the Structure, Diseases, and Injuries of the Blood-vessels. Lond., 1S47. Hare, H. A., and Holder: Some Facts in Regard to Aneurism of the Aorta, Am. J. M. Sci., Phila. and X. Y.. 1S99. cxviii. 399. Gibbons. H. W.. Jr.: Proc. San Francisco Med. Soc.. Sept. S. 1S6S: Pacific M. and S. J.. X. S.. ii, 213. Richter. C. M.: Zur Statistik der Aneurysmen. u. s. w.. Arch. f. klin. Chir.. Berl., 1SS5, xxxii. 524. Lawson. and others quoted from Richter, Arnsperger and Lobker. Le Boutillier. T.: A Case of Aneurism of the Transverse Portion of the Aortic Arch in a Girl of Xine Years, with Table of Reported Cases under Twenty Years of Age. Am. J. M. Sci.. Phila. and X. Y.. 1903. cxxv. 778. Helmstedter: Du mode de formation des aneurismes spontanes, Strassburg. 1S73. Roy. C. S.: The Elastic Properties of the Arterial Wall. J. Physiol.. Camb. and Lond.. 1SS1, iii. 125. Xote on the Elasticity Curve of Animal Tissues, ibid.. l^vS. ix. 227. Grehant and Quinquaud: Mesure sur la pression necessaire pour determiner la rupture des vaisseaux sanguins. J. de 1'Anat. et Physiol.. Par.. 18S5. xxi. 2^7. Koester: Ueber die Enstehung der spontanen Aneurysmen und die chronische Mesarteritis, Berl. klin. Wchnschr.. 1S75. 322. Fabris. A.: Experimented Untersuchungen ueber die Pathogenese der Aneurysmen. Arch. f. path. Anat.. u. s. w.. Berl.. 1901. clxv. 439. Ophiils, W.: Some Notes on Arteriosclerosis of the Aorta. Am. J. M. Sc.. Phila. and X. York, 190ti. cxxxi. 97S. 660 DISEASES OF THE HEART AND AORTA. Hirsch, J. L., and Robins, M. C.: A Case of Aneurism of the Aorta of Twenty-five Years' Duration, Maryland M. J., Baltimore, 1903, xlvi, 93. Weinberger, M.: Ueber die Diagnostik und klinischen Verlauf der mycotisch-embolischen Aneurysmen und Gefassrupturen, sowie der Influenzaendokarditis, Ztschr. f. klin. Med., Berl., 1907, xlii, 457. Libman, E.: Cases of Mycotic Aneurisms, Trans. N. Y. Path. Soc., April, 1905; and Mt. Sinai Hosp. Rep., N. Y., 1905, 481. A Case of Embolic Aneurisms, Mt. Sinai Hosp. Rep., N. Y., 1905, 488. McCrae, J. : A Case of Multiple Mycotic Aneurysms of the First Part of the Aorta, J. Path. and Bacter., Edinb. and Lond., 1905, x, 373. Clarke, T. W. : Repeated Copious Haemoptoysis from an Aortic Aneurism Extending into the Right Lung and finally Rupturing, Bull. Johns Hopkins Hosp., Bait., 1905, xvi, 98. Arnold, H. D.: Cause of Death in Aneurisms of the Thoracic Aorta which do not rupture; Report of five cases, Am. J. M. Sci., Phila. and N. Y., 1902, cxxiii, 72. Hare, H. A., and Holder, C. A.: Some Facts in regard to Aneurism of the Aorta, ibid., 1899, cxviii, 399. Broadbent, W. H. and J. H. F.: Heart Disease and Aneurysm of the Aorta, 4th edition, N. Y., 1906. Oliver, W. S.: Physical Diagnosis of Thoracic Aneurism, Lancet, Lond., 1878, ii, 406. Sewall, H.: Some Considerations other than Aortic Aneurism which determine the Occur- rence of the Tracheal Tug, Am. J. M. Sci., Phila. and N. Y., 1901, cxxii, 150. Wenckebach, K. F.: Ueber pathologische Beziehungen zwischen Athmung und Kreislauf beim Menschen, Samml. klin. Vortrage begr. v. R. Volkmann, Leipz., 1907, N. F. Inn. Med., 140-141. Smith, H. L.: A New Sign in Thoracic Aneurysm, Am. Med., Phila., 1902, iii, 814. Fran^ois-Franck: Recherches cliniques et experimentales sur la valeur comparee des signes fournis par 1'examen du pouls radial dans les aneurysmes du tronc brachio- cephalique de 1'aorta et de 1'artere sous claviere. Importance du retard du pouls, J. de 1'anatomie et de la physiol. norm, et path, de 1'homme at des anim., Par., 1878, xiv, 113. Recherches sur la diagnostic du siege des aneurismes de 1'aorta, ibid., 1879, xv, 97. Marey, E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Paris, 1881. V. Ziemmsen, A.: Ueber den Pulsus differens und seine Bedeutung bei Erkrankungen des Aortenbogens, Deutsch. Arch. f. klin. Med., Leipz., 1890, xlvi, 288. Baetjer, F. H.: The X-ray Diagnosis of Thoracic Aneurysms, Bull. Johns Hopkins Hosp., Bait., 1906, xvii, 24. Holzknecht, G.: Die RSntgenologische Diagnostik der Erkrankungen der Brusteingeweide, Fortschr. a. d. Geb. d. Rontgenstr., Hamb., 1901, Erganzungshef t , 6. Milanoff : Etude de la douleur et de quelques autres symptomes des aneurismes de 1'aorte thoracique descendente, These, Par., 1900. And reef : Contribution a 1'etude des aneurismes de 1'aorte descendente, These, Toulouse, 1904. Osier, W.: Aneurism of the Descending Thoracic Aorta, Internat. Clin., Phila., 1903, xiii ser., i, 1. Hewlett, A. W., and Clark, W. R. P.: The Symptoms of Descending Thoracic Aneurism, Am. J. M. Sc., Phila. and N. Y., 1909, cxxxvii, 792. Bostroem: Das geheilte Aneurysma dissecans, Deutsch. Arch. f. klin. Med., Leipz., 1S87, xlii, 1. Schede, Fr.: Zur Aetiologie, Verlauf, und Heilung der Aneurysma dissecans der Aorta. Arch. f. path. Anat. u. s. w., Berl., 1906, cxcii, 52. MacCallum, W. G.: Dissecting Aneurism, Bull. Johns Hopkins Hosp., Bait., 1909, xx, 9. Henschen, S. E.: Das Aneurysma Arteriae pulmonalis, Volkmann's Samml. klin. Vortrage, Leipz., 1906. No. 422-423. Albertini and Valsalva. Quoted from Gibson. Tufnell, J.: The Successful Treatment of Aneurism by Consolidation of the Contents of the Sac, Lond., 1S75. The Successful Treatment of Aneurism bj r Position and Re- stricted Diet, Trans. Med. Chir. Soc. Lond., 1874, Ivii, 83. Taylor, A. E.: The Effects upon the Blood of the Tufnell Method and the Calcium Salts in the Treatment of Aortic Aneurism, J. Exp. Med., N. Y., iii. ANEURISM. 661 Lancereaux and Paulesco: Du traitement des aneVrismes en general et de 1'aneVrisme de 1'aorte en particulier par injections sous-cutane'es d'une solution gelatineuse, Bull, de 1'Acad. de Med., Par., 1897. Futcher, T. B. : The Treatment of Aneurisms by Subcutaneous Gelatin Injections, J. Am. M. Asso., Chicago, 1900, 204. Bouillaud: Gaz. des hop., Par., 1859, 61. Chuckerbutty: Brit. M. J., Lond., 1862, ii, 61, 85. Quoted from Balfour. Balfour, G. W.: On the Treatment of Aneurism by Iodide of Potassium, Edinb. M. J., 1869, xiv, 33. Further Observations on the Treatment of Aneurism with Iodide of Potas- sium, ibid., 1870, xv, 47. Moore, C. H.: On a New Method of Procuring the Consolidation of Fibrin in Certain Incur- able Aneurisms, Trans. Med. Chir. Soc., Lond., 1864, xlvii, 129. Murchison, C.: Report of a Case of Saccular Aneurism of the Ascending Aorta projecting through the Anterior Wall of the Left Side of the Chest, ibid., 136. P6trequin: Suite et fin du m^moire concernant une nouvelle methode pour guerir certains aneurismes sans operation a 1'aide du galvanopuncture, Rec. d. trav. Soc. md. d. Indre-et-Loire, Tours, 1845, 117; also Compt. rend, de 1'Acad. d. Sc., Paris, 1845, xxi, 992. Ciniselli, L.: Osservazione di aneurismi dell' aorta trattati coll elettropuntura, Gior. d. r. Accad. di med. di Torino, 1872, 35, xii, 418; Gaz/. Med. di Milano, 1847, vi, 9. Hunner, G. L.: Aneurism of the Aorta treated by Insertion of a Permanent Wire and Galvanism (Moore-Corradi Method), Bull. Johns Hopkins Hosp., Bait., 1900, xi, 263. Rosenstirn, J.: The Surgical Treatment of a Case of Aneurism of the Arcus Aortie, with a Case cured by the Loreta-Barwell Method, Am. J. M. Sci., Phila. and N. Y., 1891, ci, 55. Murray, W.: An Account of a Case of Aneurism of the Abdominal Aorta which was cured by Compression of that Artery immediately above the Tumor, Trans. Med. Chir. Soc. Lond., 1864, xlvii, 187. Shepherd, F. J.: Digital Compression for Aneurism, Montreal M. J., 1903, xxxii, 70. Bryant, Limn and Berham, Skerritt, Paget. Quoted from Pringle, J. J.: A Case of Aneu- rism of the Abdominal Aorta treated by Laparotomy and the Introduction of Steel Wire into the Sac, Trans. Med. Chir. Soc. Lond., 1887, Ixx, 261. For details of the various ligatures see Lobker: Aneurisma, Eulenberg's Realencycl. d. ges. Heilk., Wien und Leipz., 3d ed., 1894, i, 560, or Ref. Handb. Med. Sc., or various text-books of surgery. Sheen, W.: Results of Ligature of the Innominate Artery, Ann. Surg., Phila., 1905, xlii, 1. Halsted, W. S.: Partial, Progressive and Complete Occlusion of the Aorta and other Large Arteries in the Dog by Means of the Metal Band, J. Exp. Med., N. York, 1909, xi, 373. The Partial Occlusion of Blood-vessels, especially of the Abdominal Aorta, Bull. Johns Hopkins Hosp., Bait,, 1905, xvi, 346. Matas, R.: An Operation for the Radical Cure of Aneurism based upon Arteriorrhaphy, Ann. Surg., Phila., 1903, xxxvii, 1903. J. Am. M. Asso., Chicago, 1906. Statistics of Endoaneurismorrhaphy, or the Radical Cure of Aneurism by Intrasaccular Suture, ibid., 1908, li, 1607. PART IV. i. PAROXYSMAL TACH YCAi> < *.*. COTTON in 1867 described a peculiar condition in which attacks of extreme tachycardia were present, leaving the heart quite normal in the interim. Similar cases were reported by Bensen, Nothnagel, Proebsting, Priesendorfer, Pribram, and Bristowe, who considered them to be due to a sort of vagus neurosis. Bouveret, however, regarded the condition as a distinct clinical entity, of which he was able in 1889 to collect over twenty cases from the literature, and which he designated as "essential (or idiopathic) paroxysmal tachycardia (tachycardie paroxystique essen- tielle)". According to Bouveret, this condition is characterized by attacks in which the pulse suddenly attains a rapidity (200 to 300 per minute) which is never seen in any other con- dition, even in the gravest heart failures. These attacks last from several minutes to several days or even weeks, and subside as sud- denly as they come. They sometimes recur for years and often for decades without seriously interfering with life and general health of the patient; or, on the other hand, an attack sometimes ends in death. Bouveret's clinical description was so complete that, though many cases were subsequently reported, little that was essential was added until Aug. Hoffmann in 1900 called attention to the fact that the paroxysms of tachycardia began and ceased with extreme suddenness, and showed by excellent tracings that the complete change of rate often occurred within the period of a single cardiac cycle. Moreover, he showed that this change of rate was an exact doubling, trebling, or quad- rupling of the previous rate, and ended by halving, quartering or drop- ping to one-third. For example, the normal pulse-rate being 70, the rate during an attack might be 140, 210, 280 per minute, and vice versa. Hoff- mann regarded t hi s sudden complete change of rate as characteristic of the essential or idiopathic paroxys- mal tachycardia, in contrast to the simple tachycardia of exercise, excitement, or convalescence, in which the change of rate is due to loss of vagus tone and comes on by a gradual increase of rate during a period of from one to several minutes. Such a tachycardia rarely exceeds 120 to 140 per min- ute. Kven though it may give rise to sharp attacks coming on more or loss suddenly and accompanied by palpitation, it is not to be regarded as idiopathic (essential) paroxysmal tachycardia, but will be considered under the simple nervous affections of the heart (Chapter III). 662 PAROXYSMAL TACHYCARDIA. 663 As will be seen, one cannot lay too much stress upon the importance of distinguishing between "paroxysms of tachycardia" and "idiopathic paroxysmal tachycar- dia." Only those cases should be considered in which the mode of onset and cessation of the attack is carefully given, if possible with venous pulse tracings. The mechanism involved in the attacks should also be noted. It is only in this way, and not by indiscriminate analyses of cases in which the heart occasionally becomes rapid, that an accurate knowledge of the condition can be acquired. The accurate knowledge of paroxysmal tachycardia, therefore, dates from Hoffmann's analysis of pulse tracings. FIG. 317. Venous pulse in a case of paroxysmal tachycardia (G. D. R.). (Kindness of the Johns Hopkins Hospital Bulletin.) A. During the attack (pulse-rate 144 per minute). Ventricular type of venous pulse, no a wave discernible, c, carotid wave. Time of the carotid wave. B. Tracing taken five minutes later, just after cessation of the attack. Pulse-rate 80. Venous pulse of the normal auricular type, conduction time (a-c interval) normal. C. Tracing from the same case taken during a period of irregularity a few days later, showing extrasystoles with shortened conduction time. The intervals are measured in millimetres upon a uniformly running drum. Still more accurate knowledge came with the analysis of venous tracings as well, and of tracings obtained at the moments when the attacks began and ceased. Types of Paroxysmal Tachycardia. By this means several types of venous tracings have been recorded : 1. Attacks of tachycardia in which the auricular type of venous pulse remains. At the cessation of the attack, the auricles may continue for a while at least at their old rhythm, the rate of the ventricles falling to half or less by the onset of a partial auriculo(atrio)ventricular block and a 2 : 1 rhythm (cases reported by Hoffmann, Gerhardt, Rihl, and Schmoll). There may be periods of irregularity between, especially just before and just after, attacks due to the occurrence of partial block for occasional beats. The partial block even in these cases does not persist indefinitely, but the rate of the auricles finally also becomes slow, and a 1 : 1 rhythm at the slow (normal) rate is resumed. On the other hand, there may be present no 664 DISEASES OF THE HEART AND AORTA. auriculoventricular or sinoauricular block whatever. Electrocardiograms show that during the tachycardia the pace-making area may be situated in the auricle at either the normal or at some abnormal site. In some cases of this type it may probably be situated in the cells of the auriculoventricular bundle. 2. Attacks in which the venous pulse is of the ventricular type (see page 80) with no wave due to auricular contraction, and which subside suddenly with approximate halving or quartering of the rate without signs of auriculo(atrio)ventricular block, the venous pulse between attacks show- ing only a single auricular wave for each ventricular contraction. Between attacks there may be an irregularity due to the presence of extrasystoles with shortened conduction time. Cases of this type have been studied by Mackenzie, Hirschfelder, Hay, Peabody, and others. The ventricular type represents some of the auriculoventricular tachycardias, all the cases of ventricular tachycardia and any that may be due to auricular fibrillation, as well as some of the tachycardias arising in the auricles when the con- tractions of the latter are too feeble to give rise to a wave. In the latter the true site of origin is shown by the presence of the P wave in the electro- cardiogram. A careful analysis of the pulse-rate during and between attacks shows that the rate is by no means always a definite multiple, but varies within considerable limits (as for example, from 1.7 to 2.1 : 1; 88 to 140 and vice versa 70 to 160) even when tracings are obtained from the instant of onset or of cessation of an attack. OCCURRENCE AND ASSOCIATED LESIONS. Paroxysmal tachycardia is equally common in both sexes (Bouveret, Hoffmann). It occurs at all ages, frequently beginning in early childhood and persisting for decades. On the other hand, it frequently occurs in old persons, as in G. R., who was 72 years of age. It is not infrequent in other- vise healthy pregnant women, in whom it is a very annoying feature. PAROXYSMAL TACHYCARDIA. 665 In at least half the cases the heart is free from organic lesions, but, on the other hand, paroxysmal tachycardia very commonly occurs in the course of mitral stenosis, and probably also in the sudden tachycardias of aortic insufficiency. Sometimes, as in the cases reported by Romberg, there is associated coronary sclerosis a group which seems to be particularly common. This seems to correspond to the experimental observation that shortly before death the auricles of the exposed dog's heart sometimes pass into fibrillary contractions for a short period upon the slightest mechanical irritation, as well as to the experiments of T. Lewis. The writer has encountered a num- ber of cases associated with mitral stenosis. The autopsy findings of Mackenzie and Keith, patches of fibrous myo- carditis in the vicinity of the His bundle and coronary sinus, are of great interest, but await further observations before they can be accepted as the pathogenetic lesion. On the other hand, tumors, patches of fibrosis, and arteriosclerosis in the vicinity of the vagus nucleus in the medulla, adhesions along the course of the vagus (Reinhold, Hoffmann, Pitres, Oppeiiheimer, FIQ. 319. Slightly more intense stimulation. Tachycardia, with quickened conduction, outlasting the period of stimulation. Time in seconds. Schlesinger, Pal), multiple sclerosi (Miiller), early tabes (Hirschberg) are sometimes found. However, S. Hyman, in Sir Victor Horsley's laboratory, has produced permanent lesions of the vagal nuclei in a series of dogs and monkeys without ever giving rise to paroxysms of tachycardia. Never- theless, it is conceivable that continued reflexes from irritation of nerves through pressure of tumors from hernias, intestinal parasites, etc., may increase the irritability of the heart muscle just as they often increase that of the cerebral cortex. Indeed, paroxysmal tachycardia bears certain super- ficial resemblances to a condition of " epilepsy of the heart," and is occa- sionally associated with idiopathic epilepsy (Nothnagel, Schlesinger). In a number of cases collected by Hoffmann disturbances of the digestive and pelvic organs were found, in some cases floating kidney. In some cases the attacks date from an acute cardiac overstrain; in others from an attack of rheumatism, with or without other cardiac complications. However, the writer can confirm the statement of Hoffmann, that in many cases neither the underlying condition nor the factors bringing on the attack can be discovered. Onset. The attacks themselves often occur at the moment of awak- ing from sleep, after or during defecation, during conditions of fatigue, and are sometimes brought on by nervous excitement, as was the case in the second attack of one of our patients. Mere percussion of the precordium has been known to bring on an attack (Bouveret). Change in the position of the body from the horizontal to the vertical may bring on an attack (orthostatic paroxysmal tachycardia). 666 DISEASES OF THE HEART AND AORTA. NATURE OF FUNCTIONAL DISTURBANCES. The nature of the functional disturbance is still obscure, though several theories have been advanced. Hoffmann, Lommel, Gerhardt, and Mackenzie at first believed that it consisted in the interpolation of an extrasystole between each two regular systoles, calling attention to the fact that the arterial pulse often showed an alterna- tion of large and small beats; but Bayliss and Starling, Hirschf elder, and others have been able to show that this indicates that the rate is a little too fast for the optimum contractions of the ventricles rather than that the small systoles are of abnormal origin. Hoffmann (1904) suggested that the sudden change of rate (to approxi- mate multiples or fractions of that pre-existing) represented the coming on or the passing off of a block between the site at which the cardiac im- pulses arise (remains of embryological sinus, the area bounded by the venae cavae, coronary sinus, and septum auriculorum and in front by the Eusta- chian valve) and the auricular muscle tissue a true sino-auricular block. Just as in the cases of atrioventricular block above mentioned, the attacks would thus correspond to the periods when the block has passed off, the return to normal pulse corresponding to the onset of block. However alluring this theory may be, it must be admitted that there is at present little evidence to support it. More plausible is the theory of Mackenzie (1903-04), that these attacks are brought about by a condition in which the (Purkinje) cells of the His auriculo- (atrio-) ventricular bundle initiate the rhythm of the beat instead of the sinus. This theory is founded not only upon the above-mentioned venous tracings, but also upon the statement of Gaskell that, if one " touch the auriculoventricular ring of muscle (in the frog) with the slightest stimulus, immediately a series of rhythmical contractions occurs," while touching the auricular and ven- tricular muscle causes only a single contraction in each case. In mammals, however, the evidence upon this point is very flimsy, for it has been impos- sible to stimulate the fibres of the atrioventricular bundle alone without including fibres of the auricles and ventricles. Lohmann, it is true, stimu- lated the region of the auriculoventricular bundle (including the auricular and ventricular muscle) and obtained simultaneous contractions of the auricles and ventricles, which outlasted the period of stimulation. Erlanger has obtained somewhat similar results, but does not regard them as conclusive. Hering and Rihl obtained extrasystoles with shortened conduction time and assumed that they arose in the bundle of His. Mackenzie and Keith, however, claim to have found deposits of cells whose cicatrization " irritates the bundle and renders it more excitable than the sinus. The contraction of the heart then originates from this more irritable part. Somewhat analogous changes follow in cardiosclerosis and in degener- ation of the coronary arteries." Hirschfelder, however, has been able to duplicate ex- actly the findings of Lohmann and Hering by faradic stimu- lation of the exposed dog's auricle, not in the vicinity of the auriculo- ventricular bundle, but far out upon the auricular appendix. He found that, if the right auricular appendix in the dog is stimulated with very weak faradic stimuli, no effect at all PAROXYSMAL TACHYCARDIA. 667 may be produced. If stimulus is a little stronger, the rate of both auricle and ventricle changes suddenly, within the duration of one or two cardiac cycles, to a very much more rapid rate, which varies from 1.5 to 2.1 the preceding rate. The conduction time is in some cases prolonged to about double the original rate (diminished conductivity) or short- ened to about half (increased conducfivity or perhaps origin of impulses at the auriculo- ventricular bundle). Occasionally the auricles and ventricles are seen to contract abso- lutely synchronously, which probably indicates that under these conditions the impulses are arising in the cells of the auriculoventricular bundle (auriculo ventricular tachycardia). In still other experiments the ventricle may be seen to contract before the auricle (ventricu- lar tachycardia), just as is frequently found in perfusion experiments on the excised dog's heart at a somewhat elevated temperature. When the faradic stimulation is repeated several times within a few minutes, the irritability of the heart muscle is found to be increased, so that the same intensity of stim- ulus which at first produced merely a tachycardia during the duration of the stimulus gives rise after repetition to a paroxysm which outlasts it by many seconds or even many minutes. When the faradic stimulus is increased in. intensity still more, the auricles pass at once into a state of fibrillation, which may or may not be preceded by one or two auricular extrasystoles. During auricular fibrillation in the dog the rhythm of the ventricles assumes a rate which is about the same as when responding to single coordinated contractions of the auricle, but which is frequently if not always irregular. Lewis, who has been able to control his results by means of the electrocardiograph, states that in every case of undoubted fibrillation the ventricular rhythm was irregular. The writer, in a series of experiments performed before the introduction of the electrocardiograph, has obtained regular tachy- cardias in dogs whose auricles had been strongly faradized and which, both on inspection and when the contractions were recorded by air transmission, appeared to be in a state of fibrillation. Since the border-line between rapid coordinate and incoordinate contractions can be made with certainty only by means of the electrocardiograph, it is possible that the contractions in these experiments were still coordinate and only simulated fibrillation. Lewis and Agassiz have reported cases of paroxysmal tachycardia with venous pulse of the ventricular type in which the auricular P wave was absent from the electrocardiogram though the rate remained regular. It is unfortunate that in these tracings trembling of the galvanometer thread interferes with the clearness of the curves, that the presence or absence of fibrillation of the finer type is difficult to determine absolutely, but it appears probable that waves of auricular origin can be definitely discerned. Clinical as well as experimental evidence indicates, however, as pointed out by Hirsch- felder and later by Lewis, that the difference between the coordinate and fibrillation tachy- cardia, whether of regular or irregular rhythm, is a quantitative as well as a qualitative one, and that the fibrillation represents merely a degree of irritability of the auricular muscle higher than the coordinate tachycardia, so that both paroxysmal and permanent absolute arrhythmia seem to be very closely allied to paroxysmal tachycardia. It is, moreover, not infrequent to find the latter condition passing over to the former, as was probably the case with patient W.W.C. and as is particularly common in cases of mitral stenosis. Lewis's contention, that in the auricular fibrillation the impulses arise in rapid succession in a number of ectopic foci instead of in one focus, seems to be the correct one. Unpub- lished experiments by B. S. Oppenheimcr seem to furnish a further basis for this view. August Hoffmann has recently reported a case in which the paroxysmal tachycardia induced a still more sorious condition just at the end of the attack, irregular contractions of the ventricles which gave for a moment electrocardiograms typical of fibrillation of the ventricle. There are therefore three or perhaps four conditions which may bring on attacks of experimental paroxysmal tachycardia in the dog. 1. Auricular tachycardia. 2. Auriculoventricular tachycardia. 3. Ventricular tachycardia. 4. Perhaps auricular fibrillation. In all these conditions there is a condition of increased irritability of the heart, and in most of them a region of the heart becomes the pace-maker (i.e., the impulses are e c t o p i c or heterogenetic, Lewis, or heterotopic, Hering). 