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 OXFORD MEDICAL PUBLICATIONS 
 
 DISEASES OF THE HEART 
 
 MACKENZIE
 
 OXFORD MEDICAL PUBLICATIONS 
 
 DISEASES OF THE HEART 
 
 BY 
 
 V 
 
 JAMES MACKENZIE, M.D., M.E.C.R 
 
 SECOND EDITION 
 
 OXFORD UNIVERSITY PRESS 
 
 AMERICAN BRANCH 
 
 35 WEST 32xD STREET, NEW YORK 
 
 MCMX
 
 
 PRINTED IN ENGLAND 
 
 OXFORD : HORACE HART 
 
 PRINTER TO THE UNIVERSITY
 
 PREFACE TO THE SECOND EDITION 
 
 The speedy exhaustion of the first edition of this book, and 
 the demand for its translation into a number of languages, is an 
 evidence of the interest taken in the more recent methods of 
 studying diseases of the heart. It is extremely gratifying to find 
 many investigators entering a field fidl of promise of new and 
 original observations, embracing every aspect of the circulatory 
 system. 
 
 I wish to point out that, in setting forth my own experiences, 
 I desire to keep the record of facts apart from their interpretation. 
 For this reason the numerous figures in the text represent the 
 actual facts as recorded by the movements of the heart and blood- 
 vessels, and are therefore far more trustworthy than a verbal 
 description. The interpretation of these tracings represents the 
 present state of my knowledge. These interpretations may ulti- 
 mately be proved to be incorrect, but the recorded movements 
 will continue to serve for other and more fitting explanations. 
 
 A vast amount of clinical and experimental work still remains 
 to be done to explain the variable changes in the heart's action 
 due to disease, and my explanations can, consequently, only be 
 tentative. Should other investigators prove these interpretations 
 wrong by the discovery of new facts, I shall rejoice with them, 
 for they will have shed fresh light, and will have reached a plane 
 higher than I have been able to attain. 
 
 A valuable addition to the methods for clinical and experi- 
 mental observation has been made by the recording of the electrical 
 changes caused by the contraction of the heart chambers. I am 
 indebted to my friend, Dr. Lewis, for kindly writing a short 
 appendix on this subject. 
 
 J. M. 
 
 January, 1910.
 
 PREFACE TO THE FIRST EDITION 
 
 In the following pages are given the results of observations on 
 affections of the heart, made during an active practice of over 
 a quarter of a century. As the nature of the heart affection can 
 only be inferred from the presence of one or more symptoms, my 
 special object has been to ascertain the mechanism by which the 
 symptoms are produced, to find out their relationship to organic 
 changes in the heart, to ascertain their prognostic significance, 
 and, finally, to employ them as a guide for treatment. 
 
 This line of observation has revealed many new and unexpected 
 features, and has necessitated the employment of special methods 
 and the watching of individual cases for many years. 
 
 To make the results of use in practice it has been found necessary 
 to enter into considerable detail, and it has been difficult to make 
 the account at the same time succinct and intelligible. A certain 
 amount of detail is necessary, yet too much would be wearisome 
 and perhaps confusing, hence controversy has been avoided and 
 the observations have been given with the explanation that seems 
 most reasonable. 
 
 Many methods of examination that occupy prominent places 
 in textbooks have been briefly dealt with or even ignored, not 
 because I do not recognize their usefulness in certain cases, but 
 because my object has been to deal with matters of practical 
 value in the every-day examination of patients. It may appear 
 that an unnecessary amount of attention has been devoted to 
 details, many of which can only be recognized by special apparatus. 
 But to bring conviction proof had to be elaborated. Many of 
 the seemingly trivial signs, such as the minute differences in the 
 size of a pulse beat, or a slight delay between the auricular and 
 ventricular systoles, are really of vital importance in revealing
 
 viii PREFACE 
 
 changes which have been proved to be due to very definite affections 
 of the heart. In the same manner the study of irregularities is 
 of the greatest service, as their presence is easily detected and their 
 significance has never been properly understood. A close study 
 of irregularities throws an unexpected light upon the functional 
 derangements of the heart, and affords grounds for an intelligent 
 diagnosis upon which a rational treatment and prognosis can be 
 based. 
 
 The main purpose of all my work has been to obtain a guide 
 for treatment, and my readers may be disappointed at the seeming 
 barrenness of my work in this respect. A careful search has been 
 made for the essential principles that should govern a rational 
 treatment, and if only few drugs and suggestions are given, it is 
 because the treatment of cardiac disease at present in vogue 
 requires careful revision in the light of the more accurate diagnosis 
 now made possible by means of the graphic method of examination. 
 
 In routine practice it is not usually necessary to take graphic 
 records. If one is trained to make careful and minute observations 
 by the ordinary methods, and to have these checked by graphic 
 records, one can ultimately acquire the power of recognizing the 
 majority of movements of the circulation without graphic records. 
 In regard to the tracings given in this book, a selection has been 
 made from an enormous number of observations, and are rarely 
 exceptional, but are types of the commoner forms. The interpre- 
 tation of these records may prove to be faulty, and an endeavour 
 has therefore been made to keep the actual observation separate 
 from the interpretation, so that if the latter be erroneous, the 
 recorded movements may at least remain available for future 
 workers in this field. 
 
 It was originally intended to give a more complete account of 
 the morbid anatomy of the heart, and for that purpose Professor 
 Keith has investigated a great number of hearts, of which I have 
 kept careful clinical records, but the investigation, so far, has 
 brought to both of us the conviction that before the pathology of 
 the heart can be put on a satisfactory basis a more thorough and
 
 PREFACE ix 
 
 minute examination of the post-mortem appearances in correlation 
 with the clinical symptoms is necessary. The post-mortem aspect 
 of heart disease is therefore dealt with very briefly, and my obser- 
 vations in this respect are intended to be suggestive rather than 
 conclusive. 
 
 I had intended to give the means of judging the state of the 
 heart in cases apart from those directly due to affections of the heart, 
 as in fevers, pregnancy, surgical diseases, diseases of other organs, 
 the administration of chloroform. This has only been carried out 
 to a limited extent, because, when the results came to be analysed, 
 I did not see my way clear in all cases to give satisfactory guides, 
 so that many observations have been omitted. I hesitated to 
 include my observations on chloroform administration, because 
 the matter is still very vague. I feel convinced that the reason 
 chloroform is attended with so much danger will never be solved 
 until prolonged and painstaking investigation is made during its 
 administration along the lines of observation detailed in this 
 book and I leave my remarks in this unsatisfactory state in the 
 hope that others may solve the question. 
 
 What a tool is to a workman, so should a textbook be to the 
 busy practitioner. In cases of heart affection one or two symptoms 
 are usually most prominent, and by giving clear definitions of the 
 terms employed, and by arranging the index and the discussion in 
 the text, an endeavour has been made to facilitate the rapid 
 inquiry into the meaning of any given symptom. 
 
 J. M. 
 
 17 Bentinck Street, London, W. 
 September, 1908. 
 
 a 3
 
 CONTENTS 
 
 PAGE 
 
 Definition of Terms xviii 
 
 CHAPTER I . 
 General Outline of the Principles underlying the 
 
 PRODUCTION of HeART FAILURE 
 
 § 1. The object of the circulation, and how it is attained. § 2. The importance of the 
 heart muscle. § 3. The meaning of heart failure. § 4. Reserve force. § o. Con- 
 ditions exhausting the reserve force. § 6. The nature of the symptoms in heart 
 failure. § 7. Methods adopted in describing affections of the heart ... 1 
 
 CHAPTER II 
 Fundamental Functions of the Heart Muscle-cells 
 
 §8. Myogenic doctrine. §9. Stimulus production. §10. Excitability. §11. Con- 
 ductivity. § 12. Contractility. § 13. Tonicity. § 14. Co-ordination of functions. 
 § 15. Characteristics of the functions of the heart muscle-fibres . . . . G 
 
 CHAPTER III 
 
 Development, Anatomy, and Physiology of the Heart 
 
 § 16. The primitive cardiac tube. § 17. The functions of the primitive cardiac tube. 
 § 18. The remains of the primitive cardiac tube in the mammalian heart. § 19. Func- 
 tions of the primitive cardiac tissue in the mammalian heart. § 20. Functional 
 anatomy of the heart. §21. The nerve-supply of the heart . . . . .11 
 
 CHAPTER IV 
 
 Preliminary Examination of the Patient 
 
 § 22. The patient's appearance. § 23. The patient's sensations. § 24. The patient's 
 history. § 25. The chief complaints : breathlessness, sense of exhaustion, pain, 
 constriction of chest, palpitation, consciousness of irregular action of the heart, 
 haemorrhages, cerebral symptoms ......... 20 
 
 CHAPTER V 
 Respiratory Symptoms 
 
 § 26. Breathlessness, or air hunger. § 27. The sense of suffocation. § 28. Inability to 
 stop breathing. § 29. Quiet, rapid breathing, free from distress. § 30. Con- 
 tinuous laboured breathing. § 31. Laboured breathing brought on by exertion. 
 § 32. Attacks of breathlessness (cardiac asthma). § 33, Cheyne-Stokes respiration. 
 § 34. Slow respiration. § 35. Pulmonary haemorrhage. § 36. Acute suffocative 
 oedema of the lungs ........... 26
 
 xii CONTENTS 
 
 CHAPTER VI 
 Reflex, or Protective Phenomena 
 
 PAGE 
 
 § 37. Classification of symptoms in visceral disease. § 38. Insensitiveness of the 
 viscera to ordinary stimuli. § 39. The mechanism by which pain and other reflex 
 phenomena are produced in visceral disease (the viscero-sensory reflex). § 40. The 
 purpose of visceral reflexes. § 41. Why pain is referred to regions remote from the 
 organ. § 42. The relationship of the heart to sensory nerves. § 43. The viscero- 
 motor reflex. § 44. Vagal sensory reflex. § 45. Conditions in which angina pectoris 
 is induced. § 4G. Conditions giving rise to attacks of angina pectoris. § 47. Associa- 
 tion of angina pectoris ^\^th exhaustion of the muscle of the heart. § 48. Association 
 of angina pectoris with impairment of the function of contractilitj^ § 49. Summa- 
 tion of stimuli as a cause of angina pectoris ....... 33 
 
 CHAPTER VII 
 Angina Pectoris 
 
 § 50. Conditions predisposing to an attack. § 51. Conditions inducing an attack. 
 § 52. Character and duration of an attack. § 53. The symptoms present during an 
 attack : pain, constriction of the chest, sense of impending death. § 54. The state 
 of the heart and arteries. § 55. The symptoms present after an attack. § 56. Estab- 
 lishment of a tendency to recurrent attacks. § 57. Prognosis. § 58. Treatment . 45 
 
 CHAPTER VIII 
 
 Heart Affections and a Hypersensitive Nervous System 
 
 § 59. Reaction of visceral disease on the central nervous system. § 60. Pseudo-angina 
 pectoris, a useless and misleading term. § 61. Exaggerated sensory phenomena 
 with and without valvular disease. § 62. Exaggerated sensory phenomena in 
 early cardio-sclerosis, § 63. Characteristics of the sensory phenomena. § 64. Air 
 .suction. § 65. The circulatory sjmiptoms in the X disease. § 66. Vasomotor 
 angina pectoris. § 67. Prognosis. § 68. Treatment ...... 55 
 
 CHAPTER IX 
 Instrumental Methods of Examination 
 
 §69, The sphygmograph. §70. Tlie polygraph. §71. The clinical polygraph. 
 
 § 72. The ink polygraph 67 
 
 CHAPTER X 
 
 The Po.sition and Movements of the Heart 
 
 § 73. The position of the heart in the chest. § 74. The standards for recognizing the 
 events in a cardiac revolution. § 75. Conditions of the chest-wall permitting the 
 recognition of certain movements of the heart. § 76. The natiu-e of the movements 
 graphically recorded. § 77. The apex beat. § 78. Interpretation of a tracing of 
 an apox beat due to the systole of tlie left ventricle. § 79. The auricular wave.
 
 CONTENTS xiii 
 
 PAGE 
 
 § 80. Retraction of yielding structures in the neighboiuhood of the heart during 
 ventricular systole. § 81. Liver movement due to cardiac aspiration. § 82. Epigas- 
 tric pulsation. § 83. The apex beat due to the right ventricle. § 84. Significance 
 of the inverted cardiogram. § 85. Alteration of the apex beat due to retraction of 
 the lung. § 86. The shock due to the ventricular systole ..... 75 
 
 CHAPTER XI 
 
 Examination of the Arterial Pulse 
 
 § 87. Superiority of the digital examination. § 88. What is the pulse ? § 89. Inspec- 
 tion of the arteries. §90. Digital examination of the arteries. §91. The value of 
 a sphygmogram. § 92. Definition of a sphygmogram. § 93. Events occurring during 
 a cardiac revolution revealed by the sphygmogram : (a) the systolic period, (6) the 
 diastolic period. § 94. Features of the sphygmogram due to instrumental defect . 90 
 
 CHAPTER XII 
 Arterial Pressure 
 
 § 95. The cause of arterial pressure. § 96. Methods of measuring the blood-pressure. 
 § 97. Increased blood-pressure. § 98. Hyperpiesis. § 99. Effect on the heart 
 of increased peripheral resistance. § 100. Increased arterial pressure and heart 
 failure. § 101. Treatment of high arterial pressure. § 102. Diminished arterial 
 pressure ............. 98 
 
 CHAPTER XIII 
 The Venous Pulse 
 
 § 103. What the venous pulse shows. § 104. Inspection of the jugular pulse. 
 § 105. Methods of recording the jugular pulse. § 106. The recognition of the 
 events in a jugular pulse. § 107. Description of the events in a cardiac cycle. 
 § 108. The causes of variation of pressure in the auricle and in the jugular 
 vein. § 109. Standards for interpreting a jugular tracing. § 110. The carotid 
 wave. § 111. The notch on the ventricular wave. § 112. The diastolic wave. 
 § 113. Changes due to variation in the rate of the heart. § 114. Method of analys- 
 ing a tracing. § 115. The ventricular form of the venous pulse. § 116. Conditions 
 giving rise to a venous pulse .......... 105 
 
 CHAPTER XIV 
 
 Enlargement and Pulsation of the Liver 
 
 § 117. Reflex or protective symptoms. § 118. Signs of enlargement of the liver. 
 § 119. Pulsation of the liver. § 120. Conditions producing enlargement and 
 pulsation of the liver. § 121. Jaundice. § 122. Differential diagnosis. § 123. 
 Prognosis. § 124. Treatment .......... 122 
 
 CHAPTER XV 
 
 Increased Frequency of the Heart's Action 
 
 § 125. The normal rate. § 126. Classification. § 127. Cases which respond to a call 
 upon the heart's energy by increased frequency. § 128. Cases in which the heart's
 
 xiv CONTENTS 
 
 PAGE 
 
 rate is continuously increased. § 129. Cases in which the increased frequency of 
 the heart occurs in irregular paroxysmal attacks (palpitation). § 130. The cause 
 of increased frequency of the heart's action. § 131. Prognosis .... 129 
 
 CHAPTER XVI 
 
 Diminished Frequency of the Heart's Action 
 
 § 132. Definition of the term ' bradycardia '. § 133. Normal bradycardia . . . 138 
 
 CHAPTER XVII 
 The Irregular Action of the Heart 
 
 § 134. Places where the heart's contraction may start. § 135. Classification of irregu- 
 larities .............. 140 
 
 CHAPTER XVIII 
 
 Sinus Irregularities 
 
 § 136. Character of the irregularity. § 137. Etiology. § 138. Symptoms. § 139. Asso- 
 ciated symptoms. § 140. Prognosis ......... 143 
 
 CHAPTER XIX 
 The Extra-systole 
 
 § 141. Definition of the term ' extra-systole '. § 142. Character of the irregularity. 
 § 143. Etiology. § 144. Ventricular extra-systole. § 145. Auricular extra- 
 
 systole. § 146. Nodal extra-systole. § 147. Condition of the a. -v. bundle in 
 cases showing extra-systoles. § 148. The dropping out of the beat after the extra- 
 systole. § 149. Reasons for attributing the origin of extra-systoles to affections of 
 the remains of the primitive cardiac tube. § 150. Conditions inducing extra-systoles. 
 § 151. Sensations produced by extra-systoles. § 152. Prognosis. § 153. Treatment 148 
 
 CHAPTER XX 
 
 The Nodal Rhythm (Continuous Irregularity of the 
 Heart — Paroxysmal Tachycardia) 
 
 § 154. Meaning of the term ' nodal rhythm '. § 155. Etiology. § 156. Manner in which 
 the nodal rhythm leads to heart failure. § 157. Classification. § 158. Cases in 
 which the rate is not markedly increased. Symptoms. Prognosis. Treatment. 
 § 159. Cases in which the rate is greatly increased. Symptoms. Prognosis. Treat- 
 ment. § 160. Cases in which the nodal rhythm is transient and recurrent (par- 
 oxysmal tachycardia). Symptoms. Piognosis. Treatment . . . . .166 
 
 CHAPTER XXI 
 
 Affections of the Conducting Functions of the Primitive Cardiac 
 Tissue (Heart-Block, Adams-Stokes Disease, Ventricular Rhythm) 
 
 § 161. Definition. § 162. Methods of recognizing depression of conductivity. § 163. 
 Intersystolic period (the a-c interval). § 164. Depression of conductivity without 
 arrhythmia. § 165. Influence of rest upon conductivity. § 166. Arrhythmia due
 
 CONTENTS XV 
 
 PAGE 
 
 to depression of conductivity. § 167. Missed beats due to depression of conductivity. 
 § 168. Independent ventricular rhythm due to heart-block. § 169. Effect of the 
 auricular contraction on the radial pulse. § 170. Etiology. § 171. Significance 
 of the milder forms of depression of conductivity. § 172. Symptoms. § 173. Prog- 
 nosis. § 174. Treatment ........... 175 
 
 CHAPTER XXII 
 Exhaustion of Contractility 
 
 § 175. Necessity for recognizing exhaustion of contractility. § 176. The function of 
 contractility. § 177. Conditions inducing exhaustion of contractility. § 178. Symp- 
 toms : (a) reflex, (6) changes in the heart's action. § 179. The pulsus alternans. 
 § 180. Prognosis. § 181. Treatment 191 
 
 CHAPTER XXIII 
 Dilatation of the Heart (Failure of Tonicity) 
 
 § 182. The cause of dilatation of the heart. § 183. The function of tonicity. § 184. The 
 symptoms of depression of tonicity. § 185. Dilatation of the heart. § 186. The 
 cause of functional murmurs. § 187. The consequences of dilatation of the heart, 
 and how they are brought about. § 188. Dropsy. § 189. Enlargement of the liver. 
 § 190. Oedema of the lungs. § 191. Urinary symptoms. § 192. Prognosis. 
 § 193. Treatment 201 
 
 CHAPTER XXIV 
 
 Acute Febrile Affections of the Heart 
 
 § 194. Manner in which the heart is affected in fever. § 195. The febrile heart. 
 § 196. Acute febrile affections of the heart. § 197. Symptoms in myocarditis : 
 changes in rate, changes in rhythm due to depressed conductivity of the a. -v. bundle, 
 depressed contractility, extra-systole, nodal rhythm, depressed tonicity (dilatation 
 of the heart). § 198. Symptoms in endocarditis. § 199. Symptoms in pericarditis. 
 § 200. The heart in rheumatic fever : pathological changes, symptoms. § 201. The 
 heart in pneumonia. § 202. The heart in diphtheria. § 203. The heart in septic 
 infections. §204. Treatment 214 
 
 CHAPTER XXV 
 Valvular Defects 
 
 § 205. The manner of heart failure with valvular defects. Mitral stenosis : § 206. Con- 
 ditions inducing heart failure in mitral stenosis. § 207. Murmm-s present in mitral 
 stenosis (presystolic, diastolic, disappearance of the presystolic murmur, presy- 
 stolic murmm- of ventricular origin, systolic murmur due to mitral stenosis). § 208. 
 Progress and symptoms in mitral stenosis. § 209. Occasional symptoms : paroxys- 
 mal tachycardia, haemoptysis, cerebral embolism, angina pectoris. Mitral regurgita- 
 tion : §210. Murmurs due to mitral regurgitation. §211. Conditions inducing 
 heart failure in mitral regurgitation ......... 228
 
 xvi CONTENTS 
 
 CHAPTER XXVI 
 
 Valvular Defects (continued) 
 
 PAGE 
 
 § 212. Tricuspid incompetence. § 213. Tricuspid stenosis. § 214. Disease of the aortic 
 valves. Etiology. § 215. Aortic stenosis. § 216. Aortic incompetence. § 217. 
 Prognosis in valvular affections. § 218. Treatment ...... 237 
 
 CHAPTER XXVII 
 
 Cardio-Sclerosis (Arterial Degeneration. The Senile Heart) 
 
 §219. Conditions producing cardio-sclerosis. §220. Conditions inducing degenerative 
 changes in the arterial system, § 221. Obliteration of the capillaries. § 222. Symp- 
 toms of cardio-sclerosis. § 223. Prognosis. § 224. Treatment. § 225. Aneurysm 243 
 
 CHAPTER XXVIII 
 Adhesive Mediastino-Pericarditis 
 
 § 226. Etiology. § 227. Symptoms. § 228. Prognosis and treatment .... 253 
 
 CHAPTER XXIX 
 
 Congenital Affections of the Heart 
 
 §229. Etiology. §230. Symptoms. §231. Prognosis. §232. Treatment . . .256 
 
 CHAPTER XXX 
 Heart Disease and Pregnancy 
 
 § 233. Importance of the subject. § 234. Standards for guidance. § 235. Management 
 
 of the labour 258 
 
 CHAPTER XXXI 
 
 Chloroform in Heart Affections 
 
 § 236. Conditions contra-indicating its use : respiratory embarrassment, cardio-sclerosis, 
 
 status lymphaticus. § 237. Estimation of the fitness of the patient . . . 261 
 
 CHAPTER XXXII 
 
 Prognosis 
 
 § 238. Responsibility of the medical profession. § 239. Basis for prognosis . . . 264 
 
 CHAPTER XXXIII 
 Treatment 
 
 §240. The essential principle in treatment. §241. Rest. §242. Sleep. §243. Bodily 
 comfort. § 244. Diet. § 245. Condition of the bowels. § 246. The mental factor. 
 §247. Drugs. §248. Oxygen 268
 
 CONTENTS xvii 
 
 CHAPTER XXXIV 
 
 Treatment (continued) 
 
 PAGE 
 
 § 249. The action of digitalis on the human heart. § 250. Action on dilatation of the 
 heart. § 251. Action on rate and on the nodal rhythm. § 252. Action on conduc- 
 tivity (heart-block). § 253. Action on contractility. § 254. Action on blood- 
 pressure. § 255. Digitalis in practice. § 256. Other drugs of the digitalis group 
 (strophanthus, squills, helleborein) ....... 281 
 
 CHAPTER XXXV 
 
 Treatment (continued) 
 § 257. Venesection. § 258. Exercises. § 259. Massage. § 260. Special movements and 
 exercises. §261. Baths. §262. Spa treatment. §263. Nauheim baths. §264. 
 Cause of efficacy of the spa treatment ....... 293 
 
 APPENDIX I 
 The Pulse in Angina Pectoris ....... 302 
 
 APPENDIX II 
 
 The Nodal Rhythm ......... 309 
 
 APPENDIX III 
 Paroxysmal Tachycardia of Auricular Origin , . .334 
 
 APPENDIX IV 
 Nodal Bradycardia ......... 337 
 
 APPENDIX V 
 Irregularities in Cardio-Sclerosis ...... 350 
 
 APPENDIX VI 
 
 The Effects of Digitalis on the Human Heart . . .356 
 
 APPENDIX VII 
 
 The Electro-cardiogram ........ 370 
 
 BIBLIOGRAPHY 377 
 
 INDEX 395
 
 DEFINITION OF TERMS 
 
 Although I have endeavoured in the text to explain clearly what I mean by any term, 
 yet many terms -will be employed before the reader reaches the places where they are 
 explained. For that reason I give here a brief description of the more important terms that 
 have been lately introduced or are not found in current literature, or which I have employed 
 to describe conditions that have not been hitherto recognized. 
 
 a.-c. interval is the time between the beginning of the auricular and carotid waves in tracings 
 of the jugular pulse. (Also intersystolic period described in § 163.) 
 
 Arterial degeneration is the term used to cover all forms of arterial disease. As I deal 
 with arterial disease only so far as it embarrasses the work of the heart, I use this to avoid 
 the more specific terms concerning which there is still so much difference of opinion. 
 
 Auricular venous pulse is the form of jugular pulsation where the wave due to the auricle 
 is found preceding the ventricular contraction in contradistinction to the ventricular 
 venous pulse (q.v.). Sometimes called also the normal or negative venous pulse. 
 
 Auriculo-ventricular node (a.-v. node, Knoten of Tawara) is the enlargement of the remains 
 of the primitive cardiac tissue found in the wall of the right auricle, from which the a.-v. 
 bimdle arises (Fig. 2). 
 
 Auriculo-ventricular bundle (a.-v. bundle, Gaskell's bridge, Kent's or His's bundle). The 
 remains of the primitive cardiac tissue which passes from the a.-v. node to the right and 
 left ventricles. 
 
 Card io-sclero sis. Fibrous changes affecting the endocardium and myocardium are found 
 in the majority of cases in two groups of people, those with a history of an acute febrile 
 affection — most commonly rheumatic fever — and those with evidences of arterial degenera- 
 tion. The symptoms resulting from both conditions have a great similarity, but there 
 are circumstances, such as age and response to treatment, that sharply separate them ; 
 the term cardio-sclerosis, unless qualified, will always refer to the group with arterial 
 degeneration. Fatty changes are frequently present in cardio-sclerosis, but they cannot 
 be distinguished by clinical methods. 
 
 Conductivity is the term used by Gaskell to describe that function of the fibres of the heart 
 muscle which conveys the stimulus from fibre to fibre. It is usually studied by observing 
 the time between the systole of the auricles and ventricles. 
 
 Contractility is Gaskell's term for the power of contracting possessed by the muscle. 
 
 Extra-systole is the premature contraction of the auricle (auricular extra- systole) or of the 
 ventricle (ventricular extra-systole), or both chambers together (nodal extra-systole), 
 while the fundamental or sinus rhythm is maintained. Usually the extra-systole is 
 followed by a long pause (compensatory pause). Karely the premature contraction 
 occurs between two normal beats (interpolated extra-systole).
 
 DEFINITION OF TERMS xix 
 
 Heart-block is the term used by Gaskell to signify the stoppage or blocking of the stimulus 
 for contraction in its passage from the auricles to the ventricles. 
 
 Hyperalgesia. An abnormal sensitiveness to pain, shown by a painful response to such 
 stimulation as would not normally produce pain, e. g. lightly pressing the skin (cutaneous 
 hyperalgesia) or muscles (muscular hyperalgesia) between the thumb and forefinger. 
 
 Myogenic theory. The view that the heart muscle-fibres possess in themselves the power 
 of originating and conveying the stimulus for the contraction of the heart, as opposed 
 to the neurogenic theory, where it is held that the heart acts only in response to nerve 
 stimulation. 
 
 Nodal Bradycardia is the term used for that condition of infrequent action of the heart 
 where there is no evidence of the auricular systole between the ventricular beats and 
 where the venous and liver pulses are of the ventricular form (see also Nodal Ehythm). 
 
 Nodal rhythm. In the majority of cases of continuous irregularity and paroxysmal tachy- 
 cardia it is found that the ventricular contraction precedes or is sjTichronous with the 
 auricular contraction, and hence it is inferred that the heart's contraction in these cases 
 must originate from a point that could affect both auricle and ventricle at or about the 
 same time. It is suggested that this point may be in the a.-v. node or its neighbourhood, 
 and as it is important to recognize the abnormal rhythm it is provisionally distinguished 
 by the term ' nodal rhythm '.* 
 
 Palpitation is used in a twofold sense, to describe (a) attacks of increased frequency of the 
 heart's action, (6) the sensation by which a patient is conscious of the excited and usually 
 increased frequent action of the heart. 
 
 Paroxysmal tachycardia is applied to a sudden increase in the heart's rate, usually 
 followed by an equally sudden reversion to the normal. It is due to the starting of the 
 heart's contraction at some part other than the normal. The most common form is really 
 a transient nodal rhythm. There is also a rarer form, where the stimulus arises in the 
 auricle. I therefore restrict the term to the increased frequency of the heart's action 
 due to the temporary inception of an abnormal rh3rthm. 
 
 Primitive cardiac tissue is the term applied to the tissue in the mammaUan heart which 
 represents the cardiac tube of the more primitive vertebrates. It is shown in Fig. 2, 
 and consists of the s.-a. and a.-v. nodes and a.-v. bundle. This view of the origin of 
 these structures is inferred from the consideration of certain embryological, physiological, 
 and clinical characteristics, but has not yet been fully estabUshed by embryologists. 
 
 Pulsus alternans means that form of abnormal rhjrthm where the radial pulse is perfectly 
 regular but where there is an alternation in the size of the beats, and is an evidence of 
 the failure of the function of contractility. 
 
 Pulsus bigeminus is applied to that form of pulse irregularity where every second beat is 
 an extra-systole, and is usually smaller than the preceding normal beat. The smaller 
 beat is invariably followed by a pause longer than the pause preceding it. 
 
 Sino-auricular node (s.-a. node). The term given by Keith and Flack to a small bundle 
 of tissue representing the remains of the primitive cardiac tube (portion of the sinus 
 venosus) near the mouth of the superior vena cava (1, Fig. 2). 
 
 Tonicity is the term applied to that function of the heart muscle which keeps the heart during 
 diastole in a state of slight contraction. Depression of this function results in dilatation 
 of the heart and of the auriculo-ventricular orifices. 
 
 * Resent elestro-cardiographic observatioas by Lewis leads him to conclude that the dis- 
 appearance of the evidence of the auricular contraction in cases" of nodal rhythm is often due to 
 the auricle passing into fibrillation.
 
 XX 
 
 DEFINITION OF TERMS 
 
 Ventricular rhythm. This term is applied to the ventricular contractions in cases of complete 
 heart-block. As this occurs when a lesion severs the a. -v. bundle, it is assumed that the 
 remaining fibres of the a. -v. bxindle in the ventricles start the ventricular contractions,— 
 the rate being very slow, rarely above thirty-two beats per minute. (In some of my 
 earUer witings I employed this term to describe the condition given under nodal 
 rhythm.) 
 
 Ventricular venous pulse is that form of jugular pulsation in which the auricular wave 
 disappears or coincides with the period of ventricular systole, there being no sign of the 
 auricular wave at the normal period of the cardiac cycle. Sometimes called the positive 
 or pathological venous pulse. 
 
 Viscero-motor reflex. The term used to describe the contraction of muscles of the external 
 body- wall in response to a stimulation from a diseased viscus. 
 
 Viscero-sensory reflex. The sensory symptoms (pain and hyperalgesia) evoked by the 
 stimulation from a diseased viscus of a sensory nerve in its passage from its peripheral 
 distribution in the external body-wall to the brain.
 
 DISEASES OF THE HEART 
 
 CHAPTER I 
 
 General Outline of the Principles underlying the production 
 
 OF Heart Failure 
 
 § I. The object of the circulation, and how it is attained. 
 
 2. The importance of the heart muscle. 
 
 3. The meaning of heart failure. 
 
 4. Reserve force. 
 
 5. Conditions exhausting the reserve force. 
 
 6. The natiire of the symptoms in heart failure. 
 
 7. Methods adopted in describing affections of the heart. 
 
 As the study of the condition of the heart is approached in this book 
 from a standpoint somewhat different from that usually taken in textbooks 
 on diseases of the heart, I propose to give here a brief description of the 
 principles underlying this method of study, in order that the reader may 
 the more readily appreciate the nature and symptoms of heart failure. 
 
 § I. The object of the circulation, and how it is attained. — The 
 object of the circulation is the supply of a constant stream of material capable 
 of nourishing the tissues, and of replacing the loss of energy sustained by 
 them, and the removal of such waste products as are capable of entering 
 the circulatory channels. In order to facihtate the exchange of products 
 between the blood and the tissues, a certain degree of slowing of the flow 
 takes place as the blood passes through the capillaries. As a continuous 
 pressure is required to force the blood onwards, the intermittent pressure 
 conveyed to the blood-stream by the heart is converted by the resihent 
 nature of the arterial walls into a constant pressure at the periphery of the 
 arterial system. The maintenance of the arterial pressure is the outcome 
 of the force exerted by the left ventricle, and of the resistance of the smaller 
 a,rteries and capillaries. The full force of the ventricular contraction is 
 not spent on the blood-current merely during the period of its systole. In 
 throwing the bloodj^into the arterial system, it does so with such force that 
 it distends to a sUght extent the larger arteries. The elastic coats of the 
 arteries, as soon as the ventricular systole is over, compress the column of 
 blood within them, and in this manner maintain a degree of arterial pressure 
 during the period that the ventricle is not acting. The ventricular^force 
 
 MACKENZIE
 
 2 DISEASES OF THE HEART 
 
 is thus stored up by the distension of the elastic coats of the arteries, and 
 liberated during the ventricular diastole. 
 
 The principles underlying the mode of action of the left ventricle and 
 the systemic circulation apply equally to the right ventricle and the pul- 
 monary circulation. 
 
 § 2. The importance of the heart muscle. — The heart muscle supphes 
 the force which maintains the circulation. In the normal condition, the 
 mechanism of the circulation is so adjusted that all parts combine to facihtate 
 the work of the heart and to attain the object of the circulation. Any dis- 
 turbance of that adjustment must at once entail more work upon the heart 
 muscle, inasmuch as a departure from the normal means the embarrassment of 
 the heart in maintaining the normal arterial pressure. So long as the heart 
 can overcome the impediment, and maintain the circulation in a normal 
 manner, no symptoms are evoked, but if the heart is no longer able to carry 
 on the circulation efficiently, then certain phenomena at once arise, and 
 these phenomena we call ' symptoms of heart failure '. 
 
 § 3. The meaning of heart failure. — From this consideration it will 
 be reahzed that heart failure is simply inabihty of the heart muscle to 
 maintain the circulation, and that this failure of the heart muscle is due 
 to a disturbance of the normal adjustment of the various factors concerned 
 in the circulation. This disturbance may arise in a great many ways, but 
 the end result is the same — embarrassment of the heart muscle and its final 
 exhaustion. The heart muscle, therefore, is of such prime importance in 
 what we call heart failure, that a close and intimate study of its properties 
 is essential. This will be dealt with later in some detail ; here I want to 
 call attention to a feature of the heart muscle which is the essential factor 
 in the consideration of every form of heart failure, namely, the reserve 
 force. 
 
 § 4. Reserve force. — If the part played by the heart muscle in the 
 maintenance of the circulation and the nature of the symptoms in heart 
 failure be considered, it wiU be found that the explanation of heart failure 
 can be summed up in the general statement that heart failure is due to the 
 exhaustion of the reserve force of the heart muscle as a whole, or of one or 
 more of its functions. This statement may seem so self-evident as scarcely 
 to need amplification, but, as a matter of fact, this, the essential principle 
 on which diagnosis, prognosis, and treatment should be based, is often 
 practically ignored. I shall make no apology for the continuous reiteration 
 of this apparent truism, for the simple reason that in the study of aU cases 
 of heart failure the condition of the reserve force will be found to be the 
 ultimate question.
 
 GENERAL OUTLINE OF HEART FAILURE 3 
 
 Although we recognize what reserve force is, it is not very easy to define 
 it in words. Physiologists do not seem to have given it that study its impor- 
 tance demands. Although difficult to define, its existence is proved in every 
 movement of the body, and in every effort which is made, as it is by the 
 possession of this quality that we are able Avith ease to undertake all forms 
 of effort. The estimation of the amount of reserve present is the best test 
 of the heart's condition. It is the 'premature exhaustion of this reserve ivhich 
 constitutes heart failure, and it is the heart's power to regain this reserve 
 force on which recovery from heart failure depends. 
 
 § 5. Conditions exhausting the reserve force. — I have already re- 
 marked that, in the normal condition, the adjustment of all parts concerned 
 in carrying on the circulation is essential to efficiency. Any disturbance 
 of the adjustment at once calls for an increased effort. Such calls are made 
 first on the reserve force and, if persisted in, lead sooner or later to its 
 exhaustion. These disturbances of the adjustment are extraordinarily 
 varied in character, and may arise from any one of the factors on which 
 the normal heart's action depends. It will be from this standpoint that 
 the diseases of the heart will be studied, inasmuch as it is only by looking 
 at the matter in this hght that a proper perspective is obtained in regard 
 to the significance of any abnormahty. Thus, irregular action of the heart 
 will be described from the point of view of its effect upon the efficient 
 performance of the heart, as well as the condition producing it. Valvular 
 defects will be studied not as a specific affection to be considered in them- 
 selves, but rather as a source of embarrassment to the heart muscle in its 
 work. In the same manner, arterial degeneration and high blood-pressure 
 wiU be considered as conditions that upset the normal adjustment of the 
 factors that carry on the circulation. Inherent defects of the muscular 
 wall itself wiU also be viewed in their bearing on the heart's efficiency. The 
 relative efficiency of independent functions of the muscle-fibres will be kept 
 constantly in view, inasmuch as organic lesions act deleteriously through 
 disturbing the normal harmony of these functions. Depression of the in- 
 dividual functions may arise without any gross organic lesions, and lead to 
 serious embarrassment of the circulation. "While I am far from compre- 
 hending the full effect of functional depression, for the study of pure func- 
 tional pathology is in its infancy, yet I hope the facts I detail may help 
 forward a line of observation that promises much for future investigation. 
 
 § 6. The nature of the symptoms in heart failure. — Briefly put, 
 the symptoms are produced by the exhaustion of the reserve force. The 
 first sign is invariably a subjective one, although it may for a time pass 
 unnoticed. The patient's attention is first directed to his condition by some 
 
 B 2
 
 4 DISEASES OF THE HEART 
 
 disagreeable sensation evoked when lie attempts to perform some act which 
 he had been wont to do with ease, and without distress. Such a condition 
 can be summed up as due to the too speedy exhaustion of the reserve force, 
 and manifested by a limitation of the field of cardiac response. The sen- 
 sations by which the limitation makes itself known are varied, but when 
 carefully analysed, the true nature of the heart failure is revealed. Hence, 
 I insist upon particular attention being paid to the patient's sensations. 
 
 The standard by which one measures the strength of the heart, or, more 
 properly speaking, the amount of the reserve force, is in the main personal, 
 as each individual unconsciously acquires the knowledge of what he can do 
 with comfort, and his attention is called to the fact that his range of effort 
 has become circumscribed. The observing physician can also detect signs 
 in the frequent pulse and quickened respiration, out of proportion to the 
 exertion. Other sources of information are obtained from the physical 
 examination of the patient, not only in the heart itself, but in the condition 
 of the circulation in other organs and tissues, as well as in the reflex protective 
 phenomena which appear in affections of the heart as in affections of other 
 viscera. 
 
 § 7. Methods adopted in describing affections of the heart. — The 
 ideal method in writing a book on diseases of the heart would be to take up 
 each separate lesion, and describe the symptoms that arise in consequence 
 of the lesion. But although this method is the one that has been attempted 
 by most writers of textbooks, it is impracticable in our present state of 
 knowledge. Not only are the lesions imperfectly recognized, but the symp- 
 toms themselves are usually not the outcome of the organic lesion, but result 
 from the embarrassment of the heart induced by the lesion. Thus the 
 symptoms of heart failure in a case of valvular disease are not produced 
 by the valve lesion, but by the failure of the heart muscle to overcome the 
 difficulty created by the damaged valve, and this failure may be brought 
 about in a variety of ways by the greater exhaustion of one function than 
 of another, — sometimes, for example, it is the contractile power of the heart 
 that gives way, sometimes the tonicity ; so that we get a variety of symp- 
 toms corresponding to the exhaustion of different functions. But these 
 functions may become exhausted from other causes than valvular lesions, 
 and similar symptoms may therefore be induced by organic lesions of great 
 diversity. Another reason for not following this ideal method is that it 
 is extremely rare that the heart is the seat of only one lesion, or of a lesion 
 limited to one particular part. Acute affections of the heart, for instance, 
 are often described as endocarditis or pericarditis, because there happens 
 to be a marked systohc murmur or a pericardial friction sound. But in
 
 GENERAL OUTLINE OF HEART FAILURE 6 
 
 addition to these audible signs, there may be presented a great number of 
 symptoms such as dilatation of the heart, irregular action of the heart, 
 and so forth, and these are given as being symptoms of the endocarditis or 
 pericarditis. As a matter of fact, these symptoms are not the outcome 
 of endocarditis or pericarditis, but of a myocardial affection, and the attempt 
 to give a precise description of the symptoms pertaining to each organic 
 lesion has led writers to ascribe phenomena to lesions with which they have 
 no connexion, with the result that the symptomatology of heart affections 
 is to-day confused and contradictory. 
 
 In searching for a reason for this confusion, I am incUned to attribute 
 it to the fact that the human mind attaches the greatest importance to that 
 class of phenomena which most strongly affects the senses. Many of the 
 really vital and aU-important symptoms are so subtle and so shght that it 
 takes the most careful methods to detect them, whereas a roaring murmur 
 or an irregular pulse thrusts itself upon our attention. The result is that 
 the subtle signs are ignored and aU the stress is laid upon the murmur and 
 irregularity. Murmurs and irregularities, therefore, have come to occupy 
 a far more important place in the cardiac symptomatology than their true 
 significance merits. 
 
 These considerations have led me to adopt a method which I hope will 
 place the symptoms in a proper perspective. Recognizing the fact that the 
 attention of the physician or the patient is drawn to the heart by the appear- 
 ance of one or more symptoms — and it is only by the recognition of the 
 symptoms that the diseases can be inferred, — I write this book from the 
 standpoint of the symptoms. So far as I can, I describe each symptom, 
 give its physiological meaning, and the various pathological conditions 
 with which it may be associated. Then I try to estimate its significance. 
 From the data thus obtained, conclusions are drawn as to prognosis and 
 treatment.
 
 CHAPTER II 
 
 Fundamental Functions of the Heart Muscle-cells 
 
 § 8. ]Myogenic doctrine. 
 
 9. Stimulus production. 
 
 10. Excitability. 
 
 11. C'onducti%'ity. 
 
 12. Contractility. 
 
 13. Tonicity. 
 
 14. Co-ordination of functions. 
 
 15. Characteristics of the functions of the heart muscle-fibres. 
 
 § 8. Myogenic doctrine. — While it would be somewhat beyond my 
 province to enter into a discussion of the question whether the heart contracts 
 in response to a nerve stimulus, or in response to a stimulus developed in the 
 muscle-cells, it is very necessary, in order to comprehend the meaning of 
 the signs and symptoms that arise in affections of the heart, to appreciate 
 the phenomena which are associated with the contraction of the muscle- 
 fibres. The conception of the meaning of the heart beat, which we owe to 
 Gaskell, has been supported by careful and minute analysis of the functions 
 of the normal heart muscle-fibres, and the interpretation of the symptoms 
 of heart affections in the light of this knowledge has revealed so clearly 
 their true meaning as to revolutionize the study in the human subject. 
 Even if the ' Myogenic doctrine ' be ultimately proved untenable, the 
 investigations carried out in its support have added so much of value 
 to our knowledge of the heart's action that its conception will ever be 
 associated with a great stride forward, not only in physiology, but also in 
 the recognition and treatment of diseases of the heart. It is just possible 
 that the two opposing doctrines — Neurogeny and Myogeny — may be 
 reconciled along the lines I suggest in the following brief summary of the 
 main points. I do not enter into much detail, but give such salient points 
 as are necessary to appreciate the explanation of the symptoms I give in 
 the course of this work. For fuller details the reader is referred to Gaskell's 
 article on ' The Contraction of the Cardiac Muscle ' in Schaefer's Text Book 
 of Physiology. 
 
 From the consideration of the physiology of the cell, it may be said 
 that every function possessed by a cell in the fully developed state exists 
 partiallj' developed in the primitive form. However specialized the function
 
 FUNDAMENTAL FUNCTIONS OF THE HEART MUSCLE-CELLS 7 
 
 may be, nervous, muscular, or secretory, these functions can be referred 
 back to some property possessed by the primitive cell. The cells which con- 
 stitute the primitive structure of the body all start equally endowed, and 
 it is by a gradual process of specialization that each takes on its peculiar 
 function, while as it acquires a high degree of speciahzation it gradually 
 loses those functions it no longer exercises. The functions possessed by the 
 primitive cells can therefore be deduced not only from the results of direct 
 observation, but from the specialized functions of the more differentiated 
 tissues, even if these functions be so highly developed that they bear little 
 resemblance to those found in the primitive cell. For instance, the excita- 
 bihty of the cell may become so specialized as to be responsive only to certain 
 stimuli, as heat, pain, light, sound, while all its other functions are appa- 
 rently lost. If one looks at the functions of nerve and muscle cells in the 
 fully developed state, it seems at first sight difficult to realize that they had 
 originally identical functions. The primitive cells, from which the heart 
 developed, had all the same characteristics, yet in their final evolution 
 they present widely divergent characteristics both in appearance and in 
 function. That some such modification does occur must be inferred when 
 we witness the change in function that takes place in the evolution of the 
 heart from the primitive cardiac tube. I therefore suggest as a working 
 hjrpothesis, that in the evolution of the heart muscle-fibres certain functions 
 of the primitive cell were retained, some of these being more developed than 
 others according to the duties the fibres had to perform, so that while they 
 have come to resemble muscle-fibres, they nevertheless retain in a varying 
 degree some functions which are highly specialized in the nerve-cell. 
 
 The special functions which Gaskell has demonstrated are five in 
 number, namely : — 
 
 (1) The power of producing a stimulus which can excite the heart to 
 
 contract — stimulus production. 
 
 (2) The power of being able to receive a stimulus — excitability. 
 
 (3) The power of conveying a stimulus from fibre to fibre — conductivity. 
 
 (4) The power of contracting when stimulated — contractility. 
 
 (5) The power to retain a certain amount of contraction even when 
 
 the active movement has ceased — tonicity. 
 
 § 9. Stimulus production From this point of view it is assumed that 
 
 the heart muscle-fibres, if suppHed with appropriate nutriment, possess 
 a power of internally secreting a material which is capable of stimulating 
 the fibre to contract. This material is being continually secreted, and during 
 a pause in the heart's contraction, accumulates in the heart cell. When 
 sufiicient has been stored to excite the heart to contract, the whole store
 
 8 DISEASES OF THE HEART 
 
 is used up in stimulating the muscle-cell. Immediately after the contraction 
 the store again begins to accumulate until sufficient has been produced 
 to excite the heart to further contraction. This function, being continuous 
 in its action, cannot control the rhythm of the heart, but by its co-operation 
 with the other functions a rhythmical character is given to the accumu- 
 lation and destruction of this material. 
 
