G 000 005 485 8 vIvXwXw THE LIBRARY OF THE UNIVERSITY OF CALIFORNIA LOS ANGELES GIFT OF SAN FRANCISCO COUNTY MEDICAL SOCIETY DISEASES OF THE HEART Diseases of the Heart THORACIC AORTA. BYROM BRAMWELL. M.D., F.R.C.P.E., LECTURER ON THE PRINCIPLES AND PRACTICE OF MEDICINE, AND ON PRACTICAL MEDICINE AND MEDICAL DIAGNOSIS IN THE EXTRA- ACADEMICAL SCHOOL OF MEDICINE, EDINBURGH ; PATHO- LOGIST TO THE EDINBURGH ROYAL INFIRMARY; ADDITIONAL EXAMINER IN CLINICAL MEDICINE IN THE UNIVERSITY OF EDINBURGH. LATE PHYSICIAN AND PATHOLOGIST TO THE NEWCASTLE-ON-TYNE INFIRMARY ; FORMERLY MEDICAL OFFICER TO THE TYNEMOUTH UNION WORKHOUSE HOSPITAL, THE PRUDHOE MEMORIAL CONVALESCENT HOME, THE TYNE FLOATING HOSPITAL, ETC., ETC. "WITH 317 ILXjTJSTI2,.A^TIOIsrS. NEW YORK : D. APPLETON & CO., BOND STREET. 1884. [.-/// Rights Resened.\ Library tioo 3737^ Cn fHentoriam. T. B. v.. 624142 PREFACE. In the following pages, which are based on portions of my Lectures on the Principles and Practice of Medicine, and on Practical Medicine and Medical Diagnosis, I have endeavoured to give a systematic account of the Diseases of the Heart and Thoracic Aorta.^ My attention was early directed to the diseases of the heart, for soon after entering practice I met with a long series of rare and interesting cardiac cases. During the past fifteen years I have been constantly thinking and talking about the subject, and steadily accumulating the clinical knowledge and pathological material necessary for the pro- duction of such a work. The lithographs of naked-eye objects, represent with few exceptions the hearts of patients who have been under my own care during life, and with whose clinical histories I am intimately acquainted. The microscopical lithographs are, with two exceptions, copied from sections made by myself In order to ensure absolute accuracy of representation, the naked- eye specimens were first photographed and then drawn under my immediate personal supervision, while the microscopical objects have been placed directly on the stone from my own drawings. ' The subject niattei' of the work was delivered ahnost exactly as it stands, in the form of lectures to the author's class at the beginning of the winter session 1883-84. viii Preface. I am particularh^ indebted to Professor Turner for his kindness and libcralit}' in allowing me to photograph and reproduce the rare and beautiful specimens which are shown in figs. 1 70', 171, 242, 243, 244, 262, and 281, and which are contained in the Anatomical Museum of the University of Edinburgh. I am also indebted to Professor Greenfield and Dr \V}'llic, with whose kind consent two specimens (figs 169 and 263) which came under m\- notice in the course of my work as Pathologist to the Edinburgh Royal Infirmary, are represented. My thanks are also due to Professor Pettigrew, Drs Walshe, Sansom, Galabin, Eothergill, Green, Macalister, Dudgeon, and The Executors of the late Dr Peacock, for their kindness in allowing me to reproduce some of the figures which have appeared in their respective works ; and to Messrs J. and A. Churchill, Messrs Longmans, Green and Co., and Messrs Macmillan and Co., for permitting me to cop}', or to have electrotypes of cuts, from works which they publish. I must also express my indebtedness to the numerous writers whose opinions are referred to in the text, and more especiall}- to Drs Walshe, Sibson, Sansom, and Galabin. B. B. 23 Drumsheugh Gardens. Edinburgh, .ATay 1884. CONTENTS. CHAPTER I. PACK INTRODUCTORY ANATOMICAL AND PHYSIOLOGICAL RE- MARKS—THE ARTERIAL BLOOD SUPPLY OF THE HEART — THE AUTOMATIC MECHANISM OF THE HEART — THE NERVOUS SUPPLY OF THE HEART — THE CONNECTIONS OF THE SYMPA- THETIC WITH THE HEART — THE CONNECTIONS OF THE PNEUMOGASTRIC WITH THE HEART — THE MANNER IN WHICH THE VAGUS AND SYMPATHETIC NERVES AFFECT THE HEART — THE RELATIONSHIP BETWEEN THE HEART AND THE MINUTE BLOOD VESSELS. . . . . . . . I-45 CHAPTER II. THE GENERAL PATHOLOGY OF THE HEART. . . . 46-56 CHAPTER III. THE CLINICAL INVESTIGATION OF CASES OF CARDIAC DISEASE — METHOD OF CASE-TAKING — SUMMARY OF SYMPTOMS — THE PHYSICAL EXAMINATION OF THE HEART — INSPECTION — PALPATION — PERCUSSION — AUSCULTATION — THE PHYSICAL EX- AMINATION OF THE AORTA AND GREAT BLOOD VESSELS — THE EXAMINATION OF THE PERIPHERAL ARTERIES — THE SPHVGMO- GRAPH — THE EXAMINATION OF THE VENOUS SYSTEM. . 57-295 Contents. CHAPTER IV. PACE DISEASES OF THE PERICARDIUM— ACUTE PERICARDITIS— PERICARDIAL ADHESIONS— INDURATIVE - MEDIASTINO-PERI- CARDITIS — CHRONIC PERICARDITIS — HVDROPES ICARDIUM — PNEUMOPERICARDIUM — H^MOPERICARDIUM. . . 296-359 CHAPTER V. DISEASES OF THE ENDOCARDIUM — ACUTE SIMPLE EN- DOCARDITIS — ULCERATIVE ENDOCARDITIS — CHRONIC ENDO- CARDITIS — CHRONIC VALVULAR LESIONS — MITRAL INCOM- PETENCE — MITRAL STENOSIS— AORTIC INCOMPETENCE — AORTIC STENOSIS— TRICUSPID INCOMPETENCE— TRICUSPID STENOSIS — PULMONARY STENOSIS— PULMONARY INCOMPETENCE. . 360-559 CHAPTER VI. DISEASES OF THE MYOCARDIUM — ACUTE MYOCARDITIS — CHRONIC MYOCARDITIS OR FIBROID DEGENERATION— PARTIAL ANEURISMS OF THE HEART— HYPERTROPHY AND DILATATION — HYPERTROPHY OF THE LEFT VENTRICLE— HYPERTROPHY OF THE RIGHT VENTRICLE— HYPERTROPHY OF THE AURICLES — ATROPHY OF THE HEART — FATTY INFILTRATION — FATTY DEGENERATION— SPONTANEOUS RUPTURE — NEW GROWTHS IN THE HEART. ....... 560-658 CHAPTER VII. THE CARDIAC NEUROSES — PALPITATION — INTERMITTENT ACTION— ANGINA PECTORIS. .... 659-689 Contents. xi CHAPTER VIII. PAGE DISEASES OF THE THORACIC AORTA — ACUTE AORTITIS — ATHEROMA — GENERAL DILATATION — ANEURISMS — COARCTA- TION OF THE AORTIC ARCH. .... 690-749 APPENDIX. THE CARDIOGRAPH. ..... l^^'lll INDEX. ... 775 CORRIGENDA. Page 56, three lines from the bottom, instead of 'g//fl;ged' read 'gff//ged.' Page 10, instead of ' Sedg^wick ' read ' Sedgwick.' Fig. 281, first line of description, instead of 'a bridge of muscular tissue (b) being left between them,' read 'a bridge of muscular tissue being left between them.' LIST OF ILLUSTRATIOxNS. FIG. 1 Heart of Dugong, 2 Bifid Apex in Human Heart, 3 Course of the Circulation, 4 Muscular Fibres of Heart, 5 Do., Do., 6 Diagram of Reflex Theory of Cardiac Contraction, . 7 and 8 Nerves and Ganglia on Surface of Calf's Heart, 9 Diagrammatic representation of the Coronary Plexuses, 10 Do., Do., the Cardiac Plexus, . 1 1 Semi-diagrammatic representation of the Connections of the Sympathetic with the Heart, 12 Semi-diagrammatic representation of the Connections of the Pneumogastric with the Heart, . 13 Semi-diagrammatic representation of the Nervous Supply of the Heart as a whole, 14 The Last Cervical and First Thoracic Ganglia of the Rabbit, ..... 15 Diagram of Reflex Theory of Contraction of the Blood vessels, ..... 16 Diagram of Cheyne-Stokes' Respiration, 17 to 22 Diagrams illustrative of the Mechanism of Cheyne-Stokes' Respiration, 23 Position of the Heart and Great Vessels, 24 Regions on the front of the Chest, . . Alodi 25 Area of Pulsation in a case of Congenital Displace- ment of the Heart, .... 26 Displacement of the Heart by left Pleuritic Effusion, 27 Do., Do., in Cirrhosis of the Lung, 28 Do., Do., the result of Ascites, 29 Do., Do., by an enlarged Liver, 30 Do., Do., the result of Emphysema, 31 Outline of Hypertrophied Left Ventricle, 32 Outline of Hypertrophied Right Ventricle, . 33 Relationship of the Heart to the Lungs, 34 Area of Prsecordial dulness in middle age, . 35 Relationship of the Heart to the surrounding Viscera, Owen, Original, Modified from Dalton, QUAIN, Schweigger-Seidel, Original, Pettigrew, Original, Do., I-AGK 2 Do. Do. Do. Foster, 2 4 8 9 13 17 18 17 23 24 26 Original, 42 ? 60 Original, 76 SlBSON, 94 Hed from Walshe, 96 Original, 106 SiBSON, modified. 108 Do., 109 Do., III Do., 112 Do., 1 12 Von Dusch, 114 Do., "5 SiBSON, 123 Weil, 124 Do., 126 XIV List of Illustrations. 36 Diagrammatic Representation of the Cardiac Cycle, Original, 37 Do., Do., Do., Gairdner & Sharpey, 38 Diagram of the Position of the Cardiac Valves, JModificd from Gee, 39 Diagrammatic Representation of the Cardiac Cycle, Original, 40 Diagram illustrative of Pseudo-reduplication of the Pleart Sounds, ..... Sansom, 41 to 48 Diagrammatic representation of Cardiac Murmurs, Original, 173 49 to 54 Diagrams illustrative of the direction of Pro- pagation of Cardiac Murmurs, . . . Do., 182 55 Sphygmogram in Aortic Stenosis, . . Do., 56 Do., in Mitral Stenosis, . . . Do., 57 and 58 Diagrams of the Effects of IMitral Lesions on the Circulation, .... Do., 217, 59 Diagram of the Effects of Aortic Lesions on the Cir- culation, ..... Do., 60, 61, and 62 IMahomed's modification of Marey's Sphygmograph, 63 and 64 Dudgeon's Sphygmograph, . 65 Marey's Sphygmograph applied to the Wrist, 66 to 76 Sphygmograms in Health and Disease, 77 Dudgeon's Sphygmograph applied to the Wrist, 78 to 124 .Sphygmograms in Health and Disease, 125 Mahomed's method of gauging High Tension, 126 to 138 Sphygmograms in Disease, . 139 and 140 Tracings of Jugular Pulsation, 141 to 144 Naked Eye appearances of the heart in Pericarditis, .... 145 Section through the Healthy Pericardium, . 146 to 157 Microscopical Sections from Pericarditis and Pericardial Adhesions, . 158 Pericardium distended with fifteen ounces of fluid, 159 Distention of the Pericardium with 2)% lbs. of fluid, 160 Outline of the Percussion Dulness in Pericardial Effusion, ..... Do., 161, 162, and 163 The Pulsus Paradoxus. KussMAUL, Ziemssen, and Traube, 350, 164 and 165 Early Endocarditis, 166 Vegetations on the Mitral Valve, 167 Section through the Normal Endocardium, . 168 Ulcerative Endocarditis of the Aortic Valve, 169 Do. Do. Aortic and Mitral, with Rupture of Chorda- Tendinere 170 and 170' Aneurisms on JNIitral Valve, 171 Ulceration of the anterior segment of the Mitral A'alve, 173 Ball-like masses of Micrococci, 174 Section through the aortic valve in Endocarditis, 174' Colonies of Micrococci, .... I'AGE 137 138 140 158 165 -179 •186 213 217 218 Do., 236 Dudgeon , 238 Do., 240 Original, 242-245 Dudgeon , 246 Original, 248 -277 Mahomed, 278 Original, 281 -286 '"riedreich, 292 Original, 300 QUAIN, 303 Original, 304 -306 SiBSON, 320 Do., 320 321 Traube, 350 351 Green, 365 Original 366 QUAIN 367 Onginal 402 Do. Do. Do. 403 Osler, 404 Original, 404 Osler, 404 List of Illustrations. XV Original, 405 ZlEGLER, 405 Original, 416 Do., 417 QUAIN, 422 SiBSON, 422 VTacalister , 423 Do., 423 Original, 424 Do., Do., 425 Do., 436 Do., 442 Do., 445 175 Section through the Mitral Valve in Endocarditis, . 175' Section through a Cardiac Vegetation, 176 Chronic Endo-myocarditis, .... 176' Chronic Endocarditis, .... 177 Aortic and Mitral Valve Segments, . 178 Aortic and Mitral Orifices in the Calf's Heart, 179 Base of the Ventricles in Systole, 180 Cross section of the Ventricles in Systole, . 181 Aortic and Mitral Valve Segments, . 182 Section through the Left Auricle of a Child, 183 Do., Do., 184 Effects of a Mitral Lesion on the Venous Circulation, 185 Direction of propagation of Mitral Systolic Murmurs, 186, 187, and 188 Sphygmograms in Mitral Regurgitation, 189, 190, and 191 Cardiograms in Mitral Regurgitation, Sansom & Galabin, 448 192 Pulse Tracing in Pernicious Anasmia, . . Oi-igiiial, 453 '93) ^94) 195' 196) 197) and 198 Naked Eye appear- ances of the Heart in Mitral Stenosis, . . . Do., 478 199 Direction of propagation of the Presystolic Murmur, Do., 485 200 Diagram of Diastolic Mitral Murmurs, . . Do. , 486 201 Diagram of Cardiac Murmur and Sounds in Mitral Stenosis, ..... Do., 488 202, 203, 204, and 205 Cardiograms in Mitral Stenosis, Galabin & .Sansom, 489 206 Pulse Tracing in Mitral Stenosis, 207 Aortic Valve Flaps, ..... 208 Ulceration of Aortic Valve Flaps, . 209 Atheroma and Disease of Aortic Valve Flaps, 210 Aortic Regurgitation and Dilatation of the Left Ventricle, ..... 211 Direction of propagation of Aortic Diastolic Murmurs, 212 and 213 Sphygmograms in Aortic Regurgitation, 214 and 215 Cardiograms in Aortic Regurgitation, 216 Direction of propagation of Aortic Systolic Murmurs, 217 and 218 Sphygmograms in Aortic Stenosis, . 219 and 220 Pulse Tracings in Pernicious Anaemia, 221 Direction of propagation of Tricuspid Systolic Murmur, 222 to 228 Constriction of the Pulmonary Orifice, Original, 492 QUAIN, 499 Original, 502 Do., 502 Do., 503 Do., 512 Do., 514 Galabin, 515 Original, 525 Do., 526 Do., 529 Do., 536 229 Course of the Circulation in the Fcetus, 230 Direction of propagation of Pulmonary Systolic Murmur, ..... 231, 231,' 232, and 233 Muscular Fibres in Myocarditis, 233 and 234 Sections through the Left Ventricle in Chronic Mitral Disease, 235 Atrophy of the Papillary Muscles, . 236 Endo-peri-myocarditis, 237 Subacute Myocarditis, 238, 239, 240, and 241 Chronic Myocarditis, Peacock, 544, 545 Modified from QuAlx, 546 Original, 550 Do., 562 Do., 563 Do., 568 Do., 568 Do., 568 Do., 569 XVI List of Illiistraiions. 242 Aneurism of the Left Ventricle, 243 and 244 Aneurism of the Septum Ventriculorum, . 245 Section through a commencing Cardiac Aneurism, . 246 Outline of Hypertrophied Left Ventricle, . 247 and 248 Cardiograms in Hypertrophy of the Left \'entricle, . . . 249, 250, and 251 Sphygmograms in Hypertrophy of the Left Ventricle, .... 252 Hypertrophy of the Right Ventricle, 253 Cardiogram in Hypertrophy of the Left Auricle, 254 Cardiogram in Dilatation of the Left Ventricle, 255 and 256 Atrophy of the Heart, 257 Fatty Infiltration of the Heart, 258 Fatty Degeneration of the Heart, . 259 and 260 Spontaneous Rupture of the Heart, 261 and 262 Tumours of the Heart, 263 Blood-cyst in the Heart, 264 Section of Aorta, in Atheroma, 265 Do., Do., 266 Sphygmogram in Atheroma, 267 Saccular Aneurism of the Abdominal Aorta, 268 and 269 Aneurisms of the Thoracic and Abdominal Aorta, ...... 270 Aneurism of the Sinuses of Valsalva, 271 and 272 Section through the wall of an Aortic Aneurism, 273 and 274 Obliterative Endarteritis, . 275, 276, 277, and 278 Sphygmograms in Aneurisms, 279 and 280 Sphygmograms in Aneurism, 281 Rupture of an Aortic Aneurism into the Left Auricle, 282, 283, 284, 285, and 286 Aneurism of the commence- ment of the Thoracic Aorta, 287 and 288 Aneurism of the transverse portion of the Aortic Arch, ..... 289 Aneurism rupturing into the Q£sophagus, . 290 Erosion of the Spine by the pressure of an Aneurism, 291, 292, 293, and 294 Clots from the interior of Aneurisms, 295 and 296 Sphygmograms from a case of Aneurism, . 297 and 298 Coarctation of the Thoracic Aorta, 299 Galabin's Cardiograph, .... 300 Marey's Tambour, ..... 301 Normal Cardiographic Tracing, 302 Normal Cardiographic Wave, 303 Heart Curve from the Ventricle of a Cat, Original, 576 Do., 576 Do., 577 Von Dusch, 564 G A LAB IN, 595 Original, 596 Von Dusch, 601 Galabin, 602 Do., 622 Original, 630 Do., 635 Do., 641 Do., 653 Do., 654 Do., 656 Do., 692 Do., 693 Do., 696 Do., 698 Do., Do, Do.. Do., Do., 715 Do., 716 Do.. 720 Do.. Do., Do.. Do., Do., Do., Walshe, Galabin, Marey, Galabin, Eiilayged from Galabin, Foster, 721 304 Simultaneous Tracings, from the interior of the Right Auricle and Right Ventricle, and of the Cardiac Impulse in the Horse, . . Ch.\uve.\u & Marey, 305 to 317 Cardiographic Tracings in disease . Galabin & Sansom, 735 747 754 756 759 760 761 762 763 DISEASES OF THE HEART. CHAPTER I. INTRODUCTORY ANATOMICAL AND PHYSIOLOGICAL REMARKS THE ARTERIAL BLOOD-SUPPLY OF THE HEART. THE AUTOMATIC MECHANISM OF THE HEART. THE NERVOUS SUPPLY OF THE HEART. THE CONNECTIONS OF THE SYMPATHETIC WITH THE HEART. THE CONNECTIONS OF THE PNEUMOGASTRIC WITH THE HEART. THE MANNER IN WHICH THE VAGUS AND SYMPATHETIC NERVES AFFECT THE HEART.- THE RELATIONSHIP BETWEEN THE HEART AND THE MINUTE BLOOD-VESSELS The consideration of the Diseases of the Circulatory System is a subject of great importance, for it embraces many affections which are of every day occurrence in practice, which entail a vast amount of suffering, and which are very frequently the cause of death. The diseases of the Circulatory System include^ — 1. The diseases of the Heart and Pericardium. 2. The diseases of the Arteries. 3. The diseases of the Veins. In treating of the Diseases of the Heart and Pericardium, I shall first describe the methods of clinical examination which are in common use for investigating the condition of these structures, directing attention, as I proceed, to those ' The diseases of the Lymphatics are sometimes included under this head, but they are, I think, more appropriately considered under the disorders of the Chylopoietic \'iscera. A 2 Diseases of the Heart. points in their anatomy, physiology, and pathology, which are essential for the due comprehension of our subject. After the reader has become thoroughly familiar with these points, I shall consider the individual affections of the heart and pericardium in detail. TRELIMINARY ANATOMICAL AND PHYSIOLOGICAL CONSIDERATIONS. The heart— the central organ of the circulation— may be regarded as a muscular pump ; or, speaking more accurately, it may be said to consist of two^ muscular pumps, — the systemic and pulmonary hearts respectively. Each half or pump consists of two chambers, viz., (i) a receiving chamber or auricle, and (2) a propelling chamber or ventricle. ' At an early period of fcEtal life, as in the permanent state of the Dugong * (see fig. l), the heart is so deeply cleft from the apex towards the base, as almost to give the idea of two separate ox^TiXi's..— Carpenter'' s Physiology, p. 271. In the adult heart of man, the remains of the deep cleft are sometimes seen in the form of a bifid apex (see fig. 2). Fig. I. — Heart of Dugong seen anteriorly: shows bifid apex, s, right auricle. q, right ventricle, t, left auricle, r, left ventricle, u, aorta giving off innominates, left carotid and left subclavian arteries, v, pulmonary artery bifurcating and pro- ceeding to right and left lungs. — {After Owen.) Fig. 2. Apex of the human heart (half the natural size) showing a deep cleft, A, between the two ventricles. Prcliiuinary Considerations. 3 The function of the auricle is to receive the blood which is carried to it by the great veins, to store up that blood for a brief period {i.e. the period corresponding to the ventricular systole), and to transmit it to the ventricle. The function of the ventricle is to propel the blood, which it receives from the auricle, into the great artery which arises from it, and thence through the arterial system and round the vascular circle.^ The backward flow of blood from the ventricle to the auricle is partly prevented by the auriculo-ventricular valve segments, partly, as Ludwig, Hesse, and Macalister have shown, by the contraction of the muscular wall of the ventricle itself, i.e. by the contraction of the muscular fibres which surround the valvular orifice. The backward flow from the arterial system (aorta or pulmonary artery) into the ventricle, is prevented by certain valvular arrangements, which I shall afterwards describe in detail ; while the backward flow of blood from the auricles to the veins is partly prevented by the contraction of the muscular fibres, which are placed at their points of termination, i.e. where the veins join the heart, the systemic venous circula- tion being still further protected from the ' backwash,' which not unfrequently occurs through the tricuspid, even in con- ditions of health, by the valves of the veins themselves. By these means the onward flow of blood in one — a forward — direction is accurately maintained. The course of the circulation is diagrammatically represented in figure 3, while ' the passage of the blood through the heart takes place in the following manner : — - At the commencement ot the auricular diastole (and while the ventricular systole is taking place) blood begins to flow from the great venous trunks into the auricular ' The chief cause, ol the motion of the blood, is the heart, but the onward passage of blood is also aided by the contraction of the blood vessels. This contraction is partly the result of elasticity, and partly due to an active contraction of the muscular coat. Diseases of the Heart. KIG. 3. Course of the Circulation. 5 Description o/FlG. 3. — Diagraiiintatic representation of the course of t lie circulation. ^Modified from Dal ton. ) The arrows indicate the course of the circulation. RV, the right, and LV, the left ventricles. RA, the right, and LA, the left auricles. Lungs, Liver (description in full). S, Stomach. Spl, Spleen. In, Intestines. K, Kidneys. Sc, Supra-renal capsules. P, Pelvic viscera. LE, Lower extremities. UE, Upper extremities and superficial parts of the head and neck. B, Brain. Sp, Spinal cord. PA, Pulmonary artery. PV, Pulmonary veins. AA, Branches of the ascending aorta. DA, Descending aorta. SV, Superior cava. IV, Inferior cava. 1 Cccliac axis, sending branches to the spleen, stomach, and liver. 2 Mesenteric arteries. 3 Renal arteries. 4 Arteries to the pelvic viscera. 5 Arteries to the lower extremities. 6 Arteries to brain and spinal cord. 7 Arteries to brain. 8 Arteries to spinal cord. 9 Arteries to the upper extremities and superficial parts of the head and neck. 10 Hepatic veins. 1 1 Portal vein. 12 Veins from the intestine (superior and inferior mesenteric veins). 13 Veins from the stomach and spleen. 14 Splenic vein. 15 Coronary and pyloric veins from the stomach. 16 Renal veins. 17 Veins from the pelvic viscera. 18 Veins of the lower extremities. 19 Veins from the brain and spinal cord. 20 Veins from the brain. 21 Veins from the spinal cord. 22 Veins from the upper extremities and superficial parts of the head and neck. 6 Diseases of tJie Heart. cavities ; as soon as the ventricular diastole occurs the ven- tricles dilate, the pressure in the ventricular cavities becomes negative, and blood flows from the auricles into the ven- tricles through the auriculo-ventricular (mitral and tricuspid) orifices ; before long the auricles become full of blood, and the auricular systole occurs ; the muscular contraction com- mences in the walls of the great veins, and spreads in a peristaltic manner over the auricles, which sharply contract and discharge their blood into the ventricles, distending them, and bringing the segments of the auriculo-ventricular valves into close apposition ; the muscular contraction now passes to the ventricles, the auriculo-ventricular orifices are firmly closed by the muscular contraction, to which I have alread}' referred, the valve segments are tensely stretched, the arterial valves are burst open, and the ventricles empty themselves into the aorta and pulmonary artery ; the great arteries become distended, the segments of the aortic and pulmonary valves are floated together ; the recoil of the aorta and pulmonary artery then occurs, and the aortic and pulmonary valves are closed and stretched. Now in studying both the physiology and pathology of the heart, and in investigating its diseases at the bedside, it is essential to keep this fact constantly in view, that the heart is not merely a mechanical, but that it is also a muscular pump, and that, as Professor Michael Foster so lucidly points out, its action consequently presents problems which are partly mechanical and partly vital} I cannot insist too strongly upon the importance of looking at the heart both as a mechanical pump and as a vital organ ; it is in fact the base upon which an intelligent comprehension of the physiology and pathology of the heart, and of the symptomatology, diagnosis and treatment of its diseases, must be founded. But although the heart is a muscular organ, it differs from the other muscles of the body in several important particulars. They are as follows : — ' A Text Book of Physiology, p. IJ5. Peculiarities of the Cardiac Aliiscle. 7 In \}aq first place, although the cardiac muscle is involun- tary in its action, it is transversely striated in its structure — a fact which, as Gaskell has pointed out, explains many of the peculiarities of the cardiac muscle. Dr Gaskell looks upon the heart as a specially modified portion of the vascular system ; 'the heart is to be considered,' he says, 'as a piece of artery or vein, the muscular walls of which have developed in a special manner. The keynote therefore of the peculiarities of the cardiac muscle consists in its structural position, intermediate between unstriped and striated muscle fibre. Muscular tissues exhibit three different modes of responding to stimulation according to their structure. These modes may be expressed by saying that certain muscles possess essentially the power of "tonic contraction," others the power of "rhythmical contrac- tion," and others that of " rapid contraction." A comparison of the tetanising action of a strong interrupted current upon a strip of muscle from the bladder of the tortoise and from the heart of the tortoise with the ordinary tetanus curve of the frog's gastrocnemius shows clearly the difference of the three kinds of muscular tissue. ' The unstriped muscle of the bladder contracts slowly after a long latent period, the contraction increasing steadily in force during and even after the cessation of the tetanizing current, and then the strip returns with excessive slowness to its original length. In other words, we see a prolonged tonic contraction as the result of the stimulation. 'With the striated muscle we have the well known curve of tetanus composed of the superposition of a series of rapid contractions. ' The cardiac strip gives a curve which is intermediate between the two, and may be described as consisting of a long continued tonic con- traction upon which a number of rapid contractions are superimposed. These separate rapid contractions never succeed one another so quickly as to fuse together. The cardiac muscle then, when tetanized, gives, in virtue of its relationship to unstriped muscle, a tetanus of tonicity (to use Ranvier's expression), and at the same time a series of rapid contractions in consequence of its affinity to ordinaiy striated muscle. When the vitality of the tissue is impaired by exhaustion, by injurj^, by malnutrition, the cardiac muscle loses its power of rapid contraction, and the less- specialized tonic power alone remains, the inuscle strip tetanized when in that condition contracts with a prolonged tonic contraction in the same way as unstriped muscle. ' In another respect too, the intermediate position of the cardiac muscle between the slowly contracting, slowly exhausted unstriped muscle, and the rapidly contracting, easily exhausted striated muscle, is clearly shown ; the vitality of unstriped muscle after the death of an animal is wonderfully long ; the irritability of the cardiac muscle after death is Diseases of the Heart. that of the ordinarj' striated less than this, but decidedly greater than muscles.'^ Secondly, The structure of its fibres is somewhat different from the structure of the voluntary muscles. {a) The fibres of the heart are made up of quadrangular portions (see fig. 4), each of which contains a nucleus, and each of which may, therefore, be regarded as a distinct muscle cell. Fig. 4. — Six muscular fibre-cells from the heart, magnified a,i^ diameters. (After E.A.S., Quaiii's Anatomy, Ninth Edition']. a, line of junction between two cells; b,c, branching of cells. (From a drawing by Mr J. E. Neale.) iU) They have no sarcolemma. .{c) They are longitudinally as well as transversel\- striated, and, in good sections, are seen to be composed of a number of minute rods or fibres running parallel to each other. {d^ They freely anastomose, the connections being formed ' The Journal of rhysioloi;y, vol. iv., No. 2, p. II 6. Peculiarities of the Cardiac Muscle. g by branches given off here and there, from the muscle cells of which the fibres are composed. (See fig. 5.) Fig. 5. — Muiciila)- fibres from tlie heart, magnified, showing their cross stria, divisions, and junctions. {After Schweigger-Seidel, from Quains Anatomy, Ninth Edition. \ The nuclei and cell-junctions are only represented on the right-hand side of the figure. {e) They seem to be difiercntly affected by electricity, the Faradic current, according to Zicmssen's observations, being much less efficacious in producing contractions and alterations in rhythm than the galvanic. Thirdly, its action is constant, and its contractions rhyth- mical and automatic. Amongst the vital problems connected with the heart, some of the most prominent and important are : — (i) The manner in which it receives its arterial blood supply. (2) The construction and mode of action of the mechanism, by which its contractions are produced and regulated (its lo Diseases of the Heart. automatic muscular and motor nerve arrangements), the scnsorium is informed of its condition (its scjisory nerve arrangements), the nutritive condition of its muscular fibre is maintained and regulated (its trophic nerve supply). (3) The construction and nature of the nerve arrange- ments, by means of which it is brought into relationship with the other parts of the vascular system, and with the other organs of the body. The A rterial Blood-supply of the Heart. As we all know, arterial blood is conveyed to the car- diac muscle by the coronary arteries ; and until quite recently it was supposed by many of our leading physiologists and physicians, that in consequence of the relative positions of the parts, the orifices of the coronary arteries must of neces- sity be closed during the systole of the ventricle — the valve flaps being pressed against the orifices of the coronary arteries by the blood-stream in its passage from the ven- tricle into the aorta. The recent experiments, however, of Martin and Sedgwick, seem conclusively to show that this supposed closure does not occur, and that the coronary, like all the other arteries of the body, are distended during the systole of the heart. These observers have shown, by means of careful cardiographic tracings, that the blood-waves in the coronary arteries and carotids are exactly synchronous both in normal and diseased states of the circulation. It seems certain, therefore, as Dr George Balfour and others had previously argued, that the blood is propelled into the coronary arteries during the systole of the heart. TJie Automatic McchaiiisDi of the Heart. The nervous mechanism of the heart is extremely com- plicated, and the manner in which it acts is far from being perfectly understood. It is a subject, however, of the greatest importance, and we must, therefore, consider it in some detail. Mechanisiu of tJic Hearf s Beat. 1 1 In the Jijsi place, it is necessary to remember that the con- traction of the heart is automatic, i.e. it is due to impulses arising within the heart itself, and that, in conditions of health, the action of the two sides of the heart, i.e. of the two pumps, is synchronous. Under ordinary circumstances the heart beats in a perfectly rhythmical and regular manner, the number of contractions being, in the adult male, about 72 per minute. Until recently it was supposed that the rhythmical action of the heart was entirely due to the periodical and orderly discharge of motor nerve force in the nerve ganglia, which are scattered through the organ, but recent obser- vations, more especially of some German physiologists and the brilliant researches of Gaskell, seem to show that the influence of the cardiac ganglia is not indispensable, and that the muscular fibre itself, in some of the lower animals at all events, possesses the power of rhythmical contraction. Gaskell's observations seem to prove conclusively, that, in the tortoise, the automatic action of the heart does not depend upon any special rhythmical nervous apparatus, but that it is due to a property of rhythmical contraction inherent in the muscular tissue itself. It is perhaps premature to conclude that the automatic contractions of the human heart are produced in exactly the same manner as the automatic contractions of the heart of the tortoise. We may, however, safely say, that in man, the rhythmical action of the heart must be due, either to the periodical and orderly discharge of motor nerve force from the ganglia which it contains, or to a rhythmical property possessed by the muscular tissue independently of any special nervous mechanism ; and if we may judge by analogy, the latter view is possibly the correct one. And this we may term the first step in the comprehension of the mechanism of these complicated arrangements. In the second place, it would appear that the stimulus to muscular contraction is the presence of blood, or rather the presence of blood under a certain pressure, in the cardiac 12 Diseases of the Heart. cavities.^ If the pressure is too low the stimulus is insuffi- cient, and the muscle does not contract. If, on the other hand, the pressure is too great, over-distention and a para- lytic condition may result. Indeed the recently published experiments of Sewall and Donaldson seem to prove ' that, within its working limits of internal pressure, the heart muscle has a remarkable power of accommodating the intensity of its discharges of energy, to the resistance to be overcome.' ^ 'A fact continually forced upon our attention,' say these writers, ' was the great dependence of the systole, as to its energy and completeness, upon the amount of fluid within the heart. Particularly was this noticed in regard to the thin walled sinus and auricles, when isolated in the man- ner to be described. Within tolerably low fluid pressures, the sinus and auricles become so distended as to be powerless to contract ; as the pressure within them is reduced they contract feebly, and when the quantity of blood flowing into them is only just sufficient to bring about full distension during diastole, they contract powerfully, and empty them- selves completely at each beat. As the supply of blood is further lessened by lowering the pressure flask, the contractions apparently again become feebler, and in the sinus hardly visible.' ^ The exact manner in which the cardiac muscle is stimulated by the presence of blood under a certain pressure is obscure. If the muscular contraction can occur independently of the ganglia, we must suppose either that the muscular fibre is dir-ectly stimulated by the mechanical stretching which it undergoes when the cardiac cavities become dis- tended ; or, that the contraction is indirect, and is due to stimulation of the fine nerve fibres'* which, as Schweigger-Seidel ^ has shown, form a rich plexus in the endocardium. If we grant that the ganglia are concerned in the process, we may suppose, as some physiologists have for long held, that the mechanism is a reflex one. A cardiac ganglion- cell may be regarded as the centre of a reflex arc, to which a sensory nerve fibre passes from the endocardium, and from which a motor nerve ' In some of the lower animals, the frog for instance, the heart continues to beat even after the cavities have been cleared of blood, and indeed when they are almost empty of fluid. In the frog, therefore, the presence of blood is not absolutely necessary to produce cardiac contractions, but it is nevertheless probable that the pressure of the blood in the cardiac cavities, under ordinary circumstances, acts as a stimulus, and excites the contraction of the cardiac muscular fibres. - The Journal of Physiology, vol. iii. p. 361. ' Loc. cit. p. 361. *■ This view necessarily supposes that these fine nerve fibres are motor. ' Quoted by Power, Carpenter'' s Physiology, p. 276. Automatic Mechanism of the Heart. 13 fibre proceeds to the cardiac muscle (see fig. 6) ; the reflex mechanism being thrown into action by the presence of blood, under a certain pressure, in the cavities of the organ. Fig. 6. — Diagrammatic refresentation of the reflex mechanism by which [it has been theorised) the cardiac imticle is thrown into contraction, under the influence of the blood pressure. E',E, the endocardium ; B, the blood in the cardiac cavity ; M, the muscular fibre of the heart ; G, ganglion cell, the reflex centre ; n, sensory nerve fibre conducting the impression generated by the blood pressure on the sensory nerve terminations under the endocardium to the reflex centre ; n', motor nerve fibril conducting the impulse from the reflex centre to the muscle. In the third place., the experiments of Gaskell, and of Sewall and Donaldson, seem to show that in the frog and tortoise at least, and when the heart is acting normally, the motor im- pulse originates in the sinus, and passes from the sinus to the muscular fibres of the auricle, and thence to the ventricle, the rhythm of the sinus determining that of the whole heart. Those authorities who believe that the automatic action of the heart is due to the periodical discharge of its motor ganglia, necessarily conclude, in order to explain these results, that the action of the ganglia, which are situated in the sinus venosus, is more powerful than that of the ganglia situated in other parts of the organ ; and indeed some authorities have sup- posed that the ganglia of the sinus venosus are the true auto- matic centres, while the action of the other ganglia requires to be excited reflexly, or in some other manner. The supporters of the neurotic theory further believe that the sequence of the cardiac contractions (the fact that the contraction of the 14 Diseases of the Heart. auricle follows at a regular interval upon the contraction of the sinus, and the contraction of the ventricle at a regular interval upon that of the auricle) is due to nervous influences. Dr Gaskell, whose experiments seem to show, as I have already mentioned, that the automatic rhythm originates in the muscular tissue itself, explains the fact that the contractions originate in the sinus, by the peculiar structure of the cardiac muscle in this part of the heart ; while he states that the sequence of the contraction of the ventricle to the auricle is not due to separate stimuli passing along nerve fibres from the sinus to the ventricle — not, in short, to any nervous mechanism— but to the fact that a wave of con- traction passes directly from the muscular fibres of the auricle to the muscular fibres of the ventricle, through the muscular fibres forming the auriculo-ventricular groove. The pause, or, more correctly, the alteration of rate in the progress of the contraction wave, which takes place between the contraction of the auricle and the contraction of the ventricle, is, he says, due to an alteration in the conducting power, which naturally exists at the auriculo-ventricular ring. ' This diminished conducting power or natural block, exists not only because the auriculo-ventricular muscular ring is narrow, and that a somewhat abrupt change occurs in the direction of the muscular fibres along which the contraction wave passes when it reaches and leaves this ring, but essen- tially because the structure of the muscular fibres here is different from those of the auricle or ventricle. ' The muscle fibres throughout the heart ^ are,' he states, ' of the same type, any differences which are seen are differ- ences in the prominence of the various structural peculi- arities of the cardiac type of muscle, and are not so great as the differences between unstriated and striated muscle fibres. Thus all the muscle fibres are, to a greater or less extent, transversely striated ; but the prominence of this striation varies considerably. Similarly the thickness of the fibre, the extent of parallelism of its edges, the size of the nucleus in relation to the size of the fibre, and therefore the extent of crowding ' He is speaking, it must be remembered, of the adult heart of the tortoise. A^itoniatic JMechanisiu of tJie Heart. 15 of the nuclei in any strip, all present differences in different parts of the heart. The greatest contrast is seen when the muscular fibres of the ground layer in the sinus are teased out and compared with the muscle fibres of the spongy tissue of the ventricle. The sinus muscle fibre is thin and delicate, tapering somewhat at both ends, with a large central oval nucleus which causes a distinct bulging of the fibre ; the sub- stance of the fibre shows a striation which is decidedly indis- tinct, presenting often a granular rather than a distinct banded appearance. On the other hand, the ventricular muscle fibre is boldly and strongly striated, it is much thicker than that of the sinus, its edges are parallel, and the thin elongated nucleus is small in comparison to the size of the fibre. The muscle fibres of the reticulated tissue of the auricle are not so large or so coarsely striated as those of the ventricle, though larger and much more distinctly striated than the sinus muscle fibres. Their edges also are more parallel than in the fibres of the sinus. The muscular ring forming the junction of the auricles and ventricle, and, to a certain extent, the whole junction wall joining the two auricles, are composed of muscle fibres, with a structure intermediate between the sinus and the auricle muscles. The nuclei are large, conspicuous on section both in size and number, the striation is not so well marked as in the bulged portion of the auricles, and the fibres are thin and delicate, with somewhat parallel edges. ' Such a structure as above described is very suggestive, not only as an explanation of the pauses which occur natur- ally in the course of the peristaltic wave of contraction, but also of the differences of rhythmical power exhibited by different parts of the heart.' ^ Dr Gaskell, therefore, conceives ' that the variations in the rhythmical power and in conductivity, which are characteristic of the different parts of the adult heart of the tortoise, may all be accounted for on the supposition, that the development of the muscular tissue of the originally tubular heart has not proceeded at the same rate throughout the tube, so that in the adult heart greater variations in rhythmical power arc ' Journal of riiysiology, vol. iv. pp. 72, 73. 1 6 Diseases of tJie Heart. apparent in the different sections of it, than in the original tubular heart ; the peristaltic wave of contraction which originally passed smoothly from end to end, passes finally along a tube of irregular calibre, the muscular walls of which have become so modified in their rates of contraction and conduction, as well as in the arrangement of the fibres, as to form out of a simple peristaltically contracting tube such an efficient muscular pump as is represented by the adult heart.^ ' The conception advanced above, that the rhythmical beating of the heart is due to a series of peristaltic con- tractions which start from that particular portion of the muscular tissue of the heart in which the property of auto- matic rhythm has been most largely developed, brings the heart's action into harmony with the rfest of the vascular system and with the rhythmical properties which are so often manifested by the less specialized forms of muscular tissue.'^ Space will not allow me to detail the facts and arguments on which Dr Gaskell founds this theory, which obviously has most important practical bearings on the pathology of the human heart. I would, however, strongly advise my readers to peruse the original for themselves. In the fourth place, Gaskell has distinctly proved that the ventricle is supplied with afferent nerve fibres, which are ' able to regulate the force of the auricular contractions, as well as in all probability the rate of rhythm. It is then conceivable that the function of many of the nerve fibres which pass into the ventricle is by their action upon the force of the auricular contractions to regulate the amount of blood thrown into the \-entriclc, and therefore the amount of work done by the heart.' ^ But although the movements of the heart are automatic, it is intimately connected both with the sympathetic and cerebro- spinal nervous centres ; and its action can, as each one of us so well knows, be readily affected by general nervous influences. But in order that this most important and difficult part of our subject may, if possible, be clearly understood, I must now describe the nervous supply of the heart in some detail. ' Journal of Physiology, vol. iv. p. 77. - Loc. cit. p. 80. ^ Loc. cit. p. 92. The Nervous Supply of the Heart. i 7 Delicate nerve fibres are met with in considerable numbers both on the surface and in the substance of the heart ; and nodular enlargements, which microscopic examination has shown to be true nervous ganglia, i.e. to contain nerve cells, are abundantly distributed on certain of these nerve fibres, and on the numerous points of junction which certain of the fibres make with each other. In the human subject the nerves of the heart are neither so numerous nor so distinct as in some of the lower animals, as, for example, the calf (see figs. 7 and 8) ; but even in man ' the surface and substance of the heart are enveloped in a more or less uniform plexus.' (^The Physiology of the CircnlatioUy by J. Bell Pettigrew, p. 298.) FIG. 7. FIG. 8. Fig. 7. — Nerves and gangliaon the anterior surf ace of the calf 's heart. {After Pettigrew.) a, b, pulmonary artery and aorta with nerve-plexuses and ganglia. ?', de- scending cava with nerve-plexus and ganglia, c, right auricle, d, left auricle. e. Nerves and ganglia distributed on right side of heart. /, ditto on left side. g, anterior coronary vessels covered with nerve-plexuses and ganglia. Fig. 8. — Nervcsandgangliaonthcposteriorsurfaceofthecalfs heart. {After Pettigrew, ) i, descending cava, c, nerves and ganglia on right auricle, d, ditto on left. e, nerves and ganglia on right ventricle, f ditto on left. /, great nerve-plexus and ganglia covering coronary sinus (r) and extending itself on the right (//), left (/), and posterior coronary vessels, and the right {e) and left (/) ventricles generally. The ganglia in this case are very numerous, particularly on the coronary sinus (r). B 1 8 Diseases of the Heart. Both nerve fibres and nerve cells are most numerous and most distinct in the grooves which contain the larger branches of the coronary arteries, and anatomists have consequently described a rigJit and a left coronary plexus. The coronary plexuses (see fig. 9) may be said to be composed of branches proceeding to the heart from the so-called cardiac plexus, which, to a large extent at least, surrounds the arch of the aorta. The right coronary plexus (R C P) accompanies the branches of the right coronary arter)^, and sends branches (a, b) both to the right auricle and right ventricle. It receives branches (c, d) from both the superficial (S C P) and deep (D C P ) cardiac plexuses (see fig. 10) the composition of which I shall presently describe. The left coroftary plexus (L C P), which is larger than the right, is composed of two primaiy divisions (represented as one ganglion cell in the figure), corresponding to the primary'- divisions of the left coronary artery. The branches proceeding to it (e) are almost entirely derived from the left half of the deep cardiac plexus (D'C'P'), a few filaments only (f) passing to it from the right half (DPC). The branches proceeding from it (g, h, i) are distributed to the left auricle and to both ventricles. RA aY— Fig. 9. — Diagrammatic representation of the coronary plexuses. RCr, right, and LCP, left coronary plexuses; RV, right, and LV, left ventricles of the heart ; RA, right, and LA, left auricles ; SVC, superior vena cava, a, branch of the right coronary plexus to the right auricle ; b, to the right ven- tricle ; c and d, branches proceeding to the right coronary plexus from the super- ficial, and deep cardiac plexuses respectively ; e and f, branches proceeding to the left coronary plexus from the left and right halves of the deep cardiac plexus respectively ; g, branch proceeding from the left coronary plexus to the left auricle ; h, to the left ventricle ; i, to the right ventricle, The Coronary Plexus of Nerves. 19 TJie cardiac plexus (see fig. jo, S C P, D C P and D'C'P') may be described as partly surrounding the arch of the aorta. In it all the cardiac branches of the sympathetic and of the pneumogastric and its branches, terminate, and from it, branches proceed to the heart. In this great cardiac plexus the numerous nerve filaments, proceeding to and from the heart, are re-arranged and re-distributed, and by this means the heart is brought into most intimate connection with many distant parts — a connection which the practical physician should always keep in view, for it explains many of the symptoms (apparently unconnected with the heart) which are met with in association with cardiac disease. The cardiac plexus has been artificially divided by an- atomists into two 'parts, which are respectively termed the superficial and deep cardiac plexuses. The sifpe?'Jicial car-diac plexus (S C P) lies for the most part in the concavity of the aortic arch. In it the first, or superficial cardiac nerve of the left side (I'C'N'), and the lower cervical branch of the left pneumogastric (8', fig. lo) terminate ; and from it branches (c) proceed to the right coronary plexus. It also gives a few small filaments (j and k) to the pulmonary artery and anterior pulmonary plexus of the left side. The deep cardiac plexus (D C P and D' C P'), which is considerably larger than the superficial, is situated ' behind the arch of the aorta, between it and the trachea, and above the bifurcation of the pulmonary arteiy.'i In it, all the branches of the sympathetic and pneumogastric pro- ceeding to the heart, except the first or superficial cardiac branch of the left sympathetic and the lower cervical branch of the left pneumo-gastric, terminate. The deep cardiac plexus is described as consisting of two halves (right and left). The right half{T> C P) sends branches to — (i.) The right coronary plexus (d). (2.) The right auricle (1). (3.) The left coronary plexus (a few filaments) (f). The great majority of the branches of the Icfi half (e) proceed to the left coronary plexus ; a small number (o) passing to the superficial ' Q^tain's Anatomy, Ninth Edition, vol. i. p. 661, from which I have largely drawn in this description. 20 Diseases of the Heart. cardiac plexus. A few filaments (the small branch above the letter k in fig. 12), proceed to the anterior pulmonary plexus on each side.^ V- ICN 3CN DCP RA- SV- D'C'P' Fig. 10. — Diai^raininatic rcpresentatioii of tlic cardiac plexus. The different divisions of the plexus are shown as ganglion cells. SCP, superficial cardiac plexus ; DCP, right, and D'C'P', left halves of the deep cardiac plexus ; ICN, first or superficial cardiac nerve on the right side ; I'C'N', first or superficial cardiac nerve of the left side, 2CN, right, and 2'C'N', left middle cardiac nerves; 3CN, right, and 3'C'N', left lower cardiac nerves; 8', lower cervical branch of the left ]ineumogastric proceeding to the superficial cardiac plexus, 9, 9, branches of the right pneumogastric proceeding to the right half of the deep cardiac plexus ; r'c'l' and 9', branches of the left recurrent largyngeal nerve proceeding to the left half of the deep cardiac plexus ; c, branch from the superficial cardiac plexus to the right coronary plexus ; j, k, branches to the pulmonary artery and pulmonary plexus of the left side, d and f, branches from the right half of the deep cardiac plexus to the right and left coronary plexuses, respectively ; 1, branch to the right auricle, e, branches from the left half of the deep cardiac plexus to the left coronary plexus ; o, branch to the super- ficial cardiac plexus. The other letters have the same significance as in fig. II. ' According to Pettigrew a few of the branches forming the superficial cardiac plexus pass backwards and appear on the posterior surface of the heart ; while a certain number of the branches of the deep cardiac plexus pass forwards to appear on its anterior surface {Physiology of the Circtilntion, p. 298). The Cardiac Plexus of Nerves. 21 The cardiac plexus then is a 'junction' at which impulses passing to and from the heart may be transferred from one nerve path to another, and by means of which communica- tions are established between the heart and distant parts. The ' main lines ' which pass between the nerve centres and the heart are the sympathetic and pneumogastric. In order to complete the anatomical description of the cardiac nerves, I must now detail the origin and connections of their cardiac branches. THE CONNECTIONS OF THE SYMPATHETIC WITH THE HEART. Each of the three cervical ganglia of the sympathetic sends a branch to the heart, the upper, middle, and lower eardiae nerves respectively (see fig. 1 1). The upper or siiperjicial cardiac nerve of the right side (1 C N) arises by two or more branches from the upper cervical ganglion, and some- times also by a branch from the trunk of the sympathetic, which joins the upper and middle cervical ganglia. After proceeding down the neck it enters the thorax, being directed along the innominate artery to the back of the arch of the aorta, where it terminates in the deep cardiac plexus (D C P). In its course through the neck and in the thorax, it forms numerous connections with other branches of the sympathetic and of the pneumogastric, the more important of which are — 1. A connection with the external laryngeal branch of the pneumo- gastric (l). 2. A connection with the trunk of the pneumogastric {2). 3. A connection with the recurrent laryngeal branch of the pneumo- gastric (3). It also sends some small branches to the thyroid body, and to the front of the great vessels (aorta and pulmonary artery). The upper or superficial cardiac nerve of the left side (I'C'N') arises in the same manner, and has the same course through the neck as its fellow of the right side. After entering the chest it is directed along the left common carotid artery to the front of the arch of the aorta, which it crosses, and terminates in the superficial cardiac plexus (S C P). In exceptional cases this nerve terminates in the deep cardiac plexus. 2 2 Diseases of the Heart. The middle^ deep, or great cardiac Jterve of the right side (2 C N) arises from the second cervical ganglion of the sympathetic. After entering the chest it lies in front of the trachea, and ends in the right half of the deep cardiac plexus. It forms connections with — 1. The upper cardiac branch of the sympathetic (4). 2. The recurrent laryngeal branch of the pneumogastric (5). The middle cardiac nerve of the left side has the same origm, course, and connections as the corresponding nerve on the right side. It terminates in the left half of the deep cardiac plexus. The lower cardiac nerve of the tight side arises from the third cervical ganglion, or from the first dorsal ganglion of the sympathetic, enters the thorax behind the subclavian artery, and terminates in the right side of the deep cardiac plexus. It forms connections with — (i.) The middle cardiac branch of the sympathetic (6). (2.) The recurrent laryngeal branch of the pneumogastric (7). The hnver cardiac nerve of the left side has the same origin, course, and connections as the corresponding nerve on the right side. It terminates in the left side of the deep cardiac plexus. This nerve often joins the middle cardiac branch of the same side, the common trunk thus formed, ends in the left side of the deep cardiac plexus. Description oj FiG. II. — Seini-diagraiinnatic rcprescntatioti of the connections of the sympatlietic with the heart. ICG and I'C'G', upper cardiac ganglia of the sympathetic (right and left). 2CG and 2'C'G, middle ,, ,, ., 3CG and 3'C'G, lower ,, ,, ,, icn, 2cn, 3cn, 4cn, 5cn, 6cn, yen, Sen, branches of the right, first, second, third, fourth, fifth, sixth, seventh, and eighth cervical nerves, proceeding to the sympathetic ganglia. I'c'n', 2'c'n', 3'c'n', 4'c'n', 5'c'n', 6'c'n', 7'c'n', 8'c'n', branches of the left, first, second, third, fourth, fifth, sixth, seventh, and eighth left cervical nerves proceeding to the sympathetic ganglia. IDG right, and I'D'G', left first dorsal ganglia of the sympathetic, idn branches of the right, and I'd'n' left first dorsal nerves proceeding to the first dorsal ganglia of the sympathetic. ICN right, and I'C'N' left, first or superficial cardiac nerves. 2CN right, and 2'C'N' left middle cardiac nerves. 3CN right, and 3'C'N' left inferior cardiac nerves. The other letters have the same significance as in the previous figures ( 9 and 10). TJic Cardiac Brandies of tJic Sympathetic. 2, ICG. Icn. 2cn. 3cn. 4cn. 2CG 6cn^ ■ICN I'C 3CG Scn- ldn> IDG ''H^^ ^^ 3CN I'C'G' VC'Qf 3'C'G' .I'd'n' I'D'C 3'C'N' SVC- DCP RA- av- D'C'P' 24 Diseases of the Heart. THE CONNECTIONS OF THE PNEUMOGASTRIC WITH THE HEART. Nerves destined for the heart arise from the trunk of the pneumogastric, both in the neck and in the thorax, and cardiac branches are also given off by several of its branches (see fig. 12). Anatomists consequently describe cervical cardiac, and thoracic cardiac branches of the pneumogastric. The cervical cardiac branches.— \x\ the upper part of the neck several small twigs (2) connect the pneumogastric with the upper cardiac branches of the sympathetic ; while the external laryngeal branch of the superior laryngeal nerve, which is a branch of the pneumogastric, is also con- nected with the upper cardiac branch of the sympathetic (i). In the lower part of the neck a branch of some size (8) arises from the trunk of the right pneumogastric, as it is about to enter the thorax. It is directed along the innominate artery to the back of the aorta, being usually blended into one of the branches of the sympathetic, and ter- minates in the right side of the deep cardiac plexus. This branch some- times arises from the recurrent laryngeal. The corresponding nerve of the left side (8') crosses in front of the arch of the aorta, and terminates in the superficial cardiac plexus. Both nerves (right and left) give some small twigs to the coats of the aorta. 77/^? thoracic cardiac b}-anches. — On the right side several cardiac branches (9 and 9) arise from the trunk of the pneumogastric, and from the recurrent laryngeal, and pass to the right side of the deep cardiac plexus. The corresponding branches from the left side (9') usually come entirely from the recurrent (Quain), and pass to the left side of the deep cardiac plexus. In fig. 13 I have endeavoured to represent the nervous mechanism of the heart in all its complicated details. Description of Fig. 12. — Semi-diagrammatic representation of tlie connections of tlie pneumogastric with tJie lieai-t. PI', right pneumogastric ; P'P', left pneumogastric ; rcl, rcl, right recurrent laryngeal nerve ; r'c'l', r'c'l', left recurrent laryngeal nerve ; si, s'l', right and left, superior laryngeal nerves ; el and e'l', right and left, external laryngeal nerves. I and I', communicating branches between the external laryngeal nerves and the first cardiac nerves, on the right and left sides respectively ; 2 and 2', between the trunk of the vagus and the first cardiac nerve on the right and left sides respect- ively ; 8, communicating branch between the trunk of the right pneumogastric and the lower cardiac nerve ; 8', on the right side this branch usually proceeds directly to the superficial cardiac plexus ; 9, 9, branches from the right vagus, in the thorax, to the right half of the deep cardiac plexus ; 9', branches from the left recurrent laryngeal to the left half of the deep cardiac plexus. The Cardiac Branches of the Vagus. 25 p' rcl DCP- RA- D'CT' 26 Diseases of the Heart. I'C'C 3CG IDG DCP D'C'P' The Nervous Supply of the Heart. 27 Description jf Yli;. 13. — Semi-diagrammatic representation 0/ the nervous supply of the heart. RCP, right, and LCP, left coronary plexuses ; SCP, superficial cardiac plexuses; DCP, right, and D'C'P', left half of the deep cardiac plexus; P right, and P' left pneumogastric nerves; ICG, Right, and I'C'G', left superior ganglia of the sympathetic ; 2CG, right, and 2'C'G', left middle ganglia of the sympathetic ; 3CG, right, and 3'C'G', left inferior ganglia of the sympa- thetic ; RV, right, and LV, left ventricles ; RA, right, and LA, left auricles ; SVC, superior vena cava. rcn, 2cn, 3cn, 4cn, 5cn, 6cn, 7cn, 8cn, branches of the right, first, second, third, fourth, fifth, sixth, seventh, and eighth cervical nerves, proceeding to the sympathetic ganglia. I'c'n', 2'c'n', 3'c'n', 4'c'n', 5'c'n', 6'c'n', 7'c'n', 8'c'n', branches of the left, first, second, third, fourth, fifth, sixth, seventh, and eighth left cervical nerves proceeding to the sympathetic ganglia. IDG right, and I'D'G' left first dorsal ganglia of the sympathetic, idn branches of the right, and I'd'n' left first dorsal nerves proceeding to the first dorsal ganglia of the sympathetic. si right, and s'l' left superior laryngeal branches of the pneumogastric ; EL right and E'L' left external laryngeal nerves ; rcl right, and r'c'l' left recurrent laryngeal nerves at lower part of neck, and in the thorax respectively. a, branch from right coronary plexus to right auricle ; b, branch from right coronary plexus to right ventricle ; c, branch from the superficial cardiac plexus to the right coronary plexus ; d, branch from the right half of the deep cardiac plexus to the right coronary plexus ; e, branch from the left half of the deep cardiac plexus to the left coronary plexus ; f, branch from the right half of the deep cardiac plexus to the left coronary plexus ; g, branch from the left coronary plexus to the left auricle ; h, branch from the left coronary plexus to the left ventricle ; i, branch from the left coronary plexus to the right ventricle. ICN right, and I'C'N' left, first or superficial cardiac nerves. 2CN right, and 2'C'N' left middle cardiac nerves. 3CN right, and 3'C'N' left inferior cardiac nerves. I, branch from the right, and l', branch from the left external laryngeal nerves to the superior cardiac nerves ; 2, branch from the right, and 2', from the left pneumogastric nerves to the superior cardiac nerves ; 3, communicating branch from the right, and 3', from the left recurrent laryngeal nerves to the first cardiac nerves on the right and left sides respectively ; 4, communicating branch between the right, and 4', communicating branch between the left superior and middle cardiac nerves ; 5, communicating branch between the right, and 5' between the left middle cardiac and recurrent laryngeal nerves respectively ; 6, communicating branch between the right, and 6', communicating branch between the left, middle and inferior cardiac nerves ; 7, communicating branch between the right, and 7', between the left inferior cardiac nerves and the recurrent laryngeal respectively ; 8, communicating branch between the right inferior cardiac nerves and the trunk of the pneumogastric, 8', on the left side this branch of the pneumogastric proceeds directly to the superficial cardiac plexus ; 9, 9, branches from the trunk of the right pneumogastric, and 9', from the left recurrent laryngeal nerve to the right and left halves respectively of the deep cardiac plexus. 28 Diseases of the Heart. THE MANNER IN WHICH THE VAGUS AND SYMPATHETIC NERVES AFFECT THE HEART. I have now described the construction of the mechanism concerned in the innervation of the heart, and I must next point out the manner in which that mechanism works. We have already seen that while the movements of the heart are automatic {i.e. are due to impulses arising within the heart itself), they can be profoundly modified by the condition of distant parts ; and that the impulses which produce these modifications are conveyed to the heart through certain branches of the pneumogastric and sym- pathetic nerves. Until recently, we might have summed up the effects of these impulses by saying, that impressions passing to the heart through the pneumogastric, retard, ivJiile impressions passing to the heart through the sympathetic, accelerate its movements (hence the terms 'inhibitor' and 'accelerator' of the heart which are given to the two nerves respectively) ; but recent observations seem to show that the action of the vagus on the heart is much more complicated, and that it affects not only the rhythm, but also the force of the cardiac contractions, and that it exerts a trophic influence upon the cardiac muscle. It will be necessary, therefore, to consider each of these functions separately. The Inhibitory Action of the Vagus. As the result of the laborious investigations of many able observers, physiologists have concluded : — Firstly, that there exists in the medulla oblongata a cardio-inhibitory centre, which is continually exerting a restraining influence upon the heart ; and Secondly, that the action of this cardio-inhibitory centre may be intensified, i.e., the action of the heart may be still further retarded by : — (a) Direct stimulation, i.e., by certain changes in the medulla itself. (b) Impressions passing to it from the brain. The InJiibitoiy Action of the Vagus. 29 (c) Impressions passing to it from peripheral parts (reflex stimulation). ^ Some authorities also believe that the cardio-inhibitory centre may itself be inhibited, i.e. its restraining power taken off the heart, by im- pressions passing to the medulla from other parts of the central nervous system, or from the periphery. The most important local changes which stimulate the cardio-inhibitory centre, appear to be increased blood-pressure within the cranium, and irritative lesions in the medulla or in the neighbourhood of the vagi roots, e.g. inflammatory affections at the base of the brain, etc. ; while reflex inhibi- tion of the heart seems to be chiefly brought about by impres- sions passing to the medulla from the abdominal viscera.^ It has also been supposed that the action of the heart may be inhibited by impressions passing from the heart itself. The experiments of Cyon and Ludwig, Rutherford and others, seem to show that reflex inhibition of the heart can be pro- duced in the rabbit by stimulation of the central cut end of the superior cardiac nerve, the impression passing up to the cardio-inhibitory centre in the medulla oblongata, and back, through the vagus and its inferior cardiac branch, to the heart. The superior cardiac branch arises by two roots, one connected with its superior larj'ngeal branch crosses down the neck close to the cervical sympathetic, and joins one or two branches of the inferior cervical ganglion with which it proceeds to the heart. This branch is a purely sensitive nerve ; and is in fact the sensitive nerve of the heart. On ' Whether the action of the cardio-inhibitory centre is automatic or not, is still undecided. * Powerful stimulation of any afferent or sensory nerve can probably produce reflex inhibition of the heart. Rutherford states that the cardio-inhibitory fibres of the vagus may be thrown into action by stimulating: (i). The central end of the vaso-inhibitory or superior cardiac branch of the vagus (depressor nerve) ; (2). The central end of the vagus of the opposite side ; (3). Almost any sensory nerve, in the case of warm-blooded animals ; (4). The abdominal viscera of the frog; (S). The splanchnic and sympathetic. — Lancet, Dec. 16, 1871, page 483. Michael Foster states that ' the regulative action of the inhibitory mechanism is brought into more or less close connection with all parts of the body. — A Text Book of Physiology, p. 174. 30 Diseases of the Heart. cutting it across, and stimulating its inferior (peripheral) end no effect is produced ; while stimulation of its upper (central) end causes pain, retardation of the heart, and, as I shall afterwards more particularly point out, such a striking diminution of blood-pressure, that the term depressor nerve has been given to it. The inferior cardiac branch leaves the vagus below the origin of the inferior lar)-ngeal nerve, and proceeds directly to the heart. It is a cardio-inhibitory nerve, and stimulation of its inferior cut-end gives rise to the same effects as stimulation of the vagus itself {i.e. stimulation above the origin of this branch), viz. (with weak currents) retardation of the heart from prolongation of the diastole, and (with stronger currents) complete arrest during diastole. In the rabbit the vagus gives two branches to the heart, a superior and an inferior cardiac branch (see fig. i6). Track r/7/i.fAor. \V n.raff. Fig. li,. — The last ceiT>ical and first thoracic ganglia in the rabbit. {Left side). (SoHunvhat diagrammatic, many of the various branches being omitted.)— ( .After Foster. ) Trach. Trachea. Ca. carotid arter)'. sh. subclavian artery. n. Vog. the vagiis trunk, n. rec. the recurrent laryngeal, sym. the cervical sympathetic nerve ending in the inferior cervical ganglion, gl. cerv. inf Two roots of the ganglion are shown, 7 ad., the lower of the two accompanying the vertebral arter)^ A. vert. , being the one generally possessing accelerator properties, gl. thor. pr^ The Inhibitory Action of the Vagus. 31 In the human subject, two branches of the vagus seem to correspond to the superior cardiac branch of the vagus in the rabbit ; while the inferior cardiac branch of the vagus of the rabbit seems to be (mainly at all events) represented in man by the large branch which leaves the vagus trunk at the lower end of the neck (inferior cervical branch). Now it has been supposed that these two nerves, together with the cardio-inhibitory centre in the medulla, constitute a reflex arc ; and that stimulation of the peripheral terminations of the superior cardiac nerve in the heart may generate an im- pulse which, being conveyed to the cardio-inhibitory centre, and being reflected back to the heart along the vagus, may retard the action of the heart. Whether the superior cardiac nerve has any special function of this description, other than is possessed by all sensitive nerves, is extremely doubtful ; and it seems certain that increased blood-pressure within the heart, as a whole, does not, as was at one time supposed, produce reflex inhibition of the organ. Physiologists are not yet agreed as to the exact manner in which the vagus causes inhibition of the heart. Until quite recently it was believed that while weak stimulation of the nerve prolonged the diastole, the duration of the ventricular systole being, very little affected, more powerful stimulation caused complete arrest during diastole (complete relaxation), the next systole being as it were indefinitely postponed ; and it was generally supposed that Description of fig. 14. continued. the first thoracic ganglion. Its two branches communicating with the cervical ganglion surround the subclavian artery forming the annulus of Vieussens. syi?i. thai: the thoracic sympathetic chain. n. dep. depressor nerve, which, though running by the side of the sympathetic, is really a branch of the vagus, from which it separates higher up. This is joined in its course by a branch from the lower cervical ganglion, there being a small ganglion at their junction, from which proceed nerves to form a plexus over the arch of the aorta. It is this branch from the lower cervical ganglion which possesses accelerator properties — hence the course of the accelerator filires is indicated in the figure by the arrows. 32 Diseases of the Heart. the vagus inhibited the contractions of the heart by pre- venting motor impulses being sent from the automatic gangha to the muscle, i.e. by holding in, as it were, the motor energy of the ganglia ; and this would appear to be the view which Sewall and Donaldson take. They think that their experiments 'point pretty clearly to the con- clusion, that the inhibitory action of the vagus nerve exerts itself in the same indirect way (as a motor stimulus does), influencing the ventricle by damping in sinus and auricles the excito-motor discharges arising in these parts of the heart.' ^ Dr Gaskell takes a different view. He has shown:— Firstly, that the vagus is able to modify all the great functional attributes of the cardiac muscle, viz.: — {a) The rate at which automatic contractions are pro- duced. (The automatic rhythm.) {b.) The force with which the contractions, more especially the contractions of the auricle, are carried out. (The fojre of contraction.) (c.) The facility with which the contractions are conducted by the muscular fibres. (The poiver of conduction'-.) Sccondty, that it sometimes produces depression, at other times exaltation, of function. He believes that the vagus may produce standstill or inhibition of the heart (auricles and ventricles) in the three following ways : — (i.) By producing cessation of its automatic contractions, i.e. by depressing the rhythmical power of the muscular fibres of the sinus in which the automatic rhythm originates. (This has been established in the frog, tortoise, and snake.) (2.) By reducing the force of the auricular contractions, so that they become invisible, i.e. by depressing the contraction power of the rapidly contracting reticulated muscular fibres of the auricle. (Frog.) The contractions, he states, may be ' Joitrnal of Physiology, vol. iii. p. 367. ^ In the tortoise the force of the contractions of the ventricle was uninfluenced by vagus stimulation. In the frog, on the other hand, the vagus influences the force of the ventricular as well as of the auricular contractions. The Trophic Action of the Vagus. 33 so small as only just to be visible, so that to the naked eye the heart appears to stand still. (3.) By blocking the contraction wave at the sino-auricular ring, i.e. by depressing the conducting power of the muscular fibres connecting the sinus and auricle. (Snake, tortoise, frog.) The Trophic Function of the Vagus. As I have previously remarked, Dr Gaskell has advo- cated the important theory, which Eichorst had previously advanced, that the vagus is the trophic nerve of the heart. ' Although,' he says, ' the initial effect of the vagus is to de- press some function, its final and most enduring power is to exalt, intensify, and repair that function. Thus, although it slows rhythm, yet its stimulation makes the rhythmical power last longer than it otherwise would, and makes the heart beat with regularity when it was previously irregular ; although it reduces the force of the contractions, yet its ulti- mate effect is to improve and sustain the contraction force ; although it may diminish the conduction power, yet in the end it completely repairs that power. For these reasons,' he says, ' / took upon tlie vagus as essentiatty tlie tropliic nerve oj the Jicarti^ Since this chapter was written, I have learned from Dr Gaskell that the term ' trophic,' as it is commonly used and understood, does not exactly express the function which he supposes the vagus to have over the cardiac muscle. ' I have felt,' he says, ' all along that the word trophic is somewhat misleading as applied to the results of my experiments on the action of the vagus. I wanted a word to express, what appears to me to be the fact, in the cold-blooded animals at all events, that the inhibitory process is not destructive but constructive in its nature, but could not find any good term. I have therefore used the word ' trophic,' not perhaps in its usual sense, but rather in a sense similar to Heidenhain, when he divides the nerves supplying the sub-maxillary gland into secretory and trophic' ^ Jotirnal of Physiology, vol. iv. p. 104, C 34 Diseases of the Heart. Tlic Mode of Action of t tie Vagus on ttic Heart. The exact manner in which the terminal fibres of the vagus are brought into relation with the cardiac muscle is unknown. The effects produced by vagus stimulation, and by the action of certain poisons, have led some physiologists to believe that the arrangement is an extremely complicated one ; and in order to explain these results, they have theorised that there existed an inhibitory mechanism within the heart itself, the action of which is strengthened (brought into play) by impressions carried to it by the terminal branches of the vagus, and which in its turn acts upon, i.e. inhibits the ganglionic apparatus more immediately concerned in the production of the rhythmical movements of the heart, i.e. the automatic nerve mechanism. The facts and arguments which they have advanced in support of the view that the vagus does not act directly upon the cardiac muscle, but that it acts through some intermediate nerve apparatus, are as follows : — 1. The latent period, which elapses between electrical stimulation of the vagus and the production of its inhibitory action on the heart is twenty-times longer than that which elapses between the electrical stimulation of an ordinary motor nerve, and the contraction of its muscle. viz., 3th and f^jth of a second respectively. 2. A very much stronger current is required to produce inhibition of the heart through the vagus, than is required to produce spasm of a voluntary muscle, when its motor nerve is stimulated. 3. If the action of the heart be arrested by stimulation of the vagus, the rhythmical contractions after a time return, although the stimulation of the vagus be continually kept up, a fact which may be explained either by supposing that the inhibitory fibres of the vagus become gradually exhausted by the prolonged stimulation, or that the accumulation of nerve force in the automatic ganglia becomes after a time too great to be held back, and that an explosion and muscular contraction consequently take place. 4. Continued stimulation of one vagus annuls or prejudices the action of the other. 5. ' The effects of vagus inhibition are perhaps more marked when the electrodes are placed on the boundary line between the sinus venosus and the auricle, than over the vagus trunk itself.'— iv7j/^r. 6. If during the complete relaxation which results from powerful stnnulation of the vagus, the muscular tissue be mechanically irritated, it is still found to contract. The TropJiic Action of the Vagus. 35 While the existence of an intermediate (intra-cardiac) inhibitory mechanism between the terminal fibres of the vagus and the automatic nerve apparatus they think proved by the following circumstances : — 1. When the electrodes are placed on the boundary line between the sinus venosus and the auricles, more powerful inhibition is produced than when they are applied to the vagus itself 2. After the administration of urari, stimulation of the vagus no longer produces inhibition of the heart, but stimulation in the region of the sinus venosus will still do so. 3. After the administration of atropia, neither stimulation of the vagus nor of the sinus produces any inhibitory effect. It is therefore concluded that atropia paralyses the intra-cardiac inhibitory apparatus itself 4. Muscarin and jaborandi in full doses produce exactly the same effect which is produced by powerful vagus stimulation, viz., complete arrest during diastole, an effect which is not prevented by the previous administration of urari (which, as we have seen, paralyses the terminal fibres of the vagus, but does not touch the intra-cardiac inhibitory mechanism) ; but which is prevented by the previous administration of atropia which paralysis the intra-cardiac inhibitory mechanism. Hence it is concluded that muscarin and jaborandi stimulate the intra-cardiac inhibitory mechanism. Dr Gaskell's view as to the mode of action of the vagus is different. He has shown that the action of the vagus on the cardiac muscle is in many respects identical with the action of a weak interrupted current. He believes that the nerve acts directly upon the muscular fibre itself, and he argues that the action of atropin, muscarin, and some of the other cardiac poisons to which I have referred above, can be consistently explained upon this view.^ 'Again,' he says, 'I have shown clearly that the vagus depresses and exalts all the different functions of all the different muscular tissues of the heart, whether the function in question is rhythm, contraction, conduction, tone, or excit- ability. Also, I have shown that depression of one function is not necessarily accompanied by a simultaneous depression of another function, and so also with the exaltation of function. Further, the exaltation of each function is not necessarily dependent upon a previous depression ; in each case the primary effect may, under certain circumstances, be ' youriial of Physiology, vol. iv., No. 2, pp. 114, 115, 116. 36 Diseases of the Heart. exaltation and not depression. Combining these two facts together, we are driven to accept one of two alternatives, either the vagus contains a multiplicity of fibres, which can be divided into two groups after the fashion of Heidenhain, I. Depressors (Hemmungs-fasern) ; 2. Augmentors (Ver- starkungs-fasern) ; and further, each member of each of these groups has again its own special function, so that, for instance, the rhythm-inhibiting nerve fibre is different in kind from the contraction-depressing fibre, and so on ; or else, the same trophic nerve fibre produces all the different effects observed, according to the nature of the muscle, which it supplies, and the condition of that muscle at the time. ' In this paper as well as in my previous paper, all the facts have tended strongly to prove that the vagus acts in the same manner upon the rhythm of the heart, and upon the force of its contractions, so that if separate inhibitory and accelerator nerve fibres exist for the one, separate depressor and aug- mentor fibres must exist for the other. If, therefore, it can be shown that such diminution and augmentation of the strength of the contractions are due not to different influences reaching the muscle, but to the same influence affecting the muscle when its conditions are different, then it is, to say the least, highly probable that slowing and acceleration are also due, not to different nerve fibres, but to the action of the same nerve fibre under different circumstances. In the frog, as I have previously pointed out, such a complete gradation exists between a primary excessive diminution of the contractions and a primary augmentation in consequence of nerve stimula- tion, as to render the hypothesis that such curves depend upon the simultaneous stimulation of two antagonistic nerve fibres very improbable. I have now proved in addition, that a weak interrupted current applied to the smallest strip of cardiac muscle produces the same two opposite effects, and that here the depressing effect may be removed and the aug- menting alone remain, when the condition of the muscle is altered by the application of atropin. In order, therefore, to still hold to the view of specific nerve fibres acting in opposite directions upon the force of the contractions, it is necessary to The Trophic Action of the Vagus, 37 assume, not only that those nerve fibres possess opposite quahties up to their very termination in the muscle, but that even when the muscle itself is stimulated, the relative action of these two sets of nerves still holds its ground. In addition, atropin would have to be considered as acting upon these two sets of nerve endings, and not upon the muscle, paralysing the depressor nerve endings before those of the augmentor nerves. The experiments of Luchsinger and Szpil- man,^ which lead them to the conclusion that atropin has a special action upon unstriped muscle fibre, those of Bow- ditch, already referred to, and my own, all point to the con- clusion that atropin affects the cardiac muscle directly in consequence of its affinity to unstriped muscle fibre. The whole evidence goes to show that the vagus is a constructive and not a destructive nerve, that the initial depression of function is not of the nature of exhaustion, but is preliminary to a greater functional activity. The phenomenon presented by the muscular tissue of the frog and tortoise under the influence of an induced current, is of exactly the same nature as that seen in the muscle of the snail's heart (as pointed out by Foster and Dew-Smith) when a constant or weak interrupted current is sent through it. In both cases augmentation of function occurs as well as depression ; in the one case the evidence is as strong in favour of special inhibitory and accelerator nerves as in the other. Clearly, in the case of the snail, it is simply impossible, as Foster has said, to explain such results by the presence of accelerator and inhibitory fibres in every strip of muscular tissue, when, as a matter of fact, cardiac nerves of any kind whatever have not been proved to exist. Clearly also, whatever explanation will ulti- mately be found for the action of the current upon the mus- cular tissue of the snail's heart, will also explain the same phenomena in the heart of the frog and tortoise. The problem which demands solution is essentially. Why is the condition of the muscle ultimately improved in every one of its functions by the direct application to it of a continuous stimulus, which ' Pfliiger's Archtv., vol. xxvi. p. 459. 38 Diseases of the Heart. is not strong enough to produce motor effects? and why is that improvement of function preceded in many cases by a diminution of function ? When these two questions have received a satisfactory answer, it will no longer be strange that the vagus produces throughout two opposing effects, and the action of atropin will become clear ; then the relationship between trophic and motor action will be understood, and the true functions of the ganglion cells found in connection with nerve fibres will be indicated. At present it can only be said that the vagus is the trophic nerve of the cardiac muscle, its action resembling that of a stimulus too weak to produce motor effects, and therefore it is possible that the function of the ganglion cells, in the course of the nerve, is to convert an otherwise motor into a trophic nerve.' ^ 'This argument,' Dr Gaskcll writes me, 'is based upon experiments upon cold- blooded animals; how far it applies to the warm-blooded I (Dr Gaskell) do not yet know. Eichhorst and Zander conclude that the vagus in the warm-blooded contains trophic fibres.' The action of the sympathetic upon the heart is even less clearly understood than the action of the pneumogastric, but it is believed that there exists in the medulla oblongata (or possibly above it), a centre, stimulation of which produces increased frequency of the heart's beat, and it is supposed that this accelerator, or cardiac-motor centre, as it is some- times called, may be stimulated, i.e., the frequency of the heart's beat may be increased either by direct or reflex stimuli. The influences which throw this centre into action have not been very accurately ascertained, but it is probable that emotion excites the heart through the agency of the accelerator nerves ; while diminished blood pressure within the cranium is supposed to stimulate them. Impulses generated in this centre, the action of which, be it observed, is supposed to be intermittent (and in this respect to differ from the action of the cardio-inhibitory centre, which is supposed to be constant), appear to pass down the lateral column of the cord to the lower end of the ^ Journal of Physiology, vol. iv. p. 121. The Action of the Sympathetic on the Heart. 39 cervical region, whence they pass through the nervi com- municantes, to the (?) middle and inferior cervical ganglia of the sympathetic, and thence to the heart. According to Prof. Michael Foster the accelerator nerves frequently pass along the nerves accompanying the vertebral artery, and reach the heart through the last cervical and first dorsal ganglia.' It is supposed from the long latent period which elapses between stimulation of the accelerator and the production of its specific action on the heart, that its fibres terminate in an intermediate ganglionic apparatus similar to that which I have already described in speaking of the termination of the pneumogastric. Now, although the pneumogastric acts as inhibitor, and the sympathetic as accelerator, it must not be supposed that their action is directly antagonistic. That such is not the case seems abundantly proved by physiological observa- tion. Physiologists have shown, says Dr M. Foster, that ' if during maximum stimulation of the accelerator nerves, the vagus be stimulated even with minimum currents, inhibition is produced with the same readiness as if the accelerator nerves were not acting. Vagus stimulation does not annul, but appears simply to suspend, during its continuance, the manifestation of the accelerator action.' - It may appear to some that I have entered into undue physiological detail in dealing with this subject, but it must be remembered that it is only by attention to these minute physiological details that the physician can hope to make much advance in cardiac patholog)', a subject on which our knowledge of the ordinary details of morbid anatomy is already so far advanced. The relationship between the Heart and the minute Blood-vessels. In order to conclude the description of the innervation of the heart, I must shortly direct attention to the intimate relationship which exists between the heart on the one hand ' The middle and lower cervical ganglia in man appear to correspond to the lower cervical and first dorsal ganglia in the rabbit, through which accelerator impulses have been proved to pass, as shown in figure 14. - Text Book of Physiology, Third edition, p. 175. 40 Diseases of the Heart. and the peripheral blood-vessels on the other, and to the beautiful self-adjusting mechanism by which alterations in the one are of necessity followed by corresponding changes in the other. \Vc have already seen the fundamental importance of looking at the heart both as a mechanical pump and as a vital organ ; and another point which I must now insist upon — and it is hardly of less importance whether we are studying the heart from a physiological, a pathological, or a clinical point of view, — is the necessity of taking an all-round view, so to speak, of the circulation. Indeed it is essential to remember that the heart is only a part of the vascular mechanism, and that the condition of the circulation, and consequently the condition of the heart (for the organ naturally adapts itself to the amount and kind of work which it has to perform) depend in no small degree upon the condition of the peripheral resistance, which is in its turn mainly due to the obstruction which the blood meets with, in passing through the minute arteries. In conditions of health, the minute arteries are always more or less constricted in consequence of a permanent con- traction of their middle or muscular coats, and it is to this ' tonic ' contraction that the peripheral resistance is in great part due. [The peripheral resistance depends also upon the facility with which the blood passes through the capillary system of ves.sels ; and since the blood flow through the capillaries may be influenced by alterations in (a) the condition of the capillary walls, (b) the condition of the tissues outside the capillary walls, and (c) the composition of the blood itself, all of these factors must be taken into consideration as causes of peripheral resist- ance, and of variations in the blood pressure. In con- ditions of disease, variations in the blood pressure may result from alterations in the ' capillary resistance,' but these variations are, in my opinion, never so great, either in conditions of health or disease, as those which are due to alterations in the condition of the muscular coat of the minute arteries]. Relationship of Heart and Minute Blood-vessels. 