668 DISEASES OF THE HEART AND AORTA. These attacks always subside spontaneously as suddenly as they set in, no matter how long their duration. They can sometimes, but not always, be stopped by stimulation of the vagi. In the cases studied with the electrocardiograph by Thomas Lewis and his pupils, Marris and Cohn, the paroxysms arise in the same* way as in Hirschfelder's experiments on the dog, but, probably owing to certain slight inherent differences between the dog's heart and the human heart, the most common mechanism in the one is not the same as in the other. The most common type thus far described in man has been an auricular tachycardia in which the impulses do not arise at the node of Keith and Flack but in some other area in the wall of either the right or the left auricle, as is shown by the presence of an inverted P wave (Lewis). In a number of cases the auriculo ventricular bundle probably becomes the pace-maker of the heart during the tachycardia, as is indicated in some of the reported cases by a greatly shortened conduction time (a c interval upon the venous pulse) and in others by the entire absence of a presystolic a wave, and a very high wave of short duration, synchronous with the c wave and followed by a subsidence to the normal level during the greater part of ventricular systole, often with extrasystole showing greatly shortened conduction time between attacks (cases of Rihl, Hirschfelder, Marris, and A. E. Cohn). In some cases, especially of short paroxysms, as have been reported by Thomas Lewis, the electrocardiogram may show the characteristic form of ventricular extrasystoles, indicating that in these cases either ventricle may become the pace-maker; and the same observer has reported another case in which also the ventricular type of venous pulse was present, in which the electrocardiogram showed the absence of the auricular P wave, the presence in diastole of the small wavelets characteristic of auricular fibrillation. CAROTID PRESSURE VOLUME OF VENTRICLES VENOUS PRESSURE Fio. 320. Diagram showing the effect of a paroxysm of tachycardia upon the circulation. The under- lined portion indicates the paroxysm. It will be seen from the above that clinical evidence shows an almost exact reproduc- tion of the conditions produced experimentally by Hirschfelder, Lewis, and other investi- gators, and it therefore seems almost justifiable to assume that the same mechanism, namely, increased irritability of the heart muscle and inherent cardiac nerves, is operative in both. Whether the stimulus originates in the Purkinje fibres or elsewhere seems for the present to have little practical importance. More important is the fact that Reid Hunt, Cushny and Edmunds, Garrey and Hewlett, and the writer have observed that such paroxysms may occur not only spontaneously or from direct stimulation of the heart muscle, but also upon stimulating the cardiac nerves, either accelerator or vago-sympathetic, in hearts whose irritability is already abnormally high. Hence it is natural that when the cardiac irritability is high, small reflex stimuli bring about an attack. Stimulation of Cardiac Nerves. That something more than mere neurogenic influences is essential was shown by Gerhardt and Hirschfelder. These observers paralyzed the vagi of such patients with atropine and yet produced no attack. Hirschfelder found that slight stimulation of the accelerators, by exercising his patient to the point of giddiness twenty-four hours after an attack and while his vagi PAROXYSMAL TACHYCARDIA. 669 were paralyzed with atropine, caused a slight gradual increase of pulse-rate, but nothing resembling an attack of paroxysmal tachycardia. The con- dition of extreme irritability of the cardiac muscle had evidently passed off. More recently, however, Rothberger and Winterberg have been able to produce auriculoventricular tachycardias in animals whose cardiac irri- tability has already been enhanced with barium or calcium chloride by stimulating the left accelerator nerve, so it is not unlikely that increased excitation of the latter, perhaps indeed of both accelerators, may be respon- sible for the onset of many paroxysms. The stimulation due to exercise in Hirschfelder's patient, though as intense as the condition of the patient would warrant, may not have been a crucial test as to the role of the accel- erator nerves. It is not improbable that there may be a well-marked sym- pathicotonie in many of these cases (see page 19), and it should always be carefully tested for. Paroxysmal Tachycardia from Coronary Ischaemia. Quite recently T. Lewis (Paroxysmal Tachycardia, Heart, Lond., 1909, i, 43) has succeeded in producing paroxysms of tachycardia in cats and dogs by ligating one of the coronary arteries, especially the right. These attacks come on even after section of both vagosympathetic nerves, and hence were not neuro- genic in origin. He has been able to obtain four types of abnormal cardiac cycles during such paroxysms: 1. Approximate doubling of the rates of both auricles and ven- tricles, with normal or slightly diminished conductivity; 2. Approximate doubling of these rates of these chambers, but the auricles and ventricles contract simultaneously (nodal rhythm'.'); 3 Fibrillation of the auricles with approximate doubling of rate in the ventricles; 4. Approximate doubling of rate in both auricles and ventricles, but the ventricles contract before the auricles (ventricular tachycardia). The writer has also obtained all of these four types during faradization of the auricles, so that it would appear that they may all be traced to a common cause, most probably over-excitability of the heart muscle. Moreover, Rothberger and Winterberg have obtained electrocardiograms with small irregular waves, suggestive of auricular fibrillation, from a patient with paroxys- mal tachycardia, and Professor Barker, Dr. Bond, and the writer have recently obtained a similar tracing from a patient between paroxysms, though electrocardiograms from another patient in the midst of a severe paroxysm showed apparently normal contractions of the auricles. Rothberger and Winterberg have obtained exactly similar electrocardio- grams from animals with exposed hearts in which they produced a state of auricular fibril- lation by faradization of the auricles. This coronary form of paroxysmal tachycardia is exactly similar to the cases of Romberg and Barker (page 369J, but it is by no means certain that this factor is the causal one in all cases of paroxysmal tachycardia. Paroxysmal Tachycardia and Paroxysmal Irregularity. Closely allied to the condi- tion of paroxysmal tachycardia (paroxysms of rapid heart rate with regular rhythm) is the condition of paroxysmal irregularity (paroxysms of rapid heart-rate with irregular rhythm) (Cushny and Edmunds). The latter occurs about as frequently as the regular tachycardia and is characterized by short attacks of absolute arrhythmia, which, like the regular tachycardias, sot in suddenly and subside suddenly. It differs from the latter only in the fact that during the attack the rhythm of the ventricles is absolutely irregular and the auricles are invariably in a state of fibrillation. Since Hirschfelder and also Lewis have shown that both the regular paroxysmal tachycardia and fibrillation of the auricles arise from a condition of increased irritability of the heart muscle, it is not surprising that one sometimes encounters transitional cases. in which a single paroxysm may begin as a regular tachycardia and pass abruptly into a state of auricular fibrillation. Such a case was recently met with by Dr. G. S. Bond in the electrocardiographic laboratory of the Johns Hopkins Hospital, as was also another type of transitional type in which the auricles were in a state of fibrillation but the ventricles were beating, probably independently, at a rapid regular rhythm, exactly as Hirschfelder has found from faradization of the auricles in a certain number of dogs. The electrocardiogram in this case showed that the beats of 670 DISEASES OF THE HEART AND AORTA. the ventricle arose at an abnormal site. It is probable that in this case the ventricular muscle was excited secondarily by the numerous impulses coming down from the auricles or that the same cause which increased the irritability of the latter also acted directly upon the ventricles. The symptoms and general clinical manifestations of paroxysmal irregularity do not differ materially from those of regular paroxysmal tachycardia, the most prominent feature* being the sensation of weakness and of palpitation during the attack, with signs of cardiac failure in the more severe cases. Like the regular paroxysms, they are frequently brought on by indigestion, flatulence or fatigue from overexertion. Indulgence in alcohol is some- times a causal factor, probably by inducing a state of sympathicotonie, as was the case in a patient recently under the writer's care who was in the habit of taking a pint of whiskey a day and was subject to definite attacks of this character. These were sometimes brought on by his flatulence, at other times by exertion, but they usually began several hours after the exertion was over. Between attacks the patient feels well and cardiac function between attacks is perfect. Paroxysmal irregularity is in most cases of somewhat graver import than paroxysmal tachycardia, for the transition to permanent arrhythmia is not so great, and, as inCushny and Edmunds's case, as well as, perhaps, W. W. C., cited below, there is a greater tendency for the arrhythmia to become permanent. EFFECTS ON CIRCULATION. The effect which these paroxysms of tachycardia exert upon the circu- lation is primarily due to the deficient filling of ventricles during the short diastoles. As Yandell Henderson has shown, the ventricles fill to their normal extent only when the pulse-rate is moderately slow. When the pulse becomes rapid, the ventricles do not have time to fill, and, since the period of systole is never much less than 0.2 second, it is evident that when the heart-rate is much above 200 the period during which filling can take place is very short and little blood can enter the ventricles. The volume of the heart remains small. As a result of this condition, blood stagnates in auricles and veins, venous pressure rises (to 30 cm. H 2 in one case ex- amined by Eyster and Hooker), and with it there come engorgement of the liver and oedema of the extremities. Stasis also occurs in the pulmonary veins, ushering in oedema and dyspnoea, and sometimes these symptoms of broken pulmonary compensation dominate the scene (see page 195). On the other hand, the arterial pressure falls, because, as the filling of the ventricle is small, the amount which is driven out into the arteries is diminished correspondingly. This fall in blood-pressure is usually accom- panied by pallor and often by symptoms of cerebral anaemia, exactly as occurs in hemorrhage, surgical shock, or other conditions in which the amount of blood in the arteries is diminished. Other organs also suffer from anaemia, and finally also the heart itself, which may give signs of weakening, first evinced by lowered tonus and dilatation. It is evident that hearts whose coronary arteries are sclerotic would suffer more readily than those with normal blood supply. PHYSIOLOGICAL SUMMARY. The pathological physiology of paroxysmal tachycardia may therefore be summed up as follows: Underlying causes: Increased irritability of cardiac muscle. Predisposing factors for an attack: Slight reflex stimulations of cardiac nerves. PAROXYSMAL TACHYCARDIA. 671 Condition during attack: " Doubling " or multiplication of pulse-rate, with or without auricular fibrillation. Mechanical effects on the circulation, to which these symptoms are referable: 1. Systemic stasis, high venous pressure. 2. Pulmonary stasis, high pressure in pulmonary veins. 3. Anaemia of brain, kidneys, and heart, from low arterial pressure. SYMPTOMS. Although attacks of tachycardia sometimes run their course without the patient's knowledge, it is more common for them to be accompanied by symptoms. These symptoms may be grouped as follows: 1. Symptoms of cardiac excitability. 2. Those due to engorgement of systemic veins (failure of right ven- tricle) . 3. Those due to engorgement of pulmonary veins (failure of left ventricle) . 4. Those due to cerebral anaemia. 1. Palpitation, a feeling of discomfort or oppression in the pre- cordium, and weakness are the most common symptoms. This is often worse just at the end of the attack, and may, as in Hay's case, resemble the symptoms of angina pectoris. In this case there was also hyperaesthesia of the precordium and neck. The latter may be due to engorgement of the cervical veins, as in angina pectoris it may be referred from the heart (Mackenzie). 2. Besides the above-mentioned feeling of fulness in the neck, the patient often has a similar feeling in the abdomen from dis- tention of the liver, and swelling of the feet commonly appears before the end of the attack. 3. Dyspnoea is frequent. It is striking that this may occur with- out any change in the rate of 'respiration, even in cases with severe myo- cardial changes (Romberg). No doubt this is associated with engorgement and high pressure in the pulmonary veins. It is often accompanied by cough and the expectoration of mucus, sometimes containing large endo- thelial cells with blood pigment (Herzfehlerzellen). Occasionally there is actual haemoptysis (in three of Bouveret's eleven cases) during the attack. Actual pulmonary oedema may indeed set in, as in Pribram's case, a young woman otherwise healthy, whose attacks were so severe that "the pulse became baiely palpable. The patient fell into a state of collapse, and finally oedema appeared in the lower part of the lungs. At the moment when death seemed imminent, when collapse was at its height, she gave a cry of anguish; it seemed to her as though something were taken out of her neck, and the scene suddenly changed. The pulse fell to 70, became large and full, and the collapse disappeared." On the other hand, this sudden change does not always occur, and death sometimes supervenes during the attack. The venous stasis also leads to albuminuria, though in the milder attacks the urine may be increased and of low specific gravity. 672 DISEASES OF THE HEART AND AORTA. 4. The fall in arterial pressure usually brings about symptoms of cerebral anaemia; weakness, vertigo, and even extreme nerv- ousness is the rule during the attacks, accompanied by restlessness, loss of appetite, and inability to sleep. Even syncope may occur. In a gentle- man whom the writer examined some years ago these syncopal attacks had led several prominent physicians to diagnose Adams-Stokes syndrome ; when, as was shown by the examination and subsequent observation, the cerebral ansemia resulted not from bradycardia but from tachycardia. Fortunately, these attacks have a tendency to become milder. Dr. Lyon writes, three years after the first examination, that this patient "is now able to play cards, go fishing, and do almost anything in a quiet way during attacks." PHYSICAL SIGNS. Physical signs are absent between attacks of par- oxysmal tachycardia. During the attacks the face is usually pale, the expression anxious, the pupils are equal, the veins of the neck are seen to be engorged and often to show a positive ''single' pulsation accompanying each systole (sometimes due to transitory tricuspid insufficiency), perhaps due to the feebleness of the auricular con- tractions. The tumultuous heart action is often seen in a precordial heav- ing and well-marked apex beat. The area of cardiac dulness is rarely increased except toward the end of the attack. It is usually un- changed or decreased in size, corresponding to the diminished filling of the ventricles. This diminution in the size of the heart during an attack has been seen with the fluoroscope by Hoffman, Dietlen, and others, and it can be demonstrated in the experimental paroxysms. Towards the end of severe attacks dilatation sets in from cardiac weakness. The heart sounds may be unchanged, but usually become short and somewhat muffled. There is often embryocardia. It is very common to hear a soft systolic over the right ventricle and apex, perhaps due to a mitral or tricuspid insufficiency of the papillary type. Sometimes the cardiac rhythm is irregular, owing to inability of the ventricles to follow all the impulses from the sinus and auricles or to the presence of extrasystoles. The liver often is felt to be enlarged, and often shows a systolic pulsation during attacks (tricuspid insufficiency), but ascites rarely occurs. (Edema of the ankles and feet is very frequent. CASE OF PAROXYSMAL TACHYCARDIA. (1. D. R., a hotel-keeper aged 72, was admitted to the Johns Hopkins Hospital on Feb. 22, 1906, complaining of palpitation of the heart. The family history and personal history were negative. The patient had always been a robust man, had had no infec- tious diseases and no other cardiac manifestations. The first attack of palpitation and tachycardia came on suddenly after retiring one evening twenty years before admission. It caused him great fear, but no pain. The attack lasted six hours and left him weak but other- w i s e w ell. Attacks similar in character recurred once a month until the winter of 19().~>-190G. when they became more severe and began to occur once or twice a week. During the attacks he passed large amounts of urine. He never noticed palpitation between attacks of tachycardia. PAROXYSMAL TACHYCARDIA. 673 The patient was a large well-nourished man of good color. His pupils were equal and reacted well to light and during accommodation. The thorax was rather barrel- shaped; the percussion note was hyperresonant, and the breath-sounds were clear, though distant. The cardiac impulse was neither seen nor felt, but the apex, as made out by per- cussion and auscultation, was situated in the fifth left interspace 11 cm. from the midline. The cardiac dulness extended up to the upper border of the third rib, but could not be made out to the right of the sternum. The sounds were distant, but clear. The pulse- rate between attacks was 64 per minute. It was usually regular in force and rhythm, of good volume and rather high tension; the blood-pressure ranged from 165 to 190, the minimum from 100 to 115. The abdomen was large and flabby, with considerable panniculus. Liver and spleen were not palpable. The examination was otherwise negative. The venous pulse between attacks was usually normal. On Feb. 23 and March 1 and 15 the patient had attacks of tachycardia, in which his pulse-rate rose suddenly from 80 to 88 per minute to a height of 144 to 160 per minute. The attack of March 15 began just after returning from the closet, where he had passed a soft fluid stool. Tracings made from the patient during this attack showed what is probably a ventricular type of venous pulse during the attack. When the latter ceased, however, the pulse resumed the normal auricular type. There was no sign of auriculoven- tricular block. Excitement incident to being shown at the clinic precipitated a second attack on March 15, which was not relieved by the application of an ice-bag, yawning, deep breathing, pressure on the vagus, in front of the sternocleidomastoid, nor by admin- istration of spiritus aetheris nitrosi, amyl nitrite, or digitalin. The attack ceased spon- taneously within an instant, at 3.10 p.m. On March 21 his pulse was irregular, due to the presence of numerous extra- systoles with shortened conduction time (auriculoventricular?). These subsided, however, leaving his pulse regular. On March 24 his pulse remained at 76 in spite of the administration of 2mg. atropine. Even rapid walking while he was under the influence of the atropine did not bring on an attack, nor did the administration of amyl nitrite on March 24. A very well-defined case of tricuspid insufficiency resulting from the cardiac overstrain of a prolonged paroxysm of tachycardia is exemplified by the following patient seen in consultation with Professor Barker. CASE OF LOXG-STANDING PAROXYSMAL TACHYCARDIA. W. W. C., clerk in the U. S. Patent Office, aged 29, had always been healthy except for a very severe attack of gonorrhoea six years before admission. He had no cardiac disturbance until seven years ago (one year before the attack of gonorrhoea), when he had symptoms of slight cardiac weakness which was said to be valvular (?), but these soon disappeared under treatment, so that he was able to dance and take all kinds of exer- cise without symptoms. Two years before admission he awoke one morning, after an emission, with severe palpitation and a very rapid weak pulse. He was kept quiet, an ice-bag put to his chest, and he was given strych- nine, 1.5 mg. (fQ gr.), also tincture of strophanthus. His pulse- rate dropped to 72. Three weeks later he had another emission and another attack, and since then had a large number. The attacks often come on after emissions, which leave him feeling very much depressed. They subside very suddenly and the pulse returns to normal at a bound, remaining between 70 and 100 per minute between attacks. In the present attack, however, the pulse-rate has been rapid continu- ously for over a year (since April, 19 OS), and this has been accom- panied by palpitation and great weakness, occasionally by n a u s c a and v o in i t - ing. It has not been relieved by strophanthin, digitalis, strychnine, nitroglycerin, belladonna, or potassium bromide. The patient is a pale, nervous-looking young man. The pupils are rather wide, but there are none of the ocular signs of Basedow's disease. The thyroid is not enlarged. There is no glandular enlargement. His chest is long and rather flat, but shows nothing of importance. 43 674 DISEASES OF THE HEART AND AORTA. The heart is much enlarged, the apex being located in the sixth left inter- space 10.5 cm. from the midline. It is very movable within the chest, site altering 5 cm. as the patient turns from side to side. There is a heaving impulse over the precordium, with systolic retraction of the interspaces over the right ventricle and marked systolic retraction in the epigastrium. Dulness extends above to the second inter- space at the left sternal margin, and to the right reaches 5 cm. from the m i d 1 i n e. Longitudinal diameter, 20 cm. The area of flatness extends from the apex to the level of the fourth rib and just b e y o n d the sternal margin in the fifth right interspace. The heart sounds are heard at the apex, the first being accom- panied and followed by a slight soft systolic murmur not transmitted to the axilla, while the second is fairly distinct. The second pulmonic is accentuated, the second aortic clear. There are no diastolic murmurs. The striking feature is a loud superficial blowing systolic murmur heard over an elliptical area bounded above by the level of the fourth interspace, to the left by a point 9 cm. from the midline, below by the middle third of the ensiform cartilage, and to the right by a point 1 cm. to the right of the sternal margin. This represents the tricuspid area. The heart's action is extremely rapid, about 180 per minute, and is irregular; the pulse still more so, as about 40 beats per minute are ineffectual and do not open the aortic valves. The radial pulse is therefore 140 per minute. The right jugular vein is rather full and shows a defi- nite ''single'' systolic pulsation coincident with the apex beat. This is borne out by the tracing, upon which there are no waves of auricular con- traction. The pulse is small, of rather low tension, and very irregular. The vessel wall is not sclerotic. Blood-pressure with the Erlanger apparatus: Maximal varies from 100 to 110 mm. Hg: minimal varies from 70 to 80 mm. The liver is much enlarged and extends almost to the level of the umbilicus. Its surface is smooth, the edge round and fairly soft, but it does not pulsate. His venous tracing is shown in Fig. 75, page 116. The patient improved somewhat during his stay in the hospital ; but his pulse remained rapid, he was bedridden, and died two months later. DIAGNOSIS. In the cases in which the pulse-rate is above 160 per minute the diag- nosis rarely presents any difficult}', for the tachycardias of simple nervous origin, on the one hand, and those of organic cardiac disease rarely reach that height. But in the border-line case in which the tachycardia is about 140, the diagnosis may be difficult. The crucial point in the differentiation lies in the suddenness of the change of rate, and for this it is important to have observed the beginning and the end of an attack, the sudden rise to maximum rate within a few seconds indicating idiopathic paroxysmal tachycardia, while a gradual step-like or progressive rise indicates a simple tachycardia. Thus while the patient (1. R. exemplifies the idiopathic con- dition, the following case is typical of the simple tachycardia. CASE OF SIMPLE EMOTIONAL TACHYCARDIA RESEMBLING IDIOPATHIC PAROXYSMAL TACHYCARDIA. The patient, a biological student at the University of Virginia, aged 20 years, had recovered from an attack of typhoid fever about a year before. Previously to this he had been strong and free from cardiac symptoms; but since convalescence he is t r o u b 1 e d w i t h attacks of p a 1 p i t a t i o n a n d t a c h year d i a in which the pulse-rate rises from about 60 to about 120 per minute. Slight mental excitement and even the mere mention of taking a pulse tracing suffices to bring on an attack. Before the apparatus could be applied he felt his pulse begin to rise. In the successive quarters of a minute the pulse- rate was 15, 21, 26, PAROXYSMAL TACHYCARDIA. 