 §10. Excitability. — The heart muscle depends for its contraction upon 
 its power of receiving a stimulus — that is, upon its excitabiUty. Imme- 
 diately after the heart has been stimulated to contract, the fibres are no 
 longer capable of further stimulation, excitability has disappeared, and the 
 fibres are in what is called the refractory stage. The excitability begins 
 at once to be restored, and increases very rapidly during diastole. This is 
 demonstrated by the heart being susceptible to weaker stimuli the longer 
 the time since the previous contraction. So long as the heart is capable of 
 contracting, the rate of the heart depends upon the functions of stimulus 
 production and excitability, and when the conditions are normal the equal 
 action of both functions — the stimulus material being renewed at a uniform 
 rate, and the restoration of the excitability taking place uniformly — a regular 
 rhythm of the heart's action results. Under normal circumstances, therefore, 
 the heart's rate and rhythm are dependent upon the integrity of these two 
 functions. 
 
 § II. Conductivity. — In a mass of primitive cells the individual cell 
 has a power of passing the stimulus on to neighbouring cells. This function 
 of conductivity is possessed by the heart muscle-fibres, for the stimulus 
 is passed on from ceU to cell from the point where it originated. The 
 possession of this function by the muscle-fibres of the heart gives them 
 a character which is typical of certain forms of nerve-fibres, but in the heart 
 this is not so highly developed as in the speciaUzed nerve-fibre, the conduction 
 of the stimulus not being so rapid in all cases, andmuch more easily exhausted. 
 Like every other function of the heart, it is entirely abolished after it has 
 been exercised, and it returns gradually. The rate an impulse travels also 
 varies in different fibres of the heart. Some fibres, such as the more recently 
 developed contractile fibres of the auricle and ventricle, conduct the stimulus 
 with much greater rapidity than the fibres which convey the stimulus from 
 auricle to ventricle. 
 
 § 12. Contractility — The power of contraction is the most evident 
 of all the functions of the heart. By the co-ordinated contraction of the 
 fibres of the different portions of the heart, the circulation is maintained. 
 After a contraction, this function is completely exhausted, and the power 
 returns very gradually. Within certain limits the strength of the contraction
 
 FUNDAMENTAL FUNCTIONS OF THE HEART MUSCLE-CELLS 9 
 
 depends upon the length of the period of rest preceding the contraction, 
 the function gathering strength during quiescence. 
 
 § 13. Tonicity. — The functions of the heart muscle do not differ, 
 except in degree, from those of other muscular structures, and as tone is 
 a very characteristic property of muscular tissue, it is certain that the heart 
 muscle will possess it, and it is shown by the fibres not relaxing to their full 
 length during diastole. On account of the rapid action of the heart it is 
 not easy to demonstrate this function. Gaskell^"' has shown that the degree 
 of relaxation depends on the amount of tone present, and that certain drugs 
 increase or diminish the amount of relaxation. Thus antiarin, veratrin, and 
 digitalis prevent the relaxation of the heart muscle in the frog so that 
 the heart remains longer in the condition of complete contraction, the 
 relaxation gradually becoming less and less, till finally it is almost impossible 
 to recognize individual beats. On the other hand, solutions of lactic acid 
 and muscarin produce the opposite effect, the heart becoming more and 
 more relaxed, the contraction diminishing in size till the heart stands still 
 in diastolic relaxation. Just as certain portions of the musculature have 
 certain functions more highly developed, it would not be unreasonable, as 
 Gaskell says, to expect that different parts of the heart should vary in their 
 tonicity. That this expectation is justified will be manifest when all the 
 symptoms of heart failure are considered, and it is only on recognizing that 
 the heart possesses this very important function that we can understand 
 some of the most significant features of heart failure. 
 
 § 14. Co-ordination of functions When the complicated action of 
 
 the heart is considered, it will be readily recognized that though all the 
 fibres may be endowed Avith these functions, a further speciahzation is 
 a necessity for the co-ordinated movement of the different parts of the 
 heart. If all the fibres were equally endowed, then all would contract 
 simultaneously. As it is, certain fibres at the venous end have the functions 
 of stimulus production and excitability more highly developed than others, 
 so that after a period of rest the contraction starts in them. The stimulus 
 then proceeds to adjoining fibres in such a manner that the process of 
 stimulation and contraction sweeps through the whole heart, with the 
 result that the different chambers and the different parts of each chamber 
 contract in that order and degree necessary to the efficient carrjang on of 
 the circulation. If anj^ other part of the heart be rendered more excitable 
 than the venous end, then the contraction starts there. As the stimulus 
 then does not sweep through the heart in the normal manner, the heart's 
 action is less efficient, and heart failure may thus arise. 
 
 § 15. Characteristics of the functions of the heart muscle-fibres. —
 
 10 DISEASES OF THE HEART 
 
 While the heart may be said to carry on its work in consequence of its pos- 
 session of these functions, there are other important features in each which 
 have a practical bearing on the symptoms of diseases and the principles 
 of treatment. The integrity of these functions depends on the supply of 
 suitable nutriment, and sufficient time of inactivity to recover after their 
 exercise. When a contraction takes place, all the functions have been exer- 
 cised to the full extent of the power possessed by the fibres at the moment 
 of stimulation. No heart-cell exhausts only a portion of its function ; 
 when stimulated, it uses all the energy which it possesses (all or nothing). 
 For a brief period after their exercise, the functions cease to exist : recovery, 
 however, begins at once during the period of rest,, and each function in time 
 regains its strength, so that, within certain limits, the longer the delay, the 
 more complete is the recovery, and the more efficient is the subsequent 
 action. It is by fully appreciating the effect of rest and proper nourishment 
 that we gain the best conception of the principle that should underlie our 
 treatment of heart failure. While all the functions when exercised use all 
 the force they possess, they nevertheless manifest a quaUty whereby they 
 can respond, under certain circumstances, with a greater activity. Thus 
 the rate may be suddenly increased, and at the same time the stimulus 
 passed from the auricle to the ventricle with increased rapidity, and the 
 contraction be executed quicker. These changes are to a great extent 
 under the control of the nervous system, but they imply a quaUty possessed 
 by aU these functions which is of vital importance to us in the study of heart 
 failure. For, as I have already remarked, it is this power of responding 
 to effort that gives us the clue to the real state of the heart. 
 
 When one reflects that aU the fibres of the heart are not equally endowed 
 with the same functions, and that aU the functions may not always be 
 exposed to an equal strain, it is but reasonable to conclude that conditions 
 may arise where they are unequally affected. As a matter of fact, this is 
 what commonly happens, and it is an interesting and important question 
 to consider in each case of heart failure what functions are specially at fault. 
 The significance of this question was demonstrated when Wenckebach-^ 
 showed how the irregular activity of the various functions or of the various 
 parts of the heart were made manifest by certain characteristic arrhythmias. 
 Following up the idea of exhaustion or over-excitability of individual func- 
 tions, I have sought to connect many of the symptoms of heart failure 
 with these functions. While I do not say that my conclusions are invariably 
 correct, they have led to some definite results of the very highest importance, 
 and it is along these lines that advance in our knowledge will likely follow 
 for some time.
 
 CHAPTER III 
 
 Development, Anatomy, and Physiology of the Heart 
 
 § 16. The primitive cardiac tube. 
 
 17. The functions of the primitive cardiac tube. 
 
 18. The remains of the primitive cardiac tube in the mammaUan heart. 
 
 19. Functions of the primitive cardiac tissue in the mammalian heart. 
 
 20. Functional anatomy of the heart. 
 
 21. The nerve supply of the heart. 
 
 While I take it for granted that the reader is f amiHar with tlie ordinary 
 textbook description of the anatomy and physiology of the heart, there are 
 some recent investigations which have an important bearing on the cUnical 
 investigation of heart disease which need to be considered. For that reason 
 I give here a brief resume of certain points necessary for the appreciation of 
 chnical signs. 
 
 § 1 6. The primitive cardiac tube — In an early stage of the embryo's 
 development, the heart appears as a tube. The veins from the body unite 
 into a common cavity — the sinus venosus — at the posterior end of this tube. 
 In the course of development this tube becomes bent upon itself, and from 
 it, later, pouches develop which ultimately become the auricles and ventricles 
 — the original tube still persisting and connecting them (Fig. 1). As develop- 
 ment proceeds, the sinus venosus loses its distinctive feature as a separate 
 structure to become incorporated in the termination of the superior and 
 inferior vena cavae, and a strip of the right auricle between the orifices of 
 those two vessels, and the coronary sinus. Probably the terminal part of 
 the pulmonary veins is also derived from the sinus. At the same time the 
 original cardiac tube ceases to exist as a tube but it is inferred that it persists 
 as the connecting medium between auricles and ventricles in the shape 
 of a band of pecuHar fibres — the a.-v. bundle (Fig. 2). It thus loses its 
 function as a propelling organ, which is taken up by the auricles and 
 ventricles. 
 
 § 17. The functions of the primitive cardiac tube. — The functions 
 of the primitive cardiac tube and its representative in the mammalian heart 
 need to be carefully studied, as the appreciation of the nature of its functions 
 has the most important bearing on many cases of heart failure. Its pecuUar 
 properties have been studied most fully in the heart of the frog, also
 
 12 
 
 DISEASES or THE HEART 
 
 in the toad, tortoise, crocodile, &c., but, so far, only to a slight extent in 
 the mammalian heart. In the lower vertebrates the primitive tube is still 
 recognizable in the sinus venosus, auricular canal, and aortic bulb (Fig. 1). 
 It has been found that the posterior end of this tube is the most excitable 
 portion, and in consequence of this the heart's contraction starts at the sinus 
 venosus. The remainder of the tube also possesses the faculty of starting 
 the heart's contraction, only in a less degree than the sinus. If, how- 
 ever, any part of the tube be rendered more excitable than the sinus the 
 
 Auricle, 
 I 
 
 Auricular part of 
 primitive cardiac tute. 
 
 Aorta. 
 
 Bulbar part of primitive 
 cardiac tube, included in 
 liuman right ventricle. 
 
 Bnlbus cordis. 
 
 ^^vV _ Ventricular part of 
 
 primitive cardiac tube. 
 
 Inferior vena cava. 
 
 Fig. 1. Diagram of the primitive vertebrate heart, showing the development of the auricle 
 and ventricle from the primitive cardiac tube. (Keith.) 
 
 contraction starts from that part. The pecuharity of the primitive cardiac 
 tube and its relatively greater excitability than the auricular or ventricular 
 tissue is brought out in the following experiment by GaskeU ^-^ : ' Touch 
 the auriculo-ventricular ring of muscle (i.e. the primitive cardiac tube) 
 with the sUghtest stimulus, immediately a series of rhythmical contractions 
 occurs. It is most striking to see, after removal of the septum, how 
 every portion of auricular and ventricular tissue can be explored up to the 
 very edge of the ring, without obtaining more than a single contraction, 
 while immediately the needle touches the muscular ring a series of rapid 
 contractions results.' 
 
 The possession of the power of independent contraction by the separate
 
 DEVELOPMENT, ANATOMY, AND PHYSIOLOGY 13 
 
 portions of the heart is brought out in the Stannius experiments. When 
 a ligature is apphed or a cut made between the sinus and auricle of a frog's 
 heart {A, Fig. 1), so as to sever completely the connexion, the sinus con- 
 tinues beating, and after a pause of varying duration the auricles and 
 ventricles begin to beat at a rate different from, and independent of, the 
 sinus. This rate is slower than the sinus rate, and sometimes the auricle 
 contracts before the ventricle, sometimes the ventricle precedes the auricle, 
 and very rarely they contract simultaneously. (Engelmann ^^^). 
 
 If a second Stannius hgature be apphed between auricle and ventricle 
 {B, Fig. 1), the sinus and auricle continue beating, and after a period the 
 ventricle takes on its own rhythm, slower than, and independent of, the 
 other portion of the heart. 
 
 § 1 8. The remains of the primitive cardiac tube in the mamma- 
 lian heart. — The sinus venosus, which in the primitive heart normally origi- 
 nated the stimulus for contraction, has no representative as an independent 
 structure in the human heart. Morphologists recognize that it has become 
 incorporated in the great veins near the heart, and physiologists observed 
 that the peculiar functions of the sinus venosus were found over a somewhat 
 wide distribution. Normally, the contraction starts with such uniformity 
 in a number of places that no one place can be pointed out with certainty 
 as the starting-point, though the mouth of the superior vena cava seems to 
 lead the contraction. In certain experiments dissociation can be shown,, 
 and independent pulsations start at the coronary sinus and pulmonary veins. 
 From this it is inferred that in these separate places some remains of the 
 original sinus venosus persist, the possession of which endows them with 
 the power of starting independent contractions. Until very recent times 
 no definite remains of the sinus venosus had been found. Keith and Flack ^-^ 
 have described lately a small node of tissue — the sino-auricular node 
 (1, Fig. 2) — at the mouth of the superior vena cava. This tissue consists of 
 fine delicate pale fibres faintly striated, in which branches of the vagus and 
 sympathetic nerves terminate, and is suppHed with a definite artery. These 
 observers consider that this node of tissue represents a portion of the sinus 
 venosus, from which, probably, the heart's contraction starts. Similar 
 tissue has so far not been found in the other veins. It is possible that some 
 fibres may be scattered about, but, not being grouped into a definite node, 
 they are not capable of being differentiated from the muscular fibres by 
 which they are surrounded. The further remains of the primitive cardiac 
 tissue are probably found lower down, arising in the right auricle and passing 
 across the a.-v. septum to be distributed inHhe ventricles. Although the 
 presence of this bridge was inferred in the mammalian heart by Gaskel, it
 
 14 DISEASES OF THE HEART 
 
 was not demonstrated until 1893, when first Stanley Kent^^^, then His 
 ( j unr . ) -^^, described its presence and both experimentally demonstrated some of 
 its functions. A full description of its structure and ramification was given 
 in 1906 by Tawara^-^ whose elaborate examination of the tissue has been 
 of the greatest interest and importance. This bundle rises from a node of 
 tissue — the a.-v. node (2, Fig. 2) — situated in the right auricular wall near 
 the mouth of the coronary sinus, and Colin -^"^ has recently worked out some 
 of the details connecting it with the muscle-fibres of the auricle. The bundle 
 passes over the auriculo-ventricular septum below the central fibrous body 
 and under the septal cusp of the tricuspid valve. While on the septum 
 it divides into two, one branch passing into the left ventricle and the other 
 into the right. In the right ventricle it continues its course as a narrow 
 rounded bundle in the muscle-wall of the heart, till it approaches the apex, 
 where it divides into numerous fine threads, terminating in the muscle- 
 fibres. In the left ventricle the bundle rapidly widens out into a thin 
 band which passes down to the apex splitting into fine branches. 
 
 The character of the fibres constituting this bundle varies. The fibres 
 of the a.-v. node are of the same delicate nature as those of the sino-auricular 
 node. As this bundle passes into the ventricle the fibres change, becoming 
 thicker, the greater part of the cell body being undifferentiated protoplasm 
 only faintly striated at the circumference and containing a large nucleus. 
 In their final distribution they are recognized as being the fibres described 
 long ago by Purkinje. Another pecuharity of this bundle is that it is isolated 
 from the structures in which it is embedded by a fine sheath of connective 
 tissue. There are numerous nerve structures in the a.-v. bundle which have 
 been specially studied by Gordon Wilson ^^^. He finds numerous ganglion 
 cells, abundant nerve-fibres, an intricate plexus around the muscle-fibres 
 of the bundle, and distinct vaso-motor nerves. Finally, it is mainly supphed 
 by a special branch of the right coronary artery, a fact of some significance 
 in the pathology of the heart. 
 
 § 19. Functions of the primitive cardiac tissue in the mammalian 
 heart — The functions of this bundle have been only partially explored 
 experimentally, though a fair inference of its functional action can be made 
 from clinical symptoms. Kent ^°^, His (junr.)-^*^, Erlanger ^'^, Hering -'■'^, and 
 others have demonstrated that it conveys the stimulus from auricle to 
 ventricle, for compression of the bundle interferes with the conduction, 
 while section stops all connexion, and the ventricle contracts at a rate 
 quite independent of the auricular rate, as after the second Stannius ligature. 
 An exactly similar experience is met with as a result of disease in man. 
 
 But, as has been seen, the primitive cardiac tube also possesses the power
 
 DEVELOPMENT, ANATOMY, AND PHYSIOLOGY 15 
 
 of originating the stimulus for contraction, and there is every reason to sup- 
 pose that if it be rendered more excitable the remains of the primitive cardiac 
 tissue in man will start a contraction independent of the sinus rhythm. In 
 the neighbourhood of the node there are certain centres which when stimu- 
 lated modify the heart's action. Thus Mac William ^'^^ has shown that a small 
 area in the auricle here, when stimulated, causes marked slowing of the 
 ventricular rate. Whether this is a portion of the vagus mechanism or some 
 
 Fig. 2. Section of a heart, exposing the septal wall of the right auricle and ventricle 
 and showing the position of a portion of the remains of the primitive cardiac tube. 
 1. Superior vena cava above the sino-auricular node. 2. Auriculo- ventricular node (Knoten 
 of Tawara), from which the auriculo-ventricular bundle arises. The interrupted part 
 represents the main bundle, and the continuation to 3 is the right division, where it is shown 
 in the cut moderator band. 4. Aorta. 5. Right auricle below the sui^erior caval orifice and 
 taenia terminaUs. 6. Pulmonary artery. 7. Opening of coronary sinus. (Keith.) 
 
 portion of the primitive cardiac tissue has not been determined. Lohmann ^^", 
 by irritating the a. -v. node, or its immediate neighbourhood, caused the 
 starting of the auricular and ventricular contractions together. In the 
 human subject I have attempted by a process of reasoning to show that 
 extra-systoles may arise in this tissue, and that the continual irregularity 
 recognized so frequently in the later stages of rheumatic heart affection and 
 cardio-sclerosis, may be due to the inception of the rhythm of the heart by 
 the irritated primitive cardiac tissue probably in or about the a. -v. node.
 
 16 DISEASES OF THE HEART 
 
 § 20. Functional anatomy of the heart — I mention here a few of 
 the more important features connected with the heart as a muscular organ 
 which are of importance in this cKnical study. These are based on 
 Keith's ^^*^ descriptions, who has demonstrated that the heart is built of 
 muscle bundles whose points of origin and insertion are as definite as those of 
 skeletal muscles, and whose functions can also, to a great extent, be inferred 
 with equal certainty. Naturally the separation of the different muscle 
 bundles is not so complete as in skeletal muscles, there being a continuous 
 connexion between neighbouring fibres, so that they pass gradually from 
 one system into another. 
 
 In order to appreciate how the muscle-fibres act, and also to understand 
 the changes that result from an increase in the size of the heart, it is necessary 
 to comprehend how the heart is fixed in the thorax. 
 
 The pericardium is a fairly unyielding structure fixed firmly above 
 to the cervical fascia and below to the central tendon of the diaphragm. 
 The aorta and the great veins, where they penetrate the pericardial sac, 
 receive a covering from it, and these may be regarded as fixed points. The 
 lungs also may be considered as ligaments which attach the base of the 
 heart to the whole of the chest-wall. 
 
 The contraction of the heart starts at the mouth of the great veins. It 
 has hitherto been assumed that regurgitation from the auricle was prevented 
 by the contraction of the circular fibres at the mouth of the veins. Keith 
 shows that these are too weak for the purpose, except around the coronary 
 sinus, and that regurgitation back into the superior vena cava is prevented 
 by the contraction of the broad band of muscle which sweeps over the roof of 
 the auricle — the taenia terminalis. In its contraction this muscular band shuts 
 off the vein from the auricular cavity. As the taenia is attached at the orifice 
 of the inferior vena cava and is carried over the roof of the right auricle, it 
 also aids in the closure of the inferior vena cava and the pulmonary veins. 
 The pressure of the blood in the inferior vena cava apparently renders 
 a perfectly competent closure of the inferior caval orifice unnecessary. 
 
 Arising from the taenia are a number of other muscular bands, the 
 pectinate fibres, which pass across the auricle to be fixed in the auriculo- 
 ventricular septum. In their contraction, in addition to assisting the taenia 
 in emptying the auricle, they pull up the ventricles by reason of their insertion 
 into the a.-v. septum {A, Fig. 3). 
 
 The ventricles have themselves no real fixed point, but depend for 
 security on the fixation of the vessels at the base of the heart. Immediately 
 below the origin of the aorta in the heart is the central fibrous body, which 
 is reaUy a tendon for much of the ventricular muscle. The remainder of
 
 DEVELOPMENT, ANATOMY, AND PHYSIOLOGY 
 
 17 
 
 the ventricular muscle is inserted into the a. -v. septum. The other fixed 
 point during contraction is the apex. It becomes a fixed point in virtue 
 of the peculiar arrangement of the muscles here constituting the ' whorl '. 
 A great number of fibres from different parts of the heart converge here and 
 
 Fig. 3. Sketch of the heart to show the movements of the auriculo- ventricular gi'oove during 
 auricular and ventricular systole. A, position of groove when pulled upon by the contraction 
 of the pectinate fibres of the auricle ; B, position of the groove when pulled upon by the con- 
 traction of the ventricular fibres. During the diastole the groove occupies a position midway 
 between A and B ; a, sinus portion of superior vena cava ; b, inferior vena cava ; c, is on the 
 taenia terminalis ; d, apex of the heart ; /, pulmonary artery ; i, i, pulmonary veins ; k, pul- 
 monary artery. During ventricular systole g' is pulled to g and e' to e ; h', musculi pectinati 
 during auricular systole ; Ji", during ventricular systole. (Keith.) 
 
 mutually support one another in contraction, the result being a fixed point 
 from which the fibres can exercise traction in different directions. With the 
 onset of the ventricular contraction the apex of the heart rises up and presses 
 firmly against the chest-wall. As no shortening takes place between the 
 apex and the aorta, all the parts of the heart are drawn towards the 
 line between apex and aorta. Hence it is that while during ventricular 
 
 MACKENZIE o
 
 18 ■ DISEASES OF THE HEART 
 
 contraction the apex is pushed forwards, all the other portions of the cardiac 
 surface are dragged inwards, and this explains the variation in the appear- 
 ance of a cardiogram taken from different parts of the front of the chest. 
 At the same time, as Chauveau^^^ and Keith ^^^ have shown, the ventricular 
 fibres inserted into the a. -v. septum not only diminish the size of the ven- 
 tricle, but enlarge the size of the auricle by dragging down the a.-v. septum 
 — a fact of some importance in the production of the venous pulse {B, Fig. 3). 
 
 § 21. The nerve supply of the heart — The independent functions 
 of the muscle-fibres enable the heart to execute its movements independently 
 of any nervous intervention, nevertheless nervous influences have a powerful 
 effect in modifying the activity of the various functions of the fibres. The 
 nerves of the heart are usually described as being of three sorts, namely, 
 (1) inhibitory fibres passing to the heart, (2) accelerator or augmentor 
 fibres also passing to the heart, and (3) depressor fibres passing from the 
 heart. 
 
 The inhibitory fibres are derived from the spinal bulb by the internal 
 branch of the spinal accessory nerve, and pass down in the vagus and reach 
 the heart by its cardiac branches. The effects of the vagus upon the heart 
 are varied. On division of one vagus little effect may result. If both 
 vagi be cut the frequency of the heart is much increased. If the vagus be 
 stimulated the result is curiously varied. Its action may be said in a general 
 way to depress the functions of the heart muscle-fibres, but it does not do 
 so uniformly in all cases. It usually acts first on the excitabihty of the 
 heart or on the stimulus production, so that the whole heart becomes slower 
 in its action, or the whole heart may stand stiU for a brief period. With 
 stronger stimulation, it may act on the conductivity of the fibres joining 
 auricles and ventricles, and depress this function so that the ventricle fails 
 to respond to every auricular systole. Underlying this seemingly uncertain 
 action of the vagus is a principle which is of great importance in diagnosis 
 and in treatment, namely, that if there be depression of one function of the 
 heart, vagus stimulation is liable to seize upon that function and increase the 
 depression. The fact that depressed functions are more susceptible to vagus 
 stimulation seems to be the reason for some of the discordant results arrived 
 at by experiments. 
 
 The accelerator fibres belong to the sympathetic system and have 
 their origin in the spinal cord, passing out of the cord by the white rami 
 communicantes to the upper four or five dorsal nerves. They pass 
 upwards to the inferior cervical ganglion ; from thence they pass to join the 
 cardiac fibres of the vagus, and so reach the heart. Stimulation of these 
 fibres increases the rate of the heart, sometimes very considerably, and
 
 DEVELOPMENT, ANATOMY, AND PHYSIOLOGY 19 
 
 according to Roy and Adami ^"^ they increase the strength of contraction 
 and output as well, and hence have been assumed to contain augmentor 
 fibres. 
 
 The depressor fibre is a definite nerve which arises in the heart, and, pass- 
 ing upwards, joins the vagus nerve and so reaches the bulb. Stimulation of 
 the peripheral part of the cut nerve has no effect, but stimulation of the 
 central end causes a fall of blood-pressure through reflex action on the 
 medulla oblongata. 
 
 Afferent fibres. — Such is a brief resume of the heart nerves described 
 in physiological textbooks, but the whole matter is not included here. 
 There is a great field of evidence which is entirely lost to the physiologist, 
 but which is open to the clinician. The personal sensation of the animal 
 cannot be communicated to the experimenter, nor can the changes in sensa- 
 tion that result from stimulation of the cardiac nerves be ascertained. In 
 dealing with the symptoms of heart affections it mil be shown that there 
 is unquestionable evidence of a system of nerves passing from the heart 
 to the spinal cord and the bulb. The principles involved in the production 
 of these symptoms have not been thoroughly appreciated, and I shall enter 
 more fully into their explanation when dealing with the reflex or protective 
 phenomena (Chapter VI). 
 
 Cardiac ganglion cells. — The nerve-fibres of the a.-v. bundle have been 
 referred to on p. 14. The ganglion ceUs in the heart have been studied by 
 GaskeU ^^^. He says, ' WTiat, then, are the ganglion cells in the heart ? What 
 function do you attribute to them ? That is a question which I am ready to 
 answer, and to answer with confidence, as follows : The gangUon cells in the 
 heart are part of the great group of ganglion cells which are situated on the 
 course of the small-fibred efferent nerves supplying the viscera. These ceUs 
 form the outlying vagrant groups of nerve-cells which are known by the 
 name of the sympathetic and cerebro-spinal gangha. In the case of the 
 heart, the ganglion cells are the cells belonging to the smaU-fibred efferent 
 cardiac fibres of the vagus, just as some of the cells in the ganghon stellatum 
 and in the inferior cervical ganglion are the cells belonging to the small- 
 fibred efferent cardiac fibres of the augmentor nerve. There is no more reason 
 to assign special functions to these ceUs than to any of the other peripheral 
 efferent nerve-cells. They are cells connected only with the inhibitory fibres 
 of the vagus, and as such are simply part and parcel of the mechanism of 
 inhibition, just as the corresponding cells in the ganglion stellatum are 
 simply part and parcel of the augmentor mechanism.' 
 
 c 2
 
 CHAPTER IV 
 
 Preliminary Examination of the Patient 
 
 § 22. The patient's appearance. 
 
 23. The patient's sensations. 
 
 24. The patient's history. 
 
 25. The chief complaints : breathlessness, sense of exhaustion, pain, constriction of 
 
 chest, palpitation, consciousness of irregular action of the heart, haemor- 
 rhages, cerebral symptoms. 
 
 § 22. The patient's appearance — Before entering upon the physical 
 examination of the patient, the physician ought to obtain a clear and com- 
 prehensive appreciation of the patient's own sensations. I therefore wish 
 to insist upon the importance of the preliminary examination, for it often 
 happens that a thorough appreciation of the patient's own experiences is 
 of more value in arriving at a correct estimation of the heart's efficiency 
 than the most elaborate methods of physical examination. The attempt 
 to appreciate the patient's condition should begin when first he presents 
 himself before us. On his appearance in the consulting-room, his bearing, 
 his gait, the condition of his respiration, the colour of his face, any nervous 
 peculiarity in his manner of speech and behaviour, and so forth, should 
 be noted. If he is in bed, note the position he assumes, and any change 
 in his colour or respiration in response to such exertions as talking or 
 turning over. By habit, one unconsciously notices these things, and as the 
 examination proceeds first one trivial matter, then another, may arise, 
 which helps materially in guiding the examination and in forming the 
 final opinion. 
 
 § 23. The patient's sensations. — After ascertaining his age and occu- 
 pation, ask the patient to describe the chief symptoms from which he suffers. 
 In his replies, insist upon these being precise and definite. When he refers 
 to his feelings, get him to indicate the location by placing his hand upon the 
 region ; otherwise, proud of his small anatomical knowledge, he will attribute 
 his sensations to his viscera ; and here I may add a warning to the physician 
 not to make a note of the sensations by attributing them to any viscus : 
 thus a pain should not be put down as felt in the heart, stomach, liver, or 
 lungs, but only in the region of the body indicated by the patient, for 
 it will probably be found on later examination that the pains are not felt
 
 PRELIMINARY EXAMINATION OF THE PATIENT 21 
 
 in the viscus. In other words, he should make no notes that might 
 prejudge the nature of any symptom until he has before him all the 
 evidence. 
 
 Having obtained from the patient an account of the symptoms from 
 which he suffers, a brief inquiry should be made regarding the other viscera, 
 as to the state of the digestion, the urinary secretion, the breathing, &c. 
 Particular inquiries should always be made in regard to sleep, for in many 
 patients the want of sleep induces a breakdown, and the power of a patient 
 to pass a night in comfort or otherwise, often gives important indications. 
 The condition of the brain, its power of attention, memory, dreams, and so 
 forth, are often of material value. 
 
 § 24. The patient's history — After this, I usually inquire into the past 
 history for other illnesses, the nature of employment, whether there is worry, 
 excessive indulgence in tobacco or alcohol. Guided by the information thus 
 obtained, I return again to the main complaints, and inquire when they 
 began to appear, and what induced their appearance. In all cases it is 
 necessary to find out what degree of exertion the patient can undertake 
 with comfort. As I have said, heart failure resolves itself into the question 
 of the amount of reserve force, and consequently it is at this juncture that 
 we begin to find out that amount ; therefore the factors that produce the 
 first sign of discomfort need the most detailed inquiry. The sequence of 
 the phenomena as they arise is most instructive. The patient has often 
 only a confused notion of the order of appearance of the sensations, and the 
 situation in which they are felt, and it may be necessary to postpone a final 
 opinion until a second visit, and the patient should be instructed to note, 
 should occasion arise, the individual sensations, their location, and order 
 of appearance. On a subsequent visit the account may be totally different, 
 but often one made with great precision. It is sometimes surprising to 
 observe that a patient, after an attack of agonizing pain, has but a very 
 dim idea in what region it was felt. Inquiries should be made as to the 
 presence of less obtrusive symptoms, which experience tells us to expect, but 
 which the patient often ignores, unless his attention is drawn to them. Thus 
 when he complains of a pain in the chest, is it associated with a sense of 
 constriction, or after it passes, is there a desire to micturate ? Many patients 
 have bad dreams and even delusions, and, as Head points out, the latter 
 are never elicited unless carefully inquired after. 
 
 § 25. The chief complaints — The chief complaints from which patients 
 with heart failure suffer are as follows : — • 
 
 Breathlessness. — This first appears on the patient making some effort 
 which was not previously attended with discomfort, or dyspnoea more or
 
 22 DISEASES OF THE HEART 
 
 less extreme appears without any apparent cause. The various forms of 
 respiratory trouble are described in Chapter V. 
 
 The sense of exhaustion. — Many people complain of feeling simply 
 ' done up '. The sensation may come on after a bodily or mental effort, and 
 particularly after some excitement. It may be a feeling of exhaustion in 
 general, or it may be located in some definite region, as the epigastrium, or 
 across the chest. It is a symptom common to trivial and transient condi- 
 tions of heart exhaustion, and to conditions of the utmost gravity, in the 
 latter case usually associated with other phenomena. A curious sense of 
 exhaustion referred to the legs in walking is occasionally complained of by 
 elderly people. They feel, after walking a short distance, as if they were 
 walking in water, or forcing the legs through some viscous fluid. A similar 
 condition is found in patients suffering from heart-block, and some of these 
 are never really comfortable unless in the recumbent position. 
 
 Pain may appear in all degrees of intensity, and be of slight or serious 
 import, the most severe not necessarily being the most serious, nor the 
 slightest being of the least significance. It may come on with exertion, 
 and at once bring the patient to a standstill. It may not appear until 
 some hours after the exertion which induced it. It may be felt in various 
 regions of the chest, or arms, or epigastrium, or neck. Its starting- 
 point and radiation should always be noted, as it follows frequently very 
 definite lines, which reveal its true origin. A pain may also be felt in other 
 regions, as over the liver, when there is enlargement of that organ due to 
 heart failure. 
 
 A sense of constriction or oppressio7i of the chest is a fairly common 
 accompaniment of pain, but it may appear independently of pain, and be 
 so severe as to compel a cessation from all effort. The symptoms associated 
 with pain are described in detail in Chapters VI and VII. 
 
 Palpitation is the consciousness of the impact of the heart against the 
 chest-wall. The heart is frequently also quickened in rate, though not 
 necessarily so. In neurotic people, the hammering of the heart against the 
 chest-wall is most distressing. 
 
 Consciousness of irregular action of the heart. — Allied to this is the con- 
 sciousness of irregularity. The most common form of irregularity is that 
 where there is an occasional long pause or intermission, the next beat of the 
 heart being strong, giving rise to an unpleasant sensation. So severe may 
 the shock from this strong beat be that in some people it induces a feeling of 
 exhaustion. Instead of being conscious of the strong beat after the pause, the 
 patient may be aware of the pause, and feel as if the heart had stopped, or he 
 may feel some curious sensation as a ' catch in his breath \ Irregularity
 
 PRELIMINARY EXAMINATION OF THE PATIENT 23 
 
 may give rise to a slight fluttering sensation in the chest. When the heart 
 becomes continually irregular for a short or a long period, this fluttering 
 makes the patient conscious of the abnormal action (see Chapter XX). 
 
 Haemorrhages. — Rupture of an artery due to high blood-pressure acting 
 on a degenerated artery may give rise to cerebral apoplexy, bleeding under 
 the conjunctiva, from the nose, &c. Nose bleeding is not infrequent with 
 disease of the aortic valves, and in women attacks of bleeding from the nose 
 are liable to occur at the beginning of the menstrual period. Haemoptysis 
 may occur when the lungs are engorged or when there is a rupture of a 
 blood-vessel. 
 
 Cerebral Symptoms 
 
 There are a number of symptoms produced by the brain dependent on 
 the inefficiency of the circulation. I exclude from consideration here the 
 symptoms due to lesions of the blood-vessels, as rupture. The symptoms 
 induced more directly by affections of the heart are caused by a diminished 
 supply of blood reaching the brain, and the nature of the symptoms 
 depends on the extent of that diminution and the period during which the 
 diminished supply lasts. 
 
 Dizziness or giddiness. — The first stage of transient cerebral anaemia 
 is shown by a sensation of giddiness. It is seen most characteristically in 
 elderly people (particularly in tall people), when there is arterial degenera- 
 tion. The attack usually comes on when the individual makes a sudden 
 change in his position, as in rising from a couch. The attack may be hmited 
 to a passing sensation of giddiness, or the individual may reel and stagger 
 and clutch at some object for support, or he may fall. In walking, a transient 
 dizziness may come on and the individual may stagger for one or two 
 steps. The liability to these attacks varies at different times — periods of 
 liability varying with periods when the tendency disappears. The attacks 
 occurring in elderly people have no special prognostic significance, as I have 
 known persons exhibit them over a long period of years and live to over 
 eighty years of age. Exactly similar attacks may occur where the heart 
 fails to send sufficient blood into the brain, as in paroxysmal tachycardia, 
 where the transient increased rate is accompanied by a diminished output 
 from the heart. 
 
 Loss of consciousness. — Syncopal attacks or fainting, when the patient 
 becomes limp and unconscious, occur with a diminished supply of blood 
 to the brain. This can be brought about in a variety of ways, and is 
 generally due to an alteration in the heart's action. I have made observa- 
 tions and taken tracings of several patients during syncopal attacks, and
 
 24 DISEASES OF THE HEART 
 
 have found a variety of conditions present. The most common has been 
 a slowing of the heart-rate, with great weakness of the pulse, so that 
 only a slight tracing was obtained by the sphygmograph. In one case the 
 heart was beating with great rapidity, but the j^ulse beats were small and 
 the patient lay unconscious for nearly half an hour. In another case the 
 heart became very slow in its action and irregular with beats of varpng 
 strength. The more frequent forms of syncope are preceded by a pre- 
 liminary sensation of extreme weakness and loss of sight. ' All became 
 dark ' is a very frequent expression made by the patient after recovery. 
 
 There is one form of loss of consciousness which is met with in elderly 
 people. The attacks come \vithout warning and are of momentary duration, 
 resembUng "petit mal. The individual may be sitting at his desk, when his 
 head suddenly drops on the desk, or he may be standing or walking when 
 he suddenly falls. Consciousness at once returns and he is surprised to 
 find himself in a strange posture. There is generally present extensive 
 arterio-sclerosis in these cases, with an irregular heart due to extra-systoles. 
 I am disposed to consider the attacks due to several of these extra-systoles 
 occurring in succession, so that there is a temporary cessation or a diminu- 
 tion in the amount of the blood suppljdng the brain. Similar attacks 
 occur in the early stages of heart-block, but tracings of the jugular pulse 
 enables one to distinguish the condition. 
 
 Adam-Stokes syndrome. — When the blood-supply of the brain is com- 
 pletely arrested, loss of consciousness results, and, if prolonged, epileptiform 
 contractions of the muscles of the body may result. The condition of 
 heart affection where this is seen most typically is in heart-block — when 
 the auricle continues to beat at a normal or quickened rate and the ventricle 
 stands still or beats at a very slow rate. But identical cerebral phenomena 
 may arise from other conditions when the ventricular contraction is too 
 slow, as in the condition I describe under the term ' nodal bradycardia ' 
 (p. 337), or in the long standstill of the whole heart, probably due to vagus 
 influence, as described by Laslett ^°^. 
 
 The symptoms due to a diminution of the blood-supply varies according 
 to the degree of the cerebral anaemia. Patients suffering from one of the 
 conditions just mentioned may show a variety of symptoms, as a feeling 
 of dizziness, a brief loss of consciousness, or a prolonged loss of consciousness 
 with twitchings of the muscles or even convulsions. These varying degrees 
 depend on the frequency of the ventricular systole, the milder phenomena 
 being shown when the ventricular standstill is prolonged, or when the 
 contractions are at rare intervals. Dr. O'Connor, in the case of nodal 
 bradycardia, described on p. 342, noted that his patient might have twenty
 
 PRELIMINARY EXAMINATION OF THE PATIENT 25 
 
 or thirty brief attacks of loss of consciousness in one day, and on several 
 occasions when talking to his patient he observed him suddenly become 
 pale and lose himself for a few seconds, the attack exactly resembling one 
 of petit mal. He has had his finger on the patient's pulse on several of 
 these occasions and felt it disappear. During longer pauses in the pulse 
 this patient had numerous epileptic convulsions. 
 
 Barr ^^^ has noted in a case of heart-block that convulsions occurred 
 when the pulse disappeared for twenty seconds. In tracings taken from 
 the same patient, pauses of twenty-one seconds and over were followed by 
 convulsions. With prolonged disappearance of the pulse and unconscious- 
 ness, convulsions do not always occur, and in the same individual during 
 long pauses there may be no convulsions, or there may be slight muscular 
 twitchings or wide-spread convulsive movements, under apparently similar 
 circumstances. 
 
 How long it is possible for the pulse to disappear and recovery of con- 
 sciousness to be complete has not been determined in the human subject, 
 nor can the observation of the pulse alone be relied upon to give informa- 
 tion. Leonard Hill has pointed out that the merest trickle of blood may 
 keep the brain intact, and the fact that in heart-block the auricles are 
 beating may account for a certain amount of blood reaching the brain. 
 That the auricle can send blood into the arterial system can be inferred 
 from the fact that its contraction does affect the radial pulse, as shown by 
 Figs. 122-4, pp. 183-4. 
 
 Hallucinations. — When the heart is failing the blood-supply of the 
 brain is not fully maintained and certain symptoms may be detected. 
 Thus the patient can maintain a mental effort as in reading, or in writing, 
 only for a short time, becoming easily fatigued. The memory for recent 
 events becomes impaired, and what the patient may read is imperfectly 
 retained. In more severe cases hallucinations may appear and may take 
 various forms. The patient may imagine that some one is hiding behind 
 a door and though in conversation admitting the unlikelihood of such a 
 circumstance, yet when left alone the hallucination returns with a sensation 
 of terror. Or the patient may wake up and imagine he sees objects, as an 
 arm projecting from the ceiling, or the sound of some one on the stair, 
 or of soldiers marching past in the street. Head ^^ has dealt very fully with 
 this matter, and points out that the patient usually conceals these hallucina- 
 tions until he is directly questioned concerning them.
 
 CHAPTER V 
 
 Respiratory Symptoms 
 
 § 26. Breathlessness, or aii- hunger. 
 
 27. The sense of suffocation. 
 
 28. Inability to stop breathing. 
 
 29. Quiet, rapid breathing, free from distress. 
 
 30. Continuous laboured breathing. 
 
 31. Laboured breathing brought on by exertion. 
 
 32. Attacks of breathlessness (cardiac asthma). 
 
 33. Cheyne-Stokes respiration. 
 
 34. Slow respiration. 
 
 35. Pulmonary haemorrhage. 
 
 36. Acute suffocative oedema of the lungs. 
 
 The respiratory symptoras arising in the course of heart affections are 
 so numerous, and the conditions causing them so multifarious, that it is 
 impossible to deal exhaustively with this subject. The factors concerned 
 in the production of any one of the forms of respiratory trouble are often 
 difficult to recognize, and I shall not attempt any strict analysis of these 
 factors, but limit myself to the more apparent clinical forms that accompany 
 heart affections. 
 
 § 26. Breathlessness, or air hunger — There is normally a ' desire to 
 breathe ', and under certain circumstances this may be intensified so that 
 there is a ' hunger ' for air. The sense of air hunger compels laboured 
 breathing so that the term ' breathlessness ' includes the subjective sensation 
 and the objective symptom. The centre for respiration in the medulla is 
 influenced by its blood-supply, and its nervous connexion with the peri- 
 phery. A free blood-supply is necessary to supply oxygen and remove the 
 carbonic acid, and an insufficient interchange of these gases is betrayed by 
 an increased activity of the centre, thus giving rise to breathlessness. The 
 respiratory centre is also receptive to peripheral stimulation, as from sensory 
 nerves of the skin and from cardiac and pulmonary nerves. 
 
 An absence of the sense to respire may occur for a short period as in the 
 apnoeic stage of Cheyne-Stokes respiration. John Hunter ^'^'^ gives a curious 
 account of an attack from which he suffered, when he lay pulseless but 
 conscious ; observing he did not breathe, and had no desire to do so, 
 he thought he must die if he did not breathe, and by an effort of will
 
 RESPIRATORY SYMPTOMS 27 
 
 continued to breathe until his pulse returned and the automatic respiration 
 was established. 
 
 § 27. The sense of suffocation.— This is difficult to describe, and is 
 referred usually to the upper part of the chest and throat. The mechanism 
 is obscure. It is a frequent accompaniment of heart affections, from 
 temporary weakness of the heart to the gravest forms of heart disease, and 
 its significance may be slight, or in serious heart trouble it may be a very 
 grave sign. 
 
 § 28. Inability to stop breathing — I have been struck by the fact 
 that while taking tracings of the jugular and other pulses many patients 
 are unable to stop breathing. When asked to hold their breath, they will 
 shut their mouths, but are unable to stop breathing through the nose. If 
 the nose be pinched, they then complain of distress (air hunger). This 
 condition only arises in extreme heart failm-e, and as the heart regains 
 strength we may recognize the fact by the abihty to hold the breath. 
 
 § 29. Quiet, rapid breathing, free from distress — In many cases of 
 heart failure, when the patient is lying quiet, no definite symptom can be 
 found save that of a respiration more rapid than normal. There is no 
 distress, and the symptom is apt to be overlooked. Sometimes I have 
 failed to recognize it until I have come to analyse tracings where the 
 respiratory movements had been taken. Where, as sometimes happens, 
 a patient describes certain feehngs (as angina pectoris) which we are bound 
 to recognize as cardiac in origin, but where physical examination reveals 
 no sign of mischief, the recognition of more rapid respiration may prevent 
 us from vicA^ing too hghtly the condition of the patient. This symptom 
 is of the greatest importance in patients suffering from affections of the heart, 
 particularly in mitral-stenosis, in exhausting diseases like typhoid fever, 
 and in all conditions that compel the weakly, and particularly the elderly, 
 to lie on their backs, as e. g. when suffering from a broken leg. In such 
 cases the lying in bed, while favouring the work of the left ventricle, embar- 
 rasses the work of the right by restricting the respiratory movement. As 
 a result of this restraint of the ribs, the breathing becomes shallow. The 
 effect is to retard the flow of blood through the less mobile part of the lungs, 
 and in consequence stasis at the base of the lungs results (see § 190). 
 
 § 30. Continuous laboured breathing — This occurs characteristically, 
 at the beginning of what is called ' sudden failure of compensation '. The 
 patient cannot lie down, but sits up breathing in short quick gasps. The 
 slightest exertion, such as is entailed by changing to a more comfortable 
 position, immediately aggravates the distress. This form of breathing is 
 best seen in cases of dilatation of the heart with a rapid irregular pulse,
 
 28 DISEASES OF THE HEART 
 
 and, in fact, the whole respiratory distress is often the outcome of the 
 heart taking on the nodal rhythm which is manifested by the irregularity 
 (Chapter XX). With slowing of the heart's action and other evidences 
 of cardiac improvement, the respiratory distress gradually disappears, but 
 is liable at first to be brought on readily by a slight exertion. 
 
 § 31. Laboured breathing brought on by exertion — This is a symp- 
 tom common to a great many affections besides heart troubles, but its asso- 
 ciation with a weak heart is so common that it should at all times lead to 
 an inquiry as to the condition of the heart. It may occur with every form 
 of heart affection. It is of very great use in estimating the strength of the 
 heart, as its appearance indicates in a rough way the degree of exhaustion. 
 The earlier it appears, the less the reserve power of the heart. On the other 
 hand, improvement may be indicated by the gradual return of the ability 
 of the patient to undertake with comfort greater exertion. The forms of 
 exertion that induce it are very puzzling. Some patients can lift great 
 weights, and pursue the hard work associated with their calling, yet cannot 
 walk up a slight hill without complaining of being short-winded ; or they 
 suffer in the same way on going into the cold air. Some can cycle in comfort, 
 while others cannot cycle, but can walk with comfort on the level. I cannot 
 explain these, and other peculiarities, but note them as clinical facts. 
 