41 The degree of constriction is constantly undergoing varia- tions even in health, and is subject to marked alterations in some diseased conditions ; hence the amount of resistance which the heart has to overcome in forcing the blood into the capillaries, is constantly changing ; and to meet sudden variations of this description a delicate self-adjusting nervous mechanism is provided. But in order that this part of our subject may be properly understood, I must now describe the mechanism by means of which the arterial 'tone' is regulated. There seems good reason to believe : — (i) That the tonic constriction of the muscular coats of the minute arteries is (immediately) due to the presence of a peripheral neuro-muscular or (purely) muscular apparatus, which may be thrown into action by local stimuli, the most important of which is the blood pressure. The peripheral mechanism concerned in this maintenance of arterial ' tone ' probably bears a close resemblance to the peripheral mechanism concerned in the production of the rhythmical movements of the heart. Ganglionic masses can be demonstrated in the walls of many of the minute blood-vessels, and it has been by some authorities supposed that the blood pressure produces stimulation of the muscular coats of these vessels in a reflex manner (see fig. 17) ; but in many vessels {e.g. those in the skin and muscle) no such ganglionic masses have as yet been demonstrated, and in their case we must conclude that the contraction of their muscular coats is due to direct stimulation of the muscular fibre itself, or of the terminal vaso-motor filaments which are distributed to it. The view, which supposes that the muscular fibre is itself stimulated by the blood-pressure, is probably the correct one. (2) That the action of this peripheral neuro-muscular or purely muscular mechanism is, under ordinary circumstances, maintained and regulated by impulses which are being con- stantly sent to it from centres (vaso-constrictor centres) in the medulla and spinal cord, through the vaso-motor nerves ; and that the action of these vaso-constrictor centres may be increased or diminished both by direct stimulation or in a reflex manner. In other words, the calibre of the minute arteries, and therefore the peripheral resistance may be 42 Diseases of the Heart. increased or diminished by central and peripheral causes (stimuli). Fig. 15. — Diagrammatic representation of the reflex mechanism, by which (it has been theorised) the muscular coat of the blood-vessels is tkrowti into contrac- tion, under the influence of the blood-pressure. E' E, Endothelium; B, the blood in the blood-vessel; M, the muscular coat of the artery ; g, ganglion cell — the reflex centre ; n, sensory nerve fibre, conducting the impression generated by the blood pressure on the sensory nerve terminations in the wall of the vessel to the reflex centre ; n', motor nerve fibril conducting the impulse from the reflex centre to the muscle. The vaso-motor {i.e. vaso-constrictor) centre of the medulla, which is probably bilateral, is situated immediately above the calamus scriptorius, and extends for some distance into the pons (to i or 2 m m. below the corpora quadrigemina). The conducting fibres proceeding from it are believed to pass through the lateral columns of the spinal cord, and to proceed to the blood-vessels chiefly through the sympathetic system of nerves. The vaso-motor centre of the medulla probably regulates the vascular system of the abdomen, the arteries of the skin and muscles being probably mainly supplied by vaso-constrictor fibres proceeding from the vaso-motor centres in the spinal cord. The exact position of these spinal centres is not ascertained. The action of the vaso-motor {i.e. vaso-constrictor) centres, which, it will be remembered, is supposed to be constant, may probably be intensified by : — (a) Increased blood pressure within the cranium, and local irritative lesions of the medulla. (b) Impressions proceeding from the cerebrum. (c) Impressions proceeding from the periphery. It has been ex- perimentally proved that irritation of any afferent (sensory) nerve, such as the sciatic, will produce constriction of the minute blood vessels Relationship of Heart and Minute Blood-vessels. 43 (especially those of the abdomen) and increased blood pressure, presum- ably by reflexly stimulating the vaso-motor centre in the medulla. (3) That the action of the peripheral neuro-muscular mechanism may be inhibited by nervous impulses passing to it from certain centres in the medulla, and (?) spinal cord, through the vaso-dilator nerves ; and that the action of the vaso-dilator centres, which is not constant, may be called into play by central and reflex stimulation. The calibre of the minute arteries may therefore be increased, and the blood-pressure lowered either by inhibi- tion of the vaso-constrictor, or by stimulation of the vaso- dilator centres in the medulla and (.'') spinal cord.^ It is not absolutely certain that a distinct and separate vaso-dilator centre exists ; some authorities in fact believe that the same centre may at one time evoke vaso-constrictor and at another vaso-dilator impulses ; but it seems tolerably well ascertained that there are distinct fibres for the conduction of these two sets of impressions, and for theoretical and teaching purposes it is convenient to describe and represent a distinct vaso-dilator centre. The exact course of the vaso-dilator conductors in the cord is yet undetermined, but it seems probable that they pass down in some part of the lateral columns, and reach the blood-vessels chiefly through the cerebro-spinal (and not through the sympathetic) nerves. The vaso-dilator centre in the medulla is chiefly, if not exclusively, connected with the vessels of the abdominal viscera ; and it is most readily thrown into action by stimuli passing to the medulla through the depressor nerve, and by impressions passing from the abdominal viscera through the splanchnics.'-' ' It must be remembered that the inhibitory action of the vaso-dilators on a peripheral neuro-muscular or muscular mechanism, is theoretical, and it is not definitely proved. ' It is quite possible,' as Foster says, ' that dilation may be brought about in different ways, in different cases, and so also with constriction.' — A Text Book of Physiology, p. 211. - This description of the action of the vaso-motor mechanism is not complete. It must of course be remembered, that local variations in the blood supply are being constantly required by the ever varying needs of particular times and organs, and that as Prof. M. Foster says, ' the great use of the whole vaso-motor system is not to maintain a general arterial tone, but to modify according to the needs of the economy the condition of this or that vascular area ' {A Text Book of Physiology, page 213). But in studying cardiac affections the changes in the action of the heart, which are induced by local variations of this description, may, for practical purposes, be safely ignored. Hence I have limited my description to those alterations of the vaso-motor mechanism which are sufficiently general to produce definite changes in the action of the heart. 44 Diseases of the Heart. Now, as I have previously stated, a very striking dimi- nution of blood pressure results from stimulation of the superior cardiac branch of the vagus or depressor nerve, as it has therefore been called. It is obvious, therefore, that there is an important connection between the heart and the vaso-dilator centre in the medulla, by means of which the heart and peripheral blood vessels are brought into such close physiological connection, that changes at one end of the circulation, so to speak, are at once attended by compensatory changes at the other. If, for example, the arterial blood pressure is from any cause suddenly increased, a sudden strain is necessarily thrown upon the left ventricle, and it might easily happen that the resistance in front was too great for the force of the pump. Under such circumstances paralytic distention of the left ventricle and death would follow, if it were not for the fact that the undue distention of the cavity and the effort which the heart is making to overcome the resistance, produce irritation of the terminal fibres of its sensitive nerve (the superior cardiac or depressor nerve), in consequence of which a powerful stimulus is sent to the vaso dilator centre in the medulla, with the result that a sudden dilatation, of the capacious blood-vessels of the abdomen, occurs, and that there is a rapid fall of the blood pressure. The peripheral resistance is in this manner immediately diminished, and paralytic distention of the left ventricle prevented. [Where the arterial constriction and increased blood pressure are slowly and gradually established, compensation is effected in a different manner, viz., by the gradual increase in the strength of the pump, witness the hypertrophy of the left ventricle, which occurs in cirrhotic form in Bright's disease.] It has been thought that the vaso-dilator and vaso-con- strictor centres are also connected with the cardio-inhibiting centre in the medulla ; and some physiologists have supposed that reflex inhibition of the heart might be produced by the stimulation of the sensitive nerve of the heart (superior cardiac nerve), which presumably occurs in conditions of over dis- tention of the organ. The recent experiments, however, of Relationship of Heart and Minnie Blood-vessels. 45 Ludwig and Luchsinger, and of Sevvall and Donaldson, seem to prove that this is not the case, and that increased blood- pressure within the heart, as a whole, generally weakens the inhibitory influence of the vagus. The last two observers, however, conclude ' that changes of intra-cardiac pressure, ivJien experienced by the ventricle alone' (no italics in the original), ' are without effect on the cardio-inhibitory function of the vagus.' ^ Possibly, therefore, when the ventricles only are over-dis- tended, some reflex inhibition may occur ; but, even if it does occur, it certainly must be temporary and slight, for the main effect of stimulation of the sensitive nerve of the heart is reflex stimulation of the vaso-dilator centre, and consequent diminution of blood-pressure throughout the body ; and dimi- nished blood-pressure, as we have previously seen, tends to lessen rather than to increase, the inhibitory action of the vagus. So again, in some cases of sudden palpitation, the rise in blood pressure, which would necessarily be produced by the excessive action of the muscular pump, is possibly prevented by the stimulation of the cardio-inhibitory centre. Vice versa, if from any cause the general blood pressure is suddenly diminished, the restraining influence of the cardio-inhibitory centre is removed, and the rapidity of the heart's action is increased — and the fall in blood pressure is to some extent at least counteracted. ' Journal of Physiology, vol. iii. p. 363. ^6 Diseases of the Heart. CHAPTER II. GENERAL PATHOLOGY OF THE HEART. Having directed attention to some of the more important problems connected with the physiology of the heart, I will now briefly sketch the general pathology^ of the organ. In considering the pathology of the heart, it is important to remember that it is a composite anatomical structure, and that it may be said to consist of three distinct parts, viz. :— 1. The pericardium. 2. The muscular substance or myocardium. 3. The endocardium. The affections of the heart are €\\\\&x functional ox organic; and I must now briefly describe the characteristic features of each of these great groups of conditions.^ The Functional Affections of the Heart. The main characteristics of the purely functional^ affec- tions of the heart are as follows : — (I.) They have no distinct morbid anatomy ; in other words, in the purely functional disorders no changes are to be found after death in the heart itself. ' The special pathology and morbid anatomy of the individual diseases which aflfect the heart, will be more conveniently considered when I come to treat of the individual affections in detail. ^ The distinction of organic and functional disease. In cases of organic disease distinct structural changes are found after death, but in functional disorders no such changes can be demonstrated. It is impossible, however, to draw a sharp and absolute line of distinction between these two conditions, for every functional derangement does without doubt depend upon histological or chemical changes in the anatomical elements of the affected part, and it is probable that as our means of investigation become more minute, many of the so-called functional affections will be proved to be organic. ^ The purely functional affections, in which there is no distinct morbid anatomy, are practically synonymous with the neurotic affections of the heart. General Pathology of the Heart. 47 (2.) They are often sudden in their onset, and usually temporary in their duration ; they seldom if ever destro}' life, and they are not, as a rule, followed by any permanent injurious effects. Some of the so-called functional affections do occasionally result in organic disease ; in exophthalmic goitre, for example, palpitation and accelerated action of the heart are prominent symptoms, and are for a time, at least, unattended by any perceptible physical alterations of the organ, but hypertrophy, and more especially dilatation, do in many cases ultimately occur. (3.) They are, as a rule, due to derangement of the nervous mechanism of the heart ; and the primary cause is very often located in some distant organ. In some cases, the primary lesion (if we may use the term in connection with hysteria, hypochondriasis, etc.) is cerebral. Under this head are included the derangements of the heart which are so frequently met with in hysteria, hypochondriasis, and the like. In others, the cervical portion of the spinal cord is the part at fault. Palpitation and extreme rapidity of the heart's action are occasionally met with, for example, in cases of myelitis and locomotor ataxy. In a third group of cases, the primary lesion is situated in the cervical sympathetic ; and in this group we are probably right in placing the derangements of the heart, which are such striking symptoms in the affection termed exophthalmic goitre. In a fourth group, the derangement of the heart is due to reflex irritation, the primary cause being situated in some peripheral organ, such as the uterus or ovary. While in other cases, the intra-cardiac nervous mechanism itself, or the muscular fibres, are directly affected ; the palpi- tation, irregular action, etc., which result from the use of some drugs, should probably be included under this head. (4.) The symptoms are usually referred to the heart itself, and consist of uneasy sensations, such as pain and palpitation. There are seldom any symptoms resulting from mechanical derangement of the circulation. 4 8 Diseases of the Heart. The Organic Diseases of the Heart. The chief characteristics of the organic diseases of the heart are as follows . — 1. They have a distinct morbid anatomy. 2. They are both acute and chronic ; they are often per- manent, or are usually followed by permanent structural defects ; they frequently shorten, and often destroy life. 3. They may affect either the pericardium, myocardium, or endocardium, in many cases all three structures being involved. 4. Their mode of origin is various, but the following main groups may be described : — A. In some cases the disease is /nw^n'/j^ mnZ/rtc. Under this head are included : — (rt.) The congenital malformations and imperfections, such as congenital stenosis of the pulmonary orifice and patency of the foramen ovale. {b) The mechanical ruptures of the valves which some- times, though rarely, occur independently of any previous cardiac disease.^ {c) Primary new growths of the heart, such as primary cancer and primary sarcoma. These cases are extremely rare. {d) Primary (idiopathic) inflammations of the heart, e.g., primary idiopathic pericarditis, primary idiopathic endocar- ditis, primary idiopathic myocarditis. These conditions are extremely rare, but they are occasionally met with. In many cases these so-called primary idiopathic inflammations are in reality rheumatic ; cases of pericarditis are, for example, occa- sionally met with, in which the cardiac inflammation is fol- lowed, instead of being preceded, by swelling of the joints and the other symptoms of acute rheumatism. ' In the large proportion of cases of rupture of the valves, which occur during violent effort, mental agitation, and the like, the valve, which gives way, is not absolutely healthy, but has been weakened by previous disease. General Pathology of tJie Heart. 49 (e) The local softenings, dilatations, and ruptures of the muscular substance which result from disease of the coronary arteries.^ B. In others, the cardiac disease is part and parcel of a general affection. Under this head are included : — ia) The inflammations of the pericardium, of the endo- cardium, and of the myocardium, which occur in the course of rheumatic fever, scarlet fever, Bright's disease, and many other general affections. {b}j The softening and degeneration of the cardiac muscle which occur in cases of prolonged high temperature (pyrexia), notably in typhus. (c.) The fatty degeneration of the heart, which is associated with general fatty changes throughout the body ; and the fatty degeneration which is met with in conditions of ansemia, notably in the so-called progressive pernicious or idiopathic variety. {d.) The waxy degeneration of the cardiac muscle, which is occasionally met with in the course of general waxy disease, but which is of little practical importance. (^.) The ulcerative form of endocarditis, which is in some cases closely allied to pyaemia, and in which the cardiac af- fection, though undoubtedly the most prominent and central (or local) lesion, is, in many cases, only a local manifes- tation of a general septic condition. (/!) The gummatous affections of the heart, which are occasionally seen in tertiary syphilis. {g) The hypertrophy of the left ventricle, that results from obstructed arterial circulation, and which is seen in its most typical form in the cirrhotic form of chronic Bright's disease ; and the dilatation and hypertrophy of the right ventricle, which result from obstructed pulmonary circulation, * Although I have placed these cases under the primary affections of the heart, it must be remembered that the disease of the coronary arteries, which gives rise to them, is usually part and parcel of a general arterial affection {e.g. atheroma). From this point of view, therefore, we might include local softenings, etc., in the second great group of cases. D 50 Diseases of the Heart. notably in connection with emphysema, cirrhosis of the lung, and the pulmonary congestion produced by mitral lesions. Many of the chronic affections of the heart, which at first sight appear to be primarily cardiac, i.e. to originate in the heart itself, should be included in this group. Chronic valvular lesions, for example, sometimes owe their origin to a previous attack of rheumatic fever and endocarditis. Fibroid degeneration, too, often results from a previous myocarditis ; while the rare condition, aneurism of the heart, is usually pro- duced by a local fibroid change, which in its turn may have resulted from a previous myocarditis. In other cases, valvular lesions (aortic valvular lesions more particularly) are due to atheromatous changes at the base of the aorta, which are part and parcel of a general arterial disease. C. In a third group of cases the disease of the heart is due to extension to the heart of a morbid process which has its original seat in some other organ. The extension may take place — (rt.) By direct continuity of tissue, as, for example, in those cases in which a pericarditis results from an inflammation of the pleura, or in which a mediastinal growth, a lympho-sar- coma, for instance, makes its way through the pericardium and involves the heart. {b.) Indirectly through the veins or lymphatics, as in those cases in which secondary tubercles, abscesses, cancers, or hydatids form in the substance of the heart or in the peri- cardium, the infective particles being carried to the heart from the lung or some other more distant organ. 5. The most prominent symptoms (dropsy, cough, short- ness of breath, etc.) are generally due to derangement of the venous or arterial circulation of distant parts or organs ; the symptoms, referred to the heart itself, being in most cases comparatively insignificant. Now, organic lesions of the heart chiefly affect the circula- tion in two ways, viz. : — General PatJiology of the Heart. 5 i A. By impairing the force of the cardiac muscle {cardiac pump). Lesions, such as fatty, fibroid degeneration, etc., which weaken the cardiac muscle, must of course impair its ' driving ' power, and of necessity produce retardation of the circula- tion. Lesions of this description usually involve both sides of the heart (both the right and left hearts), and affect more particularly the muscular walls of the ventricles. When the strength of the left ventricle is impaired, the amount of blood pumped into the arterial system is less than normal, while the left auricle, the lungs, the right heart, and the systemic venous circulation become over-distcndcd, and the rapidity of the whole circulation is decreased. When again the wall of the right ventricle is weakened, the amount of blood supplied to the lungs, left side of the heart and systemic arterial circulation is deficient, while the systemic venous circulation is over-distended. It is important, too, to remember that when the cardiac walls are weakened, the venous ostia (mitral and tricuspid orifices) are less firmly closed than in health, and a leakage through these orifices is apt to take place. This is probably the chief cause of the mitral regurgitation which occurs in chlorosis and many other conditions ; and this form of incom- petence we may conveniently term ' muscularl i.e. incom- petence due to defective muscular closure of the valvular orifice. Then again, when the cardiac walls are weakened, the blood pressure, which in conditions of health is opposed by the elastic resistance of the cardiac muscle, readily produces dilatation of the cardiac cavities, and this condition, i.e. dilatation, materially adds to the difficulties of the circula- tion, for the following reasons : — (a) In proportion as the dilatation increases, the walls of the cavity become thinner, and therefore weaker. {b) The greater the amount of blood which the cavity contains, the greater the amount of force required to empty it. (r.) Dilatation of the ventricles, by preventing the perfect 52 Diseases of the Heart. closure of the auricula-ventricular valves permits of regurgi- tation, and to this condition the term ' relative incompetence' is usually applied. It is probable, however, that in many cases of dilatation, defective muscular closure (the condition which produces ' miiscidar incompetence', as I term it) is a more important cause of regurgitation than the actual stretching of the valvular orifice itself. In dilatation, then, the muscular wall is not only weaker than in health, but a greater amount of work is actually de- manded of it ; and the circulation may be still further embar- rassed by regurgitation through the auriculo-ventricularorifices. It is extremely important to remember that the re- gurgitation which results from ' defective muscular closure,' and from ' relative incompetence,' is not necessarily a perma- nent condition. Indeed in many cases we can, by appropriate treatment, restore the cardiac muscle to its previously healthy state, and with the restoration of the cardiac muscle the regurgitation necessarily disappears. The condition, therefore, of the cardiac muscle, and the presence or absence of dilatation, are points of the greatest practical importance. Indeed, as we shall afterwards see, the prognosis is largely based upon the condition of the heart in these respects ; and the treatment of cardiac affections is, to a great extent, directed to maintaining the cardiac muscle in a sound and healthy state. B. By producing structural alterations in the valvular orifices, and valve flaps, ivhich interfere tvith the valvular mechanism, and prevent the steady onward flow of blood in the natural course of the circulation. These alterations constitute the great group of valvular lesions properly so called. They are usually permanent and incurable. They consist of adhesions, thickenings, contrac- tions, and ulcerations of the valve-flaps and adjacent parts, in consequence of which, narrowing {stenosis) of the valvular orifice, or imperfect closure of the valvular apparatus {incom- petence^ is produced. The two conditions (stenosis and incom- petence) are very generally combined ; in some cases stenosis, in others incompetence being the more prominent. General Pathology of the Heart. 53 Both conditions (stenosis and incompetence) interfere with the steady onward flow of blood in the normal direction, and produce diminished supply of blood to the parts in front of the lesion and vascular engorgement of the parts behind. But the manner in which these effects are produced differs some- what in the two cases. In stenosis the obstruction \% passive, the blood simply stagnating, as it were, in the cavities of the heart and parts of the circulation behind the ' block ; ' while in incompetence the obstruction may be termed active, for it is due to a ' backwash' or regurgitant current, which presses back, as it were, and arrests the advance of the blood column into the cavity of the heart, which is situated immediately behind the seat of the lesion. But further, the regurgitant current, passing as it does with considerable force into a cavity, the walls of which are relaxed and flaccid, has a stronger tendency to produce di- latation of that cavity than simple passive obstruction has — witness the condition of the left ventricle in aortic stenosis and incompetence respectively ; and dilatation adds, as we have already seen, very materially to the difficulties of the circulation. Now, from what I have said, it might be supposed that every structural alteration which produces either stenosis or incompetence of a valvular orifice, is necessarily attended by symptoms due to disturbance of the circulation ; and such in truth would be the case, if it were not for the fact, that nature adapts herself to the altered condition of things ; and that certain secondary changes are gradually established, by virtue of which the bad effects of derangement of the circula- tion are resisted, and by means of which the normal balance, so to speak, of the circulation is maintained or re-established. There is, in short, in almost all cases of valvular defect, a natural effort to compensate the lesion, the importance of which in a practical point of view, it is impossible to over-estimate. These compensatory changes consist of alterations in the heart, the object of which is to restore and maintain the balance of the circulation, and to resist the injurious effects of the lesion on the heart itself; and of certain changes in 54 Diseases of the HearL the peripheral tissues, by means of which the injurious effects of backward pressure and venous stagnation are, to some extent, prevented. The exact nature of these compensatory changes, which depend upon (i.) the valve which is affected ; and (2.) the manner in which it is affected {i.e. whether stenosis or incom- petence, is the chief lesion), will be more appropriately con- sidered when I come to treat of the individual valvular lesions in detail ; but, speaking broadly, I may say that in all valvular lesions compensation is chiefly effected by hypertrophy of the walls of the cardiac cavity or cavities, which are situated behind the affected orifice.^ When, for instance, the aortic orifice is contracted, the muscular wall of the left ventricle becomes thicker, and the ' driving ' power of the left heart being materially increased, a larger quantity of blood is propelled in a given time through the narrowed orifice than could possibly have been the case in the normal (un-hypertrophied) condition. So again stenosis of the mitral valve is followed by hypertrophy of the left auricle, but in this case (the normal function of the auricle being passive rather than active, and the resisting power of its walls — against the blood pressure — depending not only upon the muscular tissue but also upon the connective tissue layers of the endocardium), the hypertrophy consists not only of an increase of the muscular wall of the auricle, but also of thick- ening of its elastic tissue lining. By these means its resist- ing power is materially strengthened at the same time as its propelling power is increased.^ This increase of the con- nective tissue coat of the auricle is (in proportion to the amount of muscular hypertrophy) still more marked in mitral ' Alterations in the frequency of the cardiac contractions also exert an important compensatory influence, more especially, as we shall afterwards see, in the case of aortic lesions. - The reader must not suppose from this statement that all fibroid changes in the cardiac walls add to the resisting power of the organ. When the muscular tissue of the organ is replaced by fibrous tissue, as it is in fibroid degeneration, both the ' driving ' and resisting power of the organ are diminished. It is only when the muscular wall remains healthy, or is hypertrophied, that an increase of the fibrous tissue in the endocardium can possibly add to its resisting power. General PatJiology of the Heart. 55 incompetence, in which condition, as we have previously seen, increased resistance is necessary to counteract the dilating force of the regurgitant current, but in which there is no obstruction to the passage of the blood from the auricle to the ventricle. So again in aortic regurgitation, the forcible pas- sage of an abnormally large quantity of blood into the cavity of the left ventricle during its diastole (from the aorta through the incompetent valve, and from the left auricle through the mitral orifice), produces over-stimulation of the muscular fibre, in consequence of which, hypertrophy of the left ventricle is produced ; and this for a time, at least, is able to counter- balance the bad effects of dilatation, a condition which is produced, as we have already seen, by the too forcible dis- tention of the cavity while its walls are flaccid and relaxed. The hypertrophy, then, which follows and accompanies valvular lesions, is eminently beneficial, though it is not in all cases an unmixed good ; and I cannot insist too strongly upon the immense importance of this doctrine of compensa- tion. The symptoms, as we shall afterwards see, are trivial, or altogether absent, so long as the compensatory changes are sufficient to balance the bad effects of the lesion ; the prognosis is very largely based upon the amount of com- pensation and the capabilities of repair which are present ; while the treatment is in great part directed to promoting and maintaining the hypertrophy and other secondary changes, by means of which the balance of the circulation is restored and maintained in a comparatively normal condition. The amount of compensation which is possible in any given case, depends chiefly upon the following circumstances : I. TJie siiddauiess, extent, anel character of the lesion. A very extensive lesion, which occurs suddenly — rupture of the heart, for instance — may of course destroy life so rapidly that compensatory changes cannot possibly occur. Then again a severe (but not immediately fatal) lesion which occurs suddenly, is with difficulty compensated — rup- tures and ulcerations of valves are examples. In other cases, on the contrary, in which the progress of the lesion is slow and gradual, compensation is easily 56 Diseases of the Heart. established, and is very complete. In many chronic valvular lesions, for example, compensatory changes advance pari passu with the morbid process, and for a time at least, the balance of the circulation is so satisfactorily maintained, that the patient (provided that he lives a quiet and tranquil life, and does not suddenly add to the difficulties of the circula- tion) may be unaware of the existence of any cardiac defect. 2. The reparative pozvers of the patient, and especially the capabilities of compensation existing in the heart itself 3. The resisting power of the tissues, which in its turn depends upon the soundness and vitality of the individual organs, and especially upon the vaso-motor nerve tone, and the vitality of the whole organism. In young persons, where the tissues are healthy, and in persons of good nerve tone and tranquil disposition, com- pensation is satisfactorily, and, for a time at least, effectually established. Vice versa, in old people, in persons whose tissues are unsound or degenerating, more especially in those in whom the nerve tone is bad, compensation is, from the first, imperfect, and the injurious effects of the lesion are speedily manifested in the form of symptoms. The condition of the tissues, then, as a whole, and the reparative power and vitality of the patient are facts which the practical physician must ever keep prominently in view. Indeed, we may lay it down as an axiom, that in looking at cardiac cases, zuhether from a pathological or a clinical point of viezu, and more especially in considering the prognosis and treatment, it is quite as important (I might even say that in some cases it is more important) to look at the condition of the system as a zvhole, as it is to regard the condition of the heart in particular. He is in fact a poor physician who concentrates his attention upon the tissue or organ which is primarily affected ; and this statement holds good even should he succeed in arriving at an accurate estimate of the cardiac or other local lesion ; while the best physician is he who accurately guages the nature and extent of the local lesion, and at the same time takes a broad and comprehensive all- round view of the case. Clinical Exajuination of Cardiac Cases. 5 CHAPTER III. THE CLINICAL INVESTIGATION OF CASES OF CARDIAC DISEASE- METHOD OF CASE-TAKING — SUMMARY OF SYMPTOMS — THE PHYSICAL EXAM [NATION-INSPECTION— PALPATION— PERCUSSION^ AUSCULTATION— THE USE OF THE SPHYGMOGRAPH. Having considered some of the most important points connected with the physiology and general pathology of the heart, we are now in a position to take up the clinical exami- nation of the organ. And in order to make this most import- ant part of our subject as clear and intelligible as possible, I will first sketch out the method of case-taking, and the plan of examination which I am in the habit of employing in the investigation of cases of cardiac disease — and we shall, then, be in a position to consider the symptomatology and physical examination in detail. Under the head of the physical examination I shall : — 1. Describe the normal physical signs {i.e. the signs appreciable to the senses — aided and unaided — of the phy- sician, which result from the physical condition of the organ in its healthy state), and their mode of production. 2. Describe the pathological physical signs {i.e. the signs which result from the physical condition of the organ when diseased) and their mode of production. 3. Give in a short and summary manner, the leading facts, which will enable us, in any case in w^hich an abnormal physical sign is detected, to determine the nature of the lesion which is present ; for it is important to remember that few physical signs are absolutely distinctive (pathognomonic); in fact, diseased physical signs, such as increased dulness on percussion over the prscordia, may be due to several different morbid conditions. 58 Diseases of the Heart. METHOD OF CASE-TAKING. A. PRELIMINARY FACTS :— Name— Age— Sex— Married or Single- Occupation— Full I'uslal Address — Date of Admission to Hospital. B. COMPLAINTS: — (The Symptoms which bring the patient to consult the physician). C. THE HISTORY:- (i.) Of the Present Illness: — The exact date of its commencement. The exact mode of commencement. The supposed cause of the attack. The exact character of the symptoms ; the order of their appearance ; and the treatment which has been adopted, up to the time when the patient comes under observa- tion. (In acute cases take the temperature.) (2.) The Health History prior to the commencement of the present attack : — Especially a history of disease or injury likely to be followed by disease of the heart. The habits, mode of life, and general surroundings of the patient. (3.) The Family History: — Especially the occurrence of heart affections or of acute rheumatism amongst near relatives. D. THE PRESENT CONDITION :— (The date at which the examina- tion is made should be stated.) (I.) The Physiognomy of the Case :— The description of any striking abnormal appearances. The condition of the superficial vessels. The character of the breathing. The presence of subcutaneous oedema. The attitude. The general state of nutrition. The facial expression, etc. (2. ) The presence or absence of subjective symptoms referred to :— (a.) The Heart /to'/^'.— (Uneasy sensations in the region of the heart, palpita- tion, pain, etc.) {b.) Distant Organs or Parts. — (Symptoms resulting from mechanical dis- turbance of the circulation — deficient supply of arterial blood, or venous engorgement, etc.) (3.) The Physical Examination of the Heart and Circulatory Organs. The Physical Examination of the Heart. Inspection of the Pracordial Region. Observe : — (a.) Its form and configuration. {b.) The position, extent, and character of the visible impulse, especially the position of the apex beat, (r.) The condition of the integument over the precordial region. Method of Case-taking. 59 Palpation of the HcarL Note : — [a.) The exact position of the apex beat. {b.) The character of the cardiac contractions (force, rhythm, celerity, etc.) (r. ) The presence of prascordial thrills or friction fremitus. {d. ) The presence of pain or tenderness on pressure over the praecordia. Percussion of the Heart. Determine : — (a.) The area of superficial or absolute dulness. (/'. ) The area of deep or relative cardiac dulness. Auscultation of the Heart. Determine : — ((7.) The rhythm of the heart, whether regular or not. {h.) The character of the individual (first and second) sounds in the mitral, aortic, pulmonary, and tricuspid areas, as regards : — Loudness or intensity. Tone and purity. Reduplications. Murmurs, (c. ) WTiere a murmur is present, observe : — Its rhythm. Its point of differential maximum intensity. The direction in which it is propagated. Its sound characters. The Physical Examination of the Aorta and Great Vessels. Inspection. The conformation of those parts of the thorax and abdomen which are super- ficial to the aorta and great vessels, must be observed, particularly the presence of any prominence, pulsation, or tumour. Palpation. Determine : — (a) The presence of any undue pulsation in the supra-sternal notch, or of any abnormal pulsation in the thorax or abdomen. (b) The presence of thrills, tenderness on pressure, etc., in the course of the aorta or great vessels. Percussion. Note :— The presence of dulness on percussion in the course of the aorta or great vessels; its exact extent, outline, etc. Auscultation. Observe : — The character of the heart sounds, and the presence or absence of murmurs over the course of the aorta or great vessels (their rhythm, direction of propagation, etc.) 6o Diseases of the Heart. The Examination of the Superficial Arteries. Note the condition of the superficial arteries, such as the carotids, brachials, temporals, etc., by inspection, and if necessary by palpation and auscultation : and particularly observe the condition oi t/ie pulse {i.e. the radial artery) : — (a.) By the finger (palpation) as regards :— Its frequency. Its rhythm. Its volume. Its compressibility or tension. The special characters of each pulse wave (celerity, dicrotism, etc.); and the condition of the vessel (in respect to its fulness) during the diastole of the ventricle. The condition of the arterial coats. The comparative conditions on the two sides of the body (i.e. the comparison of the two radial arteries). {l>.) By the eye (inspection). (c.) By the sphygmograph. The Examination of the Venous System. inspection. Note the condition of the superficial veins, and particularly observe the condition of the jugulars as regards fulness, the presence of pulsation, etc. Auscultation. Note the presence or absence of a venous hum in the neck, over the orbit, Torcular Herophili, etc. (4.) The condition of the Respiratory, Alimentary, Genito- Urinary. Nervous, and Integumentary Systems. E. THE DIAGNOSIS. F. THE PROGNOSIS. G. THE TREATMENT— Hygienic, Dietetic, Medicinal (general and local). H. THE SUBSEQUENT COURSE OF EVENTS. The progress of the case during the patient's stay in hospital. The mode of termination of the case. The date of termination. In fatal cases the record of the post-mortem examination, and an account (when necessary) of the subsequent microscopical examination of the tissues and organs. Symptoms. 6 r SUMMARY OF THE CHIEF SYMPTOMS. Age. — Diseases of the heart may occur at any age, but some affections are more common at one period of hfe than at another. Childhood. — Congenital Alalfonnations are generally at- tended with symptoms, and are, therefore, as a rule, observed immediately or soon after birth. Many cases prove fatal during the first few weeks or months of extra-uterine exist- ence ; and severe cases, which do not die at an early stage, usually succumb at or about the time of puberty. Congenital malformations are, therefore, rarely noticed, except on the post-mortem table, in the adult.^ Acute inflammations, more especially endocarditis, are sometimes seen in children, and are probably of much more frequent occurrence than is generally supposed ; and cases of valvular disease are by no means rare before the age of puberty; mitral lesions frequently follow scarlet fever, and mitral regurgitation is present in a considerable proportion of the cases of chorea. Youth and Early Adult Life. — Functional affections of the heart are most common from the age of puberty up to the age of twenty-five or thirty, but are also, of course, met with in later life. Acute inflammations of the heart, more especially those forms which are associated with rheumatism, are also most common in early adult life. The valvular lesions, more especially the lesions of the mitral valve, which so often follow acute endocarditis, are consequently of frequent occurrence at this time. Active manhood. — The lesions of the heart and arteries, which are due to strain, syphilis, and drink, now begin to appear, aortic valvular lesions and aneurisms being espe- cially prominent. The forms of disease, which are prevalent in early adult life, also occur. ' Congenital lesions of the valves which have not interfered with the circulation, and which were not suspected during life, are not unfrequently discovered after death. In cases of this description the congenitally malformed valve is frequently the seat of disease acquired in later life— of endocarditis, chronic valvular lesions, etc. 62 Diseases of the Heart. Later Adult Life and Old Age. — Valvular lesions, which in some instances date from a former attack of acute rheumatism, and have been long latent, now begin to be actively manifested ; and all the other lesions which depend upon degenerative changes either in the heart or arteries become prevalent. Tnie angina pectoris is seldom observed before the age of forty ; fatty degeneration of the heart, dilatation, and valvular lesions of all kinds, are extremely common, and cause a large proportion of the deaths between the ages of fifty-five and sixty. In women the period between forty-five and fifty, and in males between fifty-five and sixty, seems a particularly critical one. The tendency to aortic valvular lesions, aneurism, and all the other cardiac changes which depend upon atheroma, steadily in- creases with the age of the individual ; and these affections (aneurism, apoplexy, etc.) would be still more prevalent if it were not for the inactive (strainless) lives which most old people lead, the tendency to arterial rupture being in con- sequence reduced (considering the condition of the arteries) to a minimum. Sex. — The functional derangements of the heart, which accompany hysteria and anaemia, and the cardiac affections which are met with in cJiorea and exophthalmic goitre are very much more common in the female sex.^ Those cardiac affec- tions, on the contrary, which are due to atheroma and gout, to strain, syphilis, and alcohol, are very much more prevalent in males ; aortic lesions, aneurisms, and true angina pectoris are examples in point. Occupation. — The occupation of the patient exercises a very distinct influence in the production of cardiac disease. Persons who are exposed to cold and wet, such as washer- women, firemen, cabmen, etc., are much more liable to con- tract rheumatic fever, and therefore to suffer from acute inflammatory affections of the heart and the chronic valvular ' Hysteria, chlorosis, chorea, and exophthahnic goitre are all much more common in females. Sympto7ns. 6 J lesions, which so frequently supervene upon acute endo- carditis, than other people. Blacksmiths, puddlers, paviors, and all persons engaged in laborious occupations, more espe- cially those who have to make sudden efforts, and who are therefore exposed to strain, are more liable to atheroma, aortic valvular lesions, and aneurism, than other people. Soldiers and sailors are also very often affected with arterial disease probably because they are much exposed to strain, and because they are more subject to syphilis than other members of the community, and are also frequently addicted to alcoholic excesses. The constriction of the neck and chest, which is produced by tight or badly fitting clothing and accoutrements, is probably also another cause for the pre- valence of aneurisms amongst soldiers ; the constriction pro- duces a direct mechanical impediment to the circulation, which is increased by any strain or violent exertion, such as a charge at 'the double,' or a 'forced march.' Complaints. — In order to understand the ' complaints ' of the patient, it is essential to remember that the heart is a vital organ as well as a mechanical pump. There are, in short, two great groups of cardiac symptoms. (i) In one, the symptoms are referred to the heart itself, and depend upon the fact that the patient is conscious of some derangement in its action as a vital organ. These symptoms, which may for the sake of convenience and description be termed 'vital ;' or better, 'subjective cardiac sensations', consist of: — uneasy sensations in the region of the heart; conscious- ness of excessive or disordered action (palpitation, irregu- larity, intermittent action, and the like) ; and in some cases, severe pain in the cardiac region. (2) In the other group, the symptoms are referred to some distant organ or part, and depend upon the mechanical derangements in the circulation which are produced by the cardiac lesion {i.e. derangement of its action as a mechanical pump). Giddiness, fainting, cough, shortness of breath, dropsy, dyspepsia, drowsiness, etc., are examples of this group, to which the term ' mechanicar may be appHed. 64 Diseases of tJie Heart. The mechanical symptoms arc, for the most part, due to one or other of two conditions, viz. : — (a) Defective siipply of arterial blood to distant organs and parts. — The attacks of giddiness, fainting, the feeble motor power in the lower extremities, and the muscular twitchings in the face and lower limbs, which are seen in some cases of aortic regurgitation, are good examples of this group of symptoms. (b) Venous engorgeinent of distant organs and parts. — The symptoms which are due to this cause are both numerous and important. In fact, many of the most pro- minent symptoms in cardiac cases are due to the secondary alterations in distant organs, and to the complications which result from the long-continued venous engorgements which I am now describing. Venous engorgement of the lungs, for example, produces shortness of breath, cough, haemoptysis, etc., and predisposes to the attacks of bronchitis and pneu- monia, which are so common in cardiac cases, and which are attended by characteristic symptoms. Venous engorgement of the kidneys produces marked alterations in the urinary secre- tion ; the amount of urine is diminished ; the specific gravity is high ; the urine is highly coloured, loaded with urates, and often albuminous. In the course of time a form of cirrhosis of the kidney may be established. In addition to these lung and kidney symptoms, others, due to engorgement of the liver, stomach, intestines, brain, etc., are commonly observed ; while the congestion of the subcutaneous veins, and the veins in the zualls of the scrolls cavities, produces dropsy, which is almost invariably first observed in the feet, but which may ultimately involve an extensive area of the subcutaneous cellular tissue and almost all the serous cavities of the body.^ It is of great importance to remember that the occurrence of dropsy in these cardiac cases, depends in no ' Cardiac dropsy begins in the lower extremities, because being farther removed from the heart, the circulation in them is slower than in other parts of the body. It is generally worse at night, because during the day, when the patient is standing and going about, the return current of blood has to overcome the force of gravity in its passage backwards to the heart. Symptoms . 65 small degree upon the condition of the vaso-motor nerve tone, and the general vitality — the resisting power, so to speak, of the tissues. The composition of the blood, too, is an important element in its production. In addition to the two great groups of symptoms already referred to, two minor groups may also be described : — (a) In this group the symptoms are for the most part mechanical, but inasmuch as they are irregular and accidental in their occurrence, should be distinguished from the mechani- cal symptoms which I have hitherto described. To these symptoms, which are due to plugging of distant vessels by particles of fibrine (emboli) detached from clots in the heart, or from vegetations on the cardiac valves, the term accidental may be given. The exact nature of these accidental symptoms depends for the most part upon the vessel which happens to be ob- structed, upon the size of the plug, and upon the rapidity with which the obstruction is produced. Particles of fibrine detached from the cavities or valves of the right heart produce embolic infarctions in the lungs, of which the chief symptom is haemoptysis ; limited inflam- mation of the pleura usually results, and, in those cases in which the infarction is of large size, the consolidation of the lung which it produces, can be recognised by percussion. Sudden obstruction of the main branches of the pulmonary artery — a condition which seldom occurs in cardiac cases, but which is sometimes seen after delivery, and in phlebitis, — may be followed by immediate death. In other cases, the termina- tion is not so rapid, death being preceded by intense dyspnoea, cyanosis, quick and tumultuous action of the heart, rapid elevation of temperature, etc. When the embolon is detached from the left cavities, it finds its way into some of the branches of the systemic arterial circulation. In some cases, it passes up the left common carotid artery, and lodges in the middle cerebral artery of the left side, producing right-sided hemiplegia and aphasia. In some of these cases the attack is ushered in by sudden loss E 66 Diseases of the Heart. of consciousness, in others there are epileptiform convul- sions ; in others again (and more particularly in those in which the hemiplegia occurs more gradually) consciousness is retained. In some cases the embolon lodges in the spleen ; in others in the kidney ; and, in fact, it may be carried to almost any part of the. body. The pathological character of the plug is also a point of some importance. In ordinary cases it consists, as I have already mentioned, of fibrine, and the effects which it produces are, for the most part, mechanical. In many cases of ulcerative endocarditis, micrococci abound in the vegetations covering the affected valves, and, being conveyed by the emboli to distant organs, there set up a similar infective process to that which is occurring in the heart. (b) In this group the symptoms are the result of pressure. In intra-thoracic aneurisms, and in some cases of pericarditis, for instance, prominent symptoms, such as pain, dysphagia, alterations in the voice, cough, etc., may be due to this cause. The more particular description of the symptoms, included in these four groups, will be more appropriately deferred until I come to treat of the individual cardiac diseases in detail. But it may perhaps be well, before going further, to consider a little more fully than we have yet done, dyspnoea, cough, and expectoration, three symptoms which are very common in cardiac cases, and which may be due to a considerable variety of different conditions. Dyspncea. Alterations of the breathing are frequently met with in cardiac and arterial disease. In some cases, the difficulty of breathing is only occasional, in others, it is constantly present ; in some it is due to over-exertion or other obvious exciting cause ; in others, it occurs independently of any apparent external conditions. The chief forms of dyspnoea, and the conditions which give rise to them, are as follows : — Cardiac Dyspncea. 67 1. Breathlessness on exertion (going up stairs, climbing a hill, etc.), the breathing being natural when the patient is at perfect rest. This is the most common form of cardiac dys- pncea. It occurs more particularly in mitral lesions ; in those cases in which the right cavities of the heart are dilated ; and in cases of anaemia, in which, as we have seen, cardiac symp- toms are common. (The dyspnoea in cases of anaemia is doubtless in great part due to the altered composition of the blood independently of the cardiac condition.) 2. The dyspnoea which results from alterations in position (probably from alterations in the position of the diaphragm) independently of pulmonary complications, such as bronchitis, oedema of the lungs and hydro-thorax. In many cases of advanced cardiac disease, more especially when the aortic arch, or the right cavities of the heart are much dilated, dyspnoea is readily excited by slight changes in position. It is common to find patients, breathing comfortably and quietly so long as they are sitting and at rest, unable to lie down for some time after getting into bed, on account of the dyspncea produced by the alteration in their position. In some cases the heart, after a time, accommodates itself to the altered condition of things ; the breathing quiets down, and the patient falls asleep. This form of dyspnoea is probably in many cases due to the altered position of the diaphragm, and seems closely allied to the difficulty in breathing, which cardiac patients so frequently experience after a full m.eal, when the stomach becomes distended with flatus, during attacks of dyspepsia, etc. In some cases it seems to be produced by reflex im- pressions passing from the stomach through the vagus nerve to the heart. 3. Paroxysmal attacks of dyspnoea. Sudden difficulty in breathing is occasionally met with in the course of cardiac affections. In some cases it is due to sudden over- distention of the cardiac cavities ; in others, to spasm of the glottis, produced by the pressure of an aneurism of the aortic arch upon the left recurrent laryngeal nerve ; in others, to the sudden pressure of an aneurism upon the 68 Diseases of the Heart. trachea ; in others, to the sudden oedema of the lungs, which sometimes, though rarely, results from excessive over-distention of the left ventricle ; in others to sudden distention of the right ventricle, and imperfect supply of blood to the lungs ; while in exceptional cases severe dyspnoea may be caused by embolic plugging of the pul- monary artery. In cases of this description the difficulty of breathing is intense; the patient has to sit up, and literally to fight for breath. The duration of the attack varies ; in some cases, it is onl>' temporary ; in others (as for instance, in the case of an aneurism pressing upon the trachea or primary bronchi) it may continue for several days. In many cases death terminates the attack. 4. Typical Orthopnoea. In other cases the difficulty in breathing which was first slight, steadily increases, and a permanent condition of orthopnoea, which may continue for several days, or even weeks, is gradually developed. Such a condition is common in the late stages of cardiac cases, more particularly in advanced stages of mitral disease and in dilated conditions of the right heart. The patient is more or less cyanotic. Dropsy is usually a prominent symptom, and the difficult}' in breathing depends, in many cases, upon pulmonary complications, such as hydro-thorax, bronchitis, oedema of the lungs, etc. 5. Cheyne-Stokes' Respiration : Angina sine dolore. — In some cases of cardiac disease, more particularly where the right heart is dilated and fatt}-, a peculiar form of rhythmical dyspnoea is observ^ed, to which the term Cheyne-Stokes' respiration is given, after the two physicians (Drs Cheyne and Stokes) who first described it. In this form of dyspnoea the patient experiences considerable difficulty of breathing for a few respirations. The dyspnoea gradually subsides, the respirations becoming shallower and shallower, slower and slower, until for a time — it may be for half or three quarters of a minute — they are entirely suspended ; they then gradually reappear, and become deeper and deeper, quicker and quicker, until the height of the paroxysm of dyspnoea is reached. Cheyne-Stokes Respiratio7i, 69 (See fig. 16.) The same sequence of events then recurs. The duration of the whole cycle from the height of one paroxysm of dyspnoea to the height of the next paroxysm, is usually from one to two minutes, half, or less than half, being occupied by the period of non-respiration or rest. Fig. 16. — Diagraniniatic representation of Cheyne-Stokes' Respiration. Cheyne-Stokes' respiration is not pathognomonic of any single condition ; it is a rare phenomenon, and has been observed in : — (a) advanced cases of cardiac disease (more especially, as I have already mentioned, in a dilated and fatty condition of the right heart, atheroma of the coronary arteries, and dilatation of the aorta) ; (b) certain cerebral affections (more especially lesions in the neighbourhood of the medulla oblongata) ; (c) uraemia ; and (d) very exceptionally in other conditions. Cheyne-Stokes' respiration is a very grave and ominous symptom ; it only occurs in advanced cases of cardiac disease, and is, as a rule, speedily followed by death. It is closely allied to the condition which is termed angina sine dolore. In many cases of Cheyne-Stokes' respiration the arterial tension is very markedly increased ; this was notably so in two typical cases which have come under my own observation. In some cases the condition continues for many hours, it may be for several days ; the sufferings of the patient (though not painful in the common acceptation of the term) are extreme ; he becomes much exhausted, and often very drowsy and sleepy. No sooner, however, does he dose off to sleep than he wakes with a horrid dream or with a start ; and the waking is always associated with the period of dyspnoea, i.e. it always occurs, so far as my observation goes at the height of the paroxysm of dyspncea. 70 Diseases of the Heart. In Cheyne-Stokes' respiration, then, there is an alternate condition of dyspncea and apnoea, the two conditions being separated by a gradual rise and fall in the depth and fre- quency of the respirations. The exact cause of the condition is not definitely known. Its immediate cause is, without doubt, perverted action of the respiratory centre in the medulla ; and in order to understand the manner in which this perverted action may be brought about, I must now briefly describe the nervous mechanism of respiration. It seems probable : — (i.) That the nerve impulses, which throw the respiratory muscles (the muscles of inspiration and expiration) into action, are discharged from a centre which is situated in the medulla oblongata — the so-called respiratory centre. (Respiratory centres are also situated in the spinal cord, but that in the medulla oblongata is certainly the most important, and seems to initiate the process, and to control the action of the lower, i.e. of the spinal respiratory centres.) (2.) That under normal circumstances the action of this centre is rhythmical and automatic. (This point is not ab- .solutely determined, but it seems probable that the action of the respiratory centre in the medulla is automatic.) (3.) That although the action of this centre (the respiratory centre) is automatic, its discharges (both as regards their force and frequency) may be influenced by external conditions {i.e. conditions outside the centre) ; and that amongst these external conditions the amount of oxygen supplied to this centre by the blood is certainly the chief. When the blood contains a small amount of oxygen {i.e. when it is highly venous), or when the arterial blood supply to the centre is diminished or abolished, its nerve discharges are increased, i.e. the force and (to a less extent) the frequency of the respiratory movements arc increased ; in other words, a condition of d)\spncea may be developed. The attacks of dyspnoea which occur in some cases of cirrhotic Bright's dis- ease are probably due to this cause, viz., to a diminished supply of arterial (oxygenated) blood to the respiratory centre. In chronic Bright's disease the arterial tension is Cheyne-Stokes Respiration. 71 extremely high, in consequence, it is supposed, of a spas- modic contraction of the arterioles, and we can easily suppose that when the arterioles are tightly contracted, the blood supply to the respiratory centre in the medulla may be so much diminished as to produce a condition of dyspnoea. This form of dyspnoea is sometimes called renal asthma, the term is, however, a bad one, for the condition differs from the dyspnoea of spasmodic asthma in this important particular, that there is no obstruction to the passage of air into and out of the air cells. The respirations are not only more frequent, but they are much deeper than in health — to use the expres- sive words of my friend Dr Wyllie, a patient affected with this form of dyspnoea ' looks as if he had just been running a mile race.' When, on the contrary, the blood is over oxygenated, the nerve discharges from the respiratory centre are diminished in force and frequency, and a condition of apnoea may result. A free supply of arterial blood to the medulla, therefore, produces diminution of the respiratory movements, while a diminished supply of arterial blood, or a venous condition of the blood, is attended with the opposite result. The phenomena of Cheyne-Stokes' respiration are pro- bably to be explained (in part at least) by the fact, that periodical variations occur in the amount of oxygen supplied to the respiratory centre in the medulla. Various theories have been advanced to explain the manner in which Cheyne-Stokes' respiration is produced. None of them are, to my mind, perfectly satisfactory. The best known are those of Traube and Filehne. Traiibc's T/ieory. — Traube, starting with the idea that in the different clinical conditions, which give rise to Cheyne-Stokes' respiration, there is a diminished supply of properly arterialised blood to the respiratory centre, supposed : — (i) That in consequence of the deficient supply of oxygen, the irrita- bility of the respiratory centre is so materially lowered, that a much larger accumulation than usual of carbonic acid in the blood is required to arouse it into action. 72 Diseases of the Heart. (2) That in order to provide this increased quantity of carbonic acid, the intervals between the different respiratory acts are necessarily pro- longed, and that it is in this manner that the stage of apnoea is produced. (3) That at the end of the period of apnoea, the accumulation of car- bonic acid in the blood is so great, that the respiratory centre is aroused into action ; that the stimulation is at first slow and imperfect, but that it gradually gains in intensity and strength until the discharge, which is excited by it, is so violent, that a condition of dyspnoea is produced. (4) That in consequence of the increased respiratory efforts the blood becomes oxygenated ; the respiratoiy centre is therefore no longer stimu- lated, and in consequence of the cessation of the stimulation, or possibly of the fact that its irritability is exhausted, the respiratory centre gradually ceases to discharge, and the period of apncea supervenes. Various objections may be urged against this view, but the main one —and it seems to me a fatal one— is this, that a diminished supply of properly arterialised blood to the respiratory centre would excite it to dis- charge, rather than lower its irritability. Venous blood stimulates the respiratory centre, not so much because it contains an excess of carbonic acid, as because it is deficient in oxygen. With regard to this point, Dr M. Foster says, ' There can in fact be no doubt that the action of deficiently arterialised blood on the respiratory centre, as manifested in an augmentation of the respiratory explosions, is due primarily to a want of oxygen, and in a secondary manner only, to an excess of carbonic acid.'^ , Dr Saiisom's Modijicatioit of Trauhe's TIieo>y. — Ur Sansom agrees with the latter part of Traube's theory, but supposes that the impaired irritability of the respiratory centre, which Traube attributes to a deficient supply of sufficiently arterialised blood, is of a paralytic character, and that in many cases it is due to the direct result of a cerebral lesion. ' I consider,' he says, ' that the initial lesion is paresis of the respiratory centre, and though this paresis may be produced by reflex ner\'e influence, it is usually a direct exhaustion from cerebral causes — once initiated, the explanation of the phenomena on the theory of Traube is complete.'^ With this opinion I cannot entirely agree. It is difficult to see how a centre, which is in a state of paresis or paralysis (unless we include under that head a condition of irritable weakness such as I believe to be at the root of the matter) can be excited to such vigorous action as the respiratory centre evidently is ; and it is difficult, I think, to explain by this theory the total cessation of the respiration which occurs during the stage of apncea. I differ from Dr Sansom in thinking that the irrita- bility of the respiratory centre is impaired. It seems to me that a ' A Text Book of Physiology, 3d edition, p. 340. - Diagnosis of Diseases of the Heart, p. 39. Cheyne-Stokes Respiration. ']-}y condition of irritable weakness, in which it is more irritable^ more easily excited to discharge, but at the same time more easily exhausted than in health, would more satisfactorily account for the phenomena. But to this point I will presently return. Filelijie's Theory. — Filehne believes that the vaso-motor centre, as well as the respiratory centre, is concerned in the production of the condition. He supposes : — (i) That at the end of the period of apnoea the deficiency of oxygen and the excess of carbonic acid in the blood, stimulate the vaso-motor centre ; and that in consequence of this stimulation, the arteries through- out the body (including of course the cerebral vessels) are thrown into a condition of contraction. (2) That in consequence of the diminished supply of arterial blood to the respiratory centre, which results from this arterial contraction, stim- ulation of that centre (the respiratory centre) occurs, and is manifested externally in the form of dyspnoea. (3) That in consequence of the excessive respiratory efforts, the blood becomes quickly arterialised, the stimulation of the vaso-motor centre is thereby removed ; the tonic contraction of the arteries, therefore, disappears, and the respiratory centre is again supplied with arterial blood. Its discharges, therefore, become less and less powerful, and finally, when the arterial spasm is completely removed, the respiratory centre is so freely supplied with arterial blood that it no longer discharges, and the condition of apnoea is produced. After the apnoea has continued for a longer or a shorter period, the blood again becomes venous, the vaso-motor centre is again stimulated, the arteries again contract, and the whole sequence of events is repeated. This view at first sight seems very plausible, but it is certainly incom- plete, unless we suppose that there is, in addition, some condition present which renders the discharges from the respiratory centre more easy at one period of the cycle {i.e. during the period of dyspnoea) and more diffi- cult at the other period of the cycle {i.e. during the period of apnoea) than they are in health. It fails, I think, to account for the phenomena, unless we grant that some primary alteration in the respiratory centre, such as I have indicated, is present. If the conditions which Filehne suggests are all that are required, would not Cheyne-Stokes' respiration be of more frequent occurrence than it is ? Would we not expect it to be produced in every case in which the blood is imperfectly aerated? Again, it fails, I think, to account satisfactorily for the apnoea. There are surely circumstances of every day occurrence in which the medulla is quite as freely supplied with arterial blood as it is in cases of Cheyne-Stokes' respiration during the period of apnoea, i.e. after the arterial spasm is relaxed ; and if Filehne's theory is correct, why is it that in these cases apncea is not produced .'' 74 Diseases of the Heart. I am disposed, therefore, to think with Dr Sansom, that something more is necessary, and that there must be some alteration of the respira- tory centre itself, in addition to the conditions which Filehne's theory supplies. A state of irritable weakness would, in my opinion, account for the condition. The respiratory centre in the medulla oblongata probably consists of two parts— one connected with inspiration (the inspiratory centre), the other, with expiration (the expiratory centre). Now, according to Rosen- thal (quoted by Dr M. Foster), the inspiratory centre is the seat of two conflicting forces, one tending to generate inspiratory impulses (the dis- charging portion of the inspiratory centre, as we may call it), and the other offering resistance to the generation of these impulses (the restrain- ing or inhibiting portion of the inspiratory centre), the one and the other alternately gaining the victory, and thus leading to a rhythmical dis- charge.i Further, we may probably with truth suppose that the two parts of the inspiratory centre are differently acted upon by the same stimulus ; venous blood, for instance, which excites the action of the discharging portion, depresses the action of the restraining portion, vice versa arterial blood depresses the action of the discharging portion, but strengthens the action of the restraining part. Now, if we suppose that the discharging portion is in a condition of irritable weakness, in which it is more easily excited to discharge, but in which it tends to become more speedily and more completely exhausted than in health — (or, better still perhaps, that both portions of the centre are in this abnormal condition, i.e. a state of irritable weakness), we have, I conceive, a condition of things which will satisfactorily explain the phenomena. Let us suppose, as it is simpler, a case in vvhich the discharging portion is in a condition of irritable weakness, the restraining portion remaining normal. Starting, as we did in considering Filehne's theory, with the end of the period of apnoea, i.e. with the blood in a highly venous condition (see fig. 17), we may suppose : — (l.) That the venous blood gradually excites a paroxysm of dyspnoea : — Firstly and chiefl)' by acting directly upon the inspiratory centre itself, depressing the action of the restraining portion, and arousing the action of the discharging portion, which has, during the stage of rest or apnoea, been graduall)- recovering from the condition of exhaustion occasioned by the excessive discharge, which produced the preced- ing paroxysm of dyspnoea. Secondly., by stimulating the action of the vaso-motor centre, in consequence of which the arterioles are con- tracted, and the supply of oxygen to the respiratory centre is still further diminished. (See fig. 18.) ' Text Rook of Physiology^ 3d edition, p. 336. Cheyne-Stokcs Respiration. 75 (2.) That in consequence of the excessive ifritability of the discharging portion of the inspiratory centre, the discharges become excessive, and a condition of dyspnoea is produced. (See fig. 19.) (3.) That in consequence of the iveakncss of the discharging portion of the inspiratory centre it speedily becomes exhausted— over exhausted ; and the dyspnoea tends to subside. (See fig. 20.) (4.) That in consequence of the excessive respiratory efforts during the paroxysm of dyspnoea, the blood (which was previously venous) be- comes arterialised ; stimulation of the discharging portion of the inspira- tory centre ceases ; stimulation of the restraining portion is produced ; and in consequence of the deficient stimulation and over-exhaustion of the discharging portion, the restraining portion has full swing, and the condition of apnoea is produced. (See figs. 21 and 22.) The arterialised blood acts firstly and chiefly upon the inspiratory- centre itself, strengthening the action of the restraining portion and de- pressing the action (removing the stimulation) of the discharging portion ; secondly^ by removing the stimulation of the vaso-motor centre, in conse- sequence of which the arterioles dilate, and the supply of oxygen (arterial blood) to the respiratory centre is still further increased. During the stage of apnoea, the discharging portion, which was ex- hausted by excessive action during the period of dyspnoea, gradually regains its irritability, and the condition required for its stimulation, and for the removal of the control of the restraining portion, viz., a venous condition of the blood, is, in consequence of the absence of the respirator}- movements, gradually developed. In figures 17, 18, 19, 20, 21, and 22, 1 have endeavoured to represent the changes which I suppose occur in the different periods of the Cheyne- Stokes' cycle. By this theor)- we can, 1 think, satisfactorily explain : — [a] The occurrence not only of diminished respiratory movements after the period of dyspnoea, but the complete arrest of respiration which occurs during the stage of apnoea — a point which it is difficult to explain by the other theories. {b) The remarkable fact that the respiratory centre is at one moment violently discharging, and at the next in a state of absolute quiescence. if) That the dyspnoea and apnoea follow one another with rhythmical regularity ; and that the one condition gradually passes into the other, and vice versd. It is perhaps impossible in the present state of our knowledge to ofter a decided opinion as to the manner in which the irritable weakness of the vaso-motor centre, which I have supposed is present in cases of Cheyne- Stokes' respiration, is produced. A deficient supply of arterial blood is probably in many cases one factor which aids in the production of the condition. We know that in conditions of profound aneemia, an extreme condition of irritable weakness of the spinal centres ^in which the muscular 76 Diseases of the Heart. Fir,. 17. 18. Fig. 17. — The end of the pei iod of afmva. 1. The discharging portion of the inspiratory centre is inactive but quite recovered from its previous exhaustion^d". 2. The restraining portion of the inspiratory centre (r) is still in excess = r+, but exhausted. 3. The lungs (L) are inactive. 4. The blood (B) is venous=V+ ; and a stimulus is passing : — to the dis- charging portion of the inspiratory centre (d") ; and to the vaso-motor centre (VMC) 5. The vaso-motor centre is not acting. 6. The peripheral blood vessels (b) are dilated ; and charged with venous blood ; and in consequence of the absence of oxygen, the discharging portion of the inspiratory centre is being stimulated. Fig. 18. — The cointneiue)iient of the period of dyspnoea. 1. The discharging portion of the inspiratory centre is beginning to act, and has quite recovered from its exhaustion=d" + . 2. The restraining portion is not acting and is exhausted = r. 3. The lungs (L) are moderately distended =moderate dyspncea. 4. The blood is highly venous (V + ), and a stimulus is passing :— to the dis- charging portion of the inspiratory centre, and to the vaso-motor centre. 5. The vaso-motor centre is acting, the peripheral blood-vessels are moderately constricted, and charged with highly venous blood ; a stimulus is consequently passing to the discharging portion of the inspiratory centre. Cheyne-Stokcs Respiration. n FIG. 19. FIG. 20. Fig. 19. — The period of the height of the dyspncea. 1. The discharging' portion of the inspiratory centre is acting very powerfully. 2. The restraining portion is inactive, but beginning to recover from its exhaustion. 3. The lungs (L) are acting very powerfully. 4. The blood is anterio-venous=AV ; and not stimulating any of the centres. 5. The vaso-motor centre is discharging powerfully in consequence of the previous stimulation. 6. The peripheral blood-vessels are markedly contracted, and the discharging portion of the inspiratory centre is being stimulated by the want of oxygen. Fig. 20. — The end of the period of dyspnoea. 1. The discharging portion of the inspiratory centre is acting feebly, and rapidly becoming exhausted. 2. The restraining portion has recovered from its exhaustion, but is not yet acting=r". 3. The lungs are acting feebly. 4. The blood is arterial^A, and a stimulus is beginning to pass to the restraining portion of the inspiratory centre. 5. The vaso-motor is still acting, though feebly. 6. The peripheral blood-vessels are moderately dilated, and charged with arterial blood ; a stimulus is consequently passing to the restraivuiig portion of the inspiratory centre 78 Diseases of the Heart. Fig. 21. — The period of the conimencetnent of apiiwa. 1. The discharging portion of the inspiratory centre is inactive and exhaust- ed=d. 2. The restraining portion is acting, and has quite recovered from its previous exhaustion. 3. The lungs are inactive. 4. The blood is highly arterial (A+), and a stimulus is passing to the restrain- ing portion of the inspiratory centre. 5. The vaso-motor centre is not acting. 6. The peripheral blood-vessels are dilated, and in consequence of the free supply of arterial blood the restraining portion of the inspiratory centre is being stimulated. Fig. 22. — The period of the height of the apnan. 1. The discharging portion of the inspiratory centre is inactive, but beginning to recover from its exhaustion=d'. 2. The restraining portion of the inspiratory centre is still acting powerful- ly =r"+. 3. The lungs are inactive. 4. The blood is anterio-venous (AV), and not stimulating any of the centres. 5. The vaso-motor centre is inactive. 6. The peripheral blood-vessels are widely dilated, and charged with blood, which is partly arterial and partly venous, and which stimulates neither portion of the inspiratory centre. Cheyne-Stokes Respiration. 79 power is defective, muscular nutrition impaired, but muscular irritability both to direct and reflex stimulation notably increased) is often observed ; and in many cases of Cheyne-Stokes' respiration, the arteries are tightly contracted, the face is pale, and the supply of arterial blood to the nerve centres is deficient, i.e. a condition of local anaemia is present. It is difficult, however, to suppose that a deficient supply of blood to the vaso-motor and respiratory centres is (even in these cases) the sole cause of the condition. And in those cases in which the arterial tension is not increased, and in which there is no anaemia, it is obvious that some other condition must be present. Theoretically we may suppose that the condition (irritable weakness of the respiratory centre in the medulla) may be produced b)- : — (rt.) Lesions of the medulla itself ib^ Impressions passing to it from the higher nerve centres. And, if these conditions occur, we can satisfactorily explain the mode of production of those cases of Cheyne-Stokes' respiration in which there are nervous lesions, and in which the heart is healthy. if) Impressions passing to it from the periphery, more particularly from the heart and respiratory organs through the vagi and superior laryngeal nerves. That the respiratoiy centre is powerfully affected through these chan- nels, the passage quoted in the foot-note from Prof M. Foster clearly shows ; and it is not difficult to conceive that in conditions of disease, profound modifications of the respiratory centre may in this manner be produced, more especially in those cases in which the right ventricle is affected, and the supply of blood to the lungs interfered with. Possibly then, a combined condition of defective arterial blood supply to the respirator)' centre, such as is produced by a tonic contraction of the minute arteries, together with some abnormal stimulation through the vagi or superior laryngeal nerves,^ such as we have supposed may be ' ' Among the afferent impulses which affect the automatic action of the centre ' {i.e. of the respiratory centre) says Dr Michael Foster, ' the most important are those which ascend along the vagi. If one vagus be divided, the respiration becomes slower ; if both be divided, it becomes very slow, the pauses between expiration and inspiration being excessively prolonged. The character of the respiratory movement too is markedly changed ; each respiration is fuller and deeper, so much so indeed that, according to some observers, what is lost in rate is gained in extent, the amount of carbonic acid produced and oxygen consumed in a given period remaining after division of the nerves about the same as when these were intact. Without insisting too much on the exactness of this compensa- tion, we may at least conclude from the effects of section of the vagi, in the first place, that during life afferent impulses are continually ascending the vagi and modifying the action of the respiratory centre, and in the second place, that the modification bears chiefly on the distribution in time of the afferent respiratory impulses, and not so much on the amount to which they are generated. These 8o Diseases of tJie Heart. produced by the cardiac lesion (more particularly by a dilated condition of the right heart), may be the cause of the Cheyne-Stokes' respiration which is met with in some cardiac cases. The whole subject {i.e Cheyne-Stokes' respiration) requires further elucidation. It is only by the accurate examination, and by the pubHca- tion of a considerable number of cases that we can hope to arrive at a satisfactory conclusion as to the exact nature of the condition. In order to facilitate the study of these cases I have drawn up the following memorandum showing the points to which attention should be particularly directed in the clinical examination. The points to which attention is to be directed in the clinical examination of Cheyne-Stokes' respiration. A. Preliminary /"^rc/x— Name — Age— Sex— Occupation— Address — Date of Examination. B. History. (i.) Of the present illness. — The date of commencement ; the exact mode of commencement ; the supposed cause of the attack ; the character of the symptoms ; the order of their appearance ; and the treatment which has been adopted, up to the date of the observation. (2.) The health history prior to the commencement of the present attack. (3.) The family histoiy ; especially the occurrence of disease of the heart or kidneys ; and of attacks of Cheyne-Stokes' respiration amongst near relatives. C. The present condition. (l.) The nature of the primary (main) disease. (2.) The condition :—{a) of the heart (which should be carefully and methodically examined in accordance with the plan of examination afferent impulses are probably started in the lungs by the condition of the blood in the pulmonary capillaries acting as a stimulus to the peripheral endings of the nerves, though possibly the altered air in the air cells may also act as a stimulus to the nerve endings.' . . . Again, 'if the central end of the superior laryngeal branch of the vagus be stimulated, whether the main trunk of the nerve be severed or not, a slowing of the respiration takes place, and this may, by proper stimula- tion, be carried so far that a complete standstill of respiration in the phase of rest is brought about, i.e. the respiratory apparatus remains in the condition which obtains at the close of an ordinary expiration, the diaphragm being completely relaxed. In other words, the superior laryngeal nerve contains fibres, the stimula- tion of which produces afferent impulses, whose effect is to inhibit the action of the respiratory centre ; while the main trunk of the vagus contains fibres, the stimula- tion of which produces afferent impulses, whose effect is to accelerate or augment the action of the respiratory centre.' — A Text -Book of Physiology, io\\x\\\ edition, PP- 356, 357- Cough and Expectoration. 8i previously described, see page 58) ; (i^) of the lungs ; {c) of the kidneys (amount of urine in twenty-four hours, its colour, reaction, specific gravity, presence or absence of albumen and casts) ; {d) of the nerve centres. (3.) The appearance of the patient during the attack of Cheyne-Stokes' respiration, and the sensations which he experiences. (4.) The exact character of the respiration itself. The exact duration of the whole cycle ; the exact duration of the period of dyspnoea ; the number and character (depth, etc.) of the respirations during the period of dyspnoea ; and the exact duration of the period of apnoea. The observer should endeavour to represent diagrammatically on paper the character of the respirations during the whole cycle ; preserving, so far as possible, the relative frequency and depth of the respiratory movements. (5.) The condition of the peripheral circulation. The colour of the face, during the periods of dyspnoea and apnoea, respectively. The fre- quency of the pulse during the periods of dyspnoea and apnoea. The ten- sion of the pulse during the periods of dyspnoea and apnoea. In all cases sphygmographic tracings should be carefully taken both during the periods of dyspnoea and apncea, and, if possible, a continuous tracing during the whole cycle, i.e. from the commencement of one period of dyspnoea to the commencement of another period of dyspnoea should be obtained. (6.) The treatment adopted and its effects ; in particular, the effect of nitrite of amyl inhalations, or of nitro-glycerine. (7.) The result. (8.) In fatal cases the record of the /^'^Z-wfA'/tv;/ examination. Cough and Expectoration. Cough is a common symptom in cases of cardiac disease. It generally depends upon venous engorgement of the lungs or upon the secondary pulmonary complications, such as bronchitis, oedema of the lungs, pneumonia, etc., which are, as we have already seen, of very frequent occurrence. In cases ot this description, the cough is usually moist, the character of the expectoration varying with the nature of the pulmo- nary complication. In other cases, the cough is due to reflex irritation, it is then usually dry, and often has a harsh, brassy, clanging character. Aneurisms or simple dilatations of the aortic arch, which exert irritative pressure upon the recurrent laryngeal nerve, are attended by a characteristic cough of this description. A short, dry cough is also seen in F 82 Diseases of tJie Heart. some cardiac cases (in which there are no distinct pulmonary compHcations, and in which there is no pressure upon the recurrent laryngeal nerve), and is possibly produced by reflex irritation of the terminal branches of the cardiac nerves in the walls of the heart itself. Expectoration. The character of the expectoration depends chiefly upon the exact nature of the pulmonary complication which is present. In acute bronchitis, for example, the expectorated matters are white and frothy, and consist chiefly of water}- mucus ; in chronic bronchitis the expectoration is muco- purulent or purulent ; in pneumonia it is scanty and viscid, and may present the characteristic rusty-red colour ; in very acute cedema of the lungs, a large quantity of liquid is suddenly poured out into the air-cells and minute bronchi, there is great dyspnoea, both inspiration and expiration may be attended with a loud roaring stridor, and the patient may expectorate a large quantity of frothy fluid, which in some cases is highly albuminous. Haemoptysis is not unfre- quent in the course of cardiac cases. In some it depends upon simple engorgement of the lungs, and the rupture of dilated capillaries in the walls of the air cells. In this form of haemoptysis, which is common in mitral stenosis, the blood may be expectorated in considerable quantities, and is often quite pure. In other cases haemoptysis depends upon embolic plugging of some of the pulmonary vessels (pulmonary infarctions) ; in cases of this description the blood (which may at first be pure) soon becomes of a dark colour, and is usually mixed with considerable quantities of mucus ; as the case progresses, the expectora- tion may assume various shades, and may become foetid. In other cases again, haemoptysis depends upon the rupture of an aneurism into the air passages. In cases of this description, the blood is bright and florid, and the bleed- ing may be sufficiently copious to be followed by immediate death. Comparative value of di^ event symptoms. 83 T/ie comparative significance of ' subjective cardiac sensations,' and of symptoms indicative of mechanical derangement oj the circ2ilation. In many cases of functional derangement of the heart, more especially in the great group of neurotic lesions, there are no ' mechanical ' symptoms, but the patient complains only of ' subjective cardiac sensations.' He often, too, is im- pressed with the belief that he has heart disease, and comes to the physician with the express object of having his heart examined. Persons suffering from organic cardiac disease, on the contrary, iisiially complain of the lung, stomach, and other symptoms, which result from mechanical derangement of the circulation, though they may in addition experience and com- plain of ' subjective cardiac sensations.' The practical lesson to be derived from these facts is, that persons who come to a physician complaining of their hearts, and zvho do not manifest any mechanical disturbance of the circulation, are in all pro- bability free from serious cardiac disease ; ^ while in those cardiac cases in which such symptoms as cough, shortness of breath, dropsy, etc., are present, as the result of the cardiac lesion, there is some structural alteration which has produced mechanical derangement of the circulation ; occasionally, as in anaemia, this structural alteration is temporary and curable, but in most cases it is permanent and ' organic' The reader must not, of course, conclude from this statement, that the converse proposition holds good, viz., that all persons who have an organic cardiac lesion, manifest well-marked symptoms. Such is not the case, for, as we have previously seen, many serious organic lesions are for a long time latent {i.e. are unattended by symptoms), being balanced by the compensatory changes which occur. ' True angina pectoris is a notable exception to this statement. In that con- dition intense pain, commencing in the region of the heart, and radiating up to the left shoulder and down the left arm, is experienced. The pain is attended with a dread of impending death, but there are often no other symptoms indicative of serious organic disease. 84 Diseases of the Heart. The History of the Case. History of the present illness. — In the first place, it is im- portant, if possible, to ascertain the exact date at which the symptoms, for which the patient comes under observation, com- menced. By determining this point we can, provided that he has been previously healthy, ascertain with considerable pro- bability whether the cardiac lesion is a recent one or not.