675 3 , having doubled itself within a single minute. But the change of rate was not sudden! Physiological examination was negative, heart not being enlarged and sounds normal. The case was therefore considered a simple tachycardia. A favorable prognosis was given, which was verified by the subsidence of tachycardia and palpitation within a few months. TREATMENT. Drugs. As regards the treatment of paroxysmal tachycardia various methods have been employed. The first essential is to put the patient into the best possible physical condition, to treat any aneemia, digestive disturbance, constipation, disturbance of vision, heaving, enteroptosis, or other conditions which may bring about reflex irritations; to stop the use of tea, coffee, tobacco, and alcohol, and so to arrange the life of the patient as to do away with mental excitement, worry, over-exertion, and fatigue. If necessary, a "rest cure" may be resorted to. These measures may do much to diminish the frequency of the attacks, but often the latter do not disappear altogether. Small doses of digitalis or aconite may be tried in the interim between attacks, in the hope of keeping them down by increasing the action of the vagus; or potassium bromide or valerian may be given, in the hope of quieting the nervous system ; but the desired result is only occasionally obtained. To quiet the attack after its onset drugs are of little avail. Morphine, bromides, etc., and other sedatives may diminish the in- tensity of the symptoms, but do not slow the heart-rate. The administration of a few whiffs of chloroform, of amyl nitrite, nitro- glycerin, Hoffman's anodyne, strychnine, digitalis and its derivatives (digitalin, digalen), is without effect. Though large doses of strophan- thin sometimes stop auricular fibrillation in animals, intravenous injection of strophanthin has not given satisfactory results in three cases of par- oxysmal tachycardia to whom it has been administered in the Johns Hop- kins Hospital. Aconite also, though the best stimulant for the vagus, was without clinical effect in the one case in which the writer used it. The application of an ice-bag to the precordium sometimes relieves the symptoms, but only rarely is a sufficient cardiac sedative to stop an attack, Exercise for Stopping the Attacks. Fairbrother states that he has been able to stop his own attacks by sudden or violent exercise, such as running or jumping. In like manner a young physician with mitral stenosis who was under the writer's observation suffered from paroxysms which for years resisted treatment with rest, digitalis, strophanthin, potassium bromide, aconite, pressure on the vagus, and deep breathing; but they have disappeared since he has been doing hard work in the hospital. Needless to say, such exertions in a layman should always be under the care of a physician. The paroxysms themselves may sometimes be stopped by various mechanical methods which stimulate the vagi; deep inspirations (Xoth- nagel), especially yawning, "squeezing arms and elbows tightly against the chest while holding breath and compressing abdomen" (Valsalva'a experiment with elbows compressed against chest) (Hay), s w a 1 1 o \v ing, especially of ice-water, or belching, may be successful. Max Herz has found it possible to suppress many troublesome attacks in his patients by bringing about belching in the following manner: The patient is made to sit down, fill 676 DISEASES OF THE HEART AND AORTA. his mouth with water, bend his head backward as far as possible, and swallow. This not only brings about a desire to belch, but also facilitates the eructation of a large amount of gas, and frequently brings the attack to a close. Needless to say, care should be taken that the belching does not pass over into continuous air swallowing and that the patient does not acquire this pernicious habit (see page 708). When belching fails to stop the attack, vomiting may be resorted to, and frequently proves an effectual though unpleasant method. Tick- ling the pharynx with the finger is usually sufficient to bring it about, especially after swallowing some water. Emetics need not be used. One of the oldest and best procedures (Bensen, 1880) is pressure upon the vagus just to the left of the thyroid cartilage. The nerve which is just behind the carotid artery is pressed very firmly against the vertebrae and held tightly for two or three minutes. In a considerable number of cases this stops the attack, but in many it fails, or succeeds for a moment and then the tachycardia is resumed (Priesendorfer), just as is the case in the experimental auricular fibrillation. However, when the results of all methods of treatment have been taken into account, one is inclined to share the feelings expressed by Mackenzie when he wrote: "In my early days I, too, thought I knew ho\v to stop attacks, but more extended experience has shown me that when they stopped it was from some cause unknown to me and which was independent of any means I employed." BIBLIOGRAPHY. PAROXYSMAL TACHYCARDIA. Bouveret, L.: De la tachycardie paroxystique essentielle, Rev. de Med., Par., 1889, ix, 753, 836. Hoffmann, Aug.: Die paroxysmale Tachycardie (Anfalle von Herzjagen), Wiesb., 1900. Pathologic und Therapie der Herzneurosen, u.s.w., Wiesb., 1901. Neue Beobachtungen ueber Herzjagen, Deutsch. Arch. f. klin. Med., Leipz., 1903, Ixxviii, 39. Ueber Ver- doppelung der Herzfrequenz, Ztschr. f. klin. Med., Berl., 1904, liii, 206. Rihl, J.: Analyse von fiinf Fallen von Ueberleitungstorungen, Ztschr. f. exp. Path. u. Therap., Berl., 1905, ii. 83. Schmoll, E.: Paroxysmal Tachycardia, Am. J. M. Sci., Phila. and N. Y., 1907, cxxxiv, 662. Mackenzie, J.: On the Inception of the Rhythm of the Heart by the Ventricles, Brit. M. J., Lond., 1904, i, 529. New Methods in the Study of Affections of the Heart, ibid., 1905, i, 813. Abnormal Inception of the Cardiac Rhythm, Quart. M. J., Oxford, 1907, i, 39. The Extrasystole: A Contribution to the Functional Pathology of the Primitive Cardiac Tissue, ibid., 1908, i, 182 and 481. Diseases of the Heart, Lond., 1908. Hirschfelder, A. D.: Observations upon Paroxysmal Tachycardia, Bull. Johns Hopkins Hosp., Balto., 1906, xvii, 337. Hay, J.: Paroxysmal Tachycardia, Edinb. M. J., 1907, N. S. xxi, 40. Peabody, F. \V.: A Note on the Venous Pulse in Paroxysmal Tachycardia, Arch. Int. Med., Chicago, 1909, iv, 432. Romberg, E.: Lehrbueh der Krankheiten des Herzens und der Blutgefiisse, Stuttg., 1906. The complete bibliography of cases will be found in the monograph of Hoffmann and the articles of Reinhold, Schlesinger, and Schmoll. Gerhardt, D. : Beitrage zur Lehre von den Extrasystolen, Deutsch. Arch, f . klin. Mod., Leipz., 1905, Ixxxvii, 509. Lommel, F.: ibid., 1905, Ixxxii, 495. Bayliss, W. M., and Starling, E. H.: On Some Points in the Innervation of the Mammalian Heart, J. Physiol., Camb., 1892, xiii, 407. Gaskell. W. H.: Schaefer's Text-book of Physiology, Edinb. and Lond., 1900, ii. PAROXYSMAL TACHYCARDIA. 677 Lohmann, A.: Zur Automatie der Bruckenfasern des Herzens, Arch. f. Physiol., Leipz., 1904, 431, and Suppl., 265. Bering, H. E., and Rihl, J.: Ueber atrioventrikulare Extrasystolen, Ztschr. f. exp. Path. u. Therap., Berl., 1906, ii, 510. Experimentelle Untersuchungen ueber Herzunregel- massigkeiten an Affen, ibid., 1906, ii, 525. Hirschfelder, A. D.: The Functional Disturbances in Paroxysmal Tachycardia, Arch. Int. Med., Chicago, 1910, vi, 380; Recent Studies upon the Electrocardiogram and upon the Changes in the Volume of the Heart, Interstate M. J., St. Louis, 1911, xviii, 557. Lewis, T., and Silberberg, M. D.: Paroxysmal Tachycardia Accompanied by the Ventric- ular Form of Venous Pulse, Quart. J. M., Oxford, 1911, v, 5. Lewis, T., and Schleiter, H. G. : The Relation of Regular Tachycardias of Auricular Origin to Auricular Fibrillation, Heart, Lond., 1912, iii, 173. Agassiz, C. D. S.: Paroxysmal Tachycardia Accompanied by the Ventricular Form of Venous Pulse, ibid., 1912, iii, 193. Hoffmann, A. : Fibrillation of the Ventricles at the End of an Attack of Paroxysmal Tachy- cardia in Man, ibid., iii, 213. Hirschfelder, A. D.: Contributions to the Study of Auricular Fibrillation, Paroxysmal Tachycardia, and the so-called Auriculo- (atrio-) ventricular Extrasystoles, Bull. Johns Hopkins Hosp., Bait., 1908, xix, 323. Cushny, A. R., and Edmunds, C. W.: Paroxysmal Irregularity of the Heart and Auricular Fibrillation, Am. J. M. Sc., Phila. and X. Y., 1907, cxxxiii, 66. Studies in Pathology, Quart. Publ., Aberdeen Univ., 1907. Hunt, R.: Direct and Reflex Accelerations of the Mammalian Heart, Am. J. Physiol., Bost., 1899, ii, 395. Carrey, W. E. : Effect of Chemicals on the Heart Nerves, Calif. State M. J., San Francisco, 1907. Some Effects of Cardiac Nerves upon Ventricular Fibrillation, Am. J. Physiol., Bost., 1908, xxi, 283. Henderson, Y. (with the collaboration of M. McR. Scarborough and F. P. Chillingworth) : The Volume Curve of the Ventricles of the Mammalian Heart, etc., Am. J. Physiol., Bost., 1906, xvi, 325. Pfibram, A.: Wien. med. Presse, 1882. Quoted from Bouveret. Lyon, I. P.: Personal communication. Dietlen. H.: Orthodiagraphische Beobachtungen ueber Veranderungon der Herzgrosse bei Infektionskrankheiten, exsudativer Perikarditis und paroxysmaler Tachykardie, Munchen. med. Wchnschr., 1908, Iv, 2077. Nothnagel. Quoted from Bouveret. Fairbrother, H. C.: A Remedy for Paroxysmal Tachycardia, J. Am. M. Asso., Chicago, 1909, liii, 300. Herz, M. : Ein Kunst griff zur Unterdriiokung der Anfalle yon Angina Pectoris und paroxys- maler Taohykardie, Wien. klin. Wchnschr., 1908, xxi, 803. Bensen: Berl. klin. Wchnschr., 1880. II. THYROID HEART. The cardiac disturbances associated with thyroid disease were the most striking features observed by Parry in 1815 in the first described cases of exophthalmic goitre. His first case died of heart failure. Graves (1835), Basedow (1848), Stokes (1854), and Trousseau (1856) were also impressed by the cardiac features of this disease. Trousseau found them especially important in the "formes frustes " or " atypical " forms to which he called attention, likening such cases to a defaced (" fruste ") coin. The important role which these "formes frustes" of Basedow's 1 disease play in many cases of so-called cardiac neurasthenia and hysteria has, since Trousseau, been recognized with increasing frequency, and espe- cially since Friedrich Kraus in 1899 called attention to them by introducing the term "Kropfherz" ("goitre heart" or thyroid heart), which is now widely used in Germany. FORMS OF CARDIAC DISTURBANCE DUE TO THYROID DISEASE. Strictly speaking, as shown by Rose, Schranz, and Minnich, there is some cardiac disturbance with all forms of goitre. Four main forms of cardiac disturbance may thus be distinguished, due to: I. Pressure of the goitre upon the trachea, bronchi, veins, chest, and sympathetic ganglia (in simple goitre), pneumo-mechanical goitre heart (Rose). II. Hypothyroidism (in myx oedema, cretinism, and achondroplasia). III. Hyperthyroidism (exophthalmic goitre and formes frustes). IV. Goitre secondary to the cardiac disease (goitre cardiaque, "car- diac goitre"). CARDIAC DISTURBANCES FROM PRESSURE OF THE THYROID. Potain in 1863 and Rose in 1878 reported cases of heart failure and more or less sudden death in cases in which large colloid goitres pressed upon the veins and trachea. Such a goitre has several mechanical effects: 1. It may prevent adequate filling of the lungs and thus produce emphysema, deficient aeration of the blood, and later asphyxia. The chronically deficient aeration of the blood may lead to secondary car- diac overstrain and finally to myocardial weakness. This will be enhanced by all pulmonary infections. 1 Basedow (" Bas-e-do"). Dock after a careful study of priorities advises the accept- ance of this name, which was the first unobjectionable term given and is the one most widely accepted. 078 THYROID HEART. 679 2. The goitre often presses on the sympathetic ganglia on one or both sides of the neck, thus stimulating the accelerators and bringing on a chronic tachycardia just as is produced in Basedow's disease. Miiller's muscle in the orbit may also be stimulated and exophthalmos produced. This exophthalmos is often unilateral. The condition of exoph- thalmos and tachycardia from the pressure of a simple goitre is known as pseudo-B asedo w' s disease. 1 CASE OF SIMPLE GOITRE RESEMBLING BASEDOW'S DISEASE. Such a case is represented by that reported by Potain in 1863: 2 M. K., servant girl, aged 50. Complains of palpitation, feeling of pressure in chest, attacks of suffocation, irregular menstruation. She has had goitre all her life, unaffected by iodine treatment. For some years her eyes have been larger than before. She has lost weight, has suffered from dyspnoea especially on exertion, she has throbbing of the goitre, and her legs are swollen. Her pulse is 152, irregular. Apex is in the sixth interspace 13 cm. from midline. There is heaving of the entire precordium. At the apex and over the precordium there is a meso-systolic murmur. The veins of the neck are dilated. There is a large goitre which does not pulsate and no murmur is heard over it. Digitalis is without effect, and the patient died from pulmonary oedema 11 days after admission. Autopsy showed colloid cystic goitre with some hemorrhages from stasis, slight infarction of the lungs, and a somewhat enlarged, very flabby heart. The livor, orthopnoea, asphyxia, and sudden death, as in Rose's case, are due to pressure upon the air-passages, and are to be regarded as cardiac symptoms. The respiratory origin of this suffocation is seen in the very marked inspiratory (not systolic) retraction of all the thoracic interspaces. CARDIAC AFFECTIONS OF HYPOTHYROIDISM (CARDIOPATHIA THYREOPRIVEA) (KRAUS). In all the conditions in which there is atrophy of the glandular tissue of the thyroid and diminution in the internal secretion of the gland, there are symptoms of cardiac weakness. The patients get out of breath on very slight exertion. The pulse is small and weak, but may be either slow or slightly accelerated (Kraus). This is due to the fact that the physiological vagus tone is largely due to the thyroid secretion (v. Cyon), and when it is deficient there is an overstimulation of the accelerators. However, as Kraus points out, the cardiac features in cachexia thyreoprivea arc not prominent features of the disease, and hence are of little importance in connection with diseases of the heart. Revilliod has, however, called attention to another effect of hypo- thyroidism upon the circulation, namely, early arteriosclerosis with cal- careous deposits. This effect has also been produced by v. Kiselsberg in new-born lambs from which he removed the thyroid glands. In contrast to other experimental arteriosclerosis, the arterial changes affected the intima and not the media. 1 In some cases, however, this is not due to pressure on the sympathetic but to the activation of thyreoglobulin by the iodine treatment. Occasionally, moreover, a goitre shows in one part colloid degeneration, in another hyperplasia like that of Basedow's disease. 2 Bull, de la Soc. d'Anat. de Paris, 1803, p. 87, quoted from Minnich. 680 DISEASES OF THE HEART AND AORTA. DISTURBANCES DUE TO HYPERTHYROIDISM. Basedow's Disease (also "Formes frustes," and Accidental Hyperthyroidism in the Treatment of Obesity). As stated above, these conditions present the most important cardiac features which are due to disturbed thyroid metabolism. PATHOLOGY, PATHOGENESIS, AND PATHOLOGICAL PHYSIOLOGY. The veil of mystery has been lifted from diseases of the thyroid by the hands of the physiological chemists. The surgeons Astley Cooper, Rever- din, and Kocher had found that extirpation of the thyroid for goitre led to myxoedema, and Pisenti Gley and Vassale had demonstrated that these symptoms could be prevented by feeding the dried thyroid sub- stance. But the accurate knowledge dates from the studies of Baumann and his pupils, Roos and Oswald. Thyreoglobulin and lodothyrin. Baumann, Roos, and Oswald have shown that the active principle of the thyroid is a globulin (iodothyreo- globulin) which contains all the iodine of the gland. Thyreoglobulin is at first formed within the cells free from iodine and later acquires its iodine from the blood, becoming iodized thyreoglob- ulin or iodothyreoglobulin. The cells secrete thyreoglobulin more readily after it is combined with iodine. In cases of colloid goitre when the blood content is low in iodine, the cells become loaded with the iodine- free thyreoglobulin and undergo col- loid degeneration. Iodine-free thyreoglobulin is p h y s i o - logically inactive, and the entire activity of the gland is due to the iodized thyreoglobulin. Indeed, as Baumann has shown, it is due to a comparatively simple molecular group with which the iodine is combined, and which can be split off from the rest of the globulin molecule by hydrolysis with H 2 S0 4 (iodothy rin) . Effect of Thyreoglobulin on Thyroid Structure. According to Oswald, it is the state of the thyreoglobulin which determines the histological changes in the thyroid. When the iodine-free thyreoglobulin accumulates in the cells, they become overloaded with colloid and gradually undergo colloid degeneration, so that the acini are found surrounded with the original single layer of flat epithelial cells in all stages of colloid degeneration, whose disintegration adds to the colloid within the lymph spaces and within the acini. (Oswald, Huerthle.) Fir,. 321. Photograph of a patient with Basedow's disease. (Kindness of Prof. Blood- good.) THYROID HEART. 681 An excess of the iodized product, on the other hand, stimulates the cells to hyperplasia, so that instead of a single layer of columnar epithelium the cells about the acini are found to be several layers and protrude into the lumen in irregular papillary masses suggesting adenomatous changes (Halsted, Oswald, MacCallum, Wilson). The same hyperplasia takes place as a compensatory process when a part of the gland is removed (Halsted, Marine). 1 The colloid gradually disappears from the lumen as glandular activity and hyperplasia progress and as the symptoms become more severe, and in very bad cases it may be entirely absent (Marine and Williams, Wilson). The arteries and veins are very much dilated (C. Gerhardt). When the iodine is administered in cases of colloid goitre, the excess of thyreoglobulin may be suddenly iodized and by escaping into the blood may give rise to symptoms of hyperthyroidism (palpitation tachycardia, tremor, loss of FIG. 322. Photograph of a portion of the thyroid gland removed from the patient shown in Fig. 321. (Kindness of Prof. Bloodgood.) weight, exophthalmos Basedowification of a simple goitre). When there is an excess of iodine and iodized thyreoglobulin in the blood, the symptoms are the same as arise from the administration of thyroid substance (thyreo- globulin or iodothyrin, its split product). PHYSIOLOGICAL EFFECTS OF THYROID SECRETION. The effects of excess of thyroid secretion in the blood are: 1. An increase in metabolism, especially in the oxidation processes and the breaking down of proteids in the tissues and bone, giving rise to an increase in X and P 2 5 (Fr. Miiller) excreted and in the gas metab- olism (Magnus-Levy). In man this finds its concrete expression in the loss of weight, due especially to loss of muscle substance (Baumann and Roos). 2. There is a general stimulation of the peripheral nerves both medullated and sympathetic. V. Cyon, Roos, Oswald and Kraus, and Friedenthal have shown that these substances have several distinct actions on the circulation. 1 Marine and Lenhart (Arch. Int. Mod., 1911, viii, 205) regard the epithelial hyper- plasia as indicating underactivity of the thyroid, even in Basedow's disease. 082 DISEASES OF THE HEART AND AORTA. A. They stimulate the depressor or afferent nerves from the heart, giving rise on the one hand to the cardiac sensations, palpitation, and anginal pains, and on the other hand to the vasodilation and low diastolic blood-pressure which are often observed in these cases. B. They stimulate both the vagi and the accelerator nerves. 1 The action upon the accelerators predominates, however, and tachycardia is thus produced. The vagus still remains irritable, however, and the heart can be slowed by pressure on it. The same stimulation of the other fibres of the cervical sympathetic gives rise to the peculiar ocular signs of Basedow's disease (see page 687). C. Cleghorn has shown that thyroid extract has a direct action on the cardiac muscle, increasing the size and force of the contraction, which manifests itself in the increased pulse-pressure, increased maximal pressure, and cardiac hypertrophy. FIG. 323. Drawing of a histologieal specimen from the same thyroid. The histological picture of advanced thyroid hypertrophy observed in cases of Graves's disease in which the symptoms are most marked. (Bloodgood, Surg. Gyn.aud Obstcs., August, 1905, vol. i, p. 113.) This drawing was made in June. 1903. Biochemical Evidences of Hyperthyroidism. Falta and Zuelzer, Kraus, and Frieden- thal have shown that thyroid extract directly antagonizes adrenalin in its pupillo-dilator action on the frog's eye, and that this can be used as a test for hyper- thyroid ism in clinical cases. Another important biochemical blood test for hyperthyroidism is that of Reid Hunt, who has shown that the blood of such patients increases the resistance of mice to poisoning with acetonitrile and morphine, so that the lethal dose is thus doubled. All these investigations have proved without doubt that in Basedow's disease there is an excess of thyroid secretion into the blood (as claimed by Mobius), and that the secretion is indistinguishable from that of the normal thyroid, representing a condition of hyperthyreosis (increased secretion) rather than of d y s t h y r e o s i s (altered secretion). Whether they will be of practical value in the diagnosis of the puzzling "formes frustes" remains still to be determined, since the excess of thyreoglobin in the blood of these cases may be too small for chemical recognition. 1 In most of these effects this sympathicotonie predominates, as shown by Eppinger, Falta, and their collaborators (see page 19). THYROID HEART. 683 It is possible that this anti-adrenalin action may be responsible for the brownish pigmentation (Jellinek's sign) which occurs in many cases of hyperthyroidism, especially about the eyelids. This pigmentation some- what resembles the pigmentation of Addison's disease (lack of adrenalin secretion). Kraus and Friedenthal have also found that this antagonistic action upon the frog's pupil is valuable in diagnosis, since it is given by the blood of patients with Basedow's disease, but not by the blood of neurasthenics and hysterical patients. 1 V. Cyon has shown the very important fact that injection of thyroid exact or iodothyrin causes an increased blood flow through the thyroid gland, probably thus acting as a hormone to increase its own secretion and to introduce a vicious circle: Hyperthyroidism (Basedow's disease) t 1 Increased thyroid Increased blood flow secretion through thyroid It is this increased dilatation of the arteries which gives rise to the murmurs over the thyroid in Basedow's disease (Guttmann). ETIOLOGICAL FACTORS. Basedow's disease is more common in women than in men (805 women, 175 men in Buschan's 980 cases); 60 per cent, occur in the fourth decade of life (Buschan). In Passler's 58 cases there were 4 under 15 years, 29 at from 15 to 25 years, 18 at 25 to 45 years, 7 over 45 years. Basedow's disease is very widespread, but is somewhat more rare in regions where simple goitre is common than elsewhere, perhaps owing to the lesser intake of iodine. Heredity plays some role; mental and nervous disease, diabetes, and tuberculosis are often found in the same family. In one famous family reported by Osterreicher eight out of ten children of a hysterical woman had Basedow's disease, and one of these daughters had three children with the same illness. The following list gives the predisposing factors in the series of A. Kocher and of Landstrom: Cases. Gradual onset with etiological factors unknown 2S Pregnancy 10 Chlorosis 7 At first menstruation t> After fright, shock, or grief > After fatigue S Infectious diseases (influenza alone, 7) 1 ; > Old simple goitre "> Sojourn at high altitude - Heredity 1 Appendicitis 1 Total . . .86 1 It seems doubtful whether the blood of cases with mild formes frustes contains enough excess of thvreoglobulin to give this test a hard-and-fast diagnostic significance. 684 DISEASES OF THE HEART AND AORTA. It will be seen that infectious diseases and especially influenza con- stitute the most common cause. De Quervain has found a subacute thy- roiditis quite common in these conditions, especially in influenza, typhoid fever, rheumatism (as in Parry's first case), and diphtheria, and this thy- roiditis was followed by Basedow's disease within a few months in about 20 per cent, of the cases. Boggs and Sladen have found mild thyroiditis present in most of the cases of typhoid fever in which the pulse is over 120 at the height of the fever. Tonsillitis may also be a forerunner; and Engel-Reimers has found acute thyroiditis in secondary lues leading to Basedow's disease. After pregnancy the hyperthyroidism which is normally present in that condition may increase and lead directly into Basedow's disease. The coexistence of puerperal infection, mastitis, fright, grief, or shock undoubtedly predisposes to the disease, as in the case of a girl under Friedrich Muller's care, whose symptoms began when she was suddenly deserted by her lover just after the birth of an illegitimate child. In one of v. Graefe's cases the symptoms set in within a few days following a night of sexual excesses. These factors may act by producing a reflex dilatation of the vessels in the thyroid. Thus, Trousseau writes of a woman of 53 who suffered deep grief from the death of her father. " One night, after she had been crying for a long time, she suddenly felt her eyes swell and lift up her lids, her thyroid gland increase notably in size and throb in an unusual manner; she had at the same time violent palpitation of the heart." The writer on one occasion had the opportunity to observe a case of acute enlargement of the thyroid in a man of thirty, associated with tremor, tachycardia, palpitation, slight v. Stellwag's but no other ocular sign. The disturbance followed the inges- tion of two cups of strong coffee at a time of great worry and was compli- cated by a mild attack of "grippe." The enlargement of the thyroid was sufficient to prevent buttoning the collar. It subsided entirely after 24 hours, and with it the symptoms of hyperthyroidism. It is probable that the grippe (influenza or streptococcus infection) rendered the thyroid par- ticularly sensitive. SYMPTOMS. The classical pathognomonic symptoms of exophthalmos are the well-known triad of strum a, tachycardia, and exophthalmos, or the tetrad of struma, tachyca rdia, exophthalmos, and tremor. These are well described by Parry (1815) in his first case, a married woman, aged 37, who had " caught cold in lying in, and for a month suffered under a very acute rheumatic fever. Subsequently she became subject to more or less palpitation of the heart very much augmented by bodily exercise, and gradually increasing in force and frequency till my attendance, when it was so violent that each systole shook the whole thorax. Her pulse was 196 in a minute, very full and hard, alike in both wrists, irregular as to strength, and intermitting at least once in six beats. . . . Twice or thrice she had been seized in the night with a sense of constriction and difficulty in breathing, which was attended with spitting of a small quantity of blood. She described herself also as having frequent and violent stitches of pain about the lower part of the sternum. . . . About three months after lying in, while she was suckling her child, a lump about the size of a walnut was perceived on the right side of her neck. This THYROID HEART. 