 § 32. Attacks of breathlessness (cardiac asthma) — A form of 
 respiratory distress which comes on usually in the night, sometimes suddenly 
 arousing the patient from sleep, has received the name of ' Cardiac Asthma '. 
 An attack of this sort is sometimes the first serious sign of heart trouble, 
 though on inquiry an account can usually be obtained of a period prior to 
 the attack when there was a distinct hmitation of the field of cardiac response. 
 The patient may have gone to bed in his usual health and according to his 
 usual custom, and after three or four hours' sleep he is awakened with a 
 feeling of suffocation, and an intense desire to breathe deeply. He sits up 
 in bed, and breathes in deep and laboured fashion, A sense of great pros- 
 tration may add to his suffering. Wheezing sounds may appear in the 
 chest, and he may cough up some frothy phlegm. The attack may last 
 for half an hour or longer ; then the breathing becomes quieter, and he 
 is able to lie down, though he keeps starting up, and finally assumes a position 
 with his head and shoulders raised, passing the remainder of the night in 
 uneasy slumber. Once these attacks begin they are apt to continue, and 
 the nights of the patient often become periods of great distress. The fear 
 of the attack may keep the patient awake, and should he drop off to sleep 
 he awakes with a start at the first sign of embarrassed breathing. 
 
 The class of case which shows this condition most characteristically
 
 RESPIRATORY SYMPTOMS 29 
 
 is the elderly, and those who suffer from cardio-sclerosis. Generally they 
 have a high blood-pressure, and the heart is usually regular except for the 
 presence of occasional or frequent extra-systoles. In these cases we some- 
 times find the best examples of the pulsus alternans. The cause of this 
 form of asthma is not quite clear. I have found the great distress induced 
 by this condition in many cases insusceptible to treatment, but lately 
 I have been giving massive doses of oxygen, in some cases with very gratify- 
 ing success (see p. 278). 
 
 § S3- Cheyne-Stokes respiration — In all cases of heart affection 
 where there is reason to suspect cardio-sclerosis, or where there is a high 
 blood-pressure from such causes as arterio-sclerosis and Bright's disease, 
 and where we get a history of breathlessness, quiet observation should be 
 made when the patient is perfectly still, and nothing attracting his attention. 
 Under such circumstances, the patient's breathing may occasionally be found 
 to take on a peculiar rhythmical character. Instruction should also be 
 given for the attendants to note the character of respiration during sleep. 
 
 The character of the breathing is a rhythmical variation in the size 
 of the respiratory movements — a gradual passage from a state of 
 complete or almost complete cessation to a condition of breathing where 
 the respiratory movements are deep and laboured (see Figs. 4 and 5, 
 Plate I). When the breathing gradually slows and ultimately stops, the 
 patient's mental condition frequently becomes a blank, and is accompanied 
 usually by twitching of some muscles, especially to be noticed in those of 
 the hand and arm. With the resumption of the breathing, he wakes, and 
 may resume a conversation that he had been pursuing before the slowing 
 of the breathing set in. 
 
 Usually no material change can be detected in the action of the heart 
 during the diverse phases of respiration. Sometimes, however, certain 
 changes may appear in the pulse coincident with the respiratory phases. 
 One patient with a sclerotic heart (Case 23, Appendix V) had shown 
 a weU-marked pulsus alternans for many months (Fig. 249), and towards 
 the end of his life he developed Cheyne-Stokes respiration (Fig. 6, Plate I). 
 During the respiratory phases there was a distinct increase in this form of 
 irregularity in the radial pulse. I took his blood-pressure during a period 
 of Cheyne-Stokes respiration, and found that it fell 5 to 10 mm. Hg. during 
 the apnoeic stage. This variation can be made out in the pulse tracing in 
 Fig. 6, Plate I, where it shows a greater amplitude of beat, and lowering of 
 the base line during the fall of blood-pressure, i. e. during the apnoeic period. 
 Gibson has also described a fall of blood-pressure during the apnoeic stage. 
 In Fig. 7, Plate I, there is a tracing from a patient who had hiccough as well
 
 30 DISEASES OF THE HEART 
 
 as Cheyne-Stokes respiration, and Cushny^^^, commenting on this case before 
 the Physiological Society, remarked, ' During the intervals of apnoea, the 
 rhythm of the hiccough was more rapid than during the periods of active 
 respiration, but the violence of the spasms seemed somewhat less. 
 
 ' The physiology of hiccough is still obscure, and we are not aware of any 
 record of the movements having been taken previously. It is generally 
 stated to be a reflex movement of the diaphragm, originating from some 
 abnormal irritation of the stomach. If the respiratory centre is involved 
 in the reflex, as is generally held, it must have remained excitable by nervous 
 impulses in this case when the normal chemical stimulus failed to induce 
 respiration. The slowing of the hiccough rhythm during the periods of 
 active respiration is striking, and may perhaps be analogous to the inter- 
 ference of two reflexes with a final common path (Sherrington) ; here only 
 one afferent stimulus is of nervous origin, however, the other being 
 chemical.' 
 
 Usually the patient is unaware of the occurrence of this periodic respira- 
 tion, and it causes him no distress. On the other hand, it may occasion 
 acute distress : the patient may drop off to sleep, and this form of respiration 
 gradually appears, and during the apnoeic stage the patient awakes with 
 a most distressful sensation of suffocation. So terrible is this that patients 
 extremely exhausted may spring suddenly out of bed in an extremity of 
 terror. 
 
 The great majority of cases of Cheyne-Stokes respiration are brought 
 on by, or associated with, cardio-sclerosis, arterial disease, and high blood- 
 pressure. It disappears with the sudden fall of blood-pressure due to 
 dilatation of the heart. It may be made temporarily to disappear by 
 massive doses of oxygen ; or on the inhalation of small quantities of COo 
 (Pembery *^''). Haldane and Poulton*^" have produced the condition 
 by forced breathing, and conclude that the periodic breathing is due to 
 the ' disappearance of the (indirect) excitatory effects of want of oxygen 
 in the respiratory centre '. 
 
 In the great majority of cases of arterio-sclerosis and Bright 's disease 
 it is usually the beginning of the end, the patients dying within a few months 
 or weeks, or even a few days of its onset. In a few cases I have seen it appear 
 two or three years before death. It calls for no special treatment save 
 when the apnoeic stage produces the terrible sense of suffocation ; then 
 morphia or chloral generally relieves this feature without altering the 
 respiration. 
 
 Cheyne-Stokes respiration must be kept distinct from certain other 
 forms of periodic respiration. Hibernating animals show a form of
 
 RESPIRATORY SYMPTOMS 31 
 
 periodic respiration, also some children during sleep. It appears also in 
 some cases of tubercular meningitis. 
 
 Loss of consciousness does not always ensue during the apnoeic stage 
 of Cheyne-Stokes respiration, as shown by the following instance. I saw in 
 consultation a clergyman, aged fifty, who had a paralytic seizure two years 
 previously, resulting in an ordinary hemiplegia. When I saw him he was 
 lying in bed quite conscious, extremely prostrate, with a pulse rate of 180 
 per minute, with t3rpical periodic respiration. During the apnoeic stage 
 he was quite conscious, and could talk intelhgently, his voice was faint and 
 reedy in quality, diminishing in loudness towards the end of his remarks. 
 His medical attendant told me he had suffered off and on from this condition 
 for three years. This case corresponds to a description given by John 
 Hunter ^^, who says, ' A gentleman had a singular asthmatic affection, and 
 his breathing gradually stopped and again gradually recurred, but became 
 violent, and thus constantly and alternately held two or three minutes, 
 and when the breatliing ceased yet he spoke although but faintly.' 
 
 § 34. Slow respiration — There is a number of individuals in whom 
 the respirations during rest are much slower than normal, 7 to 10 per minute. 
 The slow respiration induces an irregular action of the heart, and is described 
 in Chapter VIII. The condition is probably due to vagus stimulation, 
 and I have been able to produce it artificially by the administration of 
 digitalis. 
 
 § 35. Pulmonary haemorrhage — Bleeding from the lungs is not an 
 infrequent complication in heart failure. It is most commonly seen in the 
 terminal stages of arterio-sclerosis, with the fall of blood-pressure that 
 indicates dilatation of the heart and stasis of blood in the lungs. In these 
 cases the expectoration is either blood-stained or it is almost entirely 
 composed of lumps of dark clotted blood. Post mortem there are usually 
 found several hard patches of ecchymosed blood at the base of the lungs. 
 In the young with mitral stenosis, profuse haemoptysis may occur, and is 
 generally a sign of extreme gravity. 
 
 In other forms of heart affection, haemorrhage more or less free may 
 occur, and give the patient considerable relief, and be followed by no serious 
 consequence. In fact, if we find the patient on the whole with a fair amount 
 of reserve force, whatever the nature of the heart lesion, there need be no 
 immediate alarm from a free haemoptysis when due to cardiac trouble. 
 
 A serious form of haemoptysis arises from a pulmonary infarct, or a pul- 
 monary apoplexy ; in these cases the symptoms are extremely varied in 
 severity. Thus I have seen patients with phlebitis of the veins of the leg, 
 or after confinement, die in a few minutes with symptoms of great respiratory
 
 32 DISEASES OF THE HEART 
 
 distress. In some cases I have seen the most intense dyspnoea with gradual 
 loss of consciousness go on for four or five hours, and then suddenly the 
 dyspnoea ceases and the consciousness returns. After twelve hours the 
 patient has expectorated large quantities of pink-stained jelly-Uke mucus. 
 I have also seen cases of pulmonary infarct, as after a fracture of the tibia, 
 where the only evidence was the expectoration, for three or four days, of 
 dark-coloured blood, in small quantities at a time, followed by complete 
 recovery. Presumably the difference in the symptoms in these cases 
 depended on the size of the infarct or the extent of the apoplexy. 
 
 § ^6. Acute suffocative oedema of the lungs A peculiar form of 
 
 oedema, of which I have only seen a few cases, is that in which the patient 
 is suddenly seized with breathlessness, usually during the night, followed 
 speedily by the welling out of the mouth and nose of large quantities of 
 froth. Usually the patient succumbs within an hour of the commencement 
 of the attack. The conditions giving rise to it are obscure, and it occurs 
 in a great variety of cases. An excellent account of a case, and the literature 
 on this subject, are given by L. Williams ^°.
 
 CHAPTER VI 
 
 Reflex, or Protective Phenomena 
 
 § 37. Classification of symptoms in visceral disease. 
 
 38. Insensitiveness of the viscera to ordinary stimuli. 
 
 39. The mechanism by which pain and other reflex phenomena are produced in visceral 
 
 disease (the viscero-sensory reflex). 
 
 40. The purpose of visceral reflexes. 
 
 41. Why pain is referred to regions remote from the organ. 
 
 42. The relationship of the heart to sensory nerves. 
 
 43. The viscero-motor reflex. 
 
 44. Vagal sensory reflex. 
 
 45. Conditions in which angina pectoris js induced. 
 
 46. Conditions giving rise to attacks of angina pectoris. 
 
 47. Association of angina pectoris with exhaustion of the muscle of the heart. 
 
 48. Association of angina pectoris with impairment of the function of contractility. 
 
 49. Summation of stimuli as a cause of angina pectoris. 
 
 § 37. Classification of symptoms in visceral disease When the 
 
 symptoms of visceral disease are carefully analysed there appears a great 
 similarity in the nature and origin of certain of them, which permits of their 
 division into three groups ; — first, symptoms due to changes in the organ 
 itself — in the case of the circulatory system, changes in the movements 
 of the heart and blood-vessels ; second, symptoms observed in remote 
 organs and tissues which suffer indirectly from the primary lesion, for 
 instance, jaundiced skin in liver affections, uraemic convulsions in renal 
 disease and dropsy, oedema or albuminuria in heart failure ; third, reflex 
 or protective phenomena, which form the subject of this chapter. 
 
 While the character of the symptoms in the first two divisions depends 
 on the size and specific function of each organ, the reflex phenomena pro- 
 duced by all organs have a great resemblance. This is particularly the case 
 with all the hollow muscular organs. They have similar origins and their 
 reflexes are similar in character, and are only modified by the special develop- 
 ment of each. In spite of the seeming dissimilarity in the form and function 
 of the digestive tube, uterus, ureter, and heart, they are fundamentally 
 the same, and the reflexes associated with them are of a like nature. Hence 
 the nature of obscure symptoms in affections of the heart may be revealed 
 by an inquiry into the meaning of similar phenomena presented by these 
 organs, which have at first sight so little affinity with it. 
 
 MACKENZIE J)
 
 34 DISEASES OF THE HEART 
 
 § 38. Insensitiveness of the viscera to ordinary stimuli In order 
 
 to appreciate the reflex symptoms in visceral disease we must keep in mind 
 the functions of the nerves that supply them. 
 
 The nerve-supply of the body is included in the two great systems, the 
 autonomic and the cerebro-spinal. The autonomic includes the whole of 
 the sympathetic nerves, and certain cerebral nerves, of which the vagus 
 is the only one that concerns us here. 
 
 The tissues and organs supplied by the nerves from the autonomic 
 system are not endowed with sensation in the sense in which the term is used 
 in regard to tissues supplied by the cerebro-spinal nerves. The skin, muscle, 
 and other tissues of the external body-wall are readily sensitive to all forms 
 of stimuli that produce such sensations as touch, pain, heat, and cold, whereas 
 the viscera supplied only by the autonomic system are totally irresponsive 
 to such stimuli. Thus such organs as the heart, stomach, bowels, liver, 
 kidney, can be cut, torn, burnt, and no sensation elicited. Yet, as we know, 
 pain of a most excruciating character can arise from visceral affections. 
 Harvey ^^ describes how he touched the exposed heart of the son of Viscount 
 Montgomery and found it without sensation. Surgeons in pre-chloroform 
 days incidentally refer to the insensitiveness of the viscera. Thus Richerand ** 
 describes how, in operating in the neighbourhood of the heart, he found the 
 pericardium insensitive, and I have repeatedly verified this observation in 
 cases where the ribs have been resected. The following experience illustrates 
 the insensitiveness of the viscera, and at the same time affords an insight 
 into the manner in which visceral pain arises. 
 
 I had occasion to resect the bowel in a conscious subject under the 
 following circumstances. He had an umbilical hernia, and had worn for 
 years a pad tightly pressed over it, until the skin had ulcerated. The 
 ulceration had finally penetrated into the bowel, and his food was dis- 
 charged through the fistula. It was resolved to resect the bowel, but the 
 patient would not be anaesthetized. Observing that the skin was already 
 ulcerated, and that the tissues forming the external wall were not very 
 sensitive, so that the abdominal cavity could be opened with Uttle pain, 
 I reasoned that the after-operation could be performed painlessly. It turned 
 out as I had expected, and I was able to break down numerous old and 
 recent peritoneal adhesions, to detach them from the liver and bowel, to 
 resect a piece of bowel and mesentery, and to stitch these structures without 
 the patient experiencing the slightest sensation. But I found that he 
 occasionally groaned with pain when I was not touching him, and watching 
 to see the cause I found that the upper part of the resected bowel, which was 
 laid on one side in a warm aseptic cloth, occasionally passed into peristalsis,
 
 REFLEX, OR PROTECTIVE PHENOMENA 35 
 
 contracting from a wide tube to a thick fleshy rod ; when this happened the 
 patient groaned with pain. I asked him where he felt the pain, and he 
 passed his hand invariably over the umbilical region. I started the peri- 
 stalsis several times by slightly pinching the bowel, and each time the patient 
 felt the pain. Here before my eyes was the cause of the pain, and the seat 
 of origin of the pain was at least twelve inches away from the part in which 
 the pain was felt. 
 
 From this experience the following deductions can be made : first, 
 that the stimuli that produce pain and other sensations in the external 
 body-wall are not adequate to produce these sensations when applied to the 
 viscera ; second, that violent contraction of non-striped muscular fibres 
 can produce pain, but the region in which the pain is felt is different from 
 that in which the contracting muscle lies. 
 
 This isolated experience has been confirmed by many other observations 
 I have made, and in part confirms the experiments made by Haller^" more 
 than 150 years ago upon animals, when he showed that they were indifferent 
 to severe mutilation of their viscera, so long as the external body-wall was 
 not interfered with. 
 
 These experiences compel one to look for an explanation of the production 
 of visceral pain other than that which suffices to explain its production from 
 the stimulation of the external body-wall, and the following explanation 
 seems satisfactorily to account for the matter, and to explain the peculiar 
 nature of the sensory phenomena that arise in visceral disease. 
 
 § 39. The mechanism by which pain and other reflex phenomena 
 are produced in visceral disease (the viscero-sensory reflex) — When 
 a nerve that terminates in a sense organ is stimulated in any part of its 
 course from the periphery to the brain, a stimulus is conveyed to the brain 
 of a kind similar to that induced when the peripheral end-organ is stimulated. 
 Thus the stimulation of any part of the optic nerve or auditory nerve gives 
 rise to the sensation of light or of sound. In the same manner, if a sensory 
 nerve be stimulated in any part of its course through the brain, spinal cord, 
 or trunk of the nerve, the resultant sensation is referred to the peripheral 
 distribution of the nerve in the external body-wall. 
 
 Fig. 8 is a diagram representing the brain and spinal cord (S.C.) with 
 
 a sensory nerve (S.N.) passing from the skin (Sk) through the spinal cord 
 
 to the brain. A stimulus applied to the skin, or to the sensory nerve 
 
 between the skin and the cord, or to the sensory nerve in the cord, gives 
 
 rise to a sensation referred by the brain to the portion of skin innervated 
 
 by the nerve, though the stimulus may have affected the nerve after it had 
 
 left the skin. In the diagram, a viscus (H) is represented, and its nerve 
 
 D 2
 
 36 
 
 DISEASES OF THE HEART 
 
 (Sy. N.) is seen passing to the spinal cord. In the normal processes of life, 
 a stream of energy from the viscera is continually passing by the afferent 
 
 Fig. 8. Diagram sho^-ing the mechanism producing visceral pain. From the viscus H an 
 abnormal stimulus is conveyed by the sympathetic nerve (Sy. N.) to the spinal cord S.C. On 
 reaching the cord the abnormal stimulus spreads beyond the sympathetic centre and affects 
 nerve-cells in its immediate neighbourhood. The cells so stimulated react according to their 
 function, the sensory causing a sensation which the brain recognizes as pain, and refers to the 
 peripheral distribution of the sensory nerve (S.N.) in the skin (Sk) or muscle (31), the motor 
 (M.N.) producing contraction of the muscle (31). The abnormal stimulation may leave a 
 portion of the cord abnormally irritable (shaded portion), so that the tissues supplied by 
 nerves from that portion of the cord are hyperalgesic, and attacks of pain, as of angina pectoris, 
 are more easily provoked. 
 
 nerves to the spinal cord, and continuously playing upon the efferent nerves 
 that run to muscles, blood-vessels, and so forth. These processes are
 
 REFLEX OR PROTECTIVE PHENOMENA 37 
 
 conducted so that they give rise to no appreciable sensation. If, however, 
 a morbid process in a viscus gives rise to an increased stimulation of the nerves 
 passing from the viscus to the spinal cord, this increased stimulation affects 
 neighbouring centres. If it excites the sensory nerve represented in the 
 diagram as passing from the skin to the brain, the resulting sensation will 
 be referred by the brain, not to the viscus, but to the peripheral distribution 
 of the sensory nerve. Thus it was that when, in the course of the operation 
 which I have described, the bowel contracted, the resulting pain was referred 
 not to the bowel, but to the peripheral distribution of the sensory nerves 
 in the region of the umbiHcus — thus the pain in visceral disease is seen to 
 be of a reflex character — a viscerosensory reflex. 
 
 In the diagram there is shown a motor nerve {M.N.) arising in the cord 
 and passing to a muscle {M). The stimulus from the viscus [H) passing 
 into the spinal cord, may excite the cells of origin of the motor nerves, with 
 the result that the muscle is stimulated to contract ; hence we get the 
 viscero-motor reflex. This reflex is best seen in affections of the abdominal 
 viscera when the abdominal wall becomes hard, due to tonic contraction 
 of the muscles. 
 
 When a portion of the spinal cord becomes violently stimulated by reason 
 of a visceral affection, that portion of the cord may remain for a lengthened 
 period in an over-excitable state, so that all the nerves that arise from this 
 portion of the cord may be much more easily stimulated. This can be 
 demonstrated in many cases of visceral disease by the hyperalgesic state 
 of portions of the external body-wall, and by the exaggerated motor reflexes. 
 In such instances, stimulation of the skin or muscles, as by light pinching 
 between finger and thumb of such weak force that normally it would only 
 result in the sensation of touch, is felt by the patient as pain. Light stroking 
 of the skin with a pin head may be felt as pain, and produces very readily 
 a strong reflex contraction of the muscles whose nerves arise from the same 
 portion of the cord. A further result of this irritable focus in the cord is 
 that the visceral stimulation more readily induces pain, and not only may 
 the original attacks of pain (as in angina pectoris, renal and bihary colic) be 
 more easily induced, but stimuli from other sources may induce the attack 
 of pain. Thus in cases of gall-stones with hyperalgesia of the external 
 body-wall over the region of the liver, the ingestion of the food into the 
 stomach may give rise to much pain in the hjrperalgesic tissues. 
 
 § 40. The purpose of visceral reflexes Reflexes have been studied 
 
 with the greatest minuteness, and the work of Sherrington *^ demonstrates 
 the extraordinary variety and complexity of the spinal reflexes, but their 
 purpose has been to a great extent overlooked. The main purpose of many
 
 38 DISEASES OF THE HEART 
 
 reflexes has been either to remove the body from the reach of injurious 
 influences, or to interpose a firmly contracted muscle between the agent 
 threatening the injury and the organ. It may even be true, as Herbert 
 Spencer suggests, that the evolution of muscles and the segmentation of 
 the body was due to the necessity of protection when the external body- wall 
 changed from an insensitive hard carapace to a sensitive mobile covering. 
 The way that the protective mechanism comes into play is by exalting the 
 sensitiveness of reflexes. Thus if an organ suffer injury, as by inflamma- 
 tion, the surrounding portion of the external body-wall immediately has its 
 protective functions exalted. This is usually accomplished by increased 
 sensitiveness of the skin and underlying structures, so that touch arouses 
 at once a strong and vigorous contraction of the protective muscles. These 
 muscles themselves become much more sensitive to pain, and, as painful 
 stimuli are the most provocative causes of reflexes, acutely tender muscles 
 may remain permanently contracted. 
 
 To illustrate the meaning and purpose of visceral pain and allied pheno- 
 mena, a case of gastric ulcer may be taken. The ulcer may be situated on 
 the posterior wall and at the cardiac orifice of the stomach, while the sensation 
 of pain is referred to the epigastrium. Here the skin and muscles may be 
 found exceedingly tender to touch and light pressure. The reflex contraction 
 of the underl3dng recti muscles is extremely lively and powerful. If you try 
 gently to palpate the stomach, these muscles at once become so strongly 
 contracted that it is utterly impossible to feel what is underneath. What 
 is nature doing ? Manifestly it is interposing a most efficient barrier between 
 the intruding hand and the diseased organ — the whole being a protective 
 mechanism. Had the stomach only been sensitive, the hand would have 
 reached the stomach, but by the reflex mechanism, the external body-wall 
 is made sensitive, and the powerful reflex contraction of the muscles effec- 
 tively guards the stomach from injury. The same protective mechanism 
 is involved in joint-disease. Thus the shoulder- joint may be found immobile. 
 Put the patient under chloroform and all the muscles relax, and a grating 
 may be detected on moving the joint. It is evident that here the injured 
 joint required protection, and the muscles responded to their first and 
 primitive duty. 
 
 Pain itself, Hilton pointed out, has the same purpose, — protection. It 
 commands at once cessation of any action that induces it, and this protective 
 function is seen nowhere more clearly than in heart affections. 
 
 § 41. Why pain is referred to regions remote from the organ. — 
 In a great many instances the pain is referred to situations remote from the 
 organ giving rise to it. Thus the pain of biliary colic may be felt in the
 
 REFLEX, OR PROTECTIVE PHENOMENA 
 
 39 
 
 epigastrium, the pain of renal colic in the testicle, the pain of heart affections 
 in the arm. 
 
 The reason for this is that in the course of development the tissues, 
 that in a low scale of Hfe immediately covered the organ, have been dis- 
 placed. Thus, the pain felt in the testicle in renal calculus is due to the fact 
 that in its journey down to the scrotum the coverings of the testicle receive 
 a tw4g from the first lumbar nerve, from which the kidney is also innervated, 
 and when the centre of this nerve in the spinal cord is stimulated, as in 
 renal calculus, the pain is felt in the testicle, and exquisite pain may be 
 eUcited on pressing the testicle. On the other hand, one never finds the 
 skin of the scrotum hyperalgesic in these cases, but only the deep covering 
 of the testicle, because the scrotum is supplied by the sacral nerves. 
 
 LS9 
 
 s la 
 
 Fig. 9. Diagi-ammatic representation of a primitive vertebrate animal to show the distri- 
 bution of the sensory nerves. For clearness of comparison the number of segments is repre- 
 sented to be the same as in man, and the heart occupies the same position. Each nerve is 
 shoAvn as limited in its distribution to one segment (after Ross). 
 
 § 42. The relationship of the heart to sensory nerves.— In order 
 to appreciate the mechanism of the pain felt in affections of the heart, the 
 manner in which the upper dorsal nerves come to be distributed should be 
 borne in mind. Ross *^ has pointed out that in the primitive vertebrates, 
 before the development of the limbs, each spinal nerve is distributed seg- 
 mentally round one half of the body (Fig. 9). The upper dorsal nerves 
 are therefore entirely distributed over the body-wall and to the tissues 
 covering the heart. The upper limbs, as they bud out from the trunk in 
 their development, drag with them away from the trunk portions of the 
 cervical and upper dorsal nerves, so that parts of the first and second dorsal 
 nerves are distributed to the ulnar border of the forearm and inner surface 
 of the upper arm. Thus, a stimulus originating in the heart and affecting 
 the cord area of the first and second dorsal nerves, would be felt as pain in 
 the lowly vertebrate over the heart, whereas in man it would be felt in the 
 upper arm or in the forearm (Fig. 10). 
 
 This peculiar distribution of the nerves to the chest and arm, resulting 
 from the development of the limbs, provides a unique field for observing
 
 40 
 
 DISEASES OF THE HEART 
 
 the mechanism of many nerve processes. The character of the field can be seen 
 in the distribution of the shaded area in Figs. 10, and 12 (p. 51), which represent, 
 the one the distribution of the eruption in a case of herpes zoster affecting 
 the spinal ganglia of the eighth cervical, first and second dorsal nerves, 
 
 and the other the area in which pain was felt, 
 and in which the skin was hyperalgesic in a case 
 with the symptoms of angina pectoris. The 
 existence of these and similar associated areas 
 has been demonstrated by a variety of methods 
 clinically, experimentally, and by dissection. 
 
 We know that the efferent cardiac fibres of 
 the sympathetic pass out of the spinal cord 
 with the upper dorsal nerves. Although it 
 is impossible experimentally to demonstrate 
 the region of the spinal cord to which the 
 afferent nerves pass, clinical observation pro- 
 vides ample evidence, and this evidence demon- 
 strates that the afferent nerves pass into the 
 cord at the same regions from which the 
 efferent pass out. 
 
 The usual description given of the pain in 
 angina pectoris is that it is felt in the heart and 
 shoots into the arm, or that there are two pains, 
 a local pain in the heart, and a referred pain in 
 the arm. If, however, a careful analysis be 
 made of aU the symptoms present, facts will be 
 found that practically demonstrate that in angina 
 pectoris there is but one kind of pain, and that 
 its production is in accordance with the law 
 I have attempted to establish, namely, that it is 
 a viscerosensory reflex. It is not in every case 
 that one is able to demonstrate the truth of this 
 hypothesis, but the conclusions drawn from 
 observations made in suitable cases may legitimately b'e applied to others. 
 Shortly, these observations are, that the pain in the very gravest cases 
 may be felt in regions distant from the heart, as in the left arm ; that 
 this pain is identical in character with that felt over the heart ; that the 
 pain may originally start in parts distant from the heart and gradually 
 approach and persist over the heart, and lastly, that the tissues of the 
 external body-waU over the heart may be found extremely hyperalgesic 
 
 Fig. 10. The dotted area 
 shows the distribution of an 
 eruption due to herpes zoster 
 in the peripheral distribution 
 of the eighth cervical, first and 
 second dorsal nerves. There 
 was also a small patch of erup- 
 tion over the left scapular spine.
 
 REFLEX, OR PROTECTIVE PHENOMENA 41 
 
 after the pain has passed away. From this last fact it is inferred that, 
 inasmuch as the seat of pain corresponds to the region of hjrperalgesia, 
 therefore the pain was felt by the hyperalgesic nerves. To assume otherwise 
 is to ignore a principle that explains satisfactorily the sensation of pain 
 wherever arising. 
 
 § 43. The viscero-motor reflex — So far I have dealt mainly with 
 the viscero-sensory reflex, but no less striking evidence can be found of the 
 viscero-motor reflex among the group of symptoms included in the term 
 ' angina pectoris '. Some would limit the term ' angina pectoris ' to that 
 class of cases where, in addition to the pain, there is a sense of constriction 
 in the chest, amounting to the sensation at times as if the chest were gripped 
 in a vice, or as if the breast bone would break. I am convinced that these 
 sensations arise from spasm of the intercostal muscles, and correspond to 
 the hard contraction of the flat abdominal muscles in affections of the 
 abdominal viscera. If one watch a case of what is called ' muscular rheu- 
 matism ', where the intercostal muscles are affected, and where these muscles 
 are stimulated by the slightest movement to violent cramp-Uke contractions, 
 one cannot but be struck by the resemblance to the description given by 
 the ' gripping ' sensation experienced by patients suffering from certain 
 affections of the heart. I have watched the attacks in such cases, and could 
 find no difference between them and those where the sense of contraction 
 was the chief symptom in heart disease. 
 
 The viscero-motor reflex may be present alone, or, as is more commonly 
 the case, it may be associated with the pain. The purely viscero-motor 
 reflex is seen best in the elderly, where it may be considered a symptom 
 of one form of the terminal affections of the heart due to cardio-sclerosis 
 or old age. I have found it a precursor of steadily advancing cardiac weak- 
 ness, and although for a time considerable rehef may be afforded, the changes 
 in the heart are so advanced that in the nature of things only one end can 
 be looked for. In such cases pain may be absent. 
 
 § 44. Vagal sensory reflex — So far the symptoms I have dealt with 
 have been mainly concerned with the reflexes connected with the sympathetic 
 nerve supply. Equally instructive though less frequent symptoms can be 
 shown to arise from stimulation of the vagus. At its centre in the medulla 
 this nerve is in near relationship to the upper cervical nerves, and it would 
 seem more particularly to the sensory nerves supplying the sterno-mastoid 
 and trapezius muscles. Not only can these muscles become extremely 
 hyperalgesic in various heart affections, but the pain from heart affection 
 may be felt in the region of distribution of the cervical nerves. Pain may 
 also be felt during an attack of angina pectoris in the gums and throat—
 
 42 DISEASES OF THE HEART 
 
 due to a radiation of the stimulus from the vagus to the centre of the 
 fifth nerve. 
 
 Other very striking reflexes are sometimes met with in an attack of 
 angina pectoris. Thus during or after an attack, an abundant flow of saUva 
 and the secretion of large quantities of pale urine may occur ; both symptoms 
 I suggest are due to reflex stimulation of the floor of the fourth ventricle. 
 
 There are also good grounds for attributing some forms of dyspnoea to 
 reflex stimulation from the heart. 
 
 § 45. Conditions in which angina pectoris is induced If a large 
 
 number of cases be studied, symptoms of angina pectoris will be found to 
 arise in patients with the most diverse forms of lesion, and even in patients 
 without any evidence of cardiac disease. From among a number of con- 
 ditions, I select the following : Cases of (1) aortic aneurysm, (2) aortic 
 valvular disease, (3) atheroma of the coronary arteries, (4) myocardial 
 degeneration or enfeeblement of the heart muscle from poor nourishment 
 or over-exertion, (5) increased arterial pressure of the elderly (usually 
 associated with 3 and 4). 
 
 It would seem that identical symptoms produced from conditions so 
 diverse cannot be directly due to the organic lesion, to the aortic aneurysm, 
 to the disease of the coronary artery, or to the increased peripheral resis- 
 tance. We must therefore look for a cause common to all five conditions. 
 
 § 46. Conditions giving rise to attacks of angina pectoris In order 
 
 to find what this common cause may be, consideration of the conditions giving 
 rise to an attack of angina pectoris will help materially. In the first place, 
 it is to be noted that angina pectoris in the five conditions cited appears 
 as a late symptom, after the heart has been struggling a long time against 
 obstacles opposed to its efficient action, or after the nutrition of the muscle 
 has been impaired by gross pathological changes in the coronary artery^ 
 or when the muscle-fibres have become impaired through slowly advancing 
 degeneration of the fibres. We find, further, that many patients when at 
 rest do not suffer from pain, but that any cause inducing increased work 
 on the heart provokes an attack. Bodily exertion in any form, excitement, 
 increased peripheral resistance (as in exposure to cold air), may bring on 
 directly an attack of angina pectoris. That is to say, in predisposed 
 individuals all circumstances that throw more work on the left ventricle 
 induce an attack of angina pectoris. 
 
 § 47. Association of angina pectoris with exhaustion of the muscle 
 of the heart — Such considerations lead to the conclusion that angina pec- 
 toris arises from certain conditions of the muscular substance of the heart,, 
 when the contraction meets with a resistance greater than it can easily and
 
 REFLEX, OR PROTECTIVE PHENOMENA 43 
 
 efficiently overcome, whether a fairly strong muscle struggles against an 
 increased resistance (as when there is great peripheral resistance or a narrowed 
 aortic orifice), or when a weak or degenerated muscle has opposed to its con- 
 traction a normal or even a lowered pressure, but a pressure greater than the 
 Aveakened muscle can readily overcome. 
 
 § 48. Association of angina pectoris with impairment of the func- 
 tion of contractility — If we inquire what function of the muscle-fibres is 
 concerned in the production of angina pectoris, we shall find additional 
 confirmation for the foregoing conclusion. 
 
 I shall later deal very fully with the fact that affections of certain functions 
 of the muscle-fibres (Gaskell's functions ^2^) can be demonstrated by means 
 of graphic records of the cardiac movements. I have taken a large number 
 of tracings from patients who have suffered from angina pectoris — during 
 the attacks and when free from pain — and an analysis of these tracings 
 enables me to say with confidence that angina pectoris can occur when the 
 excitabihty, the conductivity, and the power to produce a rhythmical 
 stimulus are unimpaired. There only remain now the functions of tonicity 
 and contractility. The evidence of failure of the function of tonicity is 
 mainly shown in the dilatation of the heart, and typical attacks of angina 
 pectoris frequently occur in hearts perfectly normal in size. Therefore angina 
 pectoris may occur without any evidence of the impairment of the function 
 of tonicity. Seeing, then, that angina pectoris can occur in patients when 
 four out of five functions of the heart muscle are demonstrably intact, we 
 are led to inquire whether angina pectoris may not be due to an impairment 
 of the remaining function, that is, contractility. When we come to look for 
 facts that have a bearing on this question we find : (a) an a 'priori evidence 
 in the fact that this is the function directly concerned in suppljdng the 
 motive force to the circulation of the blood, and that it is the function that 
 will necessarily become exhausted when an excessive resistance is opposed 
 to the contraction of the heart muscle ; (&) the symptoms associated with 
 and the conditions giving rise to the characteristic sign of depressed con- 
 tractility (pulsus alternans), are of a similar nature to the symptoms in 
 angina pectoris ; (c) angina pectoris may be associated Avith the pulsus 
 alternans ; {d) in other hollow organs severe pains are evoked by contraction 
 of the muscle- wall. 
 
 From this line of reasoning I would suggest that angina pectoris is an 
 evidence of exhaustion of the function of contractility. 
 
 § 49. Summation of stimuli as a cause of angina pectoris. — 
 The fundamental functions of the heart muscle correspond to those of other 
 involuntary muscles that form the walls of hollow organs ; these functions
 
 44 DISEASES OF THE HEART 
 
 being modified to suit its special work. Like the other viscera, the heart 
 is insensitive when stimulated in a manner that provokes pain when applied 
 to the tissues of the external body-wall. I may point out that a prolonged 
 strong contraction of a hollow organ can produce pain, and that this is 
 undoubtedly the cause of the severe pain associated with renal calculus, gall- 
 stones, spasm of the bowel, and uterine contractions. Can the heart give 
 rise to pain in a similar manner ? On account of the modification of its 
 functions, the heart cannot pass into a prolonged state of contraction. 
 Immediately it contracts, the function of contractihty is abolished and the 
 muscle passes at once into a state of relaxation, and for this reason the pain 
 cannot be produced by a ' spasm of the heart '. But I suggest that the 
 heart muscle may produce pain when it is confronted with work greater 
 than what it can readily overcome — a condition which produces strong 
 peristalsis and pain in other hollow viscera. But the pain in the heart 
 arises by a sUghtly different mechanism. A skeletal muscle will contract 
 in obedience to stimulation of a sensory nerve going to the spinal centre 
 of its nerve, if a stimulus of sufficient strength be applied. If the stimulus 
 is too weak no contraction follows, but if this weak stimulus be frequently 
 and rapidly repeated, then the muscle contracts in accordance with the 
 law of the summation of stimuli. I suggest that the heart muscle induces 
 pain on the principle of summation of stimuli. If we minutely study our 
 cases we shall find that the pain rarely arises at the first exposure of the heart 
 to the effort that induces the pain ; sometimes effort has been undertaken 
 a few minutes before the pain comes on, and in certain cases it may not 
 come on for hours after the causal exertion has ceased. From such observa- 
 tion we can infer that the heart muscle was exhausted by the exertion, 
 and so great was the exhaustion of the reserve force that the heart was 
 unable to regain its reserve with cessation of effort, so that the exhaustion 
 persisted till it culminated in an attack of angina pectoris. 
 
 The reasonableness of this explanation will be more apparent after dealing 
 specially with the symptoms of angina pectoris in individual cases.
 
 CHAPTER VII 
 
 Angina Pectoris 
 
 § 50. Conditions predisposing to an attack. 
 
 51. Conditions inducing an attack. 
 
 52. Character and duration of an attack. 
 
 53. The sjrmptoms present during an attack : pain, constriction 
 
 of the chest, sense of impending death. 
 
 54. The state of the heart and arteries. 
 
 55. The s3Tnptoms present after an attack. 
 
 56. Establishment of a tendency to recurrent attacks. 
 
 57. Prognosis. 
 
 58. Treatment. 
 
 In Chapter VI, I give the reasons for assuming that the symptom complex 
 called Angina Pectoris belongs to the class of reflex protective phenomena 
 where the symptoms are evoked by a viscus reflexly stimulating certain 
 areas in the central nervous system. The stimulus from the heart to the 
 spinal cord irritates the nerve-cells in close proximity to the nerve conveying 
 the stimulus from the heart. The nerves thus irritated respond and exhibit 
 the evidence of their peculiar function — sensory nerves, by pain felt in their 
 peripheral distribution, motor nerves, by contraction of the muscles. In 
 this way we get the peculiar distribution of pain in angina pectoris, and the 
 sense of constriction of the chest-wall. This violent stimulation of the 
 spinal cord may leave, after its subsidence, an irritable focus in the cord, 
 rendering that portion of the cord more susceptible to stimulation, so that 
 it becomes easier for future attacks of angina pectoris to be provoked. This 
 irritable focus can be demonstrated to exist in some patients by the hyper- 
 algesic state of the skin and muscles, and other subcutaneous tissues in the 
 region where the pain was felt. So sensitive may this irritable focus become, 
 that an attack of angina pectoris may be provoked by a stimulation reaching 
 the focus from regions other than the heart. I have further suggested in the 
 foregoing chapter that these phenomena are not the outcome of the gross 
 lesion found in cases of angina pectoris, but are due to the exhaustion of 
 the contractile function of the heart muscle. If this view be kept in mind, 
 the examination of patients is greatly facilitated, and the grounds for 
 a rational diagnosis, prognosis, and treatment are laid. 
 
 § 50. Conditions predisposing to an attack. — That a muscle should
 
 46 DISEASES OF THE HEART 
 
 evoke disagreeable symptoms when over-fatigued is a principle applic- 
 able to all muscular structures of the body. The peculiar functional 
 attributes of the heart muscle imply a modified method of exhibiting 
 these disagreeable symptoms, which I have dealt with in Chapter VI, 
 showing how in many cases it is probably due to the law of summation of 
 stimuli. In looking at the coronary arteries in certain typical cases of 
 angina pectoris, one can reasonably infer one way in which the attacks 
 are brought about. In some cases the coronary arteries are so narrowed as 
 scarce to permit the entrance of a pin. During life the stream of blood 
 must have been greatly reduced, and if it were sufficient to supply the 
 muscle during rest, it was demonstrably insufficient while the heart was 
 in a state of activity. In this respect there seems to be a distinct affinity 
 between the origin of the pain in these cases, and in those cases of what is 
 called ' intermittent claudication ' — first described in the horse, but not 
 infrequent in man. In one of my cases of this complaint, for two years 
 the patient could not walk one hundred yards before he had to stand still 
 and rest on account of the great pain in the legs and feet, and of intense 
 coldness of his feet. On standing a few minutes the pain disappeared, and 
 his feet became warmer. Here there was a marked atheromatous degenera- 
 tion of the arteries of the leg, and the supply of blood was sufficient for the 
 muscles when at rest, but contraction of the muscles demanded a greater 
 supply than the arteries could furnish, with the result that the exhausted 
 muscles became painful, and the diminished supply of blood to the skin 
 caused a sense of coldness. Ultimately the arterial supply became so slight 
 that gangrene of the toes set in. From the foregoing illustrations a fairly 
 safe conclusion can be drawn as to the manner in which anginal symptoms 
 are provoked. It can further be safely inferred that the muscle exhaustion 
 may arise in other ways, for example, when the nutrition is poor, as happens 
 in anaemic and badly nourished people. The heart may become exhausted 
 because it is never allowed sufficient time to recover its reserve force, as in 
 individuals who are worried and overworked. Or exhaustion may arise 
 from obstruction to the work of the left ventricle, as in disease of the aortic 
 valves, and in atheroma of the arteries, especially when accompanied with 
 partial obliteration of the capillary field (§ 221). In these cases the 
 disease that has damaged the aortic valves and arteries has at the same 
 time invaded and enfeebled the heart. 
 
 In addition to exhaustion of the heart muscle as a cause of angina pectoris, 
 there has to be noted this further fact, that angina pectoris arises only in 
 connexion with exhaustion of the left ventricle. The symptoms of angina 
 pectoris are invariably associated with lesions on the ventricular side of the
 
 ANGINA PECTORIS 47 
 
 mitral orifice. In a few cases I have found angina pectoris in patients with 
 mitral stenosis after violent exertion, but it is to be noted that the blood- 
 supply to the ventricle is limited in such cases. I do not remember having 
 seen a case of angina pectoris with free mitral regurgitation unaccompanied 
 by affections of the aortic valves ; hyperalgesia of the chest-wall is, however, 
 fairly common when there is also dilatation of the heart. In several 
 instances I have noted, with Broadbent and Musser, the complete cessa- 
 tion of anginal attacks with the onset of free mitral regurgitation. In 
 such cases the attacks were due to the left ventricle struggling to overcome 
 the high arterial pressure, and the cessation was due to the dilatation 
 of the heart rendering incompetent the mitral valves, and thus permitting 
 the ventricle to ease its load (Chapter XXVII). Though freedom from 
 attacks of angina pectoris was thus acquired, a great fall of arterial pres- 
 sure resulted, leading to dropsy and gradual exhaustion (Chapter XXII). 
 
 § 51. Conditions inducing an attack — Angina pectoris is never the 
 outcome of an acute affection ; it is invariably led up to by a long period of 
 gradual exhaustion.* The onset is, in the majority of cases, induced by 
 some extra effort on the part of the heart. This need not be an effort of 
 unusual severity ; it occurs more frequently when the individual is using 
 his powers in a way which formerly required no very marked strain. The 
 cause may be of the nature of bodily exertion, mental excitement, exposure 
 to cold air, or anything that calls for more work on the part of the heart. 
 In most cases the attack does not come on at once, unless the effort is per- 
 sisted in, as in walking up a hill, and the first warnings of heart exhaustion 
 are ignored. The attack of pain may not come for some minutes or even 
 hours after the causal exertion has ceased, and when the patient has been 
 resting in bed. In some severe cases the attack of pain may come on at 
 intervals when the patient has been exposed to no exertion, particularly 
 in cases where the attacks have been frequent, and a tendency to them has 
 been established. 
 
 § 52. Character and duration of an attack The attacks may be 
 
 so shght at first as to pass almost unnoticed, and it is only after they become 
 more frequent and severe that the patient's attention is called to the fact 
 that he had previously experienced some discomfort. In the more simple 
 cases the pain may not be very severe, and, appearing after some violent 
 exertion, may never again show itself. Instead of pain it may be but a slight 
 sensation of constriction across the chest, that calls for a deep inspiration 
 
 * Except in cases of coronary embolism, of which there are several cases on record in 
 which attacks of angina pectoris were evidently due to the plugging of a coronary artery 
 (Garrod ' and Parkes Weber ").
 
 48 DISEASES OF THE HEART 
 
 to relieve the tension. The more severe attacks imperatively command 
 a cessation of all efforts, and here all degrees of suffering may be experienced. 
 Dm-ing the attack the patient may stand still in a position of rigid immo- 
 biUty, afraid to move or to speak, scarcely daring to breathe, or he may kneel 
 down and rest his head on a chair, or roll on the floor in an extremity of 
 agony, or the patient may become unconscious and, in rare cases, may die. 
 If the pain is located in the arm, he may nurse it across his chest, rocking 
 backwards and forwards. The face may become pale or flushed, and beads 
 of perspiration may roU down the forehead. The attack may terminate 
 with the expulsion of air from the stomach, unconsciously sucked into the 
 stomach during the attack (§-64). 
 
 In most cases the attack lasts for a few seconds, but it may continue 
 with great severity for several hours, yielding only to large doses of opium. 
 Such severe cases may die during the suffering. 
 