^ In some cases the point is easily determined. A patient affected with aneurism, for example, may tell you that, while making some violent exertion, he felt something give way in the chest or abdomen, and that his symptoms date from that event. In cases of acute rheumatic inflammation of the heart, there is usually no difficulty in fixing the exact date at which the rheumatic attack commenced. So, too, in some functional derangements, more especially in some forms of neurotic palpitation and the like, the attack comes on sud- denly and abruptly, the patient having been previously free from any cardiac symptoms. But in other cases, more espe- cially in the great group of chronic cardiac affections, the symptoms develop so gradually, and the case progresses so slowly, that the patient is unable to fix a definite date for the commencement of his illness. In the second place, the exact mode of commencement of the attack, the character of the symptoms, and the manner in which they are progj'essing, should be ascertained. The exact character of any apparent cause, such as violent effort, mental agitation, an attack of rheumatism or scarlet fever, should be carefully investigated. In the third place, it is important to ascertain the nature of the treatment %vhich has been adopted tip to the time ivhen the patient comes under observation. Digitalis, for example, when given in full doses, may materially modify the action of the heart ; the knowledge, therefore, that the patient had been taking large doses of digitalis, might be a point of great The fact that the symptoms are of recent origin is not proof positive that the lesion is a recent one, for grave cardiac lesions may, as I have repeatedly pointed out, he, for a time at least, unattended by any obvious symptoms. The History of the Case. 85 practical importance. In other words, the nature of the treat- ment which has been previously adopted, may give us a clew- to the nature of the case, and indicate the opinion of the previous medical attendant. The history of the state of health before the commenceinent of tlie present illness, is a point of the greatest practical importance. The patient should always be closely questioned as to the occurrence of previous attacks of rheumatism,^ more especially of rheumatic fever. When a history of acute rheumatism is elicited, it is important to ascertain if the heart was affected during the attack. The fact that the patient was leeched, cupped, or blistered over the praecordia, is important evidence in those cases in which he is unable to give us any definite information on this point. That the patient has been short of breath on exertion (on going up stairs, up a hill, etc.), since the attack of rheumatism, is also highly suggestive of a chronic valvular lesion, although he may have in other respects enjoyed good health. Scarlet fever is another disease, which is, not unfrequcntly, attended with endo- carditis ; and in children, who come under treatment for valvular lesions, it is important (more especially where there is no history of rheumatism) to inquire into this point. I might mention many other conditions which sow the seeds of subsequent cardiac or arterial disease (syphilis, for example, is an important cause of aneurism), they will however be detailed when I come to speak of the aetiology of the in- dividual cardiac diseases. The habits and mode of life, and general surroundings of the patient, are of great importance, more especially in deter- mining the plan of treatment : but these points will be more appropriately considered afterwards. ' It is important to remember that endocarditis may develop in the course of mild and apparently insignificant attacks of subacute rheumatism. Many persons, too, more especially in the lower ranks of life, do not appreciate the difference between ordinary muscular rheumatism and rheumatic fever (articular rheumatism.) It is well, therefore, in the first instance to ask the patient if he has suffered from rheumatism, and if he answer in the affirmative, to question him as to the e.xact nature of the attack 86 Diseases of the Heart. Family History. — Acute rheumatism, which is such a fertile source of cardiac valvular lesions, is much more frequent in some families than in others ; and it is in consequence of their liability to rheumatism, that the members of these families are more apt to be affected with cardiac valvular lesions than other people. But, independently of the rheumatic tendency, some persons inherit ^a tendency to disease of the heart and vascular system. For example, the late Dr Charlton of Newcastle-on-Tync, told me, that two brothers, in easy circumstances, who had not been exposed to any undue strain, and who had not suffered from rheumatism, came under his care, suffering from atheroma of the thoracic aorta, and died at the unusually early ages (for atheroma) of twenty-three and twenty-five. In these cases it was difficult to resist the conclusion that the condition was hereditary. In later life, when arterial degeneration is common, this hereditary ten- dency to atheroma is still more apparent. In some cases it seems to be due to gout ; in others it is associated with kidney disease. Those functional forms of cardiac derange- ment, which depend upon disordered innervation of the heart, are more common in persons of a neurotic temperament than in other people ; and as we all know the neurotic tempera- ment is eminently hereditary. PRESENT CONDITION. [The date at which the examination is made should be stated, for in hospital practice several days may elapse between the admission of the patient and the noting of the case.] The Physiognomy of the Case. — While the preliminary facts and previous history are being investigated, the phy- sician is both consciously and unconsciously learning many important particulars as to the nature of the case. In some cases the physiognomy not only suggests the nature of the lesion, but also indicates its severity. Attention must be particularly directed to : — I. The colour of the face (of the lips, nose, and ears more especially,). 1 he Colour of the Face. 87 2. The presence of subcutaneous dropsy (in the feet, face, and hands more particularly.) 3. The facial expression. 4. The condition of the breathing. 5. The attitude. 6. The general state of nutrition. The Colour of the Face. By observing the colour of the face we get important evidence as to the condition of the capillary circulation ; and hence as to the manner in which the circulation is being car- ried on — a point of the greatest importance in cases of cardiac disease. In some cases the colour of the face is natural ; in others it is more dusky than in health ; in others, again, it is paler than normal. Natural Colour of the Face. — In many functional affections, more particularly the neurotic disorders of the heart ; in many aneurisms ; in aortic stenosis ; in slight cases of aortic regurgitation ; and in mitral cases (more especially mitral stenosis), so long as compensation is perfect, the colour of the face may be quite natural. Blucuess of the face — Cyanosis. — Anything which inter- feres with the circulation of the blood in the lungs, with the passage of the blood through the right cavities of the heart, or which prevents the return of blood to the heart, such as pressure on the superior cava, will produce venous congestion, and hence blueness of the face. The cyanosis is most marked in those cases in which there is a backwash through the tri- cuspid, or in which the venous and arterial blood currents are intermixed, as they are in some congenital malformations. Congenital Cyanosis, in which the blueness is often extreme (hence the term morbus ceruleus, which has been given to these cases), usually depends upon some cardiac malformation, such as stenosis of the orifice of the pulmonary artery w^ith a patent condition of the foraman ovale, or upon transposition of the aorta and pulmonary artery (the aorta arising from the right, and the pulmonary artery from the left ventricle). Acquired Cyanosis. — When the cyanosis is extreme, there 88 Diseases of the Heart. is generally, in my experience, long standing disease of the lungs or disease of the right cavities of the heart, permitting of tricuspid regurgitation : the two conditions being generally combined. Cases are, for instance, not unfrequently met with in which there is a history of repeated attacks of bronchitis since childhood ; in which the patient has for years been short of breath ; in which the lungs are emphysematous or cirrhotic ; and in which the right cavities of the heart are hypertrophied and dilated. In cases of this description, there is always more or less blueness of the lips, and any increased obstruction to the aeration of the blood in the lungs (such as is occasioned by an attack of acute bronchitis, pneumonia, etc.), or any in- creased distention of the right cavities of the heart, may be attended with the most extreme degree of cyanosis. In mitral cases in which, as we have previously seen, the free circulation through the lungs is interfered with, and in which secondary changes in the right heart are so commonly observed, more or less cyanosis is usually present, but it is seldom so great as in the cases of primary pulmonary obstruction to which I have just alluded, and is often asso- ciated with some degree of ansemia. While compensation is perfect the colour of the face may be quite natural. In all of these cases, but less so, I think, in congenital cyanosis than in the other two, the face may be somewhat swollen as well as cyanotic. When the return current of blood through the superior vena cava is interfered with, as it is sometimes by the pressure of an aneurism or solid intra-thoracic growth, the lips, ears, nose, etc., are more or less livid. In these cases there is marked oedema, which is not, of course, confined to the face, but is seen in all the parts (face, neck, upper extremities, and upper part of the thoracic parieties) from which the superior cava draws its blood-supply. In consequence of the oedema, the face in the region of the eyelids, etc., is usually pale, and the condition may at first sight be mistaken for a case of Bright's disease. The marked lividity of the lips, ears, etc., and the limitation of the swelling to the area of distribution of the superior cava, at once, distinguish the two conditions. Subcutaneous Dropsy. 89 Pallor of the Face. — In cases of free aortic regurgita- tion, in which the arterial system is imperfectly distended during the diastole of the ventricle, the face is pale, generally thin, and there is often an anxious expression of countenance.^ In conditions of aiiccinia, in which, as we have pre- viously seen, cardiac symptoms and cardiac murmurs are common, the face and mucous membranes are unusually pale ; in chlorosis and progressive pernicious ancsinia, the face may be slightly puffy, and generally has a lemon yellow hue, which must be distinguished from the dingy, yellow colour, which is seen in many cases of advanced mitral disease.- Cardiac lesions are, of course, frequently met with in con- nection with Bright's disease ; and in combined cases of cardiac and renal disease, the pale, puffy face which is charac- teristic of the large white kidney, or the dingy colour of the face which is seen in the cirrhotic form of Bright's disease, may, of course, be met with. The presence oj subcutaneous dropsy. As we have previously seen, dropsy is of frequent occur- rence in advanced cases of cardiac disease (more especially mitral and right sided lesions) ; and it almost invariably com- mences in the feet.^ I have already alluded to those cases of ' This statement does not, of course, apply to those cases oi aortic regurgitation in which the mitral valve has given way. In combined cases of this description, more particularly when the mitral regurgitation is free, there may be some blueness of the lips. ^ In both ot these cases the conjunctiva may be yellow. In the former (chlo- rosis) the yellow colour is seen chiefly at the inner and outer canthi, and is due to a deposit of sub-conjunctival fat ; in the latter (advanced cases of mitral disease, tricuspid regurgitation, etc.) the yello\v discolouration of the skin is of a darker, dingier hue, and usually depends upon congestion of the liver. ^ A swollen condition of the feet, untied shoes, slit-up trousers, etc., at once suggest a cardiac lesion. The same form of dropsy [i.e. dropsy beginning in the feet) may be due to simple debility, to anything which interferes with the return current through the inferior vena cava, or to primary obstruction to the blood in the lungs, such as is produced by cirrhosis, emphysema, etc. The differential diagnosis which can generally be made without much difficulty, will be more particularly described under the head of valvular lesions. 90 Diseases of the Heart. local dropsy (dropsy confined to the face, neck, and upper extremities) due to the pressure of an aneurism or intra- thoracic growth upon the superior cava. The Facial Expression. The facial expression (irrespective of the colour of the face and the presence or absence of oedema) does not, as a rule, afford much information. In exophthalmic goitre, in which cardiac symptoms and signs are usually prominent, the projecting eyeballs at once attract attention. In some cases of aortic disease, or of aneurism, the expression may be anxious and indicative of suffering. During the paroxysm of angina pectoris, in conditions of orthopncea, and Cheyne- Stokes' respiration, an expression of horror, dread, anguish, or intense suffering, may be present. In advanced conditions of cyanosis, in which the cerebral centres are imperfectly sup- plied with arterial blood, the patient is often drowsy and the expression apathetic. The Condition of the Breathing. In cases of aortic disease there may be no disturbance of the respiration. In other cases of cardiac disease, one or other of the different forms of dyspnoea, which I have previously described (see page 66), may be present. T/ie Attitude. In acute cases the patient is usually in bed, not so much on account of the cardiac complication as on account of the primary affection (acute rheumatism, etc.) ; he usually lies on his back, and, so far as possible, avoids movement. In those cases of cardiac disease, both acute and chronic, in which the respiratory functions are seriously interfered with, the patient is unable to lie down, and a condition of typical orthopncea may be present. Frequently he will not go to bed, but sits up in a chair for days and nights— it may be for weeks— together. The position, in which he places The General State of Nutrition. 9 1 himself in order to get relief, is sometimes a striking one ; when he is sitting in a chair or on the side of the bed, the head is bent forwards, the weight of the trunk being supported by the arms, which are kept rigid, the hands grasping the thighs just above the knees ; in this position the parts are so fixed that the respiratory muscles, more particularly the extraordinary muscles of respiration, are able to act with great advantage ; in other cases, he leans over the back of a chair, or kneels on the floor, resting his head and forearms on the bed, or sits resting them on a table, mantlepiece, etc. Patients suffering from aneurism sometimes assume peculiar positions in order to remove the pressure of the sac from the surrounding parts ; in some cases of abdominal aneurism, for example, the patient can only lie on his face ; in others, he can only get relief from paroxysms of pain by resting on his hands and knees ; in others, again, the thigh is flexed upon the abdomen. But more minute and detailed description of the various attitudes which may be assumed in individual cases, would obviously be out of place here. The General State of Nutrition. The cardiac affections which seriously embarrass the respiration, and cause secondary disturbances in the liver, stomach, and other abdominal organs, are usually attended with very considerable derangement of the nutritive functions. In mitral cases, for example, after the failure of compensation, the patient becomes soft and flabby, and there is usually con- siderable emaciation ; it must of course be remembered that when the subcutaneous fat is abundant, or there is great dropsy, the emaciation may escape detection unless carefully looked for. In aortic cases the patient is usually spare, but the general state of nutrition is, as a rule, fairly well preserved. In some cases of aneurism there is no impairment of the general health ; indeed one of the most striking features is often the total want of proportion, so to speak, between the severity of the disease and the general constitutional state. 92 Diseases of the Hcaj-t. THE PHYSICAL EXAMINATION OF THE HEART AND ORGANS OF CIRCULATION. The object of the physical examination of the heart and organs of circulation is, of course, to ascertain their exact physical condition. We endeavour to determine the physical condition of the heart itself ; of the great blood-vessels within the thorax and abdomen ; and the manner in which the peri- pheral circulation is being carried on. The methods of examination which we chiefly^ employ are inspection, pal- pation, percussion, auscultation, and the use of the sphygmo- graph. THE PHYSICAL EXAMINATION OF THE HEART. The object of the physical examination of the heart is to determine — 1, The exact frequency^ rhythm, and character (whether slow and laboured, quick and irritable, etc.) of its contrac- tions. These points are determined by observing the character of the pulse ; by inspecting and palpating the praecordia ; and by auscultating the heart ; the examination of the pulse being especially valuable. 2. Its position in the thorax ; its size and shape as a luhole ; and the relative size and shape of its component parts. We determine these points chiefly by inspecting the prae- cordial region {i.e. by observing by means of inspection the position, extent, and character of the visible impulse); by palpating the praecordial region {i.e. by observing by means of palpation the position, extent, and character of the visible impulse) ; and by percussing the praecordial region {i.e. by determining by means of percussion the exact extent, shape, and outline of the cardiac dulness). Percussion is particularly valuable in determining these points. ' The cardiograph is not yet employed, even in hospitals, as one of the ordinary methods of examination ; it is not, therefore, described in the text, but in the appendix. The Physical Examination of the Heaj't. 93 3. The condition of its valvular apparatus. The condition of the valvular apparatus of the heart is chiefly determined by means of auscultation. Palpation in some cases also affords information. The exact size and shape of the heart and of its component cavities (which are, as we have just seen, chiefly determined by means of percussion), cor- roborate the information derived from auscultation ; while very important evidence as to the condition of the valvular mechanism, is also obtained by observing the condition of the circulation in front of and behind the valve which is being examined. The mode of examination will afterwards be described. 4. The state of its musciilar zualls (whether hypertrophied, dilated, degenerated, etc.). We determine this most important point by observing : — {a) The size of the heart and of its component parts (in- spection, palpation, and percussion of the prsecordia). f) The force and character of the cardiac impulse (palpa- tion of the praecordia) ; the force and character of the pulse ; the loudness and other characters of the heart sounds (auscul- tation of the prsecordia), and the condition of the peripheral — arterial and venous — circulation. Corroborative evidence is also afforded in many cases by observing the general condition of the system, and the state of particular organs, such as the lungs and kidney : profound anaemia, for example, suggests fatty degeneration of the heart ; kidney disease (especially cirrhosis), hypertrophy of the left ventricle. 5. The condition of the pericardial sac. This point is chiefly determined by means of auscultation and percussion. INSPECTION AS APPLIED TO THE EXAMINATION OF THE HEART ; INSPECTION OF THE PR/ECORDIAL REGION. By the praecordial region we understand that part of the chest wall which lies in front of the heart. It is necessary, therefore, before proceeding further, to define the exact position of the heart in the thorax, and to describe the limits of the praecordial region. 94 Diseases of the Heart. The position of the Heart in the Thorax. The heart, contained in the fibro-serous bag termed the pericardium, is placed obHquely, with its long axis from right to left, in the lower part of the anterior mediastinum (see fig. 23). It consists of four chambers, two auricles and two KiG. 23. — The heart and great vessels in situ. ^ Enlarged from Sibson. ) The lungs have been drawn aside, and the anterior surface of t-he pericardial sac removed. TJie Position of tJie Heart in tJie TJiorax. 95 ventricles ; and in the adult male, after death, is about the size of the closed fist. It rests upon the central tendon of the diaphragm, is attached above by its base to the great vessels, and is almost completely surrounded by the lungs, which, with the bony walls of the chest, protect it from external injury. The base corresponds to the junction of the upper margins of the third costal cartilages ; the apex to the 5th interspace, or the 6th rib. (In the adult male the apex-beat can usually be felt between the 5th and 6th ribs, at a point about an inch and a half below, and slightly within the left nipple.) As a zutiote, then, the heart extends vertically from the 2nd interspace above, to the 6th rib below ; and transversely, from a little within the left nipple, to a finger's breadth or more to the right of the sternum ; and this space which the heart occupies, as a whole, is called the deep cardiac region. Nearly two-thirds of the organ lie to the left, and more than one-third to the right of the middle line. Sibson points out that when the left lung is unusually large, i.e. larger than the right, the heart is situated more to the right ; and vice versa, when the right lung is larger than normal (irrespective, of course, of any disease, for we are now considering the position in health), the heart may be situated more to the left. The relationship of the Heart to the surface of the Chest. The prsecordial region (that part of the chest wall which lies in frojit of the heart) includes, therefore, the greater part of the lower sternal and left mammary, and part of the right mammary, regions. (See fig. 24.) The anterior surface of the chest, and the root of the neck, have for facihty of description and for chnical convenience, been artificially divided into the following regions : — The supra-sternal, upper sternal, and lower sternal regions, in the middle line. The supra-clavicular, clavicular, infra-clavicular, mammary and infra-mammary regions, on each side. The boundaries of these regions are as follows : — 96 Diseases of the Heart. The supra-sternal region (i. fig. 24) is situated immediately above the upper end of the sternum, and is bounded on each side by the anterior borders of the sterno-mastoid muscles ; its upper boundary corresponds to the upper end of the trachea. The upper sternal region (2. fig. 24) comprises the part of the chest which is situated behind the upper portion of the sternum. The upper boundary- of this region is represented on the surface of the chest by the upper end of the sternum, the lower end by a line drawn across the sternum at the level of the junction of the third costal cartilages ; laterally this region is bounded on each side by the corresponding edge of the sternum. Fig. 2i,. — The regions on the front of the Chest. (Modified after Walshe.) 1. Supra sternal region. 2. Upper sternal region. 3. Lower sternal region. 4>4'' Right and left supra-clavicular regions. 5' 5'- Right and left clavicular regions. 6,6'. Right and left infra-clavicular regions. 7j7'- Right and left mammary regions. 8,8'. Right and left infra-mammary regions. Relationship of t lie Heart to the Chest Wall. 97 The lower sternal region (3. fig. 24) corresponds to the lower portion of the sternum. TJie supra-clavicular region (4 and 4'. fig. 24) is triangular in shape, and is situated immediately above the clavicle ; on its inner side it is bounded by the outer side of the supra-sternal region, below by the clavicle; its third side being formed by an artificial fine drawn from the outer end of the clavicle to the upper end of the trachea. TJie clavicular region (5 and 5'. fig. 24) corresponds to the inner half of the clavicle. The infra-clavicular region (6 and 6 '. fig. 24) is bounded above by the clavicle ; below by a fine drawn across the chest on the level of the third rib ; internally by the edge of the sternum ; externally by an imagi- nary line falling vertically from the inner edge of the acromial process. TJie mani)nary region (7 and 7 '. fig. 24) is situated immediately below the infra-clavicular region ; and is bounded below by a slanting line drawn through the middle of the sixth costal cartilage ; internally by the edge of the sternum ; and externally by the vertical ' acromial line ' described above. The infra-mammary region (8 and 8'. fig. 24) is situated immediately below the mammary region ; its lower margin corresponds to the lower margins of the false ribs ; internally it is bounded by the edge of the sternum, and below that bone by the margins of the ribs ; externally by the 'acromial line.' The exact relationship of the cardiac cavities to the front of the chest is, according to Walshe, as follows : — The anterior surface of the heart is chiefly formed by the right cavities ; the tip of the left auricular appendix, and a narrow strip of the left ventricle being the only parts of the left heart, which are visible when the anterior surface is exposed in situ. The right auricle reaches into the right mammary region, mainly on the level of the third cartilage and fourth interspace, slightly on that of the second space. The right ventricle corresponds mainly to the lower sternal and left mammary regions, its inferior and nearly horizontal border stretching from the fifth right cartilage to the point at which the apex beats. The left auricle lies deeply behind the root of the pulmonary artery, little but the appendix being visible. The left vetitricle extends vertically from the third to the upper edge of the sixth left costal cartilage, and occupies a portion of the left mammary region — a comparatively narrow strip being visible anteriorly. The entire of the left ventricle, the greater part of the left auricle, and a large portion of the right ventricle towards the apex, lie to the left of the sternum. On the level of the fourth cartilage the widths of the heart substance lying on either side of the left border of the sternum are very closely the same.^ ' Diseases of the Heart, p. 4. G 98 Diseases of the Heart. Method of inspecting- tJie Clwst. The patient should be stripped to the waist, and placed directly opposite the observer, in a good light, in a sitting or semi-recumbent position. In cases of suspected aneurism, in which it is important to note the slightest elevation of the chest-wall above the level of surrounding parts, the suspected region of the chest must be well illuminated, and the observer having placed himself on the opposite side of the patient to that from which the rays of light are proceeding, should bring his eye to the same horizontal plane as the region of the chest which he wishes to examine. In this manner slight local elevations can be most readily observed. Tlie points to be observed in i)ispccting the prceeordial region are : 1. Its form and conformation. 2. The position, extent, and character of the visible im- pulse, especially the position of the apex beat. 3. The condition of the integument. (This is a point of comparatively little importance). TJie form and eonformation of tJie preeeordial region. In health the two sides of the chest are practically sym- metrical, and the left mammary region does not differ in form and shape from the corresponding region on the opposite side. Alterations in the form and conformation of the praecordial region are frequently met with in disease ; in some cases it is unduly prominent, in others it is flattened or retracted. Undue prominenee of the prcveordial region. This condition may be due to : I. Congenital or acquired alterations in the shape of the thorax, such as are seen in some cases of rickets, or in con- nection with some curvatures of the spinal column. Diagnosis. — In these cases the character of the prominence ; the presence of other associated alterations in the bony walls of the thorax, such as a well-marked spinal curvature ; and the history of the case, enable us without difficulty to determine the cause of the prominence. Undue proviinencc of the Prcccordial Region. 99 2. Abnormal conditions of the thoracic parieties in the praicordial region, such as an abscess in the subcutaneous cellular tissue, or an exostosis, or other new formation spring- ing from the ribs or cartilages. Diagnosis. — In these cases — which are rare — the diagnosis presents no difficulty. In the case of an abscess in the chest wall there is tenderness on pressure over the swelhng, and often redness of the skin of the affected part ; the history shows a recent origin, and there are no signs of disease of the subjacent viscera. Solid tumours springing front the ribs or cartilages are also unattended by evidence of cardiac or puhiionary disease ; they are usually well defined and localised, and are as a rule readily distinguished, by means of palpation, from all other causes of bulging. 3. Fluid accumulations in the left pleural sac ; solid tumours of the left lung ; solid tumours in the anterior mediastinum. Diagnosis. — Fluid accumulations in the left pleural sac, which give rise to prominence of the pracordia, also produce bulging of the whole ^ of the affected (left) side, and are attended by the characteristic symptoms and signs of left pleural effusion. Solid tumours of the left lung, and new growths in the mediastinum, seldom give rise to marked prominence of the prsecordia. When sufficiently large to produce bulging of this part of the chest wall, they are attended with characteristic symptoms and signs, which it would be out of place to enumerate here. 4. Fluid in the sac of the pericardium. 5. Increase in the size of the heart itself, especially those enlargements which are attended with marked hypertrophy of the organ. The characteristic features of prominence of the prae- cordia, due to fluid in the sac of the pericardium and enlargement of the heart itself, which are the most common causes of local bulging, and which are of course the most ' A small encysted pleuritic effusion might produce local bulging of the prse- cordia ; but such a condition is infinitely rare. A more frequent condition, but one which seldom gives rise to difficulties in diagnosis, is an empyema which is pointing. loo Diseases of tJie Heart. important, so far as our present studies are concerned, will be afterwards considered in detail. It is important to remember that the prominence which results from these causes is greater in young persons (in whom the chest walls are elastic) than in old people. 6. Forward displacement of the heart by an aneurismal or solid tumour situated behind it. This condition is ex- tremely rare. 7. The presence of an aneurism of the first portion of the aortic arch. The bulging in such cases is almost invariably above the fourth rib, but occasionally the aneurism ' points ' lower down, as in a case which I shall afterwards describe. Flattening or retraction of tJie precordial region. This condition may be due to : 1. Congenital malformation. Diagnosis. — In these cases the depression is seldom limited to the prsecordial region. It is usually symmetrical, and involves the lower sternal region, together with more or less of the mammary and infra-mam- mary regions on each side. 2. Long continued external pressure. Depression of the lower end of the sternum is sometimes seen in shoemakers, and is produced by the pressure of the ' last ' against this part of the chest. Diagnosis. — The depression which occurs in shoemakers is more cen- tral than the depression which results from cardiac affections, and in- volves the right as well as the left infra-mammary region. The central position of the depression and the nature of the patient's employment, together with the absence of any history, symptoms, or signs of local disease, are the points to which attention must be directed in making the diagnosis. 3. Retraction of the left lung, a condition which may result from pleurisy, cirrhosis of the lung, etc. Diagnosis. — In these cases the retraction or depression is not con- fined to the praecordial region, but affects the whole of the left side ; while the associated physical signs, and the previous histor}', usually afford distinctive evidence of the condition. The Visible Impulse of the Heart. loi 4. Pericarditis. — Here the depression is usually confined to the lower end of the sternum and the adjacent part of the left infra-mammary region. The depression does not occur until absorption of the inflammatory products, and adhesion of the opposed surfaces of the pericardium have taken place. It is always best marked in those cases in which the chest wall is elastic {i.e. in young subjects), and in which the ex- terior of the pericardium has become adherent to the chest wall as the result of inflammation outside the sac. The position, extent, and charaetcr of the Visible Impulse, espeeially the position of the Apex Beat. The visible impulse as a whole, and the position and characters of the apex beat in particular, must be noted — but since it is usually necessary to confirm and supplement the information derived from inspection by means of pal- pation, I shall leave the description of the cardiac impulse in health and in disease until that method of investigation has been considered. Epigastric Pulsation. Should this condition be present, it will of course be observed at this stage of the examination {i.e. during the inspection of the praecordial region) ; but since it is necessary to employ palpation to define its exact characters, it will be more conveniently considered after that mode of examination has been described. Pulsations over the Aorta and at the Root of the Neck. In addition to the visible cardiac impulse and the epigastric pulsation just mentioned, the presence or absence of pulsation in other parts of the thorax and at the root of the neck should be noted at this stage of the examination. It will, however, be more convenient to describe these pul- sations when I come to treat of the systematic examination of the aorta and superficial vessels. I02 Diseases of the Heart. The Condition of the Integument over the Pmeordia. The condition of the integument over the prsecordial region sometimes affords useful information. Cupping marks are suggestive of previous inflamma- tion ; and a history of cupping during a previous attack of rheumatic fever is very suggestive of an acute rheu- matic inflammation of the heart (pericarditis, or endo- carditis). Prcecordial Vascularity. — It is common to observe, especially after middle life, a line of minute vessels running across the chest in the neighbourhood of the praecordial region. The late Professor Laycock, who first directed attention to the condition, considered that it Avas suggestive of cardiac disease, and there can be no question but that the condition is more frequent in persons suffering from vascular lesions than in other people, but it occurs not unfrequently in perfectly healthy individuals, and is not therefore a sign of much importance. CEdcjna of the subcutaneous cellular tissue, when it is limited to the praecordial region, usually depends upon a local inflammation, and is then associated with tenderness on pressure,. redness, and the like. It may however depend upon disease of the subjacent viscera. The condition with which it is most frequently associated is a malignant intra-thoracic growth. Oedema of the chest wall and of the praecordial region is also of course seen as part and parcel of a general dropsy. PALPATION OF THE PR/ECORDIA. Palpation corroborates the information derived from in- spection, and, in many cases, enables us to ascertain with exactitude : — 1. The position of the apex beat. 2. The character of the cardiac contractions, i.e. the force, rhythm, celerity, etc., of the cardiac impulse. In some cases it also affords additional information, in- asmuch as it reveals the presence of cardiac thrills, or friction fremitus, and enables us to elicit the presence or absence of pain and tenderness on pressure over the praecordial region. Palpation. 103 Method of palpating the Chest in order to ascertain the exact position of the Apex Beat. In order to ascertain the exact position of the apex beat by means of palpation, the patient should be laid in the re- cumbent position, and the fingers of the right hand placed lightly over the front of the chest below the left nipple. The position of maximum cardiac impulse, which usually corresponds to the position of the apex beat, should then be noted, and the interspace in which the apex pulsation is situated,^ and the distance of the apex beat from the left border of the sternum ascertained. It sometimes happens that the apex beat is not ap- preciable when the patient is in the recumbent position. In these cases (the nature of which I will presently describe), the position of the apex beat can usually be ascertained by so altering the position of the patient as to bring the heart more in contact with the wall of the chest. He may be made to sit up and to lean forward, for instance ; or, he may be placed on his left side. If the latter method be adopted, due allowance must be made for the lateral displacement of the heart, which results from the alteration in position."^ ' To ascertain the exact position of the apex, the interspaces must be carefully counted from above downwards ; the forefinger of the right hand should first be made to define the position of the first interspace immediately below the clavicle (in many persons there is a well marked prominence of the sternum at the level of the second costal cartilages, which forms an easy guide to the second interspace) ; the middle finger of the same hand should then be inserted between the second and third ribs ; the second interspace having thus been ascertained, the forefinger of the right hand should be placed in it, and the middle finger should then, but not till then, be slipped over the third rib into the third interspace ; the fourth and succeeding interspaces are successively defined in the same manner, until that in which the apex beat is situated, is finally reached. The position of the apex with regard to the left nipple (in males) ; or, better, its exact distance from the left border of the sternum, must then be measured and noted. Note. — In fat or very muscular persons it may be necessary to use some force in defining the position of the interspaces in the manner just described. ^ According to Sibson, the apex beat may, in some cases, be displaced as much as two inches to the left, by turning the patient from the back on to his left side. I04 Diseases of the Heart. The position of the apex beat is of great practical import- ance, for it corresponds to the lowest point of the heart, and is in fact the means by which we are in the habit of deter- mining the lower boundar}- of the organ. TJie jionnal position of the apex beat. In the adult healthy male the apex can usually be seen and felt pulsating (over an area about an inch square) be- tween the fifth and sixth ribs, at a point two inches to the left of the sternum.^ In well nourished healthy persons, the apex pulsation is the only pulsation which is visible over the praecordia during ordinary (tranquil) action of the heart. In women with well developed mammae, in fat or muscular persons, and when the heart is acting feebly the apex beat may be invisible. Viee ve7'sd, in thin persons, or where the heart is excited or h)'pertrophied, the apejc beat is unusually well marked. The position of the apex beat varies somewhat in different healthy individuals, being sometimes situated a little higher, sometimes a little lower than the fifth inter- space. These alterations depend for the most part, as Sibson has shown, upon the length of the arch of the aorta ; and also upon the age of the individual, the form of the thorax, and the condition of the respiratory organs. In children the apex beat is usually higher, and often more to the left ; rice versd, in old people, and especially in those in whom the aorta is atheromatous and elongated, the heart, and therefore the apex beat, are lower than the fifth interspace. In strong robust persons, and in those who possess a broad and deep chest of the inspiratory type, the position of the heart and arteries, and of all their parts, is lower, while in those who are slender, and possess a narrow and flat chest of In describing the position of the apex beat, more particularly in females, the interspace in which it is situated, and its exact distance from the left border of the sternum should be stated. In males the apex beat is normally situated an inch within, and an inch or an inch and a half below the left nipple. Congenital displacements of the Heart. 105 the expiratory type, the position of these parts is higher than in the average healthy individual.^ During inspiration the apex beat (in its relationship to the chest wall) is lower than during expiration. This is partly due to the fact, that the heart descends with the descent of the diaphragm, and partly because the front wall of the chest is raised during inspiration. Congenital displaccinchts of the Heart. The heart is occasionally placed in the right side of the chest, the apex beat being somewhere in the neighbourhood of the right nipple. When this condition occurs congenitally, there is usually complete transposition of the viscera, the heart being placed on the right side, and the liver, for ex- ample, on the left side of the body. Cases of this description are not very uncommon, and two examples have come under my own personal observation. A much rarer form of congenital displacement is that in which the heart is placed on the right side, while the liver and other viscera are situated in their usual position. The following case of this description recently came under my notice ; and another case — verified by post-mortem ex- amination — has lately been recorded in the pages of the Lancet? Case I.— Congenital displacement of the heart to the right side, tJte position of the otJier viscera being normal. J. A., set. 39, a joiner, presented himself at the Cowgate Dispensary, Edinburgh, in December 1881, suffering from a dislocation of the shoulder. On stripping him, the house surgeon (Dr Christie) noticed strong pulsation just above the right nipple— while the impulse of the heart could not be felt in the usual position. Concluding that the case was one of congenital displacement Dr Christie kindly asked me to see the case ; and with his opinion I entirely concurred. The facts which I elicited were as follows : — The patient, who was some- what thin and of bad physique., stated, that he had always enjoyed good ' Sibson On the Position ami Form of the Heart. Russell Reynold's System of Medicine, vol. iv. p. 97. ■ Lancet, July 8th, 1882, p. 9. io6 Diseases of tJic Heart. health; that he had never, to his knowledge, had anything the matter with his chest. He was not short of breath, had never sufifered from palpita- tion or pain in the region of the heart, and had never had any symptoms or sensations which made him suspect that there was anything wrong with his heart. The left infra-mammary region looked flattened, the depression being greatest in the sixth and seventh interspaces. The heart impulse could not be felt in the usual position. On percussion the left infra-mammarj' region was hyper-resonant; and the normal cardiac dulness could not be detected. The respiratory murmur was audible over the usual position of the heart, but the heart sounds could not be heard. Very distinct pulsation could be seen and felt in the third, fourth, and fifth right interspaces (see fig. 25) ; there was marked dulness over the area of pulsation; and the heart sounds were loudly heard over the same part of the chest. The percussion note over the outer part of the right infra-clavicular region was impaired, but the right lung, both ante- riorly and posteriorly, seemed normal. The li\er was situated on the right side; and the stomach in its normal position — no splenic dulness was detectable. The girth of the right side of the chest was considerably larger than that of the left, the measurements being as follows : — Position of Measurement At the level of the second rib Through the nipples . . . . At the level of the seventh rib The heart's action was readily excited, tuated, but free from murmur. Right. Left 16X in. I5>^ in. i^Yz in. ilYz in. 15 in. 14 in. Both sounds were accen- FlG. 25.— Front view oj the thorax in the case of J. A. , sho'coing the area of cardiac pulsation. Displaccuicnts of the Heart. 107 Diagnosis. — The heart was obviously placed on the right side of the chest. The facts, that there was no history or evidence of lung disease, and that the girth of the right chest was considerably greater than the left seemed to show that the displacement was not due to retraction of the right lung, but that it was in all probability a congenital condition. The peculiarity of the case consisted in the fact, that the heart was the only organ transposed, the liver and stomach being placed in their normal positions.' Alterations in t/ic position of the Heart and Apex Beat winch oecnr in disease. In studying the alterations in the position of the apex beat which occur in disease, it is important to remember that the organ rests upon the diaphragm, to which it is indirectly attached by means of the pericardium, and that it is directly attached at its base to the great vessels, and behind to the roots of the lungs by the pulmonary veins. The organ therefore ascends and descends with the ascent and descent of the diaphragm ; further, it is readily displaced from side to side by lateral pressure. The alterations in the position of the heart and apex beat which result from disease, may be due either to extrinsic or intrinsic canses. A. Displacement of the Heart dice to extrinsic canses. The heart may be pnsJied to one side by fluid, gaseous, or solid accumulations or by enlargements of the surrounding viscera ; or, it may he pnlled^ to one side by retraction of the air containing viscera, i.e. the lungs ; or, again, it may, by the force of gravity, fall with the descent of the diaphragm.^ ' Breschet and Otto, quoted by Peacock, in his work on Alalformaiions of the Hitman Heart, page 2, have met with cases of this description ; but so far as I have been able to ascertain, no other cases have been recorded in English medical literature. - The contraction of the lung tends to produce a vacuum within the thorax, in consequence of which the adjacent organs, including the heart, are of course displaced (pushed rather than pulled) towards the affected side by the atmospheric pressure. ' When the diaphragm descends, the great vessels (and therefore the heart) are also dragged down by reason of their attachment to the pericardium. io8 Diseases of the Heart. The displacement may be either to the right or to the left, upwards or downwards, forwards or backwards. Displacement of the Heart and Apex Beat to the right may be due to : — 1. The presence of fluid, gaseous, and solid accumulations in the left pleural sac, or solid enlargements of the left lung. 2. Retraction of the right lung — a condition which usually results from pleurisy with effusion, cirrhosis or phthisis. Fluid in the left pleural sac (see fig. 26) is by far the most common cause of displacement to the right ; and in Fig. 26. — Displacement of the heart to the right as the result 0/ effusion into the left pleural cavity. {Modified froin Sib son.) these cases the apex beat not unfrequently corresponds to the right nipple. Extreme displacement to the right may also be due to retraction of the right lung. Sibson quotes several cases of this description,^ and I have seen more than one case in which the pulsation of the heart was situated just above the right nipple. ' Russell Reynold's System of Medi.inc, vol. iv. p. 143. Displacements of the Heart. 109 Displacciiieni of the heart and apex beat to the left may be due to : 1. Accumulation of fluid, gaseous, or solid matter in the right pleural cavity ; or solid enlargements of the right lung or right lobe of the liver. 2. Retraction of the left lung (see fig. 27). Fig. 27. — Displaceminit of the heart to the left, in consequence of retraction {cirrhosis) of the left lung. (Modified from. Sibson.) The displacement, which results from this cause is seldom so great as in the following case, in which the pulsations of the heart were observed in the left axilla. Case If. — Pleurisy : Cirrliosis {?) of the left Lung; great displacement of tlie Jieart to the left. J. M., set. 21, a fireman, was admitted to the Ne\vcastIe-on-Tyne Infirmary, under my care, on 3d December 1874, complaining of palpita- tion, shortness of breath, cough, spit, and great debility. Previous history. — The patient, who has always been very round shouldered, stated that he had enjoyed excellent health until four years ago, when he had an attack of rheumatic fever, which laid him up for fourteen weeks : he does not know whether his heart was affected or not. After this attack he enjoyed good health for some years, when he ' caught a severe cold,' in consequence of exposure to cold and wet, and was ill for several weeks with cough and severe pain in the left side, which ' caught no Diseases of tJic Heart. his breath.' These symptoms gradually subsided, and he continued in excellent health until four months ago, when his present illness com- menced with cough, spit, and shortness of breath. These symptoms have gradually increased, and he has lost a great deal of flesh. Presetit condHion—ViQ is considerably emaciated. The girth of the left chest is considerably less than that of the right, the measurements being as follows : — Position of measurement. Right. Left At the second rib i5>^ in. \i\)i'm. At the nipples I5/^ i"- I4/^ in- At the ensiform cartilage . . . 15 in. 1 5 in. The percussion note over the greater part of the left lung, but especi- ally at the base, is impaired ; increased vocal resonance, sibilant rales, and occasional large crepitations are heard on auscultation. There was also evidence of commencing consolidation of the right apex. The pul- sation of the heart can be very distinctly seen and felt in the left axillary and infra-axillary regions, the apex being apparently situated in the sixth interspace, two inches outside the nipple. The percussion note between the left nipple and the sternum is resonant, and the heart sounds are inaudible at this spot ; at the aortic cartilage the heart sounds are ver^f faint, but are much louder in the second and third interspaces on the left side. Upward displacement may be due to : (i) Anything which raises the arch of the diaphragm, such as soHd, Hquid, or gaseous accumulations in the cavity of the abdomen — ascites (see fig. 28), ovarian tumours, tympanites, enlargement of the Hver (see fig. 29), fibroid tumours of the uterus, etc. In many of these cases the displacement is partly to one side as well as upwards. Enlargement of the left lobe of the liver, for example, usually displaces the heart upwards and to the left, while great enlargement of the spleen may push it upwards and to the right. (2) Retraction of the upper part of either lung, the most common pathological condition being phthisis. Dozvmvard displacement may be caused by : (i) Anything which presses down the heart or diaphragm, such as aneurisms or solid tumours, emphysema of the lungs, etc. (see fig. 30). Displacements of the Heart. 1 1 1 Fig. 28. — Upivard displacement of the heart, the result of ascites. (2) Collapse of the abdominal viscera, and consequent descent of the diaphragm. Forivard displacement is very rare, but it does sometimes result from an aneurism (as in a case which I shall afterwards relate) or a solid tumour in the posterior mediastinum. Backivard displacement is still more rare ; it is said to be occasionally produced by tumours or inflammatory accumu- lations in the anterior mediastinum, but no case of this description has come under my personal observation. I 12 Diseases of the Heart. Fig. 29. — Displacement of the heart ufncards and to the left, the result of enlargement of the liver. {Modified frotn Sibson. ) Fig. 30. — Do7vnward displacement of the heart, the result ofpithnonary emphysema. ( After Sibson, modified. ) Displacements of tJie Heart. 1 13 B. Displacements of the apex beat due to intrinsic causes. The intrinsic conditions which may produce displacement of the heart and apex beat are — 1. Fluid in the sac of the Pericardium. — Where the peri- cardial effusion is considerable, but not excessive, the base of the heart and the great vessels are pushed upwards and backwards, and the apex is tilted upwards and outwards, so that it may correspond in position to the left nipple, or in some cases may be situated still further to the left. Where the effusion is very copious, the apex beat may be completely obscured ; while in those cases in which the amount of effusion is small (the heart itself being of normal size), or in which the heart is fixed by old pericardial adhesions, there is little or no alteration of the apex beat. 2. Alterations in the shape and size of the heart itself.- — When the left ventricle is hypertrophied (see fig. 31), the extension is chiefly downwards and outwards {i.e. to the left), and the apex beat may be situated in the sixth, seventh, or even the eighth interspace, three, four, or even five inches to the left of the sternum. In many cases it is considerably outside the left nipple. In hypertrophy and dilatation of the right ventricle, the apex beat (which is usually under such circumstances more diffused than in health), is displaced downwards and to the right (see fig. 32), and the cardiac impulse is not unfrequently best seen and felt in the pit of the epigastrium. But since epigastric pulsation may be due to several other important conditions, it will perhaps be well to enumerate them here. Epigastric Pulsation. The chief forms of epigastric pulsation are, in the order of their relative frequency, as follows : (i.) Transmitted pulsation from the heart. — This form of pulsation is generally due to enlargement (hypertrophy and dilatation) of the right ventricle, but it may also be caused by the downward displacement of the organ, which is seen in pulmonary emphysema,^ aneurism of the arch of the aorta, ' In emphysema the right side of the heart is dilated and hypertrophied, and to this cause the epigastric pulsation, which is so marked a feature in emphysema, is in part due. H 114 Diseases of the Heart. collapse of the abdominal viscera, etc. The pulsation is in these cases exactl}' synchronous with the ventricular contrac- tion, and is often transmitted through the left lobe of the liver. (2.) Pulsation of the abdoniinat aorta. — In some of these cases, as for instance in neurotic pulsation of the vessel, the aortic pulsation may be directly felt, in others it is indirectly felt, and is communicated through the liver or some solid body, such as a cancer of the pylorus, lying in front of the Fig. 31. — Hypertrophy of the left veiitiicle, shoiving the altered positio)i of the apex. (After von Dusch.) The continuous line represents the normal heart ; the dotted line the hyper- trophied left ventricle. The apex of the left ventricle is outside the dotted line a b, which is drawn through the left nipple. Displacement of the apex-beat. I I vessel. The pulsation in this form is a little behind (after) the apex beat, but this fact is sometimes with difficulty established in practice. (3.) Aneurisin of the lozt'er part of the thoracic, or of the upper part of the abdominal aorta. — This is not a common cause of epigastric pulsation. The aneurismal pulsation may be directly felt, or may be transmitted through the liver. According to Sibson, the epigastric pulsation, which is caused by an aneurism of the lower part of the thoracic or Fig. 32. — Hypertrophy of the right venti-icle. (After von Dusch.) The normal outline of the heart is represented by a continuous line : the hypertrophied right heart by a dotted line. 1 1 6 Diseases of the Heart. the upper part of the abdominal aorta, is strong during ex- piration, but is lessened, or even disappears, during inspiration. In cases of abdominal collapse, on the contrary, the epigastric pulsation is more marked when the patient takes a deep in- spiration.^ (4.) True Pulsation in the liver. — Here the pulsation is caused by a ' back-wash ' from the right auricle. The liver is always enlarged, and the pulsation is diffused through, and not simply communicated to it. Its rhythm corresponds to tlie apex beat, for the blood-wave which produces it is propelled by the right ventricle through the incompetent tri- cuspid orifice into the hepatic veins. This form of pulsation is therefore pathognomonic of tricuspid regurgitation. In some cases of this description the hepatic pulsation may possibly be due to communicated pulsation from the inferior vena cava,- for the back-wash also extends into that vessel. THE EXTENT OF THE CARDIAC IMPULSE AS ASCERTAINED BY INSPECTION AND PALPATION. In health, and during tranquil action of the heart, the apex beat is the only cardiac pulsation which is visible, and it usually covers an area of about one square inch in extent. When the heart is excited, in thin persons, and when an unusually large portion of the organ is in direct contact with the chest wall — a condition which may result from increased size of the organ, forward displacement of the heart, or retraction of the anterior margins of the lung — pulsation may be seen and felt over a large portion of the precordial region. Diffuse wave-like pulsation is seen in some cases of dilatation of the organ, and, according to some observers ^ in pericardial effusion. ' Russell Reynold's System of Med id /le, vol. iv. p. 129. Pulsation in the vena cava might also result from a communication between a large arterial trunk, such as the abdominal aorta, and that vessel ; but I am not acquainted with any case in which this condition has been observed. ' It is very doubtful whether a diffuse wave-like pulsation over the precordial region does result from pericardial effusion. Diniiuished cardiac impulse. 1 1 7 The exact character of tJie Cardiac Impulse ivith respect to force, rhythm, celerity, etc. The force of the cardiac impulse is ascertained by pal- pating the praecordia in the manner described above, and is still more accurately observed by placing the right hand over the precordial region, the left hand over the back between the scapulae, and by compressing the chest firmly between the two. The pulsation of deep-seated aneurisms can some- times be observed by this method, when the ordinary method of palpation fails to elicit any abnormal pulsation. The force of the cardiac impulse varies considerably in different cases, and depends upon: — (i) The thickness and character of the media (tissues of the chest wall, lung, etc.) which separate the heart from the hand of the observer ; (2) The force with which the heart is contracting. Diminution or absence of the cardiac impulse (as seen and felt over the prsecordial region) on the one hand, and excessive impulse on the other, do not, therefore, necessarily indicate actual diminution or actual increase of the cardiac contractions, — though they certainly suggest these conditions. Diminished Cardiac Impulse. We will first consider those cases in which the cardiac impulse, as seen by the eye and felt by the hand, is weakened or abolished. In these cases, as I have just stated, the force of the cardiac contraction is sometimes apparently, sometimes actually, weakened. The conditions ivhich give rise to diminution or absence of t/ie cardiac impulse, the force of the cardiac contractions being normal (i.e. to apparent diminution of the force of the cardiac contractions), are as follozus : — I. Undue thickness of the thoracic walls, especially the presence of a thick layer of subcutaneous fat, largely de- veloped mammae, etc.^ ' In these cases (where the subcutaneous fat is excessive) the heart may be infiltrated with fat, or in a condition of true fatty degeneration, and the force of the cardiac contractions may be actually as well as apparently diminished. 1 1 8 Diseases of tJie Heart. 2. Excessive over-lapping of the heart by the lungs. This condition is seen even in health where the thorax is unusually short and broad, and the lungs voluminous ; but it reaches its highest degree of development in pulmonary emphysema. 3. Fluid in the sac of the pericardium. When the effusion is scanty, the position and force of the apex beat may not be altered. When the effusion is more considerable, the apex is raised and carried more to the left, and the cardiac impulse as felt by the hand is weakened.^ When the effusion is very great, the apex beat may completely disappear,^ and it may be impossible, when the patient is lying on his back,"^ to feel any cardiac impulse. The conditions ivliich give rise to actual dimiiuition of the force of the cardiac contractions, and therefore of the cardiac impulse, as felt by the hand externally, are : — 1. General collapse, and anything which temporarily weakens the action of the heart — (nervous depression, exces- sive smoking, etc). 2. Structural alterations which weaken the cardiac muscle, such as fatty degeneration, fibroid degeneration, acute myo- carditis, etc. Increased Cardiac Impulse. Increased cardiac impulse, as seen and felt over the prsc- cordia, like diminished impulse, may be either apparent or real. The conditions zuhich gives rise to increased cardiac impnlsc — tlie force of the cardiac contractions remaining normal — {apparent increase^ are as follows : — I. An atrophied condition of the chest walls. This cause ' In some of these cases the visible impulse may be considerable, but the impulse, as felt by the hand, slight. - In many cases of excessive pericardial effusion, the force of the cardiac con- tractions is also actually impaired. ' The cardiac impulse can generally be felt if the patient is made to lean well forwards, or turn on to his left side. The rhythm and celerity of the cardiac impulse. 1 19 is, to a large extent, theoretical and of little importance in practice. Atrophy of the subcutaneous fat, and of the chest muscles (the lungs being normal), probably exerts little influence on the cardiac impulse as felt externally. Indeed in many of these cases the heart is itself debilitated, and as a matter of fact the impulse weakened. 2. Increased exposure of the heart. This is a frequent cause of increased pulsation, and is usually due to the retraction of the lungs, which results from pleurisy, cirrhosis, etc. ; but it may be due to forward displacement of the organ. TJic conditions ivJiich produce actual increase of the force of t/ic cardiac contractions, and therefore of the cardiac inipidse, as seen and felt externally, are : — 1. All conditions which produce temporary over-action of the heart, such as violent exertion, mental agitation, and the numerous causes of functional palpitation. 2. Hypertrophy of the heart ; particularly hypertrophy of the left ventricle. In these cases the cardiac impulse is heaving or pushing, and the whole chest may appear to be raised en masse. The Rhythm of the Cardiac Contractions. When the cardiac impulse is perceptible, the exact rhythm of the cardiac contractions can of course be ascertained by palpating the prascordia, but the rhythm of the heart will be more appropriately considered when I come to treat of the pulse. The Celerity of the Cardiac Impulse. In some conditions, the heart contracts more abruptly than in health, and the impulse, as seen and felt externally, is correspondingly sudden. This form of impulse (due to increased celerity of contraction) is chiefly seen in conditions of nervous excitement, and of ' irritable weakness,' such as is associated with anaemia and allied conditions. The area of visible impulse is often increased. In other cases the cardiac contraction, and therefore the I 20 Diseases of fJic Heart. impulse as seen and felt externally, are unusually slow and laboured (diminished celerity of impulse). This form of contraction is generally associated with hypertrophy, more especially hypertrophy of the left ventricle ; the cardiac impulse is usually strong and pushing, and in many cases the chest appears to be raised up en masse. Proicordiai thrills and friction fremitus. Vibratile sensations, of a ' soft ' trembling character, and resembling very closely the vibratile sensation which is ex- perienced on placing the hand over the back of a cat, when purring (hence the term ' purring tremor ' which has been applied to them), are sometimes felt on placing the hand over the praecordia. To vibrations of this description the term thrill is applied. The term friction fremitus is given to vibrations of a harsher, rougher, and grating character, which can be felt when the hand is placed over the chest. Thrills may be produced either in the heart itself or in the great vessels. The cardiac thrills with which we are now concerned, are usually produced by the passage of the blood stream through a stenosed or roughened orifice, and are therefore generally produced by a 'direct' current. Stenosis of the mitral valve is the most common cause of cardiac thrill. The vibratile sensation is felt in the mitral area, i.e. over the position of the apex beat ; its rhythm is (for tlie reasons which I shall afterwards explain in speaking of cardiac murmurs) presystolic, that is to say, it occurs immediately before the contraction of the ventricle, i.e. immediately before the apex beat. Aortic stenosis is the next most common cause of thrill. The vibratile sensation is systolic in rhythm, and is felt over the base of the heart and ascending thoracic aorta. Occasionally, however, the thrill is produced by a back- ward or regurgitant current. A systolic thrill over the apex is felt in some cases of mitral regurgitation ; and a diastolic thrill at the base is not at all uncommon in aortic regurgi- tation. Thrills produced at the tricuspid and pulmonary orifices are extremely rare. Percussion. 121 Friction fremitus is produced by the rubbing together of two rough surfaces. When felt over the praecordia, it may be pericardial or pleural. Pericardial friction fremitus corresponds in rhythm to the rhythm of the heart. It is a comparatively rare pheno- menon which is seen in some cases of pericarditis, more especially in those cases in which the lymph coating of the pericardial sac is tough. Pericardial friction fremitus is therefore observed towards the later periods of pericardial inflammation, i.e. when the lymph is becoming tough and organised. The clinical signiiicance of pericardial fremitus is not great, for friction vibrations are almost always more apparent to the ear than to the touch, and are therefore better studied by auscultation than by palpation. Pleural friction is sometimes felt over the praecordial region, more especially over the borders of the heart. Its rhythm corresponds to the rhythm of the respirations, and by this means it is distinguished from the friction fremitus of pericarditis. PERCUSSION. Percussion, the next method of physicial examination which we employ, is an extremely important means of in- vestigation. It is founded on the facts: — (i) that the heart is a solid organ which is in great part surrounded by the air-containing lungs ; and (2) that the ' sound ' and ' sensation of resistance,' which are obtained by percussing a solid body and an air-containing viscus, are markedly different. The object of percussion is to ascertain the size, the shape, and position of the heart ; and in order to determine these points we must endeavour to define: — (i) the extent and outline of that part of the heart which is uncovered by lung, — the area of superficial or absolute cardiac dulness ; (2) the size and outline of the heart as a whole — tJie area of deep or relative dulness, as it is sometimes termed — (the area of impaired percussion). I 2 2 Diseases of the Heart. The area of superficial or absolute eeirdiae dulncss. The size of the area of superficial or absolute cardiac dulness varies considerably, in health, with the condition of the lungs, being diminished during inspiration, and increased during expiration, and is subject to marked alterations in disease. Theoretically, it should exactly correspond to that portion of the heart which is uncovered by lung (see fig. 33), but as a matter of fact its inner (central) border does not correspond to the mid-line of the sternum, but to the left border of that bone ;^ while its inferior border cannot be accurately deter- mined by means of percussion.^ The extent of the heart, which is uncovered by king, during moderate inspiration, is seen in figure ■}^'}^. In full inspiration, the anterior border of the right lung closely corresponds to a line drawn vertically downwards through the centre of the sternum. It extends downwards as far as the junction of the sixth costal cartilage with the sternum ; the lower border of the lung leaves the middle line usually at the level of the sixth rib or sixth interspace, and passes obliquely downwards and backwards. The anterior border of the left lung closely corresponds to the mid- line of the sternum until it reaches the level of the fourth costal cartilage. At this point it passes obliquely downwards and outwards until it reaches a point which usually corresponds to the junction of the fifth rib with its costal cartilage. It then turns obliquely inwards and downwards, forms the tongue-shaped projection, which is well shown in the figure, and finally passes backwards and downwards, usually leaving the middle line at the level of the sixth rib or sixth inter-space. The area of superficial or absolute cardiac dulness is, then, more or less triangular^ in shape; the size of the triangle varying with the position of the anterior borders of the lungs. ' The sternum is an excellent conductor of sound, and it is difficult or impos- sible when one lateral half is in contact with the resonant lung, as it is during complete inspiration, to get an absolutely dull percussion sound over the other (the right) half of the bone. ^ The lower border of the heart cannot be accurately defined by percussion, for it is practically impossible to distinguish the dull sound which is due to the lower part of the heart, and the dull sound which is due to the upper part of the liver. ' In many cases, the area of superficial cardiac dulness is rather quadrangular than triangular. Area of absolute eardiac d illness. 12X The base of the triangle cannot, for the reason ah-eady given (see foot-note, page 122), be accurately defined by per- cussion, but is represented with sufficient accuracy by a horizontal line drawn from the position of the apex beat to the mid-sternum. Under normal circumstances, and during moderate inspiration, the length of the base line is about 2\ inches. Fic. 33. — Snpe7-Jicial view of the organs of the chest and abdomen from the front, shoiV/n:;- the part of the heart uncovered by Ii(ng. {Enlarged from Sibson. ) 124 Diseases of tJie Heart. Fig. 34. — The area o/pnccordial Jiilness in middle ai;v. (After Weil.) ABCD, area of superficial or absolute cardiac dulness ; AIK, area of im- paired percussion or deep dulness ; CE, lower border of right lung ; DF, lower border of left lung; G and H, upper borders of lungs ; PQ, upper border of hepatic dulness ; LM, lower border of hepatic dulness ; NO, lower border of stomach in n)oderate distention. Area of absolute cardiac di tin ess. 125 The apex of the triangle corresponds under normal cir- cumstances to the junction of the fourth left costal cartilage with the sternum. The vertical side of the triangle, i.e. the side formed by a line drawn from the apex of the triangle to the central (the sternal) end of the base line, is, under normal circumstances, about two inches in length. For the reason already given (see foot-note, page 122) it does not correspond to the mid-line of the sternum, but to the left border of the bone. The third or oblique side of the triangle, which is seldom a straight line, but generally more or less curved, as repre- sented in figures 34 and 35, is formed by drawing a line from the apex of the triangle to the outer end of the base-line {i.e., to the apex of the heart) ; it is usually about 3 inches in length. Mode of percussiug the area of superficial or absolute cardiac dulness. In seeking to determine the exact size and boundaries of the area of superficial or absolute cardiac dulness, at the bedside, it is convenient in the first place, as recommended by Sansom, to draw the base-line, i.e. to draw a horizontal line from the position of the apex beat to the mid-sternum, and then to determine the position of the vertical and oblique sides of the triangle respectively, i.e. to define the anterior margins of the lungs by means of percussion. And it is important to remember that at those points at which the absolute and relative areas of cardiac dulness meet [i.e. where the margins of the lungs terminate), the percussion strokes must be lightly struck, for otherwise the resonant note which is obtained from the thin layer of lung will be, to some extent, obscured by the dull sound which is obtained from the solid heart, which is situated beneath it. The extent of the area of absolute cardiac dulness, both in moderate inspiration, and during complete inspiration, and in complete expiration, should be ascertained if extreme accuracy is required, per- cussion being performed, while the patient holds his breath, after a moderate inspiration, a complete inspiration, and a complete expiration, respectively. 126 Diseases of tJie Heart. Fig. 35. — Atitei-ior view of the chest and abdomen, showing the position of the heart in the thorax and its relationship to the surrounding viscera. (After Weil. ) EF, edge of the right king; GH, edge of the left lung; MN, right border of the heart ; NO, lower border of the heart ; PO, left border of the heart ; Q, sinus mediastinocostalis, situated between the edge of the pleura and incisura cardiaca of the anterior border of the left lung ; R, highest point of the portion of liver covered by lung; S, lower edge of the liver; T, cardiac portion of the stomach; U, pyloric portion of the stomach ; V, small curvature of the stomach ; \V, greater curvature of the stomach. TJie area of deep or relative cardiac dulness. 127 TJie area of deep or relative cardiac dnlitcss. The area of deep or relative cardiac dulness should cor- respond to the space which the heart occupies as a whole, that is to say, it should extend vertically from the third rib or second interspace to the base-line drawn from the apex beat horizontally across the sternum, and transversely from an inch to the right of the sternum to a point slightly within the left nipple. (See fig. 35.) As a matter of fact, how^ever, it is difficult to define the exact extent of the deep cardiac dulness. As we have already seen, its lower border cannot be accurately ascertained by means of percussion. Its upper boundary runs into the dulness which is due to the presence of the great vessels (aorta, pulmonary artery, and superior cava, etc.) ; while the right and left borders of the heart (more particularly the right) are so deeply situated, that their exact position is with difficulty determined. The left border can generally be fairly well defined, — and we have an additional guide to its position in those cases in which the apex beat is well-marked, for the position of the left apex beat not only represents the lowest, but also the outermost point of the heart. (In some cases of pericardial effusion, and in some cases of hypertrophy of the left ventricle, the cardiac dulness extends farther to the left than the position of the apex beat.) When the right ventricle is dilated, the left apex beat may be ill defined or absent. In cases of this description the pulsation of the right ventricle is often best marked in the epigastrium, and the position of the apex beat affords no guide to the left border of the heart. Mode of percussing the deep cardiac duluess.— The observer should first endeavour to define the upper border of the heart by percussing from above downwards in the para-sternal line.^ He should then determine the extent of the transverse dulness at the level of the fourth rib or fourth interspace. The percussion must be forcibly made, for the borders of the heart are covered by a thick layer of resonant lung ; small differences in tone must be accurately noted, and the ' per- cussion resistance ' carefully observed. ' The para-sternal line is an imaginary line drawn vertically downwards over the front of the chest mid-way between the left border of the sternum and the left nipple. I 28 Diseases of the Heart. Alterations in the extent of the cardiac diilness %:^hich occur in disease. The area of cardiac dulness may be either increased or diminished in disease ; and both conditions — increased and diminished duhiess over the praecordia — may be either actually or apparently due to cardiac alterations. In other words, alterations in the extent of the praecordial dulness are in some cases due to alterations in the size of the heart and pericardium ; in other cases, to alterations in the surrounding viscera (more particularly in those portions of the lungs which overlap the heart), the size of the heart and peri- cardium being normal. Increased dulness over the prcecordia. Increased dulness over the praecordia may be due to : — 1. Increase in the size of the heart (hypertrophy, dilata- tion, deposits of fat on the exterior of the heart, new growths in its substances). 2. Fluid in the sac of the pericardium (pericarditis with effusion, hydro-pericardium). 3. Increased exposure of the heart — the organ itself being of normal size. Under this head are included : — (a) Those cases in which the anterior borders of the lungs are retracted from pleuritic adhesions, cirrhosis, etc. (b) Those rarecases in which the heart is displacedforwards by aneurisms or solid tumours in the posterior mediastinum. 4. Solid or fluid accumulations in contact with the heart, amongst which the following are the most important : — (a) Consolidations (from pulmonary apoplexy, pneumonia, tubercle, new growths, etc.), of those portions of the lungs which overlap the heart. (b) Fluid in the pleural sacs. (c) Solid tumours, deposits of fat, or inflammatory forma- tions in the anterior mediastinum. (d) Enlargements of the liver. (e) Aneurisms springing from the base of the aorta. Note. — It is extremely important to remember that the dulness which, under ordinaiy circumstances, results from enlargement of the heart and Increased Prcecordial D illness. 129 many of the other conditions which I have enumerated in the text, may not be present in those cases : — in which the lungs are emphysematous ; in which the anterior margins of the lungs are fixed by adhesions ; or in which there is air in the pericardial or pleural sacs. TJie differential diagnosis of increased dulness over the prcecordia. Given the presence of increased dulness over the prae- cordia, we must, of course, endeavour to determine the exact nature of the pathological condition which is present ; and in order to arrive at this conclusion, it is convenient to proceed by the following stages or steps : — Step No. I. — Is the increased dulness derived from the heart itself, or is it due to the presence of some non-resonant substance in contact with the organ ? Step No. 2. — If the dulness is due to the presence of a non-resonant substance in contact with the heart, what is the exact pathological condition which is present ? Step No. 3. — If the dulness is directly derived from the heart itself, does it result from increased exposure (apparent enlargement) of the organ, or from an actual increase in the size of the heart, including the pericardium ? Step No. 4. — If the dulness is due to an actual increase in the size of the organ, does it result from the presence of fluid in the sac of the pericardium, or from an enlargement of the heart itself? Step No. 5. — If the dulness is due to enlargement of the heart itself, is the enlargement general or partial, and what is the pathological character and cause of the condition ? Step No. I.— Is the increased dulness over the prcecordia derived from the heart itself, or is it due to the presence of some iiflji-resojiant substance in contact ivith the organ ? As a rule there is little difficulty in coming to a correct conclusion on this point. As we have previously seen, the chief pathological conditions which give rise to dulness in the neighbourhood of the heart, are: — (a) Consolidations of the adjacent portions of the lungs (apoplectic, pneumonic, tubercular, sarcomatous, etc.). I I 30 Diseases of the Heart. (b) Fluid in the pleural cavity. (c) Enlargement of the liver. (d) Tumours, or inflammatory deposits in the anterior mediastinum. (e) Aneurism of the first portion of the aortic arch. Now in most of these conditions — in the vast majority of cases met with in practice — the increased dulness is not confined to the limits of the praicordia, but extends often for a considerable distance into the surrounding regions of the chest.^ In many cases too, it does not conform to the shape of the dulness which results from an enlargement of the heart or pericardium.- There are, too, as a rule, other symptoms and physical signs indicative of the cause of the dulness. In consolida- tions of the lung, for example, cough, expectoration, and alterations of the respiratory murmur over the seat of the dulness (tubular breathing, rales, etc.), would probably be present. In addition to these positive facts the negative evidence — that there are no signs nor symptoms of disease of the heart or pericardium — confirms the diagnosis. The points, then, to which attention should be directed, in order to come to a conclusion as to the first step in the diagnosis are : — 1. The extenfand outline of the dulness. 2. The presence of symptoms or physical signs indicative of disease of the adjacent parts. 3. The condition of the heart and pericardium, as deter- mined by other methods of investigation. Step No. 2. — If the dulness is due to tJie presence of a non- ' Dulness, resulting from a limited consolidation of those portions of the lungs in contact with the heart, might of course be limited to the praacordia. In such a case the other physical signs and symptoms (negative and positive) would be quite sufficient to determine the diagnosis. ^ It would be extremely difficult, indeed in many cases impossible, to dis- tinguish the dulness due to a small tumour or inflammatory accumulation in the anterior mediastinum, from the dulness which results from enlargement of the heart or pericardium. Fortunately limited tumours of this description are rare, and the difficulty in diagnosis is therefore seldom met with in practice. Increased PrcFCordial Dtilncss. 1 3 1 resonant substance in contact ivith the heart, i^'hat is the exact pathological condition zv/iich is present F This point can only be determined by a careful and accurate survey of all the 'facts of the case' (symptoms, physical signs, etc.) ; and it would obviously be out of place to attempt to detail here the numerous symptoms and physical signs which characterise the many different condi- tions which may produce dulness in the neighbourhood of the heart. Suffice it to say, that the observer must first endeavour to determine to which group of conditions (con- solidation of the lung, fluid in the pleura, etc.), the lesion is to be referred ; and having decided that point, he must next endeavour to determine the exact pathological character of the structural alteration which is present. Step No. 3. — If the dnlness is directly derived from the heart itself, does it result from increased exposure (i.e. apparent enlargement), or from aetiial increase in the size of the organ ? By far the most common cause of ' increased exposure' of the heart is retraction of the anterior margins of the lungs, a condition which usually results from pleurisy or cirrhosis. In seeking then to decide whether the increased dulness is due to apparent or actual enlargement of the organ, attention must be particularly directed to the condition of the lungs. A history of previous pleurisy ; the fact that the anterior margins of the lungs are fixed by adhesions, and do not expand and cover up the heart during inspiration — a point which can be determined by percussion and ausculta- tion, during inspiration and expiration respectively ; or, the presence of symptoms and signs of cirrhosis, phthisis, etc., would of course be in favour of increased exposure (apparent enlargement) — an opinion which would be confirmed by the absence of symptoms and signs of pericardial or cardiac disease, or of any extra-cardiac cause of enlargement of the heart, such as cirrhosis of the kidney or atheroma. But while these are the points to which attention should be directed, in order to make a diagnosis, it must be con- fessed that a positive opinion cannot always be arrived at ; and it is still more difficult to exclude any enlargement of 132 Diseases of t lie Heart. the heart itself, in those cases in which the increased exposure is due to forward displacement of the organ. In many of these cases the heart is actually enlarged as well as dis- placed ; and in those cases in which there is no enlargement of the organ, the strong cardiac impulse which may be very noticeable, and the presence of intra-cardiac murmurs, which may be produced by pressure alterations at the valvular orifices, may make it impossible to exclude all cardiac hypertrophy. In cases of this description then (which, as I have previously remarked, are extremely rare), a positive opinion that the increased dulness is due to forward dis- placement, and not to enlargement of the heart itself, could only be ventured upon, when : — (a) There is distinct evidence of an aneurism or tumour behind the heart, i.e. of the presence of an efficient cause of forward displacement. (b) There are no signs nor symptoms of cardiac disease ; and no extra-cardiac cause of enlargement such as chronic Bright's disease. Step No. 4. — If the dulness is due to an actual increase in the size of the organ, does it result from fluid in the sac of the pericardium, or from enlargement of the heart itself? This question, which involves the differential diagnosis of pericardial effusion and hypertrophy and dilatation of the heart, will be more appropriately considered in the detailed description of pericarditis, which will be afterwards given. Step No. 5. — If the increased dulness is due to enlargement of the heart itself is the enlargement general or partial, and zvhat is the pathological character and cause of the condition ? This point, too, will be more conveniently considered under the detailed description of hypertrophy and dilatation of the heart. DIMINISHED DULNESS OVER THE PRyECORDIA. Diminished dulness over the praecordia is comparatively seldom due to diminution in the size of the heart itself; it most frequently depends upon some alteration in the lungs or adjacent viscera. The chief causes of diminished dulness Dimmished PrcECordial Dulness. jj over the praecordia are, in the order of their relative frequency, as follows : — I. Increased covering up of the heart by the lungs. By far the most common cause of this condition is emphysema, but it is sometimes due to the anterior margins of the lungs being fixed over the heart by pleuritic adhesions ; or to the fact, that the heart is pushed up under cover of the lungs by some gaseous, fluid or solid accumulation in the abdomen. In some healthy persons, in whom the lungs are very voluminous, the area of absolute cardiac dulness is much smaller than usual, and may be completely abolished during a full inspiration ; but these cases are easily recognised by the facts, that the area of cardiac dulness is present during a full expiration, and that there are no signs nor symptoms of cardiac or pulmonary disease. 2. Gaseous accumulations in the pleura, stomach, or intestines. 3. Gas in the pericardium. 4. Atrophy of the heart itself TJie dijfcrential diagnosis of diminished dulness over the prceeordia. There is not, as a rule, much difficulty in deciding this question. The steps which it is convenient to follow in order to arrive at a correct conclusion are as follows : — Step No. I. — Does the diminished praecordial dulness depend upon extra- or intra-cardiac ^ conditions } Step No. 2. — If extra-cardiac, is the diminished dulness due (a) to some abnormal condition of the lungs ; (b) to distention of the stomach and intestines ; or (c) to air in the pleural cavity (pneumo-thorax).'' The observer should remember that atrophy of the heart sufficiently great to cause diminished praecordial dulness is extremely rare, and could only be diagnosed by the method of exclusion. - ' Under the head of intra-cardiac conditions, I include abnormal conditions of the pericardium, as well as of the heart itself. - Atrophy of the heart is met with in many wasting affections, more particularly in cancer of the pylorus. In many cases of this kind (wasting diseases with atrophy of the heait) the lungs are emphysematous, and the diminished precordial dulness is partly' due to increased overlapping of the heart by the lungs. 134 Diseases of the Heart. In all cases, then, in which diminished pra^cordial dulness is met with, the practitioner should, in the first place, make a careful physical examination of the patient, paying particular attention to the condition of the lungs, stomach, and adjacent viscera. By this means he will be able to determine whether the physical signs of emphysema, pneumo-thorax, or any of the other extra-cardiac causes of diminished dulness (which I have just mentioned) are present. When the diminished dulness is due to pneumo-peri- cardium, the physical signs of that condition — which are very definite, and which I shall afterwards describe — will be dis- covered in the course of the examination. Should the result of this examination be negative {i.e. should physical examination fail to elicit any cause for the condition), he will have to ask himself whether the diminished dulness is due to a voluminous (but not emphysematous) con- dition of the lungs, or whether it is caused by atrophy of the heart itself The condition of the general health ; the state of the cardiac dulness during a full expiration ; ^ and particularly the presence of any well recognised cause of atrophy of the heart, such as cancer of the pylorus, are the points to which attention is to be directed in order to decide this point. AUSCULTATION. Auscultation is an extremely important means of phy- sical examination. It is founded upon the facts : — (i) That during each cardiac revolution certain sounds are generated within the heart. (2) That these sounds depend upon definite physical conditions, more especially upon the condition of the valve- flaps, and the manner in which they are closed and stretched. (3) That modifications in these physical conditions {i.e. alterations in the valve-flaps, and in the manner in which they are closed and stretched) are attended by correspond- ing modifications in the cardiac sounds. ' When the kings are vohiminous, hut otherwise healthy, the cardiac duhiess becomes distinctly perceptible during a complete expiration. In atrophy of the heart, a full expiration does not produce such a marked effect. A iiscultation. 