685 continued to enlarge till the period of my attendance, when it occupied both sides of her neck so as to have reached an uncommon size, projecting forward before the lower angle of the jaw. The part swelled was the thyroid gland. The carotid arteries on both sides were greatly distended, the eyes were protruded from their sockets, and the countenance exhibited an expression of agitation and distress, especially on any muscular exertion, which I have rarely seen equalled. . . . Bowels were usually lax. . . . For a week she has had cedematous swelling of her legs and thighs." (The patient died with symptoms of heart failure.) Besides the pathognomonic triad, increased nervous excitability, tremor, loss of weight, and pigmentation of the skin, especially about the eyelids, are important accessory symptoms. The chief symptoms of Basedow's disease may be grouped in the fol- lowing categories, and arranged in what is approximately the order of increasing severity. Cardiac Phenomena. Palpitation, continuous slight elevation of pulse-rate, with occasional attacks of intense tachycardia brought on by emotion, excitement, or exercise, or occasionally on awak- ening; visible pulsation and dilatation of carotid arteries; pulse collapsing; angina pectoris; hypertrophy of the heart; precordial heaving and intense pulsation; irregularity of pulse; dilatation of heart; heart failure; ascending cedema, etc. Psychic Symptoms. General nervousness, insomnia, restlessness, mental exuberance alternating with depression and melancholia, delusions and hallucinations. Ocular. Staring gaze without winking for considerable periods. Widening of palpebral slit (Dalrymple, v. Stellweg's sign), lids do not follow eyeballs perfectly, a white streak of sclera is seen between lid and cornea, especially on glancing downward or upward (v. Graefe's sign), inability to converge in looking at near objects (Mobius' sign), exophthalmos, overflow of tears, pain and feeling of tension in the eyeballs, cornea! ulceration. Peripheral Nerve Symptoms. Fine tremor (from 8 to 10 per second), especially of the finger tips, nystagmus, superficial and cog- wheel breathing, astasia-abasia, hypersesthesias and parsesthesias occasionally, inability to frown or wrinkle forehead (Jeffrey's sign) . Cutaneous from vasodilation and anti-adrenalin action). Feeling of heat, continuous and intense; lowered electrical resistance; sweating; color usually pale brownish Addison-like pigmenta- tion, especially about eyelids (Jellinek) ; flushes; localized transi- tory oedema, especially about eyelids; scleroderma. Nutritional (increased rapidity of metabolic processes loss of X and P 2 f ). Loss in weight; sometimes absolute anorexia, sometimes excellent appetite; attacks of diarrhoea, often with slimy stools; polyuria; glycosuria. Fever (varying from 9!) to 104). Blood. Slight leucocytosis without change in red blood-corpuscles or secondary anaemia; polymorphonuclears 50-55 per cent., lym- phocytes 20-25 per cent., large monon u clears S-16 per cent, (large mononulcear leucocytosis present in formes frustes). (Barker, Caro.) 686 DISEASES OF THE HEART AND AORTA. Psychic Manifestations. The psychic symptoms in hyperthyroidism have been very aptly compared to the well-known effects of over-indul- gence in coffee, increased activity of thought, restlessness, irritability, insomnia, and in the more severe cases garrulity and delusions. As men- tioned above, over-indulgence in coffee may sometimes be followed by enlargement of the thyroid. There can be little doubt that many cases of so-called neurasthenia and hysteria are due to a more or less transitory state of over-secretion of the thyroid. This is particularly true when the symptoms are accentuated at the menstrual periods, for then the thyroid secretion is increased. It is possible that, as suggested by Graves, the "globus hystericus" may be due to an acute swelling (erectile expansion) of the thyroid. Neurasthenic symptoms may, however, have a basis in hyperthyroidism in cases when this would be least expected. For example, a young physician in robust health recently complained to the writer of having suffered from insomnia and palpitation for several months, during which time he had been compelled to forego his accustomed daily exercise. On closer observation, however, he observed that at about the time his symptoms had begun he noticed a slight swelling of his thyroid which had persisted ever since, although he had no tremor. Cardiac Signs and Symptoms. The cardiac symptoms also have some similarity to those of an overdose of coffee, especially the pal- pitation. This symptom is probably due to the direct stimulation of the afferent nerves of the heart (depressor), which has been shown by v. Cyon to result from injection of thyroid extracts, iodothyroin and thyreoglobulin. Palpitation is the earliest and often the mort severe symptom. The tachycardia, like most of the signs of Basedo\v's disease, results from the stimulation of the accelerator nerves and from the degree to which this outweighs the effect upon the vagus. The pulse-rate may be continuously elevated (over 120), or the tachycardia may be latent and attacks of rapid pulse may be brought out only by slight disturbance of the equilibrium or by the administration of very minute doses of thyroid extract (Emerson, quoted by Barker). In these attacks the pulse- rate rises gradually during a few minutes and falls gradually (in contrast to idiopathic paroxysmal tachycardia), but in one case v. Hoesslin has seen sudden doubling and sudden halving of the rate. Stru- bing has found that pressure upon the vagus slows the rapid heart of Base- dow's disease, showing that there is no paralysis of that nerve. Although, as Cleghorn has shown, thyroid extract increases the force and size of cardiac contraction (the increased pulse-pressure shows increased cardiac output), the persistent over-stimu- lation of this organ draws so much upon its reserve force that it may readily suffer from overstrain and undergo acute dilatation. Afferent impulses through the depressor nerves, which are already in a state of increased irritability, may give rise to symptoms of typical angina pectoris, with referred pain down the arms and precordial hyperaisthesia. This thyroid type of angina pectoris has been described on page 379. Prolonged overstrain may result in failure of either the left or the right heart, and symptoms of pulmonary or systemic decompensation (oedema, ascites, etc.) set in. THYROID HEART. 687 The irregularity is probably due to occasional extrasystoles, though careful analyses of its nature are lacking. In one case reported by v. Hoesslin there was definite paroxysmal tachycardia with sudden onset and sudden cessation approximate halving and doubling of rate, but Hirschfelder finds that this condition is a rare one in Basedow's disease. The attacks of tachycardia and palpitation most commonly begin and end by a gradual, though rapid, change of rate, and indicate a simple exaggera- tion of physiological variations. The maximal blood-pressure is usually high, the minimal normal; the pulse-pressure increased; this shows that there is an increased systolic output with low peripheral resistance, and corresponds well with the experimental results from injection of thyroid tissue juice (Pressaft). In 10 cases of Basedow's disease Krause and Friedenthal found: Lowest. Average. Highest. Cm. H 2 O. Mm. Hg. Cm. H 2 O. Mm. Hg. Cm. H 2 O. Mm. Hg. Maximal blood-pressure ... 145 106 182 134 215 158 Minimal blood-pressure ... 85 62 89 . 5 65 . S 90 66 This accords with the writer's experience, but in the early cases and "formes frustes" the maximal pressure may not be elevated even when there is tachycardia. The heart is usually enlarged and hypertrophied, the apex impulse forcible, and the large systolic excursions impart a heaving to the whole chest. In periods of overstrain from exertion or excitement there may be transitory dilatation of the heart, and this uniformly occurs during the chronic heart failure. There is often a blowing systolic murmur heard over both ventricles and at the apex, perhaps due to functional insuffi- ciencies of the auriculoventricular valves. Heart failure is the immediate cause of death in most cases of Base- dow's disease. Ocular Manifestations. The ocular manifestations are peculiar and very characteristic. V. Graefe (1857) called attention to the fact that when the eyes moved upward and do w n w a r d the lids did not follow them perfectly, but a streak of white sclera could be seen between lids and cornea (Graefe's sign). Dalrymple and in 1867 v . S t e 1 1 w a g noted the widening of the p a 1 p e b r a 1 slits, the staring expression, the absence of winking. V. Stellwag's sign is in most cases the earliest characteristic sign of Basedow's disease. M 6 b i u s ' sign is the inability to converge the two eyes when looking at a very near object. The origin of these signs is very simple. Claude B e r n a r d , when li e first stimulated the cervical sympathetic, demonstrated that widen- ing of the palpebral slit and dilatation of the pupil resulted and that the eyeball was pushed forward. Aran and Kaufmann (1860) demonstrated that this exophthalmos resulted from s t i m u 1 a t i o n o f M u 1 1 e r ' s non-striated m u s c 1 e in the eyelid, which is innervated by the cervical sympathetic. These experiments were confirmed by a number of writers, especially MacCallum and Cor- nell (1904). The exact cotirse of the fibres of Mailer's muscle and their mode of operation has been described by Landstrom. Landstrom finds that the fibres of smooth muscle form a narrow cuff, or truncated cone, encircling the anterior portion of the orbit. The fibres at the posterior border of the cuff pass backward and are inserted into the sclerotic coat of the eyeball. The fibres forming the anterior margin of the cuff are inserted into the 688 DISEASES OF THE HEART AND AORTA. upper or lower lids, in which they run obliquely toward the palpebral slit. The middle portion of the cuff constitutes the fixed point from which the muscle acts, and is attached by short fibrous bands to the bony wall of the orbit. Contraction of this muscle therefore tends to draw the eye forward (exophthalmos) as well as to pull the lids apart (Dairy m pie and v. Stellwag's sign). The delicate coordination of lid movement and eye movement is disturbed by this added traction upon the lid (v. Graefe's sign). Moreover, the contraction of these fibres tends to keep the axes of the eyes divergent, and thus antagonizes conver- gence ( M 6 b i u s ' sign). FIG. 324. Diagram showing the relation of the various anatomical structures concerned in the production of the ocular and cardiac manifestations of Basedow's disease. A. Distribution of the branches of the cervical sym pathetic to the heart, thyroid gland, and eyelids. The arrows indicate the direction in which stimulation of the cervical sympathetic moves the eyelids and eyeball. SYM P N, sympathetic nerve plexus; SUP. C. GANG, MID. C. GANG, INF. C. GANG, superior, middle, and inferior cervical ganglia. B. Relation of Miiller's muscle to the eyeball and structures within the orbit (schematic). Muller's muscle (MULL) is shown in black. The arrows indicate the direction of its pull. TEND, tendinous attach- ment of Muller's muscle to the orbit, septum orbitale (8EPT. ORB). C. Section through the lateral portion of the orbit (semi-schematic, modified from Landstrom). ORB, orbitalis; LEV, levator palpc- brarum; CONJ, conjunctiva; SCLER, sclera; RECT MED, rectu.s medius. Muscular Changes. A fine tremor beginning in the fingers, with 8-10 contractions per second, has been shown by Marie to be almost common enough to be included among the cardinal symptoms. It is probably due to the overstimulation of the peripheral nerves, and finds its analogue in the tremor from coffee and tobacco. Tremor of the tongue and sudden movements of the tongue and lips are not as common as in alcoholism. It is probable that the muscular weakness consequent upon the katabolism of muscle proteid aids in the tremor. Astasia abasia (giving way of the legs in standing and walking) is rare, but has been reported. It represents an extreme grade of nervous disturbance. The increased metabolism of N and P 2 5 , with destruction of muscle tissue, fat, and to a lesser extent of the bones, is important and finds its expression in the general loss of weight (often 25 to 50 pounds). It is the direct result of iodothyrin intoxication. THYROID HEART. 689 Diarrhoea is common. There is often a good deal of mucus in the stools, suggesting some relation to the so-called mucous colitis. Changes in the Thyroid itself. As regards the size and appearance of the thyroid gland there is great variation. In spite of the common term of "exophthalmic goitre," the thyroid may not be prominent nor even palpable. Since there is great variation in the average size and weight of the thyroid in different regions, 25 to 33 Gm. in certain regions, 60 Gm. in others, 100 Gm. in Switzerland (Oswald), a merely palpable thyroid need be of no diagnostic importance. Increase in the size of the thyroid is equally difficult to interpret. The size of the thyroid bears a definite relation to sexual activity, and increases regularly during menstruation and pregnancy, often to a considerable degree. Indeed, in some cases of formes frustes it is not unlikely that we are dealing with slight hyperthy- roidism whose intensity is determined by these physiological factors. Increased vascularity is of great importance in differentiating between transitory and persistent hyperthyroidism. It can be demonstrated by eliciting a murmur and thrill over the thyroid when the gland is pressed upon (Guttmann). This cannot be produced in simple goitres or normal glands. SECONDARY HYPERTHYROIDISM. Moreover, it is probable that in many neurotic, toxic, and organic diseases the actions of nerves or of hormones arouse the thyroid to a second- ary activity, which may, nevertheless, be of great importance in determining the features of the case. For example, Holz has reported two cases of exoph- thalmic goitre in children in whom the disease subsided on removal of the adenoids ; one case recurred and again subsided with the recurrence and removal of the adenoids. Accordingly it is advisable not only to treat the Basedow's disease but also to look for and treat the other foci of excita- tion. DIAGNOSIS. It is evident that, though there can be little doubt as to the nature of well-developed thyroidism, there may be room for much debate regarding cases of formes frustes, for these cases must be differentiated from simple physiological hypoactivity of the thyroid. Patients should be carefully watched for the development of ocular signs, especially at menstruation, since these are practically never present in persons whose thyroid activity is normal. In cases in which symptoms are so mild, however, it is still important to bear in mind the possibility of a thyroid origin for the condition, at least in so far as an increased thyroid secretion in a y arise r e f 1 e x 1 y and perpetuate itself through the vicious circle mentioned on page 683. It is probable that on this basis the origin of many an obscure ''cardiac neurosis/' will be cleared up. Hyper- thyroidism and hysteria, sexual neurasthenias, epilepsy, tobacco poisoning, alcoholism, myocardial disease, and valvular diseases are frequently asso- ciated, and when one of these conditions is present it still remains important to look out for contributing roles on the part of the thyroid. 44 690 DISEASES OF THE HEART AND AORTA. Each case of morbus Basedowii may be considered as an autointoxi- cation due to the passage of more or less iodized thyreoglobulin from the thyroid gland into the blood. When this is secreted in large quantities, the condition is outspoken and presents many of the symptoms, among them some of severe grade. When but little excess of thyreoglobulin circulates in the blood, it may give rise to the " formes frustes" with but few symptoms and those of the milder type predominating. However, even in the most atypical cases of " forme fruste "one or more of these symptoms may reach excessive sever- ity, and the disease may persist in the form of a cardiac neurosis, a psycho- sis, a chronic enteritis, a progressive inanition, a diabetes, or even a mild relapsing fever, for long periods. The cardinal suggestive signs may be so slight in intensity as to be noticed only when the suspicion of Basedow's disease has once been aroused in the mind of the examiner, and then the coexistence of several unobstrusive features may make the condition defi- nite; as, for example, a slight staring, anxious expression in a thin, nervous woman who suffers from attacks of palpitation and precordial pain and who manifests a slight fine tremor of the fingers and a tendency to diar- rhoea. On closer examination it may be found that the lids do not follow the eyeballs perfectly and there is slight fulness of the neck, but none of these symptoms are striking. CASE OF BASEDOW'S DISEASE WITH ANGINAL ATTACKS. Mrs. K. M., housewife, aged 23. seen under treatment at the Johns Hopkins Medical Dispensary on Dec. 29, 1906, when she complained of palpitation of the heart and pain in the right chest going down the arm. She is quite nervous and sometimes has crying spells. She is a rather pale woman, fairly nourished. The gums and mucous membranes are a trifle pale. The palpebral slit is wider than normal, but lids follow eyes. Convergence is, however, not perfect. The outlines of the thyroid gland can be seen; the gland is readily palpable, but not much enlarged. The lungs were clear on auscultation and percussion. The heart was not enlarged; sounds clear. Pulse of good volume, regular in force and rhythm; blood-pressure apparently low. She was given Blaud's pills and also tincture of aconite 0.3 c.c. (fl\,v) and potassium, bromide, without relief. She was seen a number of times during the course of the next year, during which she passed through a normal pregnancy and labor. Palpitation continued. A well-marked exophthalmos developed and palpebral slits became a little wider than normal. During April, 1907, she had attacks of pain over the left side of the chest and down the front (extensor surface) of the left arm, sometimes radiating to the shoulder. During attacks there is often tenderness in the fourth left interspace, sometimes also in the fifth, about the mammillary line. It never radiates to the right of the midline. These attacks are accompanied by palpitation and the heart-rate is rapid. She also has a peculiar fluttering sensation, and occasionally an irregular beat. Tracings at this period showed normal venous and carotid pulse. She was given small doses of ergot in without relief. A week later she was given calcium 1 a c t a t e 0.6 Gm. (gr. x) after meals, after which she began to feel better at once, though never relieved by any other medicine. The remedy was, however, far from specific, and the old symptoms returned in spite of the calcium lactate. During the course of the next six months various remedies were given, none of them with marked effect. It seemed to both patient and physicians, however, that she experienced a distinct improvement in symptoms whenever calcium lactate was given and distinct retrogression when other drugs were substituted. Operation was advised but not consented to, and the patient was lost sight of. THYROID HEART. 691 ACUTE BASEDOW'S DISEASE SIMULATING MALIGNANT ENDOCARDITIS. One group of cases to which attention should be especially directed are those of very acute Basedow's disease with fever, prostration, tachy- cardia, profuse sweats, sometimes chills and slight jaundice a clinical picture very closely simulating acute endocarditis (\V. G. Thompson). These cases are rather rare, but very grave. The diagnosis depends upon the cardinal symptoms aided by a negative blood culture. PROGNOSIS AND TREATMENT. Statistics regarding the mortality of Basedow's disease vary considera- bly, as shown by the following list. V. Dusch 12 . 5 per cent. V. Graefe 12 per cent. Mackenzie 12 . 5-25 per cent. Cheadle 9 . 6 per cent. Billingham 18.1 per cent. Gaill 21 . 3 per cent. Charcot 25 per cent. Buschan (900 cases) 12.5 per cent. Thompson 10 per cent. Williamson 25 per cent. These figures err, on the one hand, because only the serious cases reach the literature, and, on the other, because most of the cases have been fol- lowed for only short periods. Williamson, who followed his cases for some years and found a 25 per cent mortality, probably approximates the truth. J. Berry gives the following statistics of 56 cases treated without operation: Complete recovery 10 Considerable improvement 24 Little or no change 8 Fatal 14 Even after recovery recurrence is the rule, so that as ex- cellent an observer as August Hoffmann states that in 23 outspoken cases he has not seen a single permanent recovery! It is evident, therefore, that at the onset of undoubted Graves's disease therapeutic interference is necessary. The best principles in inau- gurating treatment are those which may be deduced from the findings of v. Cyon's experiments, i.e., that the clinical manifestations tire due to hypersecretion of thyreoglobulin, that this is proportional to the blood flow through the thyroid, and that the thyroid secretion in the blood tends itself to increase this flow and to produce a vicious circle. The first essential of any palliative treatment, therefore, is to reduce the thyroid secretion to its lower ebb by the removal of the two stimulating causes exercise and excitement. In the mild cases a simple isolation cure, with absolute rest in the horizontal position, can sometimes so lessen the flow through the thyroid and the secretion of this gland by diminishing the size and number of heart-beats that the thyreoglobulin content of the blood falls to normal and symptoms subside. If the rest cure be prolonged, 692 DISEASES OF THE HEART AND AORTA. the slight glandular hyperplasia of early cases may subside and a permanent cure may result. Various measures assist this process, especially those which act as psychic sedatives. Psychotherapy and suggestion, in so far as they tend to lessen the elements of worry, quiet the patient's mind, and thus quiet his heart's action, may aid in tiding over a period of not too intense excitement. Similarly Mobius, the apostle of serum therapy, reports the cure of one case by hypnotism! These are, however, exceptional. Psychotherapy in Basedow's disease is to be classed among the valuable sedative measures, but not among those of fundamental therapeutics. Cold wet packs, especially before retiring, may be of considerable assistance (Eichhorst), as also the bromides and the soporifics (veronal, trional, etc.), though to a less degree. Calcium salts are often very satisfactory as sedatives. The iodobromide of calcium was used by Guptill (1874). In one case (K. M.) under the writer's care calcium lactate was the only drug which caused any symptomatic relief, but even this was not marked. Miiller and others have used quinine, especially as the hydrobromate, but in many cases it is without effect. Iodine as used by the earlier observers may sometimes exert a positively harmful influence by activating (iodizing) still more of the thyreoglobulin, and it may thus bring on an exacerbation of the condition. The effect of potassium iodide is less certainly harmful and is sometimes beneficial, but its action is uncertain. Galvanization. One of the oldest and best forms of treatment is galvanization of the cervical sympathetic, with the anode over the carotid artery and the cathode at the nape of the neck. With currents of 2-3 milliamperes, as used by Chvostek, Benedikt, Car- dew, and others, it uniformly gives a certain degree of improvement, without effecting a cure. In early cases J. O. Hirschfekler has obtained complete subsidence of symptoms in a considerable number of patients by the use of strong currents (20-30 milliamperes), the negative pole being applied over the sympathetic at the neck, the positive over the thyroid for two or three minutes. After this it is applied over the heart. This vigorous treatment seems to be the best method of applying electricity, but must be continued for several months. X=Rays. E xposure of the thyroid to the Rontgen rays was introduced by Pusey, Boggs, and Beck in America, and some- times shows favorable results. Schwartz (1908) collected reports of 40 cases, showing gain in 26, improvement in nervous symptoms in 40, exophthalmos better in 15, but struma lessened in only 8. Specific Sera. Two forms of so-called specific sera are also in use: (1) anti-thyreoidin (thyroidectin), the serum of thyroidectomized sheep (Mobius), has been in use for some years, and in spite of numerous favorable reports has been found absolutely without effect by Ewald, Mackenzie, and Striimpell. (2) Beebe has prepared an antiserum for the nucleo- proteid of the thyroid gland from animals into which the purified nucleo- proteid thyreoglobulin had been injected, in the hope of bringing about retrogressive changes in this gland. This serum has been used therapeu- tic-ally by Rogers and by W. 11. Thompson, who report distinctly favorable THYROID HEART. 