 § 53. The symptoms present during an attack of angina pectoris. — 
 The chief symptom is pain : there may be also a sense of constriction across 
 the chest, a sense of suffocation, and a sense of impending death. Occa- 
 sionally other reflexes may be present, such as a flow of saUva from the 
 mouth, and an increased secretion of urine. These symptoms are not aU 
 present in every attack, nor are they always present in the same degree. 
 There may be a shght pain or a slight sense of constriction across the chest. 
 Or the pain may be of the utmost severity, with constriction of the chest 
 so violent that the patient feels as if his breast bone was about to break. 
 
 Pain. — Pain is usually referred to some portion of the distribution of 
 the upper four left dorsal nerves in the chest and arm. Sometimes the pain 
 may be felt as low as the distribution of the sixth dorsal nerves in the epigas- 
 trium, and as high as the eighth and seventh cervical in the ulnar border 
 of the forearm and hand. It is rarely felt in similar areas on the right side, 
 and sometimes it is felt in the neck and back of the head, in the upper cervical 
 nerves, whose roots are in close association with the vagus. The pain is 
 usually felt across the chest, and may remain stationary there, or it may 
 radiate in a very definite manner into the axilla, and down the arm to the 
 ulnar border of the forearm and hand. When it does this it may stop for 
 a brief period in the upper arm or forearm, and be felt there most violently. 
 On the other hand, the pain may start in the arm and radiate to the chest, 
 where it remains with great severity for a time. 
 
 Constriction of the Chest. — Arising along with the pain, or following it, or 
 quite independent of the sensation of pain, is a sense of constriction, which 
 I have reasoned is due to the reflex stimulation of the intercostal muscles. 
 It may be so slight as to be felt only as a mere tightness across the chest
 
 ANGINA PECTORIS 49 
 
 following exertion, or it may grip the chest so firmly that the patient has 
 to stand still and take a great deep inspiration to relieve the spasm of the 
 muscles. In its most violent form it adds greatly to the suffering of the 
 jjatient when pain is also present. Thus a man aged forty-eight, who had 
 violently exerted himself, felt a pain in his chest come on gradually some 
 minutes after the exertion. As the pain increased he called on me, and 
 I asked him if he felt his chest constricted. He said ' No '. A few hours 
 later, the pain increased in severity ; then suddenly he felt his chest 
 gripped with a violence so great that it added, he said, indescribably to 
 the terror of his suffering. It was only relieved by large doses of opium. 
 Next day he felt for a short time when in bed as though that ' awful gripping 
 were coming on ', and he lay for ten minutes with perspiration pouring off 
 him, in the dread of its return. 
 
 Feeling of impending dissolution. — This, I presume, is the result of 
 violent stimulation of the nervous system comparable to what happens 
 when any other viscus is violently stimulated, as after a blow in the epigas- 
 trium, or on the testicle. On rare occasions the patient faints during an 
 attack, and in one instance a patient of mine never recovered, but died 
 during the faint. 
 
 § 54. The state of the heart and arteries — The observations of 
 NothnageP^ that contraction of the arterioles may precede an attack of angina 
 pectoris, and of Lauder Brunton^ that the peripheral arteries may contract 
 during an attack of angina pectoris, have led to some misapprehension 
 regarding the circulation in this condition. I have had the opportunity 
 of examining a large number of patients during attacks of angina pectoris, 
 in some of whom the onset occurred immediately after exertion, in others 
 some hours after exertion ; in others the attacks have conle on suddenly when 
 the patient was in bed. I have taken a large number of sphygmographic 
 tracings and a few blood-pressure observations during these attacks, and have 
 never found a single case where the arteries were constricted in the manner 
 sometimes described (see illustrative cases in Appendix I). In six cases 
 where the patient was seized with the pain in bed, and died during the attack, 
 there was not the sHghtest sign of contracted arteries. In one of these cases 
 I measured the blood-pressure during an attack shortly before his death, 
 and found that the pressure had fallen considerably. I have seen and 
 carefully studied a few cases of Nothnagel's ' vaso-motor angina pectoris ', 
 and can positively state that they come under a different category from 
 the more common forms of angina pectoris due to disease of the coronary 
 arteries (§ 66). I can only infer that cases of arterial spasm are very excep- 
 tional, and their description, fostered by the relief obtained by the adminis- 
 
 MACKENZIE -c^
 
 50 DISEASES OF THE HEART 
 
 tration of amylnitrite, has given quite a wrong conception in regard to the 
 conditions inducing an attack of angina pectoris. I have found during 
 these attacks the pulse became small, soft, and scarcely perceptible, from 
 weakness of the heart, the heart sounds becoming very faint. I have also 
 found . acceleration of the heart's rate — in one case very considerable, — 
 and occasionally the occurrence of an extra-systole, followed sometimes by 
 a characteristic pulsus alternans. In a few cases irregularities have occurred 
 whose nature I have not been able to determine satisfactorily, but in the 
 vast majority of cases I could detect no change in the heart or arteries, 
 and there never was the slightest enlargement of the heart coming on during 
 the attack. 
 
 § 55. Symptoms after an attack — The patient feels greatly exhausted 
 after the attack has passed off. Sometimes the pain does not completely 
 disappear, and an uneasy painful sensation may last. The end of an attack 
 may coincide with the expulsion of air from the stomach, and as this is 
 usually accompanied by a sense of relief, the attacks are often supposed to 
 be of gastric origin. I have watched these patients, and have no doubt that 
 the air has been sucked into the stomach during the attack. This air suction 
 is seen most characteristically in nervous people, especially women, and is 
 referred to more fully in § 64. Some patients have a desire to micturate, 
 and the urine secreted is always abundant, pale, and of low specific gravity. 
 In some patients areas of hyperalgesia of the skin appear in some portion 
 of the field in which the pain is felt. In the first attacks it may be limited 
 to a small patch, as in Fig. 11, but with recurring attacks the area may spread 
 wherever the pain is felt, as in Fig. 12. 
 
 § 56. Establishment of a tendency to recurrence of the attacks. — 
 I have already described how an irritable focus may be produced in the cord 
 after a violent stimulation from a visceral lesion (shaded area in Fig. 8, p. 36). 
 This may be manifested by an area of hyperalgesia in some part of the 
 body, and in those that exhibit this hj^peralgesia attacks of angina pectoris 
 come on with very little provocation. Even when there is no distinct 
 evidence of hyperalgesia, the stimulation of the skin or the movements of 
 the muscles of the arm may induce an attack. I have on several occasions 
 inadvertently brought on an attack while testing the sensibility of the skin 
 and deeper tissues over the praecordium. Visiting a patient one day, who 
 suffered from violent attacks, I found him feeding himself entirely with 
 his right hand. When I asked him why he did not use his left, he said he 
 was afraid to do so, as sometimes the movement of the left arm induced 
 an attack. He died a few hours after, during an attack. 
 
 § 57. Prognosis The tragic circumstances~surrounding certain cases
 
 ANGINA PECTORIS 
 
 51 
 
 of angina pectoris have so oppressed the profession and the laity that an 
 altogether exaggerated opinion has been formed of the gravity of this com- 
 plaint. If it be realized that angina pectoris is but the expression of an 
 exhausted muscle, and that the exhaustion may arise from any cause that 
 
 Fig. 11. The shaded area shows 
 the position of a patch of cutaneous 
 hyperalgesia after the first attack of 
 angina pectoris. 
 
 Fig. 12. The shaded area shows the dis- 
 tribution of the pain and cutaneous h3rper- 
 algesia after repeated attacks of angina 
 pectoris. From the same patient as Fig. 11 
 (compare the shaded area with the distribution 
 of the eruption in Fig. 10). The roman 
 numbers refer to the nerves implicated, viz. i, 
 II, and III — the first, second, and third dorsal 
 nerves, and viii, the eighth cervical nerve. 
 
 overtaxes the heart, a truer appreciation of the meaning of the symptoms 
 will be obtained. The estimation of the gravity of the cases does not depend 
 upon the violence of the symptoms. A severe attack is not necessarily 
 serious, nor is the mildest free from danger. The importance of the symp- 
 toms must be estimated by an examination of the conditions that have 
 induced the muscular exhaustion. This is, as a rule, not a matter of 
 
 E 2
 
 52 DISEASES OF THE HEART 
 
 much difficulty, if one carefully searches for a predisposing cause. The 
 age of the patient, the conditions of his or her Ufe, work, worry, nourish- 
 ment, over-indulgence in tobacco, and, in the case of women, the number 
 of children she has borne, her menstrual functions, all lead to the 
 recognition of the nature of the muscular exhaustion. If the probabilities 
 point to the absence of progressive arterial degeneration and degeneration 
 of the heart muscle, the patient may on the whole be assumed to have 
 a favourable future. If one has reason to suspect that the symptoms have 
 appeared in the early days of cardio-sclerosis, when the patient, ignoring 
 the limitation of his powers, follows the manner of his life pursued in 
 vigorous manhood, then the probabilities are that, with rest and care, the 
 heart wiU recover from its exhaustion, and be able to carry on its work 
 for many years in comfort. Where the prognosis is most serious is when it 
 occurs with marked evidence of general arterial degeneration, and where 
 there is little response to treatment, and where the attacks are induced 
 with slight provocation. These are the circumstances that would lead 
 one to look gravely upon this condition. But even when cases are so severe 
 that for months a patient may scarcely be able to walk across the floor 
 without inducing an attack, rest for a long period may restore the heart and 
 induce a cessation of the symptoms ; otherwise the condition arrived at is 
 practically beyond the possibility of recovery. 
 
 § 58. Treatment. — Treatment naturally divides itself into two heads, 
 namely, the improvement of the condition of the heart, and the giving of 
 relief during an attack. 
 
 Improvement of the condition of the heart. — For the first of these it 
 must be borne in mind that the attack is the expression of an exhausted 
 muscle, and the treatment requires a careful inquiry into the conditions 
 inducing that exhaustion. First and foremost, a stop must be put to 
 that form of exertion which has induced the attack, and any other 
 conditions that predispose to it must be avoided, such as work, worry, 
 sleeplessness, over-indulgence in food and alcohol, tobacco, and so forth. 
 The next step is to place the heart in such a position that it will regain 
 its reserve force, that is, the heart must be given less to do. This does 
 not necessarily mean that the patient should rest in bed, but he should 
 restrict his movements as much as possible. Here the habits and condition 
 of the patient will have to be considered, and each individual separately 
 treated. To stop an individual altogether from his work and engagements 
 may be most serious. It is best, as a rule, to permit him to follow some 
 particular kind of work that does not put a strain upon his heart. When 
 feasible, a complete change of habits and life, as free from over-exertion as
 
 ANGINA PECTORIS 53 
 
 possible, is most beneficial, such as a good holiday spent in the manner that 
 affords the maximum of enjoyment and requires the minimum of effort. 
 In the cases that do not yield to such limited restriction, and when the attacks 
 are demonstrably^ the outcome of an advanced exhaustion of the heart, 
 then absolute rest in bed is necessary. In other conditions the treatment 
 should follow the lines that I have laid down in the chapters upon treat- 
 ment. Of remedies and methods supposed to cure, the name is legion. 
 Happily in their prescription the above suggestions are also included, and the 
 benefit so accruing is too often attributed to the remedy or method. I have 
 in several individual patients tried various so-called remedies, and I find 
 on the whole, that if the patient is not worried, has plenty of sleep, and 
 leads a fairly restful life, he does as well without any special drug treatment 
 as he did with it. 
 
 As many patients of a neurotic type suffer from angina pectoris the mental 
 factor should always be considered. The term angina pectoris conveys to 
 their minds such fearful associations, that they readily become depressed 
 and miserable. A careful study of each case will show that in the majority 
 the attack is the outcome of a temporarily exhausted muscle and the patient 
 can have his mind relieved by the assurance that the prognosis is a good 
 one. In the after-treatment of such cases careful management is needed, 
 in order that they should not always be reminded of their complaint. Hence 
 systems of dieting, where the patient at each meal has to reflect if the 
 ingredients are injurious to his heart, should be rigidly avoided. Most 
 dietetic systems are the outcome of a fad, and based on an imperfect know- 
 ledge of digestive and metabolic processes, as in the exclusion of common salt 
 and lime salts from the meals. For the same reason ' health resorts ' where 
 people congregate and discuss their ailments should be avoided. 
 
 Treatment durmg an attack. — The slighter attacks require no treat- 
 ment. When they become more severe, rapidly acting vasodilators should 
 be administered, such as hot drinks, hot water with whisky or brandy, and, 
 best of all and most speedy, amylnitrite by inhalation. This drug is not 
 successful in all cases, but in many its action is rapid, and the relief is 
 generally complete. When it is successful, it has been inferred that the 
 patient had previously constricted arterioles, or increased arterial pressure, 
 and that the pressure was reduced, and so the heart was eased. This is 
 not the full explanation. A patient with cardio-sclerosis had an attack of 
 angina pectoris in my consulting-room. I took his blood-pressure, and 
 found it 190 mm. Hg., and then administered to him nitrite of amyl : it 
 acted instantaneously, and gave him perfect relief. After fifteen minutes 
 I again took his blood-pressure, and found that it had risen to 200 mm. Hg.
 
 54 DISEASES OF THE HEART 
 
 Though the pressure was higher, he had no pain. I inferred that the action 
 was similar to that of a man who puts on a hat that is too tight ; at first 
 there is no pain, but gradually, by the summation of stimuli, discomfort 
 comes on and increases in intensity ; he removes the hat from his head, 
 and obtains relief. He replaces the hat in the same position, and, although 
 it is as tight as before, the pain has permanently disappeared : so that the 
 temporary removal of the summating stimuli seems to be the reason for 
 the relief afforded in the particular case mentioned. 
 
 When nitrite of amyl fails to relieve the patient, we are forced to use 
 chloral or morphia in doses sufficient to give relief. I have found occasionally 
 that chloral acts beneficially not only in relieving the somewhat long attacks, 
 but in preventing the attacks recurring, when given in repeated small doses 
 of 3-5 grains and also when given at night to induce sound sleep. 
 
 In advanced cases where the suffering comes on mainly at night, it is 
 occasionally very difficult to give the patient relief. Massive doses of oxygen 
 have in some cases, as in cardiac asthma, been followed by marked benefit, 
 and should be tried (see p. 279).
 
 CHAPTER VIII 
 
 Heart Affections and a Hypersensitive Nervous System 
 
 § 59. Reaction of visceral disease on the central nervous system. 
 
 60. Pseudo-angina pectoris, a useless and misleading term. 
 
 61. Exaggerated sensory phenomena with and without valvular disease. 
 
 62. Exaggerated sensory phenomena in early cardio-sclerosis. 
 
 63. Characteristics of the sensory phenomena. 
 
 64. Air suction. 
 
 65. The circulatory symptoms in the X disease. 
 
 66. Vaso-motor angina pectoris. 
 
 67. Prognosis. 
 
 68. Treatment. 
 
 It not infrequently happens that the most common forms of disease 
 are the most difficult to describe. I attempt here the analysis and explana- 
 tion of the symptoms present in certain cases which are frequently met in 
 actual practice. As the symptoms present great variety in number and 
 intensity, numerous attempts have been made to divide them into groups, 
 and we find them under various guises, as neurotic hearts, cardiac neuroses, 
 cardiac neurasthenia, pseudo-angina pectoris. I have endeavoured to 
 find the underlying principles which provoke these manifold symptoms, 
 as their due appreciation is of prime importance in the management of 
 these cases. 
 
 § 59. Reaction of visceral disease on the central nervous system. — 
 In describing the symptoms of angina pectoris (Chapters VI and VII), I 
 have endeavoured to show that the symptoms arise from a reflex stimulation 
 of the central nervous system. But the heart and the nervous system can 
 react upon one another in other ways than by reflex stimulation. In heart 
 affections, as in affections of all other viscera, there is a tendency for the 
 central nervous system to become hypersensitive (I use this word for want 
 of a better) whereby symptoms of nervous origin are readily evoked. This 
 applies more particularly to the production of sensory phenomena, where 
 a comparatively small visceral lesion gives rise to an irritable focus in the 
 spinal cord, and to extensive suffering and widespread areas of hyperalgesia, 
 or to certain mental states where the patients sometimes become ' nervous ' 
 and apprehensive. The result of the association of heart affections with
 
 56 DISEASES OF THE HEART 
 
 these latter, may be summed up in the expression that the cardiopath 
 tends to become a neuropath. 
 
 This mental state is seen very characteristically in both men and women. 
 If they have been told that they have a murmur, or an irregular heart, 
 or if they are conscious of an extra-systole, or suffer actual distress of 
 a cardiac origin, they become extremely apprehensive. The hyperalgesia, 
 so common in the breasts of women suffering from some slight heart trouble, 
 is a constant source of worry, and some are continually imagining that 
 the abnormal soreness is an indication of serious disease. This apprehension 
 is unfortunately too often aggravated by the warnings of the physician, 
 who estimates the significance of the symptoms too seriously, or will neither 
 admit nor deny the gravity of the condition. 
 
 The combination of cardiac and nervous exhaustion may be brought 
 about in another way. People with a tendency to ' nervous debility ', or 
 who have acquired it from some other cause, may develop some cardiac 
 trouble, functional or organic. In such people, the reflex symptoms are 
 greatly exaggerated. Thus one of my patients with aortic and mitral 
 disease experienced no sensory phenomena until she developed a gastric 
 ulcer. This gave rise to great pain, and to a widespread area of hyper- 
 algesia of the skin and muscles in the left side of the abdomen. Soon after 
 this she began to suffer from pain from the heart affection, and the hyper- 
 algesia finally embraced nearly the whole of the left chest. The patient 
 lived for many years after the appearance of these symptoms, and a pyloric 
 ulcer and aortic and mitral valve disease were found on post-mortem 
 examination. 
 
 In all these cases we must exercise a great deal of judgement. It 
 frequently happens that in patients with a demonstrable cardiac lesion, 
 the symptoms are estimated too seriously, and the case looked upon with 
 greater gravity than need be. On the other hand, if there be no murmur 
 or irregularity, the case is liable to be treated Ughtly as one of ' pseudo- 
 angina pectoris ' or neurasthenia. 
 
 § 60. Pseudo-angina pectoris, a useless and misleading term. — 
 It is time the term ' pseudo-angina pectoris ' was dropped out of medical 
 literature. While it may be convenient to group under indefinite terms 
 many conditions of whose nature we are ignorant, it should be borne in mind 
 that this grouping is but provisional, and a confession of our ignorance 
 of the real nature of the complaint. With advance in our knowledge, first 
 one complaint and then another should be placed in a group whose cause 
 is definite and known. In this way many cardiac terms, such as tachy- 
 cardia, cmbryocardia, bradycardia, have been employed loosely, and noAv
 
 HYPERSENSITIVE NERVOUS SYSTEM 57 
 
 should never be employed unless a definition be given of what is 
 meant. 
 
 The term ' angina pectoris ' is employed to designate a group of sjnoaptoms 
 evoked by the heart, of which pain is the most distinctive. As angina pec- 
 toris is sometimes associated with grave organic lesions, we find such cases 
 referred to as ' angina pectoris vera '. The term ' pseudo-angina pectoris ' 
 is applied to cases in which the pain resembles that of angina pectoris vera, 
 but is due to some other cause than heart disease, or in Avhich the pain arises 
 from the heart with no organic lesion. In regard to the former class, if the 
 pain is due to some other viscus, e.g. the stomach, as sometimes happens, 
 why call it ' pseudo-angina pectoris ' ? If it is due to the stomach, why not 
 say so ? In regard to the latter class, the employment of this term is due 
 to a total misconception of the nature and mechanism of visceral pain. 
 The fundamental cause of the pain is the same in the case of the heart as 
 in that of any other viscus, and the pain is as readily induced in the heart 
 as in the stomach. As we would never dream of calhng a stomach pain 
 a ' pseudo-gastralgia ', so we need not call a heart pain ' pseudo-angina '. 
 
 I deal with the matter at length, as the employment of a fine-sounding 
 term has too often sufficed for a diagnosis, so that no inquiry into the real 
 nature of these symptoms has been undertaken. In the great majority of 
 cases when a patient complains of a pain in his chest which radiates into his 
 arm, in the area shaded in Fig. 12 (p. 51), the pain is of cardiac origin. The 
 only other conditions in which I have found pain to occupy this characteristic 
 site, was in herpes zoster affecting the upper dorsal nerves and certain 
 rare forms of gastric spasm. In one case, I thought I had to deal with 
 a case of angina pectoris until the herpetic eruption revealed the true nature 
 of the complaint. It is quite conceivable that other conditions may give 
 rise to pain having this distribution, but that is no reason for calling them 
 pseudo-angina pectoris. 
 
 The characteristic distribution of the pain and other sensory phenomena 
 at once excludes hysteria, for in the latter the symptoms do not follow the 
 anatomical distribution of nerves. When a hysterical patient feels a pain 
 in this region, it may be assumed that there is probably some cardiac trouble 
 in addition to the hysteria. 
 
 § 6i. Exaggerated sensory phenomena with and without valvular 
 disease — A great many people with a demonstrable cardiac lesion, as of 
 the aortic or mitral valves, develop sensory phenomena in an exaggerated 
 form. This is particularly seen in some women in whom the reserve force 
 is exhausted. Such folks may struggle on for a long time, working hard 
 and ignoring their earlier symptoms of a limitation of the field of cardiac
 
 58 DISEASES OF THE HEART 
 
 response, determined not to give in. Finally the nervous system shares in 
 the exhaustion, and the breakdown is brought about with an extreme 
 development of the sensory phenomena ; thus attacks of pain, sometimes 
 of great severity, may be felt across the chest and extending into the left 
 arm, or more often the complaint may be of a dull aching pain of varying 
 severity, but distinctly worse at the end of a day's work. The hyperalgesia 
 may spread over a very extensive area, and sometimes is extremely acute. 
 
 On account of the manifest lesion in the heart these cases are not un- 
 frequently diagnosed as cases of angina pectoris of a severe and dangerous 
 form, and I have known them lead a life of great restriction for many years 
 under this mistaken notion. The attacks are indeed those of angina pectoris, 
 but are not dangerous, and are an evidence of exhausted heart muscle, 
 and disappear with the restoration of the reserve force. 
 
 On the other hand, we have mothers of families with no heart murmurs, 
 who for many years have worked hard from morning till night, whose sleep 
 has been disturbed by ailing or fretful children, and who finally break 
 down with exhausted heart and nervous system. Some of my most typical 
 cases have been in young women whose sleep has been disturbed frequently 
 every night for many years to attend to an ailing parent. This constant 
 strain night and day exhausts the strength. These patients suffer from 
 heart pain, sometimes with the classical symptoms of angina pectoris 
 described in Chapter VII. 
 
 With suitable management they eventually recover, though recovery 
 is usually very protracted, the patients sometimes having to lead very quiet 
 lives for months or even years. Similar symptoms may arise in others 
 who have been exposed to worry and anxiety, or who have suffered from 
 sleeplessness, while others may suffer when there is no apparent reason for 
 the exhaustion. 
 
 § 62. Exaggerated sensory phenomena in early cardio-sclerosis. — 
 The possibility that in these cases there may be beginning cardio-sclerosis, 
 should be kept in mind, especially in cases over 40 years of age. There is 
 nothing to tell whether it is so or not, for the superficial arteries may be quite 
 normal in appearance, and the blood-pressure give no sure information. This 
 needs to be specially insisted on when these exaggerated phenomena appear 
 in women between 50 and 60. I have seen a number of patients develop 
 all the sensory phenomena in an extremely exaggerated form, becoming 
 weaker until they were unable to leave their beds ; some have become 
 unconscious, and died ; others regained consciousness, and after a time 
 sufficient strength to go about for years. After their recovery I have been 
 surprised to find an aortic systolic murmur, which had not been present
 
 HYPERSENSITIVE NERVOUS SYSTEM 59 
 
 prior to the breakdown. Some of these have remained liable to attacks 
 of angina ; one dropped down dead, and in another, who died from sub- 
 sequent heart failure, there was marked sclerosis of the heart muscle, 
 coronary arteries, aortic valves, and aorta. The diagnosis in these cases 
 depends on the response to treatment (§ 57). 
 
 § 6^. Characteristics of the sensory phenomena. — There are some 
 special points in these cases that distinguish them from those who do not 
 have the same susceptible nervous system. The suffering may not be as 
 severe as in the more grave forms of angina pectoris, but it is more lasting 
 and comes on after periods of continuous exertion. Sometimes it is limited 
 to the left arm, if that arm has been much employed in work, as in washing 
 or baking. It is frequently associated with extreme tenderness on pressure 
 of the tissues of the left chest and neck, especially the left breast, the pecto- 
 ralis major and sterno-mastoid muscles. After testing the tender skin and 
 muscles by slightly pinching the skin and muscles between the fingers and 
 thumb, the part becomes extremely sore, and the aching lasts for hours 
 afterwards. When the patient is suffering from severe pain, the mouth may 
 become dry and parched, and large quantities of pale urine may be passed, 
 as happens in cases where the angina pectoris is of very grave significance. 
 
 § 64. Air suction — Another symptom is extremely common in these 
 cases — the belching of air. One searches textbooks in vain for any hint 
 as to the nature of this symptom, and though it is extremely common in 
 all neurotic people, its significance is almost invariably misunderstood. 
 A detailed and satisfactory account is given by Wyllie,**^ and it is to this 
 article I owe enlightenment as to the meaning of this symptom. 
 
 The chief feature is the noisy expulsion of air from the stomach. Patients 
 complain of attacks of flatulence, and in these attacks seemingly expel 
 large quantities of air, but if closely watched they will be seen first to suck 
 air into their stomachs. Before expelling the air, they unconsciously close 
 the glottis, fix the muscles of the abdominal wall, then expand the chest. 
 As no air goes into the lungs, and the diaphragm is raised, the pressure in 
 the stomach becomes negative. By this process they suck air into the 
 stomach. After sucking in a quantity, they expel it with considerable 
 force, and often with a good deal of noise. Many people can do this at 
 will, others only in certain states of excitement. Some have ' attacks of 
 flatulence ' in the middle of the night, and such attacks are due to air 
 swallowing, or more correctly air suction. As Wyllie points out, these 
 attacks can be stopped by making the patient open his mouth widely, and 
 keeping the jaw propped open by a large cork between the teeth, a procedure 
 which prevents the air suction.
 
 60 DISEASES OF THE HEART 
 
 I have watched several patients during an attack of angina pectoris, 
 and when they stand seemingly immobile, they unconsciously suck air into 
 the stomach. Immediately the pain subsides the air is expelled, and the 
 patient is apt to attribute the relief he has experienced to the coincident 
 and demonstrable act. This very obvious phenomenon has led many 
 observers to imagine that the attack was gastric in origin, and hence the 
 group of gastric ' pseudo-anginas '. 
 
 This association of air suction with attacks of angina pectoris, which 
 is sometimes found in men, is extremely common in women. As air suction 
 is frequent in women, it is sometimes mistaken for a hysterical symptom, 
 and its relationship to a real heart attack is apt to be overlooked. As 
 a matter of fact, attacks of air suction are apt to arise from any exciting 
 cause, and attacks of angina pectoris readily induce them. In some it 
 occurs so readily that it may come on before the real suffering. Thus, one 
 lady who suffered from extreme arterial degeneration, had severe attacks of 
 angina pectoris, which disappeared after a long period of rest in bed. 
 When she got about again, she could walk on the level with comfort, but 
 the slightest hiU brought on discomfort, which if not heeded resulted in great 
 pain in the chest. As a rule, however, before the pain became severe she 
 began to suck in and to expel air. She would rest a minute and start again, 
 but soon had to stop, and expel ' more wind ' as she put it. 
 
 § 65. The circulatory symptoms in the X disease.* — There is another 
 class of cases of somewhat indefinite character, that needs to be recognized 
 in order to appreciate other forms of heart trouble. The class I allude to 
 will be recognized by every practitioner as they form a considerable portion 
 of the community. The individual is spare and thin ; the face is often 
 drawn and lined, sometimes even in the young. It is usually pale, though 
 in some the face is ruddy, and the nose is red in cold weather. The hands 
 are usually cold, and they teU you their circulation is feeble. They are 
 always worse on raw cold days, and feel chilly and ill after a cold bath. 
 Their complaints are extremely varied, and many have a fixed idea that 
 certain organs are at fault, and it is true that some trouble, usually slight, 
 may be found in some organ. Thus we find gastric and bowel complaints 
 extremely common, though other viscera may also be at fault and com- 
 
 * I employ the term ' X disease ' for the reason that I do not know the nature of this com- 
 plaint. Many physicians call members of this class ' neurasthenics ', and are content to leave 
 the matter there. This is simply to give a complaint a name, which is so satisfying that the 
 fact is often lost sight of that the name sheds no light upon the complaint and is nothing but 
 a cloak for ignorance. If the term ' X disease ' be employed it will be a glaring acknowledgement 
 of our ignorance, and will lead to a constant endeavour to clear up the mystery surrounding 
 these cases.
 
 HYPERSENSITIVE NERVOUS SYSTEM 61 
 
 plained of. The patient's mental condition is curious and interesting. 
 Some of them are sane, level-headed, and extremely intelligent. To these 
 the bodily suffering is nothing more than a grievous and troublesome 
 affliction. In others it leads to irritability and peevishness in temper. 
 Some become introspective, and are deeply concerned about their bodily 
 or spiritual affairs. It alters their views of material things ; cranks and 
 faddists, political, religious, and dietetic, are common among them, often 
 exhibiting strenuous enthusiasm for their particular ideas. Another aston- 
 ishing feature in these cases is the remarkable way in which a temporary 
 recovery may take place. For weeks some of these folks may go about 
 miserable and ill, taking little food, finding that little too much for the 
 digestion, and searching for some kind that will suit them — when suddenly 
 they feel better. Their recovery may last for weeks or even months, but 
 they generally relapse. 
 
 Now this peculiarity leads to another characteristic of this complaint — 
 unbounded and unreasoning belief in what they, take to be the cause of 
 their recovery, diet, drug, methods c^ exercise, operation. It is because 
 of this tendency to recover that there are so many cures. If one reads 
 between the lines of the testimonials in favour of certain remedies, empiric 
 or recognized by authority, we can see that it is this class of case that is 
 being treated. It is especially among them that faith-cures abound, and 
 these are the people who swell the ranks of Christian Scientists. Emotional 
 excitement, whether of love or religion, always relieves this kind of person, 
 and so when religion comes into play we get the various forms of faith- 
 healing. Many women feel extremely well when pregnant. 
 
 The diagnoses of medical men are as numerous and varied as the com-/ 
 'plaints of the patient. The gynaecologist diagnoses some pelvic disorder ;/ 
 jthe surgeon sees the source of all the trouble in an appendix, a dilated 
 stomach, or a wandering kidney ; while the physician recognizes the disease 
 according to the bent of his studies — a heart affection, visceral stasis, gastro- 
 ptosis, neurasthenia, atonic dyspepsia, and so forth. So minute indeed 
 ! are some of the diagnoses, that we find them classified further as cardiac, 
 gastric, mental, or renal neurasthenias. 
 
 I enter into the description of this class of case somewhat fully because 
 many of them masquerade as cases of heart disease. I have for some years 
 been inquiring into the nature of the symptoms in these cases, and here detail 
 some of the cardio- vascular phenomena, as the lack of the recognition of 
 the nature of these symptoms often leads to a mistaken diagnosis. 
 
 The most outstanding feature is cold hands, and this is sometimes asso- 
 ciated with a peculiar roughness and thickness of the skin. The fingers may
 
 62 DISEASES OF THE HEART 
 
 become white and numb ; ' dead ' is the term often appHed. Exposure 
 on a very cold day may cause the condition to be so extreme that pain in 
 the finger ends is very severe, and in one case I have seen a shght gangrene 
 follow. The nose is often red, and the association between dyspepsia and 
 the red nose is extremely common in these folks. There is very often dilata- 
 tion of the stomach, associated with accumulation of blood in the abdomina 
 veins. This latter can be demonstrated in several interesting ways. If the 
 patient be laid on his back, and very gentle pressure be steadily appUed with 
 the hands placed on the upper part of the abdomen, so as not to interfere 
 with the respiration, the veins of the neck will gradually be seen to swell 
 and the pulsation in them becomes greatly increased. In some cases this may 
 be seen to occur during quiet respiration, the swelling of the vein occurring 
 during inspiration. The cause of the swelling in this condition is that 
 pressure on the abdomen empties the abdominal veins into the right heart, so 
 that there is less accommodation for the blood returning by the superior 
 vena cava ; hence the jugular vein distends. Inspiration causing a descent 
 of the diaphragm compresses the abdominal contents, including the large 
 veins, against the unjdelding waU, and brings about the same result. 
 G. Oliver says that by putting a bag of shot (14 lb.) on the abdomen in 
 these cases he can raise the pressure in the arterial system. 
 
 The heart itself in these cases is sometimes sUghtly dilated, and there 
 may be mitral and tricuspid systolic murmurs. They are very evanescent, 
 present at one minute and gone the next. Sometimes we can detect them 
 at the beginning of an examination, and in a few minutes they have dis- 
 appeared. The rate and rhythm of the heart often varies. Sometimes 
 it is rather slow, and sometimes it is irregular, the irregularity usually 
 being respiratory, though occasionally extra-systoles are present, and then 
 the patient if conscious of them is often greatly frightened, particularly 
 if the doctor does not convincingly reassure him. Hesitation or doubt on 
 the part of the doctor hangs like a cloud over the patient. 
 
 I have been particularly struck with the slow respiration in a number of 
 these cases. It may faU as low as seven per minute (Fig. 77, Plate II), and the 
 patient be free from any distress, and quite unconscious that anything is 
 wrong. It is then that the heart rhythm is most affected, and the swelling 
 of the vein during inspiration and from pressure on the abdomen occurs 
 most characteristically. The nature of this irregularity is fully described 
 in Chapter XVIII. A healthy individual can sometimes produce this 
 irregularity by simply breathing slowly and deeply at the rate of seven or 
 eight per minute. 
 
 § 66. Vaso-motor angina pectoris — For many years I was at a loss
 
 HYPERSENSITIVE NERVOUS SYSTEM 63 
 
 to understand the cases described by Nothnagel ^^ as vaso-motor angina 
 pectoris. The term is such a fine-sounding one that it soon found its way 
 into current literature, but I could never find it employed in the sense 
 in which Nothnagel used it, nor did the cases recorded by others correspond 
 with those given by him. I have come across several patients who suffered 
 from angina pectoris, and a careful scrutiny of their symptoms leads me 
 to think that these are the kind of patient described by Nothnagel. They 
 are particularly liable to cold and chilly attacks. Occasionally the attacks 
 of chilliness persist, and, if the patients have no opportunity to warm 
 themselves, increase in intensity, until after an hour or two of misery they 
 culminate in attacks of pain in the chest, radiating into the arm. The 
 pain in severe cases persists with varying intensity until the patient gets 
 thoroughly warmed. 
 
 I deal particularly with this subject because the term ' vaso-motor angina 
 pectoris ' conveys to many minds some definite idea of what happens in these 
 cases, and though I can formulate no explanation that would, to my mind, 
 satisfactorily explain the matter, I may point out that in these cases, the 
 blood-pressure is not increased as one would expect, if the explanation were 
 merely that the heart is acting against increased peripheral resistance. 
 Although I have not taken the blood-pressure during a severe attack of pain, 
 I have taken it in a number of cases when the extremities were cold and 
 chilly and the patient suffering considerable distress, and the pressure has 
 invariably been low — about 120-130 mm. Hg. 
 
 § 67. Prognosis in cases with exaggerated sensory symptoms If 
 
 care be taken to differentiate between the patients who exhibit exaggerated 
 nervous phenomena due to progressive organic lesions, and those due to 
 exhaustion apart from a progressive lesion, the prognosis can be made with 
 fair certainty. Recovery almost invariably results in the latter class, 
 though it may be delayed for a long time. Naturally, the compHcation 
 producing the nerve exhaustion must be taken into account, and if due to 
 other visceral affections, the prognosis depends also upon their nature. 
 
 When there is an organic lesion, as cardio-sclerosis, or valvular disease, 
 on the whole the exaggerated nervous phenomena do not add to the 
 gravity, but, it has even seemed to me, act favourably in many cases, 
 for the early exhaustion is attended by such an amount of suffering, that the 
 heart is protected from more extensive exhaustion of its reserve force. 
 
 In the cases included in the groups of X disease, even when angina 
 pectoris is present, I have never found the heart trouble give rise to a 
 serious breakdown, nor have I ever found death from heart failure in this 
 type of patient. In fact, they are among the long-lived, for they usually
 
 64 DISEASES OF THE HEART 
 
 take such care of themselves that they avoid all risks and exposure to 
 danger. 
 
 § 68. Treatment. — It is of the first importance that we should appre- 
 ciate the nature of the trouble in these cases, and bear in mind the part played 
 by the nervous system. The nervous element is often the chief one to 
 be considered, and the sufferings of many of these patients are aggravated 
 by the consciousness or dread of some serious affection of the heart. Having 
 satisfied ourselves as to the real nature of the trouble, we should first of aU 
 reassure the patient. In a great many cases success in treatment depends 
 on this, and we can often see patients at once made well, or greatly improved, 
 when they become fully reassured. This is more particularly the case when 
 the patient has previously been alarmed by being told that the condition 
 was serious. The peculiar mental factor that makes this class of patient 
 the stay and support of many forms of empirical or semi-empirical treatment, 
 should be kept in mind. As suggestion plays an important part in the 
 numerous special methods of cure, it should be used inteUigently by medical 
 men, and in a legitimate manner, that is to say, the patient should be 
 reassured from the standpoint of a full knowledge of his condition. 
 
 There is a great tendency for the physician to attach too high an im- 
 portance to a case with exaggerated nervous symptoms, where there is an 
 organic lesion of the valves. I have seen many patients lead fives of great 
 restriction, with a certain amount of fear, on account of the supposed serious- 
 ness of heart trouble. Women have had attacks of angina pectoris, and 
 have been forbidden to undertake their household duties. Great numbers 
 have gone to health resorts at great expense and inconvenience year after 
 year, to perform the ' cure ', because in their days of suffering they had 
 experienced benefit. When there is a valvular murmur, we must carefully 
 inquire into the conditions that have induced the heart exhaustion and the 
 attendant suffering, and consideration of the whole of the facts wiU enable 
 us with certainty to recognize the real nature of the phenomena. We 
 can often with certainty reassure the patient that with suitable treatment 
 the suffering will, to a great extent, disappear, and that though the organic 
 trouble may persist, with intelligent management there is good ground 
 for hope of a fair restoration to health. In many cases one is able to do more, 
 to point out that the suffering is a safeguard, its first appearance being an 
 evidence that the patient is exhausting the reserve force of the heart, and 
 that such restrictions are necessary to guard against further exhaustion. 
 
 This inteUigent appreciation of symptoms is of service in other ways. 
 Thus, when patients become conscious of an extra-systole, they are often 
 subjected to long courses of treatment, usually inefficient, by their medical
 
 HYPERSENSITIVE NERVOUS SYSTEM 65 
 
 attendant, or by some special method. The mere reassurance of the harm- 
 lessness of the symptoms would have done more good than all the treatment. 
 As an illustration I cite the following experience. A professional football- 
 player consulted me because his heart ' stopped ' at times. He had been 
 seen by two doctors, who forbade him to play, and put him on digitalis and 
 strychnine. This cessation of work was a serious matter to him, because 
 if he could not complete his engagement for the season he lost the chance 
 of a benefit match, which he looked upon as a reward at the end of his services 
 as a footballer. Except that he was frightened and nervous I found him 
 in all respects a healthy man, save for a somewhat frequent extra-systole. 
 I told him he could start playing at once, and that when he was conscious 
 of his heart stopping he was to pay no attention to it. He at once resumed 
 his engagements and completed his term with no discomfort. He told me 
 that at the beginning of one match he was painfully conscious of his heart's 
 irregularity, and felt he must retire, but reflected upon what I had told him, 
 dashed into the game, and in a few minutes forgot aU about his trouble, and 
 said he never played better in his life. 
 
 I use this illustration to emphasize the fact that neither the exaggerated 
 sensory and mental sensations, nor the symptoms giving rise to them, should 
 be the guide, but what effort the heart can undertake without discomfort. 
 
 Besides reassuring the patient, steps should be made to remove him or 
 her from any conditions that conduce to the exhaustion, such as over- 
 work, worry, nursing a sick relative. Discretion must be used, and the 
 patient's circumstances considered. When the patients are well-to-do, a 
 complete change in the mode of life is often very efficacious, and they may 
 be sent away, the choice of the place depending on the patient's tastes. If 
 they can undergo some physical effort, a holiday may be recommended that 
 includes some exertion, such as hill-climbing, cycling, golfing, or ' sight- 
 seeing ' — town or country — ^provided the occupation interests the patient. 
 They may be sent to some watering-place, and may indulge in the 
 special treatment adopted there — for the sake of doing something, and 
 getting what benefit hydrotherapy may convey. My patients have gone 
 to all sorts of places, and those who went to the seaside and indulged in 
 sea-bathing got more benefit than those who frequented the more vaunted 
 inland spas, home or continental. The fife there is more bracing, and there 
 is less opportunity to meet all sorts of neurotics, and the baneful habit of 
 comparing experiences is thus not so easy to indulge in. 
 
 The vast majority of patients cannot go away and leave their posts, and 
 these form the class with which the general practitioner has often a great 
 deal of trouble. With patience and perseverance, however, much can be 
 
 MACKEXZIE -ci
 
 66 DISEASES OF THE HEART 
 
 done for them, and in many instances the doctor can give great help to some 
 of the most deserving patients he has to treat. The mother of a family has 
 to keep going, the tired daughter has to nurse the aiUng parent. In all 
 these cases there will be found, almost invariably, insufficient sleep, or sleep 
 frequently disturbed, and this is often the real cause of the trouble and 
 in addition renders the patient peevish and irritable. Much can be done 
 by suggesting different devices to promote the patient's rest. In many cases 
 we have to resort to drugs, and happily the most efficacious hypnotic in 
 these cases is also the safest, namely, bromides (particularly bromide of 
 ammonium), which should be given until the patient sleeps soundly. Often 
 they produce drowsiness and languor during the day, and the patient may 
 complain of being weaker than ever. This is no contra-indication, but the 
 contrary, for the languor induces idleness and restfulness. She does less 
 work, she is less irritable, and the heart is not so easily excited. After a 
 few weeks, if the dose be gradually diminished, it will often be found that 
 in the meantime the patient's condition has wonderfully improved. The 
 necessity of continuing her duties prevents the possibility of any immediate 
 recovery, but by the judicious administration of the bromides, patients 
 can be tided over trying periods for months or years. 
 
 ' Heart tonics ' in these cases are of little use. Even if they had the action 
 they are supposed to possess, it is doubtful if their administration would be 
 wise. It is not a whip an overworked horse needs, but rest. 
 
 The nourishment of the patient often leaves much to be desired. The 
 household duties and the cooking take away the appetite, and they content 
 themselves with stuff easily swaUowed and stimulating — hot fluids, tea, 
 coffee, and spirits. The food should be taken in small quantities and often, 
 and should be fairly dry to ensure slow mastication. It is sometimes a good 
 plan to suggest a dietary of a very simple nature. Find out what food the 
 patient prefers, and, if it is rational, so arrange the diet that every few hours 
 may bring a change, even if it be but an egg at one time, and a dry biscuit 
 and a few tablespoonfuls of milk at another. In all cases stimulants should 
 be forbidden. The great exhaustion brought about by the long weary hours 
 of work and suffering is often speedily temporarily relieved by spirits ; but 
 these are just the people who ultimately find solace in increasing quantities, 
 until the habit becomes all too powerful.
 
 CHAPTER IX 
 
 INSTRU3IENTAL METHODS OF EXAMINATION 
 
 § 69. The sphygmograph. 
 
 70. The polygraph. 
 
 71. The clmical polygraph. 
 
 72. The ink polygraph. 
 
 In the examination of the vast majority of patients, the diagnosis can 
 be made independently of graphic records. It must not be inferred from 
 this that graphic records can be dispensed Avith, for the power to diagnose 
 the great majority of cases comes through the information obtained by 
 this means. Though it is not necessary for a physician himself to take 
 records, he must be familiar with their interpretation in order that he may 
 appreciate and apply the results. 
 
 There have been many methods devised to record the movements of 
 the circulation, but here I will only deal with those which in my hands 
 have yielded very satisfactory results. The essence of a method should be 
 simplicity, for the more complicated the processes the more unsuitable 
 it becomes for practical clinical purposes. In hospitals with large staffs 
 of assistants the more elaborate methods may be usefully employed, but for 
 the practitioner who studies his own patients, the simpler the methods the 
 better. 
 
 § 69. The sphygmograph. — It is scarcely necessary to enter into 
 a full account of the construction of the various sphygmographs. They 
 have been so frequently described in textbooks that their construction is 
 famihar to all medical men. They are all practically constructed on the 
 same principle. A steel spring is laid upon the radial artery at the wrist 
 in such a manner that, while it compresses the artery, it does not obliterate 
 it. Attached directly to the spring is a long lever, or a series of small levers, 
 that magnify the movements of the spring. The free extremity of the lever 
 presses hghtly against a strip of paper, whose surface has been blackened 
 by the smoke of burning camphor or turpentine, the strip of paper passing 
 at a uniform speed by means of a clockwork arrangement. Although I have 
 worked with several instruments, I find the Dudgeon to be the handiest 
 and most useful. Into all sphygmographic records, certain errors, due to 
 
 F 2
 
 68 DISEASES OF THE HEART 
 
 defects of the instruments, creep. Some of the more elaborate instruments 
 may be freer from defect than the Dudgeon, but so long as one is cautious 
 not to read itito the tracings movements evidently due to instrumental 
 errors, the Dudgeon sphygmograph is quite serviceable for a great many 
 practical purposes, and more particularly for giving a true and accurate 
 record of the occurrence of pulse beats. 
 
 § 'JO. The polygraph. — There are many perceptible movements due 
 to the circulation that the sphygmograph fails to register, and when it is 
 required to record these movements other instruments have to be employed. 
 The method most commonly adopted has been by conveying, by means of 
 a tube containing air, the movements to be registered to a tambour on 
 which there rested a lever. The excursion of the lever is recorded on a 
 revolving drum covered by smoked paper. Two or more tambours being 
 
 B 
 
 Fig. 13. Shows the shallow cups or ' receivers ' used in taking tracings of the liver (receiver B) 
 and of the jugular or carotid pulse or apex beat (receiver E). (Half size.) 
 
 used with their levers placed one above the other, the simultaneous record 
 of different movements can be readily effected. 
 
 The elaborate and bulky apparatus required has restricted the employ- 
 ment of this method to such narrow limits, that numerous points of interest 
 in chnical medicine have been either overlooked or misunderstood. In my 
 investigations into the nature of the venous pulse, I had at first to use this 
 unwieldy instrument, but its cumbersomeness compelled me to devise 
 a much simpler and more effective apparatus. 
 