1 3 5 By means, then, of auscultation, we are able to obtain valuable information as to the condition of the valvular apparatus of the heart ; and since the mode of closure and stretching of the mitral and tricuspid valves depends, in great part, upon the condition of the walls of the left and right ventricles, and since the manner in which the aortic and pulmonary valves are closed and stretched depends upon the condition of the aortic and pulmonary blood- pressures, we have in auscultation a valuable means of ascertaining the condition of the cardiac muscle, and of the blood-pressure in the aorta and pulmonary artery respectively. Further, by means of auscultation we can observe the rhythm of the heart, and the exact frequency of the cardiac contractions.^ Auscultation, too, is the most important means which we possess of determining the presence of disease in the pericardial sac. The main objects of auscultation are to ascertain : — 1. Whether both cardiac sounds are audible or not. 2. The character of the cardiac sounds, whether normal or not. 3. If abnormal, the exact nature of the modifications which are present. But in order that these points may be thoroughly under- stood, and that the significance of their different modifica- tions may be correctly appreciated, I must now describe the normal character of the cardiac sounds, their mode of production, the nature of the alterations which they undergo in disease, and the manner in which these modifications are produced. The iioi'jiial Heart So?iiids and their mode of produetiou. During the period which elapses between the commence- ment of one ventricular contraction and the commencement ' In some cases in which the heart is acting quickly and feebly, and more especially in those cases in which some of the cardiac pulsations fail to reach the wrist, auscultation and the cardiograph are the only certain means of ascertaining the exact frequency of the cardiac contractions. 136 Diseases of the Heart. of the ventricular contraction immediately succeeding it, that is to say, during every complete cardiac revolution or cycle, two sounds are generated, which are termed respectively the first and second sounds of the heart. The two sounds are separated by periods of silence, or pauses, as they are tech- nically termed ; and the whole cardiac cycle is therefore composed of four separate parts, viz.: — 1. The first sound. 2. The first silence or pause. 3. The second sound. 4. The second silence or pause. The_/z/'i"/ sound corresponds in time to the contraction of the ventricles, i.e. its rhythm is systolic ; and it is mainly produced by the sudden tension of the auriculo-ventricular (mitral and tricuspid) valve-segments and their chordae tendirieae, partly by the contraction of the muscular walls of the ventricles.^ The second sound follows the contraction of the ventricles, i.e. its rhythm is diastolic ; and it is produced by the closure, and, more especially, by the sudden tension of the arterial (aortic and pulmonary) valve-flaps. Now, since the heart is a double organ, four sounds are in reality generated during each cardiac cycle, viz., two first sounds, produced by the sudden tension of the mitral and tricuspid valve-flaps (the mitral first sound and the tricuspid first sounds respectively), and two second sounds, produced by the sudden tension of the aortic and pulmonary valve- flaps (the aortic and ptdinonary second sounds respectively). But in as much as the action of the two hearts is, under ordinary circumstances, perfectly synchronous, the two first sounds are synchronous, and the two second sounds are synchronous ; and hence a single first sound (which is made up of the mitral and tricuspid first sounds), and a single second sound (which is made up of the aortic and pulmonary ' The tilting of the apex against the wall of the chest, the sudden tension of the walls of the ventricles, and the passage of the blood from the ventricles into the aorta and pulmonary artery, have also been thought to aid in the pro- duction of the first sound of the heart. Normal Heart Sounds. ^Zl second sounds) are heard when the stethoscope is applied over the praecordia. TJie relative duration of the cardiac sounds and silences. Under ordinary circumstances, i.e., when the heart is healthy and the pulse of normal frequency, each cardiac sound, and each silence, has a definite duration, which, for practical purposes, is sufficiently accurately expressed as follows : — If the whole cardiac cycle be divided into ten equal parts, the first sound will occupy four-tenths, the first silence one-tenth, the second sound two-tenths, and the second silence three-tenths of the whole. This measurement which is taken from Walshe {Diseases of the Heart, page 48), is a good working division, though not absolutely accurate. According to Dr Gibson ^ the average absolute duration of each phase of the entire cardiac cycle is as follows : — Auricular Systole. Ventricular Systole. ■I 12 sec. •368 sec. Ventricular Diastole. •578 sec. Entire Cycle. 1*058 sec. This division of the cardiac cycle is graphically represented in figures t,6 and 37, by reference to which the exact relationship of the cardiac sounds and silences will be more easily appreciated. Fig. 36. — Diagrammatic representation of the cardiac cycle. I = first sound. 2=second sound. A=first or short silence. B=second or long silence. ' Journal of Anatoviy and Physiology, vol. xiv. p. 237. i^.S Diseases of the Heart. Fig. 37. — Diagrammatic representation of the cardiac cycle. (After Gairdner, modified by Sharpey). TJic cJiaractcristic features of tJie individual cardiac sounds. The first sound is, as we have seen, systolic, and lasts twice as long as the second, which is diastolic ; but in addi- tion to these differences in rhythm and duration, the two sounds present certain other distinctive features. The first sound is dull, muffled, and booming in character ; it gives one the impression of being produced at some distance from the ear ; while the second sound is sharp, abrupt, accentuated, and superficial, i.e. it appears to be produced close to the ear. The syllables lupp dupp give a very good idea of the normal characters of the cardiac sounds. The characteristic features of the first sound are best heard at the apex of the heart, those of the second sound at the base. But further, the first sound which is produced in the left heart {i.e. the mitral first sound) is longer and more muffled than the tricuspid first sound ; while the aortic second is louder and more accentuated than the pulmonary. TJie points of differential niaxininni intensity of the in- dividual sounds. In order to appreciate these differences, i.e. in order to hear the sounds which are generated at any one of the four Position of tJie Cardiac Valves. 139 valvular orifices, apart, so far as is possible, from the other three, it is necessary to listen at certain points of the chest wall, which I am in the habit of terming the points of dijfcrciitial inaxinnnn intensity of cardiac sounds and nuirmnrs. The position of the points is as follows : — Mitral sounds are best differentiated at the apex of the heart. Tricuspid sounds at the lower end of the sternum, or rather at the junction of the lower left costal cartilages with the sternum. (Some authorities say the junction of the right lower costal cartilages with the sternum.) Aortic sounds at the second right costal cartilage. Pulmonary sounds at the third left costal cartilage. The fact, that the distinctive characters of any individual sound (mitral, tricuspid, aortic, and pulmonary) are not well heard if the stethoscope is placed over the exact position of the valve at which that sound is generated, is owing to the close juxta-position of the valves. According to Walshe ' a superficial area of half an inch square will include a portion of all the four sets of valves in situ; an area of about one quarter of an inch, a portion of all except the tricuspid ; ' while Sibson states that each of the higher orifices overlaps in position the orifice immediately below it. ' Thus the pulmonic orifice at its lower and right edge is situated to a slight extent in front of the upper and left edge of the aortic orifice ; the right posterior or lower flap of the aortic valve is situated in front of the upper third or two-fifths of the mitral orifice ; and the lower two-thirds or three-fourths of the mitral' orifice are behind the corresponding upper portion of the tricuspid orifice.' — Russell Reynold's System of Medicine^ vol. iv. p. 86. The exact relatiojts/iip of the valves to the surface of the c/icst is, according to the same observers (Walshe and Sibson), as follows : — Pulmonary. — According to Walshe ' ' the upper or free edge of the pulmonary valves lies horizontally, and in the mass of persons, a shade above the upper edge of the third left cartilage, the body of the valve consequently a little lower than this, — the left edge of the sternum having closely the same width of the vessel on both sides.' Aortic. — The aortic valves, according to Walshe, lie horizontally a very little further inwards, and lower than the pulmonary, corresponding to the union of the third left cartilage with the sternum. According to Sibson the upper and left border of the aortic orifice, especially during the diastole, is situated behind the lower portion of the third cartilage near the sternum ; and its lower and right border, ' Diseases of the Heart, fourth edition, p. 6. 140 Diseases of the Heart. especially during the systole, is situated behind the middle line of the sternum, on a level with the upper portion of the fourth cartilage. Mitral. — The attached edge of the mitral valve, according to Walshe, lies almost horizontally about a quarter of an inch lower than the attached bases of the aortic valves, very slightly further inwards than these, and deeper within the chest than the tricuspid valve. The attached border lies on the level of the union of the third cartilage with the sternum, nearer, as a rule, the upper than the lower border. According to Sibson the mitral orifice is seated behind the left half of the sternum, at the upper two-thirds of the lower third of that bone, on a level with the fourth cartilage, the fourth space, and the upper portion of the fifth cartilage. Tricuspid. — ' The attached edge of the tricuspid,' according to Walshe, Fig. 38. — Diagram to illustrate the position of the valvular orifices. (After Gee, slightly modified. ) Note. — The aortic valve is a little too low. Alterations of the Heart Sounds. 141 ' slantingly placed across the sternum from above downwards, and from left to right, inclines from the neighbourhood of the sternal edge of the third left interspace nearly to the sternal end of the fourth right inter- space, or fifth right cartilage ;' while Sibson states that in a healthy man with a well-formed chest, the tricuspid orifice is situated behind the lower fourth of the sternum to the right of the middle line of that bone, its upper border being on a level with the lower edge of the fourth cartilage, and its lower border being behind the lower end of the sternum, and the articulation to it of the right sixth cartilage. Mode of distingnisJung the tivo sounds of iJie heart. —Under ordinary circumstances there is no difficulty in distinguishing the two sounds of the heart ; but in some cases of disease, more particularly when the heart is acting quickly and irregularly, and when the first sound is short and valvular, it may be very difficult to say which is the first and which is the second sound. The same difficulty is also experienced in the observation of some cardiac murmurs. Now, in both cases, attention must be particularly directed to the rhythm of the sound or murmur, and to its point of differential maximum intensity. In the case of murmurs the direction of propagation is also of importance, as I shall afterwards point out. In order to ascertain the exact rhythm, the observer should listen over the prsecordia, and, at the same time, apply the fingers of the right hand over the position of the apex beat. When the apex beat is not available, the sound should be timed by the carotid pulse. The radial pulse is not suitable for this purpose, owing to the fact that an appreciable in- terval elapses between the contraction of the ventricle and the occurrence of the pulse at the wrist. Alterations in the heart sounds ivhieh occur in disease. The alterations of the heart sounds which occur in disease are either simple modifications of the normal sounds {quanti- tative changes), or absolute alterations {qualitative changes). The quantitative changes include : — I. Alterations in the loudness or intensity, and in the duration or sound characters (tone and purity) of the cardiac sounds. 142 Diseases of tJie Heart. 2. xA.lterations in the position of the points of differential maximum intensity. 3. Reduph'cations. The quaHtative changes embrace the various forms of endocardial and exocardial murmurs. Alterations in loudness or intensity} The intensity or loudness of the cardiac sounds may be increased or diminished in disease. In some cases, all four sounds (mitral, tricuspid, aortic, and pulmonary) are modi- fied ; in others, the sound produced at one valvular orifice only is affected. But although alterations in intensity are common in disease, it must not be supposed that all variations of this description are pathological. On the contrary, we know that the loudness, of the heart sounds, varies in different in- dividuals, even in health, and in the same (healthy) in- dividual under different conditions ; and that it is extremely difficult to fix upon an average healthy standard. When the alteration (from what we consider the average healthy standard) is considerable, when it is permanent, and more especially when some organic disease (either of the heart or other organ) capable of producing it, is present, there is no difficulty in deciding that the alteration is pathological. Another point which enables us to distinguish some of the pathological alterations is this, that in the physiological variations of intensity the relative degree of loudness of the different heart sounds is generally preserved, the aortic se- cond sound, for instance, being louder than the pulmonary, the mitral than the tricuspid ; whereas in some of the patho- logical variations the relative intensity of the sounds derived from the right and left hearts is perverted, the pulmonary being louder than the aortic, the tricuspid than the mitral.- ' Alterations in the loudness or intensity of the heart sounds are very often associated with alterations in the duration and sound characters ; but for con- venience of description it is better to consider each of these modifications separately. ^ In many pathological alterations the relative intensity of the sounds derived from the right and left hearts is, of course, preserved. Increased Loudness of Heart Sounds. 143 The intensity or loudness of the heart sounds, as heard over the prcecordia, is the resultant of two conditions, viz. :— (i) The amount of sound, so to speak, which is generated within the heart. (2) The facility with which the sound generated within the heart is conducted to the ear. Variations in the intensity or loudness of the heart sounds, as heard over the preecordia, may therefore be due to :— (i) Alterations in production. (2) Alterations in conduction. For convenience of description we may term the former actual and the latter apparent alterations. Let us now consider, in more detail, the pathological and clinical conditions which are associated with increase and diminution of the heart sounds, as heard over the praecordia, respectively. Increased intensitj or loudness of the heart sounds as heard over the prcBcordia. Increased intensity or loudness of the heart sounds, as heard over the prjecordia, may, as I have previously stated, be either apparent or real. Apparent increase. — In this condition, in which the heart sounds, are louder than in health, a normal amount of sound, so to speak, is generated within the heart, and the increased intensity, as heard over the praecordia, is due to the con- ditions for the conduction of sound, from the heart to the ear, being more favourable than in health. Now the pathological and clinical conditions which favour increased conduction are : — 1. Abnormal thinness of the chest wall, wasting of muscle, and especially of the subcutaneous fat. 2. Increased exposure of the heart, which, as we have already seen, may be due to retraction of the anterior margins of the lungs (cirrhosis, pleurisy, etc.), or to forward displace- ment of the heart. T44 Diseases of I he Heart. 3. Consolidation of the portions of the lungs adjacent to the heart (pneumonia, phthisis, etc.). 4. The presence of a cavity, suitable for the amplification of sound, i.e. a thin-walled cavity in contact with the heart on the one hand and with the chest wall on the other. The cavity may be situated in the lung itself (as in phthisis) ; in the pleura (as in pneumo-thorax) ; or, it may be a dilated stomach. 5. Air in the sac of the pericardium (pneumo-pericardium). In the latter cases (4 and 5) the heart sounds usually have a metallic or amphoric character, and are sometimes auto- audible. Real or actual increase. — In this condition the amount of sound which is generated within the heart, is above the normal healthy standard.^ Now, since the chief causes of the normal heart sounds are the closure, and more particularly the sudden tension of the valvular segments, it follows that anything which produces more forcible closure and more sudden tension of the valvular segments will produce an actual increase. It is necessary to add, that the valvular segments must be healthy ; where they are rendered rigid and incapable of vibrating, the cardiac sounds may be feeble, muffled, and impure, although the other conditions which favour the increased production of sound are present. In some cases all the valvular segments are more forcibly and suddenly stretched, and all the cardiac sounds are con- sequently intensified. Excited action of the heart, such as results from violent muscular effort, neurotic palpitation, ex-ophthalmic goitre, etc., is the most common cause of this condition (i.e. of increased intensity of all the heart sounds). In other cases, and these are by far the most important in a diagnostic point of view, one of the cardiac sounds only is exaggerated. ' \Yhen the conditions for conduction are unfavourable, the heart sounds, as heard over the pracordia, may be of normal, or even diminished intensity, even although the amount of sound generated within the heart is in excess. Accentuation of tJic Aortic Second Sonnet. 145 Increased intensity of tJie aortic second sound occurs in all conditions in which the blood pressure, in the aorta, is above the normal (the aortic segments must, as I have previously remarked, be fairly healthy). Increased aortic tension may result from : — (a) an obstruction to the pas- sage of blood through the arterial system, the amount of blood propelled into the arterial system (or what amounts to the same thing, the force of the cardiac pump) being normal ; (b) an excessive quantity of blood being pumped into the aorta, the peripheral resistance being normal. (When the flow through the peripheral parts of the circulation is abnormally free, an excessive quantity of blood may be propelled into the arterial system without any increase of the arterial tension resulting). The chief pathological and clinical conditions, therefore, associated with accentuation of the aortic second sound are : — 1. Obstruction to the passage of the blood through the minute arteries — a condition which occurs more particularly in chronic Bright's disease (the cirrhotic form of kidney) and in atheroma. (Dr Broadbent, Dr Mahomed, and others think that the chief cause of the obstruction in many of these cases is situated in the capillary system of vessels rather than in the minute arteries.^) In these cases the left ventricle is hypertrophied, and there is therefore a double cause for the increased aortic tension, viz., obstruction in front, and the powerful propelling force behind. 2. Atheroma, dilatation, and aneurism of the aorta. 3. Hypertrophy of the left ventricle. All cases of hypertrophy of the left ventricle are not attended with an accentuated aortic second sound. In mitral regurgitation, for example, there is usually hypertrophy of the left ventricle, but in consequence of the leak through the mitral orifice, the amount of blood pumped into the 1 aorta (by the hypertrophied left ventricle) is usually smaller than normal, the aortic tension is, therefore, diminished, and the aortic second sound j decreased. Again, in aortic regurgitation, although the hypertrophied I and dilated left ventricle propels an excessive amount of blood into the aorta, the aortic second sound is, in consequence of the incompetent i ' British Medical Jonnial^ Aug. 25, 18S3, p. 357. K 146 Diseases of the Heart. condition of llie aortic \alve and the altered condition of the aortic segments, usually completely absent, and replaced by a murmur. Increased intensity of the pulmonary second sound. — In- creased intensity of the pulmonary second sound occurs in all those conditions in which the blood-pressure within the pulmonary artery is in excess. And increased pulmonary tension, may, like increased aortic tension, be due either to obstruction in front, or increased pressure from behind, these two causes being very generally combined. The chief clinical conditions associated with accentuation of the pulmonary second sound are : — 1. Mitral lesions (both stenosis and regurgitation) which produce stagnation of the blood in the lungs. Skoda was the first to direct attention to the great im- portance of the accentuation of the pulmonary second sound in cases of mitral stenosis, and to point out that the 'amount of accentuation ' is an index or gauge of the extent of the mitral lesion. It must, however, be remembered: — (i) that this statement only holds good so long as the right ventricle is powerful and the tricuspid valve sound. In advanced stages of mitral disease the pulinonary second soimd may be less loud than at the earlier periods of the case, the explanation being either, that in consequence of the right ventricle having become feeble, or the tricuspid valve having given way, less blood is being injected into the pulmonary artery ; the blood pressure, therefore, and consequently the intensity of the pulmonary second sound, are less than at the earlier stages of the case, i.e. before the tricuspid began to leak ; (2) that in gauging the extent of a mitral lesion by the loudness of the pulmonary second sound, it is necessary to allow for pul- monary causes of accentuation. 2. Some lung affections, notably cirrhosis and emphysema, in which there is a primary ^ obstruction to the passage of the blood through the lungs. 3. Hypertrophy of the right ventricle. As I have pre- viously pointed out, hypertrophy of the right ventricle is a secondary condition which results from some obstruction Primary, as compared with the secondary cthf.XxwzXioxx, which is due to mitral lesions. Increased intensity of the Mitral First Sound. 147 to the passage of the blood through the lungs. In cases of this description there is, therefore, a double cause for the increased pulmonary tension, which produces the accentua- tion of the pulmonary second sound, viz., obstruction in front and increased pressure behind. Increased intensity of tlic mitral first sound. — When the mitral first sound is much intensified, its duration and tone are usually at the same time modified ; it is shorter than normal, more abrupt, more accentuated ; in fact it loses the distinguishing characters of the first sound, and assumes those of the second. A combined condition of hypertrophy and dilatation, together with an irritable condition of the muscular fibre, attended by increased rapidity (celerity) of contraction, are the conditions which more particularly favour the production of this form of modification. Temporary over-action of the heart (palpitation, etc.) is also a common cause of increased loudness of the mitral first sound ; but in cases of this description, the other cardiac sounds are also intensified.^ It might readily be supposed that hypertrophy of the left ventricle would produce increased loudness of the mitral first sound. Such, however, is not the case ; in fact, in solid hypertrophy of the left .ventricle {i.e. hypertrophy without dilatation), even when the segments of the mitral valve are perfectly healthy and elastic, the mitral first sound is usually weaker (more muffled) than in health (see page 154, where the cause of the muffling is explained). This fact is, I think, a strong argument in support of the valvular as against the muscular origin of the first sound. Increased intensity of the tricuspid first sound, usually de- pends upon hypertrophy and dilatation of the right ventricle. The same remarks, which have just been made regarding accentuation of the mitral first sound, apply here ; the right being substituted for the left ventricle, and the tricuspid for the mitral valve. ' The mitral segments must, for the reasons previously given (see page 144), be fairly healthy, i.e., sufficiently elastic to be thrown into vibration. 148 Diseases of the Hear I. The differential diagnosis of increased intensity of tlic heart sonnds. The recognition of the cause of the increased intensity of the heart sounds is not, as a rule, a matter of much difficult3^ The steps in the inquiry are as follows : — Step. No. I. Are all the heart sounds intensified ; or, is the accentuation limited to the sound produced at one of the valvular orifices ? Step. No. 2. If all the sounds are intensified, is the con- dition due to some temporary cause, such as over-action from excitement, neurotic palpitation, and the like ; or, is it asso- ciated with structural changes in the heart ? The points to which attention is to be directed in order to solve this question are (a) the presence of any obvious cause of temporary over-action or excitement ; (b) the con- dition of the heart after a sufficient time has elapsed to allow of any temporary over-action from nervousness, excitement, etc., to have subsided ; and especially (c) the presence or absence of any indications of organic change (such as in- creased dulness on percussion, etc.) in the heart itself Step N'o. 3. If the accentuation is confined to the sound produced at one of the valvular orifices, what is its cause ? When the aortic second sound .is accentuated, attention must be particularly directed to the condition of the urine ; the state of the superficial vessels ; the presence or absence of pressure symptoms within the thorax, and the physical examination of the aortic arch ; for renal disease, atheroma, and aneurismal dilatations of the aorta, are, as we have previously seen, the most common causes of this condition, i.e. accentuation of the aortic sound. It is important too, to note the condition of the left ventricle ; for hypertrophy of the left ventricle is another cause of increased loudness of the aortic second sound. ^ ' The hypertrophy of the left ventricle, which is associated with accentuation of the aortic second sound, is usually secondary to some form of arterial obstruction. Hypertrophy due to mitral and aortic valve lesions is not (for the reasons previously given) usually attended by increased intensity of the aortic second sound, Diminished intensity of the Heart Sounds. 149 When the pulmonary second sound is accentuated, at- tention must be particularly directed to the condition of the mitral valve, for mitral lesions are the most common (cardiac) cause of the condition. Should the mitral valve be healthy, the lungs ^ must be carefully examined, and the presence or absence of hypertrophy of the right ventricle must be noted. When the mitral or tricuspid first sounds are intensified, the condition of the left and right ventricles must be particu- larly investigated, and the causes of hypertrophy and dilata- tion looked for. DiuiinisJied intensity or loudness of tlie /wart sounds as Iieard over the pracordia. Diminished intensity or loudness of the heart sounds, as heard over the praecordia, may be either apparent or real. Apparent diminution. — In this condition, in which the heart sounds, as Iieard over the prcecordia, are less loud than in health, a natural amount of sound, so to speak, is generated within the heart, and the diminution is due, either to (a) the conditions for conduction being less favourable than in the normal state, or to (b) the heart sounds being obscured by other sounds produced within the chest, e.g. bronchitic rales.- Now the chief pathological and clinical conditions which interfere with conduction are : — 1. Excessive thickness of the chest-wall more particularly of the subcutaneous fat. 2. Abnormal over-lapping of the heart by the lungs — a condition which reaches its highest degree of development in pulmonary emphysema. 3. Fluid in the sac of the pericardium. Actual diminution. — In this condition the amount of * We have previously seen that accentuation of the puhnonary second sound is almost always due to obstraction to the flow of blood through the lungs, and that this condition may be primary., i.e. due to primary alterations in the lungs, cirrhosis, emphysema, etc., ox secondary, i.e. the result of mitral lesions. ^ In these cases it may be impossible to hear the heart sounds although the conditions for conduction are favourable. 1 50 Diseases of the Heart. sound which is generated within the heart, is less than normal. The diminution may be due to the following conditions : — 1. Less forcible closure of the valve-segments. 2. Less sudden closure of the valve-segments. 3. Structural alterations in the valve-segments, which produce loss of elasticity, or interfere with vibration.^ In some cases, all the heart sounds are weakened. In others, the sound produced at one of the valvular orifices only, is affected. The clinical and pathological conditions associated with diminished intensity of ^//the cardiac sounds are : — ■ 1. Feeble action of the heart resulting from temporary conditions, such as syncope, and the structural changes which affect the cardiac muscle in the course of an attack of continued fever, notably in typhus. 2. Feeble action of the heart resulting from permanent structural changes, such as fatty and fibroid degeneration, great dilatation of the ventricular cavities, etc. The conditions which produce diminished intensity of the individual heart sounds are as follows : — Diminished intensity of the aortic second sound. — Diminished blood-pressure in the aorta is the usual cause of this con- dition ; but it may result from rigidity of the aortic cusps.- The following pathological and clinical conditions are the usual causes of diminished blood-pressure within the aorta, ' In many of these cases the sound is impaired or replaced l)y a murmur. ■ Diminished intensity of the aortic second sound, due to this cause, is seldom observed. It probably could only occur in those cases in which the rigidity was considerable ; and, when the rigidity of the cusps is great, the aortic valve is very often incompetent, and the aortic second sound replaced by a murmur. It must, too, be remembered that forcible tension (distention) of the base of the aorta probably also takes part in the production of the aortic second sound. It is important too, to remember, that rigidity of the aortic segments is often associated with general atheroma and dilatation of the aortic arch ; and that in those conditions the aortic second sound instead of being enfeebled is usually accentuated. If the aortic segments and base of the aorta were so rigid as to be incapable of acting as good sound producers, accentuation would not, of course, be observed, even where there was atheroma and dilatation of the aortic arch ; but such a degree of rigidity is uncommon. Diminished intensity of the Heart Sonnds. 151 and hence of diminished intensity of the aortic second sound : — 1. All structural changes which impair the 'driving' power of the left ventricle, such as fatty and fibroid dege- neration of the cardiac muscle, dilatation, etc. In these cases the amount of blood propelled into the arterial system is insufficient to keep it properly distended, and the aortic blood-pressure is consequently below the normal. 2. Mitral lesions (both stenosis and incompetence.) Here again the amount of blood discharged by the left ventricle into the aorta is below the normal quantity.^ Diminished intensity of the pntvionary second sound may result from muscular weakness or dilatation of the right ventricle, or from disease of the tricuspid orifice. These conditions are almost always secondary either to mitral lesions or to primary lung aftections. Diminished intensity of the pulmonary second sound is seldom, therefore, primary. It usually happens that the pulmonary second sound is accentuated in the earlier periods of these cases ; and it is only after the secondary dilatation of the right ventricle has be- come considerable, or after the tricuspid valve has given way, that the accentuation disappears, and diminished intensity of the pulmonary second sound is observed.- Diminished intensity of tJie mitral first sound. — Weakness of the wall of the left ventricle, whether temporary or perma- nent, is a fertile source of diminished intensity of the mitral first sound. In many of these cases the wall of the right ventricle is affected in the same manner, and the sounds of the right heart are also weakened. The condition may also be due to the fact, that the valve- segments are less suddenly stretched than in health. This is probably one cause of the 'muffling' of the first sound which ' We have previously seen that the pulmonary second sound is accentuated in mitral stenosis. The contrast, therefore, between the aortic and pulmonary second sounds, is great, and is due to a double cause, viz., diminution of the aortic and increase of the pulmonary. ^ In most of these cases the diminished intensity is only relative as compared with the marked accentuation in the earlier periods. It is seldom that the pul- monary second sound is less distinct than in the average run of healthy persons. 152 Diseases of the Heart. is seen in solid hypertrophy of the left ventricle. In con- sequence of the obstruction in front (either at the aortic orifice itself or in the arterial system beyond) the contraction of the left ventricle is more deliberate than in health, and the tension of the mitral segments is more gradually effected. Some authorities have supposed that in cases of this description, the left ventricle, in consequence of being over distended, has a greater difficulty in obtaining a 'grip' of the blood, so to speak, than it has in health ; ^ and that this is the explanation of its slow and gradual contraction. I am, how- ever, disposed to doubt the correctness of this explanation. ' Loss of grip ' would be much more likely to occur in dilata- tion than in solid hypertrophy ; and dilatation of the left ventricle, as we have already seen, tends rather to produce accentuation, at the same time that it shortens the duration of the first sound. Others have explained the diminished intensity of the mitral first sound which is associated with some cases of hypertrophy, by supposing that the 'initial tension' of the mitral valve is so great that the contraction of the ventricles docs not produce the usual amount of tension, and therefore of vibration of the valve-segments. In other words, in con- sequence of the excessive intra-ventricular pressure during diastole, — a condition which we may suppose is produced by the regurgitant current in the case of aortic incompetence — the segments of the mitral valve are closed, and partly stretched, at the end of diastole, i.e. before the ventricular systole occurs.- ' Solid hypertrophy always results from some obstruction in front. The hypertrophy which occurs in mitral and aortic regurgitation is always associated with some dilatation. ^ Increased 'initial tension' could only occur in aortic regurgitation, or in mitral lesions in which the blood pressure in the left auricle during diastole was increased. Now, in mitral regurgitation the first sound is replaced by a murmur ; and in mitral stenosis, the diminution of the first sound — which is certainly present — is, I believe, due partly to the fact that the mitral segments have lost their normal elasticity, partly to the small amount of blood which the left ventricle contains, and there- fore to the diminished force with which the mitral segments are closed and ^•trctched. Altei'ations in the duration of the Heart Sounds. :)5 Another reason, which has been advanced as a partial cause for the diminished intensity of the first sound in cases of soHd hypertrophy is, that the sound which is produced by the tension of the mitral and tricuspid valves is less easily conducted through the thick muscle of the ventricular wall/ The correctness of this explanation is, in my opinion, doubtful. Structural alterations which impair the elasticity of the valve segments are also the cause of diminished intensity of the mitral first sound. This is probably one of the conditions which produce the modified first sound which occurs in mitral stenosis, to which I have already alluded. DiminisJied intensity of tJie tricuspid first sound. — Impair- ment of the force of the right ventricle (fatty degeneration, fibroid degeneration), and dilatation of the ventricular cavity, are the chief causes of this condition.- Alterations in the duration of the Jieart sounds. Alterations in duration are only noticeable in connection with the first sound. It may be either longer or shorter than in health. Inereased duration of the first sound \?, generally associated with the slow and deliberate contraction which is seen in solid hypertrophy, more especially with the solid hyper- trophy which is caused by stenosis of the aortic orifice. In addition to the alteration in duration the sound is, in these cases (as we have previously seen) more mufiled than in health. Diminished duration of the first sound is generally due to dilatation, or dilatation and hypertrophy of the left ventricle, in fact, it occurs in all conditions in which the ventricular wall is enfeebled. There is often too, in such cases, an irritable condition of the cardiac muscle, which produces increased celerity of contraction. These alterations are frequently met with in chlorosis and fatty heart.^ ' Diagnosis of Diseases of the Heart, by Dr Sansom, page 104. ' In these cases tricuspid regurgitation often occurs, and instead of a weak first sound in the tricuspid area, we have a tricuspid systolic murmur. ' In the more advanced stages of chlorosis the mitral first sound may be replaced by a systolic murmur. 154 Diseases of the Heart. Alterations in the tone of the heart sounds. Alterations in tone are often combined, as we have already seen, with alterations in intensity. The chief modi- fications in tone are as follows : — I. The heart sonnets may be more mnffled than in health} Muffling of the first sound may be due to : — (a) impaired conduction, the clinical causes of which have been already detailed (see page 149) ; (b) weakness of the walls of the left ventricle from fatty or fibroid degeneration, etc. ; (c) solid hypertrophy of the left ventricle ; and (d) alterations in the segments of the mitral valve, which impair its elasticity, but which do not give rise to regurgitation. Muffling of the aortic second sound generally results from loss of elasticity in the aortic segments, and is often asso- ciated with atheroma of the base of the aorta and disease of the coronary arteries. Impnre heart sounds. — The term impurity is given to a modification of the heart sounds, which is closely allied to muffling on the one hand and murmur on the other. In fact an impure sound may be described as a sound which has lost its normal well-defined character, which is usually of dimin- ished intensity, and which is somewhat muffled and murmur- like. An impure sound may often be transformed into a murmur by exciting the heart to more vigorous action — making the patient walk quickly up and down the room, ascend a stair, etc.- An impure sound, then, is suggestive of valvular imper- fection ; and the presence of an impure aortic second sound, more especially,^ may be a physical fact of great practical ' Alterations of this description are chiefly important in connection with the mitral and aortic sounds. - I must caution the observer against over-exciting the heart in those cases in which he desires to produce or intensify a cardiac murmur, and particularly against applying any sudden strain, or producing any sudden rise of arterial blood-pressure. An American traction machine, which I lately saw in the consulting room of a well-known London physician, seems to me especially dangerous, and verj' likely to produce rupture of a thin-walled aneurism, were such a lesion present. ' An impure first sound is of much less importance, for slight incompetence at the mitral or tricuspid orifices is frequently due to temporary and curable conditions. Alterations in the tone of the Heart Sounds. 155 importance. (Impurity of the aortic second sound generally depends, as we have previously seen, upon rigidity of the aortic cusps ; and rigidity of the aortic cusps is often associ- ated with atheroma of the base of the aorta and disease of the coronary arteries,— conditions which are frequently sus- pected, but which it may be impossible to detect by means of physical examination. Now, in more than one case of angina-like pain in the chest which has come under my own personal observation, the presence of an impure aortic second sound was the only physical alteration which could be detected, and as we shall afterwards see, when I come to treat of angina pectoris, the recognition of disease at the root of the aorta is, in suspected cases of that disease, a point of great practical importance.) 2. TJie heart sounds may be more aeeentuated than in Jiealth. The conditions, which produce modifications of this description, have already been considered, and need not again be detailed (see p. 143). 3. Higli-pitcJied, metallic, auto-audible heart sounds. When the conditions for conduction are extremely favourable ; when, for instance, that portion of lung, which covers the heart and great vessels, is consolidated or retracted, the heart sounds may be unusually loud and high-pitched. A loud and high-pitched pulmonary second sound, for example, is met with in some cases of pneumonia and pleuro-pneumonia, and probably depends, as Quincke was the first to point out, upon retraction or consolidation of the portion of lung which overlaps the root of the pulmonary artery. When a cavity, well suited for the reproduction and con- duction of sound, is in contact with the heart or great vessels on the one hand, and with the chest wall on the other, the heart sounds may have a metallic or amphoric character. In some of these cases,^ and in some cases of consolidation of the ^ A striking example of auto-audible heart sounds, depending upon the presence of a cavity in the lung, is described by Dr Smith in the Lancet for December i8, i8So. 156 Diseases of the Heart. lung, the heart sounds may be auto-audible, i.e. heard by the patient himself, and by the physician without applying the ear to the chest. A striking example of auto-audible heart sounds depending upon con- solidation of the lung came under my observation during the summer of 1 88 1. A patient who for some weeks had been suffering from a limited pleuro-pneumonia of the left base, was suddenly seized with acute pain m the left side, which was followed by quick pulse, elevation of tem- perature and rapid consolidation. The day following the occurrence of the attack, dulness on percussion and tubular breathing were present over the lower two-thirds of the left lung, and tJie heart sounds could be 7-eadtly Jieai'd, ivlien the patient sat up, ivitliout applying the car to the chest. Rednp/icatioii of the Heart Sounds. We have previously seen that although four sounds (two first and two second sounds) are generated within the heart, during each cardiac revolution, two only (a single first and a single second sound), are, under ordinary circumstances, heard over the praecordia, and that the blending of the mitral and tricuspid first sounds and of the aortic and pulmonary second sounds is due to the fact, that the action of the two ventricles is usually synchronous. Now, under certain conditions, even in health, and not unfrequently in disease, two first sounds or two second sounds are audible ; and the heart sounds are said to be reduplicated, or, as Dr Barr prefers to term it, duplicated. The exact cause of this doubling or reduplication has given rise to great debate, but most authorities are agreed — and with their opinion I entirely concur — that the condi- tion is, in the great majority of cases, due to a synchronic closure of the mitral and tricuspid valve flaps ; in short, that when the first sound is reduplicated, its two component parts, viz., the mitral and tricuspid first sounds, are individually audible ; and that when the second sound is reduplicated, both the aortic and pulmonary second sounds are separately heard. Reduplication of the First Sound. 1 5 7 It will be advisable, however, to consider the individual reduplications, their clinical significance, and probable causa- tion a httle more in detail.^ Reduplication of the First Sound. Reduplication of the first sound is rare — much rarer than reduplication of the second sound — a circumstance which is probably due, as Dr Barr has suggested, to the fact that the first sound is produced by several diff'erent factors, and that it is a sound of considerable duration. In order that the first sound may be perceptibly reduplicated, i.e. that the mitral and tricuspid first sounds may be separated by a perceptible interval, it is necessary to have a considerable degree of asynchronism between the closure and tension of the aortic and pulmonary valve flaps — a more considerable asynchron- ism than is required to produce perceptible doubling of the second sound. Further, I am of opinion that reduplication of the first sound can only occur when — in addition to asynchronism — the duration of one or other, or of both of its component parts {i.e. of the mitral and tricuspid sounds) is lessened, or when the duration of the whole cardiac cycle is very considerably increased {i.e. when the pulse is slower than in health).- Under ordinary circumstances the first sound ' While I am of opinion that asynchronism is the cause of the reduplication in most cases, I am not prepared to assert dogmatically that it is so in all. Some cases are with difficulty explained by this view, and for them, some of the many other theories which have been advocated, possibly hold true. Space does not permit me to consider the arguments for and against these various theories in detail. Those readers who are interested in the subject should consult the writings, more especially of Drs Barr and Sansom, where they will find full details. — (See articles in the Medical Times and Gazette of January and February 1877, !^nd in the Liverpool Mcdico-Clm-tirgical Journal, July 1882, by Dr Barr ; and Diagnosis of Diseases of the Heart, by Dr Sansom, p. 106, et scq.) ^ Asynchronism, without any diminution in the duration of the mitral and tricuspid first sounds, might account for the condition, if the duration of the whole cardiac revolution [i.e. of the diastolic portion of the revolution) was much increased ; if, for example, the heart were contracting 30 instead of 72 times in a minute. 1^8 Diseases of the Heai-f. occupies (roughly) ^■'yths of the entire cardiac revolution. (See fi&- 39-) Now, granting that the tricuspid first sound— as is I'"in. 39. — Diagrammatic representation of the cardiac cycle. I = first sound. 2=;second sound. A=first or short silence. B=second or long silence. probably the case — is of somewhat shorter duration than the mitral first sound, say that it occupies yVhs of the entire cardiac revolution, it is almost impossible to conceive that reduplication could be produced by asynchronism alone, that is to say, that reduplication could occur in any case in which the mitral and tricuspid first sounds and the whole cardiac cycle (the cycle for both the right and the left hearts) preserved their normal length. For if such were the case, f'yths 4- xV^''' ^•^- To^^^ ^^ ^^ entire cardiac revolu- tion, would be occupied by the reduplicated first sound, and to this we must add the interval which is required, i.e. which must separate the two component elements of the reduplicated sound, in order that each element may be per- ceived as a separate and distinct sound by the ear. Further, I may add, that reduplication of the first sound can never occur when the heart is acting quickly. The three conditions, then, which I believe to be necessar}', in most cases, for perceptible reduplication of the first sound are — (i) Considerable asynchronism in the contraction of the two ventricles. (2) Diminished duration of one or other or both of the component parts of the reduplicated sound. (3) Slow action of the heart. Reduplication of the First Sound. 159 Numerous other theories have been suggested in order to explain reduplication of the first sound, viz. : — ■ 1. That it is due to non-synchronous tension of the individual seg- ments of the auriculo-ventricular valves, owing to the absence of perfect uniformity of the contraction of the papillary muscles. — {Gutimauii.) 2. That the reduplication is due to splitting up of the first sound into its component parts of ventricular impulse and valve tension.— (//cry^f^;?.) 3. That it is due to a double mitral valve click, the true mechanism of which remains to be discovered. — {Professor UEspine}) 4. ' That the contraction of a dilated, and especially of a hypertrophied left auricle, becomes sonorous, and that the first division of the double first sound is the result of the auricular systole.' — {Dr Geo)'ge Johnson.) 5. ' That it is due to a presystolic being closely followed by a normal first sound, the presystolic sound being produced by the sudden floating upwards of the mitral curtains occasioned by the auricular systole.' — {Dr Sansfl/n.) Dr Barr has, I think, conclusively disposed of these various theories, with perhaps the exception of the last, in the article to which I have already referred. — {Liverpool Medico-Chirurgical yournal., July 1882.) Dr Sansofn's theory is the only other one, in addition to that adopted in the text, which seems to me at all probable. He explains its mechanism as follows : — ' During the interval immediately succeeding the relaxation of the ventricle, the blood, subject to the tension in the left auricle and pulmonary veins, has been pouring into the ventricular cavity; the fluid naturally finds its way in the direction of least resistance, that is, its course, when impelled towards the apex, is round the walls of the ^-en- tricle, thus coming behindxh^ curtains of the mitral valve, and bellying them out (so to speak) as the sails of a ship are bulged by the force of the wind. At the moment of auricular systole, the ventricle, as yet only partially full, is rapidly distended, the force of contraction of the auricle giving an impulse to the apex of the ventricle, and, as may of course be inferred, giving a contre-cotip to the already partially strained mitral curtains. In normal conditions such contre-coup is inaudible, but when the auricle is more than ordinarily powerful, or when the mitral valve is so changed as to give rise to the sound of membranous tension, it becomes perceptible closely preceding the sound produced by the ventricular systole — that is, the sound of complete closure of the valves guarding both auriculo-ventricular orifices plus the muscular sounds of the ven- tricles.' — {Diagnosis of Diseases of the Heart, p. 115.) Doubling of the first sound is said to occur physio- logically at the end of expiration or the commencement of inspiration ; and pathologically (though rare) it has been met with in various conditions, amongst which the following are i6o Diseases of the Heart. the chief: — functional disorders of the heart ; diseased (de- generated) conditions of the cardiac muscle ; hypertrophy of the ventricles ; dilatation of the ventricles ; valvular lesions, more especially mitral and tricuspid lesions. As I have already stated, asynchronic closure of the mitral and tricuspid valves is, in my opinion, the most im- portant cause of the condition ; and we must now consider how the asynchronism may be brought about. The first sound oi the heart is probably composed, as we have previously seen, of the sounds which are generated by : — {(i) the sudden closure and tension of the mitral and tricuspid valve flaps ; {U) the contraction of the ventricles ; and (r) the impulse of the apex beat against the wall of the chest ; ^ and all of these conditions immediately result from the contrac- tion of the muscular walls of the ventricles, which is, in its turn, due to the rhythmical discharge of motor nerve force in the cardiac ganglia. Further, we have seen that the ganglia are stimulated, to discharge, by the presence of blood under a certain tension in the cardiac cavities, and that the action of the ganglia can be held back (inhibited) or accelerated by impulses passing to the heart through the pneumogastric and sympathetic nerve trunks. Now, the theory which explains the reduplications of the heart sounds by asynchronic closure of the valve flaps necessarily presupposes that the action of the right and left ventricles is to some extent at least independent, and that the one ventricle may begin or may end contraction before the other.'^ ' The sudden tension of the valve flaps and chordce tendineae is probably by far the most important factor of the three. ^ In reference to this part of the subject Dr Barr says: ' In reply to the objec- tion which has been urged against the possibility of asynchronism, on account of the interlacement of the cardiac fibres and the observed consentaneousness of the ventricular action, I say that I have seen, felt, and heard asynchronous action, and so have no difficulty in admitting the possibility of its occurrence. I do not say that such asynchronism as exists between the auricles and ventricles is pos- sible between the two ventricles, but I do say that each side of the heart has its own proper muscular fibres, as well as those which are common to both sides ; and those proper fibres form in great part the deepest layers, and so are first Reduplication of the First Sound. 1 6 r Theoretically, therefore, we may suppose that redupli- cation of the first sound may be due either to : — (A) such accelerated or retarded action of the left ventricle as is sufficient to cause the first sound, which is generated within the left heart, to be separated by an interval, sufficient to be appreciated by the ear, from the first sound, which is gener- ated within the right heart ; or to (B) such accelerated or retarded action of the right ventricle that the same result — an appreciable interval between the first sounds of the right and left hearts — may occur.^ Further, we may presume that accelerated or retarded action of either ventricle may be due to : — ■ I. Differences in the pressure of the blood in the two ventricles by reason of which the muscular fibres of one ven- tricle are stimulated to contract before the muscular fibres of the other. It is, I think, highly improbable that this condition alone is ever the cause of a reduplicated first sound — for, as we shall see when I come to speak of reduplication of the second sound, increased pressure of the blood in either ven- tricle, generally depends upon obstruction in front ; and in such conditions, although the increased blood pressure may stimulate the affected ventricle {i.e. the ventricle which has to cope with the difficulty, and in which the increased pres- sure occurs) to commence contraction, yet by reason of the obstruction which it has to overcome, it is longer in emptying itself, and in such cases reduplication of the first sound does not of course occur. subjected to the stimulating influence of distention in producing contraction ; and in those fibres which are common to both sides, it is possible for the wave of con- traction to commence, as it were, at one extremity of the fibre and be propa- gated to the other. Each side has more or less independently its own nerve supply, its own peristaltic action, and notwithstanding that both sides are set to the same time, and that there is a complex interlacement of fibres, yet it is quite pos- sible, nay, it is an experimental fact, that one side may begin or end contraction before the other.' — {Liverpool Medico-Chirurgkal Joiiriial, July 1882, p. 206.) ' I have already expressed the view that modifications in the duration of the component elements of the reduplicated sound, or of the duration of the whole cardiac cycle, are also necessary. L 1 62 Diseases of iJic Heart. 2. Alterations of the nerve apparatus of one ventricle, by reason of which the motor ganglia of one side are rendered more or less irritable than those of the other.^ Such a condition may possibly explain the reduplications of the first sound, which are said occasionally to occur in some functional (neurotic) affections of the heart. 3. Structural alterations of the muscular fibres of one ventricle, by reason of which its contraction is more or less cjuickly effected than that of the other ventricle. In some cases of fatty degeneration (in the early stage at least) a condition of ' irritable weakness ' is sometimes met with, in which the muscular fibre is more easily excited, but in which its contraction is less sustained {i.e. of shorter duration) than in health. It is easy to conceive, therefore, that if such a change were confined to the muscular fibre proper to one ventricle, or were much more marked in one ventricle than in the other, that the first sound produced in the affected side might anticipate that produced in the normal one. So again in cases of fibroid degeneration, the contractility of the affected ventricle (granting that the change were confined to one ventricle) might, we can easily suppose, be unduly delayed, and therefore sufficient asynchronism to cau.se reduplication of the first sound, produced. Reduplication of tJic Second Sound. Reduplication of the second is much more frequent than reduplication of the first sound. It occurs as a physiological condition at the end of inspiration and commencement of expiration ; and as a pathological phenomenon it occurs in many different conditions, amongst which stenosis of the mitral valve, and primary obstruction to the flow of blood through the lungs (such as is produced by cirrhosis, emphy- sema, etc.) are the chief.- ' If Dr Gaskell's view — that the rhythmical action of the heart is due to a rhythmical property possessed by the cardiac muscle itself, independently of any ganglionic nerve apparatus — is correct, the explanation given under this head (2) will not of course hold good. ^ Reduplication of the second sound occurs in at least one-third of all the cases of mitral stenosis, and is highly suggestive of that condition. Reduplication of tJie Second Soiind. i6 o As I have previously stated, I agree with those authori- ties who beHeve that the cause of reduplication of the second sound is asynchronous closure (and tension) of the aortic and pulmonary valve flaps ; and we may theoretically suppose that the asynchronic closure may result from the fact that the systole of either ventricle is so accelerated or so delayed as to allow of an appreciable interval between the recoil of the aorta and pulmonary artery, i.e. between the production of the aortic and pulmonary second sounds. Further, we may suppose that the following conditions may produce such asynchronic contraction of the ventricles as will cause reduplication of the second sound : — 1. Derangement of the nerve apparatus of the heart, by reason of which the motor ganglia ^ of one ventricle are rendered more irritable or less irritable than those of the other. This is probably the cause of the reduplicated second sound which is not uncommon in functional (neurotic) affec- tions of the heart. 2. Structural alterations of the muscular fibres proper to either ventricle, by reason of which they are rendered either more irritable or less irritable than in health ; and by reason of which the contraction of one ventricle is, therefore, unduly accelerated or unduly retarded. (See remarks on page i6i.) 3. Differences in the pressure of the blood in the two ventricles, by reason of which the action of one is accelerated. Some authorities, who allow that asynchronic closure, of the aortic and pulmonary valves, is the cause of the redupli- cation of the second sound in mitral stenosis, have supposed that, in consequence of tiie increased blood-pressure, which is present in the right chambers of the heart, the right ventricle is first stimulated, that it first completes its systole, and that the first element in the reduplicated sound is consequently pulmonic. But with this opinion I do not agree, for, as Dr Barr points out, it does not necessarily follow th&t the ' If Dr Gaskell's view — that the rhythmical action of the heart is due to a rhythmical property possessed by the cardiac muscle itself, independently of any ganglionic nerve apparatus — is correct, the explanation given under this head will not of course hold good. 164 Diseases of tJie Heart. ventricle, which is first thrown into action, will first com- plete its systole ; for the duration of ventricular systole is not a fixed quantity. Further, we know that (within the range of its working power) the duration of the ventricular systole varies directly with the amount of resistance, which has to be overcome ; in other words, the greater the resistance, the longer the systole. (Witness the slow deliberate pulse of aortic stenosis.) And many good clinical observers positively state that the accentuated element of the reduplication is the second element, and that the accentuated or second element is heard over the area of the pulmonary artery and not of the aorta, i.e. that it is pulmonary. 4. Differences in the resistance in front, by reason of which the systole of one ventricle is rendered of shorter or of longer duration than that of the opposite one. I agree with Dr Barr and others, who think that this is the true explanation of the reduplicated second sound in mitral stenosis — that although the right ventricle is, by reason of the increased blood-pressure in the right cavities of the heart, first stimulated to contract, yet, in consequence of the obstruction to the passage of the blood through the lungs, and the difficulty which the ventricle has in emptying itself, its systole is so prolonged, that a sufficient amount of asyn- chronism is produced to allow of an appreciable interval between the aortic and pulmonary sounds ; in other words, that the reduplication is primarily due to alterations in the blood-pressure of the aorta and pulmonary artery respect- ively, and the consequent alteration in the duration of the systole of the right and left hearts ; the systole of the left ventricle being, in consequence of diminished aortic pressure, shorter, while the systole of the right ventricle is, by reason of increased pulmonary pressure, longer than in health. Numerous other tlieories have from time to time been advocated to explain the reduplication of the second sound, amongst which the following may be mentioned : — I. That the second element of the reduplication is produced by a sudden tension of the mitral curtains after the normal second sound Reduplication of the Second Sound. 165 has occurred. Dr Sansom, whose theory this is, gives the following explanation of it : — ' It seems to me, therefore, that reduplication of the second sound, in cases of mitral stenosis, can be best explained thus : — The first element of the reduplication is the normal second sound ; the tension in the aorta being feeble, it is the pulmonic element which has the chief share in the production of such second sound. The second element of the reduplication is the sudden tension of the abnormal mitral- curtains produced after the relaxation of the left ventricle. I am not prepared to say that systole of the auricle is esse7iiial to produce this sudden tension ; it may be quite possible that the reaction of the dis- tended pulmonary veins and left auricle may be sufficient to cause it. So it may occur previously to the auricular contraction, the latter occasioning or reinforcing the presystolic murmur, separated by a slight interval from the second element of the reduplication.' Dr Sansom illustrates his theory, the only one in addition to that adopted in the text which seems to me probable, by the following diagram : — Fig. 40. — Diagram illustrative of the mechanism of pseudo-reduplication of the heart sounds. {After Sansom). Ideal section through the left auricle (A) and left ventricle (V) ; M.M, mitral curtains ; the arrows show the direction of the blood current during the ventricular diastole and auricular systole. Diagnosis 0/ Diseases of the Heart, p. 1 20. 1 66 r>isi-ascs of tJic Heart. 2. Asynchronous closure of the indi\idual segments of one valve, aortic or puhnonary. — (Guttmann.) 3. That the first element of the reduplication is the * audible snap which attends the systolic closure of the valve segments, separated, by an appreciable interval, from the diastolic snap (of the arterial systole).' — (Dr George Balfour, Lancet, March 5, 188 1, p. 396.) 4. That the reduplication of the second sound originates at the narrowed orifice itself ; and that the two elements of the phenomenon in question, which form a sound which is always more or less muffled and impure, are in reality the component parts of a murmur. — (Guttmann — Hand-Book of Physical Diagnosis, p. 279.) 5. That the second element of the reduplicated sound is the sound which is produced by the contraction of the dilated and hypertrophicd left auricle. — (Guttmann, Handbook of Physical Diagnosis, p. 279.) ALTERATIONS IN THE POSITION OF THE HEART SOUNDS. The heart sounds are occasionally heard over parts of the chest at which, under ordinary circumstances, they are inaudible or only faintly heard. As a rule, such sounds are less loud than the sounds heard over the heart itself; but this is not always the case, and it occasionally happens that the abnormally placed sound, so to speak, is actually louder than the heart sounds heard over the prsecordia. The conditions which give rise to these alterations in the position of the heart sounds are as follows : — 1. Anything which renders the tissues and parts surround- ing the heart better conductors of sound, so that the heart sounds are conveyed to parts of the chest at which, under normal circumstances, they are inaudible or only faintly heard'. Consolidations of the lung, tumours in the mediastinum, and curvatures of the spine, are some of the clinical conditions which are included under this head. 2. Changes in the size and position of the heart itself. When, for instance, the left ventricle is enlarged, the apex is displaced downwards aiid to the left, and the heart sounds are, so to speak, displaced with it. So, again, when the heart is pushed to the right by an extensive left-sided pleuritic effusion, the heart sounds may be inaudible under the left, but loudly heard under the right nipple. Cardiac ^hiruiurs. 167 3. Aneurisms of the thoracic aorta. When the heart sounds are loudly heard over a part of the chest at which, under normal circumstances, they are faint or inaudible, and when the abnormally placed sound is situated over the course of the aorta, the presence of an aneurism should be suspected and the other symptoms and signs of that condition carefully looked for. In some cases of this description the heart sounds, more especially the second, are very loud {i.e. accen- tuated), over the seat of the tumour. ABSOLUTE MODIFICATIONS OF THE HEART SOUNDS. MURMURS. The alterations of the heart sounds which I have hitherto described were simple or quantitative in character ; the modi- fications which we must now consider are absolute or quali- tative. In other words, the normal heart sounds are either partly or entirely replaced by new sounds, which, in normal conditions {i.e. in conditions of perfect health and during tranquil action of the heart) are never heard over the prs- cordia. To these qualitative modifications the term niurviur is given. Cardiac uairinurs, i.e. new sounds heard either in the place of or along with the heart sounds, may be produced either outside the heart or in the heart itself. To the former the term cxo-cardial, to the latter etido-cardial, is applied. Exoca rdial Mu rui u rs . Strictly speaking the term exo-cardial murmur should include all murmurs produced outside the heart, but as a matter of fact it is usually limited to those murmurs, in reality, friction sounds, which are synchronous with the action of the heart, and which are produced either in the sac of the pericardium or in the adjacent pleura, i.e. to those exo- cardial murmurs which are heard over the praecordia. Arterial and venous murmurs, which are, of course, also exo-cardial. are classed as distinct. It is in the usually accepted — the narrow and restricted sense — that I shall make use of the term. 1 68 Vistasi's of tJie Heart. Exocardial murmurs, then, are friction sounds, which are synchronous with the contractions of the heart ; usually double (to-and-fro sounds) ; generally having the harsh, grat- ing character which friction sounds commonly possess ; as a rule heard loudest over the centre of the heart, i.e. over the anterior surface of the right ventricle, or at the base of the organ ; almost always intensified, and sometimes altered in character by the pressure of the stethoscope ; and which are produced, in the great majority of cases, by the rubbing together of the inflamed and roughened surfaces of the peri- cardium. Exocardial murmurs are, therefore, almost in- variably, indicative of pericarditis.^ Quite exceptionally a friction sound, synchronous with the action of the heart, and resembling ver\- closely (it may be exactly) the to-and-fro friction murmur of pericarditis, is produced outside the sac of the pericardium by the rubbing of the roughened outer surface of the pericardium against the front wall of the chest or adjacent surface of the pleura ; and to this sound the term pericardial-pleural-friction iminmir is applied.- Endocardial Murmurs. Endocardial murmurs, i.e. murmurs which are produced within the heart itself, are either organic ox functional. Under the former head are included all those cases in which the murmur depends upon distinct structural alterations (usually of the valvular mechanism) which can be recognised after death. Under the latter term, i.e. functional murmurs, it is customary- to describe those cases in which the murmur depends upon temporary and curable conditions, or in which no distinct alteration of the valvular mechanism can be ' Exocardial friction murmurs do not bear such an exact relationship to the sounds of the heart as endocardial murmurs. They are, however, as stated in the text, synchronous with the cardiac contractions — a point which at once distinguishes them from ordinary pleural friction murmurs. - The manner in which the pericardial-pleural-friction murmur is to be dis- tinguished from the ordinary friction murmur of pericarditis will afterwards be described. (See p. 327.) Mode of proditciion of Endocardial Miirnuirs 1 69 detected after death. The distinction is one of great prac- tical utihty, but it is not strictly accurate from a pathological point of view. We have previously s&er\,Jirst/y, that mitral and tricuspid regurgitation — conditions which are attended by well marked murmurs — frequently result from 'relative' or ' muscular ' incompetence, the valve segments being perfectly healthy ; and secondly, that the defective muscular action which produces the incompetence, depends in some cases upon temporary and curable, in others upon permanent and incurable, conditions. Now, in both cases, the murmur is un- doubtedly due to structural alterations, which, provided that the patient were to die while the murmur were still audible, could be recognised on the post-mortem table. In both cases, therefore, the murmur is, strictly speaking, organic. Provided that this fact is kept in view, it is a matter of prac- tical convenience and utility to describe the curable cases as functional, and the incurable as organic. Before we consider each of these conditions (organic and functional murmurs) in detail, it may perhaps be well to describe the manner in which murmurs are produced. Mode of production of Endocardial Murmurs. Endocardial murmurs are due to the production, within the heart, of vibrations which can be perceived by the ear of the observer ; and most authorities are agreed that the audible vibrations, which are represented externally as mur- murs, are generally (some say are always) due to the produc- tion of sonorous fluid-veins in the blood itself According to M. Chauveau, these sonorous fluid-veins are always gen- erated when the blood stream passes, zuitk sufficient force from a part of the circulatory system which is actually or relatively constricted, into a part which (in comparison with the part behind it) is actually or relatively dilated ; as, for , instance, when the blood current is forcibly driven through a , constricted mitral orifice into the ventricular cavity beyond. ' Other authorities suppose that the blood current in its pas- I sage through the heart may throw the tissue itself, over which j it passes, into vibration ; and this would appear to be the I 70 Diseases of iJic Heart. manner in which Dr Austin Flint supposes that the presys- toHc murmur of mitral stenosis is generated. The vibration of a filament or tongue of lymph in the blood current is also supposed to be the cause of some auto- audible and musical murmurs. Audible vibrations or murmurs may probably also be produced by the collision of two opposing blood currents ; when, for instance, the blood stream which is flowing back- wards through an incompetent mitral orifice meets the blood stream which is advancing into the left auricle from the pulmonary veins. The fact that a certain intensity of blood current is necessary for the production of a murmur is a point of great practical importance. We frequently find, for ex- ample, that a murmur, which depends upon organic and permanent conditions {e.g. the presystolic murmur of mitral stenosis) disappears as the case progresses, the dilated and weakened auricle (in the case of mitral stenosis) being no longer able to produce a blood wave capable of generating sound. In cases of this description, and indeed in others, in which the conditions for the production of a murmur are not as yet very perfectly developed, we can, by increasing the force of the heart's action, either temporarily by exertion (walking about, ascending a stair, etc.), or by the use ot cardiac tonics (digitalis for example), frequently convert an impure or ill-defined sound into a murmur, and can thus obtain important diagnostic evidence as to the nature of the case. It is important, too, to remember that the composition and quality of the blood seem to exercise some influence in the production of murmurs. In conditions of anaemia, for ex- ample, venous murmurs are almost invariably present, and are without doubt due to the abnormal condition of the blood.^ ' Dr George Balfour, in speaking of the mode of production of the venous hum says, ' As a venous murmur is often to be heard in certain positions, such as the torcular Herophili, where no other change is at all probable, under all the circum- stances of the case, except one involving an altered relation of the blood to its containing vein, we can have no hesitation in ascribing its production to that cause. And further, from what we know of the mode in which fluid veins are formed, we can have no difliculty in saying that this altered relation of the blood Organic Endocardial MiLrnmrs. 171 It is possible, too, that the systolic murmurs which are so commonly heard over the base of the heart,^ in conditions of anaemia, are in part at least due to the same cause. But to this point I will presently recur. Organic Endocardial iMnrmurs. Organic endo-cardial murmurs usually depend upon some defect in the valvular mechanism of the heart ; occasionally they are due to congenital imperfections and malformations ; very exceptionally to the presence of clots or vibrating fila- ments of lymph in the cardiac cavities. Organic endo-cardial murmurs are in the adult usually heard over the mitral or aortic orifices, since organic lesions of the valves, which are their most frequent cause, are usually left-sided ; but they may be produced at any of the cardiac orifices. They are either direct or indirect, that is to say, they may be produced either by the blood current as it passes onwards in its natural forward (direct) course, or by a blood-current passing back- to the walls of the vein must consist in the production of increased friction between the two, so that in those positions where there is normally a relative constriction, insufficient, however, to produce sonorous veins, the increase of friction between the wall of the vein and the layer of blood next it practically narrows the opening sufficiently to do so, by retarding the exterior portion of the blood current and leaving the central or axial portion uninfluenced. Physical laws leave no doubt as to this. It is for physiologists to explain whether it depends simply upon a watery condition of the blood or upon some other cause, and their explanation would no doubt be of the greatest importance for practical medicine.' — Diseases of the Heart, Second Edition, p. 170. ' As we shall presently see, Dr Balfour is of opinion that the basic murmurs heard in the earlier stages of anaemia are due to mitral regurgitation. But he also admits, that in the later stages, arterial murmurs may be developed, and he hints at least that the altered condition of the blood may play some part in their production. He says, for instance — ' Shortly after the appearance of the primary hsemic murmur, a tricuspid murmur and jugular undulation are found to be developed. This is naturally accompanied by a pulmonary and also by an aortic systolic murmur, the active cause in the production of both these murmurs being the large blood waves sent on by the dilated and hypertrophied ventricles.' — Ed. Medical Joiir., Oct. 1882, p. 295. 'There is also an abnormal friction between the spansemic blood and the walls of the blood-vessels, hence a rise in arterial blood -tension, hence also the formation of fluid veins at certain favoural)le points within the venous lumen, and at these points we hear the primary chlorotic murmur — the venous hum.' — Loc. cit., p. 293. 172 Diseases of the Heart. wards through an incompetent valvular orifice, i.e. by a regurgitant or indirect current. Tlie points to be observed in the Clinieal Investigation of Cardiae Murmurs are as follows : — 1. The rhythm of the murmur. 2. Its point of differential maximum intensity. 3. The direction in which it is propagated. 4. Its sound characters (loudness, tone, pitch, duration, etc.) THE RHYTHM OF THE MURMUR. By the rhythm of the murmur we mean its exact relationship to the sounds and silences of the heart. The murmur should, if possible, be ' timed ' by the apex-beat, and failing this, by the carotid pulse. When the heart is acting quickly, it may be very difficult or even impossible to 'time' the murmur correctly. The difficulty of determining the exact rhythm is also increased where more than one murmur is present, and this is more particularly the case where a presystolic is combined with a systolic mitral murmur ; the difficulty being less in the case of double aortic murmurs, for in such cases the interval between the systolic and diastolic portions of the murmur is usually quite distinct. Endocardial murmurs may occur either during the systole or the diastole of the heart, i.e. of the ventricles ; and it will now be necessary to consider each of these different murmurs, and the conditions which may produce them, in detail. Systolie Mnrniuys. Systolic murmurs correspond to the contraction or systole of the ventricles ; they more or less completely replace the first, or systolic sound of the heart, and may extend into the short silence. (See fig. 41.) They may be produced either in the left or right heart, and may be either functional or organic. They represent one or other of the following conditions : — I. Regurgitation through the auriculo-ventrieular orijiees. — (Mitral and tricuspid regurgitation.) Both of these condi- Sys^o/ic Miirnutrs. 17: Fui. 41. — Diagrammatic representation of a systolic murmur, replacing the whole of the first sound. The murmur in this and succeeding figures is repre- sented by continuous vertical lines, the normal sound by interrupted horizontal lines. I =svstolic murmur. tions are common. The former (mitral regurgitation) is often primary ; the latter (tricuspid regurgitation) is usually secondary, and due to disease of the mitral valve, or to (primary) obstruction to the passage of the blood through the lungs, such as occurs in cirrhosis, emph)'sema, etc. Now we have seen that auriculo-ventricular regurgitation may result from : — {a) Organic changes in the valve segments, such as puckerings, contractions, adhesions, ruptures, ulcerations ; these organic changes being rare on the right side, i.e. at the tricuspid orifice. {b) Muscular incompetence, i.e. imperfect closure of the valve in consequence of defecti\-e muscular contraction, the valve segments being healthy. {c) Relative incompetence, i.e. dilatation of the valvular orifice, the valve segments being healthy. And since both 'muscular' and 'relative' incompetence (which are often present in the same case) may depend on temporary and curable conditions, it follows that auriculo- ventricular regurgitation may be either organic or func- tional. 2. The formation of a fluid vein, or the production of sonorous vibrations in the tissues at the arterial orifices (aortic or pulmonary orifices), or in the first part of the arterial systems {i.e. in the commencement of the aorta or pulmonary arter}'). I 74 Diseases of the Heart. The pathological conditions associated with these basic systolic murmurs are : — {a) Constriction of the arterial orifices (aortic and pul- monary stenosis). Aortic constriction is common, pulmonary constriction extremely rare. The former is usually acquired, the latter almost always congenital.^ {b) A tongue of lymph adhering to the arterial (aortic or pulmonary) valve flaps. This is not a common cause of basic systolic murmurs, but it does sometimes occur. The murmur which it produces may be musical and auto-audible. It may disappear in the course of treatment. (r) Anaemia. Basic systolic murmurs are common in anaemia. They are sometimes heard in the pulmonary, sometimes in the aortic area. Their exact significance and mode of production, more especially of the systolic murmurs heard in the pulmonary area, have given rise to much debate ; but to this question — which is still far from settled — I shall presently recur. (See page i88.) id) Dilatation of the ascending portion of the aortic arch. In cases of this description the aortic orifice is usually diseased (constricted). A murmur may, however, be pro- duced as the blood passes from a naturally sized aortic orifice into a dilated aorta provided that it, is propelled with sufficient force to generate an audible fluid vein. It is obvious, therefore, that systolic murmurs produced at the aortic and pulmonary orifices may, like those produced at the mitral and tricuspid orifices, be either functional or organic. Diastolic Aliirnnirs. Diastolic murmurs occur during the ventricular diastole. There are at least three distinct varieties, viz. : — I. The diastolic murmurs, which occur during the period of the second sound, and which more or less completely replace it. These murmurs may, and often do, extend into the second or long pause. (See figs. 42 and 43.) ' In some cases of ulcerative endocarditis the pulmonary valve is afifected, and a systolic pulmonary murmur, representing pulmonary stenosis, is observed. Such cases are, however, extremely rare. Diastolic M7irm2irs, 175 Fig. 42. — Diagrammatic representation of a diastolic murmur, replacing second sound. 2 = murmur. Fk;. 43. — Diagrammatic representation of a diastolic murmur, replacing second sound, and extending into long pause. 2 = murmur ; B=long pause. Novv^, since the second sound of the heart is due to the closure and tension of the aortic and pulmonary valve flaps it follows, that a murmur which replaces the second sound must represent regurgitation through the aortic or pulmonary valvular orifices. And since, as a matter of practical expe- rience, we know that pulmonary regurgitation hardly ever occurs, a diastolic murmur, which replaces the second sound at the base, is, for practical purposes, pathognomonic^ of aortic regurgitation. Further, we know, as a matter of practical experience, that this murmur is almost invariably organic. Aortic regurgitation generally results from organic changes in the aortic segments (contractions, puckerings, adhesions, ruptures, ulcerations), though it is occasionally due to dilata- tion of the base of the aorta, the valve segments being ' In one or two cases a diastolic murmur has been produced in an aneurism independently of any regurgitation through the aortic valves. Such a condition is, however, so extremely rare, that for practical purposes the statement in the text — that a diastolic basic murmur indicates aortic regurgitation— may be safely relied upon. 176 Diseases of tJie Heart. perfectly healthy, ic. it is occasionally due to a condition of ' relative incompetence ' of the aortic orifice.^ 2. The murmurs which occur during" the latter part of the long silence or pause, i.e. immediately before the systole of the ventricles, and to which the term presystolic is usually given. (Fig. 44.) Fig. 44. — Diagrammatic representation of a presystolic murmur. The presystolic murmur stops abruptly with the systole of the ventricle, i.e. with the occurrence of the first sound of the heart — a fact which is at once explained when it is understood that the murmur is produced by the formation of a fluid vein as the blood is forcibly driven by the contraction of the auricle through a stenosed mitral orifice.^ Almost all authorities are agreed in thinking that the presystolic or auriculo-systolic murmur (as Professor Gairdner, who was one of the first to direct attention to its true signifi- cance, prefers to term it), is always due to organic changes, i.e. to stenosis of the mitral or tricuspid orifices. And since tricuspid stenosis is \^ery rare, a pres\'stolic or auriculo- systolic murmur, in the great majority of cases, indicates mitral stenosis. The stenosed condition is usually due to adhesion of the cusps, the chordae tendineai are often thickened, and some- ' This condition is (?) always associated with organic changes at the root of the aorta ; but it is quite possible, as Dr George Balfour points out, that a dilated aorta may contract, and so the condition of incompetence be removed. ' Relative incompetence ' of the aorta depends then upon organic changes, but it may some- times disappear under treatment. - In some cases of presystolic murmur, i.e. of mitral constriction, the first sound of the heart is replaced by a systolic murmur, and the presystolic therefore passes into the systolic murmur {i.e. is continuous with it), the two murmurs being as a rule distinguishable by their sound characters. Presystolic Muinnurs. 177 times, as it were, fused into a mass with the cusps and papil- lary muscles. The stenosis is sometimes due to calcareous deposits in the base of the valve and in the valve segments ; occasionally a mass of vegetations obstructs the orifice ; in rare cases the stenosis is caused by the pressure of a tumour, the valve segments being perfectly healthy. .Professor Austin Flint differs from the generally ac- cepted opinion, viz., that a presystolic murmur is invariably organic. While granting of course that the murmur is generally due to mitral stenosis, he thinks it by no means pathognomonic of that condition. He believes that it may occur independently of any mitral lesion, and he has recorded several cases in support of his view. In all these cases there were aortic lesions permitting of regurgita- tion ; and the question at once suggests itself, whether the presystolic murmur heard at the apex was produced at the mitral orifice at all. Might it not have been the aortic murmur heard at the apex of the heart .'' The explanation which Professor Flint gives of the production of the murmur in such cases is as follows: — 'With regard to this specimen, consider the physical conditions in life, at the instant when the auricular contraction took place. The left ventricle was filled with blood from the current passing from the auricle to the ventricle, through an unobstructed orifice, by gravita- tion, and in addition by the regurgitant current from the aorta. As a consequence the mitral curtains were floated away from the ventricular walls, and were not only approximated but in absolute contact. Recollect the physiological experiment by which it is shown that the mitral valve may be com- pletely closed by injecting liquid into the left ventricle through the mitral orifice. These conditions existing, the auricle contracts and forces an additional quantity of blood into the ventricle. This mitral direct current passes between the valvular curtains which are in apposition, and throws them into vibration precisely as the lips are made to vibrate with the breath.' ^ 3. The murmurs which occur during the first part of the ' Lancet, Jan. 27, 18S3. M 178 Diseases of the Heart. long pause, but which follow, usually with a distinct and appreciable interval, the second sound. (See fig. 45.) Fir,. 45. — Diagrammntic representation of post-diastolic murmur, which occurs in some rare cases of mitral stenosis. It is separated from the commencement of the first sound by an appreciable interval. This, which is by far the rarest form of diastolic murmur, is occasionally met with in mitral stenosis, and is doubtless produced by the blood which has been pent up in the left auricle and parts behind it, during the ventricular systole, i.e. while the mitral valve was closed, being propelled with sufficient force through the stenosed orifice to produce a fluid vein, i.e. to generate a murmur. Possibly too the negative pressure in the ventricle, i.e. the suction which occurs when the ventricle relaxes, aids in the production of the murmur.^ The period at which the murmur occurs, i.e. during the first part of the long pause, clearly shows that the contrac- tion of the auricle, which does not occur until the end of the long pause, takes no part in its production. Combination of Murmurs.