693 results, especially in the very acute cases (90 cases: 23 cured, 54 improved, 11 failed, 4 died); but other observers state that the results are no better than those in ordinary hospital practice, and further confirmation is needed. Operative Treatment. Thyroidectomy. The physiological indication for therapy in Basedow's disease is to lessen the amount of thyreoglob- ulin secreted into the blood. If the various methods intended to affect the gland as a whole are unsuccessful, the secretion may be diminished by removing a large portion of the gland (thyroidectomy). This operation was first successful in the hands of L. Rehn (1884), and has now come into quite general use, especially through the work of Mickulicz and the Kochers in Europe, and Halsted and the Mayos in America. The operation should be done under local cocaine anaesthesia. It may vary from ligature of the arteries to one-half of the gland, or this may be combined with excision of the latter; or, on the other hand, one-half of the gland may be excised and the arteries supplying a portion of the other may be ligated. The technic and results in large series of cases have been reported by A. Kocher, Landstrom, and C. H. Mayo, and many of the important details by Halsted and Evans. Kocher (1907) especially calls attention to the necessity of suiting the extent of the operation to the condition of the patient, especially the cardiovascular condition. "A systolic blood-pressure, even of 195 mm. Hg, does not forbid operation; . . . but if we find the blood-pressure below normal and the disease highly developed, we must study the condi- tion and especially note the action of the heart after exercise or excite- ment. Under these circumstances we might find a sudden, very marked dilatation of the heart, irregularity of pulse, and a blood-pressure which cannot be measured by our ordinary methods." The patient should be given a preparatory period of rest and pallia- tive treatment to prepare her for the operation, and two or more opera- tions should be done on the same patient rather than too extensive an opera- tion at one sitting. Kocher never ligates more than two arteries nor re- moves more than one-half the gland at one sitting, but these measures suffice in cases that are not too far advanced. Halsted has called particular attention to the need of preserving the parathyroid gland in order to avoid tetany. Hence he advocates tracing out the branches to these small bodies and then ligating the main artery beyond them. Both Kocher and Halsted insist upon the greatest care in the ligation of all bleeding points during the opera- tion and in draining off any small collection of serum which may collect during the healing of the wound. This greatly diminishes or obviates the intensification of Basedow symptoms which sometimes result a few days after operation (probably from absorption of iodothyreo- globulin upon the raw surface of the gland) and which may be dangerous. Halsted also found that the continuous use of an ice-bag upon the neck during a few days after the operation retards the absorption from the gland and lessens the frequency of these symptoms. As a result of this procedure in 254 patients (2 operations in 71 cases), A. Kocher has obtained great improvement in every case, with abso- lute and permanent cure in S3 per cent., and 3.5 per cent, of deaths. In the last 91 operations, since the above precautions 694 DISEASES OF THE HEART AND AORTA. had been observed, he has not had a single death! C. H. Mayo had 9 deaths in 176 cases, but only one in his last 75; and Professor Halsted's results at Johns Hopkins are equally favorable. In cases of long standing the exophthalmos never disappears, for the depths of the orbit have become filled with fat which continues to push the eye forward after the contraction of Miiller's muscle has subsided. Hypertrophy of the heart and secondary myocardial changes also remain, perhaps some cardiac weakness, but these are greatly diminished when the continuous cardiac excitation is removed. It must be admitted also that, as Tinker states, the operation requires more skill and practice than most surgical procedures, and the prognosis is therefore far better done by a man whose experience in this line is con- siderable than by a surgeon of even excellent local reputation. As regards the indication for operation, Kocher believes, that ''dis- tinct vascular symptoms (other than mere palpita- tion and tachycardia) should at once induce surgical treatment. ;; Before these have set in, the palliative method may be used for a while, and many cases may be relieved thereby or subject only to occasional recurrences. Should the mental symptoms and tachycardia persist or become more severe, the physician should recommend operation while the patient's general condition is still good, and should not wait until she is a complete physical wreck before turning over the responsibility to the surgeon. The surgeon should be allowed to operate upon the early but chronic cases which do not improve under palliative treatment. These rules apply as well to the cases of "formes frustes" as to the outspoken Basedow's disease. The persistence of psycho- and carclio- neuroses gives the indications, whether all the cardinal features are pro- nounced or not, and spontaneous recovery is no more likely to occur after the "forme fruste" has persisted than in cases where all the signs are well marked. Sympathectomy (Jonnesco's Operation). Another operation, which has been performed by Jonnesco, is the removal of the sympathetic ganglia on both sides of the neck. The result of this is usually an immediate slow- ing of the pulse, and often a cessation of other symptoms. Jonnesco reports several cases of permanent cure, but in the hands of a considerable number of later observers, among them Kocher, good results have been lacking or transitory, and this method should therefore be cast aside. BIBLIOGRAPHY. THYROID HEART. For historical details consult Dock, G.: The Development of our Knowledge of Exophthalmic Goitre, J. Am. M. Asso., Chicago, 1908, li, 1119. Troussoau, A.: Lectures on Clinical Medicine, New Sydenham Soc., Loud., 1868. Kraus, Fr.: Ueber das Kropfherz, Wien. med. Wchnschr., 1899, 416. Ueber Kropf- herz, Deutsch. med. Wchnschr., Leipz., 1906, xxii, 1889; and Berl. klin. Wchnschr., 1906, xliii, 1412. His, W., Jr.: Die leichten Formes des Kropfherzens, Media. Klin., Berl., 1906. Muller, Fr.: The Nervous Affections of the Heart, Arch. Int. M., Chicago, 1907, i, fig. 1. THYROID HEART. 695- Rose and Schranz. Quoted from Minnich, W.: Das Kropfherz und die Beziehungen der schilddrusen Erkrankungen zu dem Kreislaufsapparat, Leipz. u. Wien, 1904. Revilliod. Quoted from Minnich. Cooper, Reverdin, Kocher, Pisenti Gley and Vessale. Quoted from Oswald. Roos, E.: Einwirkung von Schilddruse auf den Stoffwechsel nebst Vorversuchen ueber die Art der wirksamen Substanz in derselben, Ztschr. f. physiol. Chem., Strassb., 1896, xxi, 19. Baumann, E.: Ueber das normale Vorkommen von Jod im Thierkorper, I, ibid., 1896, xxi, 319; and III, ibid., 1896, xxii, 1. Baumann, E., and Roos, E.: Ueber das normale Vorkommen des lods im Thierkorper, II, ibid., 1896, xxi, 481. Roos, E.: Ueber die Wirkung des Thyreoiodins, ibid., 1897, xxii, 16. Oswald, A.: Die Chemie und Physiologic des Kropfes, Arch. f. path. Anat., etc., Berl., 1902, clxix, 444. Huerthle, K.: Beitrage zur Kenntniss der Secretions- vorgange in der Schilddruse, Arch. f. d. ges. Physiol., Bonn, Ivi. Halsted, W. S.: An Experimental Study of the Thyroid Gland in Dogs, with Especial Consideration of the Hypertrophy of this Gland, Johns Hopkins Hosp. Rept., Bait., 1896, i, 373. MacCallum, W. G.: The Pathology of Exophthalmic Goitre, J. Am. M. Asso., Chicago, 1907, xlix, 1158. Marine, D., and Williams, W. W.: The Relation of Iodine to the Structure of the Thyroid Gland, Arch. Int. M., Chicago, 1907, i, 378. Wilson, L. B.: The Pathological Changes in the Thyroid Gland as related to the Varying Symptoms in Graves's Disease, Am. J. M. Sc., 1908, cxxxiv, 857. (Excellent figures.) Miiller, Fr.: Beitrage zur Kenntniss der Basedow'schen Krankheit, Deutsch. Arch. f. klin. Med., Leipz., 1893, li, 335. Magnus-Levy, A.: Gaswechsel und Fettumsatz bei Myxoedemen, Wiesb., 1896. V. Cyon, E.: Beitrage zur Physiologic der Schilddruse und des Herzens, Arch. f. d. ges. Physiol., Bonn, 1898, Ixx, 126; also ibid., Ixxi, Ixxiii, Ixxvii. Kraus, Fr., and Friedenthal, H.: Ueber die Wirkung der Schilddrtisenstoffe, Berl. klin. Wchnschr., 1908, xlv, 1709. Cleghorn, A.: The Action of Animal Extracts, Bacterial Cultures and Culture Filtrates on the Mammalian Heart Muscle, Am. J. Physiol., Bost., 1899, ii, 273. Eppinger, H., Falta, W., and Rudinger, C.: Ueber die Wechselwirkungen der Drusen mit innerer Sekretion, Ztschr. f. klin. Med., Berl., 1908, Ixvi, 1. Hunt, Reid: The Influence of Thyroid Feeding upon Poisoning by Acetonitrile, J. Biol. Chem., N. Y., 1905, i, 43. The Probable Demonstration of Thyroid Secretion in the Blood in Exophthalmic Goitre, J. Am. M. Asso., Chicago, 1907, xlix, 240. The Rela- tion of Iodine to the Thyroid Gland, ibid., 1907, xlix, 1323. Jellinek: Ein bisher nicht betrachtetes Symptom der Basedow'schen Krankheit, Wien. klin. Wchnschr., 1904. Guttmann, P. : Das arterielle Strumagerausch und seine diagnostische Bedeutung, Deutsch. med. Wchnschr., Leipz., 1893, xix. Parry. Quoted from Dock (I.e.). Buschan: Die Basedow'sche Krankheit, Wien u. Leipz., 1894. Quoted from Hoffmann. Passler, H.: Erfahrungen ueber die Basedow'sche Krankheit, Deutsch. Ztschr. f Xerven- heilk, 1895, vi, 210. Oesterreicher: Zur Aetiologie des Morbus Basedowii, Wien. med. Pr., 1SS4, xxv, 336. Landstrom, J.: Ueber Morbus Basedowii, Stockholm, 1907. Mobius, P. J.: Die Basedow'sche Krankheit, Nothnagel's Handb. der spec. Path. u. The nip., Wien, 1896, xxii. Kocher, A.: Ueber Morbus Basedowii, Mitlh. a. d. Grenzgeb. d. Mod. u. Chir., Jena, 1902, ix, 1. De Quervain, F.: Die Akute nicht eitrige Thyroiditis, Mitth. a. d. Grenzgeb. d. Med. u. Chir., Jena, 1904, ii, Supp., 1. Thyroiditis simplex und toxische Reaktiou der Schild- druse, ibid., 1906, xv, 297. Boggs and Sladen. Personal communication. Engel-Reimers: Jahrb. d. Hamb. Krankenanstalt, 1894, iii, 430. Quoted from Schmidt's Jahrb., 1895, cclvii, 23. 696 DISEASES OF THE HEART AND AORTA. Striibing: Ueber mechanische Reizung des Vagus bei Morbus Basedowii, Wien. med Presse, 1894, xxxv, 1714. V. Hoesslin, R.: Neues zur Pathologie des Morbus Basedowii, Miinchen med. Wchnschr., 1896, xliii, 25. Hirschfelder, A. D.: Contribution to the Study of Auricular Fibrillation, Paroxysmal Tachycardia, and the so-called Auriculo- (atrio-) ventricular Extrasystoles, Johns Hopkins Hosp. Bull., Balto., 1908, xix, 322. V. Graefe: Bemerkungen ueber Exophthalmus mit Struma und Herzleiden, Arch. f. Ophthalm., 1857. V. Stellwag, Carion: Ueber gewisse Innervations. Storungen bei der Basedow'schen Krankheit, Wiener med. Jahrb., 1869, xvii, 25. Mobius, P. J., 1. c. Bernard, Aran and Kaufmann, and H. Muller (Ztschr. f. wiss. Zool., 1858, ix, 541). Quoted from Landstrom. MacCallum, W. G., and Cornell, W. B.: On the Mechanism of Exophthalmus, Med. News, N. Y., 1904, Ixxxv, 733. Marie, P.: Contributions a 1'etude et au diagnostic des formes frustes de la maladie de Basedow, These, Paris, 1883. Holz: Berl. klin. Wchnschr., 1905, xlii, 91. Thompson, W. G.: A Clinical Study of Eighty Cases of Exophthalmic Goitre, Am. J. M. Sc., Phila. and N. Y., 1906, cxxxii, 835. Williamson: Remarks on Prognosis in Exophthalmic Goitre, Brit. M. J., 1896, ii. Berry, J.: Diseases of the Thyroid and Exophthalmic Goitre. Phila., 1901. Hoffmann, Aug. : Pathologie und Therapie der Herzneurosen und der functionellen Kreis- laufstorungen, Wiesb., 1901. Eichhorst, H.: Physikalische Therapie der Stoffwechselkrankheiten, Phvsik. Therap., 1906, i, 212. Guptill, C. H.: Exophthalmic Goitre successfully treated by the lodobromide of Calcium, Am. J. M. Sc., Phila., 1874, Ixvii, 125. Chvostek, Fr. : Weitere Beitrage zur Pathologie und Elektrotherapie der Basedow'schen Krankheit, W T ien. med. Presse, 1871, 1872, 1875. Benedikt, M.: Xervenpathologie und Elektrotherapie, Leipz., 1876. Cardew, H. W. D.: The Practical Application of Electrotherapeutics in Graves's Disease, Lancet, Lond., 1891, ii, 6, 64. Pusey, Boggs, Beck. Quoted from Landstrom. Schwarz, G.: Ueber Rontgentherapie der Basedow'schen Krankheit, Wien. klin. Wchschr., 1908, xxi, 1332. Mackenzie, H.: A lecture on Graves's Disease, Brit. M. J., Lond., 1905, ii, 1077. Beebe, S. P.: Preparation of a Serum for the Treatment of Exophthalmic Goitre, J. Am. M. Asso., Chicago, 1906, xlvi, 484. A Serum having Therapeutic Value in the Treat- ment of Exophthalmic Goitre, ibid., 1906, xlvii, 661. Rogers, J.: The Treatment of Thyroidism by a Specific Serum, ibid., 1906, xlvii, 655. Rehn, L.: Ueber die Extirpation des Kropfes bei Morbus Basedowii, Berl. klin. Wschnchr., 1884, xi, 11. Kocher, A.: The Surgical Treatment of Exophthalmic Goitre, J. Am. M. Asso., Chicago, 1907, xlix, 1240. With discussion by Halsted and Mayo. Halsted, W. S., and Evans, H. M.: The Parathyroid Glandules, their Blood Supply and their Preservation in Operation upon the Thyroid Gland, Ann. Surg., 1907, xlvi, 489. Jonnesco, Th.: The Enduring Results of Total Bilateral Resection of the Cervical Sym- pathetic in Basedow's Disease, Intern. Clin., Phila., 1903, 13th Ser., 136. III. MISCELLANEOUS DISTURBANCES OF CARDIAC FUNCTION THE SO-CALLED " CARDIAC NEUROSES" AND "CARDIAC NEURASTHENIA." GENERAL CHARACTERISTICS. One of the largest groups of cases seen by the clinician is made up chiefly of pale, anaemic-looking young patients, with hollow lustreless eyes and sunken cheeks, who complain of symptoms which may be divided into two categories: Symptoms. 1. Symptoms referable to sensory disturbances about the heart: palpitation, precordial tenderness, pain or constriction, pains and sensory disturbances down the arms, and, in rarer cases, of attacks resembling angina pectoris. 2. Symptoms referable to motor disturbances of the circulation, and especially to the distribution of blood in the body: cardiac arrhyth- mia, weakness, lassitude and weariness, vertigo, muscse volitantes, fainting spells, and an infinite variety of psychasthenic and nervous symptoms. This same symptom complex has already been encountered in the attacks of paroxysmal tachycardia (Chapter II.), where it has been seen to result from " arterial anemia," or the relative depletion of the arteries through dilatation of the veins, especially in the splanchnic region. Y. Henderson believes that under these conditions the viens are not overfilled, but that they too have become depleted by transudation of fluid into the lymph and tissue spaces. Mr. C. C. Cody, in the Johns Hopkins medical clinic, has found a very low venous pressure ( 2 to 7 cm. H 2 0) in a number of cases of neurasthenia and post-operative asthenia in which the above-mentioned symptoms were present. The arterial pressure in all but one of these cases was about normal, ranging from 104 to 125 mm. Hg. This same circulatory state seems to be present throughout the groups of cases about to be discussed, although the mechanisms by which it is brought about are various. Changes in Rhythm. Alterations of rhythm are very common in this group of cases (Hoffmann, Mackenzie, Reissner). They are usually associ- ated with respiration, with a slowing of the pulse during inspiration and a quickening during expiration (Fig. 325). It will be noted that this exactly corresponds to the normal centripetal action currents in the vagus (Kint- hoven, Flohil and Battaerd) which occur with each inspiration, and it is probable that in the condition of heightened excitability this (usually sub- normal) reflex stimulation becomes active. Stadler and Hirsch have been able to produce such irregularities by inflating the intestines of dogs and rabbits, but find them only accompanying dyspnoea. These observers also found that such inflations of the intestines were always accompanied by rise 697 698 DISEASES OF THE HEART AND AORTA. of blood-pressure. The writer has been able to confirm these observations. Moreover, McCaskey and Russell find that an elevation of 30 or 40 mm. Hg in blood-pressure may occur in the course of gastro-intestinal troubles, especially hyperchlorhydria and flatulence. Russell suggests that there is a relationship between chronic gastric intestinal disturbances and sclerosis of mesenteric vessels. In the cases of enteroptosis and of bathycardia a true pulsus para- dox us (diminution or dropping of beats during inspiration) may occur from the tugging upon the mediastinum, aorta, and great veins when the diaphragm is drawn down during inspiration. In rarer cases, and espe- cially those of gastro-intestinal origin, small, early beats resembling extr asystoles are present. In making the diagnosis of extrasystoles, however, great .care must be used, for it must be remembered that in the RESP. RADIAL FIG. 325. Respiratory arrhythmia in a young cigarette smoker. usual rhythmic variations in rhythm the last beat of a series with increasing rapidity may be followed by the pause due to maximal slowing, and thus an extrasystole may be simulated. On the other hand, it must be remem- bered that no experimenters have as yet been able to produce extra- systoles by stimulating the extrinsic cardiac nerves (Hering, Hoffmann, the writer and others), and therefore each case of the sort should be carefully studied with venous tracings and electrocardiograms. True ventricular extrasystoles demonstrable with the electrocardiogram are often brought on by flatulence, though many writers agree with Friedrich Miiller that the presence of definite extrasystoles is indicative of myocardial disease. Some years ago the writer had under observation a man forty years of age who was subject to palpitation and an arrhythmia brought on whenever he developed gas in the stomach or intestines. He himself was able to distinguish "large and small " beats among the palpitations, and tracings with modified Erlanger apparatus from veins and arteries bore out his impressions. It is, however, difficult to decide whether these small beats represent auricular extrasystoles or whether there is simply a rapid rhythm inter- rupted by long pauses of vagal origin. He stated that nevertheless he was able to "out- walk his doctors" at hill climbing during periods when he was suffering from both palpita- tion and arrhythmia. A moderate dose (.V mg. = gr. T ' ) of atropine caused dryness of the mouth and some vertigo, but did not greatly alter the pulse-rate nor cause the arrhythmia to disappear. The patient would not allow a larger dose to be given. If one could be certain that this dose had paralyzed the vagus the extrasystolic nature of the arrhythmia would be established, but it is most probable that the vagus was but little affected and that this evidence cannot be regarded as conclusive. It has long been customary to designate such cases as "cardiac neuroses, or, from the neurasthenic symptoms which are most striking to the physician, as "cardiac neurasthenia.'' On closer exami- nation, however, it may usually be found that both the cardiac and the neurasthenic symptoms are not primary, but DISTURBANCES OF CARDIAC FUNCTION. 699 are secondary to some visceral displacement or irritation, to some intoxication, or in rarer cases to some primary intense emotional disturbance. 1 The heart itself is sound, but, owing to the distribution of blood, does not get a chance to do the work of which it would be capable. The terms " cardiac" and "neurasthenia" are therefore both misleading, and it might perhaps be more satisfactory to desig- nate such conditions by the adjective "pseudocardiac" ("pseudocardiac enteroptosis," " pseudocardiac gastralgia," "pseudocardiac aerophagia," etc.). CLINICAL GROUPINGS. Most if not all of these "cardiac neurasthenias" are brought on by the following conditions : Alterations of the position of the heart in the thorax. a. Kyphoscoliosis, narrowness or flatness of chest. b. Cardioptosis or bathycardia (low heart), (1) due to enteroptosis (low diaphragm), (2) due to long thorax with diaphragm normal. c. High diaphragm from (1) flatus, (2) fat, (3) tight lacing. Although many cases arise in which no site of origin can be found for the symptoms, the following represents a few of the more common causes : 1. Abnormal position of the heart, a. From curvature of the spine. b. From pleural adhesions. c. Owing to a low diaphragm. 2. Visceral reflexes. a. Gastric, oesophageal and intestinal. (1) Air swallowing. (2) Gastritis, gastralgias. b. Sexual organs. (1) Sexual excesses (male or female). F e m a 1 e At onset of menses and at menopause; at menstruation; from myoma and other lesions of generative organs. Male s Gonorrhoea, prostatitis, masturbation. 3. Intoxications. Tobacco. Alcohol. Coffee. 4. Anaemia. 5. Intense emotional disturbances. ALTERATIONS IN POSITION OF THE HEART. DISPLACEMENT OF THE HEART FROM MALFORMATIONS. The displacement of the heart which occurs in kyphosis and scoliosis is often the cause of a true cardiac weakness, i.e., weakness and dyspnoea on exertion as well as from nervous causes a so-called constitutional heart weakness as Kraus terms it. 1 In many of these cases sympathicotonie or vagotonie is well marked (see page 19). 700 DISEASES OF THE HEART AND AORTA. FIG. 326. Cross section of the thorax of a flat-chested individual, showing the systolic heaving of the chest wall (broken lines) and the forces bringing it about. The outlines of the chest wall and heart during the systolic heaving are shown by the dotted lines and obliquely shaded areas. The protrusions and retractions are shown by the arrows. The patients are usually pale, rather weak, and readily become ex- hausted and cyanotic, and manifest all the cardioneurotic symptoms. The actual cause of the trouble lies not so much in the heart as in the posi- tion in which it is placed in the thorax. Pressure and tractions upon both the venae cavse and the arteries render both inflow and outflow difficult, and thus bring about a high venous and a low arterial pressure, with the symptoms which follow in its wake. Kraus and recently Herz have called attention to the cardioneurotic symptoms which occur in all narrow- chested individuals. Herz calls atten- tion to the fact that in such cases there is a tremendous lifting of the ribs and precordium with each sys- tolic erection of the heart. This is due to the short anteroposterior and especially oblique diameter of the chest, so that the heart pivoted against the posterior chest wall must push out the left anterior wall in order to complete its systole (cf. Fig. 326). As will be noted, this condition is quite different from that which results from the low diaphragm or from cardioptosis, for in those conditions the heart either beats in the long axis of the thorax, or from its mobility can adapt itself to a narrower chest. LOW HEART. Even when there are no malformations of the chest, conditions arise in which the position of the heart within the thoracic cavity is altered, and these give rise to cardioneurotic symptoms. These conditions are: I. Cardioptosis (wandering or movable heart), in which the mediastinal attachments are loose and the heart readily moves from side to side, as well as up and down. II. Bathycardia (low or unsupported heart), in which the heart lies low in the thorax because the dome of the diaphragm is lower than normal. This is sometimes due to hepatoptosis and sometimes to a congenitally low liver. III. The high heart (high diaphragm), from various causes, especially flatulence, fat, lacing, and during pregnancy. MOVABLE HEART (CARDIOPTOSIS) . Cardioptosis, or extreme mobility of the heart as shown on change of position, was first described by Glenard (1885) and by Cherchevsky (1887). The latter observer noted that, while the borders of the normal heart move 1-3 cm. when the patient turns from the left side to the right (while lying down), a certain number of cases (2.4 per cent, of all cases, according to Einhorn) are encountered in which it moves from 4-7 cm. DISTURBANCES OF CARDIAC FUNCTION. 701 without any other changes or any enlargement of the heart. As a rule, the symptoms date from some time when the patient has lost in weight, perhaps because the disappearance of mediastinal and omental fat causes the organs to become looser than before. Einhorn has found it much more common in men (18 cases) than in women (4 cases) and always associated with hepatoptosis; though in cases like that given below the element of hepatoptosis may be absent. CASE OF CARDIOPTOSIS. This, as well as the other symptoms, is beautifully illustrated by a case which the writer has recently seen in consultation with Dr. L. P. Hamburger. The patient, aged 31, had been a trained nurse since 18. Her father had died of enlarged heart and her mother died suddenly. Except for scarlet fever, whooping-cough, and measles as a child, she had been perfectly healthy until the age of 19, when a dermoid cyst of the left ovary caused profuse menstrual bleedings. This was removed and the wound drained. Adhesions formed, causing headaches and backaches and finally a nervous break-down, so that a second operation was done nine years later to relieve the adhesions. At the time of this operation she lost 14 pounds and was very nervous, and during her early convalescence had asyncopal attack during which her hands and forearms became completely blanched. One year later the patient felt her first cardiac symp- toms, suffering palpitation, and when lying down has a feeling "as though the heart were turning over" or "like a rubber bulb or sponge being squeezed out." She then feels sick and has a feeling of oppression in the chest. Physical examination shows a fairly nourished young woman of good color; pupils equal and no signs of Basedow's disease. The left lobe of the thyroid is slightly hard, but that organ is rather small. The thorax is quite well formed, not especially flat. Costal angle normal. Lungs clear. The heart is not enlarged and the sounds are clear. On turning from side to side, however, the heart moves 8 cm. The pulse is of good volume and shows a well-marked respiratory irregularity of the type described above, but no extrasystoles. The abdominal walls are soft but not especially lax; the liver does not descend when the patient stands, but the right kidney is palpable. Bromides, nitroglycerin, and strophanthus have been without avail; tincture of belladonna has somewhat quieted her cardiac symptoms. The intensity of the symptoms seems to vary with her general condition. Upon being assured of the trivial nature of her complaint, her symptoms immediately disappeared. Several months later she reported, however, that they reappeared from time to time during periods when she was fatigued or nervous. The presence or absence of symptoms was always quite independent of the mobility of the heart. In spite of her gain in weight and the improved condition under treatment, the cardiac borders moved at least 7 cm. during the periods when she was free from symptoms. Treatment. The treatment of cardioptosis presents a number of dif- ficulties. As seen from the case cited above, the symptoms depend not only upon the actual mobility of the heart but also upon the general condition of the patient's nervous system. It is the latter which deter- mines whether or not the afferent impulses from the heart shall reach the threshold of consciousness. Accordingly, the unpleasant cardiac sensa- tions may be present only when the irritability of the nervous system is increased by fatigue, anaemia, or other affections; so that relief of the latter by general measures relieves the cardiac symptoms as well, without affecting their underlying cause. The mobility of the heart itself cannot be treated directly; but it is sometimes possible, by overfeeding, to cause a sufficient deposit of fat in the mediastinum and pericardium 702 DISEASES OF THE HEART AND AORTA. to diminish the movements a little. Even when unsuccessful in this way, however, overfeeding often aids by improving the general condition, and nervous tone. GENERAL SPLANCHNOPTOSIS. The mechanism which gives rise to the cardiac symptoms of splanch- noptosis (enteroptosis) has been investigated anatomically by Keith and clinically by Wenckebach. The latter found, by means of the X-ray (fluoroscope), that the most important effect of enteroptosis was to remove the support of the liver and stomach from beneath the diaphragm. The dome of the diaphragm was thus usually seen to be flattened and to be situated a good deal lower than normal. FIG. 327. The low, normal and high hearts. (Semi-schematic.) I, first rib; X, tenth rib; VII, VIII, spines of seventh and eighth thoracic vertebrae. The horizontal line represents the "xiphisternal line" passing through the sterno-xiphisternal articulation. The small white arrow represents traction upon the trachea. A, low heart; B, normal heart; C, high heart. The normal summit of the dome in quiet expiration is just above the level of the fifth rib, and its horizontal shadow just obscures that of the tenth rib behind. Keith finds that this is normally about 1 cm. above the ''xiphisternal line,'' a horizontal line representing the level of the sternoxiphoid articulation. The upper border of the fifth rib at the junction with the cartilage is just at this level. In enteroptosis Wencke- bach is able to see the X-ray shadow of the origin of the tenth and often the eleventh rib above the dome of the diaphragm, and the latter lies well below the xiphisternal line. The writer finds that for ordinary purposes the most convenient landmarks are the xiphisternal articulation and the tip of the spine of the eighth thoracic vertebra, which is just above the upper border of the tenth rib. The xiphisternal articula- tion, the dome of the diaphragm, and the tip of the eighth tho- racic spine are normally on a level. In enteroptosis and low diaphragm the ribs drop so that first two structures are below the eighth spine, while with a high diaphragm the ribs are raised so that they are above it (Fig. 327). Effect on Respiration. The effect of this low position of the diaphragm is exerted both upon the respiration and the heart. The abdominal respira- tion, which is due to the descent of the liver, is much diminished. For when the dome of the diaphragm is flattened, shortening of the diaphragm does not push down the liver, but pulls upon the lower ribs in a hori- zontal or even upward direction. The effect of this pull upon the lower DISTURBANCES OF CARDIAC FUNCTION. 