 § 71. The clinical polygraph — This apparatus, which I have called 
 the clinical polygraph, can be used for taking, at the same time and on the 
 same recording surface, tracings of the radial pulse, with tracings of the 
 apex beat, carotid, venous, or liver pulse, or the respiratory movements, 
 and its size permits of it being carried about with the greatest facility, and 
 readily employed in general practice (Fig. 14). 
 
 The essential parts of the instrument are a small cup for receiving the 
 impressions of the pulsations, a tube for transmitting the impressions to
 
 INSTRUMENTAL METHODS OF EXAMINATION 
 
 69 
 
 a tambour and lever, the tambour being attached to a Dudgeon or Jacquet 
 sphygmograph. 
 
 The smaU cup for receiving the impressions (which will be referred to 
 hereafter as the ' receiver ') is simply a small shallow vessel, circular in shape, 
 one and a half inches in diameter and half an inch in depth {E, Figs. 13 and 
 18). The open mouth is applied over the pulsating part so that its edges are 
 closely adapted to the skin and all communication with the outer air is 
 excluded. From the roof of the receiver rises a narrow pipe, half an inch 
 in length. To this pipe is fitted an india-rubber tube three to four feet in 
 length, the other end of which is connected with the tambour. A modifi- 
 cation of this receiver is required when tracings of the liver pulse are taken. 
 The ' liver receiver ' (B, Fig. 13) is larger, being five inches in length, two 
 
 Fig. 14. The clinical polygraph, consisting of a tambour attached to 
 a Dudgeon's sphygmograph. 
 
 inches in breadth, and one inch in depth, its open edges slightly curved on 
 their long axis. A small air-hole is made at one end near the roof. In 
 employing the ' liver receiver ' the position of the lower margin of the liver 
 having been ascertained, the receiver, held in the right hand, is laid length- 
 wise across the abdomen, its lower edge being two inches below the liver 
 margin, and the end with the air-hole towards the middle line. Steady 
 continuous pressure is appUed to the lower margin of the receiver till it 
 presses deeply into the abdomen, and then the upper margin is adapted 
 closely to the skin. In this manner a considerable portion of the lower liver 
 edge is embraced by the receiver. If the forefinger of the right hand is 
 now applied over the air-hole, the movements of respiration and liver pulse 
 will be communicated to the lever. If the patient stops breathing, the liver 
 movements are alone transmitted. 
 
 The tambour (Fig. 15) supports a writing lever about six inches in length. 
 From the under surface of the tambour a pipe protrudes, which is connected
 
 70 
 
 DISEASES OF THE HEART 
 
 by the india-rubber tubing with the receiver. Screwed tightly to the bottom 
 of the tambour is a stem (B) six and a half inches in length, projecting out- 
 ward parallel to the under surface of the tambour. Half an inch of the other 
 extremity of the stem is bent almost at right angles (0), and this portion 
 fits into a slot on the upright stem that supports the movable lever of a 
 Dudgeon's sphygmograph (Eig. 14). Wlien the tambour arrangement is 
 adjusted to the sphygmograph, the tambour rests with its movable surface 
 vertical, so that the writing lever moves horizontally. For the purpose of 
 adjusting the point of the writing lever to any desired place on the record- 
 ing paper the following movements are available : The point of the lever 
 can be approximated to, or withdrawn from, any desired point by means of 
 a shding arrangement at D (Fig. 15), where the stem consists of two parts 
 clasping one another. The writing point can be made to move in the hori- 
 zontal direction, so as to write at any desired level on the paper, by means 
 
 Fig. 15. The tambour with stem for attachment to the Dudgeon or Jacquet sphygmograph. 
 
 of a joint at E (Fig. 15), which moves stiffly, and retains the position inVhich 
 it is placed. Finally, by rotating the tambour at a joint formed where the 
 stem is fixed to the under surface of the tambour, the lever can be raised 
 out of reach during the adjustment of the sphygmograph to the pulse, and 
 brought back and allowed to touch the surface of the blackened paper, 
 with sufficient deHcacy to permit its movements to be accurately recorded 
 %\ithout being restrained by too close pressure. By means of these arrange- 
 ments the lever can be moved with great facihty and accuracy in a vertical 
 and a horizontal direction, as well as made to approach or recede from any 
 given point. By this method any movement can be recorded at the same 
 time, and on the same paper, as the radial sphygmograph. One can make 
 the tambour lever write directly above or below the Avriting lever of the sphyg- 
 mograph, or, when the movements are large, a little behind, so that the two 
 levers do not come into contact during their excursions. Perpendicular 
 lines to show the relative time of the two tracings are obtained by allovWng
 
 INSTRUMENTAL METHODS OF EXAMINATION 
 
 71 
 
 the lever to make distinct marks on the paper before starting or after 
 stopping. With a pair of compasses, the relative time of any event can be 
 accurately gauged. 
 
 Some difficulty may be experienced in the employment of the clinical 
 polygraph, on account of the weight of the tambour tilting the sphygmo- 
 graph off the radial pulse, especially if the inelastic band usually supplied 
 with the sphygmograph be employed. I have long ago abandoned the use 
 of the inelastic band (placing no reliance on the pressure supposed to be 
 required to obtain an idea of the arterial pressure), and employ instead 
 an elastic band, tying the instrument to the wrist by a knot. Should any 
 slipping occur, the sphygmograph and tambour can readily be adjusted. 
 It frequently happens that the radial pulse causes such a large excursion 
 that there is no clear space on the paper for the venous or other pulsation. 
 
 Fig. 1G. The first part of the tracing shows the venous pulse from the right internal jugular 
 vein (upper tracing) taken at the same time as the radial pulse (lower tracing). The clock- 
 work being stopped, the receiver was applied over the carotid artery, and tracings of the 
 carotid and radial pulses taken. Again the clockwork was stopped, and the tambour portion 
 of the polygraph removed, and the full effect of the radial pulse was inscribed on the last 
 portion. 
 
 In such a case I either shift the sphygmograph till I obtain a tracing of less 
 amplitude (seeing that the object of taking the radial pulse at the same 
 time as the venous is to obtain an idea of the relative time), and, before the 
 paper has entirely passed through, stop the clockwork, remove the tambour, 
 and obtain a fuU-sized tracing of the radial pulse (Fig. 16). Or the venous 
 pulse may be taken a little behind the radial, and the various events dis- 
 entangled. For accurately estimating the time of the events, it is advisable 
 to take on the same paper a few beats of the carotid pulse. For convenience 
 of study, other events can be readily recorded within the Umits of a short 
 sphygraographic paper ; and a record of apex beat, venous, carotid, and 
 liver pulse may be taken at the same time as the radial sphygmogram 
 (Fig. 17). 
 
 When a long tracing is required (as, for instance, in noting the move- 
 ments of the two sides of the heart in cases of occasional irregularity), 
 a tracing paper one or two feet in length may be employed.
 
 72 
 
 DISEASES OF THE HEART 
 
 For convenience, I have had the Dudgeon sphygmograph altered so as 
 to take a paper over one inch in width, thus allowing more room for the two 
 tracings. At one time I had attached a time-marker, driven by a separate 
 clockwork as in the Jacquet, but this added too much to the weight of the 
 machine, so that it was easily displaced. Biggs has recently devised a 
 convenient Uttle time-marker which can be fixed to a Dudgeon or other 
 sphygmograph. 
 
 I have enlarged the box for holding the blackened paper, by adding 
 a compartment to contain the tambour, so that it is convenientl^'^ carried 
 on a visiting round. 
 
 Ajiex beat\ Carotid 
 
 Rt.Int.J-ug. 
 
 Fig. 17. Apex beat, carotid, right internal jugular, and liver pulses (upper tracing) taken 
 at the same time as the radial pulse (lower tracing). 
 
 § 72. The ink polygraph (Fig. 18). — Simple and useful as is the 
 instrument just described, I found it was not convenient when the move- 
 ments had to be recorded over a long period, as where the irregularities were 
 infrequent, or where they varied, or where respiratory curves were required. 
 I therefore conceived the idea of constructing an instrument that would 
 take tracings of an indefinite length, where the employment of ink would 
 enable a roll of paper to be unwound, and save as well the inconvenience 
 of blackening and varnishing. 
 
 I had considerable difficulties to overcome, but found a skilled helper 
 in Mr. Shaw, who not only comprehended and appreciated my ideas, but 
 constructed an instrument that carried them out. The case A (Fig. 18) 
 contains the clockwork for the roller which unwinds the roll of paper D, 
 and also the separate clockwork which moves the time-marking pen F. 
 B B are the two tambours, and F F their levers. The writing pens in 
 Fig. 18 are narrow-grooved wires, one end fixed to the bottom of a small 
 cistern at the free extremity of the lever. The other end of the grooved 
 wire is adjusted to barely touch the paper. The ink is put into the tiny 
 cistern, and it flows along the groove to the pen point by capillary attraction. 
 Recently these pens have been greatly improved by making a shallow 
 groove in the lever act in place of the cistern. If the pens are kept clean, 
 and the ink is free from dust, they serve their purpose most admirably, 
 and are ever ready for use. Red ink is better than the black inks, as it
 
 INSTRUMENTAL METHODS OF EXAMINATION 
 
 73 
 
 does not corrode the pens. As the radial pulse is the most serviceable 
 of standards, a special method is employed to record it. A splint (C 1) is 
 fastened to the wrist in such a manner that the pad of the steel spring 
 falls on the radial artery, and is pressed down by an eccentric wheel (18) 
 until a suitable movement is transmitted to the spring by the artery ; 
 then the broad tambour (C) is fitted on to the splint so that the knob (12) 
 falls on the moving spring. This wrist tambour is connected to the 
 tambour B by india-rubber tubing (22, 22), and the movements of the 
 
 Fig. 18. The ink polygi-aph. 
 
 radial pulse are recorded by the lever F. The shallow cup (receiver) E is 
 placed on the pulsation which it is desired to record, and the movement 
 is conveyed to the lever F of the other tambour. In this way, simul- 
 taneous with the radial pulse, a record can be obtained of the apex beat, 
 carotid, jugular, or other pulses. 
 
 To record the respiratory movements, a bag can be substituted for the 
 receiver E. 
 
 By turning the screw (3) the rate at which the paper passes can be 
 quickened or slowed at will. This is of the greatest use, for it often happens 
 that in quickly succeeding events a wider interval may be required, whereas 
 in recording respiratory movements a slow rate is best. As the time-marker
 
 74 DISEASES OF THE HEART 
 
 registers one-fiftli of a second, and is driven by a separate clockwork, the 
 rate of the recorded movements can always be ascertained with absolute 
 accuracy. 
 
 It has been suggested that another tambour should be added to record 
 a third movement, and I have tried this but have practically discarded it, 
 as, though it might be of use occasionally, it would complicate the apparatus 
 unnecessarily. Wlien one is making observations single-handed, the two 
 tambours are quite sufficient to occupy the attention. With a little practice 
 this apparatus can be used with the greatest facility. In the course of a few 
 minutes the different movements can be recorded with the patient sitting 
 up or in the recumbent position. 
 
 When the tambour is strapped to the wrist to take the radial pulse, one 
 hand is always free to start the machine, and to replenish the ink or regulate 
 the rate, the other hand holding the receiver over the movement to be 
 recorded. 
 
 The tracings in all the figures in the Plates except Figs. 90 and 103, 
 and many in the text, have been taken by this instrument.
 
 CHAPTER X 
 
 The Position and Movements of the Heart 
 
 §73. The jiosition of the heart in the chest. 
 
 74. The standards for recognizing the events in a cardiac revolution. 
 
 75. Conditions of the chest-wall permitting the recognition of certain movements of the 
 
 heart. 
 
 76. The nature of the movements graphically recorded. 
 
 77. The apex beat. 
 
 78. Interpretation of a tracing of an apex beat due to the systole of the left ventricle. 
 
 79. The auricular wave. 
 
 80. Eetraction of yielding structures in the neighbourhood of the heart during ventricular 
 
 systole. 
 
 81. Liver movement due to cardiac aspiration. 
 
 82. Epigastric pulsation. 
 
 83. The apex beat due to the right ventricle. 
 
 84. Significance of the inverted cardiogram. 
 
 85. Alteration of the apex beat due to retraction of the lung. 
 
 86. The shock due to the ventricular systole. 
 
 § 73. The position of the heart in the chest The position of the 
 
 heart in the chest, and the relations of its chambers to the chest-wall, can 
 best be reahzed from such a drawing as Fig. 19. The chief points to notice 
 are the position of the apex and how it is made' up of the left ventricle and 
 covered normally by the lung. The whole right border of the heart is made 
 up by the right auricle, and the greater portion of the anterior surface by 
 the right ventricle. The perceptible movements of the normal heart when 
 covered by the lung are due to the right ventricle, and this is the reason 
 that the apex beat, due to the left ventricle, is not obtained from people 
 with voluminous lungs. 
 
 § 74. The standards for recognizing the events in a cardiac revo- 
 lution. — Owing to their easy recognition and determined place in the cardiac 
 cycle, the carotid and radial pulses form the most certain standards for 
 finding out the place of other movements in a cardiac revolution. In 
 describing the tracings frequent references will have to be made to these 
 standards, and more particularly to that period during which the semilunar 
 valves are open, which is indicated in the tracings by the space E. When 
 it appears in the radial tracing it corresponds to the effects of the ventricular 
 systole upon the radial pulse — that is to say, to the actual pulse-wave — and
 
 76 
 
 DISEASES OF THE HEART 
 
 not to the true time of the occurrence of the ventricular systole, for the pulse- 
 wave having a longer distance to travel, the period E will be later in the 
 radial than in the apex or carotid tracings. 
 
 § 75. Conditions of the chest-wall permitting the recognition of 
 certain movements of the heart — The movements of the heart in a healthy 
 person are often so obscured by the lungs, that only very little change is 
 
 Arch of Aorta 
 
 Sup Vena Cava 
 Pericardium 
 
 Aortic Valves 
 Mitral Valves 
 Right auricle 
 
 Tricuspid valves 
 
 Border of right 
 lung 
 
 Pulmonary Artery 
 Left auricidar appendage 
 Pulmonary Valves 
 Pericardium 
 
 Left verdricle 
 Right ventricle 
 
 Border (f left 
 lung 
 
 Fig. 19. The position of the heart in the chest. (Keith.) 
 
 discernible in the external chest-wall. In many cases the lungs are so volumi- 
 nous, or the chest-wall so fat and thick, that no movement can be detected. 
 But when a large surface of the heart is directly exposed to a thin chest-wall, 
 the heart being normal or increased in size, and the lung displaced, a series 
 of movements of the chest-wall, due to the contraction and expansion of 
 the heart, can be recognized. The movements thus discernible are not the 
 same in all cases, but depend on which part of the heart's surface comes in 
 contact with the chest-wall, and other yielding structures. These move-
 
 POSITION AND MOVEMENTS OF THE HEART 77 
 
 ments take place so rapidly that it is difficult to interpret their significance 
 by the unaided senses. Many writers on this subject have drawn elaborate, 
 but nevertheless erroneous, conclusions from such unaided observations, 
 and it seems to me that accurate observations by the graphic method alone 
 can furnish a clear and definite explanation. 
 
 § 76. The nature of the movements graphically recorded The 
 
 movements of the heart that are most readily recognized are those connected 
 with the systole and diastole of the ventricles. Movements directly due 
 to the auricles are so obscured by the larger and more vigorous movements 
 of the ventricle, that it is doubtful if they are ever capable of recognition. 
 The movements most readily recognized are : first, the apex beat ; second, 
 the filling of the ventricles ; third, the emptying of the ventricles ; and 
 fourth, the shock communicated by the sudden hardening of the ventricular 
 walls as they pass into systole. 
 
 § 77. The apex beat — The chief movement, and the one which is 
 usually most apparent, is that caused by the forcible outward projection 
 of the apex of the heart during the ventricular systole — the apex beat. 
 This is generally described as ' the lowest and outermost point of the heart 
 which strikes against the chest-wall '. In healthy adults, it is usually felt 
 in the fifth left intercostal space, immediately inside the nipple line. It 
 may, however, be situated in the fourth interspace, and outside the nipple 
 line in children, and in some adults. In disease of the heart it alters its 
 situation with the increasing size of the heart. This forward thrust occurs 
 when the left ventricle is in contact with the chest. As will be shown later, 
 a movement of another description occurs when the right ventricle consti- 
 tutes the so-called apex beat. That the apex beat due to the left ventricle 
 is a distinct displacement of the heart forward can be recognized by the 
 senses of touch and sight. 
 
 During the whole time occupied by the systole of the ventricle, the apex 
 is usually kept projecting into the interspace, so that the palpating hand 
 recognizes the forward thrust, and in such a tracing as Fig. 20, the lever 
 taking the tracing is kept raised during the whole time of the outflow 
 from the ventricle (space E'). If the left ventricle is much hypertrophied, 
 the same movement can sometimes be detected in two or three interspaces. 
 If the interspaces be fairly open and the chest-wall thin, and the tip of the 
 finger be thrust into the third or fourth interspace near the sternum, the 
 right ventricle can be felt hardening, and remaining thus hardened in contact 
 with the finger during the whole period of the ventricular systole. It cannot, 
 however, be averred that in this case there is a forward thrust. The heart 
 here is always in contact with the chest-wall, and the finger pushed into the
 
 78 DISEASES OF THE HEART 
 
 interspace during the diastole in all likelihood impinges against the lax 
 ventricular wall. As soon as the ventricle hardens, the finger recognizes 
 this hardening as something pushing against it. This sensation of a thrust 
 is sometimes actually s3niclironous with an indrawing of the soft structures 
 filling up the interspace (Fig. 26). 
 
 Fig. 20. Simultaneous tracings of the apex beat and the carotid 
 pulse, showing the ' systolic plateau ' in the cardiogram during the 
 outflow from the ventricle {E'). 
 
 § 78. Interpretation of a tracing of an apex beat due to the systole 
 of the left ventricle. — A tracing of the apex beat or cardiogram is a diagram- 
 matic representation of (a) the forward movement of the apex of the heart 
 while the ventricular muscle is beginning to contract (space D, Fig. 21) ; 
 
 Fig. 21. Simultaneous tracings of the apex beat and of the pulsation in the pulmonary 
 artery, a represents the small wave due to the auricular systole. The time during which the 
 ventricle is passing into systole is represented by the space (D), emptying (E), relaxing (F), 
 filling (G). While this tracing was being taken the cylinder was rapidly rotated. The letters 
 D, E, F have reference to the same periods in the cardiac revolution as in Fig. 43 (see p. 108). 
 
 (6) the retention of the apex beat against the chest-wall while the ventricles 
 are emptying (space E, Fig. 21) ; (c) the backward movement of the apex 
 of the heart while the ventricular muscle is relaxing (space F, Fig. 21) ; 
 {d) and the gradual swelling of the ventricle during diastole (space G, Fig. 21). 
 (a) The period of commencing contraction of the ventricular muscle — the 
 presphygmic interval (space D, Fig. 21). — During this period the pressure
 
 POSITION AND MOVEMENTS OF THE HEART 
 
 79 
 
 within the ventricle is rapidly rising. The auriculo-ventricular valves close 
 as soon as the pressure within the ventricle rises above that in the auricle, 
 and the semilunar valves open as soon as the pressure in the ventricle 
 rises above that in the aorta. This last occurs at the end of the period D, 
 Fig. 21, and is usually indicated by the abrupt termination of the upstroke. 
 In Fig. 21 simultaneous tracings were taken of the pulsation in the pul- 
 monary artery and of the apex beat. As the beginning of the pulse in the 
 
 Fig. 22. Simultaneous tracings of the apex beat and of 
 the pulsation in the pulmonary artery. The letters have the 
 same significance as those in Fig. 21. 
 
 pulmonary artery indicates the opening of the semilunar valves, so it is 
 found that the end of the period D corresponds exactly with the beginning 
 of the pulsation of the pulmonary artery. When this figure was taken the 
 cylinder was rotated rapidly in order to separate the events as widely as 
 possible. When the cyHnder rotates at a slower rate, this period is repre- 
 sented by an almost perpendicular line (Fig. 22). 
 
 Fig. 23. Simultaneous tracings of the pulses of the carotid and pulmonary arteries. 
 After the third beat the cylinder was rotated rapidly. 
 
 It will be noted that the termination of the upstroke corresponds exactly 
 with the beginning of the outjBlow of the ventricle into the artery. These 
 tracings were taken from a lad suffering from phthisis of the left lung, which 
 had retracted from the heart, and through the thin chest -walls the various 
 movements could easily be observed. In the second left interspace there 
 was a marked pulsation, and tracings of this, taken at the same time as the 
 carotid pulse, left no doubt as to its being caused by the pulmonary artery 
 (Fig. 23). It will be noticed that the carotid pulse appears just a very little
 
 80 DISEASES OF THE HEART 
 
 later than the pulmonary. Here also, after a few beats, the cylinder was 
 rapidly rotated with the hand to separate more widely the different events. 
 
 (6) The period of ventricular outfloio (space E, Fig. 21). — When the 
 pressure in the ventricles exceeds that in the aorta and pulmonary artery 
 the semilunar valves open, and the blood flows out from the ventricles. 
 During this period the apex is usually kept stationary, pressing against the 
 chest-wall, and in many tracings (as in Fig. 24) it is shown by a fairly level 
 line — the systolic ' plateau '. In place of a flattened top representing the 
 period of ventricular outflow, the tracing may continue to rise (as in Fig. 20), 
 indicating that the ventricle is still slightly shifting. On the other hand, 
 the tracing sometimes rapidly descends (Figs. 21 and 22). I cannot but 
 think that this is due to the ventricle shrinking away from the interspace 
 during its systole, the receiver perhaps not being exactly over the apex. 
 I shall show later on that this shrinking can be demonstrated in various 
 places, and I have found evidence of it immediately under a diffuse apex 
 beat. The movement producing the apex beat is really a displacement 
 of the heart forward, and while the heart is thus displaced the ventricles 
 shrink as they empty themselves (see § 20). The termination of the ven- 
 tricular outflow is occasioned by the pressure in the aorta becoming higher 
 than that in the ventricle. The semilunar valves close in consequence, 
 and the ventricular muscle then relaxes ; the termination of the systolic 
 period is indicated in the cardiogram by a sudden descent. 
 
 (c) The period of relaxation of the ventricular muscle (space F, Fig. 21). 
 — With the relaxation of the ventricular muscle the apex retreats from 
 the chest-wall, as is indicated by the slanting downstroke in the tracing, 
 or where the tracing is already falling during the ventricular outflow by 
 a more rapid descent (Figs. 21 and 22). During this period the ventricular 
 pressure rapidly falls until the stage of complete relaxation, when the 
 pressure inside the ventricles becomes lower than that inside the auricles. 
 Wlien this occurs the auriculo-ventricular valves open. The apex then 
 has reached its greatest distance from the chest-wall, and in the tracing the 
 lowest point is reached. 
 
 The time of the opening of the auriculo-ventricular valves is usually 
 a very definite landmark in apex and jugular tracings, and, in consequence, 
 is a useful standard for measuring the sequence of events in tracings of 
 irregular heart action. It is recognized as the lowest point reached in tracings 
 of the apex of the left ventricle, and it is just before the fall of the wave v, 
 in tracings of the jugular pulse. Its time corresponds nearly with the bottom 
 of the aortic notch in tracings of the radial pulse. It is represented by the 
 perpendicular line 6 in man^^ of the tracings given later.
 
 POSITIOX AXD MOVEMENTS OF THE HEART 81 
 
 (d) The period of filling of the ventricles (space G, Fig. 21). — Upon 
 the opening of the auriculo-ventricular valves, the blood flows from the 
 auricles into the ventricles, and as the ventricles distend the heart pushes 
 against the intercostal space, and slightly raises the lever. Tliis period is 
 marked in the tracing by a gradual ascent. Frequently, however, the heart 
 fails to affect the tissues in the interspace during this period, so that no 
 indication of the filhng of the ventricles is obtained ; in such a tracing as 
 Fig. 20, for example, and in many others given in the text, the whole of this 
 ■period is a blank, so far as information regarding events in the cardiac 
 cycle are concerned. 
 
 § 79' The auricular wave — In some tracings from the apex there 
 is occasionally found an abrupt though slight rise immediately preceding 
 the beginning of the ventricular systole {a, Figs. 21 and 24). This is due to 
 
 Fig. 24. Simultaneous tracings of the apex beat and of the 
 radial pulse, showing the ' systolic plateau ' and the small wave 
 (a) due to the auricular systole. The third beat in the apex tracing 
 is obliterated by the movement of inspiration. 
 
 a sudden increase in the contents of the ventricle caused by the contraction 
 of the auricle, and may be termed the auricular wave. 
 
 The auricular wave is not always perceptible in apex tracings, but when 
 present it often gives valuable information. Normally, it precedes the begin- 
 ning of the wave due to the ventricular systole by about one-tenth of a second 
 (space between 1 and 2, Fig. 25). Sometimes this interval is increased, 
 and then it may indicate a delay in the passage of the stimulus from auricle 
 to ventricle (Fig. 231, p. 339). In cases of heart-block, it may be recognized 
 during the ventricular pauses (Fig. 123). Its absence may be of no signi- 
 cance, but it is to be noted that it is never seen in cases with the nodal 
 rhythm, even when immediately before the starting of this abnormal rhythm 
 it had been a conspicuous feature (compare Fig. 198 with Fig. 202, p. 332). 
 
 § 8o. Retraction of yielding structures in the neighbourhood of 
 the heart during ventricular systole — When the ventricles expel their 
 contents they must of necessity shrink. This shrinkage occurs abruptly, 
 and with considerable force. The yielding tissues in the neighbourhood 
 of the heart are dragged upon, and evidence of this dragging can be obtained 
 
 MACKENZIE n
 
 82 
 
 DISEASES OF THE HEART 
 
 from a variety of sources. John Hunter ^^^ originated the idea that the 
 systole of the ventricles would have a tendency to produce a vacuum, and 
 thus expedite the flow of the venous blood into the chest. Evidence of 
 this ' cardiac aspiration ' affecting the lungs has been obtained by a number 
 of observers. The tracings ^'^^ of Mosso and Delepine ^^^ of the movements of 
 
 Fig. 25. The apex tracing shows a slight wave, a, due to the contraction of the auricles 
 distending the ventricles and beginning one-tenth of a second before the ventricular systole. 
 For explanation of the numbered perpendicular lines see Fig. 46. 
 
 the column of air in the respiratory passages, due to the cardiac aspiration, 
 correspond exactly with those obtained from the praecordium (Eig. 26), 
 from under the liver (Figs. 27 and 28), and from the epigastrium (Figs. 
 29 and 30). 
 
 Fig. 26. Simultaneous tracings of the heart movements (upper tracing) 
 and of the radial pulse. The first part of the upper tracing was taken from the 
 apex beat in the fourth interspace immediately outside the nipple, while the 
 latter part was taken in the same interspace near the left border of the sternum. 
 In the first part the cardiogram shows a ' systolic plateau ' during the ventricular 
 outflow {E), in the other part the cardiogram is inverted, i. e. there is a depres- 
 sion during this period {E). 
 
 In Fig. 26 this drawing-in of tissues in the intercostal spaces over the 
 heart is demonstrated. It was obtained from a boy aged fourteen. The 
 apex beat was well marked in the fourth interspace outside the nipple. At 
 the same time that the apex was thrust outwards, the skin and subcutaneous 
 tissues over the same interspace inside the nipple were drawn in. In Fig. 26 
 the tracings of the apex beat were taken simultaneously with the radial
 
 POSITION AND MOVEMENTS OF THE HEART 83 
 
 pulse for four beats. The clockwork was then stopped, and the receiver, 
 which had been applied over the apex, was placed over the praecordium 
 inside the nipple, and the ' inverted cardiogram ' of the last portion was 
 obtained. The space E represents the duration of the outflow from the 
 ventricle ; and this period, which in the apex tracing shows a flattened 
 elevation, shows a great depression in that obtained from the front of the 
 heart. The ascending limb of the apex tracing corresponds to the period 
 during which the ventricle is contracting (space D, Fig. 21). This period 
 in the inverted cardiogram is represented by a slight rise, due to the shock 
 of the contracting ventricle. No blood as yet has escaped from the ventricle. 
 As soon as the semilunar valves open the blood rushes out of the ventricle, 
 the ventricles diminish in size and the yielding tissues of the interspace 
 sink in and cause the great fall, as represented in the inverted cardiogram 
 (space E, in the latter half of Fig. 26). 
 
 § 8i. Liver movements due to cardiac aspiration Not only can 
 
 this aspiration be demonstrated as affecting the pliable tissues immediately 
 in contact with the heart, but in suitable cases it can be shown to produce 
 a distinct excursion of the liver. All writers referring to this movement 
 of the liver speak of it as a downward thrust during the ventricular systole. 
 Careful tracings demonstrate that this movement is quite of the opposite 
 nature — it is a dra wing-up of the liver during the ventricular systole. In 
 Figs. 27 the apex beat is taken at the same time as the movement of the 
 liver. 
 
 The receiver taking the liver movement being applied to the under surface 
 of the organ, a retraction of the liver upwards corresponds with a fall in 
 the tracing, and vice versa. It will be seen that the movement m the liver 
 upwards takes place during the ventricular systole, while the downward 
 movement is due to the diastolic filling of the ventricle. In Fig. 28 the 
 movement of the liver is recorded at the same time as the carotid pulse. 
 It is seen that as soon as the carotid pulse appears, the liver is drawn up, 
 and remains there until the end of the ventricular systole, after which 
 the liver gradually faUs down. I do not mean that the excursion of the liver 
 is one of considerable extent, but the movement is so great as to be obvious 
 to the palpating hand. It is distinct from a pulsation of the Uver, which 
 is a periodic swelling of the liver, while this is a displacement of the hver 
 en masse. 
 
 § 82. Epigastric pulsation — The causes which may produce a pulsation 
 
 in the epigastrium are : (a) a dilated right heart ; (6) a hypertrophied left 
 
 ventricle ; (c) the abdominal aorta ; and [d) an aneurysm of the abdominal 
 
 aorta. 
 
 g2
 
 84 
 
 DISEASES OF THE HEART 
 
 In the later stages of typhoid fever and other exhausting diseases, 
 epigastric pulsation is an ominous sign of cardiac enfeeblement. The 
 movement consists of an alternate swelling and retraction of the epigastrium. 
 It is invariably assumed that this swelling or pulsation is due to the right 
 
 Fig. 27. Simultaneous tracings 
 of the apex beat and of the move- 
 ment of the liver. When the 
 ventricle empties the liver is drawn 
 up, and this causes the fall in the 
 tracing. 
 
 ' Fig. 28. Simultaneous tracings of the 
 carotid pulse and liver movement. With 
 the ajipearance of the carotid pulse there 
 is a sudden fall of the lower tracing due to 
 the liver being drawn upwards by the 
 emptying ventricles. 
 
 ventricular systole, and that it is of the same nature as the outward protrusion 
 constituting the apex beat. If this form of epigastric pulsation is carefully 
 timed wi|[i the carotid pulse, it will be found that the epigastric pulse, pro- 
 trusion, or swelling, precedes the carotid pulse, and that the retraction of 
 
 iWj 
 
 e\ Spiga^stric Pulsa-tion 
 Ra.dia,l 
 
 ^ CaLTottd 
 
 Fig. ^29. Simultaneous tracing of the epigastric pulse, due to a dilated right heart, 
 and of the radial pulse. The epigastric pulse shows a retraction during the ventricular 
 systole {E), and a jDrotrusion during the filling of the ventricle. 
 
 the epigastrium corresponds in time to the carotid pulsation. The apex 
 beat is rarely available in these cases, on account of the right heart pushing 
 the left ventricle backwards. In the tracings of the epigastric pulse (Fig. 
 29) the radial pulse is taken as the standard of time. The time occupied
 
 POSITION AND MOVEMENTS OF THE HEART 
 
 85 
 
 by the pulse travelling from the heart to the wrist being allowed for, it will 
 be found that the great fall in the epigastric pulse corresponds exactly with 
 the ventricular systole (E). 
 
 The patient from whom this tracing was taken was dying from pernicious 
 anaemia. At the post-mortem examination, a needle pushed through the 
 epigastrium, at the place where the tracing was obtained, was found to have 
 penetrated the right ventricle. 
 
 ric PulscLtion 
 
 Fig. 30. Shows the same features as Fig. 29, with the excej)lion of 
 the small wave (c) occasioned by the shock communicated to the epigas- 
 trium by the abdominal aortic pulse. A few beats of the abdominal aorta 
 are also given. 
 
 In Fig. 30 a similar tracing is given, except that there is a slight inter- 
 ruption at c, on the line of descent. This will be found to correspond exactly 
 to the time of the abdominal aorta, taken from the middle of the abdomen, 
 a few beats of which are also given. This small wave (c) is due to the impulse 
 imparted to the tissues by the pulse of the underlying aorta. Epigastric 
 pulsation, due to hyper trophied left ventricle, has the same character as an 
 apex beat (Fig. 31). Epigastric pulsation due] to the abdominal aorta 
 
 ApeocBeat 
 
 Epigastric Puls&tion 
 
 Fig. 31. Simultaneous tracings of the apex beat and of the 
 epigastric pulsation, due to a hypertrophied left ventricle. 
 
 ]3resents quite a different character from that due to a dilated right ventricle, 
 as shown in Fig. 32, where the pulse corresponds in character and time 
 with the radial pulse. An epigastric pulsation due to an aneurysm of the 
 abdominal aorta would assume the time and character of the abdominal 
 aortic pulse (Fig. 32). 
 
 § 83. The apex beat due to the right ventricle — Accepting the usual 
 clinical definition of the apex beat ' being the lowest and outermost part of 
 the heart's impulse ', a totally different form of beat is found when the right
 
 86 
 
 DISEASES OF THE HEART 
 
 ventricle causes this movement. In certain cases of dilatation of the right 
 heart, nearly the whole anterior aspect of the heart is composed of the right 
 auricle and ventricle, the left ventricle forming but a mere strip of the border 
 (see Figs. 135 and 136). This portion of the left ventricle is situated so far 
 back that it is covered by the lungs, and does not reach the chest-wall. 
 Hence it is that ' the lowest and outermost part of the heart ' in contact 
 
 Epig-PuLlsatioTx 
 
 
 / 
 
 HwJ---^-i^-~i^ 
 
 lj^^=::i^ 
 
 
 Radial 
 
 
 
 Fig. 32. Simultaneous tracings of the epigastric pulse, due to 
 the abdominal aorta, and of the radial pulse. 
 
 with the chest-wall is the right ventricle. The character of the apex beat 
 now corresponds exactly with that of the Uver movements, of the epigastric 
 pulse, due to enlarged right heart, and of the inverted cardiogram in Fig. 26. 
 In place of the outward thrust during the systole, as in the apex beat due to 
 the left ventricle, there is an indrawing of the tissues. 
 
 Fig. 33. Tracings of the apex beat, jugular pulse, and carotid pulse (upper tracing), taken 
 at the same time as the radial. The apex tracing is due to the right ventricle, and shows 
 a depression {E) during the ventricular outflow. The sharp elevation preceding E is caused 
 by the shock of the contracting ventricles. This is preceded by a small wave (o), which is due 
 to the contracting auricle distending the ventricle, and corresponds in time exactly with the 
 wave (a) in the jugular pulse, which is due to the contracting auricle sending a wave of blood 
 back into the veins. 
 
 Fig. 33 was taken from a youth, aged eighteen, with simple dilatation 
 of the heart, and free from valvular disease. There was marked pulsation 
 of the jugular veins, a few beats of which are given. The apex tracing shows 
 a great depression during the period of ventricular outflow {E). This period 
 is immediately preceded by an abrupt rise due to the shock communicated 
 to the chest by the sudden hardening of the ventricular wall. Although 
 corresponding with the period D (Figs. 21 and 22) in the left ventricular 
 apex tracings, I am inclined to think that the rise here is an instrumental
 
 POSITION AND MOVEMENTS OF THE HEART 87 
 
 fault, due to the violent shock communicated by the sudden and forcible 
 ventricular contraction. This period is preceded by a small wave (a) in the 
 tracing identical with the similar rise in Figs. 24 and 25 of the left ventricular 
 apex beat. It is due in this case, as in those, to the distension of the ventricle 
 by the auricular systole. It occupies exactly the same period in the cardiac 
 revolution as the wave (a) in the venous pulse, which is produced by the 
 systole of the right auricle. The space E in all the tracings represents the 
 period of ventricular outflow as it affects the different pulses. One can, 
 therefore, readily and with certainty refer the different events to their causes. 
 Thus we know that the wave of contraction arising in the auricle passes on to 
 the ventricle, that between the auricular outflow and the ventricular outflow 
 a period, the presphygmic {D, Fig. 21), exists, during which the ventricle 
 is contracting and raising its pressure until it opens the semilunar valves. 
 Thus the presphygmic period in the apex tracing exactly corresponds to the 
 period between the summit of the wave a in the venous pulse due to the 
 auricular systole, and that of the wave c due to the carotid pulse. A few 
 beats of the carotid are given, which can be taken as a standard of time to 
 verify all these points. The period G is due to the filling of the ventricle. 
 
 § 84. Significance of the inverted cardiogram It is asserted in 
 
 textbooks that an indrawing of the apex during systole of the ventricles is 
 a diagnostic sign of adherent pericardium. I have had several cases where 
 I have got at one time tracings of the apex beat due to the left ventricle, 
 and at other times tracings due to the right ventricle, with indrawing during 
 systole ; and at the post-mortem examination there has never been found 
 any signs of adherent pericardium. 
 
 The fact that ' the lowest and outermost point of the heart which strikes 
 against the chest-wall ' may be due to the right ventricle should be borne 
 in mind. Whenever that occurs, the cardiogram is an inverted one — that 
 is to say, there is a shrinking of the heart from the chest-wall during the 
 systole and a protrusion during the diastole of the ventricles. This is not 
 always recognizable at first sight. Being somewhat familiar with the 
 form of various apex-beat curves, I generally have no difficulty in recog- 
 nizing cardiograms due to the left ventricle. But when from a patient 
 I took Fig. 34, I certainly was misled in the first instance. The abrupt rise 
 and fall bear a close resemblance to an apex-beat curve due to the left ven- 
 tricle. Careful measurements of the radial and apex tracings show that the 
 elevation in Fig. 34 was not at the period of ventricular systole, but occurred 
 during ventricular diastole, while the systolic period {E) corresponded with 
 the fall in the tracing. It is necessary to insist upon this view, because 
 inferences drawn from the apex beat alone are liable to lead one into error.
 
 88 DISEASES OF THE HEART 
 
 Even so careful an observer as Keyt ^^'^ has mistaken the nature of such an 
 apex-beat tracing, and. imagined in consequence that he detected an extreme 
 delay in the appearance of the arterial pulse. I have observed similar 
 errors of interpretation in the tracings of other %^Titers. It follows then 
 that for a guide to any event occurring during a cardiac revolution the 
 arterial pulse is the only safe and reliable one. When the apex beat is 
 taken as a standard, careful inquiries should be directed to ascertain its 
 true nature. While it is true in the majority of instances that the cardio- 
 gram from the right ventricle is ' inverted ', I have taken tracings with 
 a systolic plateau from the third and fourth interspaces near the sternum, 
 but as I have had no post-mortem examination in these cases I am not sure 
 of the part of the heart producing these curves. The whole subject of 
 cardiography is in great need of thorough and painstaking investigation. 
 
 Apex beat\ 
 
 Radial 
 
 ^-J^^ 
 
 Fig. 34. Simultaneous tracings of the apex beat and of the radial 
 pulse. The rise in the apex tracing resembles the usual characters 
 present in a tracmg of the apex beat due to the left ventricle. On 
 analysis it is found that the elevation is during the diastole, and the 
 fall (E) during the systole, of the ventricle. 
 
 § 85. Alteration of the apex beat due to retraction of the lung. — 
 
 If one watches the progress of a case of advancing heart failure over a period 
 of years, marked changes -sviU sometimes be detected not only in the character 
 but in the position of the apex beat. In the earlier stages of heart failure, 
 due to mitral disease, for instance, the left ventricle may be pushed back 
 by the distended right ventricle, so that it is entirely covered by the lung, 
 and the apex beat may then be due to the right ventricle. In course of time, 
 from pressure of the enlarged heart, the lung is compressed and recedes, 
 leaving a large surface of the heart bare to the chest -wall. In such cases 
 the apex beat may be found in the posterior axillary line and in the eighth 
 interspace. The tracing obtained then is one due to the left ventricle. 
 
 § 86. The shock due to the ventricular systole I am of opinion 
 
 that a good deal of confusion in regard to the correct interpretation of the 
 heart movements has arisen from associating the shock conveyed to the 
 chest-wall, when the ventricles pass into systole, with the apex beat. The 
 apex beat and this impulse have become so connected that it is assumed
 
 POSITION AND MOVEMENTS OF THE HEART 89 
 
 that they are one and the same thing. The apex beat due to the left ven- 
 tricle is a movement which lasts during the whole of the ventricular systole ; 
 the shock caused by the ventricular contraction endures but a short space 
 of time, and occurs while the ventricular muscle suddenly hardens and 
 corresponds with the upstroke only of the apex beat {D, Figs. 21 and 22). 
 It is this shock which sends the lever so high in Figs. 24 and 33, at the 
 beginning of the ventricular contraction. In the tracings of the epigastric 
 pulse (Figs. 29 and 30), and of the movement from the front of the heart 
 (Fig. 26), this shock causes the sharp elevation just before the faU [E) due to 
 the emptying of the ventricle. Thus, in noting the time of the shock and 
 watching the epigastric pulse, for instance, as in Figs. 29 and 30, one could 
 see that the retraction of the epigastrium followed it. If one associated 
 the shock with the apex beat, it would therefore be assumed that the pro- 
 trusion corresponded with the systole, and the retraction with the diastole. 
 It frequently happens that this shock is the only movement of the heart 
 discernible on examining the chest. It is often markedly present in dilata- 
 tion of the heart, when the heart's surface in contact with the chest-wall is 
 entirely made up of the right ventricle and auricle. In such cases it must 
 not be assumed that the shock is the evidence of the contraction of the 
 right ventricle only. It is impossible to distinguish the shock due to the 
 right ventricle from the shock due to the left. The reason I insist upon 
 this is because the perception of this shock has been assumed to be an evidence 
 of the right heart contracting when the absence of a beat in the radial pulse 
 was supposed to indicate the absence of a contraction in the left ventricle. 
 As will be shown later, this sort of evidence is not only unreliable but 
 actually misleading.
 
 CHAPTER XI 
 
 Examination of the Arterial Pulse 
 
 § 87. Superiority of the digital examination. 
 
 88. What is the pulse ? 
 
 89. Inspection of the arteries. 
 
 90. Digital examination of the arteries. 
 
 91. The value of a sphygmogram. 
 
 92. Definition of a sphygmogram. 
 
 93. Events occurring during a cardiac revolution revealed by the sphygmogram 
 
 (a) the systolic period, (b) the diastolic period. 
 
 94. Features of the sphygmogram due to instrumental defect. 
 
 § 87. Superiority of the digital examination In the examination 
 
 of the arterial pulse, several methods may be employed, as exploration by 
 the finger, by graphic records, and by instrumental measurement of the 
 arterial pressure. By far the most important of these methods is the first. 
 There is a tendency to exalt the others at the expense of the digital, but no 
 apparatus can ever replace the trained finger. No doubt the other methods 
 can give very definite information of a limited kind, but in diagnosing the 
 patient's condition, they should only supplement the digital examination. 
 
 The mechanical methods can be of use, however, in enabling us to 
 appreciate the meaning of the sensation felt by the finger, and the attempt 
 should always be made to correlate these sensations with the results obtained 
 by the more elaborate means. 
 
 Warning must be given against estimating the patient's condition by 
 the study of the pulse alone ; any definite result obtained must only be 
 employed as one of a group of symptoms on which the ultimate opinion 
 is based. 
 
 § 88. What is the pulse ?— In order fully to appreciate the study 
 of the arterial pulse, it is essential to have a proper conception of the true 
 nature of what it is we perceive when we examine the pulse with the finger. 
 Broadbent ^^® very properly calls attention to a universal misconception of 
 what the pulse is, and points out that it is not an expansion of the artery 
 due to the blood discharged into the]aorta. Marey ^^^ says that the expansion
 
 EXAMINATION OF THE ARTERIAL PULSE 91 
 
 is so slight that many physiologists have denied its existence, and he states 
 that Poiseuille has demonstrated that in the larger arteries a slight expansion 
 with each systole does take place. No doubt the aorta and its primary 
 branches are somewhat dilated by the injected blood, but whatever the 
 expansion may be in them, in the carotid and radial it must be very minute. 
 To feel the pulse or to take a tracing, it is necessary that the artery should 
 be flattened against the bone. Lister states that it is for this reason that 
 surgeons operating in close proximity to a large artery may be utterly uncon- 
 scious of its neighbourhood, unless they inadvertently wound it or recognize 
 its pulsation by having compressed it against some resistant structure. 
 The visible movements of the artery are extremely deceptive. They often 
 give the appearance of contracting and expanding, but if the movement 
 be critically examined, it will be found to be, in reality, a displacement of 
 the artery. A straight artery like the carotid resembles somewhat a cord 
 
 FiC4. 35. The upper tracing was taken with the receiver over 
 the carotid artery, at the same time as the lower one was taken 
 with the receiver placed by the side of the carotid artery. The 
 lower tracing is the inverse of the upper. 
 
 that is periodically tightened and slightly relaxed. During the systole of 
 the ventricle, the carotid is straightened and tightened, and it becomes 
 slightly relaxed during the ventricular diastole. In persons with thin necks 
 this movement can be studied. If we place one receiver over the carotid 
 and one alongside it, and have the movements properly registered, the one 
 tracing will be found to be the exact reverse of the other (Fig. 35). If the 
 artery expanded during the ventricular systole, it would naturally thrust 
 out aU the tissues surrounding it, and the tracing from the side would then 
 be an exact duplicate of the one taken from the front of the artery. The 
 movement, then, of the beating carotid is one of displacement of the whole 
 vessel, not a dilatation and contraction of the vessel. 
 
 A similar confusion arises in studying an artery when it is tortuous. 
 In looking at the radial when it is tortuous, one can readily imagine that the 
 rising and falling of the artery is really a distension and contraction of the 
 artery. But if a suitable case be taken where in the course of the tortuous 
 artery there is a short lateral bend, the movement can be demonstrated
 
 92 
 
 DISEASES OF THE HEART 
 
 to be due to the displacement of the artery, and not due to expansion and 
 contraction of the artery. If the pad of the sphygmograph spring be placed 
 close to the artery on the concave side of the bend, and a tracing taken, 
 it will be found that during the ventricular systole the bend is exaggerated, 
 the artery being pushed farther away from the straight course, and during 
 ventricular diastole the bend diminishes. If tracings be taken of the pulse 
 in such a radial artery at the same time as the carotid pulse (Fig. 36), it will 
 be found that the radial gives an inverted tracing comparable to that in the 
 preceding figure. If the visible movement were due to the expansion and 
 contraction of the artery, the lever would, on the contrary, rise during systole 
 and fall during diastole, as in an ordinary sphygmogram. 
 