— \x\ many cases more than one murmur is present. (See figs. 46, 47, 48.) An aortic systolic murmur is very often combined with an aortic diastolic murmur, and a mitral presystolic murmur with a mitral systolic. Further, in advanced cases of aortic regurgitation, the mitral valve often becomes incompetent, and a systolic mitral murmur is heard in addition to the aortic diastolic murmur which was present from the first. Again, in the ' Goltz and Gaule believe that the negative pressure appears at the beginning of the diastole, and that it is caused by the expansion of the ventricle. ' Were this the case,' says Prof. Michael Foster, 'the ventricle might be regarded not only as a force pump driving blood into the arteries, but also as a suction pump drawing blood from the auricles and great veins.' — A Text Book of Physiology, Fourth Edition, p. 152. I Combinafion of Miirmitrs. ^79 advanced stages of mitral lesions, tricuspid regurgitation fre- quently results from the secondary changes which are estab- lished in the right heart ; while in cases of anaemia, systolic murmurs are sometimes heard at all the cardiac orifices Fig. 46. — Diagrammatic representation of systolic and diastolic murmur. ft Fig. 47. — Diagrammatic representation of systolic and presystolic murmurs. Fig. 4S. — Diagrammatic representation of systolic, diastolic, and presystolic murmurs. It is sometimes doubtful whether a cardiac sound is replaced or only obscured by a murmur, and in the case of all murmurs it is desirable, if possible, to determine whether any cardiac sound still remains. Now these points can, as Gendrin was the first to point out, sometimes be ascertained by removing the ear a short distance from the end of the stethoscope, or by so placing the instrument that the ear- piece only partly covers the external auditory meatus. By this means the sound is rendered more audible, while the murmur becomes less distinct. The fact, that the heart sound is heard, as well as the i8o D/scciscs of the Heart. murmur, shows, more especially in the case of diastolic aortic murmurs, that the valvular segments, or some of them, can still be closed and put upon the stretch, in fact, that they are still capable of generating the second sound. It does not however follow that in such cases the lesion is a trivial one. In fact, in some cases in which one valve segment only is affected (as in a case which I shall afterwards relate), the contrary holds good. The fact, then, that some sound re- mains, suggests that some of the valve segments are still sufficiently healthy to generate the normal sound. When the disease has developed slowly, as in atheromatous disease of the valve, it is probably a favourable indication, and shows that the valve is not, as yet, very seriously affected. In acute cases — such as traumatic rupture of a valve segment, or ulceration of the segments — it may be of no value whatever, but this point will be more fully discussed in treating of the prognosis of aortic regurgitation.^ THE POINT OF DIFFERENTIAL MAXIMUM INTENSITY OF THE MURMUR. From what I have previously stated in speaking of the differential maximum intensity of the normal heart sound (see page 138), it will readily be understood that in order to ascertain the valvular orifice at which the murmur is pro- duced, it is necessary to ascertain its point of differential maximum intensity. These points are shown in the diagrams (figs. 49 to 54), and are as follows : — Mitral Minima's. — The point of differential maximum intensity of mitral murmurs is the left apex-beat, wherever it may happen to be, not necessarily in the fifth left inter- space, an inch and a half below, and slightly internal to the left nipple, i.e. the position of the apex-beat in health. (See fig. 49.) Presystolic mitral murmurs are often best heard ' The observer must of course satisfy himself that the sound which remains is generated at the affected vahailar orifice. In the case of an aortic diastolic murmur, for instance, a second sound, due to closure of the pulmonary flaps, might be heard in some situations along with the diastolic murmur, and might be referred to the aortic orifice. Points of viaxinuiui intensity of MnrnitLrs. i8i slightly internal to or just above the position of the apex-beat, rather than at the apex-beat itself. (See fig. 50.) Aortic Munnurs. — The point of differential maximum intensity of aortic murmurs is the second right costal cartilage at its junction with the sternum (the aortic cartilage). A diastolic aortic murmur may however be heard loudest at the lower end of the sternum, in consequence of the fact that it is propagated downwards in the course of the blood current which produces it. (See figs. 51 and 52.) Pulmonary Murjniirs. — The point of differential maximum intensity of pulmonary murmurs is the third left costal cartilage at its junction with the sternum (the pulmonary cartilage). (See fig. 53.) Tricuspid Ahirmurs. — The point of differential maximum intensity of tricuspid murmurs is the lower end of the sternum, or rather the junction of the lower left cartilages with the sternum. (See fig. 54.) Some authorities place the point of differential maximum intensity for tricuspid murmurs at the junction of the lower riglit costal cartilages with the sternum. A systolic murmur is sometimes heard equally loud at the base and at the apex of the heart, and it may be difficult or impossible to determine, from its mere loudness, at the two points, whether it is generated at the aortic or at the mitral orifice, or at both, i.e. whether there are two separate murmurs. The question must be decided in the following manner : Firstly. The murmur must be carefully traced from one point to the other — from the apex to the aortic cartilage, for example, in the case we are supposing. If the intensity of the murmur diminishes at a point midway between the two positions {^i.e. the two points of differential maximum inten- sity), there are probably two murmurs. Secondly. The tone of the murmur at the two points must be carefully noted. If the tone differs there are probably two murmurs. Thirdly. The direction of propagation must be observed. 1 82 Diseases of the Heart. If the murmur is well propagated, both upwards over the aorta, and outwards and upwards towards the axilla, there are in all probability two murmurs. THE DIRECTION IN WHICH THE MURMUR IS PROPAGATED. Murmurs are propagated chiefly in two ways, viz. : — (i) B}- conduction, i.e. through the structures in which they are ge- nerated, and by the parts which surround those structures. {2) ^y convection, i.e. carried by fluid in the direction in which it is flowing. As a matter of practical experience and obser- vation, we know that the different murmurs which represent different vahailar lesions, are propagated in certain definite directions, which are as follows : — Mitral regU7-gitant {systolic) uiiirninrs : — These murmurs are propagated upwards and outwards towards the left axilla (see fig. 49) ; and, when organic, are often well heard at the inferior angle of the left scapula. According to Naunyn, Fig. 49.— Outline figure showing point of diflerential ma.ximum intensity (*) of the systolic mitral murmur (mitral regurgitation); and the direction in which it is propagated. The cross + , which is supposed to represent the normal position of the apex-beat, is placed a little too high. Direction of propagation of Murinurs. 18 J Balfour, and others/ the systolic murmur, due to mitral rei^ur- g-itation, is sometimes heard in the region of the pulmonar)- artery, being conducted to that part of the chest through a dilated left auricular appendix. Mitral direct {presystolic^ ninruiur. — This murmur is usually heard over a very limited area. The blood current, which produces it, is flowing directly towards the apex (or very nearly so) of the heart. (See fig. 50.) We can readily understand therefore why the presystolic murmur is usually limited to the position of the apex beat. Fig. 50. — Outline figure showing point of differential maximum intensity!*) of the presystolic mitral murmur (mitral stenosis) ; and the direction in which it is propagated. (The murmur is often best heartl a little above and internal to the apex-beat, which in the diagram corresponds to the star.*) Aortic regurgitant {diastolic) murmurs are carried down- wards by the blood current which produces them, towards the apex of the heart ; but in consequence of the fact that the sternum is such a good conductor of sound, these ' These writers say that the murmur is not heard exactly over the pulmonary area, but a little outside it, viz., at a spot an inch and a half outside the sternum, in the third interspace, just at that spot at which the tip of the left auricular appendix comes forward from beneath the cover of the pulmonary artery. 184 /h'seascs of ihc Heart. nuirmurs are well conducted down that bone, and are often heard very distinctly at the xiphoid cartilage, as represented in fig. 51. Fn;. 51. — Outline figure showing point of differential maximum intensity (*) of the diastolic murmur (aortic regurgitation); and the direction in which it is propagated. Aortic direct {systolic) murmurs are carried upwards over the course of the aorta, and the great branches which arise from it. Organic murmurs are more extensively carried in these directions than functional, i.e. anaemic murmurs. (See fig- 52.) Pulmonary regurgitant {diastolic) murmurs are so ex- tremely rare, that for practical purposes they may be almost ignored, they are propagated downwards towards the lower end of the sternum. Pulmonary direct {systolic) murmurs, which, when organic, are extremely rare, are propagated upwards and outwards, over the course of the pulmonary artery. As a rule they cannot be traced for any distance over the surface of the chest. (See fig. 53.) Direction of propaoation of Mitrnntrs. i8- Fig. 52. — Outline figure showing point of differential maximum intensity (*) of the systolic aortic murmur (aortic stenosis) ; and the directions in which it is propagated. Fig. 53. — Outline figure showing the point of difierential maximum intensity of the systolic pulmonary murmur, and the direction in which it is propagated. i86 Diseases of the Heart. Tricuspid regurgitant {systotic) munniirs are not, in my experience, extensively propagated over the chest, but are usually heard over a limited area. The direction of their propagation is probably that shown in fig. 54. Pig. 54. — Outline figure showing point of dift'erential maximuiu intensity C*) of the systolic tricuspid murmur. Tricuspid direct (^presystolic^ viurvnirs are extreinely rare, they would probably be propagated towards the apex of the heart. THE SOUND CHARACTERS OF THE MURMUR. Some murmurs are soft and blowing ; others are harsh (grating, rasping, filing, sawing, etc.) in character ; others again are whistling, cooing, and musical. Occasionally, as I have before mentioned, a murmur is auto-audible. Inorganic murmurs are usually soft ; 'direct' murmurs {i.e. murmurs due to obstruction at one or other of the cardiac orifices) are usually harsher and rougher than 'indirect' ones {i.e. murmurs due to regurgitation). But speaking generally, it may be said that the mere sound character of Functional Mumnurs. 187 the murmur is not a point of much practical importance/ either from a diagnostic or a prognostic point of view; and this is readily understood when it is remembered that the sound characters of the murmur, more especially its loudness, are largely due to the force of the blood current which produces it ; in other words, the loudness of the murmur depends to a great extent upon the condition of the cardiac muscle. When the muscular wall of the heart is weakened or degene- rated, the murmurs which are generated are faint and soft ; and in advanced cases, as, for instance, in extreme cases of mitral stenosis, no murmur may be generated at all. And since a weakened and degenerated condition of the heart muscle may be due, either to temporary and curable, or to permanent and incurable conditions, it follows that the soft- ness and faintness of the murmurs, which are produced by Its contraction, cannot be relied upon as any indication of the severity of the lesion. When, however, a harsh nnirmur gradually becomes fainter and softer, we may, as a general rule, conclude that the strength of the muscular wall is diminishing, and we may be pretty sure that this is the case, when the symptoms are at the same time increasing in severity. A faint murmur, then, associated with severe symptoms, is usually indicative of a grave lesion. FUNCTIONAL MURMURS. It is customary to include under the term functional murmurs, all those cases in which the murmur depends upon temporary and curable conditions, or in which no distinct alteration in the valvular mechanism (it would perhaps be more correct to say in the valvular segments) can be detected after death. Functional murmurs are always systolic in time, and are generally heard at the base of the heart, most com- monly to the left of the sternum, in the second interspace, i.e. in the region of the pulmonary artery. They are sometimes also heard in the aortic, mitral, and tricuspid areas. ' The presystolic murmur is a notable exception. In typical cases the sound characters of the murmur (as I shall afterwards describe in detail) are so distinct as to distinguish it from all other cardiac murmurs. 1 88 Diseases of the Heart. The exact significance and mode of production of the functional murmurs, which are audible at the base of the heart, have given rise to great debate, and are among the most unsettled points in cardiac pathology. VValshc divides the so-called functional murmurs into two great groups, which he respectively terms haemic and dynamic. Under the former he places 'murmurs originating within the heart and dependent upon an unnatural state of the blood ; ' while under the latter he includes ' murmurs which result from abnormal action on the part of the heart,' the proper valvular mechanism being healthy. And this division in- dicates the two great causes of functional murmurs, viz.: — (i) defective muscular action d\\o\\\x\^ oi mitral and tricuspid regurgitation ; and (2) an altered condition of the blood, which probably aids, at least, in the production of the pul- monary and aortic murmurs, which are met with in con- ditions of anaemia. But it will be necessary to consider the subject in more detail. Anaemia, more particularly those forms of anaemia (such as chlorosis, progressive pernicious anaemia, etc.) in which there is defective formation of blood, is the chief clinical condition in which functional endocardial murmurs occur. Now, in cases of this description the muscular fibre of the heart becomes fatty, the cardiac cavities become dilated, and the weight of the heart also becomes increased ; in fact, there is a condition of combined fatty degeneration, dilatation, and hypertrophy, dilatation being, however, much in excess of hypertrophy.^ Such a condition of the heart is just such as we would expect to produce ' relative incompetence ; ' and, as a matter of fact, all careful clinical observers are, I presume, agreed that, in cases of this description, mitral and tricuspid regurgitation do ultimately occur. yMl observers are also, I suppose, at one in thinking that arterial murmurs (pulmonary and aortic murmurs) are usually present in advanced condi- ' These changes are seen in the human subject in cases of progressive pernicious ansmia ; and they have been shown by Beau to occur in the IcAver animals alter venesection. Functional Murninrs. i8g tions of anaemia. The point which is still undecided, and which has lately given rise to so much controversy, is the nature and significance of the basic murmur, which is heard in the second left interspace, in the earlier stages of anaemia, Three theories, all of which have warm supporters, have been advanced to account for the condition, viz. — 1. That the vucrniiir is piiluionary. — The exact manner in which the murmur is supposed to be produced in the pulmo- nary artery, has not been very clearly defined by the supporters of this view ; the sudden propulsion of a large blood wave of abnormal (spanaemic) composition into the vessel, which is probably in some cases at least dilated, seems to me an efficient cause for its production. We know, as a matter of fact, that the heart, in cases of chlorosis, is not only weak, but that it is unusually irritable ; that even in the earlier stages the right ventricle is to some extent dilated ; and that the blood is markedly altered in composition. 2. That the mnrniur is due to mitral regurgitation, and that it is conducted to the anterior wall of the chest through the dilated appendix of the left auricle. — (Dr George Balfour's theory). 3. That the murmur is produeed in the pulmonary artery as the result of constriction of that vessel ; the constriction being caused by the pressure of the dilated left auricle.- — (Dr Russell's theory.) Dr Russell further believes that the systolic murmur heard in the second, third, and fourth left interspaces in the later stages of such cases, is due to tricuspid regurgitation. Before considering the arguments for and against these different theories, I may say that the question is still an open one, the balance of evidence, in my opinion, being in favour of the first or pulmonary view. I do not think, for the reasons to be presently given, that Dr Balfour has conclusively proved his point, on the contrary, there seem to me to be grave objections to his view, and I do not see that anything which has as yet been advanced, conclusively negatives the first or purely pulmonary theory. IQO Diseases of fJie Heart. Dr Balfour s Theory. The facts and arguments on which Dr Balfour bases his theory, and the facts and arguments which seem to be opposed to it may be summarised as follows : — 1. {For.) That in organic diseases of the mitral valve a systolic, basic, and apparently pulmonary murmur is often present. Admitted that this is so. 2. {For.) That this supposed pulmonary murmur is, as Naunyn was the first to suggest, not pulmonary at all, but that it is due to mitral regurgitation, and is conducted to the second left interspace through the dilated appendix of the left auricle. {Against?) While granting that, if the appendix of the left auricle were dilated and were in contact with the chest wall, the systolic murmur of mitral regurgitation would probably be conveyed to the second left interspace ; and that, as Dr Balfour points out, Naunyn's theory has been accepted a^ highly probable by many leading Continental authorities, it must be allowed that it has not been accepted as conclusively proved, more especially by many competent British observers. But even granting that it is true for some cases of organic disease {i.e. granting that cases of mitral regurgitation do occur, in which the usual symptoms and signs of that con- dition, more especially a systolic murmur audible at the apex, are present, and in which the auricular appendix is dilated and is in contact with the chest wall), it by no means follows mat the chlorotic murmur with which we are now more parti- cularly concerned is produced in the same manner. The arguments with which Naunyn supports his theory are these : — {a) {For.) That the murmur has its point of maximum in- tensity at a point an inch and a half to the left of the sternum. {Against) Speaking for myself, I have in several cases of anaemia failed to satisfy myself that the position of the maximum intensity is so sharply defined as Dr Balfour's statements seem to indicate. The murmur has seemed to me in several cases quite as loud half an inch to the left of the Functional Murmurs. 191 sternum as over the so-called auricular area, i.e an inch and a half to the left of that bone. Hayden, who is admitted to be a trustworthy observer, goes much further in this respect than I am disposed to do, for he states that the murmur is best heard at midsternum. But even granting that the point of maximum intensity of the murmur, in cases of chlorosis, is in the position which Dr Balfour describes, it does not seem to me by any means to prove that the murmur is not pulmonary. In the first place, Sibson has shown that ' in the large majority of cases' which he examined, 'the greater part (in 25 of 45 instances), or the whole (in 14 of 45 instances), of the artery, bore to the left of the sternum, and presented itself behind the upper costal car- tilages and their spaces from the first cartilage to the third space ;'^ and further, that the average breadth of the vessel in Pirogoff' s five front views of the healthy heart was an inch and a quarter.^ I see nothing improbable, therefore, in a pul- monary murmur having (in many cases) its point of maximum intensity considerably to the left of the sternum. In the second place, there seems good reason to suppose, as Dr Russell's observations seem to show, that in consequence of the dilated condition of the heart (of the right ventricle more especially) the relative position of the parts is some\vhat altered, and that the pulmonary artery may be displaced for- wards, and perhaps somewhat to the left of its usual position. (Jj) {For.) That this point does not correspond to the origin of the pulmonary artery, but does exactly correspond to the spot where the appendix of the left auricle comes up from behind, just to the left of that artery, and that in cases of this description {i.e. where the murmur is loudly heard in the second left interspace) the appendix of the left auricle is dilated, and is closer to the chest and therefore nearer to the ear than usual. {Against^ It is not proved that the appendix of the left auricle is dilated in cases of chlorosis (with which we are at present more immediately concerned). On the contrary there are, as we shall presently see, positive observations to the ' Russell V^Gyx\o\A\ System of Mediciite, vol. iv. p. 35. " //'. p. 115. 192 Diseases of the Heart. contrary ; and there are, as Dr Russell has pointed out, grave anatomical objections to the theory that the left auricular appendix is in closer contact with the chest wall, in cases of chlorosis, than in health. This point will be again referred to. But granting for the moment that cases of mitral regurgita- tion do occur, in which the left auricular appendix is dilated, and in closer contact to the chest wall than usual, and in which the systolic murmur produced at the mitral valve is heard as loudly in the second left interspace as at the apex, that is no reason for supposing that in a case of anaemia, — in which a murmur is heard in the second left interspace, and in which there is no murmur, be it observed, at the apex, and no other indication of mitral regurgitation present, — this apparently pulmonary murmur is of mitral origin. The fact that the murmur is better heard over the auricular area than over the apex — the normal position of maximum intensity for mitral murmurs — Naunyn explains by attributing it to the better conduction of the murmur along the course of the regurgitating blood current, the fluid veins producing sonorous vibrations louder at the point of impingement than at that of origin, a view which is adopted and endorsed by Dr Balfour in support of his theory. He says, 'the fluid veins formed in the early stage of chlorotic regurgitation are of low tension and but little force, hence the vibrations they originate are but slightly propagated to the left ventricle, and only with difficulty from it to the chest wall in the mitral area, where they are heard as an impure first sound. But on the other hand these vibrations are readily communicated to the wall of the auricle on which these fluid veins impinge, and are easily transmitted to the chest wall with which the auricular appendix is in contact, becoming audible in the auricular area as a distinct murmur.'^ Against this view it may be argued that if the fluid veins produce sonorous vibrations louder at their point of impinge- ment than at their point of origin in one case, why should they not do so in all .-' In other words, if this theory be cor- rect, we ought to hear the systolic murmur of organic mitral ' Diseases of tlic Heart., p. 177. Functional Alurmurs. 193 regurgitation much more frequently and much more loudly in the second left interspace than is admitted by the majority of British observers, at all events. Again, it may be asked if this explanation is correct- in cases of chlorosis, and if, as Dr Balfour admits, ' the auricle, at the moment of ventricular systole, is not only full, but somewhat tense from unusual dilatation,' and if the fluid veins produce sonorous vibrations louder at their point of impinge- ment than at their point of origin, why is it that the murmur is not heard in the back, under the left scapula, as the murmur of organic regurgitation so often is ? 3. {For.) That in some cases of mitral disease, the apparently pulmonary, but in reality auricular murmur, is occasionally actually louder than that audible in the mitral area, and that the murmur of mitral regurgitation is sometimes only to be heard in the first named situation, i.e. in the second left interspace. Dr Balfour indeed goes so far as to state that ' a more or less distinct murmur in this {i.e. the auricular) area, is one of the earliest indications of mitral regurgitation from whatever cause. '^ {Against.) While admitting that some authorities, Rosen- stein for example, support this view, it is certainly contrary to the recorded opinion of almost all the best observers in this country, and I am not prepared to admit that a systolic murmur heard in the second left interspace is, per se (as Dr Balfour states in the following passage), indicative of mitral regurgitation. ' In chlorosis,' says Dr Balfour, ' in which all these pheno- mena, to which I may now comprehensively refer under the head of cardiac dilatation consecutive to spansemia, exist only in the very slightest degree, this pulmonary or rather auricular murmur is always present, and is often — so often as to consti- tute it almost invariably — the sole sign of mitral regurgitation in these cases.'- 4. {For.) Dr Balfour claims 'that Naunyn's view is even more applicable in chlorosis than in any other form of heart affection, because the essential cardiac lesion in chlorosis ' Diseases of the Heart, second edition, p. 163. - //'/(/. p. 172. N 194 Diseases of the Heart. is muscular relaxation and progressive dilatation, hence at a comparatively early stage of the disease the dilated right ventricle has separated the left ventricle from the chest wall, while the dilated appendix of the left auricle has been pari passu brought into closer contact with it.' ^ ' The peculiar position of the murmur is due,' says Dr Balfour, ' to the altered position of the heart. ' This is due to the dilatation of the right ventricle, which dilates pari passu with the left ventricle, and, like a water cushion, separates it from the chest wall, leaving the dilated appendix of the left auricle the only part of the left side of the heart in contact with the chest wall.' - Dr Balfour further claims that the pulsation of the auri- cular appendix can be seen, felt, and graphically recorded by the cardiograph. He says — ' In this situation, the dilated appendix not infrequently gives rise to so distinct a pulsation that its movements can be traced by the cardiograph, and the history of several such cases has been published, and their car- diograms figured by my former resident, Dr George Gibson, while the pulsation is so well marked and forcible in some of these cases, that the late Dr Hughes Bennett sent me on one occasion a case of chlorosis as a case of aortic aneurism.' ^ Against these statements it may be argued firstly, that Naunyn's explanation seems more particularly to apply to those cases of mitral regurgitation in which a systolic murmur is audible at the apex, i.e. in the usual mitral area, as welt as in the second left interspace ; but that in the earlier stages ot chlorosis, the apparently pulmonary murmur is, as Dr Balfour himself admits, usually the sole sign of mitral regurgitation ; in other words, the usual evidence of mitral regurgitation, i.e , a systolic murmur in the mitral area, is wanting. Secondly, that in the later stages of anaemia (chlorosis) a true mitral murmur, i.e. a murmur audible at the apex — in the mitral area — does actually occur. This Dr Balfour him- self admits, and he explains it in the following manner: — ' Diseases of the Heart, second edition, p. 176. - Edinburgh Medical Joiirital, Oct. 18S2, p. 295. ^ Diseases of the Heart, p. 175. Functional Murnuirs. 195 ' By and by, as the regurgitation increases, and the ventricle hypertrophies, these fluid veins gain force sufficient to be com- municated through the ventricle also, hence in the later stages of chlorosis we have a mitral murmur associated with the auricular one. It is however quite possible that this murmur in the mitral area is really tricuspid, due to the increased dilatation of the right ventricle, the apex of which may even occupy the mitral area ; this not infrequently occurs in mitral stenosis, it is not an improbable event in chlorosis, and it is of little consequence which explanation we accept, the actual truth probably embracing both conclusions, being sometimes due to the one cause and sometimes to the other.' ^ Now I agree with Dr Balfour in thinking that in many cases of advanced chlorosis the systolic murmur, which is heard at the apex, is due to mitral regurgitation, but I differ from him in as much as I believe that it is a distinct murmur from that heard in the second left interspace ; and I am unable to accept the theory which he advances to explain the supposed fact that a mitral murmur may, in the earlier stages of the condition be confined to the base, while in the later stages it is heard at the apex. For is it not the fact that as cases of chlorosis (and more especially of progressive per- nicious anaemia, in which the same sequence of events occurs), advance, that the degeneration of the heart muscle increases, and that dilatation of the heart cavities, with increased feeble- ness of action, rather than hypertrophy with increased force of contraction, occurs ? If this is so, Dr Balfour's explanation obviously cannot hold good ; and he himself states that ' the essential cardiac lesion in chlorosis is muscular relaxation and progressive dilatation.'^ The order of recovery, too, seems to be opposed to this view. If the hypertrophy of the left ventricle is the cause of the mitral murmur being audible at the apex in advanced stages of the case, and if the mitral and so-called auricular murmurs depend on one and the same cause, i.e. upon mitral regurgitation, why, in cases which recover, should the basic murmur persist long after the apex murmur has disappeared .-" ' Diseases of tlie Heart, second edition, p. 177. - Ibid. p. 176. 196 Diseases of the Heart. It can hardly be suggested that the left ventricle becomes weaker during the process of recovery ; and if both murmurs depend on one and the same cause, i.e. upon mitral regurgi- tation, and if the ventricle does not become weaker, both mur- murs, surely, ought to disappear at one and the same time. Tliirdly, Dr Russell has shown that in a case of pro- gressive pernicious anaemia, in which both pulsation and bruit were present in the second left interspace during life, the auricular appendix was not dilated, and was not in contact with, but was far removed from, the chest wall, and that the pulsation, pcrcussion-dulness and bruit were respectively seen and heard over the conus arteriosus.^ Dr Balfour's counter argument against this, ' that the position of the auricle post-viortevi is no proof of its state during life, and where there is no mitral stenosis, an auricular appendix beating in the second interspace during life, may very well empty itself and contract out of sight in the act of dying,' ^ is not, to my mind, a very convincing one. In the first place, our knowledge of the normal position of the appendix (including Naunyn's own observations, which Dr Balfour quotes as one of his main arguments), has been largely acquired by the same means which were adopted in this case. And in the second place, in cases of progressive pernicious anaemia, such as this was, the heart is usually (I think I may say invariably) relaxed and flaccid after death. It seems unlikely, therefore, that in this case the appendix emptied itself and contracted out of sight. Fourthly, That when the right cavities of the heart are dilated, as Dr Balfour admits is the case, in chlorosis — the condition we are considering — the left auricular appendix is usually quite invisible from the front, a fact which Dr Russell has also urged. I have had several opportunities of verifying this statement during the past year, two of the cases being typical examples of pernicious anaemia. In none of these cases was the appendix much dilated, indeed in one of the cases of pernicious anaemia it was considerably smaller than usual. Dr Russell says — 'It is further recognised that, in ' Edinr. Medical Joiinial, Nov. 1S82, p. 408. - Ibid. Sept. 1S82, p. 197. Functional Murmurs. 197 debility, owing to dilatation of the right ventricle, the left is displaced outwards and backwards ; or a change occurs which may be regarded as a rotatory movement of the heart round its longitudinal axis ; and this must be conceded as having a displacing effect on the auricle analogous to what it has on the ventricle of the same side.' Further, Dr Russell argues that, since ' the origin or root of the appendix is overlapped in part by the pulmonary artery, so to reach the parietes the appendix has to traverse a course equal to the diameter of that vessel. Any increase in the diameter of the artery, from increase of its contents will thus place the appendix deeper in the chest.' ^ I can from personal observation testify, as Dr Russell's argument implies, that the pulmonary artery is dilated in (some) cases of pernicious ansemia, presumably therefore it is dilated in some cases of chlorosis. It must be at once conceded that pulsation is frequently to be observed in the second left interspace in cases of chlorosis. I cannot, however, say that I have ever been able to satisfy myself that it was auricular ; and, like Dr Broadbent, I am not at all convinced that Dr Gibson's latter tracings, to which Dr Balfour particularly refers (see Edijiburgh Medical jfoiirnal, October 1882, p. 294), prove the pulsation to be produced by regurgitation into the ventricle from the auricle. The tracings published by Dr Russell in the British Medical Journal of June 2, 1882, seem also opposed to Dr Gibson's view. Further, in common with Dr Broadbent, Dr Goodhart, Dr Russell and other observers, whose pathological experi- ence is not inconsiderable, I have not met with any case of cardiac dilatation — certainly not any case of anaemia, and I have had an opportunity of examining seven or eight cases, after death — in which the left auricular appendix was so markedly dilated ' as to warrant the belief that it could have been the cause of the extensive pulsation claimed for it by Dr Balfour in the second and third left spaces.' Again, Dr Russell claims to have frequently satisfied himself that the pulsation in the second interspace in cases ' Edinr. Med. Jour., Aug. 1882, p. 131. " Brit. Mcd.Jo-tir., Aug. 26, 1882, p. 354. 1 98 Diseases of the Heart. of oi'Gfanic mitral disease, is due to the dilated ri<:^ht ventricle. I can corroborate Dr Russell's statement in this respect, inasmuch as I have in several cases of right-sided dilatation — notably in a case of pernicious annemia — found that a needle passed into the second left interspace transfixed the conus arteriosus of the right ventricle, and did not transfix the pulmonary artery, as it does under normal circumstances. To the other points previously advanced in support of and against Dr Balfour's theory, the following must be added : — 5. {For.) That the pulmonary second sound is accentuated. We all, of course, know, that in mitral regurgitation, the pulmonary second sound is accentuated in consequence of the increased blood-pressure in the pulmonary artery, which results from the mitral lesion. If, therefore, the accentuation occurs in the earlier stages of chlorosis, and if it cannot be satisfac- torily accounted for in any other manner (than as the result of mitral regurgitation), we must of course admit that it is strongly corroborative of Dr Balfour's theory, always pre- mising that there is no fatal objection to that view. {Against.) Now, I at once admit that, in the later stages of ansemia, the pulmonary second sound is often intensified, and that the accentuation may be due to the mitral regurgitation which is often present in the advanced stages of that condition. In the earlier stages of chlorosis, too, I have frequently (though not invariably) found the pulmonary second sound louder than the aortic. I have been in the habit of regarding the accentuation, which occurs in the early stages of chlorosis, as apparent rather than real ; in other words, I have supposed that the aortic second sound was diminished in intensity, while the pulmonary retained its normal loudness. Possibly I may have been mistaken in this view, for the fact that the blood pressure in the peripheral arteries is increased rather than diminished in anaemia, would probably lead to accen- tuation rather than diminution of the aortic second sound ;^ and ' It is well established that the blood-pressure is increased in the earlier stages of anaemia. The increase is, I believe, due to two causes viz., (a) increased adhesions of the red corpuscles to the capillary walls, (/') contraction of the peri- pheral blood vessels, the result of anaemia of the vaso-motor centre. Functional Mni'murs. 199 I am certainly not prepared to say that true accentuation of the puhnonary second sound does not occur, even in the earHer stages of chlorosis. But even granting that the accentuation were always present and well marked, I cannot admit that it is suffi- ciently strong evidence to counterbalance the grave objections which have been advanced against the mitral regurgitation view. In particular, the objections which Dr Russell has so ably urged, and which I can not only corroborate but also strengthen, viz.: — (i) that in the most advanced stages of anaemia, as seen after death, the left auricle appendix is not dilated (in one of my cases it was actually smaller than normal) ; and (2) that when the right heart becomes dilated, as it does in conditions of anaemia, the appendix of the left auricle recedes from, rather than comes in closer contact with the chest-wall — seem to me to negative Dr Balfour's view. I feel obliged, therefore, to suppose, that if the pulmonary second sound is actually intensified, the accentuation must be due to some other cause than mitral regurgitation. One cause of the accentuation is, I believe, the diminished suction power which the left ventricle exerts in consequence of the relaxed and feeble condition of its muscular wall ; the flow of blood from the lungs to the left heart is not facilitated (on the occurrence of the ventricular diastole) as it is in health. An- other cause may possibly be found in the altered composition of the blood, though this is, to say the least, extremely doubt- ful. Dr Gaskell, indeed, whom I consulted on this matter, is inclined to think that a diminished number of blood corpuscles would facilitate rather than retard the flow of blood through the lungs; he writes — ' As to your question about the passage of the blood through the lungs in anaemia, I should think that probably the blood would pass through more easily for one reason at all events ; the experiments of Ewald (Archiv. f. Anat. u Physiologic 1877, ueber die Transpiration des Blutes) have shown that defibrinated blood passes through fine capillaryglass tubes much more easily when there are few or no corpuscles in it than in the normal condition, so, for this reason alone, the blood-flow should be more easy. On the other hand, the 200 Diseases of the Heart. anaemic condition of the blood would probably excite the vasomotor centre, and so tend to constrict the blood vessels of different vascular areas, and therefore increase arterial pres- sure. There is, however, no necessity that the pulmonary vessels should take part in such constriction, and, indeed, the evidence points rather the other way, for excitation of the vasomotor centre, either directly or reflexh', by means of the stimulation of a sensor>^ nerve, does not appear to diminish but rather to increase the flow of blood through the lungs, and similarly, I should imagine, that in the case of any excitation of the vasomotor centre, through an anaemic con- dition of the blood, no constriction of the pulmonary vessels would take place, but if anything dilation. For both reasons, therefore, it is more likely than not that the passage of the blood through the lung vessels takes place with greater facility when there are fewer red blood corpuscles.' Dv Rnsscirs Theory. Let us now turn to Dr Russell's theory. He believes : — (i) That the murmur heard in the second left interspace, in the earlier stages of chlorosis, is generated in the pulmo- nary artery. (2) That the murmur is due to a relative constriction of the vessel {i.e. of the pulmonary artery), produced by the pressure of the dilated left auricle, which is situated behind it. Now this theory necessarily presupposes that, during the ventricular systole, the pressure of the blood in the left auricle is greater than the pressure of the blood in the pulmonary artery; for otherwise the pulmonary artery could not, of course, be constricted by the pressure of the auricle. That this is so Dr Russell maintains ; and he contends that the excessive pressure (if I may so term it) in the left auricle is due to a regurgitant current being propelled into it (the left auricle), by the left ventricle through the mitral orifice. The explanation which he gives is as follows : — ' Owing to the tension in the pulmonary vessels, the fulness of the auricle must at all times be increased ; in fact, the blood Fiinctional Mttrmtirs. 201 coming from the lungs pours into it as rapidly as it empties itself into the ventricle, the result being that its cavity, al- though enlarged by sharing in the debilitating influences in existence, is already full before the ventricular systole not only prevents further relief to the tension in the pulmonary circuit, but throws back upon it (the auricle) the blood embraced by the segments of the mitral valve as they swing to close the auriculo-ventricular orifice, as well as the column of regurgitant blood from the ventricle.' ^ And again, ' The question, then, arises as to what force may act through the left auricle, and is it greater than that of the right ventricle ? Take mitral regurgitation : there a stream, at times of con- siderable magnitude, passes back into the auricle with all the force exerted by the systole of the left ventricle ; and, as we cannot assume the left auricle to be a vacuum ready to receive this regurgitating stream, there must be a backward flow through it, nearly as much greater in force than the flow in the pulmonary artery as the systole of the left ventricle is greater than the right. . . . The next question to consider is, whether the tension in the left auricle is greater than that in the pulmonary artery at the moment of ventricular systole.'- . . . ' When it is remembered that there is not only a column of blood sent with the force of the left ventricle into this tense auricle, but also that the mitral cusps, instead of being held well down into the ventricle and presenting a concavity towards the auricle, so as thereby to relieve the auricle and ' make room for the returning blood without hindrance,' must, on the contrary, owing to the enfeebled state of the papillary muscles, be allowed greater latitude of movement towards the auricle, it must be granted that the auricular tension bears a fixed relation to the strength of the left ventricle, and is there- fore greater than that in the pulmonary artery.'^ In opposition to this theory Dr Balfour maintains that ' it is absolutely impossible that the left auricle can ever so com- press the pulmonary artery ; ' . . . and ' that it is obviously impossible that the circulation could be carried on under these ' Edinburgh Medical Journal, Aug. 1882, p. 134. * Ibid. Nov. 1882, p. 411. ' Ibid. Nov. 1882, p. 412. 202 Diseases of the Heart. conditions.' It is unnecessary, I think, to detail the facts and arguments with which Dr Balfour supports these objections, and the facts and arguments which Dr Russell urges in reply, for (granting for the moment that Dr Balfour's objections are invalid) I maintain : — That even if such excessive intra-auricular pressure could occur, it certainly is not present in the early stages of chlorosis — the condition which we are now considering. Such excessive intra-auricular pressure could only be produced by extremely free mitral regurgitation. In all cases of mitral regurgitation there is probably a considerable direct obstacle (both valvular and muscular), in addition to the blood pressure in the auricle, opposed to the force of the left ventricle ; while there is no direct obstacle, but only the blood-pressure in the pulmonary artery, opposed to the force of the right ventricle. We cannot, therefore, with fairness say, because the left ventricle is much stronger than the right, it wall in mitral regurgitation raise the blood pressure in the left auricle higher than the right ventricle will raise the blood pressure in the pulmonary artery. The right ventricle, though much weaker, is acting (more especially when the tricuspid is sound) at an immense advantage, and undoubtedly propels a much larger quantity of blood into the pulmonary artery than the left ventricle propels (in any ordinary case of mitral regurgitation) into the left auricle.^ Now, there is not sufficient evidence, I maintain, to prove that any regurgitation through the mitral valve occurs in the early stages of chlorosis and anaemia, much less the free regurgitation, which would be required to produce the ex- cessive pressure in the left auricle, which Dr Russell's theory requires. The only evidence which Dr Russell produces in favour of mitral regurgitation in the early stages of chlorosis, is an accen- tuated pulmonary second sound. ' It will not be seriously denied here,' says Dr Russell, ' that in these affections there is a relative insufficiency of the mitral valve, the result of a ' The reader is referred to the original papers. See the Edinburgh Medical Journal, August and September 1SS2, p. 19S ; and November 1882, p. 409. Functional Afurmnrs. 203 debilitated and relaxed condition of the cardiac muscle, in- cluding the musculi papillares. This insufificiency, however, is not always evidenced by a bruit at the apex, the point at which mitral bruits are ordinarily audible ; but regurgitation is assumed ^ from the accentuation of the pulmonary second sound, and from the presence of a systolic murmur in the pulmonary area.' - 1 have already given, in detail, the facts and arguments which are, I consider, opposed to Dr Balfour's view, and have previously stated that the presence of a systolic murmur in the second left interspace is not, in my opinion, per se (I may add, nor when conjoined with an accentuated pulmonary second sound) sufficient evidence of mitral regurgitation. And Dr Russell himself maintains that this systolic murmur is in reality produced in the pulmonary artery. According to his own showing, then, the only evidence of mitral regurgi- tation which remains is accentuation of the pulmonary second sound. This I maintain is insufficient evidence. Since this lecture was written, Dr Russell seems to have modified the view which he originally proposed, inasmuch as he no longer insists that the increased tension of the left auricle (which his theory necessarily supposes is present dur- ing the first part of the ventricular systole) is due to mitral regurgitation. In the passage quoted in the foot-note, from his instructive paper in the BritisJi Medical Journal oi ]w\-\& 2d 1883, he suggests that the increased tension of the left auricle may be due to the incomplete emptying of the left ventricle during its systole, and consequent imperfect relief to the full auricle.^ But if this view be correct, should we not expect to hear a ■ Dr Russell is here speaking of Dr Balfour's theory ; he himself believes that the systolic basic murmur is not mitral, but pulmonary, ^ Edinburgh Medical Journal, Aug. 1882, p. 130. * ' I shall now endeavour to explain the clinical phenomena. The accentuation of the pulmonary second sound, if no lung affection be present, must be taken as indicating an abnormal accentuation of blood behind the mitral orifice. Whether this be due to the incomplete emptying of the left ventricle during its weakened systole, and consequent imperfect relief to the full auricle, or, from the first, due to a certain amount of regurgitation, or to both these causes, it is unnecessary to 204 Diseases of the Heart. systolic pulmonary murmur as a necessary accompaniment of all cases of organic mitral disease, in which the pulmonary second sound is accentuated ? We can hardly suppose that the distention of the left auricle is great in the early stages of chlorosis ; and if a small amount of distention is sufficient to constrict the pulmonary artery, and to produce a systolic murmur, should we not a fortiori expect to have a sys- tolic pulmonary murmur produced in those cases of mitral stenosis, for example, in which we may legitimately con- clude that the distention of the auricle is still more con- siderable ? It may, of course, be argued (i) that a systolic murmur is sometimes heard in the pulmonary area in cases of mitral stenosis ; and (2) that in those cases of mitral stenosis in which a systolic pulmonary murmur is not present, the left auricle is not dilated. In support of the latter proposition, it may be urged that in mitral stenosis the cardiac muscle is not degenerated, as it is in the case of anaemia, and that the left auricle, for a time at all events, is able to resist the exces- sive blood-pressure in its interior, and does not dilate. But looking at the matter from the broad ground of clinical experience, most observ'ers will, I think, agree that cases (such as mitral stenosis, mitral regurgitation, fatty heart, etc.), are frequently met with, in which the left auricle is quite as much distended as we can legitimately suppose it to be in the earlier stages of chlorosis, and in which there is no pulmonary systolic murmur. If this general proposition be granted, we must of course conclude that the pulmonary murmur, met with in the earlier stages of chlorosis, is not produced by the pressure of the distended left auricle upon the pulmonary artery, but that it is due (either wholly or in part) to some other condition or conditions. I feel obliged, therefore, to dissent from Dr Russell's theory ; and there are (as I have already pointed out in discuss here. The fact of accumulation of blood in the pulmonan- circuit, includ- ing the left auricle, is sufficient for our present purpose, and is warranted by the evidence given by pulsation at the root of the neck, by the course of the external jugulars becoming \nsible, and perhaps by pulsation appearing over the right ventricle, that a like accumulation is taking place in the right chambers of the heart and the large vessels leading to it.' Functional Murmurs. 205 detail), in my opinion, grave objections to Dr Balfour's view. I am compelled, therefore, by the method of exclusion, to fall back upon the purely pulmonary theory, and to ask whether there is any conclusive reason why the murmur should not be generated in the pulmonary artery itself, irrespective of any constriction by the pressure of the auricle, such as Dr Russell's theory implies.^ The Purely Pulmonary Theory. Dr Balfour argues that the murmur cannot be pul- monary ; — (i.) Because ' there are — in chlorosis — no causes of murmur operative at the pulmonary orifice which are not at least as active at the aortic opening, so that a pulmonary murmur would certainly be accompanied by an aortic murmur also, and the latter would, of course, be propagated along the course of the aorta, and more or less distinctly into the carotids.'^ This argument does not, however, appear to be conclusive. In the first place, we might as well say, in oppo- sition to Dr Balfour's own view — the auricular theory- — that the murmur cannot be mitral, because there are no causes of murmur operative at the mitral orifice, which are not at least as active at the tricuspid opening, so that a mitral murmur would certainly be accompanied by a tricuspid murmur ; and since it is generally admitted, and as Dr Balfour himself allows in the passage quoted below, that the tricuspid mur- mur is of later occurrence than the mitral murmur, Dr Balfour's auricular theory falls to the ground. Dr Balfour says, ' shortly after the appearance of the primary haemic murmur, a tricuspid murmur and jugular undulation are found to be developed. This is naturally accompanied by a ' There seems to me to be no sufficient evidence to justify the belief, that the murmur heard in the second left interspace, hi the ea?-ly stages of ancemia, is due to tricuspid regurgitation, as Parrot supposed. The mere presence of a murmur in that position, in the absence of the usual signs of tricuspid regurgitation, is insufficient evidence to justify such a belief. It is, however, quite possible that, in the later stages of anaemia, a tricuspid murmur ma}' be heard in this situation, as Dr Russell supposes. ^ Edinburgh Medical Journal, Oct. 1882, p. 294. 2o6 Diseases of the Heart. pulmonary and also by an aortic systolic murmur the active cause in the production of both these murmurs being the large blood-waves sent on by the dilated and hypertro- phied ventricles, as was first, I believe, pointed out by Beau.'^ In the second place, I am not prepared to admit, uncon- ditionally, that there are no causes of murmur operative at the pulmonary orifice, which are not at least as active at the aortic orifice. It appears to me quite possible that such causes may exist in the respective conditions of the two ven- tricles ; in the respective resistances which the arterial blood meets with at the orifice of the aorta and in the systemic circulation, and which the venous blood meets with at the orifice of the pulmonary artery and in its passage through the lungs ; and in the respective physical conditions (calibre, thickness of coat, relationship to the chest wall, etc.) of the aorta and pulmonary artery. In the third place, I believe that aortic murmurs are some- times present in the early stages of chlorosis, possibly they would be more frequently audible in such conditions, if it were not for the fact, that they are so soft and faint as to be obscured at the base by the pulmonary murmur, and of such low tension, and of such little force, as to be inaudible over the course of the aorta and in the carotids. (2.) Because the point of maximum intensity of the mur- mur • is not over the pulmonary artery at all, but from one to two inches to the left of the sternum, in the second interspace.'^ This argument also fails to convince me, for the reasons already detailed. (See p. 190.) (3.) Because no murmur of strictly pulmonary origin could possibly be referred to all four orifices in turn, as has been the case with the haemic murmur ; and second, because however singular a murmur of mitral regurgitation in this position may seem to be, its causation is by no means difficult to understand.'^ Neither of these reasons seems to me to exclude the pulmonary hypothesis. The mitral origin of the murmur, ' Edinburgh Medical Journal^ Oct. 1S82, p. 295. - Ibid. p. 294. ' Diseases of the Heart., second edition, p. 173. Functional Miiruiurs. 207 which Dr Balfour supports, would be as efifectually excluded by the first reason, as he argues the pulmonary origin is ; for no murmur of strictly mitral origin could possibly be referred to all four orifices in turn. The only legitimate conclusion to be drawn from the first reason is, that in chlo- rosis, murmurs may be generated at more than one orifice, a conclusion which we all allow. The second reason, even if admitted, docs not exclude the pulmonary hypothesis, but only shows that a mitral murmur can be heard in the neigh- bourhood of the pulmonary artery. I feel compelled, therefore, to differ from Dr Balfour ; for I do not see that any argument which has been as yet advanced conclusively negatives the purely pulmonary theory. As I have previously stated, the sudden propulsion of a large blood-wave, of abnormal (spanaemic) composition into the vessel, which is possibly dilated, seems to me an efficient cause for the production of the murmur ; and we know, as a matter of fact, that in cases of chlorosis these conditions are actually present— the chlorotic heart is unusually irritable and contracts with unusual suddenness ; even in the earlier stages, there is some dilatation of the right ventricle ; the blood is spanaemic, and in some advanced cases, i.e. fatal cases of pernicious ansemia, the pulmonary artery is dilated. Dr Balfour himself states, in the passage I have quoted above, that aortic and pulmonary murmurs do occur in the later stages of chlorosis, and that the active cause in .the production of both is the large blood-wave sent on by the dilated and hypertrophied ventricles. Now, if aortic and pul- monary murmurs can be produced by this cause in the later stages of chlorosis, and after, as Dr Balfour argues, tricuspid and mitral regurgitation have occurred ; should they not a fortiori be produced in the earlier stages, before, as I main- tain, there is sufficient evidence of mitral and tricuspid regurgi- tation, for would not the presence of a leak at the tricuspid and mitral orifices diminish the size of the blood-wave, and so, other things being equal, be likely to interfere with the production of, rather than to cause such murmurs ? 2o8 Diseases of the Heart. The Differential Diagnosis of Cardiac Mnnmirs. Given the presence of a murmur over the praecordia, we have to determine : — 1. Whether it is exocardial or endocardial. 2. If exocardial, whether it is a pleural, a pericardial, or a pericardial-pleural murmur. If endocardial : — 3. The valve at which it is produced, and whether it is direct or regurgitant. 4. Whether it is organic or functional. 5. If organic, the extent and gravity of the lesion. Many of these points I shall afterwards have to consider in detail, in treating of the diagnosis and prognosis of the individual cardiac affections, but it may perhaps be well, even at the risk of some future repetition, to consider the subject now as a whole, and to point out the leading facts and circumstances which enable us to form an opinion on these important questions. Step No. I. Differential Diagnosis of Exocardial and Endocardial Miinniirs. This question is, as a rule, easily determined b}' attention to the following points : — I. The Rhythm of the Mnrninr. — Pleural friction sounds are of course at once distinguished (except in the case of the peri- cardial-pleural friction murmur, which I shall presently refer to) from cardiac murmurs by the fact, that they correspond in rhythm or frequency to inspiration and expiration, and that they do not correspond to the pulsations of the heart. Exocardial murmurs (pericardial and pericardial-pleural friction murmurs) correspond in rhythm or frequency to the pulsations of the heart, but their synchronism is, as a rule, much less perfect, i.e. they do not correspond so exactly to the heart sounds, as do endo-cardial murmurs. Pericardial murmurs, when typical, are double (to-and-fro friction sounds), but the murmur of combined aortic stenosis and incompetence is also double ; hence in the majority of cases the problem resolves itself into the differential diag- nosis of these two conditions, viz., pericarditis and double Diffei'ential diagnosis of Cardiac Miirvmrs. 209 aortic disease — a point which will afterwards be considered in detail. The rhythm of exocardial murmurs is, as a rule, more variable than the rhythm of endocardial murmurs. The character and the rhythm of the murmur is apt to change from day to day, from hour to hour, or even during the actual examination of the patient, a fact which is explained by the circumstance that the relative positions of the two opposed and roughened surfaces of the pericardium may be materially modified by alterations in the position of the patient, and the pressure of the stethoscope.^ The fact that alterations in tone and rhythm can be produced by the pressure of the stethoscope is highly characteristic of pericardial murmurs. 2. Tlie sound characters of the murmur. — Exocardial murmurs are friction sounds, and, as a rule, have a harsh, grating character ; they usually appear to be superficial. But this and their other characters I have previously described. (See p. 167.) 3. The point of maximum intensity of tJic murmur, and tlie direction in w/iich it is propagated. — Exocardial murmurs are, as a rule, best heard over the centre of the right ventricle or at the base of the heart ; but they have no special points of differential maximum intensity as endo- cardial murmurs have. Exocardial murmurs are often only heard over a very limited area, and they are not propagated in any definite direction as endocardial murmurs are. (See p. 182.) 4. The associated symptoms and Jiistory of the case. — Exo- cardial murmurs appear abruptly, so to speak, and generally in the course of some constitutional affection such as rheu- matic fever, Bright's disease, etc. Endocardial murmurs may appear abruptly and in the course of rheumatic fever, ' Endocardial murmurs are sometimes only audible in one particular position. The presystolic murmurs, for example, may disappear when the patient sits up, as Professor Sydney Ringer and others have noted. Again, other endocardial mur- murs are very decidedly intensified by sitting up, walking, etc. But in these cases the rhythm of the murmur remains the same, and is not modified by alterations i'n position. O 2IO Diseases of the Heart. but, in many cases, the lesion which produces them develops very slowly. The absence of constitutional disturbance, and, especially, the fact (if such a history can be obtained) that the murmur is an old one, are strongly in favour of its endo- cardial origin. Step No. 2. The Munnur is Exocardinl ; is it a Pleural, Perieardial, or Pericardial-pleural Aluruiur ? Ordinary pleural friction is at once distinguished by the fact, that its rhythm corresponds to the rhythm of the respi- ratory movements. Pericardial-pleural friction is extremely rare. It occurs, as I have previously explained, when that portion of the pleura, which is reflected over the pericardium is inflamed ; and it is produced by the movements of the heart rubbing this rough and inflamed portion of the pleura against the anterior wall of the chest, or against the visceral pleura which is in contact with it. The points by which we are enabled to distinguish pericardial-pleural friction from ordinary pleural friction are as follows — 1. Pericardial-pleural friction is generally best heard over the borders of the heart, i.e. where the visceral and parietal portions of the pleura come into contact ; whereas ordinary pericardial friction is, as a rule, best heard over the centre of the cardiac dulness, i.e. over the centre of the anterior surface of the right ventricle. 2. Pericardial-pleural friction is, as a rule, more afl"ected by the respiratory movements than ordinary pericardial fric- tion. I have, in two cases, observed that it was decidedly increased by a full inspiration, i.e. when a larger portion of the two inflamed surfaces of the pleura were brought in con- tact. Walshe states that it is, as a rule, increased during expiration ; and in such cases the murmur is probably pro- duced by friction between the outside of the pericardium and the inside of the chest wall. When the patient takes a deep inspiration, the pericardial-pleural friction is sometimes re- placed by ordinary pleural friction. This is not pathogno- monic, for pericarditis is not unfrequently accompanied by pleurisy, and, in such cases, the pericardial friction may only Differential diagnosis of Cardiac Murmurs. 2 1 1 be observed over the praecordial region during a deep inspiration, and may then replace the pericardial friction sound. 3. In pericardial-pleural friction we should expect to find the symptoms of pleurisy, but there would be no indications of pericarditis ; and vice versa. It must not, however, be forgotten that many cases of dry pericarditis are unattended by any symptoms or signs except the to-and-fro friction murmur. 4. The pericardial-pleural friction murmur is even more variable than the ordinary pericardial friction murmur ; and may even cease with certain pulsations of the heart. Step No. J. — The IMuruiur is Ejidocardial ; at zuhich valve is it produced, and is it direct or regurgitant f The valve at which the murmur is produced is determined by observing : — 1. The point of differential maximum intensity of the murmur. (See page 180.) 2. The direction in which it is propagated. (See page 182.) 3. The effect which the lesion has produced upon the heart and circulation. It will be more convenient to con- sider this point when speaking of the character of the lesion. (See page 214.) 4. The relative frequency of the different valvular lesions. This is not a point of very much importance, for it is gene- rally easy to decide the question by the points already men- tioned (1,2, and 3) ; but in some doubtful cases, as, for in- stance, in the case of a murmur heard over the base of the heart, the fact that the pulmonary orifice is very rarely dis- eased after birth, would, supposing that we could exclude inorganic conditions, be strongly in favour of the aortic origin of the murmur. The question whether the murmur is direct or regurgitant is, of course, easily decided, by observing its rhythm. (See page 172.) When it is difficult or impossible to determine the rhythm, the sound characters of the murmur, and the effects of the lesion on the heart and circulation are the points which must be chiefly relied upon. 2 I 2 Diseases of tiie Heart. Step Xo. ^. — The Murmur is Endocardial ; is it Organic or Functional / It is sometimes very difficult, or even impossible, to give a positive answer to this question ; in other cases it is decided with the greatest ease. The difficulty is greatest in the case of mitral systolic murmurs, which result so frequently from 'muscular' and 'relative' incompetence, and in which therefore we have to decide whether the muscular weakness of the heart is curable or not. In such cases it is only by taking a broad and general view of all the features of the case — independently of the mere physical examination of the heart itself — that a correct conclusion can be arrived at. In practice, the first step in the differential diagnosis of organic and functional murmurs is to determine the rhythm of the murmur. The so-called functional murmurs are, as we have already seen, always systolic, and may be heard either in the pulmonary, aortic, mitral, or tricuspid areas. If, then, the murmur is diastolic or presystolic, we may with certainty conclude that it is organic. (As I have previously stated. Professor Austin Flint believes that a mitral lesion is not essential for the production of a presystolic murmur. The matter is perhaps of less practical moment than would at first sight appear. For since Professor Flint only claims to have noted this presystolic murmur, without mitral lesion, in cases of aortic incompetence ; and since aortic incompetence is always an organic and serious lesion, the matter is, so far as our present purpose is concerned, comparatively unim- portant, i.e. so far as concerns the decision whether the cardiac lesion is temporary and curable, or organic and incurable.) If the rhythm of the murmur does not decide the ques- tion — that is to say, if the murmur is systolic — we must seek to determine the question by attention to the following points : — (a.) Tin presence or absence of the causes of inorganic murmurs on the one liand, or of organic murmurs on the other. The structural changes of a temporary' kind which affect the heart muscle in ansemia and the continued fevers, are the great causes of the so-called inorganic or functional Differential diagJiosis of Cardiac Aliiruiurs. 2 1 3 murmurs. A murmur, then, occurring in a patient, who is neither anremic nor suffering from one of the continued fev^ers, is probably organic. The reverse proposition (that murmurs, occurrmg in persons who are anaemic or suffering from one of the continued fevers, are functional) does not necessarily hold good. This caution more particularly applies to cases of rheumatic fever in which there is a strong ten- dency to inflammatory affections of the heart, but in which functional murmurs due to anaemia and to temporary and curable alterations in the heart muscle, are also frequently developed. Murmurs, then, which develop in the course of rheumatic fever, are probably, but not necessarily, organic. It is unnecessary to detail here the ordinary symptoms of anaemia; the pallor of the mucous membranes, and the pre- sence of a venous hum in the neck, are the points of most importance. (b.) 'J fie condition of tlie Iieart and circulation. This some- times gives us important information, as in the following case : — Case. — J. B., aet. 51, was admitted to the Ne\vcastIe-on-Tyne Infirmary under my care on 29th November 1878, complaining of shortness of breath and of swelling of the feet. He was very ansmic ; a well-marked systolic murmur was audible over the aortic area ; the left ventricle was not markedly hypertrophied. The pulse was slow and deliberate, and the apex of the sphygTiiographic tracing rounded. These characters which are seen in figure 55, seemed to show that the aortic murmur was not merely haemic, but that it was due to organic stenosis of the aortic orifice. Fig. 55. — Sphygmogram from the case of |. B., referred to in the text. It must, however, be remembered, that free mitral regurgitation may be due to temporary and curable con- ditions ; and that in such cases all the symptoms and signs of regurgitation due to organic and incurable disease (viz., accentuation of the pulmonary second sound, changes in 2 14 Diseases of the Heart. the right heart, shortness of breath, dropsy, etc.), may be present. (c.) The effect of treatment. — This is a most valuable, and indeed, in some cases, the only certain means of deciding whether a murmur is functional or organic. (d.) The point of inaximnm intensity of the imirnmr and the extent of its propagation. — These points may also give us some information. Anaemic murmurs are generally basic, and are most commonly heard over the pulmonary area, often also over the aorta, more rarely at the apex. Inorganic murmurs are not so well propagated as organic ones ; aortic murmurs, therefore, which are carried into the vessels of the neck, and mitral murmurs, which are audible at the inferior angle of the left scapula, are probably organic. {e.) The history of the case. — This may be of importance ; a history of rheumatic fever would, other things being equal {i.e. in a doubtful case), be strongly in favour of the organic nature of the case. The differential diagnosis of functional and organic murmurs will be considered in further detail when the individual valvular lesions are treated of. (See chapter V.) Step No. J. — The Mnrimir is Organic ; zvhat is the extent and gravity of the Lesion ? The extent of the lesion.— 0\.\\qx things being equal, the more extensive the lesion, the more serious the case. Now, in recent cases it may be very difficult, or even impossible to determine the exact extent of the lesion. It may be impossible, for instance, to say what proportion of the symp- toms, is due to temporary conditions, and how far the morbid conditions may be restored or compensated. In chronic cases the extent of the lesion is more easily determined, and in order to arrive at a correct conclusion the following circumstances must be taken into account : — I. TJie effect of the lesion upon the heart and the circulation. — As we shall afterwards see, the great effect of all valvular lesions is to prevent the steady onward passage of the blood current. In seeking, therefore, to estimate the extent and Diffei'entiai diagnosis of Cardiac Murmurs. 2 1 5 gravity of any valvular lesion, it is necessary to examine the effects produced: — {A.) In the cavities of the heart, and in the parts of the circulation which are situated behind the lesion — the backivard effects; {B.) In the cavities of the heart and parts of the circulation which are situated in front of the lesion — the forward effects^ as they may be termed. The more marked these effects, and the shorter the period which has been required for their full development, in other words, the more rapid the progress of the case, the worse the prognosis. It will be necessary, therefore, in the next place, to consider the effects which the different valvular lesions tend to produce on the circulation in front and behind, and the symptoms which result therefrom. I say, tend to produce, for it is essential to remember that serious valvular lesions may, for a time at least, be unattended by any apparent external effects or symptoms — a point which I have already insisted upon in speaking of the important ' principle of compensation.' On the other hand it is no less important to remember, that in these cases {i.e. in cases of serious valvular lesions, which are so perfectly compensated, as to be unattended by any apparent external effects or symptoms so long as the circulation is not, so to speak, put upon the stretch) there are internal effects (such as hypertrophy of the heart, etc.) which can be detected by physical examination. The effects which the different valvular lesions tend to produce on the heart and circulation are as follows : — MITRAL STENOSIS. A. Backward Effects. (a) Blood stagnates in the left auricle, which becomes over-distended, hypertrophied, and dilated ; {b) The pulmonary veins become engorged ; {c) The lungs become congested : lung symptoms, consisting of short- ness of breath, especially on exertion, going up stairs or up a hill ; a tendency to catarrhal affections of the lungs and bronchi (especially chronic bronchitis), to oedema of the lungs, to haemoptysis, to hydrothorax, etc., are apt to arise ; id) The increased blood-pressure in the pulmonary artery produces accentuation of the pulmonary second sound ; and there is, 2i6 Diseases of the Heart. in many cases, reduplication of the second sound of the heart ; {e) The right ventricle becomes hypertrophied and dilated ; (/J Tricuspid regurgitation not unfrequently occurs with pul- sation in the veins of the neck.^ (The enlargement of the right cavities of the heart, both ventricle and auricle, and the presence of tricuspid regurgitation, can be ascertained by physical examination) ; {g) The systemic venous circulation is impeded, and the symptoms which result from this venous engorgement are often the first which attract the attention of the patient.- The peripheral parts, more especially the lips, nose, and ears, tend to become cyanotic, and the face some- what full and swollen. Dropsy, commencing in the feet (increased by standing and walking, and therefore worse at night), gradually extends upwards, and finally involves the serous cavities as well as the subcutaneous tissues of the lower parts of the body. Engorgement of the portal vessels produces congestion of the liver, stomach, and haemorrhoidal veins, with resulting enlargement of the liver, muddiness of the complexion or slight jaundice, dyspepsia, and piles. Congestion of the renal veins is attended with scanty and high coloured urine, which is loaded with urates, and often contains albumen. Interference with the return current from the brain may be attended with drowsiness and other indica- tions of mental obfuscation. B. Forward Effects. — Small and variable quantities of blood are passed into the left ventricle through the stenosed orifice ; consequently small and variable quantities of blood are pumped into the arterial system, the pulse being, there- fore, small, unequal in volume, and irregular in time. (So long as the compensation is well maintained, the volume and rhythm of the pulse ma}' not be much altered.) The occurrence of a second and imperfect ventricular contraction ' For the reasons previously given, the accentuation of the puhnonary second sound may diminish or disappear with the occurrence of tricuspid regurgitation. * In this description I have sketched the backward effects in their anatomical, rather than their chronological sequence, venous engorgement and its resulting s)TTiptoms occurring long before many of the other conditions, such as tricuspid regurgitation. Differential diagnosis of Cardiac Mnrmurs. 2 i 7 in the sphygmographic tracing, such as is shown in fig. 56, is often obscr\-ed. Pressure 3'^ oz. Fig. 56. — Irregularity of the Pulse. — W. M., ajt. 50, admitted to Newcastle Infirmary 30th November 1878, suffering from the usual symptoms of mitral disease. The heart's action was extremely irregular The left ventricle much hypertrophied. There was no rheumatic history. The symptoms were of two months' duration. I have attempted in figs. 57, 58 to represent in a diagram- matic manner, the backward effects which mitral lesions produce on the heart and circulation. A \ ^'—:/j0^ ^^S ■'^^y "] ^ V V'--; \ --A' ,# ^Ssj ^-„L n Y— i :',— - PA-^# --..,- ^^ -C-PV '- -A R4— .' »^ 1 ^ -j— -RV Li\.-{ V ^) — LV Fig. 57. — Representation of the effects of a lesion of the mitral valve (mitral stenosis in this case) on the heart and circulation. The effects of mitral regurgitation are the same, but there is, in addition, hypertrophy of the left ventricle. LV=left ventricle; L.-\. = left auricle; PV=pulmonary veins; L = lungs ; PA=puImonary artery; RV = right ventricle; RA= right auricle; V = venK cavas ; V'=venous system; B' = termination of the venous system in the systemic capillaries; A = the aorta; A'=the arterial system. The arrows show the direction of the backward pressure. The dotted lines show the effects of the obstruction (dilatation) on the different parts. 2l8 Diseases of the Heart. Fig. 58. Differential diagjiosis of Cardiac Murmurs. 219 MITRAL REGURGITATION. A. Backward Effects. — The backward effects are similar to those which are produced by mitral stenosis. As a rule grave disturbances of the circulation are manifested earlier in mitral regurgitation than in stenosis — a fact which is easily understood when we remember that in many cases the former results from degeneration and failure of the heart muscle, independently of any lesion of the valvular segments. B. Forivard Effects. — The pulse is small, and in advanced cases (i.e. after the failure of compensation), it is usually irregular. AORTIC STENOSIS. A. Backivard Effects. — The left ventricle becomes hyper- trophied in consequence of the increased effort required to force the blood through the stenosed orifice ; but so long as the mitral valve remains competent — and it usually does so even in advanced cases — there are no prominent lung symptoms, or other signs of venous engorgement. B. Forzuard Effects. — The pulse is small but of good tension, slow and regular. When the stenosis is considerable, symptoms due to defective blood-supply to the brain are sometimes observed. AORTIC REGURGITATION. A. Backward Effects. — The left ventricle becomes hyper- trophied and dilated, and in consequence of the dilatation of the cavity and the impaired nutrition of the cardiac muscle, mitral regurgitation is common towards the later stages of the case. So long as the mitral valve remains sound there are no prominent lung symptoms or other signs of venous engorgement ; should the mitral give way the symptoms characteristic of mitral regurgitation are super- added to the symptoms which I must now describe. B. Forward Effects. — At each systole of the dilated and Description of Fig. j8. Diagrammatic representation of the effects of a mitral lesion upon the venous circu- lation. The numbers and letters are the same as in fig 3. (See description page 5. ) The arrows indicate the direction of the backward current. 220 Diseases of the //earl. hypertrophied left ventricle, a large quantity of blood is pro- pelled into the arterial system, which is therefore rapidly and fully distended ; but, in consequence of the leak at the aortic orifice, this distention of the arterial system is not maintained. The pulse is highly characteristic, presenting the jerking, visible, collapsing, water-hammer character which was so ably described by the late Sir Dominic Corrigan (Corrigan's pulse.) It is generally quicker than in health. The aortic and dicrotic wave is, as a rule, feebly marked or absent, and the sphygmo- graphic tracing is, in some cases, characteristic. When the regurgitation is free, the artery may be very empty during the ventricular diastole. The face is generally pale, and usually presents an anxious expression. In advanced cases, attacks of syncope are common, and the general condition of nutrition may be considerably impaired. Pain of an angina-like char- acter is frequently observed. The amount of alteration in the pulse, more especially the degree of distention during the ventricular diastole ; the extent of the dilatation of the left ventricle ; and the condition of the mitral valve — whether competent or not — are points of great importance in estimating the gravity of this lesion. Figure 59 represents in a diagrammatic manner the effects of aortic lesions upon the circulation. ^H ^^^^H ^B^^^^^^ ■H ■^^^^^^Sv Bll ■S^^^^^ba ^^W Bll KiG. 59. — Representation of the effects of a lesion of the aortic valves (aortic regurgitation in this case) on the heart and circulation. The letters have the same significance as in fig. 57. The left ventricle is hypertrophied and dilated ; the mitral valve is as yet competent. Differential diagnosis of Cardiac Munnnrs. 221 PULMONARY AND TRICUSPID LESIONS. The effects produced by pulmonary and tricuspid lesions will be readily understood after what has been already stated in describing the effects of mitral lesions. Pulmonary lesions — which are extremely rare, except as congenital conditions — produce alterations in the right cavities of the heart and engorgement of the systemic venouscirculation. Tricuspid regurgitation (which is frequent in the advanced stages of mitral lesions, and which may also arise, as I have previously pointed out, from primary disease of the lungs, such as emphysema and cirrhosis) is always attended with marked signs of systemic venous engorgement. Venous pulsation in the neck, synchronous with the contraction of the right ventricle, is very characteristic of this condition ; and in some cases true pulsation in the liver, the result of a back-wash through the inferior cava, is observed. 2. TJie ainoiint of compensation ivhch can be produced. — In all valvular lesions there is an attempt on the part of nature to meet the difficulty. The extent to which the lesion can be compensated, and the probable time during which this compensation can be maintained, are most important points in estimating the gravity of the lesion. The capability of compensation depends upon : — {a) Tlie general reparative pozvers of the individual. — A valvular lesion of moderate extent, occurring in an individual whose tissues are prone to degenerate, or already in a state of decay, is of graver significance than a much more exten- sive lesion in a person whose tissues are otherwise healthy. if) The special reparative poiver of the cardiac uniscle. — So long as the cardiac muscle remains sound, and the hyper- trophy is good, compensation is well maintained, and the symptoms are at a minimum. But whene\-er the muscular nutrition fails, or dilatation occurs, the compensation gradu- ally fails, and serious symptoms arise. The structural sound- ness therefore of the cardiac muscle, and the presence or absence of dilatation are points of great importance in estimating the gravity of the lesion. 22 2 Diseases of the Heart. (c) The age of the patient. — Other things being equal, the younger the patient, the better the prognosis, for in young persons the reparative powers, and therefore the capabiHties of compensation, are greater than in old people. {d) The Jiabits and surroundings of the patient. — Valvular lesions are (other things, such as the condition of the tissues, being equal) much less serious in persons in comfortable circumstances than in those who are obliged to struggle for existence, and lead laborious lives. Indeed, as we shall see when I come to speak of the treatment of these affections, rest — so far as is possible — to the damaged organ is the first and most important point to be attended to. The amount of work required of the damaged heart, is a very important element in the prognosis. {e) The mental temperament of the patient is of consider- able importance. Valvular lesions are less serious in persons of a quiet and placid disposition than in persons of an excitable and anxious temperament. (/) The cEtiology of the lesion. — Valvular lesions of rheu- matic origin are, as a rule, less serious than those which result from other causes. This is probably owing to the facts, that non-rheumatic valvular lesions are often due to degenerative processes, and that persons thus affected are, as a rule, older than those affected with lesions which can be directly traced to acute rheumatism. 3. The form of valvular lesion. — We know, as the result of clinical experience, that some valvular lesions are more serious than others. Dr Walshe gives the following as the order of relative gravity, estimating the gravity not only by the ultimate lethal tendency of the different lesions, but also by the amount of complicated miseries which they inflict. (This order can onl)- be looked upon as approximate. I shall afterwards have to point out many modifications in it. There are, for instance, many different causes of mitral regurgitation, some of which are eminently curable ; others almost certainly fatal. Dr Walshe evidently alludes to the more serious forms. So again, tricuspid regurgitation may be a temporary and curable condition, though in many Diffei'cntial diagjiosis of Cardiac M2i7'miirs. 223 cases it is the most unfavourable of all cardiac valvular lesions): — 1. Tricuspid regurgitation (most grave). 2. Mitral regurgitation. 3. Mitral constriction. 4. Aortic regurgitation. 5. Pulmonary constriction. 6. Aortic constriction (least grave). The relative gravity as regards their tendency to produce sudden and instantaneous death is, however, quite different. Aortic regurgitation stands prominently out as the valvular lesion which often gives rise to immediate death, the fatal result being due to syncope ; while the other valvular lesions have no direct tendency to produce immediate death. 4. Whether the lesion is progressive or stationary. — This is an extremely important point, and it is to be determined — (a) By close observation of the case, and noting the condi- tion of the patient from time to time. {b) By comparing the duration of the case and the effects which the lesion has already produced on the heart and circulation. {c) By taking into account the nature of the morbid process. We know as the result of clinical and pathological observation, that valvular lesions, due to degenerative pro- cesses, are less likely to remain stationary than those which result from simple inflammation (endocarditis). {d) By reference to the valve which is affected, and the manner in which it is affected. Mitral regurgitation, for ex- ample, is in many cases curable, but aortic regurgitation is not. 5. The associated pathological conditions. — This is a point of the very greatest importance. In all cases in which the tissues are prone to degenerate, the prognosis is bad ; in fat, flabby individuals, a lesion— other things being equal — usually advances with more rapidity, and proves more speedily fatal than in spare and thin people. The presence of kidney disease, or of any other organic lesion, adds, of course, very materially to the gravity of the case. The points which enable us to determine the extent and 2 24 Diseases of the Heart. gravity of the lesion will be considered in further detail under the prognosis of the individual valvular lesions. THE PHYSICAL EXAMINATION OF THE AORTA AND THE GREAT BLOOD VESSELS. After having ascertained the condition of the heart itself. we must next determine the physical condition of the aorta and great blood-vessels. In actual practice it is customary and convenient to examine the condition of the arch of the aorta, and of the heart, at one and the same time ; when in- specting the praecordia, for example, to inspect at the same time the parts of the chest which lie superficial to the aortic arch ; and so on with palpation, percussion, and auscultation. In ordinary cases it is not customary to make a detailed examination of the great branches of the aortic arch, or of the descending thoracic or abdominal portions of the aorta. When, however, there is any reason to suspect disease of these structures, their condition must be carefully and methodically examined. In order to ascertain the physical condition of the aorta (both its thoracic and abdominal portions) and of its branches, we employ the same means of investigation which I have already described in speaking of the physical examination of the heart : — Firstly we inspect, palpate, percuss, and auscultate the parts superficial to the vessel. Secondly, we investigate the condition of the circulation and of the circulatory organs in front and behind ; when we are investigating the condition of the aortic arch, for instance, we direct special attention on the one hand to the condition of the pulse in the different branches arising from it {i.e. we observe the comparative condition of the pulse in the two radials and carotid arteries), and on the other to the state of the heart and venous circulation. Thirdly, we pay special attention to the physical condition of the organs and parts adjacent to the vessel. This is a point of great importance, for the chief pathological conditions in the aorta and its branches, which we are able to ascertain The Exaiuiuation of tJic thoracic aorta. 