703 ribs (Fig. 327, A) is to narrow the cross section of the thorax (Duchenne) at this level and to draw the epigastrium inward, and thus by diminishing the air capacity in this portion of the lungs to decrease greatly the effect of inspiration both in sucking air and in sucking blood into the thorax. This is the so-called ''paradoxical type of respiration. " Naturally, its effect is to diminish the intake of air and thus greatly to enhance the effect of any cardiac insufficiency. Effect on Circulation. On the other hand, the lessened up-and-down movement of the diaphragm, coupled with the relaxation of the abdominal walls, greatly diminishes the force-pump and suction-pump action by which the blood in the abdominal veins is forced onward to the thorax.. There is, therefore, a tendency for the blood to stagnate in the abdomi- nal viscera. The venous pressure becomes low. In consequence, as Henderson and the writer have shown, the filling of the heart is less complete and the systolic output is diminished. Leonard Hill has shown that if a rabbit is supported in the erect posture with feet down and head down, the blood-pressure falls and cerebral anae- mia sets in. If one presses on the animal's abdomen, the blood-pressure riP per cent, of Fleck's cases there was no ana-mia. 712 DISEASES OF THE HEART AND AORTA. to the action of a hormone arising in the ovaries and especially in the corpus luteum, which acts upon the uterus, mammary glands, and thyroid. No doubt it also has some action upon the heart, but this is still obscure, and it is difficult to determine how much of the effect is due to the ovarian secretion itself and how much to the secondary hyperthyroidism. Prognosis and Therapy. The prognostic importance of cardiac dis- turbances arising in the sexual organs varies with the primary lesion and its chronicity. In the presence of gonorrhoea or pelvic abscesses the prob- ability of a metastatic myo- or endocarditis must not be forgotten. In the presence of anaemia the development of fatty degeneration and even of insidious mitral stenosis must be borne in mind, while in the presence of myoma myocardial changes which vary from primary hypertrophy to a brown atrophy and cardiosclerosis (due chiefly to the anaemia) must be thought of. In masturbating men there is a true cardiac hypertrophy with the usual accompanying changes. These factors must, therefore, be ex- cluded before the diagnosis of a true neurosis is made and an unqualified favorable prognosis can be given. In the simple cardioneurosis or pseudocardiac sexual disturbance the cardiac outlook is favorable if the primary condition can be removed. If not the prolonged reflex stimulation of the cardiac nerves leads first to a "work hypertrophy" and then probably to cardiac overstrain and pre- mature cardiosclerotic or atrophic changes. The treatment is therefore in the field of the gynaecologist or genito- urinary specialist and not in that of the internist. Even masturbation and sexual excesses may have a basis in organic irritation and should not be regarded as entirely psychogenic without examination. These may be much helped by psychotherapy, cold baths in the morning and cold packs at night, and exercise during the day. The psychic effect of the treatment will be greatly enhanced if the impression is clinched at once by the administration of potassium or sodium bromide (1 Gm. =gr. xv, t.i.d. and before going to bed) disguised in elixir of calisaya or in com- pound tincture of gentian or of cardamom; for the patient's confidence in the outcome is gained by finding the abnormal desire to decrease at once with the onset of treatment. ADENOIDS AND RESPIRATORY OBSTRUCTION. Adenoids. The presence of adenoid growths in the nasopharynx is also of importance, not only because they interfere with the respiratory intake of air and thus bring about dyspnoea on exertion, which may simulate a true cardiac weakness, but also because attacks of mild asphyxia may occur during sleep and cause the patient to awaken suddenly with a severe palpi- tation and other cardioneurotic symptoms. Besides this, during waking hours the lesions may continue to produce reflex irritation of the cardiac nerves and give rise to cardioneurotic symptoms in the same way as do disturbances in other organs. Arrhythmia of Nasal Origin. A physiological basis for these clinical findings has been furnished by Franc,ois-Franck (1889), who found that an arrhythmia of vagal origin could be produced by stimulating the nasal DISTURBANCES OF CARDIAC FUNCTION. 713 mucosa. His studies have recently been confirmed by Koblanck and Roeder, who found that in 8 cases with arrhythmia and nasal disease there were alterations in the mucous membrane of the nasal septum in a spot opposite the middle turbinate bone. There were often nose-bleeds as well. Touching this s p o t with a blunt probe in man and animals produced a similar arrhythmia. No other area of nasal mucosa gave this reflex. The arrhythmia was characterized by series of beats with increasing rapidity interrupted by long pauses, sometimes simulating extrasystolic bigemini (Curves 1 (man) and 3 (rabbit), K. and R.), but it could not be produced after either vagus was cut. Stimulation of other mucous membranes in this manner did not give rise to such arrhythmia. The authors showed that these stimuli are carried by the septal branch of the trigeminus which lies in this vicinity, for they could not be produced after cutting the trigemini, and believe that they are carried directly from the trigeminus nucleus to that of the vagus through the fasciculus longi- tudinalis medialis. With cure of the nasal condition the arrhythmia and allied disturbances disappeared. Cardiac Asthma from Disease of Nasal Septum. Frangois-Franck also showed by careful graphic methods that stimulation of the nasal reflex can give rise to cough, laryngeal spasm, asthma, and even a reflex bronchitis, reflexes which in themselves may add to the impression of a primary cardiac disturbance. He found that these reflex conditions were more pronounced in animals with aortic insufficiency than in normal animals. The condition in man is similar, and in the presence of an organic cardiac lesion these contributing factors may play a role which determines the security of the cardiorespiratory symptoms, so that the cause of the paroxysmal dyspnoea may in some cases have to be looked for in the nose. TOXIC CARDIONEUROSES. "TOBACCO HEART." Persons who suffer from excessive use of tobacco may be divided into three classes: 1. Xon-smokers suffering from a single indulgence (acute tabagism or nicotinism). 2. Young habitual smokers, especially those who inhale cigarette smoke (subacute nicotinism). 3. Old habitual smokers, especially of cigars and pipes, who suffer from the patho- logical changes produced in the arteries (especially the coronary arteries) and myocardium, and partly from the added effects of the nicotine. PHYSIOLOGICAL EFFECTS. The physiological effect of smoking has recently been studied by Lee, as well as by Bruce, Miller, and Hooker. Lee found that ordinary tobacco smoke obtained from 1000 Cm. tobacco contained nicotine 1.165 Gm., pyridine bases (chiefly pyridine and collidine) 0.14S Gm.. IK'X O.OS Gm., XH 3 0.36 Gm., CO 410 c.c. The chief toxic product is therefore nicotine. The composition varied considerably with both the quality of the tobacco and the mode of smoking. The greater part of the nicotine at the seat of combustion is destroyed, and that 714 DISEASES OF THE HEART AND AORTA. which reaches the mouth is volatilized by the hot gases while passing over the unburned area. Accordingly a thick cigar has the worst effect, since it acts as a chimney leading the gases to the mouth, while in a thin cigar, " stogie," or cigarette they escape into the surrounding air. (In cigarette smoking inhaling the smoke more than compensates for this difference in combustion.) In long-stemmed pipes much of the nicotine condenses before reaching the mouth. Lee found that in non-smokers the first effect of smoking a cigar was to produce a rise of 10-20 mm. Hg in the maximal blood-pressure, which was often associated with palpitation. Within five minutes after this the maximal blood-pressure fell 50 mm. Hg, and this fall was accom- panied by pallor, sweating, weakness, and colicky pains in the abdomen, as well as by the appearance of muscse volitantes, irregularity and weakness of the pulse, or, in other words, the symptom complex of arterial anaemia. In more habitual smokers, those of the second group, a single cigar produced only the rise of blood-pressure and palpitation. The subacute symptoms, therefore, come on only as the result of excessive indulgence. In old habitual smokers these observers found either no effect whatever or only a slight rise of pressure resulting from a strong cigar, without any of the disagreeable symptoms. Lee's observations have been repeated by Bruce, Miller, and Hooker, who found that smoking increases the maximal, minimal, and pulse-pressures in man, though later these return to normal. The cardiac output, therefore, seems to be increased at first, as Lee had found in cats. Bruce, Miller, and Hooker also found that the volume of the hand always decreased during smoking (vasoconstriction), whereas Lee found that the volume of the cat's intestine also decreased. It is probable that a little later there occurs, in man, a dilatation of the abdominal vessels, but it is not yet certain that it does so. The chief sufferers from tobacco are the young cigarette smokers who inhale the smoke and thus soon suffer immediately from the physiological effects of the nicotine. They complain of weakness, giddiness, intense palpitation and tachycardia (from continued stim- ulation of the cervical ganglion cells) , and often of irregularity of the heart, which may be very distressing. It is most noticeable that the intense sensory disturbances occur without any motor insufficiency of the heart. Thus, a young man of 20 years, an habitual inhaler of cigarette smoke, recently consulted the writer, complaining of fatigue, giddiness, muscse volitantes, intense palpitation, but, on further questioning, stated that he was in the habit of running a quarter of a mile every evening for exercise, and after this exercise he had neither palpitation nor shortness of breath! Needless to say, he improved at once after stopping tobacco. On the other hand, all sufferers from nicotine are not free from motor symptoms nor do they recover so readily. In many cases the nicotinism is supplemented by the use of alcohol, and secondary myocardial changes, and in the older persons arteriosclerotic changes, have been superinduced. In the middle-aged smokers the symptoms are chiefly those of angina pectoris and precordial pain. Very commonly this is a true angina of cora- nary sclerosis, but there is a certain number of cases in which the unpleasant symptoms completely subside upon cessation of smoking. DISTURBANCES OF CARDIAC FUNCTION. 715 It would be a very fascinating hypothesis to believe that in such cases the effect of smoking is to produce a transitory constriction of the coronary arteries and this to cause the symptoms, but, on the contrary, some recent experiments upon dogs, done under the writer's direction by Dr. George Bond, have shown that the flow through the coronary veins is actually increased by smoking. 1 It is probable, therefore, that in early tobacco poisoning at least, the sensory symptoms are due to stimulation of the cardiac nerves and not to ischaemia of the myocardium. The commonness and insidiousness of coronary sclerosis, however, render it difficult to decide in any individual case whether the effect is entirely functional or has also a basis in arterial changes. COFFEE AND TEA. The palpitation, tachycardia, and tremor which result from over- indulgence in coffee and tea are familiar to most persons from personal experience. They often manifest themselves in chronic forms and cause cardioneurotic symptoms. Precordial pain and tenderness are quite com- mon. Foote and Simpson, under D. R. Hooker's direction, have found that when a person accustomed to coffee takes a cup of it there is a transi- tory rise in maximal and minimal blood -pressure and a slight vasoconstriction of the hand. In persons unaccustomed to coffee these changes are much more intense. Indeed this partial immunity to coffee is very transitory, for the writer has found that after discontinuing its use for several months a single cupful would give rise to palpitation, tachycardia, and insomnia, while a few months before and a few months later two cups could be taken at a time without producing symptoms. Coffee, like tobacco, gives rise to sensory cardiac symptoms by increasing the irritability of the nerves without causing any motor insuf- ficiency, and consequently the patients, as a rule, do not show muscular or cardiac fatigue on exertion in spite of the symptoms. Tea. Owing to its content of caffeine, tea causes the same symptoms as coffee, but is less extensively used in large quantities. In England, however, similar cases are occasionally reported. ALCOHOL. Palpitation and the other symptoms of "cardioneurotic" (pseudo- cardiac) weakness also occur in persons who take alcohol in quantities that are just in excess of their tolerance, and the possibility of this cause must be borne in mind. In some individuals, as in Reissner's case, palpi- tation and irregularity may follow the ingestion of a single glass of wine, without any symptoms of intoxication setting in. That these conditions may continue without the patient's recognizing the cause is a common experience, and a considerable number of cardioneurotic cases result from this unintentional over-indulgence in alcohol. Women and young persons are more sensitive than men. The functional power and endurance of the heart muscle is, moreover, weakened by alcohol; and acute dilatation may set in from comparatively slight exertion. If the use of alcohol is long continued, it may lead to fatty and nbrinous rnyocardial change, but this in mild cases subsides when the cause is removed. Bond registered the outflow from the coronary veins by the drop methoc 716 DISEASES OF THE HEART AND AORTA. SIMPLE EMOTIONAL CARDIONEUROSES. As has been seen, by far the greatest number of so-called cardioneurotic cases are of postural, reflex, or toxic origin. However, it still remains beyond question that emotional disturbances alone, or in conjunction with other conditions which in themselves are not sufficiently intense to pro- duce symptoms, may give rise to cardioneurotic symptoms. Palpitation and even precordial pain are almost universal after severe emotional disturbances and shocks and during periods of worry. The motor effects are usually shown by tachycardia, though occa- sionally arrhythmias may occur. This the writer has observed upon him- self on an occasion of intense emotion, during which the pulse became extremely rapid and seemed either to drop an occasional beat or to give rise to an extrasystole. When the cause of the worry was removed, within five minutes the pulse again became regular, so that the arrhythmia could not be accurately studied nor has it recurred at any other time during the four years that have elapsed. Similar cases are found in the literature (Reissner). In rare cases an emotional shock may cause death, even when the heart is otherwise healthy (Gibson), but the nervous mechanism by which this is brought about is not clearly understood. It is probably a condition of exaggerated vaso- motor shock arising in response to a cortical stimulus, just as it may result from over-stimulation of a peripheral nerve. In most cases of the sort, however, the heart and especially the coronary arteries are already diseased (see page 369). BIBLIOGRAPHY. CARDIAC NEUROSES. Hoffmann, Aug.: Pathologie und Therapie der Herzneurosen, Wiesbaden, 1901. Mackenzie, James: The Study of the Pulse and Movements of the Heart, Edinb. and Lond., 1903. Diseases of the Heart, Lond., 1908. Reissner, O.: Ueber unregelmassige Herztatigkeit auf psychischer Grundlage, Ztschr. f. klin, Med., Berl., 1904, liii 234. Einthoven, W., Flohil, A., and Battaerd, P. J. T. A.: On Vagus Currents examined with the String Galvanometer, Quart. J. Exper. Physiol., Lond., 1908, i, 243. Stadler, E., and Hirsch, C.: Meteorismus und Kreislauf (eine experimentelle Unter- suchung), Mitth. a. d. Grenzgeb. d. Med. u. Chir., Jena, 1906, xv, 449. McCaskey, G. W.: Diseases of the Digestive Organs in the Pathogenesis of Arterial Hyper- tension, N. Y. M. J., 1906, Ixxxiv, 76. Russell, W.: Arterial Hypertonus, Sclerosis, and Arterial Pressure, Phila. and Edinb., 1908. Hering, H. E.: Zur experimentellen Analyse des unregelmassigen Pulses, Arch. f. d. ges. Physiol., Bonn, 1900, Ixxxii, 1. Miiller, F.: The Nervous Affections of the Heart, Arch. Intern. Med., Chicago, 1903, i, 1. For an excellent general discussion see Wenckebach, K. F.: Ueber Pathologische Beziehungen zwischen Atmung und Kreislauf, Samml. klin. Vortr., Leipz., 1907, Nos. 465 and 466. Kraus, F.: Ueber konstitutionelle Herzschwache (discussion), Deutsch. med. Wchnschr., Leipz., 1905, xxxi, 1986, 2081. Herz, M.: Herzmuskelinsumcienz durch relative Enge des Thorax (oppressio cordis), Verhandl. d. Kong. f. innere Med., Wiesb., 1908, xxv, 292. Einhorn, M.: Cardioptosis and its Association with Floating Liver (Proc. N. Y. Acad. Med., Jan. 15, 1903), Med. Record, N. Y., 1903, Ixiii, 647 (with excellent bibliography). DISTURBANCES OF CARDIAC FUNCTION. 717 Mosse: Demonstration eines Falles von idiopathischer Bathycardie, Deutsch. med. Wchn- schr., Leipz., 1900, Ver. Beil. 266. Janeway, E. G.: Bathycardia, Trans. Asso. Am. Physicians, Phila., 1903, xviii, 5 (also discussion by Osier). Keith, A.: The Nature and Anatomy of Visceroptosis, Lancet, Lond., 1904, i, 551, 631, 709, 818. A Method of Indicating the Position of the Diaphragm and Estimating the Degree of Visceroptosis, J. Anat. and Physiol., Lond., 1908, xlii, 26. Hill, L.: The Mechanism of the Circulation, Schafer's Text-book of Phsyiol., Edinb. and Lond., 1900, ii, 46. Erlanger, J., and Hooker, D. R.: An Experimental Study of Blood-pressure and of Pulse- pressure in Man, Johns Hopkins Hosp. Rep., Baltimore, 1904, xii, 147. V. Frey, M., and Krehl, L.: Untersuchungen iiber den Puls, Arch. f. Physiol., Leipz., 1890, 31. Hoppe-Seyler, G.: Zur Kenntniss der Magengiihrung mit besonderer Berucksichtigung der Magengase, Deutsch. Arch. f. klin. Med., Leipz., 1892, 1, 82. Wyllie, J.: On Gastric Flatulence, Edinb. Hosp. Rep., 1895, iii, 21. Special Report on Diseases of Cattle, U. S. Dept. of Agriculture, Washington, 1904. Special Report on Diseases of the Horse, ibid., 1903. Kuthan, F.: Die Obstipation und ihre Einfluss auf die Herztatigkeit, Zentralbl. f. innere Med., 1906, xxvi, 1076. Veit: Aetiologie und Symptomatologie de Myome, Handb. d. Gynakol., 1898, ii. Strassmann and Lehmann. Quoted from Fleck. Fleck, G.: Myom und Herzerkrankungen in ihren genetischen Beziehungen, Arch. f. Gyna- kol., 1904, Ixxi, 258. Kelly, H. A., and Cullen, T. S.: Myomata of the Uterus, Phila., 1909. V. Rosthorn, Lenhartz, Link, Schott, Krehl, Klemperer, Groedel, Janowski, Fellner: Discussion of " Die Beziehungen der weiblichen Geschlechtsorgane zu inneren Erkran- kungen, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1908, xxv, 29. Lazarus: Die adenoide Vegetationen und ihre Beziehungen zur dilatativen Herzsclrwache, Festschr. f. Leyden, 1902. Frangois-Franck, Ch. A.: Contribution a 1'etude experimentale des nevroses reflexes d'origine nasale, Arch, de physiol. de 1'homme et des anim., Par., 1889, 5e Se>. i, 538. Koblank and Roeder, H. : Experimental^ Untersuchungen zur reflektorischen Herzarhyth- mie, Arch. f. d. ges. Physiol., Bonn, 1908, cxxv, 377. Lee, W. E.: The Action of Tobacco Smoke, with Special Reference to Arterial Pressure and Degeneration, Quart. J. Exper. Physiol., Lond., 1908. i, 335. Bruce, Miller, and Hooker: The Effect of Smoking on the Blood-pressures and the Volume of the Hand, Am. J. Physiol., Bost,, 1909. Foote and Simpson: Unpublished experiments, communicated by Dr. D. R. Hooker. Gibson, G. A.: The Nervous Affections of the Heart, Edinb. and Lond., 1905. Muller, L. R.: Klinische Beitrage zur Physiologie des sympathischen Nervensystems, Deutsch. Arch. f. klin. Med., Leipz., 1907, Ixxxix, 432. INDEX Abdominal aorta, aneurism of, 648 Abdominal pain from distended liver, 215 in tricuspid insufficiency, 490 Abscess of heart-muscle, 304 Absolute arrhythmia, effect of digitalis in, 127 (see also Arrhythmia) Acapnia, Cheyne-Stokes breathing from, 208 in cardiac dyspnoea, 205 in shock and fevers, 48 Accelerations, reflex, 101 Accessory heart-sounds, 158 Accidental murmurs in splanchnoptosis, 704 Acetonitrile test for hyperthyroidism, 682 Aconite, 254 pharmacological action of, 254 therapeutic use of, 254 with digitalis, 255 Aconitin, 254 Acrocyanosis, 360 Acroparsosthesia, 360 Adams-Stokes disease (see also Adams- Stokes svndrome; Heart- block), 553 auricular fibrillation in, 569 auricular heart sounds in, 554, 570 blood-pressure in, 41 differential diagnosis of, 570 effect of atropine in, 568 effect of iodides in, 573 effect of posture on, 574 electrocardiogram in, 565 etiological factors, 568 experimental, 556 lesions of auriculoventricular bundle in, 564 occasional confusion with paroxysmal tachycardia, 571 prognosis in, 572 relation of heart-block to, 561 stoppage of ventricles in, 564 stoppage of ventricles in tor- toise, 555 sync-opal bradycardia, 553 treatment of, 573 X-ray examination in, 570 Adams-Stokes syndrome (Adams-Stokes disease), 553 from extrasystoles alone, 567 Adams-Stokes syndrome without lesion of auriculoventricular bundle, 566 Adenoids as cause of Basedow's disease, 689 asthma due to, 712 cardiac disturbances due to, 712 Adherent pericardium, 598 absence of symptoms from intra- pericardial adhesions, 598 anginal attacks in, 377 ascites and hydrothorax in, 601 ascites in, 601 Broadbent's sign (retraction of ribs) in, 602 cardiac dulness in, 602 cardiolysis for, 608 diastolic shock in, 603 effect on circulation, 599 fixation of lung borders in, 603 hallucinations in, 601 hydrothorax in, 601 indications for cardiolysis, 60S paradoxical respiratory ratio in, 602 physical signs of, 602 polyserositis in, 607 pseudocirrhosis of liver in, 607 pulse in, 602 pulsus paradoxus in, 602, 605 reduplication of first heart sound in, 604 Riegel's pulse in, 604 Riess' gastric sounds in, 604 sites of adhesions, 599 sounds over stomach in, 604 third heart sound and shock in, 603 treatment of, 607 X-ray shadows in, 605 Adhesions, pleural, simulating adherent pericardium, 603 Adrenalin, 255 Administration in heart failure, 255 production of aneurism with, 623 test for hydrothyroidism, 6S2 Adrenals, hypersecretion in arteriosclerosis, 344 Afferent impulses, 17 Air in pericardial cavity (pneumopericar- dium), 592 Air-swallowing, 708 719 720 INDEX. Air-swallowing, in angina pectoris, 382 treatment of, 382 Albuminous expectoration, test for, 206 Albuminuria, 212 Alcohol as cause of arteriosclerosis, 340 Alcohol, cardiac weakness from, 715 in cardiac disease, 224 Allorrhythmias, 98 classification of, 99 neurogenic, 99 occurrence of, 101 production of, 101 reflex, 98 from nose, 101 from stimulation of gastric walls, 101 Amyl nitrite, action of, in man, 256 administration in angina pectoris, 381 in cedema of the lungs, 207 aortic insufficiency, 467 Anacrotic pulse, 68 Anastomosis of blood vessels in the treatment of thromboangitis obliterans, 365 Anaemia in cardiac overstrain, 189 in endocarditis, 403 Anatomical terms, synonymous, xxvii Aneurism, 619 age of occurrence, 621 angina pectoris in, 377 blood-pressure in, 632 brassy cough in, 628 characteristics at various sites, 635 classification of, 619 delay of pulse wave in, 632 development of, 625 diagnosis of, 644 differentiation from tortuous arteries, 644 dilatation of pupils in, 631 dissecting, 645 pathology and pathogenesis, 645 symptoms and signs, 646 dulness over, 630 dysphagia in, 629 electrolysis in (Moore-Corradi method), 0 embolic, 624 erosion from, 625 etiology, 620, 624 experimental, 623 experimental production of, 659 experimental surgery of, 659 frequency of, in women, 621 inequality of pulse in, 632 ligature of, method of Antyllus, 656 method of Brasdor, 657 method of Hunter, 656 low diet (Tufnell's) in, 649 mesarteritis in, 623 Aneurism, multiple, 621 murmur in, 629 mycotic, 624 of abdominal aorta, 648 pain in, 648 paralysis in, 649 rupture of, 649 tumor in, 648 of the heart, 312, 635 of the pulmonary artery, 647 signs of, 647 pain in, 629 pulsations in, 630, 631 role of syphilis in, 620 rupture of, 625, 627 shock in, 629 sites of, 620 spontaneous clotting in, 627 suffocation in, 628, 629 symptoms of, 628 tracheal percussion shock in, 631 tracheal tug in, 631 treatment by compression, 656 by obliteration of sac (Matas), 658 by occlusion with metal bands, 657 use of calcium chloride in, 650 use of gelatin in, 650 use of potassium iodide for, 650 venesection in, 649 wiring of (Moore's), 650 X-ray examination in, 634 Angeioneuroses, 360 treatment, of 364 Angina pectoris, 370 and palpitation, 372 diagnosis of, 380 diet in, 382 differentiation from abdominal disease, 381 due to coronary sclerosis, 374 from tobacco, 379, 714 Heberden's description of, 370 hysterical, 378 importance of diet in, 382 in acute dilatation, 376 in aneurism, 377, 629 in children, 377 in hyperthyroidism, 379 in valvular diseases, 376 referred pains in, 373 sudden death in, 374 symptoms of, 370 theobromine in treatment of, 254, 382 treatment of, 254, 381 varieties of, 374, 378 vasomotor, 377 Anginal pain, theories as to causation of, 375 Antagonistic muscles, contraction of, 189, 268 INDEX. 