 What we recognize then as the pulse is the sudden increase of pressure 
 within the artery pressing against our finger when we compress the artery. 
 With the cessation of the ventricular systole the resistance to our finger 
 steadily diminishes until the next ventricular systole suddenly rises. 
 
 Fig. 36. Simultaneous tracings of the carotid and radial pulses. The radial tracing was 
 taken by placing the pad of the sphygmograph by the concave side of a bend of the tortuous 
 radial artery. During systole the artery receded from the sphygmograph and returned during 
 diastole, and hence the tracing obtained is an ' inverted sphygmogram '. 
 
 Broadbent ^^^ uses the folloAving apposite illustration : ' Such a pulsation can 
 be felt on a large scale by placing the foot on the inelastic leather hose of a 
 fixe-engine in action, in which there can be no expansion.' 
 
 To speak of the pulse as being the expansion and contraction of the 
 arterial walls, or ' the swinging backwards and forwards of the arterial wall ', 
 is not only to use language of exaggeration, but to convey a totally erroneous 
 conception of what the pulse reaUy is. 
 
 § 89. Inspection of the arteries — Inspection of the arteries reveals 
 in health but little movement. Conditions giving rise to forcible action of 
 the left ventricle may render the pulse visible in some of the superficial 
 arteries. Exertion, excitement, or the febrile state may induce visible 
 beating of the carotids, while this is a marked feature when the arteries are 
 tortuous and atheromatous, and in such a disease as exophthalmic goitre. 
 In free aortic regurgitation, not only is there marked pulsation of the carotids, 
 but pulsation is visible in numerous superficial arteries in various situations.
 
 EXAMINATION OF THE ARTERIAL PULSE 93 
 
 The tortuous character of superficial arteries is visible in arterial degene- 
 ration. 
 
 § 90. Digital examination of the arteries — It is usual in the routine 
 examination of the pulse to place two or three finger tips on the radial 
 artery near the Avrist. The fingers are laid on the artery, and moved upwards 
 and downwards and across the artery, at first gently, and then with more 
 pressure. By this procedure a knowledge of the size of the artery and the 
 conditions of its walls is acquired. Steady pressure being applied in order 
 to obliterate the pulse, the force required to attain this gives an idea of 
 the arterial pressure, and of the character of each individual pulse-wave. 
 It is a good thing to practise the digital examination of the pulse with 
 sphygmographic tracings taken at the same time. By this means, the 
 character of the pulse will be better appreciated by the finger. 
 
 The condition of the walls. — We recognize the yielding nature of the 
 arterial coats in healthy arteries. In degeneration of the coats the arterial 
 walls may be universally thickened, or contain bead-like patches of induration 
 as in atheroma, or the artery may have become a rigid tube as in calcareous 
 degeneration. 
 
 The size of the artery. — The variations in size depend entirely upon 
 the degree of relaxation of the muscular coat of the artery. A large artery 
 is not necessarily significant of a strong pulse, nor a small artery of a weak 
 pulse. An increase in the size of the artery frequently implies diminished 
 opposition to the work of the heart. The size of the artery can sometimes 
 be readily appreciated by lightly rolling it under the fingers. At other times 
 it can only be detected when the pulse is elicited by firm pressure at the 
 place where we expect to find it. This difficulty may occur where there 
 is a good-sized artery embedded in a fat, well-padded wi'ist, or where the 
 artery is small and contracted. On the subsidence of a fever, a notable 
 diminution in the size of the artery can often be readily recognized. 
 
 The arterial 'pressure. — The trained finger is as yet the best guide we 
 have in judging the pressure within an artery. The knowledge necessary 
 to determine what is normal and what is abnormal, can only be acquired 
 by the constant study of the pulse. The finger tips become so educated 
 in course of time that we readily appreciate the sensation conveyed in 
 compressing an artery (see Chapter XII). 
 
 The pulse-rate. — The reckoning of the pulse-rate should be made at 
 a late stage in the examination. When abnormally quicls, it should be 
 again counted when the patient has regained his composure. It is best 
 enumerated in two separate half-minutes, to ascertain if the heart is acting 
 quite steadily. In children, unless asleep, abnormal frequency is often
 
 94 DISEASES OF THE HEART 
 
 very unreliable as a guide, as the presence of the doctor often keeps up a con- 
 tinued excitation of the heart. While the rate of the pulse normally indicates 
 the number of the contractions of the left ventricle, it sometimes happens 
 that these are so weak that some of the pulse-waves are not perceptible to 
 the fingers. In such cases the pulse is usually slow or irregular in rhythm. 
 To appreciate the significance of the pulse-rate, due regard should be paid 
 to the age and idiosyncrasies of the patient, and to the ailment from which 
 he suffers. 
 
 The size of the pulse-wave. — The trained finger can recognize a great 
 variety in the apparent volume of the wave itself. Some waves seem to 
 roU up under the finger, passing gradually away, while others pass quickly, 
 giving a mere flick to the finger. 
 
 The impact of the pulse-ivave on the finger. — This may be quick and 
 abrupt, and the pulse-wave quickly disappear (pulsus celer), or the impact 
 may approach the finger gradually and gradually subside (pulsus tardus). 
 Although the pulse-wave occupies such a short space of time, yet the sensitive 
 finger readily recognizes these different features. 
 
 The rhythm of the pulse. — The beats usually follow one another at 
 regular intervals, and should be of equal strength. The divergencies from 
 the normal rhythm are numerous, and the usual terms employed to distin- 
 guish them are, in my opinion, both unsatisfactory and misleading, but 
 this subject is fully entered into later. In estimating the rhythm of the 
 pulse, one's whole attention should be concentrated upon the observation. 
 If one does not exclude other thoughts from the mind, a variation in the 
 pulse rate and strength may apparently be felt. This is due to a failure 
 to appreciate the pulse during a remission of the attention. I have not 
 only been conscious of this myself, but in cases where it was important to 
 note the fact, as in pneumonia, I have found my colleagues describing 
 irregularity as being present, when careful examination revealed a perfectly 
 regular pulse. 
 
 The two radial jmlses compared. — Finally, the two radial pulses should 
 be compared, and any difference in the character of the beats noted. 
 A difference in the strength of the two pulses may be due either to an 
 abnormal distribution of the arteries on one side, or to an interference with 
 the lumen of a vessel on one side. A difference in the character of the pulse 
 usually occurs only in the latter case. The two most frequent conditions 
 altering the character of the pulse on one side, are the presence of an 
 aneurysm or of an atheromatous plate, diminishing the lumen of the vessel, 
 on the proximal side of the place where the pulse is examined. 
 
 § 91. The value of a sphygmogram — Although the sphygmogram
 
 EXA^IINATION OF THE ARTERIAL PULSE 95 
 
 represents the variations in arterial pressure, and although it can give 
 information in this respect, yet there are so many sources of error, that it 
 cannot be trusted implicitly. Its greatest service is in giving an accurate 
 record of the movements of the left ventricle. However eloquent may be 
 the words of a writer, he cannot in a page convey as clear an idea of the 
 rhythm of a heart as a simple pulse-tracing, and if writers had given us 
 more pulse-tracings their works would have been greatly enhanced in value. 
 It is because it gives us a permanent and accurate record, that a tracing of 
 the arterial pulse is of such great value. When we seek to find the nature 
 of any movement of the circulation by recording it graphically, the arterial 
 pulse is the best and most useful standard by which we can find its position 
 in the cardiac cycle, as will be shown later. 
 
 § 92. Definition of a sphygmogram. — When the spring of a sphygmo- 
 graph is so accurately adjusted on an artery that it does not obliterate 
 the artery when the arterial pressure is at the lowest, and still slightly com- 
 presses the artery when the arterial pressure is at the highest, the spring 
 will oscillate with each variation of pressure within the vessel. This oscil- 
 lation being communicated to the lever and recorded on the tracing-paper 
 gives us a series of wavy lines, which represent the variations of the pressure 
 within the artery. A sphygmogram may therefore be defined as a diagram- 
 matic representation of the variations of pressure within an artery. If 
 we knew exactly the amount of pressure exercised by the spring, we should 
 be able to obtain the value of each movement. But the possibilities of error 
 are so numerous that it is useless to draw conclusions from the amount of 
 pressure supposed to be exercised. From the examination of a tracing 
 we obtain information on three different points : first, concerning the rate 
 and rhythm of the heart's action ; second, concerning the sequence of certain 
 events occurring in a cardiac revolution ; third, concerning the character 
 of the blood-pressure within the artery. 
 
 § 93. Events occurring during a cardiac revolution revealed by the 
 sphygmogram. (a) The systolic i:)eriod. — If we take a sphygmogram we 
 can divide the cardiac cycle into two periods : one {E, Fig. 37) during which 
 the aortic valves are open and the ventricle pours its contents into the aorta, 
 and another {G, Fig. 37) during which the aortic valves are closed and the 
 ventricle is in diastole. For the sake of convenience in describing sphygmo- 
 grams these two periods \vill be referred to as the systolic and diastolic 
 periods, although in the space G the presphygmic and postsphygmic periods 
 of the ventricular systole are included (Fig. 43). The character of the systolic 
 portion varies very much in different individuals. These variations depend 
 mainly on the amount of resistance offered by the arteries to the ventricular
 
 96 
 
 DISEASES OF THE HEART 
 
 systole. In such a tracing as Fig. 37 there is first an abrupt rise (p), then 
 a faU followed by a continuation of the wave (s) at about the same level. 
 This period is usually described as being divided into two, the abrupt rise 
 being spoken of as the primary or percussion wave, and the latter portion 
 as the tidal or predicrotic wave (the papillary wave and outflow remainder 
 wave of Roy and Adami). This division has led to the idea that these 
 represent two different events in the pulse itself. As a matter of fact, the 
 
 Fig. 37. Sphygmogram of the radial pulse. The space E 
 is the period of ventricular systole when the aortic valves are 
 open ; the space G the period of ventricular diastole ; s is the 
 pulse-wave due to the ventricular systole ; n the aortic notch ; 
 d the dicrotic wave ; and p a wave due to instrumental defect. 
 
 abrupt rise 2^ above the level of the wave s is due to instrumental defect, 
 and the whole period E is occupied by the ventricular pressure forcing blood 
 into the arterial system, and corresponds with the period E in Fig. 43. In 
 cases where the arterial pressure is low relatively to the strength of the 
 ventricular systole, these two waves are so blended together that so-called 
 percussion and tidal waves can no longer be differentiated (Fig. 38). The 
 whole of this period E in the tracing will hereafter be referred to as the 
 systolic period, and the wave s as the systolic wave, as it represents the 
 
 Fig. 38. The letters have the same significance as in Fig. 37. 
 
 period of ventricular systole when the ventricle and arterial system are in 
 free communication. 
 
 (6) The diastolic period. — With the closure of the aortic valves, the 
 arterial pressure faUs rapidly to the bottom of the aortic notch 7i (Figs. 37 
 and 38). In the tracings this is seen to be at the beginning of the diastolic 
 period. This fall is interrupted by a distinct rise in the pressure represented 
 by the dicrotic wave d. There has been a good deal of discussion concerning 
 the cause of the dicrotic wave. The following explanation seems to me the 
 most probable. The semilunar valves are so delicately constructed that
 
 EXAMINATION OF THE ARTERIAL PULSE 
 
 97 
 
 they readily respond when the pressure on one side rises above that on the 
 other. As soon as the aortic pressure rises above the ventricular the valves 
 close. At the moment this happens the valves are supported by the hard, 
 contracted ventricular walls. The withdrawal of the support by the sudden 
 relaxation of these walls will tend to produce a negative pressure wave in 
 the arterial system. But this negative wave is stopped by the sudden 
 stretching of the aortic valves, which, on losing their firm support, have now 
 
 Fig. 39. A strong- beating ventricle has jerked tlie lever high above the true systolic wave, 
 and the falling lever has made an artificial notch on the systolic wave s. The true pulse curve 
 is probably represented in the dotted tracing. 
 
 themselves to bear the resistance of the arterial pressure. This sudden 
 checking of the negative wave starts a second positive wave, which is pro- 
 pagated through the arterial system as the dicrotic wave. After the dicrotic 
 wave the arterial pressure-curve gradually falls. Occasionally there are 
 slight waves in the fall, but these are of doubtful import. 
 
 § 94. Features of the sphygmogram due to instrumental defect. — 
 In the study of sphygmographic tracings one has always to bear in mind that 
 
 Fig. 40. The forcible changes in pressure have exaggerated the height and depth 
 
 of all the waves. 
 
 certain features may be due to the instrument itself. Speaking generally, 
 these instrumental features occur where there are sudden and forcible 
 changes in the arterial pressure. The most frequent of these is the jerking 
 up of the spring by the systolic wave itself. Then the next most frequent 
 is the formation of a notch on the tracing of the systolic wave, due to the 
 sudden fall of the spring after being jerked high up, as in Fig. 39. Occa- 
 sionally one finds the aortic notch artificially deepened by the sudden 
 lowering of the pressure, as in Fig. 40. 
 
 MACKENZIE jj
 
 CHAPTER XII 
 
 Arterial Pressure 
 
 § 95. The cause of arterial pressure. 
 
 96. Methods of measuring the blood-pressure. 
 
 97. Increased blood-pressure. 
 
 98. Hyperpiesis. 
 
 99. Effect on the heart of increased peripheral resistance. 
 
 100. Increased arterial pressure and heart failure. 
 
 101. Treatment of high arterial pressure. 
 
 102. Diminished arterial pressure. 
 
 § 95. The cause of arterial pressure — When the left ventricle 
 contracts it drives the blood into the arterial system. The escape through 
 the arterioles and capillaries is retarded, so that the blood continues to flow 
 after the ventricle has ceased to contract. As a consequence of this, the 
 arteries are slightly distended during ventricular systole, and their elastic 
 coats compress the column of blood within them after the ventricular systole 
 is over, and thus maintain a degr.ee of arterial pressure during the period 
 in which the ventricle is not acting. The ventricular force is thus stored up 
 by the distension of the elastic coats of the arteries, and hberated during 
 the ventricular diastole. 
 
 The chief factors therefore concerned in the maintenance of arterial 
 pressure are the ventricular systole, the peripheral resistance, and the elastic 
 recoil of the arteries. The viscosity of the blood is also a factor in the 
 raising of the arterial pressure. 
 
 § 96. Methods of measuring the blood-pressure Of late years 
 
 many instruments have been devised to measure the arterial pressure. 
 The majority are constructed on the principle of compressing the brachial 
 artery with an air-bag embracing the upper arm. Air is pumped into the 
 bag, and its pressure is measured by a mercury manometer in connexion 
 with it. When the pressure is raised sufficiently to obliterate the radial pulse, 
 we obtain the only really trustworthy standard, and it is this I refer to here- 
 after as ' arterial or blood pressure '. Attempts have been made to estimate 
 the systolic, mean, and diastolic pressures by observing or recording the 
 movements communicated to the column of mercury by the compressed 
 artery. It is found that, during the gradual compression of the artery, 
 oscillations due to the pulse beat occur in the mercury. These oscillations 
 begin, gradually reach a maximum, and gradually decrease as the pressure
 
 ARTERIAL PRESSURE 99 
 
 is raised or lowered. Far-reaching deductions have been drawn from the 
 changes in these oscillations. I think, if the cause of these oscillations be 
 properly appreciated, no safe deductions can be drawn as to what is called 
 the systolic, mean, or diastoUc pressures. When the pressure within the 
 air-bag corresponds to that of the artery, the arterial pulse communicates 
 its impact to the air in the bag, and thus induces the oscillation of the 
 mercurial column. The size of these oscillations depends on the amount 
 of movement of the arterial wall. Let the Hnes, A, B, Fig. 41, represent the 
 walls of the artery, and for simpUcity assume that the pressure is applied 
 to one side only of the vessel. It is found that a pressure of 160 millimetres 
 obliterates the arterial pulse, the wall A being flattened down on B with such 
 force that no blood passes through, and there is no oscillation of the mercurial 
 
 Fig. 41. Diagram to show the nature of the oscillations of the mercurial column in esti- 
 mating the blood-pressure. A and B represent the walls of the brachial artery. At 160 the 
 lumen of the artery is obliterated by the pressure of an air-bag embracing the upper arm. As 
 the pressure is gradually lowered in the bag, each beat of the artery produces a movement of 
 the mercury in the manometer, the movement being represented by the elevations in the 
 diagram. With diminution of pressure there is at first a gradual increase in the extent of the 
 movement followed by a gradual decrease until the pressure in the air-bag ceases to compress 
 the artery. From this it is shown that there is no definite period which can be said to corre- 
 spond to the systolic, diastolic, or mean blood-pressure. 
 
 column. When the pressure is lowered to 150, a small wave escapes during 
 systole which raises the wall to a slight extent, and gives rise to a small 
 oscillation. At 140 a larger wave escapes, but the pressure of 140 is still 
 sufficient during a portion of diastole to flatten the wall A against B. At 
 130 the pressure no longer flattens the wall A against B, but the flow 
 escapes during diastole, and the oscillation reaches its maximum. With 
 the gradual lowering of the pressure, the maximum oscillation persists. 
 At 110 the artery is fully distended during systole, and only partially 
 compressed during diastole, but the pulsation is still maximal. As the 
 pressure falls there is a decrease in the compression of the artery and 
 a corresponding decrease in the size of the oscillation, until the pressure 
 fails to compress the artery sufficiently to produce any movement. From 
 this way of looking at the matter, it wiU be realized that at no definite period 
 
 h2
 
 100 DISEASES OF THE HEART 
 
 can we tell when the record represents a systolic, a mean, or a diastolic pres- 
 sure, and that the maximal oscillation may last through a considerable 
 range of pressure with nothing to guide one to the moment when any definite 
 pressure could be ascertained. The diagram may not represent the condition 
 of affairs in every case, and a limited usefulness may possibly be found in 
 noticing the period of maximal oscillation and its decline, but so far, I think, 
 no very reliable conclusion can be drawn. 
 
 The force required to obliterate the pulsation in the radial artery is fairly 
 easily ascertained, and from it certain limited inferences may be drawn. 
 It is doubtful if it represents the actual arterial pressure within the artery, 
 for an escape can take place imperceptible to the finger, and certain external 
 conditions may affect the pressure. It is usually assumed, for instance, 
 that the arterial wall and its coverings offer such a slight resistance as to 
 be negligible. Russell ^^^ on the other hand, asserts that the thickening or 
 contraction of the artery may have a very considerable effect, and that 
 thick, sclerosed, and contracted arteries may offer such resistance that 
 a considerable proportion of the pressure may be spent in overcoming it, 
 OUver ^2 has shown that the pressure obtained by instruments may vary in 
 different arteries in the same individual, while L. Hill's observations ''^ show 
 that the arterial wall can have only a very slight influence in the instru- 
 mental observation of the blood-pressure. 
 
 There are a great many different instruments devised to take the arterial 
 pressure. Most of them are somewhat cumbrous, and some patients resent 
 the disagreeable sensation produced by compressing the upper arm. Hence 
 these methods are not likely to receive that general application which the 
 need for ascertaining the blood-pressure requires. L. Hill has recently 
 invented an extremely simple and practical method. In place of a cuff 
 surrounding the upper arm, he uses a small bag which is compressed over 
 the radial artery until the pulse disappears below the place of compression. 
 The bag is connected with a very simple manometer, which can be carried 
 in the waistcoat pocket. 
 
 Erlanger ^* and Gibson '^^ have invented methods for graphically record- 
 ing the blood-pressure. The tracings from Gibson's apparatus seem very 
 instructive, but I have no experience in the use of his apparatus. 
 
 A great deal has been written about blood-pressure and its estimation 
 in practical medicine, but it must be confessed that much of it has been 
 of little practical value, and much careful observation, extending over many 
 years, on individual patients, will be necessary before any sure and certain 
 result is obtained. The remarks I make on the subject are based on the 
 examination of numerous patients in the endeavour to ascertain some sure
 
 ARTERIAL PRESSURE 101 
 
 foundation on which to base the application of the method in the chnical 
 examination of heart affection. 
 
 § 97. Increased blood-pressure — In many cases, one can corro- 
 borate by instrumental observation the knowledge previously acquired by 
 the finger, that the pressure in the arteries increases in certain diseased 
 conditions, as Bright's disease, and with advancing years. As the increased 
 pressure of advancing years is associated with arterial changes, the question 
 of cause and effect is a very difficult one to solve. On the one hand, the 
 changes in the blood-vessels undoubtedly tend to raise the blood-pressure, 
 wliile it is contended that these are induced by the blood itself containing 
 ingredients that provoke a contraction of the arterioles, in consequence of 
 which the muscular coat hypertrophies. A rise in pressure seems to induce 
 atheromatous degeneration, and this in turn causes a rise in pressure, and 
 thus a vicious circle may be formed. The fact is undoubted, that arterial 
 changes and high blood-pressure are very frequent phenomena in advanced 
 life. The changes are so insidious that they rarely come under consideration 
 until they are well established. One may infer, indeed, that such changes 
 are occurring in middle life, when one notices a tortuous temporal artery, 
 but it is rare that the condition gives any cause for anxiety until it is well 
 established. 
 
 It is a mistake, and one made not infrequently, to begin treating the 
 high blood-pressure as if it were a disease. Happily the efforts employed 
 to reduce the blood-pressure are usually of little value. In order to appre- 
 ciate the meaning of high blood-pressure, it is well to consider the condition 
 associated with its production, for I think it has a significance beyond that 
 of being a manifestation of disease. 
 
 I have already pointed out that the arterial pressure is maintained 
 chiefly by the force of the left ventricle, the peripheral resistance, and the 
 elastic recoil of the arteries. The necessity for the pressure is the regular 
 and equable supply of blood to the organs and tissues. Between the heart 
 and tissues there is an intimate association, whereby the supply to the 
 tissues and organs is moderated by their requirements — the heart beating 
 more forcibly and more rapidly, and the peripheral resistance diminishing 
 when there is an urgent need, by the exercise of the functions of the organs. 
 With advancing age, thi'ee great changes occur in the blood-vessels. The 
 elasticity of the arteries diminishes. The result of this is that there is no 
 longer the same equable maintenance of the pressure during diastole. The 
 arteries approximate the condition of rigid tubes where the force exerted 
 by the left ventricle is not sufficiently stored up in the elastic coats, to be 
 liberated during diastole. The loss of this assistance necessitates increased
 
 102 DISEASES OF THE HEART 
 
 force of the ventricular contraction, and therefore an increase of the pressure 
 during ventricular systole. In the arterioles there may be an increase of 
 the muscular tissue, and this implies an increase in functional activity 
 with an increase of the peripheral resistance. These are the two factors 
 that are generally assumed to be the cause of increased blood-pressure, 
 but there is a third which has not received that consideration to which it is 
 entitled, namely, the diminution of the capillary field. This can be recognized 
 in various ways, as, for instance, the thinning and wasting of the skin and 
 subcutaneous tissues, and by the absence of oozing in surgical operations. 
 The manner in which it raises the blood-pressure is simply by narrowing 
 the passage of outflow (see § 221). 
 
 § 98. Hyperpiesis. — In the routine examination of patients we meet 
 occasionally with some, usually middle-aged, sometimes young, who show 
 considerable fluctuations in blood-pressure. Periods of high arterial pressure 
 (hyperpiesis of Clifford Allbutt ^^) may be associated with some discomfort, 
 as mental dullness, headache, &c. These periods can be cut short by a smart 
 purge, bodily exercise, &c., or they disappear from no ascertainable cause. 
 It is possible the periods of high arterial pressure are due to faulty metabolism, 
 but they will be found to recur in spite of the greatest care in diet. It is 
 said by some that these periods of high blood-pressure are the cause of 
 arterial degeneration, but, with an imperfect knowledge of all the factois 
 we are not in a position to decide. 
 
 § 99. Effect on the heart of increased peripheral resistance. — 
 I have mentioned that the connexion between the heart and the tissues is so 
 intimate that the demand from the tissues is responded to by stronger con- 
 traction of the heart. When, therefore, one or all of these causes increasing 
 the peripheral resistance are in action, the heart, in order to supply the 
 tissues with blood, has to exert more force in its contraction. It accommo- 
 dates itself to its ever-increasing burden by calling upon its reserve, and the 
 only evidence that it has more to do is in the hmitation of its field of response. 
 One can almost say, when an individual realizes the fact that a hill is not 
 climbed with the ease and comfort with which it used to be done, that already 
 the heart is meeting an increased peripheral resistance, and there is already 
 a slight exhaustion of its reserve force. This, as we know, is a very gradual 
 and long-continued process, beginning insidiously in the fourth decade of 
 life, and coinciding with the time at which athletes abandon the exercises 
 that call for long and severe exertion. 
 
 As the changes that increase the peripheral resistance tend slowly but 
 surely to advance, the work of the heart becomes ever greater, the field of 
 response becomes more limited, till finally the patient's attention is called 
 
 I
 
 ARTERIAL PRESSURE 103 
 
 by some disagreeable sensation to the fact of the great limitation, and so 
 we get heart failure. The peculiar feature of the heart failure that arises in 
 this way is, that the function of the heart that has most work to do usually 
 fails, namely, the function of contractility, so that it is in these cases of 
 high arterial pressure that we meet the most typical symptoms associated 
 with failure of the function of contractility. 
 
 But this is not all. The changes that have taken place in the arterial 
 walls in the periphery have at the same time been affecting the arteries 
 of the heart, with the result that the muscle-fibres are imperfectly nourished 
 and degenerate. It is in these cases of long-standing high blood-pressure 
 that we find the most striking evidence of degenerative changes in the heart 
 muscle associated with arterial degeneration, and it is wonderful how long 
 a heart extensively degenerated can maintain a high blood-pressure. 
 
 Such cases of degenerated arteries and long-continued high blood-pressure 
 end by a degenerated artery giving way and causing cerebral apoplexy, 
 or by failure of the heart. The latter may come about in various ways : by 
 a sudden change in the inception of the heart's contraction — for it is in these 
 cases we frequently find the extra-systole and nodal rhythm — by gradual 
 exhaustion of the contractihty, often with angina pectoris, and on rare 
 occasions by rupture of the heart. There may occur a somewhat sudden fall 
 in the arterial pressure from dilatation of the heart. When this occurs there 
 is a sudden change in the character of the symptoms which I have given 
 in some detail in the chapter on dilatation of the heart (Chapter XXIII). 
 
 § 100. Increased arterial pressure and heart failure From such 
 
 considerations it will be realized that we may have heart failure without 
 fall of blood-pressure, and this consideration brings clearly into view the 
 fact that heart failure in these cases is primarily a matter of exhaustion of 
 reserve force. In cases of valvular disease, as H. Starling ^' points out, there 
 may be marked failure of the heart with little or no fall in blood-pressure, 
 and recovery may ensue with little or no rise in blood-pressure. It will 
 be found, however, in these cases that the heart failure is not associated 
 with a loss of the function of tonicity. When dilatation occurs, then there 
 is usually a faU of blood-pressure, and recovery, when it takes place, is 
 accompanied by a rise of blood-pressure. 
 
 §101. Treatment of high arterial pressure. — It is an almost universal 
 custom to treat the signs of heart failure with ' cardiac tonics '. By cardiac 
 tonics are usually meant drugs or methods that are supposed to raise the 
 blood-pressure. Hence, when any disorder that implies inefficient action 
 of the heart is met, such drugs as digitaUs, or some methods of exercise and 
 baths supposed to raise the blood-pressure, are resorted to. It is manifest.
 
 104 DISEASES OF THE HEART 
 
 from the consideration of tlie causes that induce high blood-pressure, that_ 
 this treatment is iiuoiix'ct. Happily the methods and drugs have far less 
 effect than is supposed, and as rest is usually enjoined at the same time 
 the good results are due more to unconscious adoption of the best principle 
 of treatment than to the efforts that are supposed to be remedial. Manifestly, 
 in heart failure induced or aggravated by high pressure, the best line of treat- 
 ment is to ease the load and give the heart rest, to regain some store of 
 reserve force. Now there is a tendency to rush to the opposite extreme, 
 and to endeavour to reduce the blood-pressure by administering drugs of 
 the vaso-dilator class. Luckily, the administration of these drugs is of 
 little effect, and little or no permanent lowering can be obtained by their 
 use. It is manifest that with changed arteries, and a diminished capillary 
 outflow through obliteration of the capillary vessels, a high blood-pressure 
 is necessary to supply the organism with blood. If it were possible to 
 reduce the blood-pressure permanently in a man who for years had a blood- 
 pressure of 180-200 mm., the result would be impaired nutrition of the 
 organism. If the final breakdown of these patients be watched, it will not 
 infrequently be found that the blood-pressure does fall to 150 or 140 mm. Hg., 
 and the result is at once the appearance of the signs of extreme heart failure 
 — dropsy, enlarged liver, oedema of the lungs, &c. So serious is the signifi- 
 cance of a fall of blood-pressure in patients with cardio-sclerosis, even with , 
 attacks of angina pectoris, that the persistent fall of pressure is an evidence I ' 
 of the final exhaustion of the heart, though the anginal attacks may cease. ' 
 
 The principle I pursue with most success is to place the patient under l/ 
 conditions that give the heart less work to do, carefully avoiding ' cardiac Ij 
 tonics ' and ' vaso-dilators ', restricting the diet, evacuating the bowels, 3,ndAfl 
 permitting such exercise as the patient can undertake without distress,'|| I 
 according to the lines laid down in the chapter on treatment. 
 
 § 102. Diminished arterial pressure — The question of low pressure 
 and its significance is an extremely puzzling one. Here again one meets the 
 confident assertion, ' In hypotonic conditions give cardiac stimulants or 
 vaso-constrictors.' The matter is, however, far more complicated, and 
 I am only dimly groping after the true principles of treatment in these 
 cases. In dilatation of the heart, as best seen in mitral disease, the fall of 
 pressure may be considerable, and the administration of drugs of the 
 digitalis group has undoubtedly a most beneficial effect in improving the 
 patient's condition, and in raising the blood-pressure. But this is due to 
 the special effect that digitalis has upon the function of tonicity, both in the 
 heart and the arterial muscle-fibres. But in low pressure associated with 
 other conditions the drug is often of little avail.
 
 CHAPTER XIII 
 
 The Venous Pulse 
 
 § 103. What the venous pulse shows. 
 
 104. Inspection of the jugular pulse. 
 
 105. Methods of recording the jugular pulse. 
 
 106. The recognition of the events in a jugular pulse. 
 
 107. Description of the events in a cardiac cycle. 
 
 108. The causes of variation of pressure in the auricle and in the jugular vein. 
 
 109. Standards for interpreting a jugular tracing. 
 
 110. The carotid wave. 
 
 111. The notch on the ventricular wave. 
 
 112. The diastolic wave. 
 
 113. Changes due to variation in the rate of the heart. 
 
 114. Method of analysing a tracing. 
 
 115. The ventricular form of the venous j^ulse. 
 
 116. Conditions giving rise to a venous pulse. 
 
 § 103. What the venous pulse shows. — The consideration of the 
 circulation has so far been mainly concerned with the effects of the contrac- 
 tion of the left ventricle. When the apex beat is studied, or the characters 
 of the arterial pulse analysed, our purview is limited almost entirely to the 
 doings of the left ventricle. The arterial pulse indeed gives us a direct 
 knowledge of the left ventricle's action during but a portion of the cardiac 
 cycle, namely, during the period when the aortic valves are open. When 
 they are closed, we are no longer directly cognizant of what is happening 
 in the left ventricle. We come now to the study of a subject which gives 
 far more information of what is actually going on within the chambers of 
 the heart. In the venous pulse we have often the direct means of observing 
 the effects of the systole and diastole of the right auricle, and of the systole 
 and diastole of the right ventricle. The venous pulse therefore presents 
 a greater variety of features, and may manifest variations due to disease 
 which the study of the arterial pulse fails to reveal. 
 
 § 104. Inspection of the jugular pulse — In examining a patient for 
 pulsation in the jugular vein, it is generally best that he should lie down, 
 though in some rare cases, where the veins are greatly distended, the pulsa- 
 tion can only be recognized when the patient sits up. The pulsation is 
 most commonly limited to the internal jugular veins, and these veins, lying
 
 106 DISEASES OF THE HEART 
 
 alongside the carotid arteries, are never visible, being covered at the root 
 of the neck not only by the skin and sterno-mastoid muscle, but by a variable 
 quantity of adipose tissue ; one therefore recognizes the venous pulse only 
 by the character of the movements communicated to the structures covering 
 the vein. In that form of the venous pulse in which the principal wave is due 
 to the auricular systole, the sudden collapse of the tissues covering the vein 
 is more striking than the protrusion. If one further carefully times this 
 coUapse, it will be found to be synchronous with the arterial pulse. The pulse 
 in the internal jugular vein is often mistaken, even by experienced observers, 
 for * beating of the carotids '. But the carotid pulse is always abrupt and 
 sudden in its protrusion of the covering tissues, and gradual in the shrinking. 
 Furthermore, when one finds a small radial pulse and a large pulsation in 
 the neck, one may safely conclude that the neck pulsation cannot be carotid, 
 unless under very exceptional circumstances (as aneurysm). When the 
 pulsation is in the more superficial veins, as the external jugular, facial, 
 or superficial thoracic veins, the collapse of the vein synchronous with the 
 carotid pulse is usually easy of recognition. In another form of venous 
 pulse, where the pulsation is due to the ventricular systole, the engorge- 
 ment of the veins is usually so great, the arterial pulse so small, and the 
 cardiac mischief so evident, that the recognition of the venous pulse is 
 comparatively easy. 
 
 § 105. Methods of recording the jugular pulse Usually the move- 
 ments of the vein are best recorded with the patient lying down, the shoulders 
 slightly raised, the head comfortably supported by a pillow, and turned 
 shghtly to the right in order to relax the right sterno-mastoid muscle. The 
 receiver [E, Figs. 13, p. 68, and 18, p. 73) is placed over the jugular bulb 
 immediately above the inner end of the right clavicle, with just sufficient 
 pressure to shut off the interior of the receiver from the outer air. One may 
 have to shift the receiver about to get the best movement. The relation 
 of the jugular bulb to the surrounding structures is shown in Fig. 42, where 
 the circle above the clavicle indicates the position of the receiver. 
 
 Sometimes better tracings are got higher up in the neck or from the left 
 side. In great engorgement of the veins it may be possible only to get 
 a tracing when the patient is sitting up. The continued action of the 
 sterno-mastoid in laboured breathing may prevent a tracing of the jugular 
 pulse being obtained. 
 
 § 106. The recognition of the events in a jugular pulse There 
 
 is still much that is obscure about some of the details of the venous pulse, 
 and several of these are still the subject of controversy. In the following 
 interpretation I deal with the salient points which have thrown most light
 
 THE VENOUS PULSE 
 
 107 
 
 upon the obscure features of the heart's action. The movements of the 
 venous pulse are usually more numerous than those of the arterial, and in 
 the tracings a number of waves are present. As each of these indicates 
 a rise of pressure in the veins, the tracing can only be properly interpreted 
 when the force producing each rise of pressure is known ; and for this 
 purpose the time of appearance of each wave in the cardiac cycle must be 
 
 R ^ inaomiaate veia 
 
 Fig. 42. Shows the relation of the internal jugular vein to the carotid and subclavian 
 arteries, and to the sterno -mastoid muscle. The circle represents the position of the receiver in 
 taking a tracing. The spot at a is one inch from the internal end of the clavicle. (Keith.) 
 
 established. This is done by taking tracings of the venous pulse, at the 
 same time as some movement whose position in the cardiac cycle is definite, 
 and the arterial pulse, carotid or radial, is the most reliable. The apex 
 beat is often useful and convenient, but care is necessary in the employment 
 of the apex beat, as has already been pointed out (§ 84). 
 
 § 107. Description of the events in a cardiac cycle — In the diagram 
 (Fig. 43) there is represented a series of movements due to various forces
 
 108 
 
 DISEASES OF THE HEART 
 
 that occur during one cardiac cycle. If a wave be found in the vein, and if 
 its time of occurrence be ascertained by referring to the place it would 
 occupy in this diagram, we can usually find its cause by noting what force 
 is operative at that period. It must be added that while this diagram repre- 
 sents with fair accuracy the chief events in a cardiac revolution, it is 
 not asserted that it is correct in every detail. Authorities are not quite 
 
 Fig. 43. Semi-diagrammatic representation of the 
 auricular, ventricular, and aoi-tic pressures during one 
 cardiac revolution. D, the presphygmic period of the 
 ventricular systole ; E, the sjihygmic or pulse period ; 
 F, the postsphygmic period. The figures 1, 2, 3, 5, and 6 
 have the same significance as those in Fig. 46. The 
 divisions on the bottom line represent tenths of a second. 
 (After Frey.) 
 
 agreed on several smaU points, but it is sufficient for the purpose I have 
 in view. 
 
 What we have here presented are, the curves representing the variations 
 of (1) the pressure within the auricle ; (2) the pressure within the ventricle ; 
 (3) the pressure within the aorta. The spaces embraced by the perpendicular 
 lines represent respectively the time during which the semilunar valves are 
 open [E) and the auriculo-ventricular valves are shut {D, E, F). I would
 
 THE VENOUS PULSE 
 
 109 
 
 direct attention to the presphygmic period D, when the ventricular pressure 
 is rising, but has not yet opened the aortic valves ; and to the postsphygmic 
 period F, where the ventricular pressure is falhng after the closure of the 
 aortic valves. The curves indicating the pressures are approximately 
 correct, but are utilized here to show the periods when variations take place 
 in the pressure. Though the events in the diagram represent what happens 
 in the left side of the heart, there can be no doubt that the changes on the 
 right side are of the same character. 
 
 § 1 08. The causes of the variation of pressure in the auricle and 
 in the jugular vein.— The auricular pressure in Fig. 43 shows a series of 
 rises and falls, and these correspond to those in a venous pulse (Fig. 44), 
 The forces operative in producing the variations in the auricular pressure 
 
 Fig. 44. Simultaneous tracings of the jugular and radial pulses and of the carotid and 
 radial. The elevations a and v, and falls x and y in the jugular tracing correspond to those 
 in the auricular pressure-curve in Fig. 43. 
 
 are also acting in producing the jugular pulse. (The curves of auricular 
 pressure by different physiologists are very perplexing, some getting a 
 rise of varying duration during ventricular systole. I select Frey's as the 
 simplest and probably the truest.) 
 
 The auricular ivave (a) and fall {x). — The rise a in the jugular pulse, Fig. 44, 
 corresponds with the first abrupt rise a in the auricular pressure-curve, 
 Fig. 43, and both are due to the systole of the auricle. Neglecting the wave c 
 for discussion later, the fall x in the jugular pulse corresponds to the fall x 
 in the auricular pressure-curve, and occurs at the time the ventricle is in 
 systole. The fall is due to three factors : (1) the relaxation of the auricle 
 after its systole ; (2) the dragging down of the a. -v. septum by the ventricular 
 muscle, enlarging the auricular cavity as described in § 20, and Fig. 3 ; 
 (3) the diminished intrathoracic pressure in consequence of the expul- 
 sion from the chest of the contents of the left ventricle. When there is a 
 delay in the ventricular contraction, the factors may l)e separated as in
 
 110 
 
 DISEASES OF THE HEART 
 
 Fig. 112, p. 177, where x is due to the first factor, and x' to the second 
 and third factors. 
 
 The ventricular wave {v). — The rise v, after the fall x (Fig. 44), is due 
 to the storing of blood in the auricle during the time of the ventricular 
 systole, and corresponds with the second rise {v) in auricular pressure-curve 
 in Fig. 43. The termination of this rise in both figures is sudden, and due 
 to the opening of the auriculo-ventricular valves. While the beginning of 
 this rise is very variable, its termination is one of the most certain periods in 
 the cardiac cycle, indicating as it does the time of the opening of the tricuspid 
 valves. The variableness in its beginning is due to the fact that it owes its 
 origin to the quantity of blood stored in the auricle during ventricular 
 systole, and this varies in individual cases, and also in the same individual. 
 
 Fig. 45. Simultaneous tracings of the jugular and carotid pulses, showing that the waves 
 in the jugular correspond in time with the waves of increased auricular pressure in Fig. 43. 
 In this patient the tricuspid valves were partially destroyed and the orifice therefore markedly 
 incompetent, so that there was free tricuspid regurgitation. The wave v is therefore partly 
 due to blood regurgitating from the right ventricle. 
 
 with exertion and respiration. The blood comes mainly from the periphery, 
 pouring into the auricles through the veins. When the auricle becomes filled, 
 the surplus distends the superior vena cava and jugular, and hence appears 
 in the tracing as a wave. Another source is sometimes regurgitation through 
 the tricuspid orifice (see § 212). It is necessary to bear this in mind, as the 
 failure to recognize how tricuspid regurgitation would be manifested in the 
 venous tracing has led to a total misconception of the meaning and nature 
 of the ventricular form of the venous pulse. It has been assumed that in 
 tricuspid regurgitation the blood sent back into the veins would appear in 
 the jugular at the same time as in the carotid. In this assumption the effects 
 of a dilating auricle between the ventricle and veins has been overlooked ; 
 as a matter of fact, what happens is merely an increase in the amount of 
 blood accumulating in the auricle during the ventricular systole, and this 
 causes the appearance of the wave v to be somewhat premature. Thus, for 
 instance. Fig. 45 is from a case where there was a damaged tricuspid valve.
 
 THE VENOUS PULSE 
 
 111 
 
 so that regurgitation took place, and the wave v is seen to be of small size, 
 beginning early in the time of the ventricular systole (period E). 
 
 I call this wave {v) the ventricular wave, because of its association with 
 the systole of the right ventricle. Thus the termination of the wave is due 
 to the relaxation of the right ventricle and opening of the tricuspid valves ; 
 it is often made up of blood sent back through the incompetent tricuspid 
 orifice by the systole of the right ventricle ; though this wave may be small 
 and of brief duration in the auricular form of the venous pulse, it becomes 
 increased in size and the main or only wave in the ventricular form of the 
 venous pulse. 
 
 Fig. 46. Tracings of the jugular pulse, apex beat, carotid and radial 
 pulses. The perpendicular lines represent the time of the following events : 
 1, the beginning of the auricular systole ; 2, the beginning of ventricular 
 systole ; 3, the appearance of the pulse in the carotid ; 4, the appearance 
 of the pulse in the radial ; 5, the closing of the semilunar valves ; 6, the 
 opening of the tricuspid valves (compare with Fig. 43). 
 
 The fall (y) in Figs, 43 and 44 is due to the blood, that has been stored 
 in the auricle during ventricular systole, flowing into the ventricle after 
 the opening of the tricuspid valves. Then as the ventricle becomes filled, 
 stasis in the auricle and veins takes place, causing the rise between y and a, 
 Figs. 43 and 44, till the auricle again contracts. 
 
 § 109. Standards for interpreting a jugular pulse Such are briefly 
 
 the main factors concerned in the production of the auricular form of the 
 venous pulse. It is at times difficult to interpret the tracings, so that it is 
 necessary to have definite standards to help in deciphering certain obscure 
 features. 
 
 In Fig, 46 I have placed below the jugular pulse, tracings representing 
 the apex beat and the carotid and radial pulses, to show the relation in time 
 of certain events in these various movements. The numbered perpendicular
 
 112 
 
 DISEASES OF THE HEART 
 
 lines indicate the simultaneous events in the jugular pulse, the apex beat, 
 the carotid, and the radial pulse. The perpendicular lines facilitate the 
 comparison of the tracings at definite points in the cycle, and have the 
 same significance in the later tracings : 1, the beginning of the auricular 
 systole ; 2, the beginning of the ventricular systole ; 3, the opening of 
 the semilunar valves and the appearance of the carotid pulse ; 4, the 
 beginning of the radial pulse ; 5, the closing of the semilunar valves ; 
 and 6, the opening of the tricuspid valves. The time is recorded in fifths 
 of seconds in this and other tracings. 
 
 Although the carotid pulse and the apex beat can sometimes be usefully 
 employed as a standard, it will be found that the radial pulse is, on the whole, 
 
 Fig. 47. Simultaneous tracings of the jugular and the radial pulses in the first part of the 
 tracing and of the carotid and the radial in the latter part. The jugular pulse is of the auricular 
 type, a, auricular wave ; c, the carotid wave ; v, the ventricular wave ; x, the auricular 
 depression ; y, the ventricular depression. These letters have the same significance in all 
 the other tracings, and the numbered perpendicular lines have the same significance as those 
 in Fig. 46. 
 
 the most convenient in practice. A certain loss of time takes place in the 
 transmission of the wave to the radial pulse, and this can be estimated by 
 taking simultaneously with the radial a few beats of the carotid, as in Figs. 
 44 and 47, in which the space between 3 and 4 shows the loss of time between 
 the appearance of the carotid and the radial pulse. This loss being allowed 
 for, one can always find a definite period in a jugular tracing which corre- 
 sponds to any event occurring in the neck due to the ventricular systole. 
 T also employ a very useful period, namely, that portion of the ventricular 
 systole during which the semilunar valves are open (period marked E in 
 all the tracings). Its duration can be found in the radial tracing, extending 
 from the beginning of the upstroke to near the bottom of the dicrotic notch. 
 It corresponds to the time between the perpendiculars 3 and 5 in all the caro- 
 tid, jugular, and apex tracings given here. In the neck the period E begins
 
 THE VENOUS PULSE 
 
 113 
 
 with the carotid pulse. There is a slight delay between the opening of the 
 aortic valves and the carotid pulse, but it is so short (one-fiftieth of a second) 
 that it may be ignored. The space E in the radial tracing begins about 
 one-tenth of a second behind the same period in the neck. 
 
 Another important standard is that of the opening of the tricuspid 
 valves (perpendicular 6 in all the tracings), which in jugular tracings is always 
 indicated by the beginning of the fall of the wave v. In the apex tracing 
 this event occurs at the bottom of the fall, after the systolic plateau, as in 
 Fig. 25. 
 
 § no. The carotid wave — In the tracing in Figs. 44 and 47, in addi- 
 tion to the waves a and v, which have already been described, there is another 
 wave marked c. In Fig. 42 it will be seen that the subclavian and carotid 
 arteries lie in such close proximity to the jugular vein that the receiver 
 
 Fig. 48. Shows a diastolic wave h in the jugular tracing. Rate 48. 
 
 covers a portion of these arteries. In consequence of this, the stroke of 
 the arterial pulse affects the tracing from the jugular, and produces the wave 
 c, which I have caUed the carotid wave. A' considerable amount of discussion 
 has taken place in regard to the cause of c, but if an observer will carefully 
 take tracings higher and higher up in the neck, he can easily satisfy himself 
 of its nature, for it gradually assumes the character of a tracing from the 
 carotid artery. The recognition of c as due to the carotid (or carotid and 
 subclavian) helps much in the analysis of tracings from the neck, particularly 
 when there is a delay between the auricular and ventricular systole, the dura- 
 tion of the a-c interval being the best measure of the delay. (Experimental 
 observations show that faint waves may occur in the veins about the time 
 of the carotid wave, produced in some obscure way by the systole of the 
 ventricle, but the carotid and subclavian impact is the main, and for 
 practical purposes the only one, that need be considered.) 
 