225 by means of physical examination, are dilatations (simple and aneurismal) and the chief symptoms and physical signs in these conditions are often due to the pressure of the dilated blood vessel upon adjacent parts, and to the displacements which are caused thereby. INSPECTION APPLIED TO THE EXAMINATION OF THE THORACIC AORTA. The patient should be placed in a good light, and the surface of the chest carefully inspected, more especially those parts which are superficial to the course of the aorta, and at which the vessel comes nearest to the surface (the sternal end of the second right interspace in particular). But in order that this and other points connected with the physical exami- nation of the thoracic aorta, and the symptomatology of its diseases, may be thoroughly understood, it will perhaps be well for me to describe briefly the anatomical course of the vessel and its relations, which are of importance from a prac- tical and clinical point of view. Aiiatoiiiical course and relations of the tlioracic aorta. The thoracic aorta arises at the junction of the third left costal cartilage with the sternum, i.e. nearly opposite the point of union of the upper and lower sternal regions, and terminates in the abdominal aorta beneath the pillars of the diaphragm, or more exactly, on the anterior surface of the last dorsal vertebra. The thoracic aorta has been divided, for descriptive purposes, into two portions — the aortic arch and the descending thoracic aorta. The aortic arch is described as consisting of three parts — the ascendi)ig, transverse, and descending portions. The ascending portion of the aortic arch arises from the base of the left ventricle, on a level with the lower border of the third left costal cartilage, at its junction with the sternum, and passes upwards and to the right until it reaches the upper surface of the second right costal cartilage at its junction with the sternum (occasionally encroaching upon the inner edge of the first interspace), where it terminates in the transverse P 2 26 Diseases of the Heart. portion. For the greater part of its course it is enclosed in the membranous sac of the pericardium. In the first part of its course it is deeply situated, being covered by the root of the pulmonar\- artery, and being closely related posteriorly to the cavity of the left auricle. After emerging from under cover of the pulmonary artery, it comes in close relation- ship with the sternum and second right costal cartilage, being separated from these structures by the sac of the peri- cardium, the cellular tissue and fat of the mediastinum, and (when the lungs are expanded) by the thin anterior margin of the lungs, more especially of the right lung. The supe- rior vena cava lies in contact with it on the right side ; the pulmonary artery diverges from it on the left side, while be- hind it is placed the root of the right lung. The cardiac plexus and many of its branches, as they proceed to their terminations in the coronary plexuses, are closely related to the root of the aorta. This is a connection which is of great practical importance ; while the facts that the co- ronary arteries arise from the root of the aorta, and that the root of the aorta is directly continuous with the aortic valves, and therefore with the heart, are points the import- ance of which, from a practical clinical point of view, is self- evident. TJie transverse portion of the arch of the aorta commences at the junction of the upper edge of the second right costal cartilage with the sternum, and crosses almost horizontally through the upper sternal region, on the level of the first interspace, passing backwards and downwards deeply into the chest. The transverse portion terminates in the descend- ing portion of the aortic arch, at the lower border of the left side of the body of the fourth dorsal vertebra. The transverse portion of the aortic arch is separated from the surface of the front of the chest by the mediastinal fat and connective tissue, by the remains of the thymus gland, during inspiration by a small portion of the right pleura and anterior border of the right lung, and by the left pleura and anterior border of the left lung. The left pneumo-gastric, the left phrenic and superficial cardiac nerves, and the left superior Anatomical course of t/ie thoracic aorta. 227 intercostal vein, cross in front of this portion of the vessel. On the right side, at its origin, it is closely related to the superior vena cava, the right pneumo-gastric and phrenic nerves. From its upper convex surface arise the great blood vessels destined for the head and neck and upper extremities (the innominate, left common carotid, and left subclavian arteries), and in close relation with its upper surface lies the left innominate vein. In the concavity beneath its lower surface the bifurcation of the pulmonary artery and the cardiac plexus of nerves are situated ; the recurrent branch of the left pneumo-gastric winds round the concave lower surface of the vessel to which the obliterated ductus arteriosus is attached. Posteriorly the trans- verse portion of the arch of the aorta is in close contact with the left recurrent laryngeal nerve, as it ascends through the thorax to the neck, with the trachea and bifurcation of the bronchi, the oesophagus, thoracic duct, and more deeply with the bodies of the vertebrae. The descending portion of the aortic arch commences at the junction of the bodies of the fourth and fifth dorsal vertebra;, and passes downwards in close contact with the left side of the body of the fifth dorsal vertebra, until it terminates at the lower end of the body of that vertebra, in the descending thoracic aorta. The descending thoracic aorta passes downwards in contact with the spinal column ; in the upper part of its course it lies on the left side, in the lower part of its course on the anterior surface of the bodies of the vertebra;. It terminates in the abdominal aorta at the level of the twelfth dorsal vertebra. On the right side of the vessel lie the thoracic duct and the large azygos vein. On the left side the vessel is covered by the left pleura and left lung. In front of it are placed the root of the left lung and the posterior surface of the peri- cardium, and, therefore, the posterior surfaces of the left auricle and left ventricle. The oesophagus is at first on the left side of the aorta, lower down it makes its way in front of the vessel. At its termination the thoracic aorta is enclosed in the opening formed by the crura of the dia- phragm. 2 28 Diseases of the Heart. In health, inspection gives no information as to the condi- tion of the thoracic aorta ; in other words, neither pulsation nor prominence can be seen on those parts of the surface of the chest which correspond to the position of the vessel under- neath. When, however, the vessel is diseased, more especially when it is affected with aneurismal dilatations, local promin- ence and pulsation at the part of the chest, corresponding to the position of the aneurismal dilatation, are often observed. In order to detect slight elevations of the chest wall and slight pulsations, a special method of inspection is neces- sary ; instead of placing himself in front of the patient and looking straight on to the surface of the chest, the ob- server should place himself at one side of the patient — the opposite side to that from which the rays of light are pro- ceeding — -and should then bring his eye to the same hori- zontal plane as the surface of the chest which he wishes to examine. If the illumination is good, slight elevations and pulsations, which might easily escape observation by the or- dinary or full-face method of inspection, can b}' this means be readily detected. The most frequent position for aneurismal or aortic pulsa- tion is the second right interspace close to the sternum ; for, in the first place, the ascending portion of the aortic arch is more liable to be affected by aneurismal dilatation than any other part of the vessel ; and, in the second, comparatively small aneurisms are apt to produce bulgings at this spot, for the aorta is here very superficial. Aneurisms may, however, affect the vessel in any part of its course, and may 'point' at any part of the chest with which the dilated vessel comes in contact. Further details on these points will be afterwards given. (See Chapter VIII.) In some cases of aortic dilatation and aneurism, pulsation is seen in the supra-sternal notch. PALPATION APPLIED TO THE EXAMINATION OF THE THORACIC AORTA. In health the pulsation of the aorta can sometimes be felt in the supra-sternal notch, but in no other position. Percussion of t lie thoracic aorta. 229 When the vessel is dilated, more especially when a saccular aneurism is in contact with the chest wall, pulsation can often be felt over the position of the sac. When the chest wall is bulged forwards, the alteration in level can often, of course, be detected by the finger as well as by the eye. To detect slight superficial pulsations (those pulsations, for example, which are produced by an aneurismal sac which is in contact with the chest wall, but which has not as yet produced perforation or prominence), the fingers of the right hand should be lightly placed over the seat of the suspected dilatation. In some cases in which the aneurism is deeply seated, and in which there is no superficial pulsation, forcible, deep-seated and expansile pulsation can sometimes be detected by forcibly compressing the chest during expira- tion, between the two palms, one hand being placed on the front and the other on the back of the chest. When the transverse portion of the arch is dilated or aneurismal, pulsation can often be very readily felt in the supra-sternal notch, — the head should be bent well forwards so as to relax the sterno-mastoids, and the forefinger of the right hand placed in the supra-sternal notch, and pushed down- wards behind the manubrium sterni. Vibratile thrills can be felt over the course of the aorta, more especially over the position of the ascending portion of the aortic arch, in some cases of dilatation and aneurism. PERCUSSION APPLIED TO THE EXAMINATION OF THE THORACIC AORTA. Percussion of the healthy aorta }aelds only negative re- sults. At its origin the vessel is overlapped by the pulmonary artery, and even when the percussion note is impaired over the part of the chest corresponding to the root of the aorta, as it is, for example, in very full expiration, the dulness is of course derived from both vessels. After the aorta emerges from under cover of the pulmonary artery, although it lies close under the sternum, its position and outline in health cannot be definitely determined by means of percussion, for on percussion over the manubrium sterni in the healthy 230 Diseases of the Heart. condition, a n:iore or less resonant note is obtained. In the subsequent part of its course the vessel is so deeply situated as to preclude the possibility of detecting its presence by this means of investigation. When the aorta is dilated or affected with aneurism, per- cussion often yields most important results ; the extent and position of the dulness depend, as we shall afterwards see, upon the size and position of the sac, more especially upon its relation to the lung and to the chest-wall. The percussion resistance is often increased over a dilated or aneurismal aorta, the resistance being greatest in those cases in which an aneurismal sac, filled with laminated clot, lies in close con- tact with the chest wall. AUSCULTATION APPLIED TO THE EXAMINATION OF THE THORACIC AORTA. In health two sounds can usually be heard when the stethoscope is placed over the course of the thoracic aorta. Over the ascending portion of the aortic arch these sounds closely resemble the normal heart sounds, only that they are less loud, the first sound more especially being weaker than the first sound as heard over the heart itself Over the descending portion of the thoracic aorta the sounds are usually very faint and distant. The sounds heard over the aorta undergo the same quan- titative and qualitative alterations, which have previously been described in detail in treating of the modifications of the cardiac sounds ; and since the sounds, which are heard over the aorta, more especially those heard over the ascending and transverse portions of the aortic arch, are for the most part composed of the sounds produced within the heart, propagated through the aorta to the ear of the observer, it follows, that alterations of the heart sounds (more particularly those alterations which are due to disease of the aortic valves), will be heard over the course of the aorta. In other words, it is essential to remember that murmurs heard over the aorta are very frequently due to disease of the cardiac valves, and not to disease of the aorta. Ansailtation of the tJioracic aorta. 231 Alterations of the sounds heard over the aorta (both quan- titative and quahtative modifications) may, however, be due to disease of the aorta itself; and in cases of this description, the heart sounds, as heard over the heart itself, may be per- fectly normal. When, for example, an aneurism of the aorta approaches the surface of the chest, the aortic or cardiac sounds are much more clearly and distinctly heard over that part of the chest, which corresponds to the position of the aneurism, than they would be under normal circumstances. In some cases, the change is merely a quantitative one ; in others, a murmur is heard. But I must defer the more de- tailed description of the character of the sounds in cases of this nature until I come to treat of aneurismal and other dilatations. In other cases in which the aorta itself is healthy, the aortic sounds appear to be louder than in health, in conse- quence of the fact that they are more easily conducted to the ear than in the normal condition. When, for example, a solid tumour lies in contact with the aorta on the one hand and with the chest wall on the other, an apparent increase of this description is frequently observed. On the other hand, ap- parent diminution is produced by all those conditions, such as emphysema, for example, which interfere with conduction. I need not, however, go into details with regard to these points, but must refer the reader to what has been already stated with regard to the modifications of the heart sounds. When the aorta is compressed and constricted, a systolic murmur may be generated. THE EXAMINATION OY THE PERIPHERAL ARTERIES. In all cases of cardiac and arterial disease it is of the greatest importance to observe the condition of the peripheral and superficial arteries, and to ascertain the manner in which the circulation is being carried on in these vessels. By observing the colour of the skin we obtain important information as to the condition of the peripheral circulation (both arterial and venous), but this point has been already considered in treating of the physiognomy of cardiac cases. 232 Diseases of the Heart. The radial is the artery which is usually examined, but the condition of the carotids, temporals, brachials, etc., and the character of the pulse in these vessels should also be noted. I mustj therefore, now describe the manner in which we observe the pulse and the characters which it presents both in health and disease. And in order that the subject may be thoroufjhly understood (for it must be remembered that important modifications of the pulse are met with independ- ently of any cardiac or arterial disease) I shall take a some- what comprehensive view of the subject, and shall not limit the description altogether to the alterations which are met with in disease of the heart and aorta. THE EXAMINATION OF THE PULSE, INCLUDING A DESCRIPTION OF THE SPHVG.MOGRAPH. At each contraction of the left ventricle, some five or six ounces of blood are suddenly propelled into the aorta, and a blood-wave is generated, which is rapidly propagated through the arterial system. The temporary distention of the arterial walls which is caused by this blood-wave, can be felt by the finger or measured by the sphygmograph, and is termed the pulse. The exact character of the arterial expansion, i.e. of the pulse, varies in different cases, and depends partly upon the mode of contraction of the left ventricle, and the amount of blood which it propels into the aorta, and partly upon the condition of the arterial system. It is evident therefore that in the examination of the pulse we have an important means of investigating tJie condition of the heart and of the arterial system ; and since the condition of the arterial system is to a large extent regulated by the vaso-motor nerve apparatus, we are enabled, by the observation of the pulse, to obtain in many cases valuable information as to the condition of the nerve tone {i.e. the general tone of the system); the frequency and strength of the pulse being chieflly vauable in this respect. ' Text- Booh of Physiology, by Professor .M. Foster, p. 157. The Examination of iJie pulse. 233 The radial is the artery which is usually examined, and in speaking of the pulse the radial pulse is meant ; but, in cases of cardiac and arterial disease, the condition of other vessels (the carotids, temporals, brachials, etc.) should be noted. MODE OF OBSERVIXG THE PULSE. We observe the characters of the radial pulse by means of— (1) the finger {palpation) ; (2) the eye {inspection) ; (3) the sphygmograph. (l) PALPATION, OR THE EXAMINATION OF THE PULSE BY THE FINGER. The correct observation of the exact characters of the pulse by the finger is a matter of extreme difficulty, and is only acquired by long practice. Since, however, it is the method which is not only always available, but which yields far more useful and important information than any other, the student should spare no pains to make himself master of it. Two or three fingers should be applied over the artery where it becomes superficial at the lower end of the radius, and the condition of the pulse noted as regards — {a) its frequency ; {b) its rhythm ; (^) its volume ; {d) its compressibility or tension ; {e) the special characters of each pulse wave (celerity, dicrotism, etc.) ; the condition of the vessel (in respect to its fulness) during the diastole of the ventricle, i.e. between the beats ; (/) the condition of the arterial coats. {g) la cases of suspected aneurism or intra-thoracic tumour a comparison of the two radial pulses should be made. 234 Diseases of the Heart. (2) INSPECTION OF THE PULSE. In well-nourished individuals the radial pulse is hardly, if at all, visible when the circulation is tranquil ; but in emaciated subjects, and during cardiac excitement, its pulsation can often be distinctly seen. Pulsation is very visible in certain cases of disease, notably in conditions of high tension; in atheroma, where the artery stands out as a rigid, tortuous cord ; and in aortic regurgitation, where the pulsation is visible, jerking, and collapsing, and the artery tortuous (the locomotive pulse). In conditions of vaso-motor relaxation with excited action of the heart, the pulse in the peripheral vessels (the radial for example) may present the visible, jerking, collapsing character of aortic regurgitation ; but the marked (visible, jerking, col- lapsing) pulsation in the large vessels, e.g. the carotids, which is 60 characteristic of aortic regurgitation, is not observed. (3) THE EXAMINATION OF THE PULSE BY MEANS OF THE SPHYGMOGRAPH. The exact characters of the pulse, i.e. of its individual waves, and of their relationship to one another, are graphically demonstrated by means of the sphygmograph. The instru- ment is chiefly useful as an indicator of the manner in which the circulation is being carried on, and of the general con- dition of the vascular system ; it sometimes gives im.- portant diagnostic evidence, as in the earlier stages of chronic Bright's disease (especially the cirrhotic kidney), and in some aneurisms; but it is comparatively useless and superfluous as a means of diagnosing individual cardiac affections. But although its (direct) diagnostic value is limited, it sometimes enables us to form a more correct opinion than we could otherwise of the severity of a lesion or case ; in pneumonia, and typhoid fever for example, it may afford most useful prognostic information, and the same may be said of many cardiac affections. I must repeat, however, that the examina- Sphygmogi'aphic examination of the p2ilse. 235 tion of the pulse by means of the sphygmograph is altogether secondary and subordinate to the ordinary examination by the finger. FORMS OF SPHYGMOGRAPH. Mahomed's modification of Marey's^ Sphygmograph, and Dudgeon's^ Sphygmograph, are the best forms. (Dr W. J. Fleming of Glasgow introduced a 'simple form of transmis- sion sphygmograph' some years ago. I have not had an opportunity of using this instrument, which is described and figured in the Journal of Anatoviy and Pliysiology, vol. xii. p. 144). For home practice or hospital work I prefer Mahomed's modification of Marey's instrument, as I think it permits of more accurate adjustment of the pressure ; but for general practice Dudgeon's instrument is undoubtedly most con- venient ; it is extremely portable, easily applied in any position of the patient, and is only one-third of the cost of the larger instrument. With it excellent tracings may be obtained, and its inventor claims that it gives a more accurate and natural representation of the up-stroke than can be obtained by Marey's instrument.^ ' This instrument is made by Krohne and Sesemann, 8 Duke Street, Man- chester Square, London. ^ Dr Dudgeon's instrument is made by Mr J. Ganter, and may be obtained through any instrument-maker. ' Dr Dudgeon claims the following advantages for his instrument : — r. It magnifies the movements of the artery in a uniform degree, viz. 50 times. 2. The pressure of the spring can be regulated from i to 5 ounces. 3. It requires no wrist-rest, and may be used with equal facility whether the patient is standing, sitting, or lying. 4. With it a tracing of the pulse can be made almost as quickly as the pulse can be felt with the finger. 5. Its sensitiveness is so great that it records the slightest deviation in form or character of every beat. 6. Its construction is so simple, that if accidentally broken any watchmaker can repair it. 7. It is so small [2h by 2 inches), and it is so light (4 oz. ), that it can easily be carried in the pocket. 8. It is only one-third of the price of the imperfect and cumbrous instruments hitherto offered (o the profession. 236 Diseases of J he Heart. DESCRIPTION OF THE SPHYGMOGRAPH. MaJiomed's modification of Mareys Spliygviograph consists of- I. A steel spring, A (see figs. 60, 61, and 62), which rests on the artery, and which moves up and down with each movement of the vessel. One end of the spring, A' (see figs. 61 and 62), is so attached by a hinge to the framework of the instrument that vertical (up and down movement is alone permitted. To the under surface of the free end of the spring an ivory pad. A", is fixed. The ivory pad rests on the arter)-. Fig. 60. — Ma/ioiiied^s Alodification of Mareyi's Sphygmograph. A, points to the steel spring ; A', to its point of attachment to the framework ; B, the first lever ; B', its point of attachment to the steel spring A ; C, the writing lever ; C', its free end, which carries a pen ; C", its point of attach- ment to the framework ; D, the screw for bringing the turned up free end of lever B in contact with lever C ; E, the screw for increasing the pressure ; F, the dial on which the amount of pressure is indicated ; G, the slide carry- ing the strip of smoked paper; H, the clockwork, which is wound up by a screw on the opposite side to that shown in the figure ; I, I, parts of the instrument over which the straps, which fix it to the arm, are passed. 2. An arrangement of levers, by means of which the move- ments of the steel spring {i.e. of the artery) are magnified and recorded on a piece of smoked paper. There are two levers. The lower one, B, is so hinged by its proximal end, B', to the middle of the steel spring, that up and down mo\ement is alone permitted. The free end of this lever iB", figs. 61 and 62) is The SphyginoQ^rapJi. 237 turned up at a right angle, and ends in a rounded or knife-shaped edge. Through the free extremity of this lever, B (just before it terminates in the turned up end, B"), a screw D is passed. The point of the screw is always (by the force of gravity) in contact with the steel spring, which rests on the artery. And since the screw D and the lever B are practically the same, it follows that every mo\ement of the artery is of necessity com- municated to the turned up extremity B", of the lever B. The object of the screw D is to raise or lower the turned up edge of the lever B, so that it may, whatever the position of the steel spring, be in proper con- tact with the writing lever C, in other words, in order that it may always communicate the movements of the steel spring, i.e. of the artery, to the writing lever C. The second lever, C, is so fixed at its distal end, C", to the frame- work of the instrument, that vertical movement is alone possible. The free end of this lever, C, carries a pen which records its movements on a strip of smoked paper propelled past it at a fixed rate by means of clockwork. In order that the movements of the steel spring may be communicated to the writing lever, the knife-edge of lever B must be in contact with lever C, as shown in figure 61. This is effected, as has been already stated, b\' alteration of the screw D. Fh;. 61. Fig. 62. Fig. 61.— Scheme showing the essential parts of the instrument 7vhen in -woi-king ordet — i.e. the turned up knife-edge B" of the short lever in contact with the writing lever C. Every movement of the steel spring, at A", i.e. of the artery, will, when the knife-edge, B", is in this position, be communicated to the writing lever. The letters have the same significance as in fig. 60. N.B. — (The framework of the instrument has been removed). Fig. 62. — Scheme showing the essential parts of the instrument after increase of the pressure. The knife-edged B" is no longer in contact with the writing lever, and the movements of the steel spring A", i.e. of the artery, are no longer communicated to it. In order to put the instrument into working order the knife-edge B" must be raised to the position indicated by the dotted lines. This is effected by means of the screw D. 3. An arrangement by which the amount of pressure exerted by the steel spring on the artery can be regulated and measured. This is a most important part of the instrument, and is the modification made by Mahomed. It consists of an eccentric, E, by depression of which, as shown in fig. 62, a definite degree of pressure can be made upon 2:;8 Diseases of the Heart. the steel spring. The amount of pressure exerted is shown on a dial (F, in fig. 6o) in ounces troy. The eccentric (see figs. 60, 6 1, 62) is depressed by turning the screw E (see fig. 60). 4. A clockwork, H, which propels at a fixed rate a slide G, to which a strip of smoked paper is attached. 5. A framework to which the various parts of the in- strument are fixed, and by means of which the instrument is fastened to the arm by straps (K, K, fig. 65). Dudgeon's Pocket SpJiygmograpJi (see fig. 63) consists of: — I. A steel spring, A (see fig. 64), which rests upon the artery, and moves up and down with each movement of the vessel. One end of the spring (a) is tirmly attached to the framework of the instrument, the other (C) is turned up at a right angle. To the under extremity of the steel spring a button, B, which rests on the arterj-, is fixed ; and to the turned up extremity C a short rod (D) is firmly attached. Fig. 63. — Dudgeon's Sphygmograph. 2. An arrangement of levers by means of which the movements of the steel spring, i.e. of the arter\-, are The Sphymograph. 239 magnified and recorded on a strip of smoked paper propelled by clockwork. At right angles to D, and connected with it by the axle E, rises the upright stem F. Every upward movement of the steel spring causes the upright F to mo\-e forwards. At the top of F is a loop in which a rod K lies. This rod is connected at the axle H with a bent rod having a counterpoise I. When the upright F makes a forward movement, the oblique rod K also swings forwards by the weight of its counterpoise. To the lower end of K the needle L is attached by the hinge M, and its point describes on the smoked paper, which is propelled by the clockwork machinery at a uniform velocity, a graphic representation of the movements communicated to it. Fig. 64. — Scheme showing the different parts of Dudgeon's Sphygmograph. The description of the figure is given in the text. 3. An eccentric, by means of which the pressure can be increased from one to five ounces. 4. A clockwork, by means of which a strip of smoked paper is propelled at a fixed rate under the writing lever. 5. A framework, by means of which the instrument can be attached to the arm.^ ' For further particulars respecting Dr Dudgeon's instrument, see his book, The Sphygmograpli ' !40 Diseases of the Heart. DIRECTIONS FOR TAKING A SPHYGMOGRAPIIIC TRACING WITH MAREY'S instrument.^ I. Place the Patient in proper position. — He should be seated by the side of a low tabic, his arm resting on the pad (a double inclined plane), as represented in fig. 65, the fingers semiflexed into the palm. If the fingers are quite extended the arterj' is too much stretched, and jerking movements of the tendons, which interfere with the tracing, are apt to occur. If the fingers are quite flexed, the rigidity of the tendons prevents the perfect appHcation of the instrument. The position should be as easy as possible, for it is essential that the arm be kept at perfect rest. The shirt sleeve should be turned up ; and it must be loose, lest it interfere with the circulation through the arm. C Fig. 65. — Marey's Sphygmograph applied to the wrist. 2. Mark the exact position of the artery ivitJi ink or pejieil. — The ink line should be prolonged to the ball of the thumb, i.e. below the instrument when /// situ. By this means we can, without removing the sphygmograph, ascertain if the ivory pad is still in proper position, i.e. exactly over the artery. ' For further information on the subject the student is referred to Dr Ma- homed's papers in the Irlcdical Times and Gazette (January 20th, 1872, and fol- lowing numbers), and in Gant's Surgery (vol i., page 52), to which I am indebted for much of my information on the subject, and from which some of the following lules for the application of the instrument are derived. JMarcy's SphygmograpJi. 241 Before applying the sphygmograph, the harmless nature of the procedure must be explained to the patient, for it is of the greatest importance to avoid anything which will excite or disturb the action of the heart. Some persons become considerably agitated, thinking that an operation is about to be performed. (One of my patients left the hospital rather than have the instrument applied.) In such cases a pre- liminary application to a fellow-patient or nurse is advisable. 3. Apply the ifistminent, having previously screwed up the clockwork and placed the pressure at zero. — The ivory pad must be accurately applied over the very centre of that part of the artery which lies at the inner side of the styloid process of the radius. By compressing the vessel at this spot, where it is superficial and rests upon bone, we can be quite certain that the entire pressure of the spring will be exerted upon it. The instrument is then firmly strapped to the arm. The straps should be unyielding — not elastic. The slide carrying the strip of smoked paper is next to be fitted into the frame, Care must be taken that the paper is firmly and evenly stretched. This is best efi'ected by first accurately fitting it and doubling its edges over the frame, then removing and smoking it over a piece of burning camphor, and finally fitting it to the frame again. The paper should not be over- smoked, and the point of the pen must not press too heavily against it, or friction will prevent free movement, and the tracing will be imperfect. 4. Adjust the pen. — The point of the pen is then (by means of the screw D, see figs. 60 and 62) to be brought level with the centre of the strip of smoked paper, as shown in figs. 60 and 65. 5. Regulate the presstire by means of the screw L, until the maximum amount of movement of the writing lever is obtained.^ There is a certain pressure, depending upon the am.ount of expansion which is going on in the artery, at which the tracing is best marked. If the pressure is too ' The reader must not forget that every alteration of the pressure, i.e. every alteration in the position of the steel spring necessitates a fresh adjustment of the writing lever by means of the screw D. 242 Diseases of the Heart. little, i.e., if the steel spring just touches the artery in its ex- panded state, the rise of the lever will be insignificant ; if, on the other hand, the pressure be too great, the artery cannot expand to its full amount, and the tracing will be imperfect, — the up stroke shortened (see fig. 66), and the perfect development of tiie secondary waves of the tracing interfered with. Fig. 66. — Tracing taken iinaer too great pressure. The up-stroke is cut short, and the perfect development of the tracing prevented. If the tracing is satisfactory, the name of the patient, the date, the nature of the disease, and the amount of pressure which is required for {a) the perfect development of the tracing, and {b) the complete obliteration of the pulse in the artery (the latter being the gauge of the strength of the pulse) should be inscribed upon the slip of smoked paper by means of a needle or other fine-pointed instrument, and the tracing rendered permanent by dipping it in a rapidly dr}-ing varnish.^ Character of a good tracing. — In a good tracing the apex (b, fig. 67) is pointed ; and the best tracing is that in which the Fig. 67. — A^or-nal Piilsc J racing. up-stroke is tallest and the apex most pointed. It occasionally happens that the apex is rounded, as in some aneurisms ' The varnish recommended by Mahomed is made by macerating an ounce of gum benzoin in five ounces of rectified spirit ; the mixture, which should be frequently agitated, is allowed to stand for two days, and the clear liquor then poured off from the insoluble constituents of the gum. Dr Dudgeon uses the crystal varnish of photographers, or a varnish consisting of one ounce of gum damar and six ounces of rectified benzoline Marey's Sphyginograph. 243 (see figs. 68 and 69), and in a few cases of aortic stenosis (see fig. 70) ; but this is so extremely rare, that a tracing in which the apices are rounded should always be regarded as imperfect, unless it has been verified by repeated and careful readjustments of the instrument, and by repeated alterations of the pressure.^ Fig. Pressure 2.\ oz. 68. — Aneuris7/i of Left Axillary Artery {left radial tracing). — L. G., set. 63, admitted to the Newcastle Infirmary 7th March 1878, with a large aneurism of the left axillary artery. The apex is rounded ; all the curves are obliterated. Pressure 3 oz. Fig. 69. — Aneu7-ism of Left Subclavian (left radial tracing). — J. M., set. 50, ad- mitted to Newcastle Infirmary 5th September 1878 : all the waves in the left tracing are obliterated. Fit Pressure l^ oz. 70. — Aortic Stenosis. — J. B., set. 51, admitted to Newcastle Infirmary 29th November 1878, suffering from anaemia and dropsy. There was a well- marked aortic systolic murmur ; the left ventricle was not hypertrophied. The pulse tracing seems to show that the murmur was organic. FiG. 71. — Pressure i^ oz. t'lG. 72. — Pressure 25 oz. Fig. 71. — Aortic Stenosis and Dilated Aorta. — J. C, puddler, aet. 25, admitted to Newcastle Infirmary 20th February 1879. The patient had been under observation for four years previously. Marked thrill and loud systolic murmur over base of heart and over aortic region. Heart moderately hypertrophied. Pressure = i|^ oz. Fig. 72.^ — Tracing taking from the same patient with a slightly increased pressure ; the apex is now pointed. ' In most cases of aortic stenosis a pointed apex can be obtained by careful adjustment and regulation of the pressure. (See figs. 71 and 72.) 244 Diseases of the Heart. Dr Galabin points out that 'if the tracing of any pulse taken at a low pressure show a very marked primary summit, whose proportionate magnitude is modified by increase of pressure, then the tracing taken at the higher pressure more closely represents the pulse-wave. The form of trace at the lower pressure may, however, have much significance, and in these cases the whole of the information to be derived from the sphygmograph cannot be compressed into one curve, but requires at least two for its expression, namely, that trace which has the greatest amplitude, and another taken at a higher pressure.'^ The cJiicf points to be attended to therefore in order to get a perfect tracing are : (i) The accurate adjustment of the instrument, and (2) The proper regulation of the pressure. The following tracings, which were taken consecutively from the same pulse, illustrate the eff"ects of different degrees of pressure. Speaking generally it may be said that pulses of high tension require a considerable amount, and pulses of low tension a small amount of pressure for their perfect development. But to this general rule there are some ex- ceptions. In atheroma, for example, the amount of pressure required to obliterate the pulse is usually considerable, the arteries are abnormally full, but the condition is not necessarily one of high tension." In cases of atheroma the development of a pointed apex is often interfered with, unless a small amount of pressure be employed. I n comparing the tracings from diff"erent arteries, — the two, radials, for example, — a procedure which is desirable in all ' yoiirnal of Anatomy and Physiology, vol. x. p. 306. * In the first edition of this lecture I stated that the pulse in atheroma is one of low tension. This is not always the case. I should have said, that for the perfect development of the trace, a low pressure is (as a rule) required ; and that the amount of pressure required to extinguish the pulse in atheroma is not a criterion of the- blood pressure, i.e., the tension of the pulse, for where the vessel is rigid a considerable amount of pressure is required to overcome the resistance of the arterial wall, and it is only after the rigidity of the arterial wall is overcome that the pressure is fully exerted upon the arterial contents. Marey 's Sphygmog raph . 245 cases of supposed aneurism or solid intra-thoracic growth, the best obtainable tracing from each pulse should, in the Jirst place, be taken, all the conditions (with the exception of the pressure) such as the position of the patient, the tight- ness with which the instrument is strapped to the wrist, etc., being so far as is possible the same ; and in this connection it is very important to remember that when the heart's action becomes excited as the result of emotional or other causes, the character of the tracing may be materially modified, as is shown in figs. /T,, 74, 75, and '/6. Tracings slioiild, tJierefore, always be taken if possible during tranquil action of the heart. In the second place, two tracings (one from either radial) should be taken with all the conditions, including the amount of spring pressure, the same. Fig. 73. — Pressure 2^ oz. Fig. 74. — Pressure 2^ oz. Figs. 73 and 74 — Alterations in the Pulse-tracing as ihe result of Cardiac Ex- citement. — A. M., aet. 48, admitted to the Newcastle Infirmary suffering from obscure spinal symptoms. The heart became excited, and the tracing shown in fig. 74 was taken immediately after that shown in fig. 73, the instrument in the meantime remaining in situ. The spring pressure was the same in each case. KKl-vh Fig. 75. — Pressure 3 oz. FiG. 79. — Pressure 3 oz. Figs. 75 and 76. — -Alterations in the Pulse-tracing -which result from Cardiac Excitement. — Figs. 75 and 76 show two tracings from a case of chlorosis. Case : E. F., ret. 19, admitted to Newcastle-on-T>Tie Infirmary 3d March 1878. The tracing shown in fig. 75 was taken on 8th March ; the tracing shown in fig. 76 was made three minutes later, the instrument having re- mained in situ ; the heart had become excited. Pressure in both cases = 3 oz. 246 Diseases of the Heart. DIRECTIONS FOR THE APPLICATION OF DUDGEON'S SPHYGMOGRAPH. Dr Dudgeon gives the following directions for the application of his instrument : — ' I. Wind up the clockwork, used to drive the smoked paper along, by means of the milled button at the back of the clockwork box. '2. Insert one end of the smoked paper (smoked side uppermost) on the right-hand side of the instrument, between the roller and small wheels. '3. Make the patient hold out either hand open and in an easy posi- tion, the fingers pointing towards you (see fig. ']'])^ and direct him not to move the wrist or fingers. Fig. 77 — Mode of apply iu^i^ Dudgeon's Sphygviograph. '4. Ascertain the precise spot where the radial arterj' beats at the wrist, close behind the eminence of the os trapezium. ' 5. Slip the band, the free end of which has been drawn through the clamp, over the paitent's hand. '6. Apply pressure to the spring by turning the spring-regulator so that the number of ounces, or portions of ounces, you wish, is pointed to by the indicator. The pressure may be altered at will when the instru- ment is fixed on the arm. Dudgeons Sphygviograph. 247 ' 7. Place the bulging button of the spring exactly over the artery, its long axis parallel to the course of the artery, the box containing the clockwork resting lightly on the forearm above. '8. Retaining the instrument in its place with the left hand, draw the band through the clamp with the thumb and forefinger of the right hand, holding back the clamp with the other fingers of that hand ; when the requisite tightness has been obtained, which will be known by the point of the needle working freely over the centre of the smoked paper, screw up the clamp with the left hand, so as to fix the in- strument. '9. Set the smoked paper in motion by pushing towards the right the small handle on the top of the clockwork box. ' 10. Let the paper run through, and do not touch the instrument or the patient, unless to support his hand in your own right hand, to secure perfect steadiness. ' II. Catch the paper as it passes out of the instrument in your own left hand. ' 12. Stop the clockwork as soon as the paper has passed.' — The Sphygmograph, p. 67. Having now described the sphygmograph and its mode of application, I will next consider the characters of the normal pulse tracing, and the modifications which occur in it. ANALYSIS OF A SPHYGMOGRAPHIC TRACING. A pulse tracing consists of a series of curves, each one of which corresponds to one beat of the pulse, and each one of which corresponds (in time) to a complete cardiac revolu- tion, i.e., the time which elapses from the commencement of one ventricular systole to the termination of the ventricular diastole. Each individual pulse curve, a to a' (fig. ']i), may be artificially divided into the following parts : — 1. A line of ascent {a to b^. 2. An apex {b). 3. A line of descent {b to a'). This division is convenient for descriptive purposes, but a more natural division is that which separates each pulse wave into two portions (i and 2, fig. 78) corresponding in time to the systole and diastole of the left ventricle respectively. I will now describe each of these different parts. 248 Diseases of tlic Heart. The line of asecnt or upstroke'' {a to b fig. 'j'i) represents the sudden distension of the arterial system which is pro- duced by the contraction of the left ventricle at the com- mencement of the ventricular systole, i.e. when the aortic segments are suddenh' opened. It is probably also partly due to the inertia of the instrument ; and, in some cases, as in atheroma (where the vessels are extremely rigid), to impulse or shock. Pressure 3 oz. Fig. 78. — SpJivi^inographie Tracittg of Norma! Pti/se. — Male, set. 25, admitted to the Newcastle Infirmary suffering from psoriasis, (l.) Line of ascent, up-stroke or percussion stroke = a to b. (2,) Apex = 3. (3. ) Line of descent = ^ to a'; d?= aortic or dicrotic wave ; ^ = aortic notch; ^ = tidal wave. A B = base or respiratory line. l=Systolic portion of the tracing, i.e. with reference to the systole and diastole of the ventricle, not of the artery. 2 = Diastole portion of the tracing. (Note — Dr Mahomed tells me that he thinks the tidal wave in this tracing is rather too sustained, considering the amount of pressure, viz. 3 oz.) The direction of the up-stroke (whether vertical or oblique) depends (chiefly) upon : — 1. The suddenness of the ventricular systole. 2. The condition of the aortic segments. 3. In some degree, the facility with which the blood wave is propagated from the base of the aorta to the radial artery, and 4. The condition of the arterial (radial) coats. In the normal tracing the up-stroke is nearly vertical, for the contraction of the ventricle occurs suddenly, and there is no undue resistance in the aortic segments. When the ventricular contraction is more sudden than in ' It is belter, I think, not to use the term percussion stroke, proposed by Mahomed, for unless the arteries are rendered extremely rigid by atheroma, per- cussion or shock probably takes litt le or no part in the produciion of the up-stroke. Analysis of a Sphygmographic Tracing. 249 health, as it is, for example, in some cases of aortic regurgi- tation, and in conditions of cardiac excitement, the up-stroke is quite vertical, or (in tracings taken with Marey's instrument) it may even slope backwards. (See figs. 79 and 80.)^ Fig. 79. — Pulse-tracing dn7-ing Cardiac Fig. So. — Aortic regurgitation. E.xcitement. Vice versa when the ventricular contraction is slow and hesitating, -as in some cases of cardiac debility; when the aortic cusps are rigid ; when the arteries are obstructed either by internal or external causes, such as the pressure of a tumour, the presence of an atheromatous patch (at the orifice of the innominate in the case of the right radial for example) ; or, when a globular aneurismal dilatation is situated between the heart and the vessel {i.e. the radial), the up-stroke may be oblique. (See figs. 81 and 82.) Pressure \\ oz. Fig. 81. — Aortic .Stenosis. — J. B., Kt. 51, admitted to Newcastle Infirmary 29th November 1878, suffering from anaemia and dropsy. There was a well- marked aortic systolic murmur ; the left ventricle was not hypertrophied. The pulse-tracing seems to show that the murmur was organic, and not hsemic. Pressure 2\ oz. Fig. 82. — Aneurism of /eft Subclavian. — ^J. M., fet. 50, admitted to Newcastle Infirmary 5th September 1878 ; all the waves in the tracing are obliterated. ' In cases of hypertrophy of the left ventricle with high arterial pressure, the ventricular contraction may be laboured and prolonged in order to overcome the obstruction, but the commencement of the contraction is sudden, and the up-stroke veriicdl. 250 Diseases of the Heart. The hcigJit of the up-stroke represents the degree of dis- tension of the vessel, and depends upon — 1. The force and (to a less degree) the suddenness with which the aortic cusps are raised, i.e. upon the force (_and sud- denness) of the contraction of the left ventricle, less the resist- ance offered by the aortic valve-cusps. 2. The extensibility of the arterial coats, which in its turn depends upon the condition of the arterial tunics (their elasticity or rigidity), and the state of the vaso-motor system. 3. The amount of compression which is applied to the artery, i.e. the spring pressure of the sphygmograph. The up-stroke is tall in simple nervous palpitation, and in cases in which a large amount of blood is suddenly thrown into the arterial system by a hypertrophied left ventricle. In free mitral regiirgitation the left ventricle may be considerably hypertrophied, but the up-stroke is short, for in such cases the large leak at the mitral orifice prevents the distention of the arterial system. So, too, in Bright's disease and atheroma, a powerful (hypertrophied) left ventricle may fail to produce a tall up-stroke, owing to the unyielding condition of the arterial wall. Vice versa, the up-stroke is sJwrt where the left ventricle is weak or acting feebly, and in all conditions in which a small amount of blood is being pumped into the arterial system, as in aortic stenosis and mitral lesions. The apex of tJic tracing, or ^\-\q. primary ventricular luavc^ {b in fig. yd>) as it may be termed, is, in the great majority of tracings, — both normal and pathological — pointed ; in fact, as I have previously remarked, a rounded apex is so extremely rare, that any tracing in which the apices are rounded should be regarded with suspicion, and should never be accepted as the best attainable (most perfect) tracing without careful readjustment of the instrument and alteration of the pressure. ' The term 'percussion wave'' is applied to the apex by Mahomed. Analysis of a Sphygmogvapliic Tracing. 251 A rounded apex does, however, occasionally occur. It is met with in some aneurisms ; the angles of the pulse curve are, as it were, flattened out (obliterated) either in the passage of the blood wave through the sac of the aneurism, or by alterations at the mouths of the vessels arising from the sac, or as the result of the pressure of the aneurismal sac on the vessels arising from it. A rounded apex is also seen in some cases of aortic stenosis; but in these cases, and in cases of atheroma, a pointed apex can, I think, usually be obtained by accurate adjustment of the instrument and careful regu- lation of the pressure. The line of descent. — In the normal pulse tracing the line of descent {b to a' in fig. 78) is gradual,^ and is interrupted by one or more secondary waves, the most important of which is the dicrotic. The direction of the line of descent depends upon — {d) the facility with which the blood passes out of the arteries ; {b) the rapidity of the heart's action ; and (to a much less extent) {c) the condition of the arterial coats. In the normal condition of things the blood takes some time to flow from the arterial system into the capillaries, the recoil of the arteries is gradual, and the line of descent is sloping. When the outflow from the arterial system is more difficult than in health, as for example, in the cirrhotic form of Bright's disease, the line of descent is still more gradual. Vice versd when the outflow from the arterial system is very rapid in consequence of a dilated condition of the small arteries and capillaries; and in aortic regurgitation, in which the arteries suddenly collapse in consequence of the back flow through the aortic valves, the line of descent becomes more and more vertical in proportion to the freeness of the outflow and the rapidity of the action of the heart. The dicrotic wave, or the aortic systolic ivave, as it may be called, is usually present in a normal pulse tracing, and ' The line of descent is sloping, because the recoil of the artery is gradual. In this respect there is, therefore, a marked difference between the up-stroke and the line of descent 252 Diseases of the Heart. corresponds to that period of the cardiac cycle which imme- diately follows the closure of the aortic valve cusps : while the point of the tracing which immediately precedes it {e in fig. 78), and which is generally, but not universally,^ believed to correspond in time to the closure of the aortic segments, is termed the aortic notch. Where the vaso-motor tone is very good, and the arterial tension high,— as it is in some healthy persons, — the dicrotic wave is very feebly marked or altogether absent. (See fig. ^l) Fig. 83. — Pulse fracinq; of good tension (/pressure 3 oz. ) The pulse is slightly irregular, but otherwise normal ; the dicrotic wave is scarcely perceptible. The exact cause of the dicrotic wave has given rise to much debate ; but most physiologists are agreed that it is in great part due to the recoil current from the closed aortic valve, — an opinion which is con- firmed by cHnical observation. Dr Galabin, while agreeing that the great cause of the dicrotic wave is a recoil current from the aortic valves, thinks that its production is aided by the inertia of the fluid. - Dr Roy differs from this opinion. As the result of careful experiment, he suggests that the secondar)' waves which appear in the unopened artery under normal blood-pressure, are the result of an active vemii- cular contraction of the muscular coat of the arteries. He completely rejects the theories which would ascribe these undulations to reflected, ' A TVx/ y9^(7.^^/'/2)'J/o/c^l', 4th edition, by Professor Michael Foster, p. 172. * Dr Galabin explains the mode of production of the dicrotic wave in the following manner : — ' The first cause of the dicrotic wave is that which has been very generally accepted as depending upon the aortic valves. For let us con- sider a section of artery close to the valves. When the influx from the heart suddenly ceases at the end of systole, the fluid for an instant continues to flow away out of the section on account of its acquired velocity, and the pressure in the section, therefore, rapidly falls, and the artery contracts. As soon as the velocity of the fluid is checked bythe pressure in front, a reflux takes place, which, being stopped by the valves, causes a second increase of pressure and second expansion. This is propagated as the dicrotic wave into the periphery, and may itself again call out a second similar oscillation or tricrotic wave, which is not unfrequently seen in the pulse. Even in the total absence of aortic valves, the reflux, meeting with the current entering the ventricle, may cause a second Analysis of a Sphygmjgrapliic Tracing. 253 opening and closing waves, etc., or in fact to secondary' waves at all, of whatever character. The tracings which he obtained from the opened arter)' of a rabbit, under a normal blood-pressure, never showed 'the slightest trace of secondary waves superposed on the primary' or pulse wave,' although the instrument he used was quite delicate enough to record them did they really exist.' — Michael Foster's Journal of Phy- siology, 1879-80, p. 76. The dicrotic wave is absent or feebly marked in free aortic regurgitation. (See figs. 84 and 85.) Fig. 84. — Pressure -i\ oz. Fig. 85. — Pressure 3 oz. Fig. 84. — Aortic Regurgitation. — Case: G. A., jet. 56, admitted to Newcastle Infirmar}' 21st February 1878, suffering from shortness of breath and swell- ing of feet. Had been iU for three months. The face was pale and anxious, lips slightly dusky. Double aortic murmur ; heart considerably h}-per- trophied ; apex beat between 6th and 7th ribs, 3 inches below and 2 inches outside left nipple. Considerable hypertrophy and engorgement of right heart. Died 5th March 1878. Aorta very atheromatous ; aortic valves very incompetent ; segments shrunken, turned in towards the ventricle ; coronary arteries much obstructed ; cardiac walls fatty ; left ventricle dilat- ed ; pericardium adherent. The arteries were practically empty during the ventricular diastole. a-^=up-stroke ; (J=apex ; <-= tidal wave ; t/ indicates the position of the aortic wave, which is absent in this tracing. Fig. 85. — Aortic Regurgitation. — Taken from the same patient as No. 84, after ad- ministration of digitalis. The letters have the same significance as in fig. 84. increase of pressure or dicrotic wave, although this will be much less than in the former case. If the fluid in the tubes be air instead of blood or water, its mo- mentum is so small that its velocity is checked instantly at the end of systole, and there is no perceptible dicrotic wave. If, on the contrary, mercurj' be taken, both the dicrotic and succeeding waves become enormous, on account of the great momentum of the fluid, as was shown by Marey. The fluid remaining the same, the oscillation will be more ample the greater the initial velocity, and the more slowly that velocity is checked. Thus dicrotism is promoted by a sudden action of the heart, and also by distensibility of arteries, by lowness of arterial pressure, and by freedom of outflow. I think that in considering this origin of the dicrotic wave, sufficient attention has not generally been paid to the important part played in it by the inertia of the fluid, and to the fact that the aortic valves, although extremely important, are not absolutely essential.' — Journal of Anatomy and Physiolog)', vol. x. p. 303. 2 54 Diseases of the Heart. It is also faintlv marked in some pulses of high tension, and in some cases in which the elasticity of the arteries is much impaired, as in advanced atheroma. It is sometimes greatly exaggerated, and the pulse is then said to be dicrotic (see figs. 87, 88, and 89). Pressure 3 oz. P'lG. 87. — Dicrotism. — A. H., a?t. 32, admitted to Newcastle Infirmary 21st March 1878, with an enormous scrofulous kidney. There were occasional rigors. This tracing was made during a rigor, the temperature being 100° F. Fig. 88. — Irregular and Dicrotic Pulse in Pneumonia. — ^J. R., set. 68, admitted to the Newcastle Infirmary 28th December 1878. Died 31st December. Croupous pneumonia, limited to the upper lobe of the right lung. No cardiac affection. Fig. 89. — Dicrotic Pulse from a case of Rheumatic Fever. Degrees of dicrotisvi, and t/ieir significance. — Various degrees of dicrotism occur, 'to which terms have been ap- plied indicating the relation of what is known as the " dicrotic notch" to the respiratory line of the tracing' (Mahomed).^ ' Cantos .Surgery, vol. i. p. 56. The Dicrotic JFave. 255 They may be said to represent the relative condition of the artery at the point where the sphygmograph is appHed, as regards its fulness or state of distention at the commence- ment, and at the termination of the ventricular systole re- spectively. (a) When the dicrotic wave is well marked, but the aortic notch C is above the base line A B (see fig. 90), the pulse is called dicrotic. In this condition the artery is more dis- tended at the end of the ventricular systole than it is at the commencement. Fig. 90. — Dicrotic Pulse. ( After MaJiomed. ) A B,=base line ; C, = aortic notch. Fig. 91. — Fully Dicrotic Pulse. (After Mahomed.) A B,=base line; C,= aortic notch. (^) When the .aortic notch C reaches the level of the respiratory or base line A B, the pulse is called y>///^' dicrotic. In this condition the artery is apparently no more distended at the end of the ventricular systole than it is at its com- mencement, and it is apparently less distended than it is during the ventricular diastole^ (see fig. 91). (c) When the aortic notch C sinks below the level of the ' This does not of course imply that the arterial system, as a whole, is more empty at the end of the ventricular systole than it is during the ventricular diastole, but simply that the vessel at the point where the observation is taken, apparently presents such a condition ; I say apparently, for the depression of the curve at the end of the ventricular systole is doubtless in part due to the sudden fall of the lever itself 256 Diseases of t lie Heart. respiratory line A B, the pulse is called Jiyperdicrotic. (See fig. 92). In this condition the artery (at the point of obser- vation) is appare7itly less distended at the termination of the ventricular systole than it is at its commencement. Fig. 92 — HyperJkrotic Pulse. { After Malioiiied. ) A B, = base line ; C,=aortic notch. When dicrotism is well marked, i.e., when the pulse is fully dicrotic, each cardiac cycle is (apparently) attended by two pulse beats, hence the term dicrotic, or double pulse. Tlic conditions ivhich favour dicrotism arc : — 1. A low condition of arterial tension. 2. Freedom of outflow from the arterial system, i.e. through the capillaries. (Both of these conditions are usually due to one and the same cause, viz., loss of vaso-motor tone). 3. A sudden sharp ventricular systole. 4. Elasticity of the arterial walls. According to Dr Burdon Sanderson, 'dicrotism is cha- racteristic of that condition of the circulation in which the arterial pressure is diminished, while the venous is increased. It denotes that the capillary current, instead of being con- stant in its rate of movement, is markedly accelerated during diastole, and retarded during the diastolic interval.' Dr Roy thinks that the dicrotic wave of fever, which is associated with reduced blood-pressure, is due to a secondary and, most probably, reflected wave. He found that any considerable reduction of the medium blood- pressure, from whatever cause, leads to the appearance of a dicrotic pulse-wave in tracings both from the opened and unopened arter^^ This form of dicrotism,' he savs, 'must not be confounded, as is often Causes of Dicrotisin. 257 done, with those undulations more or less marked, which gave to the pulse curve in health its characteristic outline. The dicrotism from re- duction of blood-pressure, as it is seen in tracings from the now opened arteiy, is characterised by the fact, that it does not disappear when the extra-arterial pressure is raised nearly as high as the blood-pressure, showing that it is really due to a secondary and most probably reflected wave.' — Micliacl Foste7''s yoiirnal of Plivsiology, 1S79, 1880, p. 80. Clinically, the pulse is dicrotic in cases in which the nerve tone (vaso-motor system) is feeble. Many persons who apparently enjoy good health have dicrotic pulses Such persons are easily 'knocked up,' are unable to undergo any severe and prolonged strain, and are most unfavourable subjects for an attack of continued fever ; in them a severe pneumonia, or an attack of typhus, would almost certainly be fatal. A comparatively slight elevation of temperature in such persons causes the pulse to become />///)' dicrotic or even hypcrdicrotic. (See figs. 93, 94, 95.) Fig. 93. — Pressure 3 oz. Fig. 94. — Pressitre 3 oz. Fig. 95. — Pressure 4 oz. Fig. 93. — Dicrotism. — A. H., £et. 32, admitted to Newcastle Infirmary 21st March 1878, with an enormous scrofulous kidney. There were occasional rigors. This tracing was made during a rigor, the temperature being 100" F. A draught of hot milk was administered, and the tracing, shown in fig. 94, was taken. Tracing fig. 95 a few minutes later. Fig. 94. — HyperdicrotisDi. Fig. 95. —Hyperdicrotism. The great clinical condition with which dicrotism is associated is pyrexia. Where a considerable elevation of temperature (I02°-I04° Fahr.) continues for some time, as in enteric and typhus fever for example, the pulse usually becomes dicrotic. A dicrotic pulse under such circumstances indicates the free administration of stimulants. Hypcrdicrotism is (as a rule) only seen in cases of high fever with great exhaustion, but in debilitated subjects it may, as I have previously remarked, be produced by slight R 2^^ Diseases of the Heart. elevations of temperature. In the hyperdicrotic pulse the second (dicrotic) beat is cut short by the up-stroke of the ventricular systole of the next beat. If the rapidity of the hyperdicrotic pulse is increased the second beat is lost altogether, and the pulse is then said to be mojwcrotic. (See fig. 96.) Fig. 96. — Monocrotic Pulse. (After Riegel.) The prcdicrotic, true tidal, or second ventricular systolic wave. Between the apex of the tracing and the aortic notch a second wave (see fig. 78) is often, but not always, seen, Dr Mahomed thinks that it corresponds to the steady onward passage of the blood which results from the ventricular systole, hence he has termed it the true tidal wave. It is sometimes called the predicrotic w'dLWQ, because of its relationship to the dicrotic wave. It may, I think, with advantage be termed the second ventricular systolic wave, for it occurs after the apex or first ventricular systolic wave, and during the systole of the ventricle. The essential condition, which favours the production of the second ventricular systolic wave, is increase of the arterial tension during the ventricular systole. This condition (in- creased arterial tension) is usually due to difficulty of arterial outflow as in Bright's disease (see figs. 97 and 98), and in atheroma (see fig. 99); but it may also result from an excessive amount of blood being propelled into the arterial system at each ventricular systole. An excellent clinical example of the latter condition is seen in aortic regurgitation, in which a powerful and dilated ventricle propels a large quantity of blood into the arterial system, producing high tension during systole, with a well-marked predicrotic luave, but in which the The Predicrotic Wave. 259 arterial pressure during the ventricular diastole is extremely feeble.^ J'l-t'ssiirc 3 oz. Pressure 4 oz. F'lo. 97. — Chronic Brighfs Disease. — I), (.i., s-t. 40, admitted to Newcastle Infirmary 5th September 1878, sutit'ering from renal dropsy (large white kidney). The pulse is one of high tension ; the tidal wave is strongly marked. Fin. 98. — Acute Bright' s Disease. — Tidal wave strongly marked, from a patient admitted to the Newcastle Infirmarv under the care of Dr Drummoncl. Fig. 99. — Atheroma and Aneurism of Aortic Arcli. — J. D., set. 52, admitted to Newcastle Infirmary 2lst February 1878, suffering from aneurism of the ascending portion of the aortic arch and atheroma. The tidal wave is very strongly marked. There was no perceptible difference between the two pulses. Vice versa the second ventricular systolic wave is absent in those cases in which the arterial tension during the ventricular systole is low. Now, low tension during the ventricular systole may be due either to an insufficient amount of blood being pumped into the arterial system during the ventricular contraction, a condition which is seen in cases of cardiac weakness, mitral disease, etc. ; or, it may result from an abnormally free outflow from the arterial system during the ventricular systole, a condition which is ' Dr Galabin (forrtierly) supposed that the separation of the primary, or so called ' percussion ' and tidal waves did not really exist in the artery, but was produced in the trace by the velocity acquired by the sphygmograph in the sudden primary up-stroke. Further observation, Restates, 'has convinced him that, although this explanation applies to many cases, it yet does not express the whole truth, and that in some instances at least there is a real first secondary wave or oscillatory expansion in the artery, i.e. the tidal or predicrotic wave.' — yournal of Anatomy and Physiology, vol. x. p. 299. 26o Diseases of the Heart. due to a dilated condition of the small arteries and (?) capil- laries. In such cases the pulse rapidl}' falls a\va\' during the ventricular systole, in other words, after the first distention of the arterial wall there is a quick and rapid collapse, which is only arrested by the occurrence of the dicrotic wave; and this is, as we have seen, chiefly a recoil wave from the closed aortic valves. A rapid collapse of this description is best marked in the dicrotic and hyperdicrotic pulse of fever, and in con- ditions of vaso-motor debility and relaxed vessels. Hence it will be easily understood why in these cases the second ventricular systolic wave is not present. h IG. \oo.— Irregular Fiilse in mitral regurgitation, with hypertrophy of the Left Ventricle. — In the tallest curves the tidal wave, a, is well-marked, while it is absent in the smaller ones. The letters <^7. a. point to the predicrotic wave. Pressure 4^ oz. Fig. ioi. — General Atheroma. — J. U., a?t. 60, admitted to Newcastle Infirmary 2 1 St October 1878. The radials were very tortuous and rigid ; there was no valvular lesion. The tidal wave only occurs every alternate beat. It not untVequently happens that the predicrotic wave is present in some pulse curves of a tracing, but absent in others. This condition, which depends of course upon the fact that the arterial pressure during the ventricular systole is greater during some pulsations than during others, is especially frequent in mitral stenosis, in which condition a varying amount of blood is apt to be discharged into the cavity of the left ventricle, and thence into the arterial system. (See fig. 100.) Occasionally the predicrotic wave occurs every alternate beat, as show^n in fig. loi ; in that case the irregu- larity was probably due to nervous causes. The Predicrotic W'az'c. 261 Other secondary waves sometimes occur in the lower part of the Hne of descent. Their exact cause is obscure, but so far as is at present known, they are of little practical importance. These waves are probably as a rule due to the inertia of the instru- ment. Occasionally a small wave is seen to occur immediately before the up-stroke, i.e. immediateh' before the contraction of the ventricle. Possibly it may be due to the contraction of the left auricle. Respiratory or base li)u\ — In a normal tracing the lowest points of the up-strokes of succeeding pulse waves are on the same horizontal plane (see hg. "'i), and a line drawn through the bases of the up-strokes is called the base or respiratory line. The latter term (respiratory line) is applied to the base line because inspiration and expiration exert, sometimes even in health, but notably in some cases of disease, a marked influence upon it. During a full and sudden inspiration the arterial tension is lowered, and the base line falls ; during expiration, on the contrary, the arterial tension is increased, and the base line rises. In cases of spasmodic asthma and severe dx'spncea the base line max* be very uneven. (See figs. lOi, 102.) Preisiirc 3I 01. Fig. 102. — Uneven Respiratory Line. — |. K., itt. 31, adniittecl to Newcastle Infirmary 26th December 187S, sufterinc; from acute bronchitis. Fig. 103. — Uneven Respiratory Line (from a ease of Spasiiiodie Astliina). The tracing was taken during the paroxysm. 262 Diseases of the Heart. In the normal pulse-tracing, during ordinary (tranquil) respiration, each consecutiv'^e pulse curve is an exact repeti- tion of the preceding one; in other words, the pulse is regular in time, the different pulse waves are equal in volume, and the individual character of succeeding pulse curves, in respect to the different parts of which they are composed, is the same. When the pulse-tension is low, or when the respiration is active, succeeding pulse curves are seldom quite identical, but are more or less modified by inspiration and expiration, as described above. Having analysed the normal pulse tracing, and described the more important modifications which it undergoes, I will next proceed to consider the character of the pulse in health and disease. THE FREQUENCY OF TME PULSE. The frequency of the pulse is determined by counting the number of pulsations which occur in a minute. To insure accuracy, the pulse should be counted for a whole minute, and not for a quarter of a minute, as is sometimes done. In some cases in which the pulse at the wrist is very feeble, the frequency of the cardiac contractions can be best deter- mined by auscultation over the praecordia. The exact frequency of the pulse can also be determined by means of the sphygniograpb. Mahomed's modification of Marey's instrument is so constructed that four inches of the shde are propelled past the point of the writing lever in ten seconds. In order, therefore, to ascer- tain the frequency of the pulse per minute, the number of pulse waves in four inches of the tracing must be multiplied by six. Dudgeon's instru- ment is also constructed, so that six times the number of pulsations, traced on the slip of paper, give the number of beats per minute.' In counting a veiy rapid pulse, Dr Abbot describes, in the Neiu York Medical Record for August 12, 1882 (quoted in the Medical Times and Gazette., September 30, 1882), a method which he adopted for counting the heart's action during some experiments he performed with alcohol on birds. He found that he was unable to count by the usual mode ' These measurements only hold good so long as the slide is travelling at full speed. To insure accuracy, therefore, the clock-work should be fully wound up before the tracing is taken. The Frequency of the Pulse. 26 v) when the cardiac contractions exceeded 240 per minute, whereas, by the method he now describes, he easily counted 280. ' During a definite part of a minute, usually one-fourth, dots were made with a lead pencil upon a sheet of paper, syitchronous with the hearfs beats, as heard over the cardiac region. The dots were then counted. A pulse oi four hundred could be taken in this way, provided each pulsation were distinct enough to be discriminated by the touch. The indistinctness of the separate pulsations alone fixes the limits to the use of this method, as the human Jiand is capable of making intelligently and with accuracy at the rate of 450 dots per minute, for thirty seconds, which rate is probably beyond not only that of the human heart, but also of the pulse of any of the lower animals available for experiment. I have had a sufficient experience with this method,' he says, 'to know that it is of practical value, especially with children. All movements, whether of the body or not, that can be seen, felt, or heard, can be thus counted up to 400 or 500 per minute, provided that they are sufificiently distinct to be discriminated.' Frequency in health. — The normal frequency varies in dif- ferent individuals, and in the same individual under different circumstances. The average normal rate in the adult male in a state of rest is 72, but there are many exceptions. In some persons the pulse rate is habitually as high as 100, in others as low as 50. In practice, therefore, such idiosyncracies must be kept in view. The pulse is quicker in children than in adults, but it quickens slightly again in old age ; it is quicker in women than in men. The pulse rate is increased by active exercise (bodily or mental). It varies, too, with the position of the body, being quicker in the standing than in the sitting, and in the sitting than in the recumbent posi- tion. Its frequency also varies with the time of day, being lower in the early morning hours. It is decreased during sleep and increased after a meal. It varies with the tempera- ture of the body, and is to a slight extent influenced by the atmospheric pressure. The frequency of the pulse is also profoundly influenced by emotional disturbances, and by the mental condition, hence it is often difficult to get a proper estimate of the pulse-rate in children and nervous persons, the mere presence of the doctor being sufficient to increase the frequency by 10, 20, 30, or even 40 beats. Due allow- ance must of course be made for this and other disturbing- 264 Diseases of tJic Heart. causes. It is often a good plan to count the pulse at the end of the visit, or at all events to allow sufficient time for any temporar\' alteration in the pulse-rate to have dis- appeared. TABLE OF THE AVERAGE PULSE RATE AT DIFFERENT AGES. Foetus in utero, Child newly born, 1st year, „ 2d year, „ 3d year, 7th — 14th year. 14th — 20th year, 2 1 St — 60th year, Old age, about 140 140—135 120 — 1 10 105 — 100 100 — 85 85— 80 80— 72 70— 75 75- 80 Alterations in the pulse-rate, ivJiicli oceiir in disease. The pulse-rate may be either increased or diminished by disease. The pulse-rate is increased in : — I. Pyrexia (increased temperature). — As a general rule the amount of increase varies with the height of the tem- perature. According to Dr Aitken, an increase of tem- perature of one degree above 98° Fahr. corresponds with an increase of ten beats of the pulse per minute, as shown in the following table : — Temp. Fahr. Pulse-rate. Temp. Fahr. Pl Ise-rate 98° 60 103° I 10 99° 70 104° 120 100° 80 105° 130 101° 90 106° 140 102° 100 Exceptions. — In some cases of typhoid, especially in its earlier stages, and in meningitis, the pulse may be slower than natural. At the commencement, too, of some cases of pericarditis the frequency of the pulse is diminished — (Stokes). 2. Conditions associated zuit/i extreme debility.— This is chiefly the case where there has been some previous elevation of temperature, or where the nerve irritability of the heart is increased. Increased Frequency of the Pulse. 265 3. Cases in ivhich the vagus is paralysed or the cervical sympathetic irritated — In these cases the nerve balance of the heart is deranged, and the pulse-rate increased. In a few cases (as for instance, in exophthalmic goitre in which the sympathetic is irritated, and in the later stages of basilar meningitis, in whicli there is probably paralysis ot the vagus), the nerve derangement depends upon organic disease ; but in the large majority of cases, as in hysteria, in which affec- tion the pulse frequency may be enormousl)' increased, the condition is a functional one. 4. Some cases of organic cardiac disease, especially mitral regurgitation (see fig. 104), and (to a less extent) in aortic regurgitation (see fig. 105). Pressure 3 oz. Fig. 104. — Mitral RegurgUat ion. — M. A. C, aet. 16, admitted to Newcastle In- firmary 24th January 1878, suffering from cough and shortness of breath, dating from an attack of rheumatic fever two months previously. Heart's action very rapid (120-130). The first sound appeared to be reduplicated ; a systolic murmur was audible at the apex when the heart became slower. Fig. 105. — Pulse tracing from a Case of Aortic Regurgitation ^ The Clinical Significance of Increased Frequency of the Pulse, Increased frequency of the pulse, when not merely tem- porary, is very suggestive of pyrexia ; it is, however, per se, an unreliable sign of fever, for, on the one hand, fever may be present without any increase (a diminished pulse-rate being, as I have already pointed out, sometimes met with, as in the earlier stages of typhoid and in meningitis) ; and, on the other, increased frequency of the pulse may occur without 2 66 Diseases of the Heart. fever, or even with a low temperature, as in pro-agonistic collapse. In order to ascertain the cause of the increased frequency of the pulse, the first step is to take the tempera- ture. If there is no pyrexia, the causes mentioned under heads 2, 3, 4 must be looked for. A slow pulse may be due to — 1. Functional derangement of the heart. — This is pro- bably the cause of the slow pulse which occurs in jaundice, in some cases of gout, etc. Non-febrile jaundice usually produces a retarded action of the heart and diminished arterial tension. The pulse may fall to 50, 40, or even 20 beats in the minute, and it may also be irregular. Dr Wickham Legg and others believe, that the slowness of the pulse is produced by the presence of unchanged biliaiy acids in the blood. Dr Murchison has seen a slow pulse (36-60 per minute) in cases of hepatic disease in which there was no jaundice. 2. Organic lesions of the heart, such as fatty degenera- tion of the left ventricle and aortic stenosis. In the former case (weakness of the ventricular wall) a slow pulse is perhaps exceptional, and is only seen when the patient is at rest. Any exertion which throws a strain on the beat, is attended in these cases with a quick, rather than with a slow, pulse. In the latter case (aortic stenosis) the left ventricle has difficulty in emptying itself, its contraction is prolonged and somewhat laboured, and the frequency of the pulse is diminished. 3. Lesions of the nervous system, in which the cardio- inhibitory centre in the medulla or the branches of the vagus which pass from that centre to the heart are irritated (stimulated). In some cases the condition is a temporary (functional) one, as for example, in those cases in which a slow pulse is associated with a neuralgic headache (megrim); in others, as for example meningitis (in the earlier stages of which the pulse may be abnormally slow), the lesion is organic. 4. The rapid defervescence of fever ; the pulse-rate may in these cases rapidly fall from a high rate to a point much below the normal. DimmisJied Frequency of the Pulse. 267 5. Reflex stimulation of the cardio-iiiJiibitory centre in the medtiUa. — The reflex impulse may in all probability be generated by powerful stimulatio*i of any peripheral nerve ; but it most frequently arises in the alimentary tract. The slow pulse which is so frequently seen in the earlier stages of typhoid, is probably due to reflex inhibition of the heart^the local lesion of the intestine stimulates the mesenteric nerves, producing an impulse which travels to the medulla, and is reflected down the vagus to the heart. TJie Clinical Significance of a Sloiv Pulse. A slow pulse per sc {i.e. without any associated signs or symptoms) is of little practical importance, the most frequent cause (provided that it does not depend upon idiosyncracy) is a temporary functional derangement of the heart. The possibility of the condition being due to irritation of the vagi must be remembered, and the symptoms of disease at the base of the brain or in the course of the vagus looked for. In other cases {i.e. where there are associated signs and symptoms) the clinical significance of a slow pulse entirely depends upon the cause of the condition, and the prognosis must be guided accordingly. Variability of the pulse-rate. The pulse-rate is in some cases liable to very marked fluctuations. In the convalescent stage of fevers, for example, and in conditions of debility, the pulse-rate is very variable ; these changes are readily produced by any trivial movement or mental excitement. I have noticed the same liability to rapid changes in the pulse-rate in the earlier stages of some cerebral cases. Extreme variability of the pulse-rate has also been noticed after concussion of the spine. ^ ' Dr Guinoiseau, quoted in the Medical Times and Gazette, relates in the Bulletin de Th^rapeutiqiie, February 28th 1882, the case of a man who had received a concussion of the spine from a fall from a carriage on May 9th, 1881. lie recovered, and was able to resume his occupation, which was laborious; but a peculiarity in his pulse remained. Examined on October 8th, it was found that his pulse was 49 when recumbent, 73 when seated, and 109 when standing ; and on November ist the pulse-rate in these positions was respectively 45. 57, and 77. 268 Diseases of the Heart. THE RHVTH>[ OF THE PULSE. The normal pulse (during tranquil respiration) is perfectly regular (the individual pulse waves being of the same duration and volume, and presenting the same features as regards individual curves) ; but departures from the normal are com- mon, indeed in some persons who enjoy perfect health, the pulse is habitually irregular. Such idiosyncracies are more common in old than in young people. The alterations in rliythvi 7u/iic/i occur in disease can of course be observed by the finger, but are best studied by means of the sphygmograph. They ma\- consist of altera- tions in time, alterations in volume, or differences in the sphymographic characters of the individual pulse curves. Time irregularities. — P\\\ degrees of time irregularity are met with. In some, the alteration is only occasional, occurring every ten, twenty, or thirty beats ; in others, the normal rhythm of the pulse is very much altered or entirely lost. (See fig. io6.) Fir,, 106. — Extreme iri-ei;ularity of the pulse from a Case of Pneumonia. Five pulse waves are shown in the tracing, which was taken twenty-four hours before death. The irregularity sometimes consists in the omission of a beat (see figs. 107, 108) ; the pulse is then said to be 'inter- mittent.' Intermission of the pulse ma\' be due either to arrest of the contraction of the left ventricle- a condition which is not uncommon as the result of simple nervous derangement, and is then of comparatively little importance ; or, it mav be owing to the fact that some of the ventricular The R/iyt/uH of the Pulse. 269 contractions fail (are too feeble) to raise the aortic valves and send into the arteries a pulse wave of sufficient strength to be felt at the wrist. Fu;. 107. — Intermittent Pulse. ssnre 4 oz. Fig. 108. — hiterniittent Pulse. — J. B., a?t. 38, admitted to the Newcastle Infirmary nth July 1878, suffering from mitral regurgitation. The heart was much hypertrophied. Tracing made 6th January, when patient was much im- proved and attending as an out-patient. This latter condition, which is a very serious indication of heart-failure, is chiefly met with in those cases in which the heart-walls are degenerated (dilatation, fatty and fibroid degeneration), but is also seen in some mitral lesions. M Marey, quoted by Mahomed, Gufs tlospiial Reports, 1879, P- 397> gives the following explanation of this condition : — ' In a heart in which mitral regurgitation occurs, blood is forced out of the ventricle in two directions during systole ; one portion passes through the aortic orifice, the other is driven backward into the auricle. Now, when the heart is dilated, it sometimes occurs that the ventrical contraction is not of suf- ticient strength to overcome the arterial resistance and raise the aortic valves ; it finds it easier to force all the blood backwards through the incompetent mitral, which thus plays the part of a safety valve. Meantime this intermission, which is caused in the pulse, allows time for more blood to flow out of the arterial system through the capillaries, and when the next contraction of the heart occurs, it finds the arterial pres- sure considerably decreased, and it is now able to open the valves and cause another pulse-wave to pass through the arteries." 2 70 Diseases of tJie Heart. In some cases the irregularities occur at fixed intervals, i.e. every two, three, or four beats. One of the most inte- resting- of these is the pulsus bigcuiinus of Traube, in which the pulse waves run in pairs. (See figs. 109 and 1 10.) In other cases three pulsations occur together in a group, constituting the so called pulsus trigcuii)ius. (See fig. in.) Fig. 109. — Pulsus bige minus Fig. 1 10. — Pulsus bis^oninus. Fig. 1 1 1 . — Pulsus tris^eniimus. Irregularity in volume. — Irregularities in volume (see fig. 112) depend upon the fact that unequal quantities of blood are discharged into the arterial system at different contractions of the left ventricle. The condition is usually associated with irregularity in time, for when the time between the ventricular contractions varies, the amount of Irregularity of tJie Pulse. 271 blood which the left ventricle has to discharge will be apt to vary too. KiG. 112. Differences in the sphyginograpliic cJiaracters of ijidividiial pulse waves depend upon differences in arterial tension, which in their turn may be due either to — I. Different quantities of blood being propelled during successive contractions of the left ventricle into the arterial system, the causes of which condition I have already considered. Pressure 3f oz. Fig. 113. — Uneven Respiratory Line. — J. R., ret. 31, admitted to Newcastle Infirmary 26th December 1878, suffering from acute bronchitis. 2. The effects of respiration. During tranquil respiration the respiratory or base line is, as I have previously stated, a straight line. During deep inspiration and expiration, even in health, and in many pathological conditions in which the respiratory movements are profoundly affected, the ' base line' becomes very uneven (see figs. 113 and 1 14), and the sphygmographic character of successive pulse waves is 272 Diseases of the Heart. different ; expiration increases the pulse tension and lessens the frequency of the pulse ; inspiration lowers the tension and increases the Ac qucnc}' Fig. 114. — Uneven Respirato)y line (/rem a Case of Spasmodic Asthma). The tracing was taken during the paroxysm. In extreme cases the pulse-wave may be entirely absent during inspiration. This is the pulsus paradoxicus of Kuss- maul. The most striking examples of this condition are seen where fibrous adhesions pass between the thoracic parietes and the roots of the aorta and great vessels. During a full inspiration these fibrous bands are stretched, the vessels are constricted, and the pulse-wave is unable to reach the wrist. The pulsus paradoxicus has also been noted in cases of pericarditis without constricting adhesions ; also in cases of stenosis of the air-passages. I Fig. 115. — Geyieral Atheroma. — J. I),, at 60, admitted to Newcastle Infirmary 2 1 St October 1878. The radials were very tortuous and rigid ; there was no valvular lesion The tidal wave only occurs every alternate beat. 3. Differences in the resistance which the blood stream meets with in the peripheral vessels. This cause is proba- bly rare, but it is difficult to account for such a pulse tracing ' At the beginning of inspiration the arterial pressure falls ; it soon, howe\er, begins to rise, but does not reach the maximum until some time after expiration has begun. The fall continues during the remainder of expiration, and passes on itito the succeeding inspiration (Foster, page 344). In speaking of the cause of the respiratory undulations, Foster says, * We may conclude then, that the respiratory undulations of blood-pressure are of complex origin, being partly the mechanical results of the thoracic movements, possibly also produced by the alternate expan- sion and collapse of the pulmonary alveoli, but probably, in addition, brought about by a rhythmical variation of the vascular peripheral resistance, the result of a rhythmical activity of the vasomotor centre. ' —Third edition, p. 348. Irregiilaritv oj the Pulse. 2y2> as that shown in fig. 115), unless we suppose either a rh}'th- mical difference in the strength of the successive cardiac con- tractions, or a rhythmical difference in the peripheral resist- ance ; in both cases the primary cause is evidently nervous, and I see no reason why a rhythmical alteration in the peri- pheral resistance due to vaso-motor causes might not occur. TJic clinical significance of inequalities of rhythm depends entirely upon the cause of the condition. Occurring /^r j-^, without any associated signs and symptoms of disease, the condition is of no practical importance. When there are other signs and symptoms the prognosis depends entirely upon their cause. The chief pathological conditions associated luith irregu- larities in time and volume are — I. Functional derangements of the heart, such as are pro- duced by hysterical conditions, venereal excess, gout, tobacco, tea, etc. Physiologists have shown that when the excised heart is fed with rabbit's serum its action is apt to become intermittent. This in- termittence is possibly due to the chemical action of the serum. 'Various chemical substances in the blood ("natural or morbid),' says Michael Foster, 'may thus affect the heart's beat, by acting on its muscular fibres, its reflex or automatic ganglia, or its intrinsic inhibitory apparatus.' ' 2. Mitral lesions, both stenosis and regurgitation, especially after compensation has failed. (See figs. 116, 117, 118 and 1 19.) l^iessiire 3| oz. I-IG. 116. — Irregularity of the pulse. — W. M., a-t. 50, admitted to Newcastle In- firmary 30th November 1S78, suflering from the usual symptoms of mitral disease. The heart's action was extremely irregular. The left ventricle was much hypertrophied. There was no iheumatic history. The symptoms were of two months' duration. ' A Text-Book of Physiology, third edition, p. 178. S 2 74 Diseases of the Heai't. Fu;. 117. Figs, i 16 and 117 were two consecutive tracings taken on loth December, after the patient had improved under digitalis The intermittent action of the heart is well shown in fig. 117 Fig, Pressure 4 oz 118 — Mitral Regurgitation. — S B , jet. 58, admitted to Newcastle Infirmary 25th February 1878, suffering from cardiac dropsy. There was a well- marked mitral systolic murmur, which disappeared under treatment. The heart was considerably enlarged (hypertrophied and dilated). I Press t4it 3 oz Fig. 119. — Irregular and Jnterinitteitt Pulse — O. M , £Pt. 40, admitted to the Newcastle Infirmary suffering from cardiac dropsy. The heart was very much enlarged ; apex beat 4^^ inches below and 3 inches outside left nipple ; systolic mitral murmur. There has been a good deal of debate with regard to the rhythm of the pulse in mitral stenosis. The majorit)' of observers are, however. agreed — and with their opinion I entirely concur — that the pulse is irregular. Dr Sansom — than whom no better authority could be quoted — says, ' We may conclude, therefore, that a pulse tracing which shows irregularity in the diastolic periods, sometimes missed pulsations, and, as described by Dr B. Foster, the occasional appearance of a small abortive pulsation in the line of descent, is very strong evidence of the existence of mitral stenosis.' — {Diagtiosis 0/ Diseases 0/ the Heart, p. 269.) Dr Mahomed, who was, I believe, the first to describe this peculiar rhythm as characteristic of mitral stenosis, has since somewhat modified his views. The Vol It me of the Pulse. 275 He says, 'Although it is very commonly present in this disease, perhaps more commonly than in any other valvular lesion, nevertheless it is not so much a sign of stenosis of the valves as of dilatation of the ventricle. It is true, that in the typical cases of mitral stenosis the ventricle is not dilated, but I am unable to say whether this irregularity only occurs in cases in which dilatation exists.' — Gufs Hospital Reports, 1879, p. 401. 3. Degenerations of the cardiac walls. In cases of fatty and fibroid degeneration, and, in fact, in all conditions in which there is much degeneration of the left ventricle, the heart's action may be very irregular. 