721 Aorta, dextroversion (Rechtslage) of, 525 hypoplasia of, 547 stenosis of isthmus, 545 adult type, 546 signs of, 547 treatment of, 547 type of new-born, 545 Aortse, primitive, 514 Aortic area, 156 Aortic disease in pregnancy, 509 Aortic facies, 457 Aortic insufficiency, 450 amount of blood regurgitating, 453 and mitral stenosis, differentiation between, 439 asthma from lesion of nasal septum in, 713 blood-pressure in, 40, 455, 462 cardiac impulse in, 457 cardiac outline in, 458 Cheyne-Stokes respiration in, 456 diagnosis of, 466 diastolic murmur in, 459 double murmur (Duroziez's) over the arteries in, 460 Flint's presystolic rumble, 461 functional, 450, 452 hallucinations in, 456 historical, 450 mitral insufficiency in, 467 organic, 450 pathological physiology of, 452 precordial pain in, 456 presystolic thrill in, 457 prognosis, 466 propagation of murmurs in, 460 pulmonary circulation in, 455 pulse in, 462 pulse-rate in, 455, 464 relation of collapsing pulse to blood-pressure, regurgitation, and resistance, 463 rupture of valves, 451 sclerosis of aortic valves, 451 symptoms, 456 treatment, 466 of anginal attacks in, 469 use of digitalis and strophanthus, 467 venesection in, 468 X-ray shadow in, 458 Aortic sclerosis, 349 Aortic stenosis, 471 anacrotic pulse in, 476 arrhythmia in, 477 atheromatous, 471 auscultation, 474 blood-pressure in, 477 cardiac outline in, 474 congenital, 544 Aortic stenosis, endocarditic, 471 etiology of, 472 extrasystoles in, 477 failing compensation in, 473 intraventricular pressure in, 473 occurrence of, 472 palpation, 474 pathological anatomy, 471 percussion, 474 pulsus tardus in, 472, 475 symptoms of, 473 thrill and murmur in, 474 treatment of, 478 with aortic insufficiency, 472 X-ray examination in, 474 Aortitis, 349 acute, 333 tuberculous, 340 Apex beat, mechanics of, 141 method of recording, 141 "mixed type," 143 time of, 141 Apex in mitral insufficiency, 415 aortic insufficiency, 457 Apnoea, derivation of, in cardiac and pul- monary diseases, 206 Apoplexy, blood-pressure in, 40 Arches, visceral (branchial), 515 Arrhythmia, 97 absolute, 118 differential diagnosis of, 123 effect of, on circulation, 127 from emotional excitement, 716 from lesions of nasal septum, 712 in increased intracranial tension, 102 in myocarditis, 315 in tricuspid insufficiency, 492 of psychic origin, 102 permanent, electrocardiogram in, 121 respiratory, 102 sinus, 98 vicious circle of, 123 youthful type, 101 Arterial pulse, 62 Arterial tension, 25 Arteries, changes in, in congenital heart disease, 526 normal changes in, 327 sounds in, 170 strength of walls of, G21 tortuous, resembling aneurism, 644 Arterionecrosis, experimental, from adrena- lin, 343 from tobacco. 342 from toxins, 342 in animals, 342 Arteriosclerosis, 327 blood count in, 349 blood-pressure in, 40, 347, 348 clinical manifestation of, 345 722 INDEX. Arteriosclerosis, diet in, 350, 351 etiology of, 340 experimental, 343 following infectious diseases, 340 in children, 344 in hypothyroidism, 679 intermittent claudication from, 345 nervous symptoms from, 345 nitrites in, 352 of abdominal aorta, 346 of abdominal vessels, 344 of retinal vessels, 346 potassium iodide in, 352 pulse in. 347 role of salt in, 344 salvarsan in, 352 second heart sound in, 349 syphilitic, 341 theories of, 327, 343 treatment, 350 use of warm water in, 351 venesection in, 352 X-ray examination, 346 Arteriosclerotic changes in vasa vasorum,328 lesions, classifications of, 330 distribution of, 344 Arteritis, acute, 333 tuberculous, 340 Artery, compression of, sources of error in, 28 Ascites, 211 in adherent pericardium, 601 Asphyxia, effects of, 38 Aspiration of hydrothorax, dangers in, 212 technic of, 212 (see also Para- centesis) Astasia abasia in Basedow's disease, 688 Asthma, cardiac, 204 Asthma from lesions of nasal septum, 713 Atrioventricular bundle (see Auriculoven- tricular bundle) Atrophy of the heart, 289 Atrophy and cardiosclerosis, 294 Atropine, effect of, in heart-block, 559 effect of, on changes in tonus, 17 effect of, on extrasystoles, 114 test in heart-block, 568 use of, in pulmonary crdema, 207 Auricles, fibrillation of in mitral stenosis, 444 Auricles, mitral stenosis in paralysis of, 431 Auricular fibrillation, 118 Auricular fibrillation, arrhythmia in, 196 cardiac overstrain in, 196 venous pulse in, 79 Auricular paralysis, venous pulse in, 79 in mitral stenosis, 431 Auriculoventricular bundle, anatomy of, 556 clamping of, 557 lesions of, in Adams-Stokes disease, 564 physiology of, 556 Auriculoventricular valves, transmission of murmurs from, 165 Auscultation, 150 in suprasternal notch, 156 methods of, 154 through the stomach tube, 158 Azygos vein, role in hydrothorax, 211 Bacterial vaccines in treatment of endo- carditis, 397 Basedow's disease, 678, 680 acute, 691 anginal attacks in, 690 arrhythmia in, 687 astasia abasia in, 688 blood count in, 685 blood-pressure in, 41, 687 calcium salts in, 692 diagnosis of, 689 in "formes frustes," 690 etiological factors, 683 eye signs, 687 Dalrymple, 687 Mobius, 687 v. Graefe, 687 v. Stellwag, 687 force of heart in, 686 galvanization of cervical sympa- thetic, 692 Jeffrey's sign of, 685 loss of weight in, 688 metabolism, 685 mortality in, 691 psychic symptoms, 686 psychotherapy in, 692 relation to hysteria, 683 secondary to adenoids, 689 specific sera in, 692 spontaneous recovery in, 691 sympathectomy for (Jonnesco), 694 sympathicotonie in, 682 symptoms and signs of, 684 tachycardia in, 686 thyroidectomy for, 693 indications for, 693 results of, 693 treatment of, 691 tremor in, 688 triad and tetrad of symptoms, 684 wet packs in, 692 X-ray treatment of, 692 Bath treatment, advisability of, 277 Baths, electric, 276 mud, 276 Baths, Nauheim, artificial, 274 Nauheim, natural, 274 peat, 276 physiological action of, 274 INDEX. 723 Baths, precautions of, 274, 275 Bathycardia, 707 Beer in cardiac disease, 224 Belts, effect of, in producing cardiac over- strain, 190 Bicycle riding, effect of, on heart, 189 Bigeminal pulse, 114 causes of, 117 Bigeminus, 112 full, 112 shortened, 112 Bleedings in congenital heart disease, 529 Blood count in congenital heart disease, 533 Blood flow through muscles during exercise, 185 Blood, residual, 15 Blood, viscosity of, 59 apparatus for clinical determination of, 59 factors influencing, 60 Blood-pressure, 25, 197 apparatus, Erlanger's with Hirsch- f elder's polygraph attachment, 73 apparatus, forms of, 30 changes in exercises of speed, 186 determination of, auscultator method for, 33 of maximal, 28 of minimal, 28 Erlanger, 28 Janeway, 33 Masing, 29 Sahli, 30 Strasburger, 32 oscillatory method, 33 palpatory method, 32 effect of digitalis on, 239 effect of exercises of strain on, 188 end pressure, 25 in aortic insufficiency, 455 in Basedow's disease, 41, 687 in chronic nephritis, 42 in different parts of the vascular system, 34 in normal individuals, 33 in paroxysmal tachycardia, 668, 672 in various diseases, 39 lateral pressure, 25 maximal, 26 minimal, 26 normal, 33 physiological factors influencing, 35 variations in, under pathological conditions, 38 variations in, under physiological conditions, 37 venous, 50 Blowing diastolic murmur in mitral stenosis, 437 Blue babies, 529 Bradycardia, 69 in Adams-Stokes disease, 553, 569 Brain tumors, blood-pressure in, 40 Brandy in cardiac disease, 224 Brauer chamber in operations on heart, 615 Breath-holding test, 206 Breathing, Cheyne-Stokes, 208 Broken compensation as indication for in- ducing labor, 507 blood-pressure in, 42 functional valvular insufficiencies 'n, 195 pseudo-elephantiasis in, 210 pulmonary, 195 systemic, 194 venous pressure in, 197 Broken pulmonary compensation in mitral insufficiency, 413 Bronchitis in mitral insufficiency, 420, 423 Cachexia, blood-pressure in, 50 Caffeine, 253 in angina pectoris, 382 in cup of coffee, 225 Calcification in arteriosclerosis, 329 of the intima, 332 pathogenesis of, 329 Calcium chloride for aneurism, 650 Calcium salts as cardiac tonics, 253 effect of, on cardiac contraction, 2 in Basedow's disease, 692 Calomel, 226 Camphor, 252 Canalis auricularis, 515 Capillaries, changes in, in congenital heart disease, 526 determination of the pressure in, 51 malformation of, in congenital heart disease, 527 Capillary pulse in aortic insufficiency, 457 Carbon dioxide, effects of, 38 use of, for anginal pain, 229 use of, in cardiac dyspnoea, 229 Cardiac and adrenal hypertrophy, 284 Cardiac area, diameter of, 147 Cardiac asthma, 204 from coronary sclerosis, 369 from nasal disease, 205 in aortic insufficiency, 456 Cardiac chambers, coordination of, 9 Cardiac cicatrices, 312 Cardiac dilatation, mountain sickness as cause of, 182 recovery from, 183 transitory, 182 fright as cause of, 182 Cardiac disease, accumulation of fluid in, 209 724 INDEX. Cardiac disease, renal changes in, 212 symptoms of, 203 Cardiac diseases, acute, blood-pressure in, 50 Cardiac disturbances due to myoma, 711 due to sexual disorders, 710 in females, 710 in males, 710 from lesions of nasal septum, 712 from masturbation, 710 reflex, 708 air-swallowing in, 708 associated symptoms, 708 gastro-intestinal, 708 relation to menstrual flow, 711 sexual, treatment of, 712 Cardiac dulness area in children, 148 relative, 145 Cardiac dyspnoea, morphine and strychnine in, 205 Cardiac efficiency, functional tests of, 197 Cardiac facies, 215 Cardiac failure with a small heart, 197 Cardiac flatness, 148 absence of, 148 fixation of area of, in adherent pericardium, 603 pear-shaped, in pericarditis with effusion, 588 variations in, 148 Cardiac impulse, 141 course of, 5 in aortic insufficiency, 457 mechanics of, 141 movements in, 142 origin of, 5 protodiastolic wavelet on, 142 Cardiac muscle, tonicity of, 13 Cardiac nerves, action of, 17 effect of exercise on, 20 excision of, 20 tonic action of, 17 Cardiac neurasthenia, 697 Cardiac neuroses, 697 arrhythmia in, 697 classification of, 699 sexual, 710 symptoms of, 697 venous pressure, 697 Cardiac overstrain, anaemia in, 180 as cause of Adams-Stokes disease, 569 auricular fibrillation and arrhyth- mia in, 196 cases of, 177 chlorosis in, 180 diagnosis of, 183 dilatation of heart in, 181 extrasystoles in, 182 mountain climbing as cause of,180 precordial pain in, 181 Cardiac overstrain, primary, 177 etiology of, 180 sexual excess as cause of, 180 tight belts as cause of, 180 Cardiac plexus, 20 Cardiac rhythm, alterations in, 97 Cardiac shadow, 133 as an index of cardiac volume, 17 Cardiac tonicity, effect of, on regurgitation, 453 Cardiac tonus in functional insufficiency, 410 Cardiac volume, cardiac shadow as an index of, 17 Cardiohepatic angle (Ebstein's) in pericar- dial effusion, 587 Cardiolysis for relief of adherent pericar- dium, 608 Cardiometer, 11 Cardiopathia thyreopriva (hypothyroidism), 679 Cardioptosis, 700 Cardiosclerosis, 313 Cardiosclerosis and atrophy, 294 Cardiosphygmograph, 73 Cerebral thrombosis, blood-pressure in, 40 Chest, flat, in congenital heart disease, 532 Cheyne-Stokes breathing, 208 from acapnia, 208 treatment of, 209 types of, 208 Chlorosis in cardiac overstrain, 180 Choc en dome, 457 Cholera, blood-pressure in, 50 Chronic hypertension, 42 Chronic hypertrophy of the heart, blood- pressure in, 40 Circulation in foetus, mechanics of, 519 Circulation, mechanism of, 34 pulmonary, 51 Claudication, intermittent, 359 Clubbed fingers in congenital heart disease, 531 Coffee, effect of, 715 prohibition of, 225 Coitus, avoidance of, in cardiac disease, 509 Cold applications over the heart, 220 Collapse, blood-pressure in, 50 hypotension in, 50 Collapsing pulse, 68 in aortic insufficiency, 463 in arteriosclerosis, 348 Compensation, broken, hydrsemia in, 60 broken pulmonic, 194 broken systemic, 194 symptoms of broken, 194 Compression of the artery, sources of error in, 28 Concato's arch in pericarditis with effusion, 588 INDEX. 725 Concretio pericardii cum corde, 598 Connective-tissue proliferation, interfas- cicular, 312 Constipation, effect on heart, 709 Constricting the femoral arteries, rise of blood-pressure on, 198 Constriction, effect of, in producing cardiac overstrain, 190 Contractility, diminished, in pulsus alter- nans, 106 Contractions of heart, maximal, 5 Conus arteriosus, dilated, in mitral stenosis, 433 Convulsions in congenital heart disease, 529 Coordination of the cardiac chambers, 9 Cor biatriatum triloculare, 506 Coronary arteries, distribution of, 366 ligation of, 366 sclerosis of, 367 vasomotor nerves in, 367 Coronary circulation, physiology of, 366 Coronary sclerosis in patients with paroxys- mal tachycardia, 369, 665 symptoms of, 368 Corrigan's pulse, 68 "Corset heart," 704 Corsets, effect of, in producing cardiac over- strain, 190 Cough, 209 (brassy, stenotic, paretic) in aneurism, 628 Cyanosis, blood-pressure in, 42 in congenital heart disease, theories of, 530 in pulmonary stenosis, 529 in tricuspid stenosis, 498 Dalrymple's sign in Basedow's disease, 687 Death from labor, cause and frequency of, 504 Death from sudden emotion, 716 Degeneration, calcareous, 302 hyaline, 302 parenchymatous, 302 waxy, 302 Delusions, 216 from digitalis poisoning, 216 typical, 216 Determination of the blood-pressure, aus- cultatory method for, 33 Dextrocardia (dcxiocardia), electrocardio- gram in, 549 relation to transpositions in embryo, 548 Dextroversion of the aorta, 525 Diaphragm, high, 707 high, in fat persons, 707 Diarrhoea, blood-pressure in, 50 Diastasis and diastole, 11 Diastole and diastasis, 11 position of the valves in, 12 Diastolic closure of auriculoventricular valves, 12, 79 Dicrotic notch, time of, in cardiac cycle, 78 pulse, 68 wave, 66 of pulse, 66 Diet, 223 effect of, on viscosity, 60 in cardiac disease, 223 Karell's, 224 lacto-vegetarian, 224 limited milk, 224 restricted liquids (Karell), 224 restriction of salts, 224 Digalen, 234 Digestive disturbances, 215 Digitalis, 176, 233 action of, 236 on coronary arteries, 237 stage of incoordination, 238 stage of irregularity, 238 therapeutic stage, 238 administration in fresh mitral endo- carditis, 423 and nitrites, 248 and strophanthus in aortic insuffi- ciency, 467 arrhythmia and heart-block caused by, 237 contraindication to, 249 derivatives of, 247 drugs of series, 234, 235 on normal heart, 236 on the blood-pressure, 239 on tonicity, 240 flavoring of, 245 hallucinations from, 250 in arrhythmia, 243 in auricular fibrillation, 120, 320 in heart-block, 573 in second stage of mitral insufficiency, 424 intramuscular administration, 246 intravenous administration, 246 in weakened hearts, 243 methods of administration, 245 period of administration, 246 poisoning, delusions from, 216 preparations of, 234 choice of, 245 rectal administration of, 246 standardization of, 234 Digipuratum, 247 toxic affects, 237 Digitoxin, 234 Dilatation of the heart, acute, angina pec- toris in, 376 acute, pain due to, 375 726 INDEX. Dilatation of the heart, from constriction, 190 in cardiac overstrain, 181 in myocarditis, 305 physiological factors bringing about, 191 transitory, 182 Diphtheria as cause of endocarditis, 389 blood-pressure in, 48 Diplococcus rheumaticus, 387 Displacement of the heart, 699 Drugs, mode of action on circulation, 233 Duct of Cuvier, 514 Ductus arteriosus (Botalli), closure of, 541 factors causing persistence of, 541 open, 526 patent, 540 diagnosis of, 544 murmur in, 542 pathogenesis of, 540 pulsus paradoxus in, 543 respiratory interchange in, 544 signs of, 542 symptoms of, 542 treatment of, 544 X-ray shadow in, 542 role in fcetus, 520 Ductus venosus, atrophy of, 520 Duroziez's double murmur over the arteries in aortic insufficiency, 460 Dysentery, blood-pressure in, 50 Dyspnoea, 203 in congenital heart disease, 529 mechanical changes in circulation, 203 Ebstein's cardiohepatic angle in pericardial effusion, 587 Netopia cordis, 521 Ectopic impulses, 112 Efferent impulses, 17 Effusion in pericarditis, 585 Electricity, 228 in treatment of angina pectoris, 383 Electrocardiogram, 81 cause of waves upon, 90 form of, 89 in auricular fibrillation, 121 in extrasystoles, 113 in heart-block, 565 in hypertrophy of left ventricle, 94 in hypertrophy of right ventricle, 94 in mitral stenosis, 93 in paroxysmal tachycardia, 664 in situs transversus, 550 Electrocardiograph, 81 installation of, 84 Embolism in mitral stenosis, 442 in patent foramen ovale, 540 pulmonary, 207 Embryocardia, 158 in paroxysmal tachycardia, 672 Emotion, arrhythmia from, 716 effect of, on the heart, 716 Emptying of the heart, 10 Endarteritis, 333, 340 Endocarditic vegetations, bacterial origin, 385 development of, 385 Endocarditis, 385 anaemia in, 403 cerebral embolism in, 394 cerebral type, 394 choked disk in, 394 chronic, 386, 392 chronic infective, 395 cocci (streptococcus viridens) in, 395 complications of, 401 differential diagnosis of, 395 digitalis in, 402 due to pyogenic cocci, 388 effect on circulation, 390 from miscellaneous infections, 389 gonorrhceal, 389 influenzal, 389 involvement of valves, 398 jaundice in, 393 malignant, 391, 392 complications, 392 brain symptoms, 392 embolic aneurisms, 392 enlarged spleen, 392 hsematuria, 392 heart failure, 392 petechia>, 392 retinal hemorrhages, 392 treatment, 396 frequency of, 392 valves involved in, 392 microbes producing, 387 mural, 386 palliative treatment of tonsils in, 404 pathological physiology of, 390 pathology of, 386 pneumococcic, 389 prophylaxis, 403 reinfection, 401 retinal hemorrhages, 394 rheumatic, 387, 397 septicsemic, 393 simple acute, 391, 397 compensation in, 401 course of, 399 pathology of, 399 signs, 400 symptoms of, 399 statistics of, 397 INDEX. 727 Endocarditis, subacute, 397 syphilis in, 390 treatment of, 402 typhoidal type, 394 ulcerative, 386 Endocardium, atheroma of, 390 pockets of, in aortic insufficiency, 525 Endothelial cells in sputum, 209 Endurance, exercises of, 187 Energy, waste of, in fatigue, 187 Enteroptosis (see Splanchnoptosis) Epilepsy, blood-pressure in, 40 Ergot, 255 Ergotism, resemblance to Raynaud's dis- ease, 361 Erosion of bone by aneurism, 625 Erythromelalgia, 360 Erythromelia, 363 Exercise, choice of, 272 effect of, on blood-pressure, 38 Schott, 269 systems of, in therapeutics, 267 test of cardiac function, 198 Exercises, effect of, on size of heart, 189 of endurance, 187 circulation in, 187 mechanics of, 185 of speed, mechanics of, 185 of strain, 188 effect on blood-pressure, 188 mechanics of, 267 Exophthalmic goitre (see Basedow's disease) Exophthalmos from stimulation of sympa- thetic, 687 Extrasy stoles, 107 auricular, 112 auriculo(atrio)ventricular, 114 auriculo ventricular, lesions in, 117 diagnosis of, 125 effect of atropine on, 114 electrocardiogram in, 112 experimental production of, 113 heart sounds in, 114 in cardiac overstrain, 182 in myocarditis, 316 ineffectual, 114 neurogenic, 108 palpitation with, 113 prognosis, 117 treatment, 117 stimuli causing, 113 venous pulse in, 112 ventricular, 109 Face, oedema of, 210 Facies, aortic, 140 cardiac, 140, 215 mitral, 140 Fatigue, effect of, on energy used up, 187 Fats, diminished absorption of, 215 Fatty degeneration of the heart, 292, 297 etiology, 299 nature of, 298 pathological anatomy of, 297 prognosis, 300 rupture of the heart in, 300 strength of heart with, 299 symptoms and signs of, 300 treatment, 300 Fatty degeneration of the intima, 332 Fatty infiltration of the heart, 292, 293 cardiac conditions associated with, 294 etiology, 295 nature of the fatty deposit, 293 physical signs of, 295 treatment of, 295 Fetal heart sounds, graphic record of, 158 Fevers, acapnia in, 49 Filling of the heart, 10 of the ventricles, 11 First sound at aorta, 154 cause of, 153 character of, 153 duration of, 154 in suprasternal notch, 154 reduplicated, 158, 159 Fluid in cardiac diseases, accumulation of, 209 Fluoroscope, 132 diagnosis by, 135 Foetus, circulation in, 519 Football playing, effect of, on heart, 189 Foramen ovale, development of, 517 effect of patency on circulation, 539 open, 526 patent, 538 crossed embolism in, 540 occurrence and pathogenesis, 538 paroxysmal cyanosis in, 540 signs of patency, 540 symptoms of patency, 539 treatment of, 540 vicious circle in, 528 Formative stimulus in arteriosclerosis, 327, 330 Fragmentation of muscle fibres, 303 Friction in pericarditis, 582 pleuropericardial, 582 Functional mitral insufficiency, 408 Functional tests of cardiac efficiency, 197 ofcardiacinsufficiency, value of, 199 relation of, to mode of life, 199 Gallop rhythm, presystolic, 159, 160 protodiastolic, 159, 161 Galvanometer, string, 85 thread, 85 728 INDEX. Gastric ferment action, 708 Gonococcus as cause of endocarditis, 389 Graefe's sign in Basedow's disease, 687 Graves's disease (see Basedow's disease) Gymnastics, 267 fundamental principles of, 267 Hsemopericardium, 591 from cardiac tumors, 324 Hemoptysis from pulmonary stasis, 207 in pulmonary insufficiency, 482 Hsemosiderin in Herzfehlerzellen, 209 Hallucinations, 216 in adherent pericardium, 601 Headaches in congenital heart disease, 529 Heart, changes in position of, 149 changes in size of, 149 development of, early stages, 513 dilatation of, from constriction, 190 diminution in size of, in exercise, 189 disease and matrimony, 511 congenital, 513 blood count in, 533 etiological groupings, 522 flat chest in, 532 groups of lesions in, 521 syndrome of, 522 displacement of, 699 effect on circulation, 700 emptying of, 10 endothelial tube in embryo, 514 failure, mechanism of, 193 filling of, 10 high, 708 effect on circulation, 708 treatment of, 708 xiphisternal line with, 708 insensibility of, 372, 613 lesions, congenital, classification of, 521 low, 700, 707 signs of, 707 metastatic involvement of, 324 mobility of, in cardioptosis, 700 muscle, properties of, 1 structure of, 1 muscular tube in embryo, 514 non-perforating injuries of, 616 normal mobility, 700 nourishment of, 367 relaxation of, 13 sensory symptoms about, 213 small, in cardiac failure, 197 sound, first, reduplication of, in adhe- rent pericardium, 604 second aortic, in arteriosclerosis, 349 second, in mitral insufficiency, 419 third, causation of, 161 Heart, third, in adherent pericardium, 603 sounds, accessory, 158 causes of, 153 clinical diagram for, 153 digital imitation of, 170 graphic record of, 150 reduplicated, 158, 159 reproduction of, 152 split, 159 three-chambered, 526 tuberculosis of, 322 tumors of, 323 work of, 36 wounds of, 611 cause of death from, 612 experimental surgery of, 611 hemorrhage in, 615 murmurs in, 613 operative treatment of, 613 spontaneous recovery in, 611 suture of, 614 symptoms of, 613 X-ray examination of, 613 Heart-beat, origin of, 2 role of salts in, 2 theories of, 4 Heart-block (see also Adams-Stokes dis- ease), 104, 553, 555 asphyxial, 560 auriculoventricular, 104 complete. 105, 559 effect of atropine on, 559 effect of vagus on, 559 extrasystoles simulating, 572 factors affecting degree of, 557 stoppage of ventricles, 558 from cutting interauricular sep- tum, 554 functional, 104 in infectious diseases, 568 interventricular, 105 in tortoise, 555 irregular rhythm in, 561 organic, 104 partial, 105, 559 effect of heart rate in, 559 from digitalis, 569 relation to Adams-Stokes syn- drome, 561 role of vagus in, 564 sino-auricular, 105 treatment of, 573 with auricular fibrillation, 569 with rapid ventricular rate, 570 Hemisystole, 105 Hemorrhage, blood-pressure in, 50 fall of blood-pressure in, 50 from the lungs, 207 in mitral disease, 207 in congenital heart disease, 207 INDEX. 