 The true venous curve would follow the dotted line in Figs. 46 and 47. 
 
 UACEBNZIE J
 
 114 
 
 DISEASES OF THE HEART 
 
 § III. The notch on the ventricular wave. — In a great many cases 
 the wave v has a notch on it just before its termination (perpendicular 
 line 5 in Fig. 44). It corresponds in time to the closure of the semilunar 
 valves, and the following rise in v occurs between the closure of the semi- 
 lunar valves and the opening of the tricuspid valves (postsphygrriic interval, 
 
 o-C. "C '^'^ 
 
 a c ^ i d a c 
 
 v/ V . V 
 
 Fig. 49. In increase of the heart's rate the period between y and a becomes shortened, so 
 that the auricular wave, a, follows immediately after v (compare with Figs. 47 and 48)[. 
 
 F, Fig. 43), The exact cause of this notch is still a matter of dispute — 
 no satisfactory explanation being yet forthcoming. I have often employed 
 it as a useful guide in measuring the period when the semilunar valves 
 close, and it is represented by the perpendicular line 5 in all the tracings. 
 
 Fig. 50. With gi'eat increase in the rate the waves v 
 and a become blended. 
 
 § 112. The diastolic wave — Occasionally a wave may be detected in 
 slow-acting hearts shortly after the opening of the tricuspid valves {h, Fig. 
 48). A. G. Gibson '^''^ and Hirschfelder '^^^ describe this as due to the inrush 
 of blood into the ventricle floating up the cusps and causing a transient 
 closure of the tricuspid valves. Thayer*"^ and Gibson also describe 
 a sound heard occasionally at this time.
 
 ; THE VENOUS PULSE 115 
 
 § 113. Changes due to variation in the rate of the heart When 
 
 the heart's rate increases the shortening of the cycle takes place mainly 
 at the expense of the diastolic period. In the venous tracing the first 
 effect is shown by the disappearance of the period of stasis, the wave a 
 following immediately on the ventricular wave v (Fig, 49) ; with still greater 
 increase in the rate, v and a become blended (Fig. 50). 
 
 Tig. 51. In tracings from the neck the small wave, a, due to the 
 auricular systole may be the only evidence of the jugular pulse. 
 
 § 114. Method of analysing a tracing.— In the tracings given so far 
 the waves have been distinct and well marked. It often happens that the 
 jugular pulse is extremely small, so that we only get a slight movement 
 due to the auricle, the main portion of the tracing being due to the carotid, 
 
 Fig. 52. The movements in the neck seemed dancing vibrations but an analysis of a tracing 
 refers each movement to a definite cause. 
 
 as in Fig. 51. At other times the movements of the neck seem mere dancing 
 vibrations, and the record obtainable shows a series of small undulations. 
 But with the radial pulse as a standard, one can definitely assign each 
 undulation to the force producing it. Thus in Fig. 52 we can analyse the 
 tracing by the following procedure : Make a downstroke (4) parallel with the 
 perpendicular line at the beginning of the radial tracing, at the beginning of 
 a radial pulse beat. As the carotid pulse occurs nearly one-tenth of a second 
 
 I 2
 
 116 DISEASES OF THE HEART 
 
 before the radial, draw the perpendicular line 3 one-tenth of a second in 
 front of 4. Measure the distance from the perpendicular line at the beginning 
 of the tracing to 3. Draw a downstroke in the jugular tracing at the same 
 distance from the one at the beginning. This will be found to fall at the 
 beginning of a small wave, which therefore must have been due to the 
 carotid, and so mark it c. The auricular wave occurs one-fifth of a second 
 in front of c, and so the wave a can only be due to the auricular systole. 
 In Fig. 46, p. Ill, it was shown that the opening of the tricuspid valves 
 (perpendicular line 6) often coincides with the bottom of the dicrotic notch 
 in the radial tracing. If now a perpendicular line (6) be drawn at this 
 
 Fig. 53. Simultaneous tracings of the jugular and carotid pulses, showing one large wave 
 V, synchronous with the carotid pulse, and due to the ventricular systole, and one large fall, y, 
 synchronous with and due to the ventricular diastole. There is no sign of an auricular wave, 
 and the jugular pulse is therefore of the ventricular type, and the rhythm of the heart is 
 continuously irregular. 
 
 period in the jugular tracing, it wiU be found to faU at the end of a wave, v, 
 which must therefore be the ventricular wave. 
 
 By strictly following such a method as the foregoing, httle difficulty will 
 be experienced in analysing the great majority of tracings, 
 
 § 115. The ventricular form of the venous pulse In Figs. 53 and 
 
 54 are tracings of the jugular pulse. At a glance these are recognized to be 
 totally different from the form of the venous pulse just described. The 
 waves, V, in Figs. 53 and 54 are due to the blood being forced back 
 through the tricuspid orifice into the veins by the contraction of the right 
 ventricle. In a sense its origin is identical with the wave, v, in the auricular 
 venous pulse as in Figs. 44 and 45, but appears earlier in the cardiac cycle 
 (synchronous with the carotid pulse) because there is not now a dilating 
 auricle interposed between the vein and ventricle. When we come to analyse 
 tracings of the ventricular venous pulse with a standard movement, as in
 
 THE VENOUS PULSE 
 
 117 
 
 Fig. 53, we discover there is no evidence of an auricular wave, nor of a fall 
 corresponding to the fall x in the auricular venous pulse — in other words, 
 there is one great wave (v) synchronous with the ventricular systole, and 
 one great fall (?/) synchronous with the ventricular diastole. Another point 
 to be noticed is that the rhythm frequently is irregular, and that when 
 there is a long diastolic period there is a rise in the tracing due to the vein 
 filling, as after the long pauses in Fig. 54. 
 
 There are two conditions which produce the ventricular form of the 
 venous pulse : — 
 
 (1) Great distension and paralysis of the right auricle. Here there is 
 great engorgement of the right heart so that the auricle becomes embarrassed 
 
 Fig. 54. Simultaneous tracings of the jugular and radial pulses, showing the ventricular 
 jugular pulse, i. e. one large wave, v, synchronous with and due to the ventricular systole, and 
 one large fall, y, synchronous with and due to the ventricular diastole. The rhythm of the heart 
 is continuously irregular. When there are long pauses the tracing of the jugular gradually rises 
 before the next large wave, on account of stasis in the veins. When the pause is short there 
 is no sign of stasis, or only a slight wave, as on the second beat, where it might simulate a wave 
 due to the auricle, but the real cause is seen to be stasis in the veins when the pause is longer. 
 
 injts action, and the a wave in the jugular pulse diminishes in size and 
 disappears, while the v wave increases in size and occupies the whole period 
 of ventricular systole. With recovery and diminution of the engorgement 
 the auricular wave reappears. It is to be noted that the rhythm in these 
 cases is always regular. This manner of production of the ventricular 
 venous pulse is however very infrequent, far less common than what my 
 earher observations led me to suppose, for the vast majority of cases of the 
 ventricular venous pulse are due to 
 
 (2) A change in the starting-point of the heart's contraction. In con- 
 sequence of its great importance I deal with the matter in detail, and adduce 
 further proof of the nature of the change in Appendix II. For the sake of 
 brevity, I summarize here the facts which show that the, ventricular venous 
 pulse is usually an evidence of the starting of the rhythm of the heart at 
 some place other than at the mouth of the veins. For reasons to be given later, 
 I assume that this starting-place is in or about the a.-v, node (Fig. 2),
 
 118 DISEASES OF THE HEART 
 
 and hence refer to this rhythm of the heart, where there is a ventricular 
 venous pulse, as the ' nodal rhythm '. 
 
 The onset of the nodal rhythm is characterized by : — 
 
 (a) Change of the venous and liver pulses from the auricular type to the 
 ventricular. 
 
 {b) The disappearance of all other evidence of the auricular systole from 
 its normal place in the cardiac cycle (as the disappearance of a presystolic 
 murmur, and the absence of an auricular wave in the tracing from the 
 apex beat). 
 
 (c) In many cases there is a continued irregularity in the heart's action. 
 
 It so happened that my earher cases of the ventricular form of the venous 
 and liver pulses were all secondary to disease of the mitral valve, and at the 
 post-mortem examinations I found the right auricle enormously distended 
 and the muscle-fibres greatly atrophied, so that I surmised that the auricle, 
 like an over-distended bladder, had become paralysed. This view seemed 
 to be confirmed by the results of careful observation of individual patients 
 extending over many years, the auricular wave never putting in an appear- 
 ance at its normal period in the hundreds of tracings I had taken. This 
 view I expressed in my book on the Pulse ^^, but shortly after writing it a 
 few cases came under my observation that gave me grounds for suspecting 
 that * auricular paralysis ' was not the only condition that gave rise to the 
 ventricular form of the venous pulse. 
 
 I therefore began an inquiry into all forms of arrhythmia, and collected 
 a large number of cases. From amongst these I was able to differentiate 
 a group of over six hundred cases in which the irregularity was of a disorderly 
 nature, as in Figs. 53 and 54. Over one-half of these cases had a venous 
 pulse, and in every case it was of the ventricular form. In more than fifty 
 cases the disorderly rhythm had started while the patient was under observa- 
 tion, and it invariably accompanied the sudden change of the jugular pulse 
 from the auricular form to the ventricular. 
 
 In a careful analysis of a great number of my cases, I found that in some 
 there was only the large wave, lasting from the time of the opening of the 
 aortic valves to the opening of the tricuspid valves, as in Figs. 53 and 54. 
 On the other hand, there were others in whom there could be seen in the 
 jugular veins in the neck two movements during ventricular systole — the 
 first movement short and abrupt, followed by a larger movement. These two 
 movements appeared in the tracings (a' and v in Figs. 55, 56, 210, and 211). 
 The time of the appearance of a' was exactly that of the carotid in the 
 majority of cases (perpendicular hne 3 in Fig. 55). In a few instances 
 I found this wave a little earlier. Thus, in Fig. 56 it appears before the
 
 THE VENOUS PULSE 
 
 119 
 
 carotid and corresponds with the beginning of ventricular systole, as is 
 shown in Fig, 57. The patient from whom this tracing was taken is described 
 in the Appendix II (Case 7), and she had shown this form of jugular pulse 
 
 Fig. 55. The jugular pulse is of the ventricular form and shows two waves, a' and v, 
 during the period of ventricular systole (3 to 6). The wave a' appears at the same time as the 
 carotid pulse (perpendicular line 3), and is due to the auricle contracting during the ventri- 
 cular systole. There is a notch in the v wave (perpendicular line 5) corresponding to the notch 
 in the v wave in Figs. 44 and 45. 
 
 for over five years. At the post-mortem examination, the taenia terminalis 
 of the auricle was hj^pertrophied ; it can therefore be inferred that the 
 auricle must have contracted. There Avas never any sign of the auricular 
 
 Fig. 56. Ventricular venous pulse. There are two waves (a' and f ) in the jugular puke, 
 and the wave a' appears slightly before the carotid (perpendicular line 3), and is due to the 
 auricle beginning to contract at the same time as the ventricle. 
 
 wave before the carotid pulse, and I therefore concluded that the wave 
 a' in Figs. 56 and 57 must have been due to the auricular systole, and that 
 in these cases the auricle and ventricle contracted almost simultaneously 
 (see also Case 12, Appendix II).
 
 120 
 
 DISEASES OF THE HEART 
 
 Assuming this interpretation to be correct, it will be found that the wave 
 a' appears at the same time as the carotid (perpendicular line 3 in Fig. 55). 
 As the ventricle is in systole before the aortic valves open, the ventricular 
 contraction must have preceded the contraction of the auricle which pro- 
 
 FiG. 57. Tracings of the ventricular venous pulse and of the apex beat. 
 There are two waves, a' and v, in the venous pulse, and the wave a' is seen 
 to appear at the beginning of ventricular systole. The sounds of the heart 
 (1 and 2) are represented under the apex tracing, and the shading after 2 repre- 
 sents the mitral diastoUc murmur. During the short pause it fills up the whole 
 period between the first and second sounds, whereas when the pause is long, it 
 stops some distance before the first sound. 
 
 FiQ. 58. Tracings showing the normal ventricular and auricular movements from a dog's 
 heart. The downward movement represents the contraction. The perpendicular lines, a, 
 indicate the beginning of auricular systole, and, in the ventricular tracing, are seen to precede 
 the ventricular contraction. Compare with Fig. 59. (Cushny.) 
 
 duced the wave a'. On the other hand, in such a rare instance as that 
 shown in Figs. 56 and 57 the auricle and ventricle must have started together. 
 A remarkable confirmation of this view has been recently obtained by 
 Cushny ^^' and Lewis. In experimenting on the dog they have been able 
 to produce in various ways an abnormal rhythm of the heart agreeing
 
 THE VENOUS PULSE 121 
 
 exactly with the description given above — that is, the ventricle started 
 one-tenth of a second or less before the auricle (see Figs. 58 and 59), or the 
 ventricle and auricle started simultaneously. Lewis has demonstrated the 
 disappearance of the auricular systole from the normal place in the cardiac 
 cycle in cases of nodal rhythm by means of electro-cardiograms (see Fig. 279, 
 Appendix VII). 
 
 § Ii6. Conditions giving rise to a venous pulse To a great extent 
 
 we are even at this day quite at a loss to explain all the conditions that give 
 rise to a venous pulse. Most people in good health show it, while in cases 
 of marked heart failure it may be entirely absent. Some people when in 
 
 VentYicle ^' «•' ^' 
 
 mamammim 
 
 .1 «'' ft'' a-' 
 
 tTTrTTTTTTl 
 
 8 
 
 Fig. 59. Tracings of the movements of the ventricle and auricle from a dog's heart, 
 poisoned by aconitin. The perpendicular lines, a', indicate the beginning of auricular systole, 
 and in the ventricular tracing are seen to follow the beginning of the ventricular contraction. 
 Compare with Fig. 58. (Cushny.) 
 
 robust health show no signs of it, but if they become slightly debilitated 
 the venous pulse may appear in the neck. In some cases of pernicious 
 anaemia the venous pulse may be a very prominent symptom, in others it 
 may never appear. Some women during pregnancy develop a large venous 
 pulse, others only develop it during the puerperium, while others never 
 show the slightest sign of it. In irregular action of the heart it may assume 
 in certain cases, enormous proportions ; in other cases there is not the 
 slightest sign. A man may show it during one attack of heart failure, and 
 during another and more grievous attack it may be absent. 
 
 I have endeavoured to find out the reason for this variability, but 
 though in some cases I have been able to connect its appearance and dis- 
 appearance with definite changes in the heart, yet on the whole the matter 
 is one which still puzzles me.
 
 CHAPTER XIV 
 
 Enlargement and Pulsation of the Liver 
 
 § 117. Reflex or protective symptoms. 
 
 118. Signs of enlargement of the liver. 
 
 119. Pulsation of the liver. 
 
 120. Conditions producing enlargement and pulsation of the liver. 
 
 121. Jaundice. 
 
 122. Differential diagnosis. 
 
 123. Prognosis. 
 
 124. Treatment. 
 
 The symptoms arising from enlargement of the liver due to heart failure 
 receive Httle consideration from clinicians, and are very frequently over- 
 looked or misunderstood. To a certain extent, this is due to the fact that 
 this enlargement may appear at such an advanced stage of cardiac failure 
 that the diagnosis and treatment can be determined without paying 
 particular attention to the Hver symptoms. Graham Steell ^^^ includes the 
 enlargement of the liver as one of the cardinal symptoms of heart failure, and 
 Salaman^-* has given a very suggestive analysis of the pathological changes 
 and the conditions inducing them ; but clinicians generally have dealt with 
 the subject in a most perfunctory manner. While it is true that the con- 
 ditions producing these liver troubles imply an advanced stage of heart 
 failure, yet the recognition of the symptoms have an important bearing 
 on diagnosis and treatment in many cases. The symptoms due to changes 
 in this organ are not always easy to understand, but that is no reason for 
 ignoring them. 
 
 § 117. Reflex or protective symptoms Usually in the early stages 
 
 of liver enlargement we find evidences of the intervention of the protective 
 mechanism (see Chapter VI). While the Hver may be only one or two 
 inches below the ribs, the muscle wall of the upper part of the right half of 
 the abdomen becomes hard and tender. This tenderness is invariably put 
 down to the hver itself, and the manner in which this * tenderness ' is 
 usually demonstrated is by eliciting pain on pressing the finger into the 
 patient's abdomen. But if the extent of the hyperalgesia and the size of 
 the liver be mapped out, it will be found that the former is far more 
 extensive than the latter, and sometimes extends round to and affects the
 
 ENLARGEMENT AND PULSATION OF THE LIVER 123 
 
 erector-spinae muscles. In some cases the skin and subcutaneous tissue 
 also become tender, but they rarely become so sensitive as the muscles. 
 Sometimes there seems an increased tenderness where the liver is reached, 
 but this wiU be found to be due to the more effective compression of the 
 muscle between the finger and the liver. There are many other ways 
 by which the resourceful observer can demonstrate the tissue in which the 
 tenderness is present. 
 
 The consequence of this muscular hyperalgesia is manifested in various 
 ways. If the patient is going about he may suffer severe pain across the 
 upper part of the abdomen or in the back, this probably being due either 
 to increased engorgement of the liver or to the increase of the pain in con- 
 sequence of the exercise of the hyperalgesic muscles. This tenderness and 
 rigidity of the abdominal muscles interferes with the respiration of the 
 patient. He cannot breathe deeply, and attempts to do so are painful, 
 hence there results rapid and shallow breathing, with further embarrassment 
 of the right heart and a tendency to pulmonary stasis. 
 
 With long-continued persistence of the enlargement, all the sensory 
 phenomena disappear, the abdominal wall becomes lax, and sometimes 
 the edge of the Uver can be grasped. 
 
 § Ii8. Signs of enlargement of the liver — It is not always easy 
 to make out the enlargement of this organ. The contracted muscles often 
 prevent the palpation, and even percussion helps but little. Ascitic and 
 gaseous distension add further to the difficulty. But with care and gentle- 
 ness in palpation one may overcome the resisting muscles. Even when the 
 edge of the liver cannot be made out, the peculiar sense of resistance conveyed 
 to the exploring hand may reveal the enlarged liver. Other methods may 
 be adopted, such as pushing the liver forward with one hand while the other 
 explores the front. When the muscles relax and the hyperalgesia disappears, 
 there is no difficulty in finding out the enlarged Hver, except when there is 
 great distension of the abdomen. 
 
 § 119. Pulsation of the liver — When the liver is enlarged from heart 
 failure it not infrequently pulsates. If the abdominal muscles are lax, 
 there is no difficulty in recognizing this. If one hand presses on the liver 
 behind and the other is laid on it in front, the latter is heaved up and down 
 with the pulse. Even where there is a considerable amount of muscular 
 contraction, exploring the edge of the liver with the liver receiver will 
 often reveal the pulsation (§ 71). 
 
 There are two forms of liver pulse, corresponding to the two forms of 
 venous pulse — an auricular. Fig. 60, and a ventricular, Fig. 61, the latter being 
 an evidence of the nodal rhythm. When a liver pulse and a jugular pulse
 
 124 
 
 DISEASES OF THE HEART 
 
 are both present in the same individual, they are always of the same form. 
 In Fig. 62 a tracing of an am-icular jugular pulse is taken simultaneously 
 with a tracing of the auricular liver pulse. In Fig. 63, the tracing of the 
 
 LiveT 
 
 
 T I f 
 
 a 
 
 
 
 a 
 
 
 
 
 
 
 
 
 \ 
 
 V 
 
 arts 
 
 \ 
 
 
 1 
 
 
 1^ 
 
 
 
 Ij 
 
 Fig. 60. The liver pulse is of the auricular form and shows a well-marked 
 
 auricular wave, a. 
 
 ventricular jugular pulse is seen to be identical with the liver pulse in 
 Fig. 61, both tracings being from the same patient. 
 
 § 120. Conditions producing enlargement and pulsation of the liver. 
 — I have already remarked on the variety of conditions producing the jugular 
 
 Fig. 61. The liver pulse is of the ventricular form, showing no auricular wave. 
 
 pulse, and there is a Mke difficulty in understanding the conditions which 
 give rise to liver enlargement. Cases otherwise identical in their symptoms, 
 and' suffering from heart failure due to the same cause, may, diifer in this 
 
 
 
 Jit.l7-lt..Ju(/. 
 
 
 rt „ 
 
 ^ n '^n 
 
 : ■ 1 i..l 
 
 a 
 
 
 a? as ' j - 
 
 ' 1 1 
 
 ! . -^ 
 
 
 
 Liver ! 1 
 
 a 
 
 a 
 
 a a. 
 
 AtAa 
 
 I\jAAM 
 
 A A 
 
 X 
 
 X 
 
 
 
 Fig. 62. Simultaneous tracings of the jugular and liver pulses, showing 
 the correspondence between the waves a and v, and the absence of the carotid 
 wave c from the liver pulse. 
 
 particular, some showing enlargement of the hver and others faihng to do 
 so. Similarly it is not always quite clear why some pulsate while others 
 do not. To a certain extent, I think this is due to the condition of the right
 
 ENLARGEMENT AND PULSATION OF THE LIVER 125 
 
 auricle. It takes some force to distend the liver, and normally the right 
 am*icle has not sufficient strength, so that as long as the right auricle contracts 
 and dilates in its normal place in the cardiac cycle it prevents the ventricle 
 exercising its force on the liver. When, however, the ventricle starts the 
 rhythm, it drives the blood through the incompetent tricuspid orifice with 
 such force that the liver pulsates. It is in the cases of nodal rhythm that 
 we most frequently find the liver pulsating. When the nodal rhythm is 
 transient the liver may quickly enlarge and pulsate, and with cessation of 
 the attack as quickly subside and cease to beat — the liver pulse being of the 
 ventricular form (Fig. 207). 
 
 Reasoning that it requires some force greater than the normal strength 
 of the right auricle to produce pulsation of the liver, I at first drew the 
 
 Fig. 63. Simultaneous tracings of the jugular and radial pulses. The jugular pulse is of 
 the ventricular form and is identical with the liver pulse in Fig. 61, both being taken from the 
 same patient. 
 
 conclusion that an auricular liver pulse indicates hypertrophy of the right 
 auricle, and as this occurs most characteristically in cases of tricuspid 
 stenosis, I regarded the auricular liver pulse as diagnostic of tricuspid 
 stenosis. All the cases that had shown this auricular liver pulse during life, 
 whose hearts I examined 'post mortem, showed tricuspid stenosis. But I have 
 now had a number of cases showing this form of liver pulse, in which I doubt 
 if I am justified in assuming tricuspid stenosis. Volhard^'^ describes the 
 auricular liver pulse in pericardial effusion, and Wenckebach ^^^ in a case of 
 adherent pericardium. 
 
 § 121. Jaundice. — Jaundice is a frequent accompaniment of enlarge- 
 ment of the liver ; though of itself of little importance, it should be kept 
 in mind that a slight jaundice may be misleading. Many patients with 
 .advanced heart failure and with the nodal rhythm get rapidly thinner. 
 In these the liver is sometimes greatly enlarged, so that the wasting of the 
 patient, the enlargement of the liver, and the jaundiced tint, present the 
 features of malignant disease of the liver, and I have seen cases presenting 
 these symptoms thus wrongly diagnosed.
 
 126 
 
 DISEASES OF THE HEART 
 
 § 122. Differential diagnosis — Many writers refer to an ' arterial 
 pulsation ' of the liver, and I have often wondered what they mean, par- 
 ticularly as no details are ever given. I have never found any condition 
 that could come under this heading, and I suspect that some observers 
 have mistaken the movement of the liver, when it is pulled up and down 
 with the systole and diastole of the ventricle, for a pulsation, particularly 
 as it is sometimes mentioned in connexion with aortic regurgitation. 
 Wherever there is much cardiac enlargement, movement of the liver is 
 produced. Even in patients with normal hearts but with lax abdominal 
 wall, this up-and-down movement can be recognized. It has already been 
 referred to in § 81. Here I need only point out that the conditions in 
 which it occurs are generally very different from that of the heart failure 
 in which the true liver pulsation occurs. A tracing of this movement 
 
 Fig. 64. Tracings from the abdominal aorta and the liver. The liver pulse is of the 
 
 auricular type. 
 
 sets the matter at rest, as the fall due to the ventricular systole does not 
 begin until the opening of the aortic valves and the expulsion of blood from 
 the chest, which is practically synchronous with the carotid pulse. In the 
 ventricular form of liver pulse, on the other hand, there is a rise during 
 ventricular systole. A tracing of the liver movement can be distinguished 
 from the auricular liver pulse in that the fall in the latter case precedes the 
 carotid pulse. 
 
 There is generally little difficulty in distinguishing the pulsation of the 
 abdominal aorta from that of the liver pulse. In cases where the ventri- 
 cular liver pulse is present, it is very rarely that the abdominal aorta can 
 be felt, and the characters of the tracings are not likely to be confused. 
 The auricular form of liver pulse is still more distinct in character from that 
 of the abdominal aorta, as shown in Fig. 64, 
 
 § 123. Prognosis. — Liver enlargement and pulsation from cardiac 
 disease indicate a very advanced stage of heart failure. In cases where the 
 heart failure is secondary to a rheumatic affection of the heart with mitral
 
 ENLARGEMENT AND PULSATION OF THE LIVER 
 
 127 
 
 disease, it may only appear during the attacks of heart failure to which 
 the patients are liable. The enlargement subsides with improvement, and 
 if the heart's restoration be good the patient may have no signs of the liver 
 enlargement for many years. Some patients with the nodal rhythm 
 
 Fig. 65. Simultaneous tracings of the apex beat 
 and of the liver pulse. The liver edge was below the 
 level of the umbiUcus, and the pulsation of great size. 
 
 secondary to rheumatic affection of the heart may for years have a big 
 pulsating Uver (Fig. 65), in others the enlargement appears during temporary 
 heart failure. In some of these the exhibition of digitalis may cause the 
 subsidence of the liver in a couple of days. Fig. 66 was taken from the liver 
 
 Fig. 66. Tracings of the liver and radial pulses during a period of extreme heart 
 
 failure (nodal rhythm). 
 
 of a man which was pulsating as low as his umbilicus. In a couple of days 
 all signs of the liver below the ribs had gone. The enlarged liver coming 
 on in paroxysmal tachycardia, i.e. transient nodal rhythm, is a very serious 
 symptom, as it indicates marked dilatation of the heart. Also in the heart 
 failure due to cardio-sclerosis with the permanent nodal rhythm, it is a very
 
 128 DISEASES OF THE HEART 
 
 grave symptom, as the heart failure is due to extensive degeneration of the 
 cardiac muscle, and therefore does not respond to the influence of rest 
 and digitalis. Enlargement of the liver in muscle failure due to chronic 
 alcoholism is a bad sign. 
 
 § 124. Treatment. — Though no treatment is directed specially to the 
 liver enlargement, the effect of the rigid tender muscles in embarrassing 
 the respiration should be borne in mind, and suitable attempts made to put 
 the patient in a comfortable position so that he can breathe more easily, 
 and the pain due to the enlarged liver should caU for the cessation of all 
 exertion that induces it. A smart mercurial purge may sometimes afford 
 considerable relief.
 
 CHAPTER XV 
 
 Inceeased Frequency of the Heart's Action 
 
 § 125. The normal rate. 
 
 126. Classification. 
 
 127. Cases which respond to a call upon the heart's energy by increased frequency. 
 
 128. Cases in which the heart's rate is continuously increased. 
 
 129. Cases in which the increased frequency of the heart occurs in irregular paroxysmal 
 
 attacks (palpitation). 
 
 130. The cause of increased frequency of the heart's action. 
 
 131. Prognosis. 
 
 § 125. The normal rate — The rate of the heart varies very consider- 
 ably according to age, sex, and individual peculiarities. At birth, the rate 
 is usually from 130 to 140 per minute. With advancing years the heart 
 slows down gradually : between nine and ten the average is about ninety ; 
 at twenty, about seventy-four ; at thirty, from sixty-six to seventy-six : 
 it remains at about this latter rate until over fifty, when it gradually begins 
 to increase in frequency. At all ages very considerable variations may be 
 met with. 
 
 The heart's rate is greatly increased by exertion, even in those who are 
 in good training. Deane found the pulse-rate over 200 per minute in 
 a professional dancer, at the end of a dance. It quickly subsided to the 
 normal rate. According to Pembrey and Todd the increase in rate is 
 somewhat greater in the trained than in the untrained, but the decrease 
 in the rate to normal is more rapid in the trained man. 
 
 § 126. Classification — In considering the conditions that give rise 
 to increased frequency of the heart's action, we are confronted with such 
 a great number that it is impossible to deal with them all. What I propose 
 to deal with here is the abnormal increase of pulse-rate, and certain con- 
 ditions other than febrile which induce the rapidity of the pulse. These may 
 fittingly be discussed in three groups : (1) Those cases in which the heart 
 responds to a call upon its energy by increased frequency ; (2) those cases in 
 which the heart-rate is continuously increased ; (3) those cases in which the 
 periods of increased rapidity take place in irregular paroxysmal attacks. 
 
 § 127. Cases which respond to a call upon the heart's energy by 
 increased frequency. — The cases in the first of these groups, those in 
 
 MACKENZIE fr
 
 130 DISEASES OF THE HEART 
 
 which the heart responds to an increased call upon its energy by increased 
 frequency, show in reality but an exaggerated form of the normal condition. 
 When we find that a patient is seized with palpitation or rapid heart action 
 after mounting a few steps, we recognize as abnormal that which would have 
 been regarded as normal in an individual who had run half a mile at the 
 top of his speed. In other words, this increased rate is an evidence that the 
 field of the heart's response to effort is greatly reduced. A further deduction 
 can be made from observing these patients, viz. that exhaustion of the 
 reserve force heightens the excitability of the whole heart, for not only 
 is the rate increased, but the contraction sweeps through the heart with 
 greater rapidity and the systoles of the chambers are of shorter duration. 
 The increased frequency should always lead one to seek the cause from 
 which it arises. The conditions underlying it are too numerous to mention, 
 but they all in the end point to enfeeblement of the muscle of the heart. 
 In all exhausting diseases, and after convalescence from such a w^asting sick- 
 ness as typhoid fever, the heart's rate can be greatly increased by even very 
 moderate exertion. In the various anaemias (chlorosis, pernicious anaemia, 
 maUgnant cachexia) the rapid heart action is very often the symptom to 
 which the patient's attention is first called. In organic affections of the 
 heart, as in the various forms of myocarditis, in fatty degeneration of the 
 myocardium, and in valvular disease when there is only a small amount of 
 reserve force in the muscle, increased frequency of the pulse on exertion is 
 extremely common. Many of the patients whose ailments are included in 
 the foregoing groups, when at rest, have a pulse beating about or not much 
 above the normal rate. The heart then seems to be capable of sustaining 
 the demands of the circulation, but seems to be working near the top of 
 its reserve energy. On exertion this reserve energy is speedily exhausted, 
 and in order to make up for its inability to respond to the demand of the 
 tissues for more blood by giving stronger ventricular contractions, it responds 
 by giving a greater number of feebler and less complete contractions. 
 
 In addition to the increased rate there is usually hurried and laboured 
 respiration, and this too occurs whether a strong heart is overstrained by 
 a great effort, or a weak heart by a slight effort. Not infrequently in elderly 
 people, before the interference with respiration can arise, the patient in 
 making an effort is stopped by a feeling of weight or oppression within the 
 chest, or even by pain striking across the chest, sometimes severe, sometimes 
 slight, but in all cases imperiously demanding a cessation of the effort. 
 
 It is as impossible to indicate with any approach to accuracy when a pulse- 
 rate is abnormal on moderate exertion as it is to indicate what the pulse- 
 rate should be in health under similar circumstances. The increase is often
 
 INCREASED FREQUENCY OF THE HEART'S ACTION 131 
 
 so marked that its recognition is beyond dispute. Thus, in making a patient 
 sit up or turn over in bed, a rise of five to ten beats a minute may not be 
 worthy of much attention, but if the increase is fifteen to thirty beats then 
 there is distinct evidence that we have to do with some condition that has 
 exhausted the heart's reserve power. This increase of the pulse-rate beyond 
 the normal on moderate exertion does not give any clue to the nature of the 
 condition that has reduced the heart's reserve power. As already indicated, 
 these conditions are so numerous that an examination for other symptoms 
 must be undertaken to discover them. 
 
 § 128. Cases in which the heart's rate is continuously increased. 
 {a) Valvular disease. — The second division, in which the heart main- 
 tains a frequency beyond what we recognize as within the limits of health, 
 also includes a great variety of heart conditions. We have among these 
 the series of valvular diseases of the heart, with the muscle exhausted, 
 it may be from struggling against the obstruction caused by the valve lesion, 
 or with the muscle itself degenerated. Not only do such hearts respond 
 to effort with marked increase in frequency, but even during rest the heart 
 may beat with abnormal rapidity, regularly or irregularly. This forms 
 a very important factor in arriving at an estimate of the strength and 
 condition of the organ. The other symptoms of heart failure present will 
 help in indicating the stage at which the patient has arrived. 
 
 (6) Affections of the myocardium. — Apart from patients with mani- 
 fest valvular disease of the heart, there are many whose pulse is rapid, 
 and in whom no disease of the heart can be detected by physical signs. 
 The chest- wall may be thick and fat, or the lungs so voluminous that the 
 actual size of the organ cannot be satisfactorily defined. The sounds, 
 though free from murmur, may be so slightly modified that no certain infer- 
 ences can be drawn from them. Yet that serious mischief is present is 
 but too often demonstrated by watching the after-history of these cases. 
 If we exclude for the present the consideration of certain neurotic conditions, 
 the cause of the quickening in all cases is really associated with a want of 
 strength in the muscular wall. In valvular disease this is usually spoken 
 of as failure of compensation. In degeneration of the wall, fatty or fibrous, 
 the weakening of the wall is directly due to this degeneration. In the 
 great series of hearts overstrained from excessive exertion, the weakness 
 of the wall is the principal cause of the whole train of symptoms associated 
 with the failure of the heart. In arriving, therefore, at an estimate of the 
 value of the pulse quickening, a consideration of the other symptoms present 
 will be necessary to recognize what is the cause of the increased pulse-rate 
 in each special case. The circumstances, age, and condition of the patient, 
 
 k2
 
 132 DISEASES OF THE HEART 
 
 will help much in recognizing the rapid pulse due to actual degeneration of 
 the heart-wall. But there is a series of cases in which it is difficult to account 
 for the rapid pulse, especially when it occurs in the apparently strong in the 
 prime of life. In these cases there is generally a history of hard work or 
 periods of excessive muscular exertion. Sometimes the condition receives 
 a special name, as ' the soldier's heart '. Medical men whose practice lies 
 amongst workpeople subjected to such muscular exertion are familiar with 
 a similar condition. The heart overstrain is most evident amongst those 
 with a tendency to obesity and who indulge rather freely in alcohol. 
 The symptoms are mainly a quickened pulse and shortness of breath on 
 exertion. Examination of the chest is often fruitless, the chest being large 
 and deep, and the lungs often voluminous. Much improvement results 
 from care and rest, and appropriate treatment. 
 
 (c) Pregnancy. — It may be noted that these symptoms are often 
 present in pregnant women, but there the cause is but temporary, and a 
 certain amount of recovery follows delivery. But in my experience there 
 is often left a certain amount of cardiac weakness, shown by a distinct 
 limitation of the field of cardiac response. 
 
 {d) Alcohol. — In all obscure cases of rapid heart action, the question 
 of over-indulgence in alcohol should be carefully inquired into. The patients 
 often try to hide their habits in this respect, but the physician can generally 
 find a clue in the manner of the individual, his facial aspect, tremulous 
 muscles (especially the tongue), want of appetite or nausea in the morning, 
 and that tout-ensemble which leads the experienced physician to suspect 
 the secret alcoholic. Accompanying the rapid pulse and other phenomena 
 there are often a sinking sensation in the epigastrium and sense of exhaustion 
 on exertion, and breathlessness. The heart may be only slightly enlarged, 
 or there may be great dilatation, usually accompanied by enlargement of 
 the liver and tenderness of the tissues covering it. With abstinence from 
 alcohol these cases in the early stages quickly recover, but with continuance 
 of the habit all the characters of severe heart failure supervene. 
 
 (e) Neurotic cases. — There is a group of people who exhibit a rapid 
 pulse in whom no heart lesion can be detected, and whose future history 
 demonstrates that no serious cardiac lesion existed. These people exhibit 
 other symptoms more prominently associated with the nervous system, 
 and are described in Chapter VIII. 
 
 (/) Exhausting diseases. — It is always well to bear in mind that a 
 persistent quick pulse may be the earliest symptom of an attack of tuber- 
 culosis or of the onset of malignant disease. A patient may complain for 
 months of weakness, with an absence of the sense of well-being, with no actual
 
 INCREASED FREQUENCY OF THE HEART'S ACTION 133 
 
 suffering. After a time the development of other symptoms demonstrates 
 the cause of the abnormal pulse-rate. In the young, particularly, persistent 
 high frequency of the heart's action in the absence of any demonstrable 
 heart lesion should always awaken the suspicion of a latent tubercular 
 affection. I have watched such cases for months, and puzzled over the 
 cause of the rapid heart-action, until the true nature of the complaint was 
 revealed by some definite sign such as the pointing of a psoas abscess or a 
 pulmonary haemorrhage. In most exhausting diseases (malignant diseases, 
 pernicious anaemia, tuberculosis) the pulse-rate is continuously quickened. 
 The frequent heart-action may usually be taken to indicate a severe infection 
 and a serious condition. 
 
 Fig. 67. From a female aged forty, suffering from exophthalmic goitre. Rate 120. ' 
 
 Fig. 68. From a female aged twenty-two, suffering from exophthalmic goitre. Rate 120. 
 
 (g) Exophthalmic goitre. — The essential features arising from the circu- 
 lation in many cases of exophthalmic goitre, it seems to me, are the 
 abnormal and persistent dilatation of the arterioles, and a heart acting 
 with a force relatively great to the resistance opposed. These are indicated 
 by the rapid and forcible pulse-wave felt by the finger, and the visible 
 pulsation of the superficial arteries and the carotid. The corresponding 
 sphygmographic features are a high upstroke and rapid fall, so that the 
 dicrotic notch is near the base line (Figs. 67 and 68). The rate of the 
 pulse may be greatly increased, up to 140-160 per minute. The same 
 factors, the unusually forcible injection of the blood into the arteries of 
 low blood-pressure, are present in aortic regurgitation. Though the beating 
 of the carotid is due to similar causes in the two cases, the low arterial 
 pressure at the end of diastole is different. In exophthalmic goitre the 
 dilatation of the arterioles and capillaries is the sole cause, whereas in 
 aortic regurgitation there is in addition the backward flow into the ventricle 
 through the incompetent valves. The condition of the circulation in 
 exophthalmic goitre is also comparable to that in some forms of sthenic 
 fever, where the heart beats forcibly and the arteries are relaxed. 
 
 Another evidence of the relaxation of the arterioles is to be found in the
 
 134 DISEASES OF THE HEART 
 
 subjective sensation of warmth felt by some sufferers from exophthalmic 
 goitre. They rarely complain of cold in winter, however lightly clad they 
 are, and this is not infrequently the cause of matrimonial disputes, for while 
 the ailing wife feels warm in bed during winter with few blankets, the healthy 
 husband feels the cold keenly. This feehng of warmth has supplied me with 
 the indications for the only treatment of this class of case that I have foimd 
 both grateful and beneficial to the patient, namely, the periodic stimulation 
 of the vaso-motor nerves by cold baths. Whenever the feehng of warmth 
 has been present I have found these baths do good, and when there is 
 nervousness and muscular tremor the administration of the bromide of 
 ammonium has been of great service. 
 
 § 129. Cases in which the increased frequency of the heart 
 occurs in irregular paroxysmal attacks — This class includes cases of 
 ' palpitation ' and ' paroxysmal tachycardia '. There are quite a number of 
 different conditions included under these terms, and no clear idea is usually 
 given of what is meant. A very useful and practical division may be based 
 on the manner in which the heart's contraction starts. In the vast majority 
 of cases of transient rapid heart-action, the heart's action is perfectly normal ; 
 the rapid action of this class will be spoken of here as ' attacks of palpitation '. 
 In another class of patient the heart's contraction does not start at the 
 normal place ; to this latter class the term ' paroxysmal tachycardia ' is 
 limited, and the cases are described in the sections on ' nodal rhythm ' 
 (p. 309) and auricular tachycardia (p. 334). 
 
 The rate in the first class rarely exceeds 170 beats per minute, and the 
 rhythm is regular except for the presence of an occasional extra-systole ; in 
 the latter class the rate may at first exceed 200 beats per minute, and the 
 rhythm is frequently irregular. (Concerning the records of extreme fre- 
 quency sometimes quoted, I may say I have never met with cases approach- 
 ing 300 per minute, nor have I come across a single instance of a published 
 tracing recording such a speed. They may be pubHshed, but I have not 
 seen them. I have a suspicion of any estimate made of a pulse-rate over 
 200 unless graphically recorded, because I doubt if the human mind is 
 capable of accurately distinguishing between events occurring at a speed 
 over 200 per minute, and I doubt if any one could articulate or mentally 
 distinguish the individual numbers at a rate of 300 per minute.) 
 
 In the following paragraph I describe under ' palpitation ' the more 
 common forms of temporary rapid action of the heart. 
 
 Palpitation. — This may occur in people suffering from a great variety 
 of complaints. The patient is usually conscious of the change in the heart's 
 action, feeling the rapid beats and sometimes describing them as gentle,
 
 INCREASED FREQUENCY OF THE HEART'S ACTION 135 
 
 sometimes as hard and hammering. These latter sensations may occur 
 with httle or no increase in frequency. In cases of valvular disease with 
 limited reserve force, slight physical effort or mental excitement may 
 readily induce an attack. Even in the healthy, certain mental states may 
 induce an attack, while when the system is weakened from disease the 
 liabiUty to attack is much increased. It is in certain neurotic subjects, 
 particularly females, that one sees the complaint attain its most distinctive 
 features. There may be no organic affection of the heart, and though 
 frequent attacks may ultimately induce exhaustion of the reserve force. 
 
 Fig. 69. During an attack of palpitation. Kate 105. 
 
 yet, as a rule, they do not appreciably shorten life. Anything that startles 
 the patient, whether a sudden noise or mental perturbation when awake, 
 or uncomfortable dreams when asleep, readily induces an attack. But 
 it may supervene from more obscure causes, evidently caused by reflexes 
 from organs more or less remote (stomach, uterus), or from undiscernible 
 sources. When a severe attack comes on the patient may become painfully 
 aware of the violent action of the heart. She prefers to sit upright, draws 
 deep inspirations, and moves uneasily from side to side, with the hand 
 pressed over the heart. It is accompanied by sensations of a distressing 
 nature, such as a sense of suffocation, and a fear of impending dissolution. 
 When it subsides it leaves the patient exhausted. 
 
 Fig. 70. Tracing of the normal pulse of the patient from which Fig. 69 was obtained. 
 
 Rate 64. 
 
 During the attack the pulse is usually increased in frequency. The artery 
 may be of fair size ; sometimes, however, it is very small. The impact of 
 the pulse-wave on the finger is sudden and sharp and of extremely brief 
 duration. The tracing Fig. 69, taken during an attack of palpitation, 
 shows a high upstroke with a great fall, so that the arterial pressure at 
 the bottom of the dicrotic notch is nearly as low as at the end of the 
 diastohc period — an evidence that in addition to the excited heart there 
 is great relaxation of the arterial wall. Fig. 70 is from the same patient 
 when the heart was acting quietly.
 
 136 
 
 DISEASES OF THE HEART 
 
 We occasionally meet with patients in whom the pulse is extremely 
 rapid for a period, sometimes for a few minutes, sometimes for a few 
 hours, with no other sensation than that of exhaustion, the attack quietly 
 subsiding (Fig. 71). The causes are so obscure that it would be mere 
 guesswork, in the majority of cases, to attribute it to any one cause. 
 
 § 130. The cause of increased frequency of the heart's action. — 
 Apart from cases due to nerve excitation, and the nodal rhythm, it is 
 extremely difficult to account properly for this abnormal quickening. All the 
 parts of the heart participate in the excitability. It is not due merely to a 
 dilatation of the heart, for we may have hearts greatly dilated that show no 
 marked rapidity of action, and there may be hearts of normal size which may 
 for a long time beat with great rapidity. Apart from the neurotic cases, it 
 might be assumed that an intoxication of the heart, or a deficiency in some 
 
 Fig. 71. Simultaneous tracings of the radial and jugular pulses. The rhythm is normal, 
 the rate 164 per minute. There is an auricular extra-systole (a' and c' in the jugular tracing 
 and r' in the radial). 
 
 nutriment, is the fundamental cause that renders the tissues more irritable. 
 That the whole tissue is involved, and not merely the cardiomotor centre, 
 is demonstrated in many cases by the quicker contraction of the chambers 
 and the accelerated conduction of the stimulus from auricle to ventricle. 
 Thus, in Fig. 71 the tracing shows a very minute a-c interval, while notwith- 
 standing the abnormal rapidity of the heart's action, the excitability of 
 the auricular muscle was so great that a premature auricular systole actually 
 appeared. 
 
 § 131. Prognosis. — A number of people whose hearts beat too fre- 
 quently show no sign of heart trouble. We then can gauge their condition 
 by their reserve force. Apart from cases with a previous rheumatic 
 history, or of serious heart mischief, I have found that people with con- 
 tinuous rapid hearts gradually recover so far as the heart's condition is con- 
 cerned, and even cases of exophthalmic goitre may gradually recover with 
 the heart slowing down. If an alcoholic will but mend his ways before
 
 INCREASED FREQUENCY OF THE HEART'S ACTION 137 
 
 he has induced organic changes in his other organs, the heart shows a won- 
 derful power of recovery. Manifestly, in the other ailments, as tubercular 
 and mahgnant diseases, the future progress of the case is to a certain extent 
 independent of the heart affection. I -do not like the continued rapidity 
 in cases with valvular lesions, as it implies a serious impairment of the 
 myocardium, and if they do not respond to treatment they generally 
 speed on to a fatal issue.
 