4. Some affections of the central nervous system, such as meningitis, in which alterations in the condition of the intra- cranial circulation, such as result from sudden changes in position, etc., may cause alterations in the rhythm as well as in the rate of the heart's contractions. THE VOLUME OF THE PULSE. The vohnne of the pulse, which depends upon — (i) the size of the artery (radial, carotid, etc.) which is being ex- amined ; (2) the amount of blood which is propelled into the artery at each ventricular systole ; and (3) the tonicity of the arterial wall, i.e. the condition of the vaso-motor apparatus, — may be appreciated by the finger, but is accurately measured by means of the sphygmograph. In hcaltJi the volume of the pulse varies from time to time, and is of course different in different individuals. There are also many modifications in disease. A laro;e pulse, i.e. a pulse of large volume, is seen in the following conditions : — I. In many cases of fever during the earlier^ periods of the attack, when the heart is acting powerfully, and propelling a large quantity of blood into vessels, the tonicity of which is already somewhat relaxed.'^ ' During the stage of rigor the pulse is small. ^Towards the termination of cases of fever, i.e. after the contlition lias con- tinued for some time, the pulse vessels become still more relaxed, and the pulse becomes small. It is often under these circumstances dicrotic. 276 Diseases of the Huari. 2. In atheroma, when the elasticity of the arterial walls is impaired and the vessels are dilated. 3. In some cases of hypertrophy, and in some cases of simple cardiac excitement. (See figs. 120 and 121.) 4. In aortic regurgitation the systolic portion of the tracing is of large volume, but the diastolic extremely small. Press ui-e 2^ cz Fig. I20 — .Alteratw7ts in the Piihe-traciu^s as the result of Caruiac Excitement — A M, set 48, admitted to the Newcastle Infirmary suffering from obscure spinal symptoms. The heart became excited, and the tracing shown in fig. 120 was taken immediately after that shown in fig 73, the instrument in the meantime remaining in situ The spring pressure was the same in each case J'ressitre Fig. 121 — Hypertrophy of Left Ventricle — A. T , an. 54, admitted to Xewcasth Infirmary suffering from cirrhotic kidney. A small pulse is met w ith : I. In those conditions in which the amount of blood dis- charged by the left ventricle is below the normal amount. Under this head are comprised : — The Tension of the Pnlse. 277 {a) Cases (such as inanition) in which the total amount of blood in the body is reduced in quantity. (See fig. 122.) {b) Cases of mitral disease, more especially regurgitation and stenosis after the failure of compensation. (See fig. 123.) In the former (mitral stenosis) the left ventricle does not receive the usual (normal) amount of blood from the auricle ; in the latter case, some of the blood which ought to be discharged into the aorta flows back into the auricle through the incompetent valve. Pressure 2 oz. Fig. 122. — Small Weak Pulse. — ^J. M., set. 18, a soldier, admitted to the New- castle Infirmary 23d January 1879, suffering from abscess of the liver and pericarditis. The heart was displaced upwards and to the left. Pressure 3 oz. Fig. 123. — Mitral Regurgitation. — M. A. C, ast. 16, admitted to Newcastle In- firmary 24th January 1878, suffering from cough and shortness of breath, dating from an attack of rheumatic fever two months previously. Heart's action very rapid (120-130). The first sound appeared to be reduplicated ; a systolic murmur at the apex, audible when the heart became slower. {c) Cases of aortic stenosis(see fig. 124); the size of the pulse being in proportion to the narrowing of the orifice. Pressure \\ oz. Fig. 124. — Aortic Stenosis. — J. B., set. 51, admitted to Newcastle Infirmary 29th November 1878, suffering from anaemia and dropsy. There was a well- marked aortic systolic murmur ; the left ventricle was not hyptrtrophied. The pulse-tracing seems to show that the murmur was organic. 278 Diseases of the Heart. {d) Conditions of cardiac debility, both temporary and permanent. (See fig. 122) Conditions of collapse are good examples of the former ; the pulse in collapse being small and thready, while fatty and fibroid degeneration of the left ventricle, with dilatation, are types of the latter. 2 In those cases in which the vessels are unduly con- tracted, as in peritonitis, the cirrhotic form of kidney disease, and the cold stage of fevers, i.e. during the rigor. The Compressibility or Strength of the Pulse is a point of great practical importance, for in many cases it indicates the condition of the vaso-motor nerve apparatus, and hence of the general tone of the system. The strength of the pulse is measured by the finger or by means of the sphygmograph, the amount of pressure required to obliterate the pulse-wave being (provided the arterial walls are healthy) the true indication of the pulse-strength.^ Dr Mahomed gauges high tension in the following man- ner: — 'A line must be drawn from the apex of the up-stroke to the bottom of the notch preceding the dicrotic wave (fig. 125, A C). No part of the tracing should rise above this line ; (After Afa/ioined.) Fig. 125. — Afa/iflii/€d\<: method of gauging high tension. The tidal wave rises above the dotted line drawn from the apex A, to the aortic notch C. if it does, then the pulse is one of high pressure. The height of this notch is another good gauge of pressure ; the higher it is from the base line of the tracing the higher is the pressure, the nearer it approaches the line the lower is the pressure. ' When the arterial walls are inelastic and rigid, as in cases of atheroma, the amount of pressure required to obliterate the pulse is not a true criterion of its strength, for a certain (often a considerable) amount of pressure must be applied before any influence is exerted upon the blood wave itself. The Tension of the Pulse. 279 Lastly, the duration of systole compared to that of diastole may perhaps be reckoned an important sign.' Dr Mahomed believes ' that there is a normal length of systole for a pulse of a given frequency, and that the length of the systole is increased if the arterial pressure is increased.'^ I am in the habit of considering a pulse of high tension as synonymous with a strong pulse, and vice versa a pulse of low tension v/ith a weak pulse. - In vigorous health the strength or tension of the pulse is considerable, but there are great differences, even in persons who present all the external appearances of good health ; while alterations in the tension of the pulse are common in disease. A pulse of higJi tension may be either large or small, the pulse of chronic Rright's disease (especially the cirrhotic form), in which the heart is notably hypertrophied, is illus- trative of the former ; the pulse of peritonitis is an excellent example of the latter. A ivcak pulse, or pulse of lozv tension, is also very common in disease, and is also of great importance. A pulse of low tension is usually associated with feeble action of the heart and a relaxed condition of the blood vessels. It may be either small or large ; the former — a small pulse of low tension— is seen in mitral lesions and towards the terminal period of fever; the latter — a large pulse of low tension — is also seen in some cases of fever (as for instance in certain stages of rheumatic fever), and in many persons who enjoy apparent good health, but in whom the vaso-motor tone is below par. As a general rule, a slow pulse is a pulse of higher tension than a quick pulse, and vice versa, but such a relationship is by no means constant or necessary. ' Gnys Hospital Reports, 1879, p. 371. " I, therefore, differ from Dr Mahomed, who considers that hardness or incompressibiliiy is the least constant character of the high pressure pulse. ' It is not unfrequent,' he snys, 'to find tw^r/)/// vessels associated with a weak or failing heart, the pulse is then often small and feeble, it is very easily com- pressed, and is described as a small weak pulse, which is thought usually to require stimulants ; the reverse, however, is the case ; bleeding or purging will be well burne by such patients, and the result will be most satisfactory,' 28o Diseases of the Heart, The clinical significance of the tension of the pulse. — The tension of the pulse is of great importance, both for diagnosis, prognosis, and treatment. Dr Mahomed, for example, has shown that in many cases of chronic Bright's disease there is in all probability a stage of the disease in which the urine is healthy (free from albumen, casts, etc.), but in which there is persistent high arterial tension, and further, that by reducing this condition of high tension the subse- quent structural affection of the kidney may be prevented. So, too, a hard pulse associated with cardiac pain (angina pectoris) indicates a serious condition, and urgently calls for treatment. On the other hand, a pulse of low tension is no less important both for prognosis and treatment. Persons whose vaso-motor tone is below par, i.e. who have weak pulses, bear severe (especially acute) disease badly ; while a weak, and especially a dicrotic pulse in a case of fev^er, requires the free use of stimulants. The Sphygmographic Characters of the in- dividual Pulse-waves. — Most of these points, which are of considerable practical importance, such as dicrotism, have been already fully considered; the following must also be observed: — (i) The relative duration of those portions of the tracing which correspond to the ventricular systole and diastole.— -\n the normal condition the ventricular systole occupies, as we have previously seen, about ^^ of the entire cardiac revolution. This relationship is altered in certain cases of disease. When the heart is acting very rapidly, the diastole is relatively more reduced than the systole, and the proportional duration of the systolic to the diastolic portion of the tracing is increased. Increased temperature of the blood, has, as Dr Paul Chap- man ^ has shown, a distinct influence in shortening the dura- tion of the ventricular systole; and the same authority has observed, on coming out of a Turkish bath, 'that although ^ B litis h .Medical Journ-il, August 1 9, 1 882, p. 300. Character's of Individual Pulse Waves. 281 the pulse-frequency may actually increase, the systole length- ens as the patient cools.' So, too, in aortic regurgitation, the systolic portion of the tracing is usually longer than the diastolic. (2) The relative conditioti of the vessel (as regards its ful- ness) during systole and diastole. — In some cases the systolic portion of the tracing is relatively very much larger than the diastolic. A good example of this condition is seen in aortic regurgitation (see fig. 126), in which the artery is fully dis- tended during systole, but comparatively very empty during diastole. Pressure 2j oz. Fig. 126. — Aortic Regurgitaticn. — Case: G. A. , ast. 56, admitted to Newcastle Infirmary 21st February 1878, suffering from shortness of breath and swell- ing of feet. Had been ill for three months. The face was pale and anxious, lips slightly dusky. Double aortic murmur ; heart considerably hyper- trophied ; apex between 6th and 7th ribs, 3 inches below and 2 inches out- side left nipple. Considerable hypertrophy and engorgement of right heart. Died 5th March 1878. Aorta very atheromatous ; aortic valves very in- competent ; segments shrunken, turned in towards the ventricle ; coronary arteries much obstructed ; cardiac walls fatty ; left ventricle dilated ; peri- cardium adherent. The arteries were practically empty during the ventri- cular diastole. a-(^=upstroke ; iJ=apex ; f=tidal wave ; d indicates the position of the aortic wave, which is absent in this tracing. An empty condition of the arterial system during the ventricular diastole is often associated with a failing heart, and is a serious indication (see figs. 127 and 128). When the pulse \s fully dicrotie, the artery at the point of observation is apparently^ as empty at the end as it is at the beginning of the ventricular systole, and is apparently more empty at the end of the ventricular systole than it is during the ventricular diastole. Again, in hyperdicrotism the artery ' See foot note on page 255. 282 Diseases of (he Heart. at the point of observation is apparently still more empty at the end of the ventricular systole. Fig. 127. — P}-essttre 2 oz. Fu;. 118. — Pressure 2^ oz Fig. 127. — Weak Pulse. — R. R., x\.. 17, admitte I to Newcastle Infirmary 2 1st February 1878, sutiering from iilii^pathic anaemia. Died 12th April. There was a systolic (antemic) mitral murmur. The pulse-tracing resembles that of mitral regurgitation (see tig. 104). Tracing made 23d February. Fig. 12S. — Pros^ressive Pernicious Anctvtia. — .Same patient (see fig. 127). Tracing taken 19th March. The artery is almcjst empty during diastole. In other cases on the contrary (in chronic Bright's disease, for example), the diastolic portion of the tracing is unduly sustained. A persistent pulse is usually a pulse of high tension, and vice versa a pulse uhich rapidly falls away under the finger is a pulse of low tension. THE CONDITION OF TDK ARTERIAL COATS. The condition of the arterial coats with regard to the presence or absence of atheroma, is a point of great practical importance, for atheroma of the superficial arteries — the radial, temporal, etc., — is almost invariably associated with similar disease of the aorta, and very often with disease of the cerebral vessels. The presence or absence of atheroma may be of diagnostic importance, as for example, in a case in which the diagnc^is lay between an aneurism and a solid intrathoracic tumour. Atheroma in the superficial vessels is indicated by : — (i) Rigidity of the arterial coats; the vessel generally ' stands out like a cord,' is markedly visible and tortuous, while its coats feel thick under the finger. To determine whether the arterial coats are actually thickened or not, the artery should be firmly compressed and emptied by one finger, while the other finger searches for the vessel below the compressed point. When the vessel can be distinctly 1 Comparison of the Two Radials. 28 J felt, even though empty of its contents, its walls are obviously thickened and diseased. This is an important point, for all arteries which are firm and hard, and which stand out like cords, are not thickened. (2) The presence of a well marked tidal wave, the tension of the pulse being high {i.e. the pulse with difficulty obli- terated) but a low pressure being usually required for the production of the best tracing {i.e. the first ventricular wave being very easily extinguished). The Comparison of the two Radial Pulses is useful in the diagnosis of some cases of aneurism and intra- thoracic tumour. The two pulses must be compared as regards ; {a) their synchronism as to time ; {b) the character of their respective pulse waves. Differences in time between the two pulses are most easily appreciated by the fingers. In health the two radial pulses are of course synchronous, but in some conditions of disease, as for example, where the sac of an aneurism is situated in the course of the circulation, the pulse wave is retarded, and is consequently delayed at one wrist. Differences in the cliaracter of the pnlsc zvaves in the tzuo wrists may also be detected by the finger, but are much more accurately observed by means of the sphygmograph. The precautions which should be taken in comparing the two pulses have been already described. (See page 244.) Differences in the tivo pnlses may be due to : — 1. Irregular distribution, such as high division of the radial artery. In such cases there is a notable difference in the size of the vessel in the two wrists, or indeed it may apparently be altogether absent on one side. The condition is easily recognised by observing the condition of the brachial arteries on the two sides, and by feeling for the position of the abnormal vessel. 2. The presence of an aneurismal sac in the course of the circulation on one side. The alterations produced by the passage of the blood wave through a globular elastic aneu- rismal sac, consist in retardation of the pulse-wave and 284 Diseases of the Heart. flattening of its curves. In well marked cases the up-stroke is sloping, the apex rounded, and the secondary curves entirely obliterated. (See figs. 129 and 130, which represent the pulse tracings on the two sides, from a case in which a large aneurism involved the axillary artery on the left side of the bod}'.) Pressure 3 oz. Fig. 129. — Atieiirism of Left Axillary Artery (left radial tracin;;). — L. G., set. 63, admitted to the Newcastle Infirmary 7th March 1878, with a large aneurism of the left axilhry artery. The apex is rounded; all the curves are obliterated. Pressure 3 oz. Fig. 130. — Aneurism of Left Axillary Artery (right radial ). — Right radial tracing for the same patient. The pulse is intermittent, but all the curves are well marked. Fig. 131. — (Right radial. ) Pressure \oz. FiG. 132. — (Left radial. ) Pressu7-e\oz. Figs. 131 and 132. — Aneicrism of Ascenditig portion of Aortic A7xh. — J. D., aet. 50, admitted to Newcastle Infirmary sufTering from a large aneurism of the ascending thoracic aorta and atheroma. There is no important difference between the two pulses. Differences in the pulse tracings from the two wrists are not of course observed in all aneurisms. When the aneurism involves the aortic arch below the origin of the innominate the pulse-wave in the two wrists is the same, though the sphygmographic tracing on each side may be modified ^ (each ' The alteration in these cases is seldom so great as in aneurisms more peri- pherally seated (aneurisms of the innominate or subclavian foi example). CoDiparison of the Tzvo Ra dials. 285 pulse-wave being affected, quoad its curves, in a like degree). Figs. 131 and [32 illustrate this point. Again, it may so happen that an aneurism is situated on the vessel of each side, or that an aneurism is so filled up with clot that the pulse-wave is very little if at all affected in its passage through it. Such was the fact in a remarkable case of multiple-aneurism which I have recorded in the Edtiibi/n^h Medical Jonmal for June 1878, p. 1076. The pulse-tracings from the two radials were in that case almost identically the same. (See figs. 133 and 134.) Fig. 133. — (Right radial. ) Pressure l oz. Fig. 134. — (Left radial). Pressure t^ oz. Figs. 133 and l^A. — Case of Multiple- Aneurism. ~^\. F., aet. 64, admitted to the Newcastle Infirmary i8th February 1878, suffering from symptoms of intra- thoracic pressure. Died loth March. Post-?7iortem showed dilatation and small aneurism of aortic arch. Fusiform aneurisms of the innominate, left common carotid and left subclavian arteries, just above their origins. The aneurisms were filled with firm clots, through which a straight narrow channel for the blood remained. When the aneurismal sac involves the transverse portion of the aortic arch be':ween the innominate and the left sub- clavian (the circulation through the innominate being inter- fered with), the right radial pulse is normal, but the left may be modified. When the aneurism involves the innominate, the right subclavian, or right axillary artery, the right radial pulse presents the aneurismal characters, while the left is normal. Vice versa when the left subclavian, or left axillary artery is affected, the left radial pulse will be modified, but the right normal. The alteration in the two radial pulses may be of con- siderable diagnostic importance Figs. 135 and 1 36 represent, for instance, the right and left pulse-tracings of a patient who was admitted to the Newcastle-on-Tyne Infirmary, under 286 Diseases of the Heart. my care, suffering from dyspepsia. There was no complaint of any thoracic trouble. On taking a tracing of the left radial (I was at that time working at the sphygmograph, and taking tracings of every case admitted to hospital) I was, of course, at once struck with its aneurismal character, and on careful physical examination found decided dulness, faint pulsation, and marked accentuation of the cardiac sounds over the chest at a point corresponding to the origin of the left subclavian artery. F'IG. 135. — (Leflradial). Pressure t,oz. Fir,. 136. — (Right radial). Pressure 2,^ oz. Figs. 135 and 136. — Aneurism of Left Suhclavlan. — J. M., aet. 50. admitted to Newcastle Infirmary 5th September 1878 ; all the waves in the left tracing are obliterated. Fig. 137. — (Right radial.) Pressure 2\oz. Fig. 138.— (Left radial.) Pressure2\oz. Figs. 137 and 138. — Difference in the radial pulses, the result of pressure by an intra-thoracic tumour on the innominate artery. J. F., Kt. 50, admitted to the Newcastle Infirmary 24th January 1878. 3. The pressure of a tumour (solid or aneurismal) on the vessels of one side (on the innominate, or left subclavian for example). (See figs. 137 and 138.) 4. Differences in the calibre of the ves.sels on the two sides (innominate and left subclavian) such as are produced by obliquity oi origin due to disease (aneurismal dilatation of the aortic arch, etc.), or to the presence of an atheromatous patch at the mouth of the vessel or in its course. 5. Local disease in one radial artery. Asynclironism of tJic radial pulse zvith the cardiac con- tractions has been already alluded to. (See page 268.) The Condition of the J 'e nous Svstenr. 287 THE EXAMINATION OF THE VENOUS SYSTEM. T have repeatedly directed attention to the fact that many of the most prominent symptoms in cardiac cases are due to obstructed venous return ; in mitral cases, for example, as soon as compensation fails the whole systemic venous circulation becomes engorged, with the results which will be afterwards described in detail. In cases of this description, the engorge- ment is, for a time at least, passive ; but should the tricuspid valve become incompetent, either as a secondary consequence of mitral disease or as the result of primary changes in the lungs or right cavities of the heart, a backward or regurgitant current is propelled into the venae cavae, and an active ob- struction to the venous return is added. Again, in some cases of thoracic aneurism, and in some cases of solid intra-thoracic tumour — conditions which are sometimes with difficulty dis- tinguished — the return current through the superior vena cava is interfered with, and a venous congestion, limited to the territory of that vein, is produced. It is obviously, therefore, of the greatest importance to ascertain, in all cases of cardiac disease, the exact condition of the venous circulation, and this we endeavour to do: — (i) By observing the colour of the skin of the peripheral parts, more especially of the ears, lips, nose, fingers, toes, etc. — a point which has been considered in treating of the physiognomy of the case (see page 87). (2) By noting the presence or absence of dropsy in the subcutaneous cellular tissue and serous cavities — a point which has also been considered (see page 89). (3) By noting the presence or absence of symptoms pointing to venous engorgement of the internal organs, such as the lungs, liver, stomach, kidneys, brain, etc. (4) By examining the physical condition of the large venous trunks, in particular, the condition of the jugular veins. Inspection, palpation, and auscultation are the chief means which are employed in order to ascertain the condition 288 Diseases of I lie Heart. of the superficial veins. When a venous pulse is present valuable information is in some cases afforded by the tracings obtained of it. Inspection of the veins of the neck. In conditions of health, more especially in well nourished individuals and during tranquil respiration, the external jugular veins are scarcel}', if at all, visible. During forced expiration, more especially in thin persons, they become distended and stand prominently out. All of us have pro- bably noticed the great distention of the veins of the neck in some of our public singers after sustained and powerful efforts. Distention of the ju^nlar veins is of common occurrence in disease, and is produced by all conditions which interfere with the return of blood to the heart. In practice we find that distention of the jugular veins chiefly depends upon the following conditions : — 1. Mitral lesions. 2. Diseases of the lungs (such as cirrhosis, emphysema, etc.) which interfere with the passage of the blood from the right to the left sides of the heart. 3. Disease of the right side of the heart. 4. The pressure of aneurisms and solid intra-thoracic growths upon the superior vena cava. 5. Pericarditis and inflammation of the cellular tissue of the mediastinum. — In some cases of adherent pericardium and of indicative mediastino-pcricarditis, the current of blood to the heart is interfered with and the jugular veins are distended. 6. Plugging of the superior vena cava — an extremely rare condition, which is generally due to disease of the venous coats, produced by external pressure, e.g. the pressure of an aneurism or intra-thoracic growth. In distention of the jugulars due to the central causes, i.e. to disease of the heart or lungs, the distention is not constant but varies with the condition of the respiration, being most marked during expiration, least marked and usually com- Distention of the Jiigula}' Veins, 289 pletely absent during inspiration. (The distention of the veins of the neck, which is due to adherent pericardium, occurs during- the depression of the chest wall which corresponds to the systole of the ventricles ; the distention of the veins rapidly collapses and disappears during the diastole of the ventricles. The distention is due to the fact, that during the systolic depression of the chest wall, the cavity of the chest is diminished in size, and a mechanical hindrance offered to the return current of blood through the superior vena cava. During the diastolic rebound, on the other hand, the cavity of the chest is suddenly distended, a suction force is exerted, and the previously engorged veins are, in consequence, suddenly emptied. In indurative mediastino- pericarditis, the distention of the veins of the neck is due to the pressure of bands of inflammatory adhesions upon the vena cava superior ; and since the obstruction only occurs during inspiration, the jugular veins become distended, in- stead of collapsing, during inspiration, as they do in health ; the distention rapidly subsides during expiration, that is, when the constrictive bands are relaxed, and the obstruction to the blood in the superior cava is removed.) Its amount, too, varies with the position of the patient. When sitting or standing, the distention is less than when lying down, owing to the fact that in the erect position of the head, the return of the venous blood to the heart is favoured by the force of gravity. The distention is usually greater on the right, than on the left side of the neck, and is generally much more apparent in the external than in the internal jugulars. Exceptions to both of these statements do, how- ever, occasionally occur.^ The swollen external jugular veins have often a knotted appearance, the irregular enlargements corresponding to the position of the venous valves. As the result of distention of the external jugulars, the face (more especially the lips, ears, and nose) becomes cyanotic, and the features swollen, but the swelling is never very ' I have seen a case of tricuspid regurgitation in which the distention and pulsation in the internal jugulars were much greater than in the external. T 290 Diseases of t lie Heart. great.^ In consequence of the venous distention, the brain becomes congested, and symptoms of carbonic acid poisoning, viz., drowsiness, mental obfuscation, and ultimately coma, are apt to supervene. When the distention is due to a central cause, i.e. to disease of the heart or lungs, the venous engorgement is not limited to the territory of the superior cava, but its effects are also seen in the lower extremities and great organs of the abdomen, i.e. in the territory of the inferior cava. Indeed, as we have previously seen, swelling of the feet is the first symptom in many of these cases, and is generally observed before the distention of the jugulars is noticeable. When the distention depends upon a local, as distinguished from a central cause, i.e. upon direct obstruction to the return current through the superior cava, the symptoms and signs of venous engorgement are of course limited to the two sides of the head and neck, the upper extremities, and the upper parts of the thoracic parieties. When the obstruction is great, and particularly in those cases in which it is complete, the parts from which the superior cava draws its blood may become remark- ably oedematous, and it is in cases of this description that the peculiar, hard, brawny swelling, to which the terra ' collar of flesh,' has been applied, is observed. As I have previously pointed out, the swelling df the face, which is due to obstructed venous return through the superior cava is readily distinguished from that which is met with in renal dropsy, and with which it might at the first glance be confounded, by the facts : — (i) That the face is not only swollen but is also cyanotic. (2) That the swelling involves, and is limited to, the terri- tory of the superior cava. (3) That there is no kidney disease. (4) That there are symptoms and signs of aneurism, intra- thoracic growth, or other local pathological condition likely to obstruct the vein or produce disease of its coats. ' The swelling is never so great as in cases of obstmctiun of the superior vena cava from direct pressure. PiLlsation in t/ic Jugulai^ Veins. 291 Pulsation in the jugular vci)is. — In conditions of health there is no perceptible pulsation in the jugular veins, but in cases of disease, rhythmical undulations and pulsations, more particularly in the external jugulars are sometimes met with. In some cases these pulsations are only apparent ; in others they are real, and represent a true venous pulse. Apparent pulsation. — When the jugulars arc distended, as the result of a central obstruction, i.e. of disease of the heart or lungs, a rhythmical undulation, corresponding in time to the movements of inspiration and expiration, is generally observed. The vein is distended during expiration and collapses during inspiration. This apparent pulsation is at once distinguished from a true venous pulse by its rhythm. In indurative mediastino-pericarditis, as has been described above, an 'apparent' pulsation is sometimes seen in the veins of the neck ; but it differs from the ordinary form of ap- parent pulsation, inasmuch as the vein is distended during inspiration and empty during expiration. In some cases of adherent pericardium, the veins of the neck are distended during the systole of the ventricles, as I have described above. This pulsation, which is of course only apparent and due to simple passive distention, must be dis- tinguished from true pulsation of tricuspid regurgitation in which a ' back-wash ' is propelled into the veins at each systole of the right ventricle. In other cases, undulations which correspond in time to the cardiac contractions are observed. In some of these the undulations are due to impulses communicated to the dis- tended veins by the subjacent arteries ; in others, they are due to the fact that the contraction of the right auricle com- municates an impulse or shock to the blood in the superior vena cava, which is propagated to the jugulars. It is also said that the contraction of the right ventricle, even when the tricuspid is sound, may communicate a shock through the tightly stretched tricuspid valve, to the blood in the right auricle, which may be propagated, through the vena cava superior, to the jugulars. It is improbable, however, that any marked undulation in the jugulars can be produced in this way. 292 Diseases of the Heart. Apparent pulsation of this description, i.e. apparent pulsa- tion of the jugular veins synchronous with the contraction of the heart, is readily distinguished from true jugular pulsation produced by a back-wash, i.e. from pulsation indicative of tricuspid regurgitation, by compressing the vein in the middle of the neck, and observing the condition of the portion of vein which is placed below the finger, i.e. between the heart and the compressed point. If the pulsation is real, it will still be observed in the vein below the finger, for with each systole of the right ventricle the vein is again filled from below by the back-wash. If the vein remains collapsed and empty, the pulsation is only apparent. True pulsation of systolic rhytJnn is due to a stream of blood being propelled into the vein at each systole of the right ventricle. This condition is of extreme importance, and in- dicates tricuspid incompetence ; it also shows that the valves at the point of junction of the internal jugular and subclavian veins are incompetent. Jugular pulsation of this description ij.e. true jugular pulsation indicative of tricuspid regurgitation), is sometimes associated with pulsation of the inferior vena cava, the effects of which have been previously described. The exact chararacter of the jugular pulse-wave is, as Friedreich has shown, of some practical importance. In an extremely able paper on ' The Auricle in Health and Dis- ease,' Dr Gibson has directed attention to this point ; and has figured some of Friedreich's tracings (see figs. 139, 140) ' The Fig. 139. Fig. 140. Fig. 139. — Jugular pulse tracing showing the presence of the auricular wave a. (After Friedreich.) Fig. 140. — Jugular pulse tracing after paralysis of the auricle ; the auricular wave a, in the preceding figure is no longer present. (After Friedreich.) Pulsation of the Pei^ipheral Veins. 293 one shows,' he says, ' three waves, a, b, and c ; the other only two, b and c. Bestowing our attention mainly upon the first wave, a, which is caused by the systole of the right auricle, we find in it an index of the state of the auricular muscle. So long as it is shown in tracings from the jugular, the auricle is comparatively healthy ; when it disappears it is a certain proof of paralysis of the auricle, and if it should reappear it gives evidence of a return of contractile power. In this way the auricular wave in the jugular veins is of very considerable practical interest. The large wave, b, is caused by the systole of the ventricle, and the third wave, c, is reflected from the interior of the heart, in the same way as the dicrotic wave in the radial tracings of aortic regurgitation first shown by Naumann.'^ Tnie pulsation of presystolic rliytJun. — When the venous valves are incompetent in consequence of over-distention of the veins, pulsation of presystolic rhythm is sometimes ob- served. It is produced by the contraction of the right auricle and may occur independently of any systolic 'backwash' representing tricuspid regurgitation. Pulsation, like distention, is usually more marked in the right than in the left side of the neck, and is generally more perceptible in the external than in the internal jugulars. Pulsation in the peripheral veins, such as the veins on the back of the hand, is occasionally though rarely observed. It is seen, for instance, in some cases of aortic regurgitation, and is due to the fact that the pulse wave is not obliterated in the arteries as in health, but passes right on to the veins through the capillaries. Prof Michael Foster gives the following lucid description of the ways in which it may be produced : — ' To recapitulate : there are three chief factors in the mechanics of the circulation, (i) the force and frequency of the heart-beat, (2) the peripheral resistance, (3) the elasticity of the arterial walls. These three factors, in order to produce a normal circulation, must be in a certain relation to each other. A dis- turbance of these relations brings about abnormal conditions. ' Edinburgh Medical Journal, Aug. 1882, p. 126. 294 Diseases of the Heart. Thus, if the peripheral resistance be reduced beyond cer- tain Hniits, while the force and frequency of the heart re- main the same, so much blood passes through the capillaries ' at each stroke of the heart that there is not sufficient left behind to distend the arteries, and bring their elasticity into play. In this case the intermittence of the arterial flow is continued on into the veins. An instance of this is seen in the experiments on the sub-maxillary gland, where sometimes the resistance offered by the minute arteries of the gland is so much lowered, that the pulse is carried right through the capillaries, and the blood in the veins of the gland pulsates. A like result occurs when, the peripheral resistance remaining the same, the frequency of the heart's beat is lowered. Thus the beats may be so infrequent that the whole quantity sent on by a stroke has time to escape before the next stroke comes. Lastly, if, while the heart's beat and the peripheral resistance remain the same, the arterial walls become more rigid, the arteries will be unable to expand sufficiently to retain the surplus of each stroke or to exert sufficient elastic reaction to carry forward the stream between the strokes ; and in consequence more or less intermittence will become manifest.'^ Palpation uf the superficial veins is not a method of physical examination of much consequence, except in those cases in which the vein is plugged by a coagulum. In cases of this description, the vein can be felt as a firm rigid cord, and there is usually at the same time tenderness on pressure. In cases of well marked venous pulsation, such for instance as is due to tricuspid incompetence, the pulsations can be felt as well as seen. In some cases of anaemia, in which the venous hum which I shall presentl}' describe is well marked, a thrill can be felt when the finger is placed over the veins at the root of the neck. Auscultation of the veins. — In a considerable proportion of cases, even in apparent health, and notably in conditions of anaemia, a continuous humming murmur, to which the term ' A Text Book oj Fhysioloy. P'ourlh edition, p. 131. AiLsciLltatioii of the l^cins. 295 bruit de diab/c, or huviniing-top imirnmr, has been given, is heard in the veins. In many cases it closely resembles the roaring sound which is heard when a shell is placed close to the ear. It is usually best heard at the junction of the internal jugular and sub-clavian veins, is intensified by the pressure of the stethoscope, by turning the head forcibly to the opposite side,^ and by a deep inspiration."^ The murmur is generally louder on the right side. It is usually continuous, but in some cases is only produced on deep inspiration, and in such cases is, therefore, intermittent. In conditions, of anaemia venous murmurs may be often heard in other situations, as, for example, over the torcular Herophili and eyeball. ' When the head is turned to the opposite side, the muscles and fascia are put upon the stretch, the vein is compressed, and its channel narrowed. ^ A deep inspiration quickeus the flow of blood to the heart, and favours the production of fluid veins. 296 Diseases of the Heart. CHAPTER IV. DISEASES OF THE PERICARDIUM; ACUTE PERICARDITIS; PERICARDIAL ADHESION; INDURATIVE MEDIASTINO - PERICARDITIS ; CHRONIC PERICARDITIS; HYDROPERICARDIUM ; PNEUMOPERICARDIUM. Haying made ourselves acquainted with the introductory parts of our subject (the anatomy, physiology, pathology, and clinical examination of the heart), we are now in a position to study the individual diseases in detail. It will be convenient to consider : — (i.) The diseases of the pericardium. (2.) The diseases of the endocardium. (3.) The diseases of the myocardium. (4.) The neurotic affections of the heart, which include the purely functional disorders of the organ. (5.) The diseases of the great blood-vessels. The congenital malformations of the heart, which are usually treated under a distinct head, will be described under the diseases of the endocardium and myocardium. THE DISEASES OF THE PERICARDIUM. The morbid conditions of the pericardium, which are of practical and clinical importance are : — 1. The inflammatoiy affections and their results (peri- carditis, adherent pericardium, indurative mediastino-peri- carditis). 2, The effusions of fluid (of a non-inflammatory character) into the sac (hydropericardium, haemopericardium). I I Pericarditis. 297 3. The collections of air or gas in the sac (pneumo- pericardium). Coitgenital deficiencies and malformations (diverticula) of the peri- cardium occasionally occur, but are seldom suspected or recognised during life. In a few cases the whole pericardial sac has been absent, more frequently, limited deficiencies or imperfections in it have been observed. New groivtJis (tubercles, sarcomatous and cancerous tumours) occa- sionally affect the membrane ; and parasites and free bodies (which usually have resulted from previous inflammatory deposits or new growths) are vzry exceptionally found in the sac. But it is not neces- sary to describe these conditions separately. Unless they give rise to pericarditis (which they frequently do) they are unattended by any distinct symptoms or physical signs, and cannot be recognised during life. PERICARDITIS. Definition. — Inflammation of the pericardium. Like all other forms of inflammation, pericarditis may be either acute, sub-acute, or chronic. As a matter of practical convenience it is only necessary to describe separately the acute and chronic forms. ACUTE PERICARDITIS. Definition. — Acute inflammation of the pericardium. Varieties. — Many different varieties of the disease may be described. We may, for example, make an aetiological sub- division, and divide cases of pericarditis into two great groups, v\z. primary and secondary, and then again subdivide each of these groups into still smaller ones, as, for instance, into cases of tranviatic pericarditis, rhenmatic pericarditis, idiopathic pericarditis, and the like. Or, we may make a pathological division, in accordance with the extent of the inflammation {diffuse and circumscribed'^ pericarditis), or in accordance with the character of the inflammatory product (Jibrinoiis, purident, ' The division into diffuse and circumscribed is theoretical rather than practical, for in acute pericarditis, at all events, the inflammation is almost invariably diffuse. 298 Diseases of the Heart. hccmorrhagic, etc). Or again, \vc may take a clinical (or rather a clinico-pathological) basis, and divide cases of peri- carditis into dry and vwist, in accordance with the amount of effusion and the condition of the cardiac dulness. Etiology. — Acute pericarditis may occur at any period of life, but it is rarely met with in young children ; it is most common between the ages of fifteen and twenty-five. It is slightly more common in men than in women, and is most frequently observed in persons who follow outdoor occupa- tions, more especially those who are exposed to cold and wet, and to great variations in temperature ; facts which are pro- bably explained by the circumstance that men, and especially men who are exposed to cold and wet, are more frequently affected with acute rheumatism than other members of the community. In women it is much more common amongst young serv^ant girls and washer-women than in those engaged in any other occupation. Over-action of the heart seems to predispose to the condition. Primary pericarditis is extremely rare. It may be due to:— (a) Traumatic injuries, such as wounds of the sac, blows on the front of the chest, etc. (b) Primary new growths (sarcomata, carcinomata, etc.) in the pericardial tissues. These primary new growths are ex- tremely rare. (c) Exposure to cold and wet, independently of acute rheumatism or of any other diseased condition. This is probably the rarest of all the causes of pericarditis. The following is a case in point ; it is also interesting from the fact that until shortly before death there were no symptoms in- dicative of serious disease. Case — Latent idiopathic pericarditis j death. A girl, jet. 17, who had previously enjoyed good health, but who had never menstruated, complained of uneasiness in the upper part of the abdomen, and of constipation. The tongue was slightly furred, the pulse Aitiology of Acute Pericarditis. 299 a little quick, but there was nothing to direct attention to any serious disease within the chest. A dose of castor oil was prescribed, and nothing more was heard of the case for a few days. I was hurriedly sent for, and found the patient dead. She had passed a somewhat restless night, but had got up to breakfast as usual ; had suddenly complained of feeling faint, and had fallen back dead. All the organs were healthy, with the exception of the heart. The pericardium was distended with turbid fluid, and both surfaces of the pericardium— both visceral and parietal layers — were covered with a layer of recent lymph. (See fig. 141.) The case was therefore one of pericarditis ; and syncope was the immediate cause of death. On inquiry I ascertained that the patient had waded in the sea a fortnight previously, and that for some days afterwards she had been a little hoarse. There was no histoiy of rheumatism. So trivial were the symptoms, in this se\'ere and acute case, that the patient was able to go about her occupation — that of a baker's assistant — until two days before her death. Secondary pericarditis is a comparatively common condi- tion. It occurs : — (a) In the course of some general affections. The disease- par excellence with which it is associated, and of which it is, as it were, part and parcel, is acute rheumatism. Indeed, a large proportion of the cases of acute pericarditis, met with in prac- tice, are rheumatic. It is more apt to occur in first than in subsequent attacks of rheumatic fever, and in severe rather than in mild cases. Pericarditis also occasionally occurs in the course of scarlet fever. It is a somewhat common com- plication in Bright's disease, more especially the cirrhotic form ; and in cases of that description is not unfrequently the immediate cause of death. It is sometimes met with in pyaemia, purpura, and scurvy. (b) As the result of the direct extension to the pericardium of an inflammation or new growth which has originated in some of the adjacent organs or parts. This is one of the most common, probably the most cominon cause of peri- carditis which proves fatal during the acute stage.^ The primary inflammation or new growth may originate in the pleura, lung, bronchial glands, tissues of the mediastinum, the cellular tissue of the neck, or in the structures below the ' Rheumatic pericarditis is, perhaps, relatively more frequent, but is very seldom fatal. 300 Diseases of the Heart. diaphragm, i.e. in the cavity of the abdomen. An abscess of the Hver, for example, may by direct extension through the diaphragm (and without bursting into the sac) give rise to an inflammation of the pericardium. (c) As the result of secondary deposits of a tubercular, sarcomatous, or cancerous nature in the structure of the pericardium, the primary new growth being situated at a distance, and the secondary deposits being carried to the pericardium by the veins or lymphatic vessels. Pathology and Morbid Anatomy. — The naked eye and microscopical appearances which are seen in cases of acute pericarditis vary with : — (i.) The extent of the inflammation. (2.) The stage of the inflammation. (3.) The amount and kind of exudation. The extent of the infiavimation. — In the great majority of cases the inflammation is general, and involves the whole extent of both layers of the pericardial sac. In rare cases the inflammatory process is limited in distribution. In recent cases of this description, the chief morbid appearances are usually to be found at the base of the organ, around the roots of the great vessels and auricular appendages. In other cases, more particularly when the inflammation is of some duration or has become chronic,^ inflammatory adhesions, of limited extent, are found at or near the apex, on the posterior surface, or it may be on any part of the Organ. The stage of tJie infainniation, and the amount and kind of exudation. — In pericarditis the primary vascular changes (dila- tation and stasis) which characterise all inflammations are quickly followed by the pouring out of inflammatory exuda- tion matters into the serous cavity or sac. The naked eye appearances are as follows : — In the earliest stages, which it must be observed we seldom ' To avoid repetition, the pathological appearances which are seen in sub-acute and chronic pericarditis are included under this description. Fig. 141. Eearijrom a case of recent Pericarditis. (^Natural size.) The surface of the organ is coated with lymph, which is easily detached. The letter, a, points to a portion of the heart covered by lymph; b, to a detached shred of lymph; c, to a portion of the heart from which the lymph has been removed. M'LA«»iCu«i Fig. 142. — Front view of the heart in a case of acute pericarditis. {Natural size.') The front of the parietal perirardiura, which was verj- much thickened, has heen cut away; a wedge-shaped portion has heen removed froiri the apex of the left ventricle for microscopical examination. [^ote. To be seen properly this di-awing should be held about two feet from tlie eve. ^''*" ^fhZ^vTvwlh VZ '?/'«^/?i'^'''"'-.«'-^''^^- its svrfa^e is covered v^M l s> \!->a •Sa 'S I" Fig. 150. — A portion of the preiinruui.n .'i/'wn in Jig. 149 more hirildy magnijied, about 250 diameters, showing the juriction of the fpindlt ccUed tisxite, and the li/mph layer. Large masses of lymph (/, /,) are Lecomiug converted into spindle cells («, s.) Fig. 151. Fig. 152.- ----"s-iiV' ^ / -<:- .XS ■^1 ^^ m^"^. Fig. 1 51. — A portion of the central lymph layer of trie preparation shovm in fg. 149, magnified about 200 diameters, showing lymph thi-eads (a), leucocytes (6), and large epithelial cells (c). Fig. 152. — Another portion of the central lymph layer of the preparation shown in fig. 149; showing collections of red blood corpuscles (o), surrounded by lymph threads (6). M°L>u>JCii.>tNcljT> Fig. 153. — A portion of tlie spindle-celled layer from the section represented in fig. 149, more hiyhly magnified (about 250 diameters'). a, spindle cell ; b, capillary vessel ; c, leucocyte. Fig. 154. — A porlion of the preparation shown in fig. 149, at the junction of the mjiocardium and Kpindle-ceUid layer, magnifie.il about SOO diameters; showing leucocytes between the muscular fibres, proliferation of the nuclei of the muscular fibres and disappearance of their fibrillx. s, spindle cells; v, vessel transversely divided; m, m, proliferating nuclei of the muscular fibres ; /, leucocytes between the muscular fibres. M=UiaNlCuM«i«s,ljTnoUoi WW Fig. Ibb.— Section through a portion of adhererti pericardium of old Uandinn maonified about £50 diameters. ^ ^ . a, a portion of the parietal pericardium ; b. b, delicate connective tissue bundles passing between the parietal pericardium (a) and the \nsceral pericardium which is not shown in the figure ; c, c, nuclei of connective tissue ; d, d, collections of epithelial cells ; e, e, blood-vessels. ' » > " M°|ju>i '^ "^ 3 fc <& o ■i ■§' g p< '^ S' « ^ „ ^ > a as &i ."S O O "■ CD :B ^ Eh Sj3 .okT i*S(^A.^^-»'^.^i 1 /v ^m Vi£ Fig. 157. — Section Virough the thickened pericardium, the result of old pericarditis, nutgnified about 180 diameters. The superficial parts of the pericardium contain nuijierous spindle cells arranged parallel to the surface, which is covered with a beautiful layer of epithelium, much rounder in shape and more distinct than that covering the healthy pericardium. p, surface of pericardium from which the epithelium has become detached ; e, epitheliimi ; /, leu- cocytes lying in a depression on the surface: .t, spindle cells; I', leucocytes below the layer of spindle cells ; b, b, large vessels ; m, muscular fibres of the heart. M'LxolCuKxm&Lirnc^ Epn* Symptoms oj Acute Pericarditis. 307 In secondary cases of pericarditis therefore, the cHnical picture is made up, or, more correctly, it may be made up (for as we shall presently see, the symptoms due to the inflammation of the pericardium itself are sometimes entirely absent) of. — A. Symptoms due to the primary disease. B. Symptoms due to the pericardial inflammation itself, viz. : — (i.) General symptoms due to the pericardial inflamma- tion, such as fever. (2.) Cardiac symptoms proper. Under this head we have to consider: — {ai) The 'subjective cardiac sensations,' or the symptoms which result from the derangement of the heart as a sensitive, vital organ. (^.) The symptoms which may result from the derange- ment of the cardiac pump — the mechanical symptoms, as I am in the habit of terming them. {ci) The symptoms, which sometimes result from the pressure of the enlarged (distended) pericardial sac upon sur- rounding parts {i.e. pressure symptoms). {d.) Accidental symptoms due to complications, or to the extension of the inflammatory process to adjacent parts. Syjnptoms due to tJie primary disease. — It would be out of place here to describe in detail the symptoms which charac- terise the many different diseases with which inflammation of the pericardium may be associated. I must, however, emphasise the importance of looking out for the symptoms, and more especially for the physical signs of pericarditis, in all of those diseases, such as acute rheumatism, Bright's disease, etc., in which we know that inflammation of the pericardium is apt to occur. A trivial pain over the prse- cordium, for instance, which under ordinary circumstances, and in many diseased conditions, might be almost ignored, should, in a case of acute rheumatism or Bright's disease, excite grave apprehension, and necessitate minute and careful examination of the heart. And this statement is all the more necessary because of the fact, that the symptoms due to the ^^ o8 Diseases of the Heart. primary disease (notably so in acute rheumatism) are often very striking, and are apt to overshadow and obscure the symptoms, due to the inflammation of the pericardium — symptoms which arc in many cases sHght. Syniptojiis due to tlie pericardial inflaniuiation itself. — The nature and gravity of the symptoms, which depend upon the inflammation of the pericardium itself, depend upon the following conditions : — (i.) The extent and severity of the inflammation. (2.) The condition of the cardiac muscle, and of the val- vular apparatus of the heart. (3.) The amount and character of the effusion. (4.) The constitutional temperament (susceptibility), and the previous state of health of the patient. (5.) The manner and degree in which the cardiac nerves and ganglia, on the surface of the heart and around the root of the aorta, are affected by the inflammatory process. In those cases in which the inflammation is not very severe; in which the cardiac muscle is not implicated; in which the amount of effusion is small ; in which the patient was in fair health previous to the attack ; and in which he is not of an unduly susceptible temperament, the symptoms may be extremely slight or altogether absent. Indeed, from the frequency with which we find pericardial thickenings and localised adhesions after death, it is probable that many cases of this description pass entirely unnoticed. The case, which I have narrated on page 298, shows that even in severe and fatal cases of pericarditis, the symptoms may be very slight. General syviptoins due to tlic pericardial inflammation — fever. — The fever is, as a rule, slight or moderate, and presents no characteristic features. The tongue, bowels, and urine pre- sent the usual alterations which are met with in fever. When the pericarditis occurs in the course of a febrile disease, such as acute rheumatism, the increase of fever due to the inflam- mation of the pericardium is seldom sufficiently great to arrest attention. In purulent pericarditis the fever may be high, and present the irregular ups and downs which, when ■ Syiupionis of Acute Pericarditis. 309 associated with rigors and sweatings, are so characteristic of suppuration. When the inflammation extends to the pleura, and more especially to the lung itself, the fever is proportion- ately increased. In some cases there is hyperpyrexia,^ and in these cases grave cerebral symptoms, the exact nature of which I shall presently describe, are usually developed. The frequency of the pulse is, as a rule, considerably increased, the amount of increase in the earlier stages being proportionate to the amount of fever. In exceptional cases the pulse may be slower than normal. In the earlier stages it is sometimes full and bounding, and of high tension, but more frequently irritable and soft. In all cases of peri- carditis there is a tendency to failure of the pulse and to the production of dicrotism ; and this is more especially the case where the myocardium is implicated. When endocarditis and valvular complications are present, the characters of the pulse may, of course, be profoundly modified, the exact characters depending upon the nature of the valvular com- plication. Cardiac symptoms proper. — Subjective cardiac sensations, which result from derangement of the. heart as a vital, sensi- tive organ, such as pain in the region of the heart, a feeling of tightness or constriction about the chest, and (occasionally) palpitation or intermittent action of the heart, are experienced in the great majority of cases of pericarditis. Cardiac symptoms of this description are suggestive of the presence of pericarditis, but they are not distinctive of that condition. In short, the student should distinctly understand that the symptoms of pericarditis {i.e. the symp- toms as distinct from the physical signs) are by no means characteristic. According to Sibson's elaborate statistics, pain of a more or less continuous character is present in three-fourths of the ' The exact cause of the hyperpyrexia is not known. It is much more common in cases of rheumatic fever, complicated with pericarditis, than in cases which are unattended with that condition. The statistics of the Clinical Society of London seem to show that the pyrexia is not associated so frequently, as was formerly supposed, with suppression of perspiration. 3IO Diseases of tJic Heart. cases of rheumatic pericarditis. It is most marked in cases of ' dry' pericarditis, and usually disappears when the effusion becomes copious. Its intensity is not as a rule great, but in some cases ' the suffering and distress over the heart are so great as to drown all other complaints.' In a considerable proportion of cases there is pain and tenderness in the pit of the epigastrium ; and in some cases there is also tenderness on pressure over the region of the heart itself^ In exceptional cases a constrictive pain in the chest, radiating to the left shoulder and down the left arm, and resembling the pain of angina pectoris, is met with. It pro- bably depends upon the fact that the cardiac nerves (branches of the cardiac or coronary plexuses) are irritated by the inflammatory process. One of the most marked cases of angina pectoris which I have ever seen, was attended with, and apparently depended upon pericarditis. The following is an abstract of it : — Case — Angifia pectoris; perica?'difis of obscure origin. The patient was a ship-captain, iist. 49, of a florid complexion and sanguine temperament. He had suffered from syphilis, and had perhaps indulged somewhat too freely in alcohol, but had been in vigorous health up to the occurrence of the attack. The pain commenced gradu- ally in the region of the heart, and continued more or less constantly for a fortnight. It was severe throughout the attack, and was, as a general rule, confined to the region of the heart ; ever)' now and again — some days several times in the twenty-four hours — it became greatly intensified, and assumed the characteristic features of angina pectoris. During the earlier days of the attack nothing of importance was detected in the condition of the heart, but well marked pericardial friction subsequently developed. At the end of a fortnight the pain and pericardial friction ' Sibson concludes, probably with truth, ' that the pain on pressure below or at the side of the ensiform cartilage is in these cases due, not to peritonitis, but to inflammation of the fibrous structure and pericardial or inner surface of the central tendon of the diaphragm, where it forms the floor of the pericardial sac, and the lower and anterior portion of that sac' The same authority states, ' that if the pain over the heart is increased or excited by pressure over the region of the organ, it may, with an approach to certainty, be attributed to nflammation of the pleura, especially if the pain on pressure is complained of, not before, but at the time of or after the first presence of the friction sound.' — Russell Reynold's System of Medicine^ vol. iv. pp. 230 and 224. Symptoms of Acute Pericarditis. 31 1 both disappeared, and the patient apparently made a complete recover)-. I am unacquainted with the after progress of the case, and I ha^•e never been quite able to satisfy myself as to the exact cause of the attack. The aortic second sound was throughout the attack, and also subsequent!)-, somewhat accentuated, and I have often surmised that the cause of the pericarditis was the pressure of an aneurism originating immediately above the sigmoid valves. Mechanical symptoms, which result from disturbance of the action of the cardiac pump (such as pallor or lividity of the countenance, irregularity and failure of the heart's action, the pulsus paradoxicus, faintness, difficulty of breathing, ortho- pnoea, etc.) are usually observed in severe cases. They may be due to one or other of the following conditions : — {a) Effusion into the sac of the pericardium sufficiently copious to embarrass the action of the heart, and to interfere with the course of the circulation. A large effusion, more especially if it is rapidly poured out, may seriously interfere with the course of the ciixulation, by compressing the thin- walled auricles, the venae cavae, and pulmonary veins, and so prevent the due supply of blood to the aorta and pulmonary artery. The right auricle and superior cava, iti consequence of the comparative thinness of their walls, are affected most by the pressure. In consequence of the pressure on the superior cava, the veins in the neck become distended, and the greater the pressure on the superior cava the greater the distention of the veins. In cases of pericarditis, fulness of the veins of the neck is, therefore, suggestive of co- pious effusion, more especially when there is no evidence of endocarditis or over-distention of the right cavities of the heart. {bi) Inflammation of the cardiac muscle. ici) Endocarditis and associated valvular lesions. Mechanical symptoms are only seen in severe cases of pericarditis (cases with copious effusion), or in those cases in which the inflammation of the pericardium is associated with disease of the muscular walls or valvular mechanism of the heart. In fact, in any case of pericarditis in which mechanical symptoms were prominent, we would probably be 3 1 2 Diseases of tJie Heart. correct in concluding that there was something more than mere inflammation of the pericardium present {i.e. that either myocarditis or endocarchtis was present.) Pressure symptoms. — When the effusion is very extensive, the greatly distended pericardial sac may press upon the oesophagus and produce difficulty in swallowing (dysphagia), or upon the trachea or left bronchus, and cause cough and difficulty in breathing. These symptoms are aggravated by the recumbent, and relieved by the sitting posture. Aeeidcntal symptoms, due to the extension of the inflam- ination to surrounding parts (other than the myocardium or endocardium), or to the presence of complications, are of common occurrence. In a considerable proportion of cases, pleurisy, with its attendant symptoms and signs (pain in the side, etc) develops. In a few cases, pneumonia or pulmonary apoplexy is met with.^ In rare cases, more especially in rheumatic pericarditis, cerebral symptoms and hyperpyrexia occur. Hyperpyrexia is, according to the elaborate report of the Clinical Society of London, much more frequent in males than in females, and is much more common in a first than in subsequent attacks of rheumatic fever. The nervous symp- toms met with in connection with it are in the order of their relative frequency as follows : — * delirium (in all phases), insomnia, restlessness, muscular tremors, involuntary dis- charges, subsultus tendinum, coma (a late symptom), head- ache, tremor of tongue, deafness, tonic spasms (in two cases of tetaniform character), risus sardonicus, convulsions, flocci- tation, tinnitus aurium, giddiness, drowsiness, vomiting, silli- ness of manner, fearfulncss, hesitating speech, chorea, hyper- jEsthesia.' 'The delirium, which is the most frequent symp- tom met with in these cases, sometimes precedes, sometimes ' Pleuritic pain was present in one half of Sibson's cases of rheumatic peri- carditis. He says that it may Ije due to two causes, viz.: — one, the extension of the inflammation through the fibrous structure of the pericardium to the pleura covering it ; the other, the occurrence of pulmonary apoplexy with its attendant pleurisy. — Russell Reynolds, vol. iv. p. 233. Syiuptonis of Acute Pericarditis 0^6 accompanies, and sometimes follows the onset of the hyper- pyrexia.' One half of the cases of hyperpyrexia, collected by the Clinical Society, terminated fatally. The duration, after the development of the nervous symptoms, varies from a few hours to three, four, or five days. In addition to the delirium which is associated with hyperpyrexia, Sibson, Austin Flint, and others, have described a peculiar form of mental derangement, characterised by a state of taciturn melancholia and (according to Austin Flint) a suicidal tendency. According to Sibson's observations, the cases of pericarditis, in which this peculiar form of mental aberration was met with, were almost always complicated with endocarditis, and in some cases chorea subsequently developed ; and Sibson suggests that the condition is due to embolic plugging of minute vessels of the cerebral cortex. This form of delirium differs from the delirium which is associated with hyperpyrexia, in as much as it is not associ- ated with fever, its duration is much longer (from three weeks to three months, according to Sibson), and in the fact that the majority of cases, which are not complicated with chorea, terminate in recovery. In a third group of cases of pericarditis, a form of delirium which resembles more or less closely delirium tremens, is met with. This form is, according to Sibson, usually asso- ciated with moderate fever, and occurs in persons of an anxious nervous disposition, in those who have been addicted to alcoholic excess, or who have been exposed to want and pri- vation. It is sometimes seen in connection with hyperpyrexia. /;/ addition to tJic syiuptonis already ennnierated, the following may be added : — Alteration of the eountenanee. — In a large proportion of cases the facial physiognomy is altered. In some the face is flushed.^ This condition is seen more especially in the earlier stages of rheumatic cases {i.e. in cases in which the ' Sibson suggests that flushing and pallor of the countenance may in some cases be due to reflex disturbance of the vaso-motor centre, the pericardial inflam- mation acting as the peripheral source of irritation. 314 Diseases of tJie Heart. action of the cardiac pump is not as yet embarrassed), and is generally associated with profuse sweating. In others, the face is pale, pinched, and anxious; and there may be other indications of collapse and nervous exhaustion, such as nausea, vomiting, restlessness, insomnia, a weak thready or irregular pulse, etc. Severe pain in the region of the heart or in the joints, and sudden failure of the heart's action, as the result of copious effusion, myocarditis, valvular complications, etc., are the most frequent causes of this state of depression. In others, again, the countenance is more or less dusky, livid, or congested. This condition is generally seen in the later stages of the case, and is associated with obstructed venous return, the causes of which I have already described in speaking of the mechanical symptoms. (See p. 311.) Cough, hoarseness, and aphonia. — A short, dry, irritable cough is often present, and in some cases there is hoarseness or aphonia. The latter symptoms probably depend upon irritation of the left recurrent laryngeal nerve as it winds round the root of the aorta. ^ Physical signs. — The physical condition of the pericardium is ascertained by the same means by which we ascertain the condition of the heart itself, and it is important to remember that, under normal circumstances, the opposed surfaces of the sac are in close contact, and move smoothly and noiselessly one upon the other, and that the signs derived from the physical examination of the pericardium are entirely negative. In other words, the size and shape of the pericardium corre- spond, in conditions of health, exactly to the size and shape of the heart itself, and the outlines of the two structures cannot be distinguished by means of percussion, while on listening over the pericardium the sounds of the heart are alone heard.- ' In a case observed by Baeumler (quoted by Bauer, Zienissen's Cyclopaedia, vol. vi. p. 603), double paralysis of the vocal cords, due to the pressure of a large pericardial effusion upon both recurrent nerves, was observed. * It has been stated that, during violent action of the heart, a friction sound is sometimes produced within the normal pericardium, but in common with other observers I am disposed to doubt the statement. Phydcal signs of Acute Pericarditis. 3 1 5 Now in pericarditis the physical conditions are entirely altered, and it is only by keeping the nature of the altera- tions prominently in view, that it is possible to understand in- telligently the alterations in the physical signs which occur when the membrane is inflamed. These alterations are as follows : — Firstly, the surfaces of the pericardium become covered with a layer of lymph, and the rubbing together of the two opposed rough and inflamed surfaces {i.e. of the visceral and parietal layers of the sac), which occurs during the systolic and diastolic movements of the heart, is attended with the production of vibrations, w^iich are heard, through the stetho- scope as friction-sounds or murmurs, and can, in some instances, be felt by the hand placed over the prsecordium as friction fremitus. Pericardial friction-sounds and pericardial friction fremitus may be termed tlie pJiysical signs zuliic/t result from roughening of the membrane. Secondly, fluid is poured out into the interior of the sac. In many cases the distention of the sac is sufficiently great — {ci) To give rise to increased dulness on percussion over the praecordium, and to enable us, in some cases, to differentiate, by means of percussion, the outline of the pericardium from the outline of the heart. (/;) To produce such displacement in the position of the heart, that the cardiac impulse and the apex beat are either altered from the normal position or (in rare cases) completely effaced — physical facts which we determine by means of palpation. ((f) To cause lateral displacement of the lungs, and down- ward displacement of the diaphragm and therefore of the left lobe of the liver. id) To cause, more especially where the effusion is con- siderable and the chest wall elastic, bulging of the praecordium and widening of the intercostal spaces corresponding to this part of the chest. ie) By compressing the auricles and veins, to cause disten- tion of the veins of the neck, and to interfere with the natural J 1 6 Diseases of tJic Heart. course of the circulation — effects which I have already alluded to, and which are of course manifested by distinct symptoms and physical signs. The physical signs which are due to the conditions enumer- ated under headings a, b, c, d, and e, may be termed ihc physical signs wJiich result {or rather ivJiicJi may^ result) from effusion into the sae. Now in some cases the effusion is never sufficiently great to produce increased dulness on percussion, and the other physical signs which I have termed ' the physical signs which result from effusion into the sac' In other cases, when the patient first comes under observation, the effusion is not as yet sufficiently extensive to alter the percussion outline of the heart, although it subsequently may become so. In others again, although sufficiently extensive to produce increased dulness at an earlier period of the case, it has already been in great part absorbed before the patient comes under observa- tion. In all of these cases the physical signs will simply be those which are due to roughening of the walls of the sac, in short, those of the so-called dry"^ form of pericarditis. In the so-called moist variety of pericarditis, on the con- trary, the physical signs are not merely those which result from effusion into the sae. The pericardial friction usually continues throughout the period of effusion. Moist peri- carditis is, therefore, characterised by physical signs resulting both from effusion into the sac and roughening of the peri- cardial membrane. Let us now consider some of the more important of these physical signs a little more in detail. Character of Pericardial Friction Sounds. Rhythm. — In typical cases pericardial friction is double, a to-andfro sound, as it has been termed, the to and fro corre- ' I say may result, for unless the effusion is considerable, some of them at all events (distention of the veins of the neck, for instance), are not produced. ^ The somewhat artificial division into dry and moist, is especially useful in describing the physical signs. Dry pericarditis may be defined as pericarditis in which the amount of effusion is not sufficiently extensive to be detected by means of percussion ; while moist pericarditis may be defined as pericarditis in which the effusion is sufficiently extensive to be detected by means of percussion. Physical signs of Acute Po'icardiiis. 3 i 7 spending to the rubbing of the two rough surfaces of the membrane during the systole and the diastole of the heart re- spectively. The synchronism with the heart sounds is seldom very exact, and in this respect there is, as we have previously seen, an important distinction between pericardial and endo- cardial murmurs. The two divisions of the sound are, as a rule, of equal duration, the systolic portion being generally louder than the diastolic. Occasionally the pericardial friction sound is single, and it is then systolic {i.e. it corresponds rather to the first than to the second sound of the heart). In some cases it is triple, and presents 3. presystolic as well as a systolic and diastolic rhythm. Point of inaximuni intensity and direction of propagation. — Pericardial friction is usually best heard over that part of the heart which comes in most direct and forcible contact with the front wall of the chest. Under ordinary circumstances, therefore, the friction is first and best heard over the front of the right ventricle, that is to say, over the lower end of the sternum and the adjacent costal cartilages. In many cases the friction sound is limited to the pra^cordial region, and very often to the part of the chest wall which corresponds to the exact point of the sac at which the friction is produced ; though, as Sibson has shown, when the vibrations are directly communicated to the sternum, as they are most likely to be in cases of dry pericarditis {i.e. when there is no intervening layer of lung tissue or of fluid between the point of their pro- duction and the front wall of the chest), the friction sound may be conducted in various directions by the sternum and costal cartilages, which are attached to it — the sternum acting as a sounding board. Pericardial friction sounds have no de- finite and distinct lines of propagation as endocardial murmurs have. Sound Character. — In the majority of cases the sound, as the i&rva frietion murmur suggests, is harsh, and gives one the distinct impression of being produced by the rubbing together of two rough surfaces. In many cases it is actually grating or creaking (resembling the sound produced by the creaking of new leather ' bruit de cuir neuf") ; exceptionally it is soft in 3i8 Diseases of t lie Heart. character. It is usually superficial, i.e. it seems to be pro- duced immediately under the ear. In addition to these characters, which are usually of themselves quite conclusive, pericardial friction is almost invariably intensified, and in many cases its sound characters are absolutely altered by the pressure of the stethoscope; the effect of this pressure being of course to bring the two roughened surfaces of the pericardium in closer and firmer contact one with the other. Pericardial friction sounds, too, are very apt to undergo spontaneous alterations in character (rhythm, tone, area, etc.), and this is more particularly the case in the earlier periods of the inflammation, and depends of course upon the fact that the physical conditions within the sac (amount of exudation, etc.), are then undergoing rapid alterations. When the friction sound is loud, the normal heart sounds are, as a rule, completely obscured by it ; when the friction sound is soft the normal heart sounds may, as it were, be heard through it. In those cases in which endocarditis and valvular complications are present, valvular murmurs are some- times audible in addition to the pericardial friction sounds. The loudness and tone of the pericardial friction sound seem to depend upon: — (i) the force with which the two opposed surfaces of the roughened pericardium are rubbed together, and the amount of movement which takes place between them, that is to say upon the force with which the heart is contracting, and the amount of the external resistance opposed to its contraction, which in its turn depends upon the position of the organ in the thorax, and especially the relationship of the organ to the front wall of the chest ; and (2) the amount and consistency of the lymph. Vigorous action of the heart ; close contact of the organ with the front wall of the chest, more especially of the right ventricle with the sternum ; a small amount of fluid in the sac ; and a thick layer of tolerably tough lymph on the two opposed surfaces of the pericardium, seem to be the conditions which favour the production of loud pericardial friction ; and other things being equal, the louder the friction sound the more extensive the area over which it is propagated. Physical signs of Acute Periccn-ditis. 319 Dulness on Percussion over tlie Prceconiiui/i. The dulness which is due to effusion into the sac of the pericardium presents certain important characteristics. Its extent depends upon the amount of effusion into the sac, the more extensive the effusion the greater the dulness. The condition of the anterior margins of the lungs is also of considerable importance ; when the lungs are very voluminous, as in emphysema, or when their anterior margins are fixed to the front wall of the chest by adhesions, the dulness is by no means so extensive as when they are normal and can be readily pushed aside and compressed by the enlarging sac. The fonn and outline of the dulness correspond to the form and outline of the pericardial sac ; and since the peri- cardium is not reflected at the base of the heart, but includes in its narrower, upper part a considerable portion of the great vessels, it follows that the area of dulness which results from distention of the sac is pyramidal (more correctly a truncated pyramid, the apex being above, the base below) or pear- shaped — the stalk of the pear corresponding to the upper and narrower part which surrounds the great vessels, the body of the pear to the lower part of the distended sac which surrounds the heart itself. The peculiar shape of the dulness is of great diagnostic value ; and another point which is equally import- ant as an indication of pericardial effusion, but which unfor- tunately is not always present, is that in some cases the area of dulness extends beyond, i.e. further to the left than the apex-beat — z.^. the left apex beat. In figure 158, the shape of the pericardium, when artificially distended with fluid, is shown ; in fig. 159, the appearance which the sac may present when greatly distended in disease. In fig. 160, the character- istic pear-shaped outline, which the dulness presents, is well seen. Some recent writers differ from the usually received opinion, that the form of the area of cardiac dulness is characteristic of pericardial effusion. Thus Dr Rotch, in the Supplement to Ziemssen's CyclopcBdia of the Prac- tice of Medicifte, page 363, says, 'Bauer's opinion, that the triangular shape of the area of dulness depends upon the shape of the pericardial sac, has not been substantiated by later observations, the theory of Duchek having been found to be more correct, namely that in cases uncomplicated by 320 Diseases of the Heart. pleuritic adhesions it is the retraction of the edges of the lungs which determines the shape of the absolutely dull area and that therefore the so-called triangular figure can be produced by an enlarged heart as well as a pericardial effusion.' Fig. 158. Fig. 159. Fic;. 15S. — Pericardium distended intojifteen oiiiiees ofjiuid. (After Sibson.) P'lG. 159. — Case of pericarditis in 'which the sac contained 3^ ll)s. of fluid. Altered Position of the Heart and Apex Beat. The effusion at first collects at the sides of the heart, at the bottom of the pericardial sac, and around the great Physical Signs of AciUe PeTicarditis. 321 Fig. 160. — Outline of percussion dulness in a case of pericardial effusion. (After Sibsoii.) vessels. As it becomes more and more copious the sac becomes, of course, more and more distended, and the heart is pushed upwards, the apex being tilted towards the left. In consequence of this alteration in the position of the heart, the position of the cardiac impulse is altered, the lower boundary of the impulse being situated in the fourth or even the third, instead of in the fifth interspace, as it is in health. The apex beat not unfrequently corresponds to the left nipple, and in some cases it may be situated slightly above, and to the outer side {i.e. to the left) of the nipple. When the effusion is copious, the apex beat is usually impaired in force or altogether effaced. In exceptional cases, owing to the fact that the heart is enlarged, as the result of previous disease, or tied down, as the result of previous pericarditic adhesions, the position of the heart and apex beat is not altered. When the effusion is absorbed, the heart and with it the cardiac impulse and apex beat usually return to the normal position. An exception to this, the general rule, X 32 2 Diseases of the Heart. occurs in some cases in which adhesions are formed while the heart is still in its displaced position. In consequence of the alteration in the position of the heart, which occurs in most cases of copious effusion, the area of the pericardial friction sounds, which we have previ- ously seen persist, as a rule, through the period of effusion, is also displaced upwards. The to-and-fro murmur may, therefore, be heard in the third or fourth interspaces, and considerably to the left of the sternum instead of over the lower end of the sternum and the adjacent lower left costal cartilages, as it is in cases of ' dry' pericarditis. When the fluid is absorbed, and the heart returns to its normal position, the area of friction moves downwards with it. Prominence or bulging of the preeeordinni and sivelling in the pit of the epigastrium are sometimes observed when the effusion is copious. Decided prominence of the prsecordial region only occurs when the chest wall is elastic, and is therefore most commonly seen in young subjects ; it would be more frequent in women than in men if it were not usually obscured by the prominence of the left mamma. The lower left intercostal spaces are widened, and some observers have described fluctuation in them, but this condition (fluctuation) is probably very rarely (if ever) present, in acute pericarditis. General survey of the symptoms and pliysical signs. — Let us now take a brief general survey of the symptoms and signs of acute pericarditis ; and remembering that acute inflam- mation of the pericardium is usually secondary, let us omit for the purposes of description the symptoms which are due to the primary disease, and limit the description to those which result from the inflammation of the pericardium itself It will be self evident from what I have already stated, that cases of acute pericarditis vary very considerably in the severity of the symptoms, and in the nature of the physical signs which they present. The following types of the disease may be described : — I. Cases of latent periearditis. — In these cases the symp- toms are extremely slight or altogether absent, and in many Symptoms of Acute Pericarditis. 6^6 cases of this description the condition entirely escapes notice. The effusion is for the most part slight, but the case which I have related on page 298, shows that a considerable effusion may be unattended by any marked symptoms. Latent pericarditis very rarely indeed proves fatal ; the case to which I have just alluded shows, however, that death does occasionally occur from syncope. 2. Uncomplicated cases of dry pericarditis zvJiich are at- tended by distinct symptoms. — In these cases there are no mechanical symptoms ; pain in the region of the heart is the chief complaint ; the countenance may present evidence of suffering, but the general constitutional symptoms are not, as a rule, severe. On auscultation the characteristic pericardial friction murmur is heard over the praecordium (usually over the lower end of the sternum and adjacent costal cartilages, though in some cases it is much more diffused) ; there is no distinct increase of the percussion dulness ; friction fremitus is occasionally felt over the prsecordial region. 3. Cases of moist pericarditis in zvJiicJi the effusion is not sufficiently copious to seriously embarrass the action of the heart, and in ivhich there is no myocarditis or endocarditis. In this group, which includes a large number of the cases of acute pericarditis met with in practice, subjective cardiac sensations due to derangement of the heart as a sensitive, vital organ (such as pain, constriction of the chest, palpitation, etc.), are present, but mechanical symptoms (see page 311) are either slight or altogether absent. The physical signs vary with the stage of the disease. Pericardial friction is the first physical sign which can be observed ; in a short time, usually in a few hours, dulness on percussion is developed and gradually assumes the characteristic outline, which I have previously described in detail (see page 319); when the effusion is copious the whole cardiac impulse is raised, the apex beat displaced upwards and to the left, the force of the apex beat being usually impaired and sometimes altogether effaced ; with the elevation of the heart the area of pericardial friction is also elevated ; in young subjects the precordial region may be more prominent than in health. As the 324 Diseases of the Heart. effusion is absorbed, the area of cardiac dulness gradually diminishes, the apex beat regains its normal position, and the friction murmurs, which during the period of effusion are, as a rule, strictly limited to the area of dulness, and usually to the area of the cardiac impulse, may become more diffused, and are sometimes heard over the whole of the sternum and adjacent parts of the chest. In exceptional cases friction fremitus may now be felt when the hand is placed over the praecordium. 4. Cases of moist pericarditis in zvJiich the effusion is suffi- ciently copious to seriously embarrass the action of the heart, and cases of pericarditis (either dry or moist) which are complicated, with symptoms due to myocarditis or to endocarditis. The cases included under this group are attended with grave symptoms indicative of serious interference with the course of the circulation, and with serious failure of the action of the heart, such as marked pallor or livid ity of the counten- ance, faintness, extreme exhaustion, an unusually rapid, weak, irregular, and dicrotic pulse, considerable distention of the veins of the neck, considerable dyspnoea or orthopnoea, dropsy, etc. The physical signs up to a certain point are the same as those described as characteristic of the third group, viz., the physical signs proper to a considerable and usually progressive pericardial effusion. When the heart begins to fail the friction murmur usually becomes diminished in intensity ; and altera- tions in the rhythm of the heart (irregular action, etc.) may be heard on listening over the prsecordium. With the occurrence of endocarditis valvular murmurs are developed. It must not, however, be supposed that valvular murmurs are only heard in those cases of pericarditis which are included under this group. In a large proportion of the cases of peri- carditis (of the rheumatic cases at all events) which have been included in groups i, 2, and 3, endocardial murmurs are also present. In this group I include those cases in which in addition to the valvular murmurs, symptoms due to valvular lesions are present, i.e. when the valvular lesion is sufficiently severe to mechanically interfere with the course of the circulation. Clinical His lory of A title Pericarditis. 325 Onset, Course, and Termination. Onset. — The onset is in many cases insidious, pain and dis- comfort in the region of the heart being very generally the first symptoms which attract attention. In other cases, the attack is ushered in by a feeling of chilliness and by the usual malaise, etc., which so frequently attend the commencement of febrile diseases, very exceptionally there is a distinct rigor. In some cases nausea and faintness are the first symptoms. Course. — In acute cases the inflammation of the pericar- dium rapidly runs its course, — a fact which explains the fre- quent alterations in the physical signs which are met with in the disease. In the course of three or four days the effusion has usually reached its height ; the period during which the sac remains fully distended, is, as a rule, brief, in most cases absorp- tion begins to occur within a few hours after the effusion has reached its highest point. Unless the case should become chronic, which it only does in exceptional cases, the period during which the effusion is stationary, so to speak, is seldom longer than two or three days. The period of absorption and resolution generally occupies several days. The whole duration of the attack, from the commencement to the dis- appearance of friction, is usually from one to three weeks, though many exceptions to this rule occur, in some cases the duration is shorter, in others much longer than that specified. Termination. — The natural termination of inflammation of the pericardium, is recovery with the formation of adhesions i.e. with partial or total obliteration of the sac. Occasionally, but very rarely in cases of rheumatic origin, death occurs during the acute stage ; in a few cases the condition becomes chronic. But to these points I shall again refer in speaking of the prognosis. Diagnosis. — In considering the diagnosis of pericarditis, it is essential to remember that the symptoms are only sugges- tive but not distinctive ; and that inflammation of the pericar- dium can only with certainty be recognised by means of the physical signs. Friction sounds, synchronous with the action 3 26 Diseases of the Heart. of the heart, and increased dulness on percussion of the form and outline, which have been previously described, are the physical signs of greatest importance ; but neither of them is, when taken singly, absolutely conclusive, for on the one hand there are certain conditions in which sounds are heard re- sembling those produced in an inflamed pericardium, and on the other, there are several conditions in which dulness on percussion, resembling more or less closely the dulness due to pericarditis, is present. Steps in the diagnosis of pericarditis. — When a case of supposed pericarditis comes under observation, we have there- fore to determine : — 1. Is inflammation of the pericardium actually present? 