729 Hemorrhage in pulmonary insufficiency, 207 in wounds of heart, 615 intracranial, blood-pressure in, 40 Heredity in arteriosclerosis, 342 Herzfehlerzellen, 209 Heterogenetic impulses (see ectopic) in extrasystoles, 110 in paroxysmal tachycardia, 667 Hiccough-in pericarditis, 581 High diaphragm, 707 heart, 708 Hippocratic fingers, 531 His bundle, anatomy of, 556 Hoarseness in pericarditis, 581 Hormone action in cardiac symptoms, 712 Hydropericardium, 591 Hydrotherapy, 274 in arteriosclerosis, 351 Hydrothorax, 211 in adherent pericardium, 601 production of, 211 Hyperdicrotic pulse, 68 Hypermyotrophy, arterial, 334 Hypertension as factor in production of arteriosclerosis, 343 and arteriosclerosis, 45 chronic, 42 and cerebral circulation, 46 effects upon circulation, 45 treatment of, 46 diseases with, 39 Hyperthyroidism, 680 acetonitrile test for, 682 adrenalin test for, 682 angina pectoris in, 379 effect on heart muscle, 682 effect on nervous system, 682 vicious circle of, 683 Hypertrophied heart, reserve force of, 288 Hypertrophy, 279 adrenal, 284 and abdominal arteriosclerosis, 284 electrocardiogram in, 285 of auricles, 288 Hypertrophy and arteriosclerosis, 283 cardiac, 284 concentric, 281 excentric, 281 from overdrinking, 283 from work, 282 in chronic nephritis, 283 of the auricles, 288 of the heart in Basedow's disease, 687 of the left ventricle, 285 of the right ventricle, 285 pathological anatomy of, 279 prognosis, 288 reserve force, 288 sites of, 281 types of, 281 Hypertrophy and arteriosclerosis, work, 282 Hypotension, 48 disease with, 48 failure of vasomotor centre in, 48 Hypothyroidism, effect on circulation, 679 Hysterical angina, 378 Ice-bag over heart, 221 contraindications to, 221 effect on pulse rate, 221 Impulses, afferent, 17 efferent, 17 Increased intracranial pressure, blood-pres- sure in, 40 Infectious diseases as causes of arteriosclero- sis, 340 as causes of Basedow's disease, 684 hypotension in, 48 Influenza as cause of Basedow's disease, 684 as cause of endocarditis, 389 Inhalation of carbon dioxide, 229 oxygen, 228 rarefied air, 230 as cause of myocarditis, 308 Injuries of heart, 616 Insufficiency, mitral, 407 of valves in broken compensation, 195 Intermittent claudication, 359 Interstitial pneumonia, 209 Interventricular septum, defects in, 534 patent, 534 murmur in, 536 with pulmonary stenosis, 525, 529 Intima, calcification of, 332 fatty degeneration of, 332 Intranasal tracings, 81 Intravenous injections in treatment of endo- carditis, 397 of strophanthin, 247 Intraventricular pressure, 25 lodothyrin, 680 Irregularity (see Arrhythmia) permanent, 120 Irritability in cardiac disease, 216 Jaundice, catarrhal, in broken compensa- tion, 215 in endocarditis, 393 Jellinek's sign of Basedow's disease, 683 Joffroy's sign of Basedow's disease, 685 Kinematographs, 137 730 INDEX. Labor (see Pregnancy) and pregnancy in persons with heart disease, prognosis, 505 cardiac overstrain during, 504 cause of death during, 504 Langendorff ' s perfusion apparatus, 3 Laryngeal paralysis in aneurism, 628 Lead poisoning, blood-pressure in, 40 Left auricle, pressure in fetal life, 520 Liquids, restriction of, 224 in arteriosclerosis, 351 Liver, abdominal pain from distended, 215 presystolic pulsation in tricuspid steno- sis, 498 pulsation of, in tricuspid insufficiency, 492 in tricuspid stenosis, 497 signs simulating cirrhosis of, in adhe- rent pericardium, 607 Low heart, 707 Lungs, hemorrhage from, 207 Magnesium sulphate, 226 Manometers, 30 aneroid, 32 compressed air, 32 spring, 32 Marching, effect of, on heart, 189 Massage, 227 Masturbation, effect of, on heart, 710 Matrimony and heart disease, 509, 510 Meals, effect of, on blood-pressure, 38 Measles, blood-pressure in, 48 Mechanical factors in the production of mur- murs, 163 Mechanism of the circulation, 34 Mechanogymnastics, 271 Media, calcification of, 337 degeneration of, 337 hypertrophy of, 334 Medial changes in aneurism, 623 Mediastinopericarditis, 598 Meningitis, blood-pressure in, 40 Menstruation, relation of, to cardiac symp- toms, 711 Mental distraction, 219 exertion, effect of, on blood-pressure, 38 Mesarteritis, 334 Mesaortitis, syphilitic, 334 Metabolism, increase from thyroid secretion, 681 Micrococcus rheumaticus, 387 Micrograph, 76 Mid-diastolic rumble stenosis, 436 in aortic insufficiency, 459 in mitral stenosis, 436 Mill-wheel murmur in pneumopericardium, 592 Mitral area, 156 Mitral disease, pulmonary complications of, 413 Mitral facies in mitral insufficiency, 415 Mitral insufficiency, 407 and tuberculosis, 422 arrhythmia in, 420 blood-pressure in, 419 broken compensation in, 425 broken pulmonary compensation in, 413 broken systemic compensation in, 414 cardiac area in, 416 complications, 422 digitalis in, 424 early administration of digitalis in, 423 functional, 408, 409, 410 lungs in, 420 mechanics of circulation, 410 murmur and sounds in, 417 cesophageal tracing in, 81 physical examination in, 415 Mitral insufficiency, organic, 407 outward displacement of apex in, 415 papillary, 408, 409 pathology of, 407 prognosis in, 425 propagation of murmur, 418 pulmonary stasis in, 411, 422 pulse in, 419 purgation in, 424 re-education of heart muscle in, 423 relative, 409 second heart sound in, 419 second stage of, 413 stages of, 412 stasis in left auricle, 410 statistics of, 407 systolic murmur in, 417 third stage of, 414 tonicity of the heart in, 414 treatment, 422 treatment of second stage of, 424 treatment of third stage, 425 with mitral stenosis, 435 without symptoms, 412 X-ray shadow in, 416 Mitral stenosis, 427 anaemia in, 443 and aortic insufficiency, differen- tiation between, 439 and tricuspid stenosis, 441 arrhythmia in, 444 auricular fibrillation in, 444 blood-pressure in, 50 blowing diastolic murmur in, 437 bronchitis in, 443 INDEX. 731 Mitral stenosis, cardiac outline in, 433 complications, 441 congenital form, 428 diagnosis, 438 diastolic murmur in, 437 digital and phonetic imitation of the heart sounds in, 435 dilated conus arteriosus in, 433 disappearance and reappearance of presystolic rumble in, 431 effect of auricular contraction on filling of ventricles, 430 embolism in, 442 endocarditic form, 428 etiology, 428 historical, 427 laryngeal paresis in, 431 mid-diastolic rumble in, 436 operations on mitral valve, 447 paralysis of auricles in, 431 pathological physiology of, 429 pathology of, 427 presystolic rumble in, 433 thrill and systolic tap in, 432 prognosis, 447 pulmonary oedema in, 446 pulmonary tuberculosis, 443 pulse in, 438 quality and production of the sounds, 434 role of oedema and anaemia in, 428 sclerotic form, 428 snapping first sound in, 434 stages of, 437 symptoms and signs, 431 third heart sound in, 436 thrombosis in left auricle in, 442 treatment of, 442, 443 tuberculosis in, 428 volume of ventricles in, 429 with mitral insufficiency, 428, 435 X-ray shadow in, 434 Mitral valve, atheroma of, 409 demonstration of action of, 12 hemorrhage in, 409 malformation of, 551 tests for sufficiency, 408 Mitralized pulse, 420 Mobility of heart, 150 Mobius' sign in Basedow's disease, 687 Monckeberg's arteriosclerosis, 337 Moore-Corradi method in treatment of aneurisms, 650 Morbus coeruleus, 528 Morphine, dangers from, in myocarditis, 321 in cardiac dyspnoea, 205 Mountain climbing, Oertel's, 272 Movements, passive, 268 Movements, resisted, 268 Schott, 268 Murmur at back in patent ductus Botalli, 532 attack in mitral insufficiency, 418 diastolic, in pulmonary insufficiency, - 482 mitral, differentiation from accidental and tricuspid, 418 digital imitation of, 417 phonographic tracing of, 417 propagation of, 418 Roger's systolic in open septum ventric- ulorum, 536 systolic, in aortic stenosis, 474 in mitral insufficiency, 417 in tricuspid insufficiency, 490 Murmurs, 163 accidental, 166 causation of, 168 differential diagnosis of, 167 nature of, 168 time of, 166 arterial, 173 cardiopulmonary, 166, 169 character of, 164 combined, 172 differentiation between cardiopulmo- nary and other accidental murmurs, 170 functional, 166 ha^mic, 166, 168 mechanical factors in the production of, 163 phonetics of, 163 single, 172 tabulation of, 172 transmission of, to chest wall, 165, 418 venous, 173 Muscle fibres in the ventricle, arrangement of, 9 Myocardial changes, distribution of, 303 Myocarditis, 302 acute, arrhythmia in, 306 alcoholic, 309 and nephritis, 318 arrhythmia in, 315, 316 bronchitis in, 316 catalase in, 318 chronic, 312 blood-pressure in, 315 diagnosis of, 310 differential diagnosis in, 319 dilatation in, 305 diphtheric, 308 extrasystoles in, 316 hypersensibility to digitalis, 311 influenzal, 80S* morphine in, 321 murmurs in, 316 pathological physiology of, 314 rheumatic, 304, 307 732 INDEX. Myocarditis, signs and symptoms of, 307 strychnine in, 312 symptoms and signs of, 316 treatment of, 310, 320 weakness of heart in, 306 Myocardium, affections of, 302 syphilis of, 322 Myoma as cause of cardiac weakness, 711 Nasal disease, cardiac asthma from, 205 Nasal septum, arrhythmia from lesion of, 712 asthma from lesion of, 713 Nauheim treatment, 220 Nephritis and myocarditis, 318 blood-pressure in, 40, 42 Nerve-fibres producing changes in tonus, 16 Nerves, accelerator, 19 sympathetic, 19 Neurasthenia, cardiac, 697 Nitrites, 255 action of, 256 and digitalis, 248 effect of, in hypertension of intracranial origin, 40 effect of on the circulation, 257 use of, in angina pectoris, 381 in aortic insufficiency, 467 in arteriosclerosis, 352 Nitroglycerin, 255/257 mode of administration, 257 tolerance to, 257 Nodal rhythm, 118 Node, auriculoventricular, of Tawara, 556 sino-auricular, of Keith and Flack, 8 Oarsmen, longevity of, 193 Obesity, diet in, 296 high diaphragm in, 294, 707 of the heart, 292 physical signs of, 295 treatment of, 295 with cardiac atrophy and cardiosclero- sis, 294 with coronary sclerosis, 294 (Edema, 209 effect of drugs and diet on, 210 fluid, salt content of, 210 lymphagogue substance in the blood in, 210 of face, 210 of heart muscle, 194 pulmonary, 206 treatment by drainage, 211 types of, 209 Oertel's mountain climbing, 272 (Esophageal auscultation, 158 of mitral murmur, 418 CEophageal tracings, 80 in mitral insufficiency, 81 Orthodiagraph, 135 Orthopercussion, 145 Orthoplessimeter, 146 Orthopncea, 204 mechanical changes in circulation, 204 Ossification in arteriosclerosis, 329 Outflow during systole, 11 Oxygen inhalations of, in treatment of cardiac diseases, 228 "Pace-maker" of the heart, 5 Pain down the arms, 214 on swallowing in pericarditis, 581 precordial, 214 referred from cervical ganglia, 214 sensations, paths traversed by, 372 Palpation of heart, 144 Palpitation, 213 and angina, 372 cardiac sensations in, 213 with extrasystoles, 113 Papillary insufficiency, 409 muscles, fatiguing of, 77 in propagation of mitral murmur, 418 Paracentesis abdominis, 211 pericardii, 593 Paradoxical respiration in enteroptosis, 703 Pararrhythmias, 98, 123 Paroxysmal irregularity, 669 Paroxysmal tachycardia, 127, 662 associated lesions, 664 auricular fibrillation in, 666 belching in, 676 cardiac dulness during attacks, 672 cerebral anaemia in, 672 coronary sclerosis in, 665 diagnosis of, 674 differentiation from simple tachy- cardia, 674 doubling of rate in, 662 drugs in, 675 dyspnoea in, 671 effect on circulation, 668 embryocardia in, 672 fall of blood-pressure in, 668 from ligature of coronary arteries, 669 fulness of neck in, 671 heterogenetic impulses in, 667 in coronary sclerosis, 369 inactivity of cardiac nerves in, 9 inception of rhythm by auriculo- ventricular bundle, 668 interpolated extrasystoles, 666 irregularity, 118 INDEX. 733 Paroxysmal tachycardia lesions in auriculo- ventricular bundle in, 665 lesions in vagus nucleus, 665 occasional confusion with Adams- Stokes disease, 572 precordial pain in, 671 rise of venous pressure in, 668 sino-auricular block, 557 stimulation of vagi in, 668 sudden exercise in, 675 swallowing in, 676 symptoms of, 671 theories as to origin, 666 treatment of, 675 tricuspid insufficiency in, 673 types of, 663 venous pulse in, 663 vomiting in, 676 Parry's disease (see Basedow's disease) Passive movements, 268 Patent foramen ovale, 538 pathogenesis of, 538 Pathological conditions, variations in blood- pressure under, 38 Percussion, 144 errors in, 146 methods of, 145 Perfusion of excised mammalian heart, 4 Periarteritis, diffuse, 340 Periarteritis nodosa, 337 Pericarditis, 578 adhesive (see Adherent pericardium), 598, 602 blood-pressure in, 50, 583 etiology of, 578 friction at back in, 583 friction sound in, 582 hiccough in, 581 hoarseness in, 581 pain on swallowing in, 581 precordial pain in, 581 purulent, 591 simple fibrinous, 581 diagnosis of, 583 prognosis in, 585 treatment of, 584 signs of, 581 symptoms of, 581 tuberculous, 592 fluid in, 592 with effusion, 585 amount of fluid, 585 blood-pressure in, 589 cardiac outline, 587 drainage in, 595 Ebstein's cardiohepatic angle in, 587 effect on circulation, 585 enlargement of liver from, 588 Pericarditis with effusion, fulness of inter- spaces in, 587 irrigation of pericardium in, 596 paracentesis of, 593 pericardiotomy in, 595 position of heart in, 588 Rotch's sign in, 587 signs at back in, 588 signs of, 587 symptoms of, 586 treatment of, 593 X-ray examination of, 589 Pericardium, adherent, 377, 598 development of, 518 Peripheral resistance, 65 Peritonitis, blood-pressure in, 48 Petechise in endocarditis, 393 Phenolsulphonphthalein test for renal in- sufficiency, 212 in chronic hypertension, 42 in myocardial weakness, 318 Phosphorus poisoning, effect of, on heart in fatigue, 190 Phthisis, blood-pressure in, 48 Physiological conditions, variations in blood- pressure under, 37 Physical examination, 140 Physico-chemical phenomena, rhythmicity in, 1 Pigmentation in hyperthyroidism (Jellinek's sign), 683 Placenta, vessels to, 514 Pleurisy, blood-pressure in, 50 Pleuropericardial friction, 582 Pneumococci as causes of endocarditis, 389 Pneumonia as cause of pericarditis, 578 blood-pressure in, 48 interstitial, 209 Pneumopericardium, 592 Polycythgemia, blood-pressure in, 41 Polygraph, Gibson, 74 Mackenzie, 73, 74 Marey, 73 Uskoff, 30 Position, changes in, 149 effect of change of, on blood-pressure, 37 on electrocardiogram, 93 Posture, effect of, on pulse-rate, 198 Potassium iodide, 259 effect of, on viscosity of blood, 60 for aneurisms, 650 in angina pectoris, 381 in arteriosclerosis, 352 mode of administration, 259 supposed effect on viscosity of blood, 259 salts, effect of, on cardiac contraction, 2 thiocyanate, 261 therapeutic use of, 261 734 INDEX. Precordial pain, 214 in angina pectoris, 371 in cardiac overstrain, 180 in hyperthyroidism, 690 in pericarditis, 581 Pregnancy and labor, pulmonary oedema in, 503 aortic disease in, 509 as cause of Basedow's disease, 683 blood-pressure in, 41 Pregnancy, broken compensation in, 506 effect on pulse and blood-pressure, 503 hypertrophy during, 503 termination of, 508 in broken compensation, 507 treatment of heart lesions during, 506 tricuspid insufficiency during, 504 Presphygmic period, 10 Presystolic gallop rhythm, resemblance to mitral stenosis, 439 rumble, disappearance and reappear- ance of, in mitral stenosis, 431 (Flint's) in aortic insufficiency, 461 in mitral stenosis, 433 in tricuspid stenosis, 499 Presystolic gallop rhythm, 160 Protodiastolic gallop rhythm, 161 Pseudo-anginal pain, 375 Pseudo-aortic insufficiency, 457 Pseudocardiac disturbances, 699 Psychic disturbances, 215 Psychotherapy in Basedow's disease, 692 Puerperal infection as cause of Basedow's disease, 684 Pulmonary area, 156 Pulmonary artery, aneurism of, 647 blood-pressure in, 156 blood-pressure in, before birth, 51 development and maldevelopment of, 524 sclerosis of, 350 vasomotor nerves in, 52 Pulmonary circulation, 51 action of drugs on, 52 Pulmonary embolism, 207 Pulmonary hemorrhage, 207 Pulmonary insufficiency, diagnosis of, 484 diastolic murmur in, 383 etiological factors, 481 forms of, 480 functional, 480 haemoptysis in, 480 pathological physiology, 481 prognosis in, 484 pulse in, 483 signs of, 4.82 symptoms of, 482 treatment of, 484 with pulmonary stenosis, 532 Pulmonary oedema, 206 artificial respiration in, 206 in mitral stenosis, 446 in pregnancy and labor, 504 signs of, 206 treatment of, 207 Pulmonary pressure , 52 conditions affecting, 52 Pulmonary stenosis and atresia, causes of r 522 diagnosis, 533 due to endocarditis, 522 due to maldevelopment of branchial arches, 523 duration of life in, 533 statistics of, 522, 533 Pulmonary stenosis in open interventric- ular septum, 525 pathological physiology of, 527 systolic murmur, 531 treatment of, 533 with patent interventricular sep- tum, 525, 529 Pulsations, inspection of, 630 over chest, 144 over veins, 70 Pulse, anacrotic, in aortic stenosis, 476 arterial, 62 characteristics of, 26 curve, significance of, 65 dicrotic, 62 discrepancies in examining, 64 examination of the, 62 form, 65 in aortic insufficiency (Corrigan, water- hammer, collapsing), 462 qualities of the, 62 rate, 67 effect of ice-bag on, 221 effect of posture on, 198 relation to temperature, 67 Riegel's, 103 types of, 68 anacrotic, 68 bisferiens, 68 collapsing, 68 dicrotic, 68 hyperdicrotic, 68 normal, 68 tardus, 68 venous, 70 wave, inequality and delay of, in aneu- risms, 632 Pulse-pressure, 26 Pulsus alternans, contractility diminished in, 106 Pulsus irregularis perpetuus, 118 Pulsus paradoxus, 103 Pulsus tardus in aortic stenosis, 472, 475 Pupils, inequality of, in aneurism, 631 INDEX. 735 Purgation, 225 in broken compensation, 225 rise of venous pressure during, 226 Purgatives, 226 Quiet in treatment, 219 Radiographs, stereoscopic, 137 technique of, 136 Rarefied air, inhalation of, 230 Raynaud's disease, 360 pathology of, 361 Rectal administration of digitalis, 236 Reduplicated heart sounds, 158 Re-education of heart muscle in mitral in- sufficiency, 423 Referred pains in angina pectoris, 373 Reflex cardiac disturbances, 708 air-swallowing in, 708 associated symptoms, 708 gastro-intestinal, 708 Relative insufficiency, 409 Renal complications of cardiac diseases, 212 Residual blood, 15 Respiration, method of recording, 73 paradoxical type, 703 Respiratory ratio, 206 in adherent pericardium, 602 Rest in bed, 220 Retina, arteriosclerosis of, 346 dilatation of veins of, in tricuspid insuf- ficiency, 490 Retinal changes in congenital heart disease, 530 Rheumatic fever as cause of pericarditis, 578 foci of myocarditis in, 304 Rheumatism, blood-pressure in, 48 cocci causing, 387 Rhythmicity, physico-chemical phenomena in, 1 Riess' sign of adherent pericardium, 604 Right ventricle, tonicity of, 53 work of the, 51 Rise of blood-pressure on constricting the femoral arteries, 198 Rotch's sign of pericardial effusion, 587 Rupture of aneurism, 625 "Safety-valve" action of tricuspid valve, 487 Sajodin, use of in cardiac disease, 259 Salts, restriction of, 224 Salts, role of, in origin of heart beat, 2 Salvarsan, use of in cardiac disease, 260 Sauerbruch chamber in operations on heart, 615 Scarlatina as cause of endocarditis, 389 blood-pressure in, 48 pericarditis from, 579 Schott movements, 268 effect of, in reducing cardiac dila- tation, 271 precautions in, 269 Second sound, 154 Second wind, 186 Sensory stimulation, effect of, on blood- pressure, 38 Septum auriculorum, 516 Septum interpositum, 517 Septum ventriculorum, 516, 534 patent, effect on circulation, 535 prognosis in, 537 signs of, 535 symptoms of, 535 systolic murmur in, 536 trauma as cause of, 534 treatment of, 537 tuberculosis in, 534 Sexual cardiac disorders, 710, 712 Sexual excess as cause of Basedow's disease, 684 Shock, acapnia in, 49 blood-pressure in, 48 diastolic, over aneurism, 644 Sino-auricular block from cooling sinus, 5 in mammals, 105 in paroxysmal tachycardia, 666 Sino-auricular node of Keith and Flack, 6 Sinus allorrhythmias, characteristics of, 103 Sinus as "pace-maker" of the heart, 5 Sinus region in mammals, anatomy of, 5 Sinus reuniens, 516 Sinus, role of, in mammals, 7 Sinus wave on venous pulse, 79 Situs transversus, 548 Skull, fracture of the, blood-pressure in, 40 Sleep, effect of, on blood-pressure, 38 importance of, 219 Smallpox as cause of endocarditis, 389 Smoke, tobacco, composition of, 713 Smoking, effect of, on circulation, 714 precordial pain from, 714 I Snapping first sound in aortic insufficiency, 461 in mitral stenosis, 434 Sounds, alteration of, by pressure, 155 in arteries, 172 over veins, 172 Souther's tubes, 211 Spa treatment, 220 Sphygmobolometer, Sahli, 30 Sphygmogram, the absolute, 64 Sphygmograph, clinical, 62 Dudgeon, 63 v. Jaquet, 63 736 INDEX. Sphygmograph, Marey, 63 Roy and Adami, 63 Sphygmography, errors in, 63 Sphygmomanometer, v. Basch, 26 Erlanger, 28 Gibson, 30 Hill and Barnard, 27 Lauder Brunton, 32 Marey, 26 Pachon, 32 Potain, 27 v. Recklinghausen, 26 Riva-Rocci, 27 Tycos, 32 Sphygmoscope, Pal, 30 Sphygmotonometer, v. Recklinghausen, 32 Uskoff, 30 Splanchnoptosis, 702 abdominal binder in, 704 air-cushion for, 705 blood-pressure in, 703 corset in producing, 704 effect on circulation, 703 effect of, on respiration, 702 level of diaphragm, 702 overfeeding in, 705 pulsus paradoxus in, 704 syncope from, 703 tracheal tug in, 703 treatment of, 704 Split sounds, 159 albuminous in pulmonary oedema, 206 Sputum, prune-juice, 207 Squills, 236, 241 Stair climbing, beneficial effects of graded pauses, 272 Stasis, effect of, on producing cardiac oedema, 194 Stelhvag's sign in Basedow's disease, 687 Stenosis of isthmus of aorta, 545 Sterilization of patients with broken com- pensation, 509 Stethoscope, binaural, essentials of, 155 differential, 155 monaural, 154 telephone, 150 Stomach, sounds over, in adherent pericar- dium (Riess), 604 Stoppage of ventricles, 558 in Adams-Stokes disease, 564 Strain, effect of, on the heart, 192 exercises of, 188 Streptococcus, in endocarditis, 388 in myocarditis, 304 viridens (endocarditis cocci) in chronic endocarditis, 395 Strophanthin, 236, 247 Strophanthus, 235, 241 Strychnine, 250 and digitalis, 402 Strychnine, clinical effects, 250 effect on blood-pressure, 251 effect on cardiac tonicity, 250 in cardiac dyspnoea, 205 indications for, 252 pharmacological action of, 250 preparations of, 250 Sudden death in angina pectoris, 374 from emotion, 716 Suture of wounds in heart, 614 Suture of blood-vessels for thromboangitis obliterans, 365 Swimming, effect of, on heart, 189 Sympathectomy in Basedow's disease, 694 Sympathetic nerves, relation to exophthal- mos, 687 stimulation by thyroid secretion, 681 Sympathicotonie, 19, 356 in Basedow's disease, 682 Symptoms of adherent pericardium, 601 of cardiac disease, 203 Syncope in paroxysmal tachycardia, 672 from extrasystolic arrhythmia, 572 in Adams-Stokes disease, 553 Synechiae pericardii, 598 Syphilis as cause of arteriosclerosis, 334, 341 as cause of endocarditis, 390 in etiology of aneurism, 620, 624 of the myocardium, 322 with precordial pain, 322 Systole, outflow during, 11 treatment of, in cardiac diseases, 259, 260 Wassermann reaction in, 323, 451 Systolic murmur in mitral insufficiency, 417 retraction along left cardiac border, 415 retractions over heart, 143 Tabagism, 714 Tachycardia, paroxysmal, 662 Tea, effect of, 715 prohibition of, 225 Teleroentgenography, 136 Tests, functional, of cardiac efficiency, 197 Theobromine, 253 in angina pectoris, 254, 382 Theocin, 254 Theophylline in angina pectoris, 382 Theories of heart -beat, 4 myogenic, 4 neurogenic, 4 Third heart sound, frequency of, in normal individuals, 163 in adherent pericardium, 604 in aortic insufficiency, 451 Third heart sound in mitral stenosis, 436 mechanism producing, 162 INDEX. 737 Thread galvanometer, 82 Threshold percussion, 145 Thrill, systolic, in aortic stenosis. 474 in congenital heart disease, 531 in mitral insufficiency, 416 Thrills, mechanics of, 144 Thrombi in cardiac chambers, 321 in mitral stenosis, 321 Thromboangitis obliterans, 362 differentiation from angeioneuro- ses, 362 Thyreoglobulin, 680 Thyroid gland changes in Basedow's disease, 689 size of normal, 689 Thyroid heart, 678 formes frustes, 678 from pressure, 678 (hypothyroidism), 679 in simple goitre, 678 Thyroid secretion (see Hyperthyroidism),682 of thyreoglobulin and iodothyrin, 680 physiological effects of, 681 relation to histological structure, 680 Thyroidectin, 692 Thyroidectomy, 693 Tobacco angina, 379 Tobacco, effect of, on circulation, 714 on coronary circulation, 715 "Tobacco heart," 713 Tobacco, precordial pain from, 714 prohibition of, 225 Tobacco smoke, composition of, 713 Tonicity, effect of digitalis on, 240 effect of, on cardiac overstrain, 191 on residual blood, 191 factors producing changes in, 16 of the cardiac muscle, 13 of the heart in mitral insufficiency, 414 of the right ventricle, 53 Tonograph, 30 Tonsillectomy in endocarditis, 404 in mitral insufficiency, 423 Tonsillitis as cause of Basedow's disease, 684 as cause of endocarditis, 403 Tonus (see Tonicity) Tortuous arteries, 346 Tracheal percussion shock in aneurism, 631 tug in aneurism, 631 Training at end of treatment, 273 effect of, 186 Trauma as cause of thoracic aneurism, 624 cardiac, 611 lesions due to, 617 of heart, 616 Treatment of heart failure, general princi- ples, 219 relation of, to occupation, 273 Tricuspid area, 156 Tricuspid insufficiency, arrhythmia in cases of, 492 blood-pressure in, 492 diagnosis of, 494 effect on circulation, 487 functional, 486 in paroxysmal tachycardia, 672 organic, 486 pathological physiology, 487 pulse in, 492 symptoms of, 489 systolic murmur in, 490 treatment of, 494 variations in murmur, 491 venous pulse in, 488 Tricuspid stenosis, 496 cyanosis in, 498 diagnosis of, 499 effect on the circulation, 497 etiology of, 496 occurrence of, 496 pathology of, 497 presystolic rumble in, 499 pulmonary infarction in, 499 treatment of, 501 Tricuspid valve, demonstration of action of, 12 malformation of, 551 opening of, 78 Trigeminal pulse, 114 Truncus arteriosus, 514 division of, 517 Tuberculosis as cause of arteritis, 340 as cause of endocarditis, 389 in persons with mitral stenosis, 428 in pulmonary stenosis, 532 of the heart, 322 Tumors of the heart, 323 hsemopericardium from, 324 Typhoid fever as cause of Basedow's disease, 684 blood-pressure in, 48 Uremia, blood-pressure in, 40 Urine, albumin and casts in, 212 amount of in cardiac disease, 212 chloride metabolism in, 212 Vagotonie and sympathicotonie, 19 Vagus currents, with heart-beat, 213 with respiration, 213 Vagus effect in producing heart-block, 554 Valve, Eustachian (of the inferior vena cava), 516 Valves, abnormality of, 551 Valves, auriculoventricular, diastolic closure of, 76 738 INDEX. Valves in veins, inclosure of, 71 movements of, 10 position of, in diastole, 12 Valvular areas in auscultation, 156 Vasa vasorum, changes in, in arteriosclero- sis, 328 Vascular crises, blood-pressure in, 40 Vascular sounds, 172 Vasomotor angina, 377 Vasomotor crises, 356 hypotensive, 360 use of nitrites in, 356 Vasotonin, 258 Veins, cardinal, 514 sounds over, 173 umbilical (omphalomesaraic), 514 visible pulsations in, 70 vitelline, 514 Venesection, 221 contraindications to, 222 effect of, in hypertension of intracranial origin, 40 effect of, on the circulation, 222 in aortic insufficiency, 468 in arteriosclerosis, 352 in pulmonary cedema, 207 technique of, 221 Veno-auricular junction, anatomy of, 7 Venous pressure, 197 determination of, 50 effect of, on filling of the heart, 14 in broken compensation, 197 in neurasthenics, 697 in paroxysmal tachycardia, 668 Venous pulse, 70 abnormal types of, 79 diastolic, 79 double, 70 in auricular fibrillation, 79 in auricular paralysis, 79 in extrasystolic arrhythmias, 109 in heart-block, 569 in paroxysmal tachycardia, 663 information furnished by, 80 negative, 70 physiological, 70 positive, 80 presystolic, 79 relation to atmospheric pressure, 71 technique of tracings, 71 visual examination of, 79 visual examination of, differential diagnosis of arrhythmia by means of, 79 Venous tracing, interpretation of, 76 Ventricle, left, pressure within, 25 Ventricle, right, tonicity of, 53 Ventricle, third, 524 Ventricles, filling of, 11 Ventricular muscle, anatomy of, 9 Viscosity of the blood, 59 apparatus for clinical determina- tion of, 59 factors influencing, 60 diet, 60 hydrsemia, 60 number of red blood-cells, 60 Volume curve, method of recording, 11 Vomiting, blood-pressure in, 50 Von Graefe's sign in Basedow's disease, 687 Walking in treatment of heart lesions, 271 regulation of speed and respiration, 272 Water-hammer pulse, 68 Weather, effect of, on cardiac symptoms, 203 Whiskey in cardiac disease, 224 Wiring treatment of aneurism, 650 Work hypertrophy, 282 Work of the heart, 36 Work of the right heart, 51 Worry, effect of, on circulation, 716 Wounds of the heart, 611 control of hemorrhage from, 615 results of operation, 616 suture of, 614 Wrestling, effect of, on the heart, 189 Xiphisternal line as sign of level of dia- phragm, 702 X-ray, cardiac shadow, 133 examination in oblique axes, 134 of adherent pericardium, 605 of sclerotic arteries, 346 magnification of shadow, 132 methods of examination, 132 oblique illuminations, 133 pulmonary shadows, 133 shadow in aneurism, 634 Zander exercises, 271 Slip THE LIBRARY UNIVERSITY OF CALIFORNIA Santa Barbara THIS BOOK IS DUE ON THE LAST DATE STAMPED BELOW. Series 9482