2. If the case is one of pericarditis, what is the cause of the condition, and what is the character of the effusion ? 3. Is the case complicated with myocarditis or endocar- ditis? Step No. I. Is the case one of pericarditis? — In some cases it is easy to decide this point, in others difficult. When a patient, who has been previously in good health, is attacked with an acute illness, more particularly with one or other of those affections, in the course of which acute pericarditis is apt to occur ; and when a to-and-fro friction murmur and increased dulness on percussion, are present over the praecordium (more especially when the increased dulness on percussion is rapidly developed under, as it were, the eye of the observ-er), the diagnosis is self-evident. In other cases the diagnosis is difficult ; and it will be neces- sary to consider in the next place, the conditions in which sounds resembling pericardial friction, or dulness resembling, more or less closely, that produced by pericarditis is present ; and the means by which they are to be distinguished. The differential diagnosis of pericarditis with friction, and the other conditions with which it is likely to be cojifounded. The typical to-and-fro friction murmur of pericarditis is of course, sx-nchronous with the action of the heart, and it is Diagnosis of Acute Pericarditis. 327 by this means at once distinguished from ordinary pleuritic friction. Cases are, however, occasionally met with in which a pleuritic murmur is of cardiac rhythm. In \\\q first place, therefore, we must consider : — The dijfereiitial diagnosis of perica^-dial friction and peri- cardial-pteurat friction. In some cases it is impossible to pronounce a positive opinion, but the distinction can generally be made by atten- tion to the points detailed in the following table : — Table I. TJie Differential Diagnosis of Pericardial Friction and Pericardial-pleu rat Friction. Pericardial Friction. Pericardial-pleural Friction. Where audible. Usually heard over the centre Usually heard over the borders, of the right ventricle. more especially the left border, of the heart. Effect of respira- Seldom much affected by the Always more or less affected by Hon. respiratory movements, never the respiratory movements; completely arrested by hold- often completely arrested on ing the breath. Never act- holding the breath; often con- ually* converted into ordinary verted into ordinary pleural friction by a full inspiration friction by a full inspiration or deep expiration. or deep expiration. * Note — This point is not of much importance, for true friction is not unfrequently accompanied by pleurisy, and in cases of this des- cription the pericardial friction may on a full respiration, be masked (though it is not actually replaced) by the ord'nary friction sound. In the second place, pericardial friction is sometimes soft in character {i.e. it lacks the harsh characters which friction sounds typically possess) ; and since a double murmur is very frequently generated at the aortic orifice, we must now con- sider the differential diagnosis of the double murmur which is due to pericarditis on the one hand and to combined aortic stenosis and incompetence on the other. The points of dis- tinction are given in table II. 128 Diseases of the Heart. Table II. Tlie Differential Diagnosis of the Pericarditis, and the Double Stenosis and Incompetence. Double Murmur of Pericarditis. Double Mil mm r due to Murmur due to Aortic Position ofmaxi- miun intensity. Usually loudest over the right ventricle and lower half of the sternum. Area where audi- Usually heard over a limited ble, and direction area, and not propagated over of propagation. the course of the aorta, and into the vessels of the neck. Relationship to the heart sounds. Does not replace but only obscures (more or less com- pletely) the heart sounds; and is not exactly synchronic with them. Double Murmur of Aortic Stenosis and Incompetence. Although the diastolic portion of the murmur is often heard loudest over the lower end of the sternum, it is also well heard at the base of the heart. Usually heard over an exten- sive area, and propagated over the course of the aorta, and (usually) into the great vessels of the neck. Does actually replace (but not always completely) the heart sounds, and is always exactly synchronic with them. Variability. Effects of exter- nal pressure. Pulse. Apt to vary from day to day, or from hour to hour, both in respect to its position and sound characters ; the inter- val between the systolic and diastolic portions is not al- ways of the same duration, and not always distinct. Almost invariably altered in character by the pressure of the stethoscope, when soft is often converted into a rough friction sound. Remains constant as regards its position and sound charac- ters ; the interval between the systolic and diastolic por- tions is always of the same duration and is distinct. Uninfluenced by the pressure of the stethoscope. Not jerking, visible, collapsing Is jerking, visible, collapsing, or tortuous. and often tortuous. Condition of the Not much altered in size unless Icftvcntricle; out- previously diseased. Dulness, line of dulness ; pear-shaped withwell-marked force and position stalk. Apex beat feeble or of apex beat. effaced, tilted upwards and to the left. .Etiology. Usually developed acutely in the course of acute rheuma- tism, Bright's disease, etc. Almost invariably hypertro- phied and dilated — Dulness, heart-shaped without well- marked stalk. Apex beat strong, displaced downwards and to the left. May be developed acutely as the result of rheumatic or septic endocarditis, but is usually developed very gra- dually as the result of ather- Diagnosis of A cute P erica rditis. 329 In the //;/;'<:/ place a pericardial friction murmur is some- times (instead of being double) single and systolic ; and in such cases it may be mistaken for a murmur generated within the heart itself, i.e. a systolic mitral, tricuspid, aortic, or pul- monary murmur. These are the cases in which pericarditis is liable to be mistaken for endocarditis ; the mistake is most likely to be made when the pericardial murmur is soft in character. In table III., p. 330, I have detailed the points of distinc- tion between typical pericarditis and typical endocarditis, while in table IV., p. 331, is given the differential diagnosis of those cases of pericarditis, in which the murmur is single, systolic, and soft, and of the mitral, tricuspid, aortic, and pul- monary murmurs which are present in cases of chronic valvular lesions, anaemia, etc. In the fourth place, we must consider the differential diagnosis of increased dulness due to pericarditis and increased dulness due to other conditions. Simple serous effusion into the sac of the pericardium (hydropericardium) and enlarge- ment of the heart itself (more especially dilatation of the heart), are the conditions included under this group which are most likely to give rise to difficulty. TJie differential diagnosis of increased dulness due to peri- carditis and simple dropsy of the pericardial sac. In both of these conditions the form and outline of the dulness are the same, but the diagnosis can usually be made without difficulty, by attention to the points detailed in table v., p. 332. The differential diagnosis of pericardial effusion a)id enlarge- ment of the heart itself, is a point of considerable practical im- portance ; for an enlarged (more especially a dilated) heart has been more than once punctured under the impression that the case was one of effusion into the pericardial sac. The points to which attention should be directed in making the distinction are shown in table VI., p. 333. 130 Diseases of the Heart. Table III. TJic Differential Diagnosis of Acute Pericarditis and A en te Endocarditis. I. Chai-aders of the murmur. {a) Rhythm of murmur. [b) Sound char- acters. (c) Position of maximum in- tensity. {d) Direction of propagation. (^) Variability. (/) Effectsof pres- sure. 2. Outline of dul- ness on per- cussion. Pericarditis. In typical cases a double (to- and-fro) murmur, which ob- scures, but does not actually replace the heart sounds, and which is not exactly syn- chronic with them. Excep- tionally the murmur is single and systolic. In typical cases a harsh friction sound ; exceptionally, soft ; superficial. Usually over the right ventricle, but only accidentally, having its point of differential max- imum intensity in the mitral and tricuspid areas. Usually very limited in area, and not propagated in any of the definite lines of pro- pagation of endocardial mur- murs. Character liable to change (position, loudness, harsh- ness, etc.,) within brief pe- riods of time. Almost always intensified, and often modified in other re- spects, by the pressure of the stethoscope. Area of dulness often increased, and pear-shaped (see p. 321). J. Impulse, apex- Feeble or effaced ; if much beat. effusion apex tilted upwards * and to the left. Endocarditis. In the majority of cases the murmur is single and systolic, occasionally double (aortic). The murmur replaces one or other of the heart sounds, and is exactly synchronic with it. Note. — Exception in the case of pre" systolic murmurs, which are how- ever rarely due to acute endo- carditis Usually soft and blowing, deep- seated. In the mitral, tricuspid, aortic or pulmonary areas. May be heard over an extensive area, and propagated in cer- tain definite directions (see table VIII., p. 527). Character more constant. Not modified by pressure. Dulness not, as a rule, much increased ; its exact outline depends on the cavity or cavi- ties of the heart which are enlarged. Impulse may be strong ; apex in normal position. If the left ventricle is hypertrophied , apex displaced downwards and to the left ; if the right ventricle is enlarged, impulse may be in the pit of the epi- gastrium. 4. Pain over the pracordia^ and tenderness in epi- gastrium. Usually present. Usually absent. Diagnosis of Pericarditis. 331 til ^5 a— X. ^0 -ii r^"^ O p! Is S-3 sS g s ^ 1 a-" .- Sao S ^ P< t3 D c rt s o 0.0 "as !-"£ o a -rt o c °i: "• c • . .-. oj rt C C tJ ' 3 ii S ° S 4-. «= H y S ?. j3 > rt I. o'^'S o 3 ^~ ° 3 — > c t3 " rt £? T3 rt n,g C 3 g 3 6 C O en " o-a 13,2 mI? <^ c Si33^ i; a o S O 3 a O 3 ai • - X 3 V V o ;— C/) T3 pig ;3 -5 c •^1 1 3 o 2 2 6-0 o c o bB u S c c -o o 0.0 "It r- *^ Ui IS i ^ ^b- s'^ ^ ^s •s'S .^ s S .^ b ^ e- ■S s ^ i; 1^ 0-, k ^ llll 332 Diseases of the Heart. Table V. The Differential Diagnosis of increased Dulncss due to Pericarditis and Hydropericardiuni . Pericarditis. Pericardial fric- Usually present, even at the iion. height of the effusion ; always present at some stage of the case, i.e. before or after the height of the effusion. Subcutatuous Usually absent, unless com- dropsy ajid cffii- plications (great venous en- sion into other gorgement from pressure, scrolls sacs. valvular lesions, Bright's disease, etc.) Fever. Usually present. Hydropericardiuni. Absent. Hydropericardium is part and parcel of a general dropsy, and usually a late event in that condition. Absent, unless some complica- tion. Pain over pra- cordia, and ten- derness oil pres- sure in epigas- trium. ALtiology. Usually present. Usually occurs in the course of acute rheumatism and cir- rhotic Bright's disease, etc. Seldom observed. Usually in the terminal stages of mitral lesions ; or, in the course of Bright's disease, more especially the acute form, and the large white chronic variety. The differe)itial diagnosis of pericardial effusion and of dila- tation of the heart. — The difficulty chiefly occurs, when the patient comes under observation with the pericardial dulness already developed, and more especially in those cases in which it is stationary and chronic, and when there is no peri- cardial friction. In both conditions (pericarditis with effusion and dilatation of the heart) there is increased dulness on per- cussion over the prsecordia, a feeble impulse, usually feeble sounds, and often dyspnoea, venous engorgement, dropsy, etc. In order to arrive at a correct conclusion, an accurate examin- ation of the heart, and careful inquiry into the previous history of the case, and the other points detailed in the following table are indispensable Diagnosis of Pericarditis. Zo o J Table VI. TJie Differential Diagnosis of increased Dtdness dne to Pericarditis and Dilatation of the Heart. Pericarditis with Effusion. Dilatation of the Heart. Outline of Did- Dulness pear-shaped, and en- ness. largement chiefly upwards. Dulness not pear-shaped, and enlargement chiefly down- wards. Rate of develop- Oftenrapid, and then character- me7it of Dill- istic. ness. Usually very slow ; though a rapid dilatation of the heart sometimes occurs. Imptilse and apex- The impulse, when present, is Impulse can usually be felt to beat. in the 3d or 4th left inter- the left of the lower end of space ; apex beat tilted up- the sternum, or in the epi- wards and outwards, or gastrium. effaced. Relation of did- Dulness may extend to the left ness to left apex- of the left apex-beat. beat. Auscultation. Pericardial friction maybe pre- sent ; when absent, sounds are obscured. Pain over pra- Often present. cordia atid ten- derness in epi- gastrium. Pulsation in the May be present if endocarditis veins of the neck. complicates. Aetiology. Fever Usually acute, in course of acute rheumatism, cirrhotic Bright's disease. Often present. Dulness does not extend to the left of left apex beat. Pericardial friction not present ; sounds short, but usually clear. Usually absent. Often present when right heart dilated. Usually chronic ; often associ- ated with chronic valvular lesions, fatty and fibroid de- generation, anaemia, etc. Absent unless from some com- plication. The differential diagnosis of increased dulness due to pericardial effusion and hypertroph)- of the heart, can usually be made without difficulty. (See table VII.) 134 Diseases of the Heart. Table VII. The Differe7itial Diagnosis of increased D illness due to Pericarditis and Hypertrophy of the Heart. Pericarditis with Effusion. Outline of dul- See remarks in Table VI. Hypertrophy. See remarks in Table VI. Rate of develop- Usually rapid. ment. Impulse; apex- beat. Pulse. Impulse, when present, is in the 3d or 4th left interspace, and is feeble ; apex tilted upwards and outwards, or beat effaced. Weak and quick ; maybe para- doxical. Pericardial fric- Often present. tion. Usually slow. Impulse powerful ; if left ven- tricle hypertrophied, apex displaced downwards and outwards ; if right ventricle hypertrophied, apex dis- placed downwards and in- wards, beat may be in the epigastrium.. Character of the pulse depends on the side of the heart which is hypertrophied, and the cause of the hypertrophy. When left ventricle hyper- trophied, and no aortic ob- struction or mitral regurgi- tation, the pulse is large and powerful. Absent. Prognosis. — In considering the prognosis of pericarditis, we have to take into account, firstly, the danger to hfe involved by the attack itself {i.e. the immediate prognosis), and secondly (in those cases which recover), whether the ad- hesions, which almost always remain, to a greater or less ex- tent, after a severe attack of pericarditis, will be likely to produce any permanent or after bad effect upon the action of the heart. The remote prognosis is practically, therefore, synonymous with the prognosis of ' adherent' pericardium. TJie immediate prognosis. — The danger to life depends upon the following conditions :— (i) The CBtiological cause of the condition. — Uncomplicated cases of rheumatic pericarditis almost always recover. Peri- Prognosis of Ac life Pericarditis. 335 carditis due to traumatic injury, wounds of the sac, etc., is less serious than pericarditis which follows the rupture of an abscess (in the liver for example) into the sac. Peri- carditis occurring in the course of Bright's disease is very generally fatal ; the prognosis is still worse in cases of purpura and scurvy ; while tubercular is almost invariably, and cancer- ous pericarditis always fatal. (2) The severity of the associated diseased condition, and of tJie pericardial inflammation itself. — Other things being equal, a dry is less serious than a moist pericarditis, while in the latter form, the more copious the effusion, the worse the prog- nosis. In both varieties, however, tJie condition of tJie cardiac muscle, and the state of the valvular apparatus, are the two most important (cardiac) elements which determine the prognosis, the presence of myocarditis being especially unfavourable. The form of the pericarditis, whether acute or chronic, is also of importance, chronic pericarditis being very often fatal. When the effusion consists of pus, the prognosis is also much more unfavourable than in simple cases. (3.) The presence of complications, and the previous state of health of the patient. — The opinion must of course be based upon the exact nature of the complication. Hyperpyrexia, with severe cerebral symptoms, occurring in the course of rheumatic pericarditis is a very serious complication ; while the fact that the heart was diseased before the attack of pericarditis commenced, adds considerably to the danger. Other things being equal, a robust, healthy person will be more likely to survive an attack of pericarditis than a weakly delicate individual. But we find many exceptions to this general rule. (4.) The age of the patioit. — In very young or very old subjects, the prognosis is much more unfavourable than at other periods of life. Treatment. — In considering the aetiology, I have pointed out that in a large proportion of cases, pericarditis is second- ary ; and that, in some cases, the inflammation of the peri- cardium occurs in the course of certain ereneral affections 336 Diseases of the Heart. (acute rheumatism, Bright's disease, etc.) ; in others, it is due to the direct extension of pre-existing inflammation from some neighbouring organ or part (the pleura, mediastinum, lung, etc.) ; while in a third group of cases, it results from the secondary deposits of a tubercular, sarcomatous, or can- cerous nature in the tissues of the pericardium. Now, in treating the many different primary affections, which are included in these three groups, it is essential to keep this tendency to pericarditis prominently in view, to protect the patient most scrupulously from everything likely to act as an exciting cause or to arouse the inflammation of the peri- cardial sac, in short to adopt, so far as we are able, a preventa- tive plan of treatment. It is no less important in managing the primary affec- tions, to examine the heart carefully from time to time, and to look out for the first symptoms and signs of local mischief, in order that we may, if possible, cut short and allay the pericardial mischief as soon as it appears ; while, in treating cases of secondary pericarditis, after the pericardial inflamma- tion has fully developed, one of the points to which attention must be prominently directed is the treatment of the primary affection. Tlie prevention of pericarditis. — Speaking generally, we may say that the best method of preventing secondary peri- carditis is to remove as soon as possible the primary affection, guarding the patient at the same time from everything which is likely to excite the inflammation of the pericardium itself. Some of the primary affections, in the course of which pericarditis is apt to occur, such for instance as chronic Bright's disease and cancer, resist our present therapeutic means of cure ; and in them we must content ourselves with guarding the patient against exposure to cold, and anything which will excite or depress the action of the heart. Others, as for example, acute rheumatism and some cases of local inflammation in the neighbourhood of the pericardium, can be successfully controlled by a well directed and energetic plan of treatment. In acute rheumatism, for instance, we Ti-catnieui of Acute Pericarditis. 337 endeavour to cut short the attack by saturathig the system with sahcin or saHcylate of soda ; allaying excessive pain, should it be necessary, by hypodermic injections of morphia ; guarding the patient from cold by placing him in blankets and a flannel night gown to absorb the excessive perspiration, by warming the stethoscope and avoiding any undue exposure of the pr^Ecordium in making a routine examination of the heart ; and carefully avoiding everything which will be in the least likely to excite or injuriously depress the action of the heart.^ It would be out of place to detail here the manner in which the different primary affections are to be dealt with, I therefore pass to the treatment of the pericardial inflammation itself The treatment of tJie pericardial inflammation itself. — In dealing with a recently developed case of pericarditis, it is essential to remember, as Dr Sturges has so ably pointed out, and as I have for a long time been in the habit of teaching, that an inflammation of the pericardium differs from many other inflammations in this important particular, viz., that although it seldom is of itself directly fatal, it frequently is ' I am aware that statistics seem to show that salicin and salicylate of soda do not prevent rheumatic pericarditis and other cardiac complications. It will not, however, be disputed, that the rheumatic symptoms proper (the fever, the joint affection and the pain) are speedily relieved by these drugs ; and I find it difficult to believe that any plan of treatment, which is able to cut short the rheumatic fever itself, will not in many cases prevent the occurrence of pericarditis, provided that it is energetically enforced before the pericardial inflammation is established. Sibson's observations as to the influence of pain and cardiac excite- ment in the production of rheumatic pericarditis seem to lend additional support to this view. The difficulty in arriving at a conclusion from statistics as to the influence of salicin in preventing rheumatic pericarditis and other cardiac com- plications is considerable. In many cases, no doubt, the signs of pericarditis are first detected after the salicin plan of treatment has been commenced, but it is unfair to lump all cases together, and to say that salicin does not prevent rheumatic pericarditis ; in some, the pericarditis was without doubt actually present though undetected or undetectable before the treatment was commenced ; in others, the pericardial inflammation was developed before the system was properly saturated with the drug. It is only the remainder, viz., those in which the pericardial inflammation developed after full saturation of the system that can be legitimately adduced in evidence ; and we want, I think, more information on this point. (This subject is afterwards considered in greater detail, see p. 3^^-) 338 Diseases of iJie Heart. followed by secondary changes, which cripple the vitality of the patient, and which lead to the subsequent disease, and it may be to an early death. A lung, for example, which has been affected with croupous pneumonia, however severe, is (in the great majority of instances) to all intents and purposes as sound as it was before ; but a heart after a severe attack of pericarditis is, in many cases, permanently damaged, in consequence, not only of the adhesions which remain, but also — and this is much more important — because of the strong tendency which the inflammatory process has to make its way to the deeper structures, and to leave permanent structural alterations in the muscular walls of the organ. As soon, then, as there is any evidence of local mischief, it is all important to do what we can to cut short and allay the inflammatory process in the pericardial sac. The patient should, if possible, be placed in a well venti- lated and airy room, the temperature of which must be con- tinuously kept between 65° and 70° Fahr. Absolute rest in the recumbent position must be rigidly enforced, and every- thing which tends to excite the action of the heart avoided. A full dose of quinine, in combination with morphia, as recommended by Professor Robert Bartholow,^ should be administered ; and local means employed to restrain those vas- cular changes which accompany eveiy inflammation. In robust and previously healthy individuals, and more especially in those in whom the pnlse is strong and tense, the local abstraction of blood should be practised, six, eight, or ten leeches being applied over the proecordial region. The continuous application of cold to the region of the heart by means of ice-bags is next recommended, more especially by German writers. Personally, I have no experience of this plan of treatment, for, in common with most English physicians, I have been in the habit of recommending warm applications or a mustard poultice, followed by the continuous application of ' Bartholow recommends the administration of a full dose of quinine (15-20 grains of the sulphate) with a quarter to half a grain of morphia, ' and the cin- chonism should,' he saj's, ' be maintained by repeated smaller doses, for twenty- four hours or longer.' — Practice of Medichu, second edition, p. 237. I Treatment of Acute Pericarditis. 339 heat, by means of hot poultices or fomentations, to the prai- cordia, I can easily conceive, however, that in suitable cases (in robust and previously healthy individuals, and quite at the commencement of the attack) the continued application of cold may be beneficial. Excessive and violent action of the heart should be restrained by the frequent administration of small doses of aconite^ or veratrum viride. The administration of aconite is recommended by Pro- fessor Sydney Ringer ' in pericarditis accompanied with violent throbbings and extreme pain.'"' Pain in the region of the heart should be relieved by subcutaneous injections of morphia ; and even in those cases in which there is little or no pain, the administration of small doses of opium or morphia is often very beneficial. I must repeat, that depletion, continuous cold, aconite and veratrum viride are only permissible in robust and previously healthy individuals, especially in those in whom the pulse is strong and tense ; and also, that it is important in all cases in which these remedies are employed, to keep a watchful eye upon the condition of the heart and pulse, for it is essential to avoid anything which depresses the action of the heart. Leeches, continuous cold, aconite and veratrum, are useful so long as they are employed merely to moderate exces- sive action, they are injurious when they are pushed beyond this point, and allowed to produce depression. The treatment appropriate to the primary affection must, at the same time be persevered with. There is, however, one very important exception to this general rule, viz., that in rheumatic cases the further administration of the pre- parations of salicin (more especially salicylate of soda, for, according to Dr Maclagan, salicin itself does not depress the heart) should be dispensed with. The diet should be light and nutritious, consisting chiefly of milk and soups. As soon as the excessive action of the heart has been moderated, or, if at the end of twenty-four or thirty-six hours ' In cases of albuminuric pericarditis (pericarditis occurring in the course of rright's disease) opium if given at all, must be administered cautiously. ^ Handbook of Therapeutics, ninth edition, p. 472. 340 Diseases of tJic Heart, the inflammatory process is not arrested, the aconite or vera- trum should be discontinued ; and it is, in many cases, advis- able to discontinue the ice-bags, and to apply poultices, fomen- tations, or soothing liniments, containing opium, chloroform, belladonna, etc., to the pr.xcordium.^ The subsequent treatment of the case must be modified in accordance with the form of the disease (whether dry or moist), the severity of the attack, the general constitutional state, etc. It is difficult to lay down general rules applicable to all cases. The following, however, may be said to be the chief indications for treatment. 1. To allay the inflammatory process. — The same general measures should be continued as were recommended in the earliest stages of the attack (absolute rest, the avoidance of anything likely to excite the action of heart, a light diet, etc.). When the fever is considerable, the quinine may be continued, with or without a diaphoretic. Warm poultices or anodyne fomentations are to be continually applied to the praecordial region. 2. To relieve symptoms. — Pain is to be relieved by local anodyne applications, or the internal or subcutaneous ad- ministration of opium or morphia. Sleeplessness, which is often a distressing symptom, is also best relieved by an opiate at bedtime. Where there is no pain, chloral, or chloral combined with bromide of potassium, may be substituted ; personally I prefer opium or morphia, for chloral is apt to have a depressing influence upon the heart. Xausea and ' Modifications in the vascularity of the pericardium may probably be produced in two ways by means of external application, viz. : — (i.) Directly, through the communications which exist between the subcutane- ous vessels of the chest wall and the vessels on the outside of the pericardial sac. By depleting the subcutaneous vessels by means of leeches, we deplete at the same time the vessels on the outside of the pericardial sac ; and by producing dilatation of the subcutaneous vessels by the application of a warm poultice, we draw blood from the vessels in the exterior of the pericardium which communicate with them. (2.) Indirectly, by reflex nervous impulses. This is probably the more im- portant of the two, for by this means we can probably act not only upon the exterior of the visceral pericardium, but also upon the interior of the parietal pericardium, and indeed upon the vascularity of the heart itself. Trcatniciit of Acute Pericarditis. 341 sickness, which arc not unfrequent, and are often distressing symptoms, are best reheved by sucking ice, the appHcation of a mustard bhster to the pit of the epigastrium, and the internal administration of champagne, brandy, morphia, or hydrocyanic acid. Dyspncca is often met with in the later stages of the attack ; it may depend, as we have previously seen, upon many different conditions, amongst which failure of the action of the heart, valvular complications, the pressure of a large pericardial effusion upon the trachea or left bron- chus, and lung complications (such as pleurisy and pneumonia) are the chief. Each of these forms of dyspnoea will, of course, require a special plan of treatment. When, for instance, the shortness of breath is due to failure of the heart's action, cardiac tonics and stimulants should be freely administered ; when the dyspnoea is urgent, and when it depends upon the mechanical pressure of a large effusion, aspiration of the peri- cardium should be practised. Hyperpyrexia is, as we have previously seen, occasionally developed in the course of rheumatic pericarditis. Prompt measures should be at once taken to reduce the temperature, and amongst these the cold-bath treatment appears to be by far the best. The patient should be immersed in a bath at 95°-ioo° Fahr., cold water should gradually be added until in the course of twenty minutes or half an hour the tem- perature of the bath is reduced to 60° Fahr. If there is any tendency to cardiac depression, it is a good plan to give a small quantity of brandy both before and after the bath. The patient should at once be removed from the bath if any serious symptoms of cardiac depression arise. In private practice, or when it is inconvenient to immerse the patient in a bath, the application of iced-cloths, in the manner recommended by Professor Sydney Ringer,^ may be substituted. 3. To sustain the strength of the patient, and in particular should any indications of cardiac failure arise, to stimulate and strengthen the action of the heart. This is a most important indication, for one of the great ' Handbook of ThcrapcuiUs, ninth edition, p. 6i. 342 Diseases of the Heart. dangers in pericarditis is failure of the action of the heart. A watchful eye should always be kept upon the pulse and venous circulation. When the heart's action is irritable and weak, digitalis or convallaria majalis should at once be administered, the dose depending, of course, upon the special circumstances of each case. Alcoholic stimulants (brandy), carbonate of ammonia, or spirits of chloroform, should be given in those cases in which there is rapid failure of the heart. 4. To promote absorption of the inflammatory products. — In the majority of cases, the inflammatory products are more or less rapidly absorbed soon after the acme of the effusion has been reached ; but this is not always the case, and it is often desirable to assist the natural process of absorption. With this object, iodide of potassium, diuretics (especially digitalis, and convallaria majalis), and if the patient's strength per- mits, diaphoretics are administered internally ; counter irri- tants (tincture of iodine, small and frequently repeated fly- blisters, etc.) are applied over the praecordia ; while the greatest attention is paid to the condition of the general health, the treatment in fact should, so far as possible, be of a tonic character, the object being to raise the gen- eral tone of the system, and in particular to sustain and strengthen the action of the heart. Digitalis and convallaria majalis, which are both powerful cardiac tonics and active diuretics, are particularly useful. The diet should be light, and at the same time as nutritious as possible ; the bowels must be regulated ; and the ventilation of the patient's room carefully attended to. It is particularly important to avoid all causes of mental depression, and in short to keep the patient as cheerful and hopeful as possible. 5 . When the effusion is progressing so rapidly or is so exten- sive as to seriously embarrass the action of the heart and endaiiger life, or when it refuses to be absorbed by ordinary treatment, to zvithdraiu the fluid by aspirating the pericardial sac. It is unnecessary again to detail the symptoms, which result from the pressure of a large pericardial effusion upon the heart itself and upon the surrounding structures, or the Treatment of Acute Pericarditis. 343 manner in which a pericardial effusion is to be distinguished from the other conditions with which it is Hkely to be con- founded, for these points have already been considered (see pages 329, ctseq.). I therefore pass on to say that the operation has now been performed in a large number of cases with com- plete success ; the result has been most favourable in rheumatic cases associated with rapid effusion into the sac ; it is much less favourable in non-rheumatic forms, and especially when the condition has become chronic. Dr John B. Roberts of Philadelphia, who has directed special attention to the subject, states that of thirty-five cases in which the operation has been performed since the year i860, ten recovered and twenty-five died, giving a mortality of 71-42 per cent. 'In the twenty- five instances where death occurred subsequent to the tapping serious disease is stated to have existed in all the cases except three. In other words, out of the whole thirty-five cases operated upon, there were thirteen cases of pericardial effusion where other diseases did not seem to act as a complication, and of these ten recovered and three died. This would give a mortality of 23 per cent.' Dr Roberts not only recommends that the operation should be performed 'whenever the effusion whether it be serum, pus, or blood accumulates so rapidly or in such quan- tity that it threatens to destroy life, and refuses to undergo absorption by ordinary treatment ; ' but he even advocates its use as a palliative method of relief, in cases in which the pericardial inflammation depends upon, or is associated with incurable organic conditions. The sac should be punctured with the aspirator, and with the strictest antiseptic precautions. In selecting the point of puncture we must avoid the heart itself, the dia- phragm, the internal mammary artery, and, if possible (though this is a point of much less importance) the left pleura. In most cases the needle should be inserted in the fifth left interspace, midway between the nipple line and the sternum, just above the junction of the sixth rib with its ' These statistics, which are detailed in Dr Robert's work on Paracentesis of the Pericardium, page 97, were brought up to the year 1880. 344 /^/scascs of the Heart. costal cartilage. When the heart is enlarged or tied down by adhesions, the puncture should be made in the sixth inter- space, or, as Sibson suggests, between the ensiform cartilage and the seventh costal cartilage. The following are the directions which it is advisable to follow in performing the operation : — (i.) Place the patient in the recumbent position, so as to allow the heart to fall away from the front wall of the chest. (2.) See that the apparatus is in working order and per- fectly clean. It is a good plan to draw a stream of carbolic solution through it before attempting to insert it into the sac. (3.) Count the interspaces accurately from above, down- wards. (4.) Percuss and auscultate over the seat of the proposed puncture, and satisfy yourself that it is dull on percussion, and that the dulness does not depend upon the presence of the heart. (5.) Introduce the needle of the aspirator with a firm plunge ; if the skin is thick, or if you are using a large needle, a preliminary incision through the skin with a sharp bistuory is advisable. The needle should be directed at first directly backwards, and then backwards and downwards in order to avoid wounding the heart. (6.) If after exhausting the apparatus no fluid passes, withdraw the needle, wash it out, and if you feel sure of your diagnosis reintroduce it. (7.) It is advisable, unless there is any indication to the contrary, to draw off all or a large portion of the fluid at one sitting. (8.) After the needle is withdrawn a piece of lint should be fixed by adhesive plaster over the superficial wound. (9.) If pure blood flows through the instrument, if the heart has been wounded, or if any untoward symptoms, such as acute pain, dyspnoea, etc., should arise during the process of aspiration, the needle should at once be withdrawn. 6. WJioi tJic effusion eonsists of pus to lay open tlie sae, nneier strict antiseptic preeautioiis, and to insert a drainage tube. AdJierent Pcricardiuiu. 345 When the effusion consists of pus the case should, in short, be treated as any other internal abscess. Both physicians and surgeons are becoming every day more and more convinced that whenever there is an internal collection of pus it should if possible be evacuated ; and a collection of pus within the sac of the pericardium forms no exception to the general rule. As yet the operation has only been twice performed success- fully. The details of the last case, that of Dr West, will be found in the Lancet for April 28, 1883, p. 728, to which the reader is referred for further information on the subject. ADHERENT PERICARDIUM. The recovery from an attack of acute pericarditis is seldom complete, for in most cases some adhesions between the visceral and parietal layers of the sac remain. Sometimes the whole sac of the pericardium is obliterated, more fre- quently the adhesions are partial. The adhesions are permanent,^ and since they are in some cases followed by secondary changes in the heart and circulation, and therefore by permanent bad effects upon the health of the patient, I must now describe the nature of the secondary changes, the symptoms and physical signs to which they give rise, and the manner in which peri- cardial adhesions are to be recognised during life. The effects ivhicJi pericardial adJicsions produce upon the heart, and the symptoms to which they give rise, depend more particularly upon the following conditions : — 1. The extent and character (more especially the density) of the adhesions. 2. The condition of the muscular walls of the heart after the attack of pericarditis has subsided. 3. The condition of the valvular apparatus of the heart. When the adhesions are limited in extent, when the myocardium and valvular apparatus remain healthy, the adhesions produce little or no effect upon the condition of the heart, and are unattended with symptoms. ' It occasionally happens that the adhesions are afterwards broken down by the movements of the heart. 346 Diseases of the Heart. When, on the contrary, the adhesions are universal and dense, when the pericarditis is compHcated with myocarditis, and an increase of the intermuscular fibrous tissue remains after the attack has subsided, the muscular walls of the heart usually undergo degeneration, the muscular fibres becoming atrophied^ in consequence of the pressure which the fibrous tissue (both on the surface and in the substance of the organ) exerts upon them during its cicatrisation.- In these cases very grave symptoms, indicative of failure of the heart muscle, which I shall describe in detail when I come to speak of the effects of myocarditis (see p. 564), are observed.^ In other cases, again, the heart becomes hypertrophied ; indeed it used to be supposed that an adherent pericardium, by embarrassing the action of the organ, necessitated in- creased force of contraction, and consequently produced hypertrophy. We now know that although this is the se- quence of events in some cases, partial atrophy of the muscu- lar fibres and dilatation rather than hypertrophy are usually observed. In many cases a combined condition of partial atrophy with dilatation, and of partial hypertrophy results ; and in a certain number of cases more or less general hyper- trophy is found. This result (hypertrophy) is usually due to associated valvular lesions, though it may be the direct result of the pericardial adhesions independently of any valvu- lar lesion ; it is most likely to occur in those cases in which the pericardial sac is adherent to the front wall of the chest as well as to the surface of the heart, and in which the myo- cardium is healthy.^ In cases of this description {i.e. adherent pericardium with ' In many of these cases the weight of the heart and the thickness of its walls are not diminished, in fact they may be increased. The atrophy of the muscular fibres can, in such cases only be detected by microscopical examination. - The fibrous tissue which remains after a pericarditis, contracts just as the fibrous tissue in a cicatrix does. ^ It must be remembered that increased thickness of the cardiac walls, and increased weight of the organ, do not necessarily indicate true hypertrophy, i.e. an actual increase of the muscular tissue. The increased weight may be due to an increase of fibrous tissue and fat, and may actually be associated with atrophy of the true muscular elements, as I have observed above. Physical signs of Adhei'ent Pe^'icardiuni. 347 hypertrophy) the symptoms are usually those of the valvular lesion which is so often present, and on which, to a consider- able extent at least, the hypertrophy depends. The physical signs of adherent pericardium. — In some cases, more especially when the adhesions are partial and confined to the interior of the sac, the condition is not attended with any distinct physical signs, and cannot^ therefore, be recog- nised during life ; in other cases, there are very distinct physical signs which clearly indicate the nature of the con- dition ; while in a third group of cases, the physical signs are equivocal or indistinct. The physical signs characteristic of adherent pericardium are best marked in those cases in which — (i) The adhesions within the sac are extensive or universal. (2) The exterior of the sac is adherent to the chest wall and to the anterior margins of the lungs. (3) The heart is acting powerfully, i.e. is hypertrophied. The condition of the anterior margin of the lungs, more especially of the left lung, is also an important point. When the anterior margins of the lungs are tied down by adhesions, the physical signs are more distinct. When, on the contrary, the lungs have free play, and still more when they are vo- luminous or emphysematous, the physical signs of adherent pericardium are obscure and indistinct. When there are extensive adhesions both on the interior and exterior of the pericardial sac, the heart is, as it were, rigidly fixed in the cavity of the chest, and the free play of its natural movements is interfered with. In consequence of this alteration in its physical condition, the following altera- tions in the physical signs are observed : — ( I ) Systolic depression, instead of systolic protrusion of the apex beat ; and in many cases a systolic depressioji of the lozver end of the sternum and adjacent costal cartilages. — In conse- quence of the adhesions, the ventricles, during their contrac- tion, pull directly upon the diaphragm and front wall of the chest, and it is to this traction, aided, of course, by the 34S D/scascs of t lie Heart. external pressure of the atmosphere, that the systoHc depres- sion of the apex beat and front wall of the chest is due. This systolic depression is most marked when the chest wall is yielding {i.e. in young subjects), and when the ventricles are acting powerfully {i.e. when the heart is hypertrophied) ; vice versa it is absent or indistinct when the cartilages are ossified, and when the heart is acting feebly {i.e. the muscular walls of the heart degenerated, its cavities dilated, etc.) Systolic depression, instead of depression of the apex beat, is not absolutely distinctive of pericardial adhesions, as Friedreich has shown ; and Bauer says — ' We may state in general terms that systolic pitting at the site of the apex beat may be present in all cases in which the normal movement of the heart downwards and to the left, with elevation of the apex, is hindered, provided at the same time the lungs do not sufficiently approach each other, and the contraction of the heart is powerful enough to force the apex away from the chest wall. Under such circumstances the pitting follows, as a matter of course, from atmospheric pressure." (2) Permanent depression of the precordial region. — This condition, in which, as it were, the temporary systolic depres- sion has become fixed and permanent, is only observed in those cases in which the chest wall is elastic, and in which the pericardium is extensively adherent to the heart on the one side and to the chest wall on the other. (3) A diastolic rebound of the chest zvall. — This is a most distinctive sign of adherent pericardium, and it is due to the fact that after the depression of the lower end of the sternum and adjacent costal cartilages has taken place, and when the ventricle begins to relax, the natural elasticity of the chest wall causes a rebound, which can be distinctly felt by the hand as an impulse during the diastole of the heart. (4) Absence of the apex beat.— In some cases of adherent pericardium the apex beat is absent. This condition is most likely to occur when the heart is acting feebly, or when the lungs are adherent over the position of the apex beat. In some cases in which systolic depression of the apex beat is observed, it is impossible to feel the pulsation of the ' Ziemssen'.s Cyclop. has developed during the present attack), and in which the symptoms and signs of valvular lesion are rapidly developed, there is of course no difficulty. The occurrence of a presystolic mitral or tricuspid, or of a diastolic aortic or pulmonary murmur, under such circumstances, is quite conclusive, whether the murmur is attended with cardiac symptoms or not, for these murmurs always depend upon mechanical changes in the valve flaps or valvular orifices. 384 Diseases of the Heaii. There is much more difficulty when, as is usually the case, the murmur is systolic. I have already detailed in full the reasons which lead me to regard a mitral systolic murmur or impure first sound, occurring in the early stages of an attack of acute rheumatism, and in a person previously free from cardiac disease or marked anaemia, as highly suggestive of acute endocarditis. The same murmur (a mitral systolic murmur) when it occurs in the later stages of the attack, is possibly anaemic in character, more especially if the patient is markedly anaemic, and if the development of the mitral murmur is preceded by a pulmonary sj-stolic murmur ; but it is impossible to give a positive opinion on the point. The murmur may be organic ; and the wise physician, while hoping for the best [i.e. that it is anaemic), will take every precaution, and treat the patient as if the murmur depended upon organic disease. A basic s)'stolic murmur, aortic or pulmonary (but especially the latter), which develops late in the attack, and when the patient is anaemic, is very generally functional. Murmurs which are loud and well propagated are generally organic, musical murmurs are always so. Step No. J. — // inf animation of the endocardium is present, is that inflammation of the simple or ulcerative form ? The consideration of this question must be deferred until the ulcerative form of endocarditis has been described. (See page 41 1.) Prognosis. — In forming the prognosis the following points must be taken into account : — (i) The nature and severity of the primary affection with which the endocardial inflammation is associated. (2) The state of the heart itself (3) The condition of the other tissues and organs. In rheumatic endocarditis, the immediate result is usually favourable, but some cases die, as we have seen, during the acute or subacute stages of the disease. Symptoms indicative of grave mechanical derangement of Proojwsis of Aaite Endccarditis. 385 the circulation, and of failure of the heart, such as dyspnoea, dropsy, cyanosis, a quick, weak, and irregular pulse, are very serious indications. Cases in which aortic regurgitation is acutely established are, as a rule, more serious than those in which the mitral valve is affected. Pericarditis, and more particularly myocarditis, add to the gravity of the attack. The existence of previous valvular dis- ease, other things being equal, materially increases the danger. The ultimate prognosis is in a large proportion of cases unfavourable, for many patients, who recover from the acute affection, ultimately suffer and die from chronic valvular disease. The prognosis should always, therefore — even in the mildest cases — be guarded, for so long as the slightest indica- tions of endocarditis are present, it is impossible to be certain that serious valvular lesions may not remain. The disappear- ance of the systolic apex murmur, which is the most common physical sign of endocarditis, is, of course, the most favourable indication. It is not, however, proof positive of the cure of the endocarditis, for, as Dr Sansom has shown, the regurgita- tion may have been due to an affection of the myocardium rather than of the endocardium ; the corpuscular infiltration of the myocardium may be absorbed ; the valve may become competent ; but the endocardial cicatrix, so to speak, may continue to contract, and a murmur indicative of organic valve disease may in a short time be established. In all cases, therefore, the heart should be examined from time to time during the period of convalescence. The character of the murmur and the condition of the heart must, of course, be taken into consideration. A soft valvular murmur, which is not well propagated, and which is not attended by any marked accentuation of the pulmonary second sound or by secondary changes in the right heart, very often disappears without leaving any organic change behind. Vice versa the lesion is a serious one in those cases in which the murmur is heard below the angle of the left scapula, in which the second sound is accentuated, and more especially in which there are secondary changes in the right heart (increased dulness result- ing from dilatation, a systolic tricuspid murmur, etc.). BB J 86 Bisrasc's of tJic Heart. A murmur, which continues after convalescence is fully established, may, in exceptional cases, disappear at the end of some months. As a rule, however, such a murmur, and the organic changes on which it depends, are permanent. The extent and severity of the lesion which remains, vary greatly in different cases. Each case must of course be judged on its own merits in accordance with the principles which will be described when I come to treat of chronic valvular lesions. Treatment. — As in the case of pericarditis, it is necessary to consider both the prophylactic and curative treatment of the affection. Prophylactic treatment. — Since acute simple endocarditis is seldom primary, but usually occurs in the course of some other disease, our prophylactic measures must be directed : — (i) To ivarding off or preventing the primary affection zuith ivhich it is apt to he associated. Space does not allow me to enter into details as to the manner in which acute rheumatism, chorea, scarlet fever, measles, diphtheria, pyaemia, puerperal fever, and the other affections with which endocarditis is apt to be associated, are to be prevented. The prophylactic of these affections consists, of course, in avoiding the causes — both predisposing and exciting — which produce them. The reader who wishes further information on this subject must consult some of the standard works in which the aetiology of these affections is fully treated of. (2) To aire the primary affection, luhen once it is established, as speedily as possible, and in particular to adopt sncJi a plan of treatment as is most likely to prevent inflammation of the endo- cardium . Applying this indication to the treatment of acute rheu- matism, which is, as we have repeatedly seen, by far the most common cause of acute endocarditis, we must endeavour to cut short the rheumatic attack, to allay the pain and fever as speedily as possible, and to enforce a rigid system of rest, for, as Sibson has shown, the relief of pain and suffering, together Treatment of Acute Endocarditis. 387 with absolute rest, exerts a most beneficial influence in pre- venting cardiac complications. Sibson's observations on this point are, I think, of extreme importance, and have a very direct bearing upon the treatment of acute rheumatism bysahcin and its compounds. I make no apology, therefore, for quoting what he says in full. He states : — 'We here find that in the series of cases of acute rheumatism that were treated by a system of absolute rest, the proportion of those that were attacked with endocarditis was slightly less than that of those that were not so treated. Thus far the comparison is but slightly in favour of the treatment of acute rheumatism by a rigid system of rest ; and this would seem to suggest that a certain and a very large proportion of cases of acute rheumatism are habitually and in- trinsically attacked by endocarditis. When, however, we extend the comparison, and ascertain the proportion in which those cases of endo- carditis, not previously so affected, acquired permanent valvular disease, so as to injure health during the remainder of life, and to shorten life itself, we discover that the series of cases not treated by a system of absolute rest were thus permanently injured in a far larger proportion of cases, amounting to more than twice as many, or in the ratio of eight to three, than in those that were treated by rest. 'If we pursue the inquiry further, so as to discover the relative extent to which the interior of the heart was inflamed in the two series of cases, we discover that there was but one instance, or i in 24, of those with endo- carditis and without previous valvular disease, of the series treated by a rigid system of rest, that gave definite evidence of inflammation of both the aortic and mitral valves, while in 19 instances in 127, or i in 67 of the same kind of cases that were not treated by a rigid system of rest, there was direct evidence of aortic regurgitation. In nine, or rather ten, of those cases that were not treated by rest, there was a mitral murmur, and therefore direct evidence of inflammation of the mitral vahe ; but in the remaining nine cases there was also evidence of mitral endocarditis in the shape of a tricuspid murmur, or prolongation of the first sound, with intensification of the pulmonic second sound, and obstacles to the flow of blood through the lungs.^ The whole chain of e\idence points ' There will probably be considerable difference of opinion as to the exact value which these physical signs possess as evidence of acute endocarditis. In the absence of any obstruction in the lungs, they are indicative of some embarrassment in the left heart. Now, considering the frequency of acute endocarditis in acute rheumatism, and the frequency with which a systolic mitral murmur and permanent evidence of valve disease spring, as it were, directly out of these physical signs, I am personally disposed to think that when they are met with in the early stage of the attack, and are unassociated with anaemia and basic cardiac murmurs, that they are suggestive of endocarditis, but certainly not a distinct proof of its presence. 388 Diseases of the Heart. then, I think, irresistibly to the conclusion that the extent, severity, and permanent ill effects of the endocarditis were much greater in the series of cases that were not rigidly treated by rest than in the series that were so treated." Now for the relief of the joint affection and the reduction of the temperature, there is, I suppose, a concensus of opinion, that the sahcyHc treatment is better than any other. Twenty to thirty grains of saHcin or salicylate of soda given every two hours, succeed, in a large proportion of cases, in completely removing the joint affection, and in reducing the temperature within forty-eight hours. If then Sibson's observations and deductions are correct, this drug ought to exert a very beneficial influence in preventing cardiac complications. If it does not exert such a beneficial influence, we must, I think, conclude that, while relieving the joint affection and fever, it actually exerts a prejudicial effect on the heart, rendering the endocardium more liable to be affected, and neutralising the protective influence which the relief of the joint affection and fever ought, according to Sibson's observations, to produce. The most extensive observations which have as yet been published on this point, are those which were brought forward at the great debate before the Medical Society of London in the year 1881 ; and it seems to have been pretty generally concluded, that the result of the statistics then brought forward was to show that salicin and its compounds do not exert the protective influence in warding off cardiac complica- tions which we would a priori have expected. Personally I have considerable hesitation in accepting that conclusion as correct, more particularly as some of the leading speakers in that debate (Drs Hilton Fagge, Broadbent, Douglas Powell, Havilland Hill, and Herman), seemed, on the whole, to think that the influence of the salicylic compounds in preventing endocarditis was favourable, and also for the following reasons : — - ' Russell Reynolds' System of Medicine, vol. iv. p. 527. * I state these reasons with great diffidence, for I am fully aware that it is often extremely difficult to form correct conclusions upon figures and facts with which one is not personally familiar. Those who were present at the debate, and more particularly the speakers who were familiar with all the facts (for in analysing Trcatiiicut of Acute Endocarditis. 389 In the fij'st place, the result of that debate was almost entirely based upon hospital cases ; and, as Dr Douglas Powell very justly, I think, observed, and as Dr Maclagan^ has pointed out, it is almost impossible to determine this question by the results of hospital practice. In a large proportion of hospital patients, endocarditis — as evidenced by a systolic apex murmur — is already developed on the patient's admission. These cases must, of course, be ex- cluded in any inquiry as to the influence which salicin has in preventing endocarditis. Again, there is good reason for supposing, as I have previously pointed out in detail (see p. 379), that endocarditis is present at the time of the patient's admission, in many cases in which there is no murmur, but in which a bruit subsequently becomes audible. These cases must also be excluded, for, as Dr Maclagan puts it, ' this saving action (of the salicyl compounds) cannot be got unless they are given in adequate quantity before the poison has begun to act on the hearti^ It may, of course, be said, and the argument doubtless has some force, that the salicyl com- pounds should not only prevent, but that they should also allay the endocardial inflammation even after it is developed. There are not the same fallacies in deciding this point, and there seems to be a very general opinion that these drugs have no influence in this direction. Dr Fagge 'fully admits that salicylic acid seems to have no power of controlling or arresting the cardiac complications of acute rheumatism when once they have developed themselves.'^ Dr Maclagan believes that when endocardial complica- tions occur, ' the treatment by salicylate of soda occasionally increases the patient's danger. I refer especially,' he says, ' to those cases more numerous than is usually supposed, in which the muscular substance of the heart is the seat of in- flammation. Myocarditis has, for its pathological condition, such a large number of cases as were analysed by some of the speakers in this debate, it is of course impossible to go into every detail), were, of course, much more likely to come to a more correct conclusion than I can possibly do. ' Rheitviatisia, p. 271. ■ Locks cit. p. 269. ^ La7icet, Dec. 17, 1881, p. 1033. 390 Diseases of the Heart. thickening-, softening and enfeeblement of the n:mscular walls, chiefly those of the left ventricle. If to this enfeeblement is added that which sometimes follows the administration of salicylate of soda, the patient's condition is thereby rendered more serious, and the continuous administration of the salicylate might turn the scale against him.'^ It must be particularly noted that Dr Maclagan does not believe that salicin has this depressing influence on the heart. Dr Broad- bent is so strongly of opinion that salicyl and its compounds are useless in the cure of endocarditis, that the moment he recognises any cardiac inflammation he discontinues their administration.- In the second place, all endocardial murmurs are not indicative of endocarditis, in the later stages of acute rheu- matism more especially, when anaemic murmurs are most apt to arise, there may be great difficulty in deciding whether endocarditis is present or not. In the tJiird place, observers are by no means agreed as to the value which is to be attached to different endocardial murmurs as signs of endocarditis. It is difficult, therefore, to compare the results of different physicians who may attach very different values to the same facts. It is still more difficult to compare the observations made to-day with the obser\'ations made twenty or thirty years ago. Although personally I am inclined to attach very great importance to apex systolic murmurs, arising in the early stages of acute rheumatism and zvitliont basic systolic (pul- monary) murmurs, as indicative of acute endocarditis, I think it would be wise to base our inquiry upon the number of cases in which permanent valvular lesions — as to the symptoms and signs of which there is very general agreement — remain, rather than upon the frequency with which endocarditis occurs during the attack. The nature of the valve lesion which remains is also a point of some importance, for, as Sibson has shown, aortic regurgitation requires for its produc- tion (as a general rule) a greater degree of endocardial inflammation than mitral lesions. ' Lancet, Jan. 14, 1882, p. 59. ' Laucet, Jan. 28, 1882, p. 158. Treatment of Acute Endocarditis. 391 There is another reason why endocarditis — as evidenced by an apex systohc murmur — should not be taken as the standard in estimating the value of the salicyl compounds in preventing rheumatic endocarditis ; for if, as most observers admit, these drugs (salicin according to Dr Maclagan excepted) exert a special depressing influence upon the heart, their use is very likely to be attended with such relaxation of the cardiac muscle as will produce mitral regurgitation (from muscular or relative incompetence) independently of endocarditis. For these reasons it is, I think, difficult to decide the question by means of hospital statistics ; and more especially to estimate the results by the frequency with W'hich endo- carditis is supposed to occur during the attack of rheumatic fever. The inquiry should, I think, be based upon the number of cases in which permanent valvular lesions remain. Cases in which cardiac lesions were known or suspected to have existed previously, or cases in which the patient had previously suffered from rheumatic fever, should be rigidly excluded. The exact nature of the resulting valvular lesion should be stated. Instead of comparing hospital cases in which, as we have seen, endocarditis is so often established before the patient comes under observation, the inquiry should be based on the results of private practice, those cases only being selected in which the patient comes under observation at the very commencement, say within the first twenty-four hours of the attack.^ To be absolutely accurate, the result would have to be based upon a very large number of cases, all observed by one thoroughly competent, reliable, and unprejudiced observer. But since it is impossible for any single observer to meet with ' Cases which come under the care of the practitioner within twenty-four hours of the development of the attack would, as Dr Hilton Fagge pointed out in introducing the discussion on the salicylates before the Medical Society of London, be ' of far more than the average severity, since persons affected with the milder forms of the disease would often wait for a time before seeking medical advice.' That no doubt in some respects is an objection ; but the advantages of such a method of inquiry are, I think, so far as our present purpose is concerned, so much greater than those which any other method is likely to afford, that I do not hesitate to recommend it strongly to the profession. 392 Diseases of t lie Heart. an}'thing like a sufficient number of cases to serve as an adequate basis of results, the inquiry would of course have to be entrusted to a number of observers of known accuracy, and it would be of the utmost importance that they should all make their observations on exactly the same plan. In the present position of therapeutics we would hardly, I think, be warranted in making a series of investigations with the view of testing the efficiency of different drugs, for I thoroughly agree with Dr Hilton Fagge in thinking, that we would not be justified in withholding salicin and its com- pounds from our patients at the commencement of rheumatic fever unless there were some special contra-indication to the use of the drug. But we might, I think, determine much more satisfactorily by this means than by any other, the proportion of cases in which permanent valvular lesions follow the sali- cylic plan of treatment ; and this, I believe, is the most important point which we wish to decide with regard to the treatment of acute rheumatism. Having determined the point in the case of the salicylates, we would have a fixed standard with which to compare any other method of treat- ment which may in the future lay claim to be superior to that which at present we believe to be the best. The method of case-taking recommended by the Col- lective Committee of the British Medical Association, should be used, with the following slight additions necessary for the special purpose in hand : — Method of case-taking in acute rheumatism, with the object of determining the frequency 7vith -which perma7ieni ca^-diac valvular lesions folloiu the salicylic plan of treatment. Note A. Only those cases of acute articular rheumatism are to be recorded in which : (i) The patient was previously free from cardiac valvular disease. (2) The attack of rheumatic fever is a first attack. (3) The treatment is put into force within twenty-four hours after the first manifestation of symptoms, i.e. of joint pain. B. In all cases salicin to be used and not salicylate of soda ; and the drug to be given after the manner laid down by Dr Maclagan, viz. : ' at least thirty grains every hour till there is decided evidence of action, and then the dose should be diminished slowly.'i ' RheuniatisJH, p. 272. T^'-eatment of Aciite Endocm-ditis. 393 C. Whenever any of these directions are departed from, the exact nature of the modification introduced must be specified on the card. D. \xi addition to the points specified by the Collective Investigation Committee of the British Medical Association, the following particulars must be added : — Condition of the heart (i) at the end of convalescence ; and (2) six months subsequently, as regards : — (a) Position of apex beat. (b) Force of impulse. (c) Murmurs (their rhythm, points of differential maximum intensity, direction of propagation, and sound characters). (d) Condition of pulmonary second sound — normal — increased. (e) Subjective cardiac sensations. (f) Signs of mechanical derangement of the circulation. In the treatment then of acute rheumatic endocarditis, I would strongly advise the administration of full doses of pure salicin after the manner recommended by Dr Maclagan, and I cannot help thinking that if this treatment were vigorously carried out in the earlier stages of the attack, the frequency of endocarditis and other cardiac complications would be materially diminished. Some authorities recommend that full doses of alkali (thirty grain doses of bicarbonate of potash every two or three hours until the urine is alkaline) should be combined with the salicin, and they adduce in support of this plan of treatment the highly favourable results, as regards the cardiac affection, obtained by Drs Fuller, Dickenson and others. Some again, in addition to the salicin, advise the local application of blisters to the joints, as recom- mended by Dr Davies. Personally I am in the habit of wrapping the affected joints in cotton wool, or cotton wool sprinkled with belladonna and chloroform liniment, as recommended by Sibson. When the pain is very severe a hypodermic injection of morphia should be administered, and repeated, if required, for some hours must necessarily elapse before the beneficial effects of the salicin become apparent. A rigid system of rest must at the same time be strictly enforced, the greatest care being taken to avoid an)-thing, such as mental anxiety, worry, or agitation, which is likely to excite the action of the heart. The patient must of course be 394 Diseases of the Heart. placed in blankets. During the acute stage, the diet must be entirely liquid, and should consist chiefly of milk. The con- dition of the bowels must also be attended to. I do not, as a rule, prescribe a purge quite at the commencement of the attack ; it is better, I think, to wait a day or two until the acutencss of the joint affection has subsided. The patient should not be allowed to leave his room for the purpose of evacuating the bowels, it being of the greatest importance to avoid exposure to cold. If the salicin fails after a fair trial (four or five days), I would advise the administration of quinine in combination with alkalis. However mild the attack, or however rapid the return to health, the patient should be kept in bed for at least a week after the joint affection and the pyrexia have completely subsided. During convalescence all sources of cardiac excitement, both bodily and mental, must be carefully avoided. Tonics, more particularly quinine, iron and arsenic, should be pre- scribed. The greatest care must be taken to avoid exposure, or anything which is likely to bring on a relapse. These are the chief measures which I would recommend in a case of acute rheumatism uncomplicated by the symptoms or signs of acute endocarditis. But before leaving the pro- phylactic treatment of rheumatic endocarditis, I must again direct attention to the fact which Sansom, Barlow, and others have so justly emphasised, that endocarditis not unfrequently arises in the course of mild rheumatic attacks, and that in children more especially, in whom the tendency to inflam- mation of the endocardium is so much stronger than it is in adults, the most trivial rheumatic manifestations should always be carefully attended to. I cannot too strongly endorse Dr Sansom's teaching on this most import- ant point. The propJiyladic treatment of choreic endocarditis. — There are, as I have previously pointed out, ample grounds for believing that endocarditis is of frequent occurrence in chorea. Now, in dealing with cases of chorea, it is of the greatest Treatment of Acute Endocarditis. 395 importance to keep this fact in view ; for although, as a rule, the endocardial inflammation completely subsides, leaving the heart free from organic change (so far as our means of clinical investigation can detect, and as the future progress of the case amply proves), in some cases valvular lesions are (either immediately or in future life) established.^ The same general rules as to avoiding all cardiac strain and excitement, exposure to cold, and other conditions likely to act as exciting causes of endocarditis, and which have been already mentioned in speaking of the prophylaxis of rheumatic endocarditis, are equally applicable here ; and it is the more necessary to insist upon this point, since chorea is too generally regarded as a trivial affection. The patient should be kept in bed during the attack. Arsenic, chloral, and bromide of potassium, are the remedies which I have found most useful. The bowels must be carefully attended to ; but I must refer the reader for details of the treatment of chorea to works on general medicine. The prophylaxis of endocarditis in scarlet fever, measles, diphtheria, pnej'peral fever, pyceniia, etc. — We know of no special means by which the occurrence of endocarditis can be prevented during the acute stages of these affections, other than the ordinary means of treatment which it is advisable to adopt for the treatment of the primary disease. It is especially important, as Dr Sansom has pointed out, to direct attention to mild cases of scarlet fever, measles, and other febrile diseases in children, and to protect the patient, more especially during convalescence, from exposure to cold, and the other exciting causes of endocarditis.^ The treatment of the endocardial inf animation zvhen it has ' Dr Barlow has suggested that the greater frequency of mitral stenosis in young women than in young men may be due to the fact that girls suffer much more frequently from chorea than boys. Be that as it may, it is, I think probable, that in some cases, at all events, the endocardial changes established during an attack of chorea, and apparently completely recovered from, may afterwards be the starting point of serious valvular disease. ' Lettsomiafi Lectures, p. t,i. 396 Diseases of tJie Heart. arisen. — Theoretically our first indication is to cut short and allay the inflammatory process. As a matter of practice this indication cannot be satisfactorily carried out, for, in the first place, the inflammation has already made considerable progress before it can, with any approach to certainty, be recognised ; and in the second place, we cannot bring the depletory and other local measures which are useful in the early stages of most inflammations, to bear with any certainty upon the interior of the heart. General venesection, the internal administration of tartar emetic, and other remedies of a similar description, which used to be so lavishly employed in the early stages of internal inflammations, are especially out of place here, for one of the most important indications which we have to carry out is to avoid anything which will seriously depress the action of the heart. As soon as rheumatic endocarditis is distinctly recognised, it is advisable, as Dr Broadbent has pointed out, to discon- tinue the administration of salicylate of soda. This remedy docs not appear to possess any curative action so far as the endocardial inflammation is concerned, and it does seem in many cases to produce cardiac depression. There is not, according to Dr Maclagan, the same (positive) objection to salicin, which may still be continued after the endocardial inflammation is recognised, provided that the joint affection necessitates its use. It is of the utmost importance to keep the heart, so far as it can be kept, at rest. With this end all bodily movement ^ and mental excitement must be avoided ; excessive action or irritability of the heart must be moderated, and for this purpose belladonna and digitalis are the most useful drugs. Unless the joint affection continues, the pyrexia is seldom suffi- ciently great to require any special means of treatment. For the reduction of temperature salicin should first be tried, and if that drug fails, as it not unfrequently does in the presence of a cardiac complication, recourse must be had to quinine. In the majority of cases this treatment is all that is ' In those cases in which the joint affection still continues, the patient instinctively avoids all bodily movement. T7'eatme?it of Acute Endocarditis. 397 required in addition to the dietetic and other measures suit- able to treatment of the primary affection. In severe cases, when the valvular apparatus is seriously damaged, or when the inflammation of the endocardium is com- plicated with pericarditis or with myocarditis, other measures may be called for. One of the most important indications in bad — and in fact in all — cases, is to look out for symptoms of cardiac failure, and, when nccessar}^, to strengthen and stimulate the action of the heart. Digitalis, brandy, ammonia, and ether, are the remedies which are most useful for this purpose. When the right heart becomes seriously embarrassed, local depletion by means of leeches is often most useful. But these measures will be more particularly detailed when I come to treat of valvular lesions. (See p. 474.) Should thrombi form in the cardiac cavities, the internal administration of ammonia may be tried, as first recom- mended by Dr B. W. Richardson. Ten to fifteen drops of the liquid ammoniae may be given internally every two or three hours ; or ten grains of the carbonate of ammonia may be administered in a table-spoonful of the solution of the acetate three or four times daily, as recommended by Bartholow. Embolic and other complications must of course be met by appropriate remedies as they arise. Space does not allow me to go into details here. ULCERATIVE ENDOCARDITIS.^ Synonyms. — Septic Endocarditis, Infectious Endocarditis, Diphtheritic Endocarditis, Endocarditis Maligna (Virchow), Arterial Pyaemia (Wilks). ' Professor Osier objects to the tenii 'ulcerative,' because, on the one hand, there may be no actual ulceration of the valves in cases which present the character- istic features of the disease during life, and on the other, endocardial losses of substance may occur without these symptoms. I have retained the term, Jirsf/j/, because it is the title most generally used in this country- ; secondly, because ulcer- ation, though not invariably present, is in most cases a characteristic feature, and represents, so to speak, the highest degree of development of the local lesion ; and thirdly, because the term represents a mere pathological fact, and does not suggest any theory as to the causation of the disease, as the terms septic, infectious, and diphtheritic do — an important point when we consider the difference of opinion which exists as to the aetiology and pathology of the affection. 39B Diseases of tJic Heart. Definition. — An acute inflammation of the endocardium, which is characterised, pathologically — by the formation of fun- goid vegetations and (usually) ulcerations of the endocardium ; clinically — by great prostration, frequency of pulse, fever of an irregular or suppurative type, symptoms of a typhoid or pyaemic character, together with enlargement of the spleen, and the local manifestations of embolic infarctions of various organs. The invariable termination, so far as at present known, is in death. Micrococci frequently abound in the cardiac vegetations. Aetiology. — There is considerable difference of opinion as to the nature and cause of ulcerative endocarditis. Some observers regard the micrococci, which are met with in the cardiac vegetations, and in many cases also in the embolic infarctions of distant organs, as the cause of the disease, and think that they (the micrococci) gain entrance into the blood from an external wound or an abrasion, or through the gastro-intestinal tract or air passages. There seems to be little doubt that in some cases the cardiac lesion is simply one manifestation of a general pyemic or diphthe- ritic condition. In some puerperal cases, for instance, as Rosenstein points out, ' undoubted diphtheritic affections have been seen in the mucous membrane of the uterus and vagina. And in these very cases the likeness between the diphtheritic matter found on the genitalia and that which covers the endo- cardial abscess is so strong, and parasitic organisms have been detected with such certainty in both cases, that nothing but the most stubborn incredulity could deny a connection brought about by the blood, between the affection of the genitalia and the endocardial centre.' ^ Others, while admitting that micrococci are very generally, if not invariably, present in the cardiac lesion, think that they are rather the consequence than the cause of the affection, or at all events that their presence is accidental ; in other words, they believe that the cardiac vegetations form a suitable nidus in which the micrococci can develop. In support of this view ' Zlemssett's Cyclojxcdia, vol. vi. p. 70. Aitiology of Ulcerative Endocarditis. 399 they state that micrococci are frequently found in the vege- tations of rheumatic endocarditis. Osler,^ for example, who is one of the most powerful advocates of this view, states : — * Micrococci are not peculiar to the vegetations of the ulcerative form of endocarditis, but exist in the small beadlike out- growths of the rheumatic and other varieties of the disease, as Klebs was the first to point out. My experience tallies with his ; in seven specimens of verucose or plastic vegetations which I have examined all contained micrococci. ... So far as my observation goes, the micrococci do not exist in the blood during the course of the malady. Nor are they con- stantly found in the infarcts. The occurrence of micrococci in the warty vegetations of rheumatic endocarditis, and in the extensive ulcerative outgrowths so frequently met with in old sclerotic valves, are facts strongly opposed to the view of their specific poisonous nature. The micrococci appear to be identical in these cases, though Klebs states that those of rheumatic endocarditis are larger and have a brownish tint. I cannot say that these differences have been constant in the specimens which I have examined. It seems a pertinent question to ask, if in the malignant form of endocarditis, the micrococci are so potent, why in other cases in which they are equally prevalent, should they be inert } Of course it may be urged that the micrococci may be of different kinds or pos- sess diverse qualities, or that the resistance offered by the tissues to their penetration varies in different cases, or that it is only in weakened and debilitated states that those little bodies thrive. There is, I think, something worthy of attention in this latter view. If we study the conditions under which endocarditis develops, we find almost invariably that the patients are the subject of some other constitutional affection, which, as we say, predisposes to it. What determines the precise form of the endocarditis, we do not know, but the soft endocardial vegetations form a suitable nidus for the develop- ment of micrococci. They appear in fact to be just as much normal components of endocardial outgrowths as the fibrin • Transactions of the Interiiatioual Medical Congress of Londoti, 1 88 1, P 345- 400 Diseases of iJie Heart. fibrils, which are usually deposited and among which the micrococci abound. It is evident that these structures are common elements in a series of endocardial processes which display totally different symptoms and arise under different conditions. How far they are responsible either for the de- velopment of the endocarditis or for the subsequent characters which, in the grave form it assumes, the evidence does not, I think, warrant as yet a very positive opinion.'^ To sum up, ulcerative endocarditis does not appear to be a specific infectious disease in the same sense that typhoid, scarlet fe\er and smallpox are, for, so far as I am aware, inoculation experiments have failed to reproduce the disease. In some cases the endocardial lesion appears to be a manifestation of a general p}-aEmic or diphtheritic con- dition. In these cases, an unhealthy wound, diphtheritic ulcer, or diseased patch of mucous membrane, is the original source of infection, to which the cardiac lesion is secondary, though the infective emboli, which become detached from the cardiac vegetations and ulcerations, will of course aggravate the pyaemic condition. In other cases the cardiac lesion is the primary local source through which the system becomes impregnated. This group includes cases originating in the course of acute rheumatism and old standing valvular disease, and in it we may provision- ally include those cases in which the origin is obscure, and in which the primary cause of the endocarditis is unknown. To these cases the term ' arterial pyaemia,' proposed by Dr Wilks, seems very appropriate. In them, owing to a depraved con- dition of the vital forces, and of the heart in particular, the resisting power of the tissues is diminished. On the occur- rence of endocarditis (as the result of rheumatic or other causes) micrococci, which we must suppose are always cir- culating in the blood, but which in a state of health are unable to multiply and establish themselves in the tissues, find a suit- able nidus, and develop first in the cardiac vegetations and subsequently in distant organs and parts. In these cases, ' Transactions of the International Medical Congress of London, l88r, p. 346. Etiology of Ulcerative Endocarditis. 401 the cardiac lesion is the local source of infection through which the blood becomes poisoned and the pyaemic condition established. It is probable, as Dr Murchison has suggested, that, in some instances in which the symptoms of ulcerative endo- carditis are observed, the local lesion is not cardiac, but is situated in some part of the arterial system. The following are the chief conditions with which ulcerative endocarditis appears to be associated : — 1. Ac2ite or subacute rheumatism. — The exact frequenc}^ with which this association occurs has yet to be determined. Rosenstein's view that the majority of cases of ulcerative endocarditis occur in the course of acute rheumatism does not appear to be correct, for Osier found, on analysing the reports of fifty-seven cases, that in fifteen only, or 26.3 per cent, was any mention made either of acute rheumatism or of previous rheumatic attacks. In the rheumatic cases there is almost invariably, in addi- tion, a previous history of ill health or depressed condition of the system such as follows want, exposure, the abuse of alco- holics, etc. 2. Otd standing cardiac disease (valvular lesions, fibroid thickening of the cardiac walls). — It is probable that in man}^ of these cases, the endocarditis is also rheumatic, A depressed condition of the system seems in these cases also to be an important factor in determining the form which the endo- cardial inflammation ultimately assumes. The low organ- isation and defective vascularity of chronically diseased valves probably also favour the production of ulceration, as Virchow was the first to point out. 3. Pyccuiia, puerperal fever, dipJitJieria. — There seems to be no doubt, as I have already mentioned, that in some cases the endocardial ulceration is only one manifestation of a pyaemic condition, which has its original source of infection at the periphery in the shape of an unhealthy wound, ulcerated or diphtheritic mucous membrane, etc. In the majority of cases, however, in which pyaemic symptoms are associated with en- docarditis, the sequence of events is probably different, the CC 402 Diseases of t lie Heart. cardiac lesion being the priman' event to which the infection of the whole system is secondary. 4. Injuries iiiiattcndcd with local suppuration. — Osier has described a case in which ulcerative endocarditis followed a fractured leg (simple fracture unattended with local suppur- ation), and in the cases which he anah'sed he found a con- siderable number in which there was a history of some injuiy or wound. In cases of this description, in which it is clearly proved that the local wound or injury did not act as a local source of pya^mic infection, we can only suppose that the injury had a depressing influence on the system which favoured the production of the ulcerative rather than the simple form of endocarditis, the endocardial inflammation being probably due to some other condition or conditions. 5. Sypiiilis. — -In some of the recorded cases the patient suf- fered from syphilis before the onset of the attack. Possibly, therefore, in some of these cases the endocarditis was in the first instance syphilitic, and in consequence of the depraved condition of the system, and low resisting power of the tissues, it assumed the ulcerative form. In addition, there remain a considerable number of cases in which the cause of the condition is obscure. Age, sex, and occupation. — Like the simple form of endo- carditis, and like acute rheumatism, the affection seems more common in young than in old people. Males, because of their being more exposed to depressing external influences, alcoholic excesses, etc., are probably more liable to be attacked than females, though many writers state that the liability to the affection is equal in the two sexes. Persons whose occupa- tions necessitate exposure to cold, want, and other injurious external influences, probably suffer more frequently than other people, but no particular trade seems to predispose to the disease. Pathological anatomy. — In the majority of cases the left heart is the chief or only seat of the lesion, but the right heart is much more frequently affected than in simple endocarditis. As in the simple form of inflammation, the valves are the % X ll ^' ^^ ^^Ajl Fig. 168. "'^: jlortic Valve in a case of Ulcerative Etidocarditis. (^Natural size.') The Aortic Cusps are thickly coated with vegetations; two of the segments are ulcerated through (pieces of whalebone being placed in the apertures); the letter, a, points to a small depression (commencing aneurism), surrounded by minute vegetations, at the base of the Aorta ; it has evidently been produced by the vegetation, b, which at every systole would be forcibly washed against the base of the Aorta at this spot. M