 CHAPTER XVI 
 
 Diminished Frequency of the Heart's Action 
 
 § 132. Definition of the term ' bradycardia '. 
 133. Normal bradycardia. 
 
 § 132. Definition of the term ' bradycardia ' — The term ' brady- 
 cardia ' has been used when the arterial pulse was slow, and from this it has 
 been inferred that the whole heart was slow in its action. The result of 
 this usage has been to employ the term in many cases quite inappro- 
 priately. Thus it is most commonly used in association with the condition 
 known as ' heart-block ', a condition, as will be shoAvn later, where the 
 ventricle alone beats slowly, the auricle pursuing a normal or even 
 accelerated rate. 
 
 In order to differentiate between the different forms of slow pulse-rate, 
 it is necessary to make observation of the movements of the various chambers 
 of the heart. If this is done, it will be found that the cases of diminished 
 frequency of the pulse can be divided into four classes : (1) Those where 
 all the chambers of the heart participate in the slow action (normal brady- 
 cardia) ; (2) where the slow pulse-rate is due to a missed beat, the ventricle 
 having contracted, the resulting pulse-wave being too feeble to reach the 
 wrist (described in § 142, Figs. 85 and 86) ; (3) certain cases of nodal 
 rhythm where the auricle has ceased to beat, or does so synchronously with 
 the ventricle (nodal bradycardia described in Appendix IV, p. 337) ; (4) 
 where the stimulus is blocked between auricle and ventricle so that the 
 auricle beats at its normal rhythm, and the ventricle does not respond 
 to the auricular systole, but pursues an independent and slow rhythm 
 (heart-block, described in § 168, Figs. 122 and 123) ; (5) where the vagus 
 slows the heart, producing standstill of the whole heart for irregular periods 
 (p. 24). 
 
 § 133. Normal bradycardia — This only occurs when all the chambers 
 of the heart participate in the slow action. The demonstration of the 
 character of the slowing is best shown by tracings of the jugular pulse 
 with the radial (Fig. 48, p. 113) or apex beat (Fig. 72, p. 139), where the 
 auricle is seen to beat at the same rate as the ventricle. I have never
 
 DIMINISHED FREQUENCY OF THE HEART'S ACTION 139 
 
 found this form of slow heart beating under forty per minute, though some- 
 times we meet with single pauses lasting nearly two seconds (Fig. 79, p. 146). 
 There is a number of people in the enjoyment of perfect health, whose 
 pulse beats regularly about fifty per minute. Those of whom I have kept 
 a record were mostly tall men. In a great many people of spare habit, 
 who suffer also from the X disease (§ 65), the heart-rate may fall under 
 fifty beats per minute. In some of these a rise of temperature of one or 
 two degrees may actually make the pulse beat slower. There are other 
 conditions which may induce a slowing of the heart's pulse, such as increased 
 arterial pressure in Bright's disease, in gout, and in certain cases of arterial 
 
 Fig. 72. Simultaneous tracings of the jugular pulse and apex beat, showing the participa- 
 tion of auricle and ventricles in true bradycardia. Rate 50 per minute. 
 
 degeneration. In pregnancy the pulse may also be occasionally slow. 
 Jaundice is said to have a considerable power in slowing the pulse, but 
 I myself have never found it. 
 
 Occasionally we find patients losing their memory, and the pulse will 
 be found to be very slow — between forty and fifty beats per minute. Further, 
 certain phases of respiration may slow the pulse, and also the exposure of 
 the body to the cold air or to cold baths. So far as I have observed, I have 
 never found any serious result from such slowing of the heart, and I have 
 watched patients whose pulse may frequently be found about fifty per 
 minute, for fifteen and twenty years.
 
 CHAPTER XVII 
 
 The Irregular Action of the Heart 
 
 § 134. Places where the heart's contraction may start. 
 135. Classification of irregularities. 
 
 Irregular action of the heart is of importance in indicating the mechan- 
 ism of many of the heart's actions, and a knowledge of this mechanism is 
 essential to the proper diagnosis of pathological changes. As it is a subject of 
 some complexity, I give in this chapter a brief review of the more important 
 points bearing upon irregular rhythm, and a classification of the more 
 common forms. 
 
 Irregularities are of such great frequency, and their presence so readily 
 recognized by both patient and physician, that it is necessary clearly to 
 recognize their meaning and significance. Until a few years ago their nature 
 was shrouded in obscurity, and in consequence the mystery regarding 
 them in a great measure oppressed both patient and physician. The fact 
 that in some instances irregularity was of serious import led to the sup- 
 position that all irregularities are signs ©f some grave mischief. In con- 
 sequence of this many patients are subjected to unnecessary fears, made to 
 carry out elaborate methods of treatment, and have imposed upon them 
 burdensome and unnecessary restrictions. 
 
 The advance that has been made in the knowledge of this subject within 
 recent years positively constitutes a revolution. By the combined efforts 
 of clinicians and experimental physiologists, what was recently a complete 
 mystery is now one of the best understood matters in the whole science of 
 medicine. Not only has the scientific aspect been followed out thoroughly, 
 but by watching individual cases for years and noticing the changes that 
 have taken place with advancing years, and observing how people with 
 irregular hearts have borne the stress of life, I have endeavoured to obtain 
 a clearer conception of the bearing of the different irregularities upon the 
 future history of the patient. 
 
 § 134. Places where the heart's contraction may start. — The start- 
 ing-place of the heart's contraction is in the remains of the sinus-venosus 
 that have been incorporated in the veins, such as the node of tissue described
 
 THE IRREGULAR ACTION OF THE HEART 141 
 
 by Keith and Flack at the mouth of the superior vena-cava (1, Fig. 2, p. 15). 
 In describing the functions of the primitive cardiac tube (of which the 
 above-mentioned node is a portion) it was pointed out that any part of the 
 structure was capable of starting the contraction, and that it was because 
 the venous end was the more excitable that the normal rhythm started 
 there (p. 12). When another part of this primitive tube becomes from 
 any cause more excitable than the sinus portion, then the contraction 
 starts at that more excitable part, and an abnormal rhythm results. If 
 a break should occur in the extension of the primitive tissue, the two divi- 
 sions of the heart will beat separately and independently, as is shown in 
 the Stannius' ligature (p. 13). In what is called ' heart-block ' such 
 a separation occurs, and auricle and ventricle beat at independent rhythms. 
 For practical purposes, we can therefore reasonably assume four places 
 where the contraction of the human heart can start : — 
 
 (a) At the mouth of the great veins where the remains of the sinus 
 venosus still persist, giving rise to the normal or sinus rhythm. (6) At 
 the a.-v. node, where auricle and ventricle contract simultaneously, (c) In 
 the a.-v. bundle on the ventricular side of the a.-v. node, where, while the 
 auricle contracts in obedience to the sinus rhythm, the ventricle contracts 
 independently, {d) In the auricular tissue, where some part of the primi- 
 tive tube seems to persist. 
 
 § 135. Classification of irregularities. 
 
 (1) Sinus irregularities. — The heart's contraction arising normally in 
 the remains of the sinus venosus is set to a regular rhythm. The sinus 
 tissue may be excited or depressed as by nerve influence, and irregularities 
 may then occur. This form of irregularity is characterized by a varying 
 length of the cardiac cycle, mainly of the diastoUc portion, the pidse beats 
 being always of equal size or nearly equal size, and presenting no ' imper- 
 fect systoles ' or ' missed beats '. The variation usually corresponds with 
 certain phases of respiration. It is most frequent in the young, but is 
 occasionally present in adult life (see Chapter XVIII). 
 
 (2) Extra-systoles. — Here an auricular or ventricular systole, or both 
 together, may start prematurely and independently of the sinus rhythm. 
 They occur occasionally in an otherwise regular heart ; a premature beat 
 of the radial pulse is felt, followed by a long pause, or there may simply 
 be a long pause (intermittent pulse). Sometimes these extra-systoles may 
 occur with greater frequency, even every second beat being of this nature 
 (pulsus bigeminus). When they are so small as to be imperceptible to the 
 finger, it might seem as if the heart were beating extremely slowly. On aus- 
 cultation synchronous with the premature beat, two short, sharp sounds are
 
 142 DISEASES OF THE HEART 
 
 heard — the first and second sound of the premature or extra-systoHc contrac- 
 tion. These sounds are very characteristic of this condition (Chapter XIX). 
 
 (3) Nodal rhythm. — In advanced disease of the heart from rheumatism 
 and cardio-sclerosis, the starting-place of the contraction is no longer at 
 the sinus, but in some part lower down, where the auricle and ventricle 
 are stimulated to contract for the most part simultaneously. Beats of 
 varying size follow one another at varying intervals ; sometimes the irregu- 
 larity is extreme, sometimes scarcely perceptible, but careful analysis will 
 usually show variations in the length of the cardiac cycle. This irregularity 
 is usually associated with marked diminution of the heart's power, sometimes 
 extreme, at other times only indicated by a limitation of the field of cardiac 
 response when the patient makes an effort. It may occur at all ages. The 
 heart's rate is as a rule more frequent than normal and it may be extremely 
 rapid temporarily (paroxysmal tachycardia) or continuously ; when con- 
 tinuously rapid, it may slow down and beat about seventy to ninety per 
 minute. In some cases it is less frequent than normal (nodal bradycardia, 
 p. 337). 
 
 (4) Irregularities due to failure of the conducting power of the primitive 
 bundle. — This is due to the ventricular systole dropping out in consequence 
 of the stimulus for contraction not reaching the ventricle. This condition 
 is rare, but may occasionally occur in influenza and other infectious com- 
 plaints, and in old and recent rheumatic hearts, especially after digitalis, and 
 in cardio-sclerosis. A more extreme form of the condition is known as 
 heart-block. This condition may be suspected when there is a complete 
 pause in the radial pulse with absence of heart sounds (Chapter XXI). 
 
 (5) Depression of contractility {pulsus alternans). — Irregularities due to 
 the failure of the contractile power of the ventricle are usually regular 
 in rhythm — the beats varying in strength only. The most common form 
 is that where a strong beat alternates with a weak, the rate being quite 
 regular (Chapter XXII, § 179).
 
 CHAPTER XVIII 
 
 Sinus Irregularities 
 
 § 136. Character of the u'regularity. 
 
 137. Etiology. 
 
 138. Symptoms. 
 
 139. Associated symptoms. 
 
 140. Prognosis. 
 
 § 136. Character of the irregularity. — As the primitive cardiac tissue 
 at the mouth of the great veins possesses in a degree higher than any 
 other part the power of rhythmically producing the stimulus for con- 
 traction, the rhythm of the whole heart follows normally the time set by 
 this portion of the primitive tissue. While normally this rhythm is a 
 fairly regular one, as a matter of observation we find a great many people 
 who show a variation, sometimes slight, sometimes marked, in the duration 
 
 Fig. 73. Simultaneous tracings of the jugular and radial pulses, showing 
 the agreement in rhythm of the right auricle and ventricle (waves a and v) with 
 the radial pulse, in the sinus form of irregularity. The irregularity is seen to be 
 due to variations in the length of the diastoUc period (spaces O). 
 
 of the cardiac cycle. There is a much greater constancy in the duration of 
 the systolic period of the cardiac cycle than of the diastolic. With the 
 quickening of the pulse-rate, the shortening of the period of the cardiac 
 cycle takes place almost entirely at the expense of the diastolic portion. 
 In sinus irregularities it is the variation in the length of the diastolic period 
 that is the chief characteristic. In the quickened pulse we find the duration 
 of the diastolic period reduced, so that with increase of rate this irregularity 
 disappears. On the other hand, when the heart gradually slows in its action 
 this form of irregularity is prone to occur, so that we find it best in the young 
 and in some adults after a febrile attack or during slow respiration. Typical 
 instances of sinus irregularity are given in Figs. 73 and 74. In Fig. 73
 
 144 DISEASES OF THE HEART 
 
 the irregularity is seen to be due to variations in the length of the diastole 
 of the heart (period O), the systolic period (E) remaining constant. The 
 jugular tracings show that the right auricle (a) and ventricle (v) participate 
 in the same irregularity as the radial pulse. 
 
 § 137. Etiology. — It is generally agreed that this irregularity is of 
 vagus origin. Normally there is a certain degree of inhibition maintained 
 by this nerve, but its centre may become unusually susceptible to impulses 
 from other parts, and these are transmitted reflexly to the heart. This is 
 well seen in some cases where the vagus is more excitable. In certain cases 
 the reflex stimulation of the vagus will produce an alteration of the heart's 
 rate, as in Fig. 75, Plate I, where it is shown that the act of swallowing 
 quickened the heart-rate for a few beats, and then caused a slowing. 
 A more striking illustration of the reflex effect of swallowing on the heart 
 is found in Figs. 258 and 259, Plate IV, where it not only slowed the sinus 
 
 
 Fig. 74. Simultaneous tracings of the jugular and radial pulses, showing that the auricle 
 participates in the irregularity, and that there is no premature contraction during the long 
 pauses (sinus irregularity). 
 
 rhythm, but depressed the conductivity of the a. -v. fibres, so that the 
 stimulus from auricle to ventricle was occasionally blocked. In Fig. 76, 
 Plate I, a vagus effect is shown after the patient has taken three deep 
 and hurried respirations. This patient was under the influence of digitalis, 
 but here the effect is purely upon the sinus, showing a slowing of the rate. 
 In these tracings it is further to be noted that the vagus effect is not 
 immediately produced and does not at once pass off, but lasts some little 
 time. Thus, in Figs. 75, Plate I, 258 and 259, Plate IV, there is shown 
 a secondary slowing some seconds after the swallowing, and in Fig. 76, 
 Plate I, the slowing comes gradually on after the hurried respirations. The 
 reason I dweU upon this is because this sinus arrhythmia is often distinctly 
 respiratory in origin, though the pulse variations do not always correspond 
 with identical phases of the respiration, as in Fig. 77, Plate II, where the 
 slowing occurs at different phases of the respiratory movement. 
 
 In the dog this irregularity is very common, and disappears on section 
 of the vagus. An irregularity identical with Fig. 79, due to vagus stimu- 
 lation, is shown in Fig. 78.
 
 SINUS IRREGULARITIES 
 
 145 
 
 § 138. Symptoms — This irregularity is easily recognized. To the 
 finger the pulse-rate is continually changing, usually with respiration, and 
 the beats are equal in strength. On auscultation the sounds are heard 
 clear and distinct, and the interval between the first and second sounds is 
 constant. By the ear, the varying difference in the diastolic period can be 
 made out more easily than by the pulse. In rare instances the slowing 
 may occur at rare intervals and affect only one or two beats, as in 
 Fig. 79, and there may be at first some difficulty in recognizing the 
 nature of the irregularity, but when the condition of the patient in other 
 
 Fig. 78. Shows the effect of vagus stimulation in the dog's heart. The down- 
 ward movements in the tracing of auricle and ventricle are due to the systole. 
 The vagus was stimulated at s, and produced a standstill of the whole heart 
 (Cushny). 
 
 respects is taken into account, the nature of the irregularity can be 
 inferred with certainty. Such an irregularity from any other cause would 
 show evidence of severe heart trouble (as heart-block or the nodal 
 rhythm), whereas in such cases there is no evidence of heart trouble, or 
 but the very slightest. Tracings of the jugular pulse at once determine the 
 nature of the irregularity, by showing that the auricle is also subject to the 
 same influence. 
 
 § 139. Associated symptoms — These are merely incidental, the 
 
 MACKENZIE T
 
 146 
 
 DISEASES OF THE HEART 
 
 irregularity itself causing no subjective symptom. When some incidental 
 phenomenon such as syncope appears, an undue importance may be attached 
 by the physician to the irregularity. Many young folks have syncopal 
 attacks, and this irregularity, being the only abnormal feature found by 
 the physician, is often the ground on which unnecessary alarm and 
 unnecessary treatment are based. 
 
 Although in the vast majority of cases the slowing of the heart, 
 presumably due to vagus action, gives rise to no symptoms, particularly 
 in the young and when of respiratory origin, yet the period of 
 standstill may be at times so long as to produce an effect on the 
 brain. The patient from whom Fig. 79 was taken had attacks of 
 giddiness at times, and the pauses in the heart's action were often longer 
 
 Fig. 79. Occasional slowing of the Avhole heart due to inhibitory nerve influences on the 
 sinus. The a-c interval (space A) is not affected by the variations in rate. (Compare with 
 
 Fig. 78.) 
 
 than that figured here. Laslett ^^^ records a case and gives numerous 
 tracings in which the standstill was frequently so long that the patient 
 lost consciousness. 
 
 In the vague condition which I have described as the X disease (§ 65) 
 the respirations are often slow, falling sometimes to seven per minute. When 
 this occurs, the pulse invariably shows this irregularity (Fig. 77, Plate II). 
 It has also been found present in neurasthenia, and some go so far as to 
 diagnose neurasthenia by this irregularity alone. Nicholson '^^* has demon- 
 strated its presence in infants, Watson WiUiams -^^ in healthy schoolboys, 
 and Deane ^^^ in athletic soldiers, and I have found it in a great number of 
 healthy individuals, so that one can safely look upon its association with 
 neurasthenia as merely incidental. It is this form of irregularity which 
 is present in tubercular meningitis. 
 
 § 140. Prognosis. — There is no reason for attaching importance to 
 this irregularity, and no condition should be considered more grave 
 because of its presence. After a febrile attack it may usually be looked
 
 SINUS IRREGULARITIES 147 
 
 upon as a favourable sign. Its presence in tubercular meningitis adds 
 nothing to the seriousness of the condition. 
 
 The presence of this sinus irregularity may even afford grounds for 
 a favourable prognosis when it occurs in the young after recovery from 
 rheumatic fever, even though there may be a mitral systolic murmur, 
 for it is not present when there is exhaustion of the heart muscle. 
 
 Treatment. — It calls for no special treatment, nor should any attempt 
 be made to treat this symptom alone. 
 
 l2
 
 CHAPTER XIX 
 
 The Extra-systole 
 
 § 141. Definition of the term ' extra-systole '. 
 
 142. Character of the irregularity. 
 
 143. Etiology. 
 
 144. Ventricular extra-systole. 
 
 145. Auricular extra-systole. 
 
 146. Nodal extra-systole. 
 
 147. Condition of the a.-v. bundle in cases showing extra-systoles. 
 
 148. The dropping out of the beat after the extra-systole. 
 
 149. Reasons for attributing the origin of extra-systoles to affections 
 
 of the remains of the primitive cardiac tube. 
 
 150. Conditions inducing extra-systoles. 
 
 151. Sensations produced by extra-systoles. 
 
 152. Prognosis. 
 
 153. Treatment. 
 
 § 141. Definition of the term * extra-systole ' There are so many 
 
 conditions that simulate extra-systoles, that a good deal of confusion exists 
 in regard to what really constitutes an extra-systole, and it is therefore 
 necessary to define the term. As the stimulus for contraction arises normally 
 in the remains of the sinus venosus at the mouths of the great veins, and as 
 the stimulus passes from these places to the auricle, then to the ventricle, 
 
 Fig. 80. The small beats are due to extra-systoles. 
 
 80 that there is normally a sequence of stimulation and contraction of sinus, 
 auricle, and ventricle, I would suggest that the term ' extra-systole ' should 
 be limited to those premature contractions of auricle or ventricle in response 
 to a stimulus from some abnormal point of the heart, but where otherwise 
 the fundamental or sinus rhythm of the heart is maintained. 
 
 § 142. The character of the irregularity The extra-systole is 
 
 usually recognized by the occurrence of a premature beat in the radial 
 pulse followed by an abnormally long pause, as is shown in Fig. 80, where
 
 THE EXTRA-SYSTOLE 
 
 149 
 
 the two small beats are extra-systoles. It may appear only at rare intervals, 
 or it may occur at frequent irregular intervals, or regularly after every 
 1, 2, 3, 4, or more, normal beats, as in Figs. 81, 82, 83, 84. 
 
 Fig. 81. Pulsus bigeminus due to an extra-systole occurring after each normal beat. 
 
 Fig. 82. Extra-systole occurring after every two normal beats. 
 
 Fig. 83. Extra-systoles occurring after every three normal beats. 
 
 Fig. 84. Extra-systoles occurring after every four normal beats. 
 
 The ventricular contraction causing the extra-systole may be so weak 
 that no wave is perceptible to the finger in the radial, though it may be 
 detected in the sphygmogram, as in Fig. 85. In some cases it may even 
 not appear in the sphygmogram, but the heart's sounds, or a tracing of the 
 apex beat at the same time, show that during the long pause in the radial 
 pulse the ventricle contracted, but not with sufficient strength to send a wave 
 into the radial artery (Fig. 86). 
 
 In these cases the pulse is described as ' intermittept *, or, if the extra-
 
 150 
 
 DISEASES OF THE HEART 
 
 systoles occur regularly after each normal beat, the pulse at the wrist appears 
 extremely slow, and the case may be put down as ' bradycardia ', or heart- 
 block. It may be differentiated by the observation of the jugular pulse or 
 apex beat, or by auscultation. 
 
 Fig. 85. Slow pulse feeling to the finger about 30 per minute. The small waves (r') are 
 due to extra- systoles and were not perceptible to the finger. 
 
 The extra-systole is easily recognized on auscultation. The regular 
 sequence of sounds is interrupted by two short, sharp sounds (if very feeble, 
 
 
 Apex 'beat 
 
 
 ^r\ r\r\ 
 
 Af\ n y^ 
 
 r\n 
 
 yuV^ 
 
 ^\l^n 
 
 y n 
 
 r-f- 
 
 -J^^-^-J^ 
 
 ~JM 
 
 Radial 
 
 
 Fig. 86. Simultaneous tracings of the apex beat and of the radial 
 pulse. There are two beats of the apex to one radial pulse. 
 
 only one sound may be heard) followed by a long pause, as is represented 
 in the diagrams, Figs. 87 and 88. 
 
 iiiiaiMiB 
 
 Fig. 87. Diagram representing the sounds of the heart 
 with occasional extra-systoles. 
 
 § 143. Etiology. — In seeking for an explanation for the occurrence of 
 extra-systoles, I collected a large number of instances and then sought 
 for some basis of classification. Hitherto the classification has to a great 
 extent been based on the results of experiments, but I found in the human
 
 THE EXTKA-SYSTOLE 151 
 
 heart many variations which did not coincide with experimental results. 
 After trying various methods, I took up the idea that the remains of the 
 primitive cardiac tube in the human heart might preserve the functional 
 peculiarities of the original tube. One of these peculiarities is the power 
 possessed by any part of the tube, if rendered more excitable, to start the 
 heart's contraction before the sinus. As the primitive tube in the heart is 
 represented at the mouths of the great veins, in the auricle, in the a.-v. node, 
 and in the a.-v. bundle after it leaves the node (Fig. 2), I reasoned that while 
 the normal rhythm started at the veins, premature contractions might 
 start in the remains in the auricle, a.-v. node, or bundle. Examining my 
 tracings with this view in mind, I found that the vast majority readily 
 fell into this classification. 
 
 A further proof was found in the fact that in many cases the power 
 of conduction in the a.-v. bundle was impaired, implying an invasion of 
 this system by the disease, a view further supported by post-mortem 
 examinations. 
 
 Fig. 88. Diagrammatic representation of the sounds of the 
 heart in a case of such rhythmical irregularity as is represented in 
 Figs. 81, 85, and 86. 
 
 Wliile I do not assert that this view is proven to be correct, I use it, 
 as it brings out more clearly the salient points of the varied forms of 
 extra-systole, I claim no originality for this suggestion, as the possibility 
 of arrhythmias arising at the a.-v. bundle has occurred to many people. 
 
 § 144. Ventricular extra-systole — (The place of origin of ventri- 
 cular extra-systoles is assumed to be in the a.-v. bundle beyond the a.-v. 
 node or in some part of its branches in the ventricular wall.) The simplest 
 form of extra-systole is that where a premature contraction of the ventricle 
 is interpolated between two normal beats. 
 
 In Fig. 89 there are two small waves r' in the radial, which are due to 
 extra-systoles of the left ventricle. In the tracing from the neck the waves 
 c are due to the carotid, the waves a are due to the auricle, and the waves c' 
 are due to the extra-systoles and correspond to r' in the radial. The diagram 
 intercalated between the radial tracing and the tracing from the neck 
 shows the relationship of the different events. The downstrokes in the 
 upper compartment represent the beginning of the auricular systoles, and 
 the downstrokes in the lowest compartment represent the beginning of the
 
 152 
 
 DISEASES OF THE HEART 
 
 carotid pulse beats, while the slanting lines in the middle compartment 
 represent the time between the beginning of the auricular and carotid 
 waves (the a-c interval). In the cardiac cycles, apart from those in which 
 the extra-systoles r' and c' occur, the ventricular contraction follows 
 regularly on the auricular, and it is assumed that the sinus rhythm governs 
 the contraction of the auricle. The extra-ventricular contractions are seen 
 to start independently of the auricular contraction — that is, they are extra- 
 systoles of the ventricle. The same features are to be recognized in Fig. 90, 
 Plate II, where there are four extra-systoles (r' in the radial, and c' in the 
 jugular tracing) ; it will be seen that the auricular wave appears at regular 
 
 Fig. 89. Simultaneous tracing of the jugular and radial pulses, showing the interpolation 
 of ventricular extra-systoles (c', c' and r', r') represented in the diagram by the downstrokes -f- -t-. 
 The downstrokes in the space As represent the auricular waves (o) in the jugular, and the 
 downstrokes in the space Vs represent the carotid waves c, and the slanting lines connecting 
 them represent the a-c interval. 
 
 intervals, and that the extra-systoles are interpolated between two normal 
 beats. 
 
 In Fig. 91, Plate II, there is an extra-systole during each of the irregular 
 periods B and C. In the jugular tracing the carotid wave c follows the 
 auricular wave a, but during the two irregular periods the carotid wave c' 
 precedes the auricular wave a', a fact brought out clearly in the intercalated 
 diagram. We can prove that c' is due to the carotid, because it occurs 
 at the same time after the preceding carotid wave that the radial beat r' 
 appears after the preceding radial beat. The auricular wave a' appears at 
 the normal auricular interval, and the auricle pursues its wonted regular 
 rhythm while the ventricle is contracting prematurely and independently. 
 
 In the irregular period B the interval between a' and the following c is 
 greatly lengthened (space A^). The reason of this delay is shown in the 
 diagram to be due to slower passage of the stimulus from auricle to ventricle
 
 THE EXTRA-SYSTOLE 
 
 153 
 
 — a fact of great importance, which will be dealt with in discussing the 
 condition of the conductivity of the auriculo-ventricular bundle. 
 
 In the irregular period (7, there is a much longer pause in the radial 
 tracing after the extra-systole r', and the intercalated diagram shows that 
 this is due to the fact that the ventricle does not respond to a stimulus 
 after a'. The difference between the irregular periods B and C is seen, 
 therefore, to be due to the fact that in the irregular period B the ventricle 
 responds to the stimulus from the auricular systole after the extra-systole, 
 whUe in the ii-regular period C the ventricle does not respond. 
 
 The irregular period C represents the most common form of extra- 
 systole, and its appearance in grapliic records is usually easily recognized 
 by the presence of the long pause after the premature beat r'. 
 
 Fig. 92. Represents a common form of ventricular extra-systole. There is a long pause 
 after the extra-systole (r'). In the jugular tracing and in the diagram this is seen to be due 
 to the failure of the stimulus from the auricle (a') to provoke a ventricular contraction. 
 
 Thus Fig. 92 is a very characteristic example, and the intercalated 
 diagram shows a regularly acting auricle and the premature and independent 
 ventricular contraction with no response to the auricular systole after the 
 premature ventricular contraction, which accounts for the long pause. 
 
 Simultaneous occurrence of the normal auricular systole and of the 
 ventricular extra-systole. — In the illustrations I have given of the ventricular 
 extra-systole (as in Figs. 89 and 92), in the jugular tracing the carotid wave 
 c' was seen to precede the auricular wave a'. In these instances the normal 
 rate was rather slow. In most instances, however, they fall together — the 
 auricular contraction occurring during the ventricular contraction. In 
 consequence of this the auricle cannot empty its contents into the ventricle, 
 and hence a big wave is sometimes sent into the jugular. In patients with 
 a well-marked jugular pulse, this is readily recognized by the eye. In 
 other cases the jugular pulsation is only to be seen when this big wave is 
 sent back.
 
 154 
 
 DISEASES OF THE HEART 
 
 In Fig. 93 the waves a and a' are due to the auricular systole, and_^occur 
 at regular intervals. The waves a' are, however, much larger than the 
 waves a, and the reason for the increase in size is found in the fact that at 
 that time the ventricle was also in systole, causing the extra-systole. ^ In 
 Fig. 94 a simultaneous record of the apex beat and jugular pulse shows 
 the premature contraction of the ventricle o at the same time as the large 
 
 Fig. 93. Simultaneous tracings of the jugular and radial pulses. The small beats x x x 
 are extra-systoles. The auricle preserves its rhythm during the irregular periods in the radial 
 pulse.' The wave a' is the auricular wave during the premature contraction of the left ven- 
 tricle. The absence of the ventricular wave v, after the wave a', indicates that the right 
 ventricle had contracted early, evidently synchronous with the premature contraction of the 
 left ventricle, the large wave following a' being due to stasis. 
 
 auricular wave a', so that here also we have evidence of the simultaneous 
 contraction of auricle and ventricle during a ventricular extra-systole. 
 When there is a large jugular pulse, the increased size of the auricular wave 
 occurring during the extra-systole of the ventricle may not be so marked 
 as in Fig. 95. 
 
 Apexl>eat 
 
 dfp a C 
 
 mint. Jugular 
 
 Fig. 94. Simultaneous tracings of the apex beat and of the jugular pulse, showing the 
 rh3rthmical appearance of the auricular wave during the irregular periods in the apex tracing. 
 The small beats o o o are extra-systoles of the ventricle. 
 
 § 145. The auricular extra-systole — (The suggestion put forward 
 here is that, in the production of the auricular extra-systole the stimulus 
 arises in the primitive tissue incorporated in the auricle— the exact site 
 being still undetermined.) 
 
 When an extra-systole arises in the auricle, the sounds of the heart and 
 the radial tracing present exactly the same features as when a ventricular 
 extra-systole occurs, and it is only by a simultaneous record of the jugular
 
 THE EXTRA-SYSTOLE 
 
 155 
 
 pulse that the one can be differentiated from the other. In Figs. 96 and 97 
 the radial pulse shows premature beats {r'), which can be readily identified 
 as extra-systoles. 
 
 In the jugular tracings the carotid wave c' is preceded by an auricular 
 wave a', and the only inference that can be^drawn is that a' is due to an 
 
 Fig. 95. Shows three ventricular extra-systoles in the radial (r') while the auricle pursues 
 its regular rhythm (o and a'). The downstrokes 3 and 4 represent the time of the carotid and 
 radial pulses. 
 
 extra-systole of the auricle, which is followed by an extra-systole of the 
 ventricle, producing the carotid and radial beats c' and r'. 
 
 In such instances as these the auricle is supposed to contract in reply to 
 a stimulus from some source other than the sinus, and the long pause after 
 the extra-systole is due to the fact that the stimulus from the sinus arising at 
 
 Fig, 96. Shows auricular extra-systoles (a') followed by ventricular contractions (c', r'). 
 The arrows in the diagram represent the sinus stimulation and the long pauses after the extra- 
 systoles are seen to be due to the fact that the auricle did not respond to the sinus stimulation. 
 
 its normal time fails to provoke the refractory auricle to contraction. This 
 is brought out in the intercalated diagram in Fig. 96, in which, above the 
 upper space, are arrows representing the sinus stimulation. In the diagram 
 it mil be seen that there is no response to the sinus stimulation after the 
 extra-systole, but that auricle and ventricle remain quiescent till the following
 
 156 
 
 DISEASES OF THE HEART 
 
 sinus stimulation excites them to a contraction. In these two illustrations 
 the irregular period is equal to two cardiac cycles, the explanation being 
 obvious from the study of the diagram in Fig. 96. In most cases of auricular 
 extra-systole, the irregular period is less than two cycles, as is shown in Figs. 
 98 and 99. The reason given by Cushny ^^^ and Wenckebach -^, and usually 
 
 Fig. 97. Shows an auricular extra-systole a'. The numbers represent tenths of a 
 second and the irregular period (r') equals two normal periods. 
 
 accepted, is that the stimulus arising in the auricle passes back to the sinus 
 and stimulates the sinus so that its stored energy is exhausted, and it begins 
 to build up anew the stimulus material. As soon as it has again reached 
 the excitable stage, it starts off the contraction. Thus in the diagram 
 
 Fig. 98. Shows two premature or extra-systoles of auricular origin ( x ). The waves c' in 
 the jugular tracing occur at the same time as the small premature beats (-f) in the radial 
 tracing, and are therefore due to the carotid. These are preceded by premature waves o' due 
 to the auricle. The interval a'-c' (space ^3) is greater than the average a-c interval (^2)- ^'^^ 
 is much greater than the following a-c interval (A^). 
 
 (Fig. 100), representing the events in Fig. 99, the stimulus is represented 
 coming down from the sinus to the auricle, but at the extra-systole ( + ) 
 the stimulus is represented by an arrow passing back to the sinus, so that 
 the sinus responds to the retrograde stimulation. After this premature stimu- 
 lation, the sinus rests for a normal period, and starts off again at the normal
 
 THE EXTRA-SYSTOLE 
 
 157 
 
 rhythm. This irregular period, due tp the auricular extra-systole, is so. 
 frequently shorter than two normal beats that this is usually assumed to be 
 the manner in which it is brought about. While it offers a plausible ex- 
 planation, it cannot be said in any sense to have been proved, and there are 
 other possibilities which need consideration before it can be finally accepted. 
 
 Fig. 99. Shows an extra-systole of axiricular origin at a'. 
 
 the diagram, Fig. 100. 
 
 This tracing is interpreted in 
 
 As, however, they are still speculative, it would not be convenient to discuss 
 them here. 
 
 § 146. The extra-systoles arising in the auriculo-ventricular 
 node (nodal extra-systole). — So far the recognition of extra-systoles as 
 ventricular or aiiricular has been comparatively easy. There is a 4;hird 
 class which has hitherto not been sufficiently considered, and which, in my 
 opinion, has been wrongly interpreted. The characteristic feature of these 
 
 Fig. 100. Diagram representing the events in Fig. 99. The extra-stimulation at -f is 
 represented arising in the auricle, passing back and disturbing the sinus rhjrthm. Note the 
 lengthened a-c interval after the auricular extra-systole. 
 
 extra-systoles is that auricle and ventricle contract prematurely and together. 
 In Figs. 93, 94, and 95, it was demonstrated that auricle and ventricle con- 
 tracted together when the ventricular extra-systole appeared at the same 
 time as the normal auricular systole. In these cases the auricle could be 
 demonstrated to contract at its normal period. In another class of cases 
 it can be demonstrated that both auricle and ventricle contract prematurely 
 and together, the auricular wave appearing at the same time as the arterial
 
 158 DISEASES OF THE HEART 
 
 pulse. Thus in Figs. 101 and 102, the auricular waves a' in the jugular 
 appear prematurely, and obscure the appearance of the carotid waves, — 
 the time when the latter were due can be ascertained by measuring the time 
 between the extra-systole in the radial pulse, and the preceding beat. That 
 the auricle did not contract at its normal time is evident by the absence of 
 any wave at the time of the arrow in the intercalated diagram of Fig. 101 
 
 Fig. 101. Shows a nodal extra-systole (a' and r'), the auricular and ventricular systoles 
 as shown in the diagram are premature and simultaneous. 
 
 during the irregular period, which is the time when it was due. Here then 
 we have evidence that both auricle and ventricle contracted prematurely 
 and simultaneously. In the ventricular and auricular forms no difficulty 
 is found in recognizing that the extra-stimulation must have affected either 
 one chamber or the other, but in this form we have to consider where a stimu- 
 
 FiG. 102. Shows two nodal extra-systoles (a'), the auricular waves a appearing prema- 
 turely and at the same time as the extra-systole in the radial. 
 
 lation could arise that would at once affect both chambers. If all the possi- 
 bilities be considered, we are driven by a process of exclusion to attribute 
 the source of this stimulation to the tissue that joins auricle and ventricle, 
 and almost to a certainty to that portion described as the auriculo-ventri- 
 cular node (2, Fig. 2). This will be brought out more clearly in the later 
 discussion.
 
 THE EXTRA-SYSTOLE 159 
 
 In many cases it is difficult to tell whether the stimulus producing the 
 extra-systole arises in the ventricle at the same time as the normal auricular 
 systole, or whether they have contracted together in response to an abnormal 
 stimulation. In the latter case the abnormal stimulation affects the auricle 
 at the same time that the normal was due, so that we do not get the proof 
 of the premature contraction of the auricle. My reason for this suggestion 
 is that sometimes we meet with a variety of extra-systoles in the same 
 patient, indicating that at one time the auricle is prematurely stimulated, 
 at another time the ventricle, and again both ventricle and auricle together. 
 This is well seen in Fig. 103, Plate II, where three forms of extra-systole 
 occur. The wave a' in the irregular period C is manifestly an auricular extra- 
 systole followed by a premature carotid wave c', which corresponds in time 
 to the extra-systole in the radial tracing. In the irregular period B, the 
 
 Fig. 105. Shows two nodal extra-systoles. Diuing the irregular period A, the large 
 auricular wave a' appears at the normal auricular period, while during the irregular period B, 
 a' and r' occur prematurely and synchronously. 
 
 auricular wave a' appears at its normal interval, but in the radial tracing there 
 is seen an extra-systole which appears at the same time as the wave a' . This 
 is undoubtedly a ventricular extra-systole. In the irregular periods A and D, 
 the conditions are not the same. The wave a' here has quite a different 
 appearance from that in either B or C, being broader at the top. It is 
 difficult to be certain whether it appears before the normal auricular systole 
 was due, as there is a little sinus arrhythmia — the pulse periods not being of 
 equal duration. The absence of the extra-systole in the radial does not 
 imply that the left ventricle did not contract, for, as we shall see later, the 
 ventricle may contract so feebly that a pulse-wave does not reach the wrist. 
 That they are probably nodal extra-systoles can be inferred from the nature 
 of the extra-systoles that occurred from time to time in the patient. Thus the 
 typical auricular extra-systole in Fig. 99 is from the same patient. Fig. 104, 
 Plate II, is also from the same patient, and shows two irregular periods in 
 which the large wave a' appears before a normal auricular systole is due.
 
 160 DISEASES OF THE HEART 
 
 From this I suggest that this wave is of the same nature as that of a' in the 
 irregular periods A and D, Fig. 103, Plate II, namely, due to a premature 
 and simultaneous contraction of auricle and ventricle. The suggestion that 
 the abnormal stimulation may afifect auricle and ventricle at the time the 
 normal auricular stimulus is due is supported by such a tracing as Fig. 105. 
 There are here two irregular periods, A and B, due to extra-systoles. The 
 extra-systole in A is only slightly premature, and the large wave a' appears 
 at the time the normal auricular wave was due. The extra-systole in B 
 appears earlier, with the result that the large wave a' appears before the 
 time the normal auricular systole was due, so tha?t here auricle and ventricle 
 contracted simultaneously and prematurely. 
 
 This explanation of the occurrence of the extra-systole arising in the 
 auriculo-ventricular node is not the one usually accepted. It has been 
 assumed that these cases are really ventricular extra-systoles, and that the 
 stimulus has passed back and prematurely stimulated the auricle, ' a retro- 
 grade extra-systole ' as it has been called. But that this explanation is 
 not tenable can be proved on several grounds. As was shown in Figs. 89, 90 
 Plate II, 91 Plate II, and 92, there is no tendency for the stimulation 
 from the ventricular extra-systole to afifect the auricular rhythm. If the 
 stimulus does travel back, the rate backward must be much greater than 
 that at which the normal stimulus travels forward, for as shown in the 
 diagram, in Fig. 101, the time of the ventricular systole is exactly at the 
 same time as the auricular. That this time should be shorter is very unlikely 
 for two reasons — (1) the auriculo-ventricular bundle would be stimulated 
 by the ventricular extra-systole so soon after its conductivity had been 
 exercised, that it would not have recovered, and a backward stimulus would 
 therefore be delayed, just as the normal stimulus was delayed after the 
 extra-systole in Fig. 89. (2) The simultaneous and premature contraction 
 occurs in patients in whom the conductivity of the auriculo-ventricular 
 bundle is impaired, as I shall show presently. 
 
 § 147. The condition of the a.-v. bundle in cases showing extra- 
 systoles — From what I have said, there are three forms of extra-systole 
 all arising demonstrably from different places in the heart. Moreover, 
 certain individuals exhibit all these forms, and it is therefore reasonable 
 to infer that all these are due to some common cause. When all the possi- 
 biUties are considered, the suggestion that the primitive tissue is the seat 
 is the most plausible, and the question then arises, is there any further 
 evidence to be elicited as to the condition of this primitive tissue ? 
 
 The only clinical evidence of the condition of the primitive tissue is to 
 be found in measuring the rate at which the stimulus for contraction passes
 
 THE EXTRA-SYSTOLE 161 
 
 along the a. -v. bundle from auricle to ventricle. This rate is found by measur- 
 ing in jugular tracings the time between the beginning of the auricular wave 
 and the beginning of the carotid wave — the a-c interval (between lines 
 1 and 3 in the tracings of the jugular pulse as in Figs. 47 and 48), as I have 
 called it. This interval is occupied by three events : (1) the systole of the 
 auricle ; (2) the transmission of the stimulus from auricle to ventricle ; (3) a 
 minute portion of time taken up by the interval during which the ventricular 
 pressure is rising before the opening of the aortic valves. As (3) is practically 
 constant, any variation in the duration of the a-c interval can be attributed 
 to a variation in the rate of the stimulus conduction in the a. -v. bundle 
 (see § 163). In normal individuals, this period very rarely exceeds one-fifth 
 of a second. In hearts acting too frequently, this interval is usually less, 
 sometimes one-tenth. One may suspect something wrong with the a.-v. 
 bundle when this period is one-fifth of a second when the heart is beating 
 rapidly, for the stimulus that quickens the heart-rate will also quicken the rate 
 of conduction when the a.-v. bundle is intact. In healthy slow-acting 
 hearts, in which there is a variation in the heart's rate, it is found that whether 
 the heart's pauses are short or long, the a-c interval preserves a remarkable 
 constancy. The best instance of this is found in the young, and in those 
 healthy adults in whom there is present the sinus form of irregularity. Thus 
 in Fig. 79, p. 146, the long pause is due to a standstill of the whole heart, 
 and is a very typical example of ' sinus irregularity ', probably of vagal 
 origin, and here the constancy of the a-c interval (spaces A) is very well seen. 
 
 On the other hand, if we look at the interval between the auricular extra- 
 systole a' and the following carotid wave c' in Figs. 98 and 99, we find it 
 markedly increased. This implies that the conductivity in the a.-v. bundle 
 had not recovered from its previous stimulation, and the slowness of recovery 
 is the proof of inefficiency. In cases of ventricular extra-systole, as in 
 Figs. 89, 90 Plate II, and 91 Plate II, and in cases of extra-systole arising 
 at the a.-v. node, as in Fig. 101, we find frequently a distinct shortening of 
 the a-c interval after a long period of rest, and a lengthening when the period 
 of rest is short. This is well illustrated in Fig. 106, Plate II, where after the 
 long pause the a-c interval becomes less than one-fifth of a second {A^), 
 but with each succeeding beat it gradually lengthens (.^^ Ar^ A^) until it 
 exceeds one-fifth of a second in duration. In elderly people in whom extra- 
 systoles occur, this variation in the conductivity of the a.-v. bundle is almost 
 always present. I have also met with an increase of the a-c interval, and 
 extra-systoles after rheumatic fever. 
 
 § 148. The dropping out of the beat after the extra-systole. — In 
 most instances there is a long pause after the extra-systole — the so-called 
 
 MACKENZIE J^J
 
 162 DISEASES OF THE HEART 
 
 compensatory pause (pulse intermission). The reason given by Engelmann, 
 and usually accepted, is that the ventricle is so exhausted after the preceding 
 contraction that it is refractory to the following normal stimulus. While this 
 may be the explanation when the extra-systole is produced experimentally, 
 it does not hold good for the spontaneous extra-systole in man. In Figs. 89, 
 p. 152, and 90 Plate II, and in the irregular period -B of Fig. 91, Plate II, there 
 is no compensatory pause, because, as can be seen from the intercalated 
 diagrams in Figs. 89, and 91 Plate II, the stimulus from the auricular 
 contraction immediately following the extra-systole did get through and 
 stimulated the ventricle. In each case, however, the stimulus took a much 
 longer time to pass from auricle to ventricle. Ih Fig. 91, Plate II, the 
 stimulus failed to get through during the irregular period C, for there is no 
 ventricular response to the auricular contraction after the extra-systole. In 
 these and in many similar instances, it is manifest that the reason the ventricle 
 does not contract in response to the stimulus from the auricle after an extra- 
 systole, is that the stimulus is blocked in its passage over the a.-v. bundle. 
 Hewlett 202 lias recently recorded a case in which the ventricle did not respond 
 to the stimulus from an auricular extra-systole, and the same explanation 
 is given by him. From the foregoing considerations, I make the suggestion 
 that the compensatory pause is not due to the ventricle being refractory, 
 but to the a.-v. bundle being refractory and not conveying the stimulus to 
 the ventricle, which therefore stands still tiU the next physiological stimulus 
 comes down from the auricle. 
 
 § 149. Reasons for attributing the origin of extra-systoles to 
 
 affection of the remains of the primitive cardiac tube (i) An 
 
 a priori reason, in the fact that the primitive tube possesses a greater 
 excitabiHty than the auricular and ventricular tissue, and that therefore 
 an abnormal stimulus is more likely to arise in this tissue. 
 
 (2) It satisfactorily accounts for the three forms of extra-systole, especi- 
 ally when in any individual two or more forms arise. It seems more 
 reasonable to assume that the one organ or tissue being degenerated gives 
 rise to an extra stimulus, now at the auricular portion, now at the ventricular 
 portion of the bundle, and now at the a.-v. node, than to say it arises now 
 in the auricle, and now at the ventricle, and again at some other part of the 
 ventricle which propagates a stimulus back to the auricle. 
 
 (3) The frequent association of extra-systole with impaired conductivity 
 of the a.-v. bundle impHes an affection of the tissue in question. It may be 
 objected that an extra-systole is an evidence of exalted function, while 
 impaired conductivity is an evidence of depressed function. GaskeU has 
 shown that the rate at which a stimulus passes across a bridge of heart
 
 THE EXTRA-SYSTOLE 163 
 
 muscle can be retarded by narrowing the bridge over which the stimulus 
 for contraction has to pass. In the cases of associated depressed conduc- 
 tivity and extra-systole, there is destruction of some part of the bundle, 
 while the degenerative process which does this, renders the part more 
 irritable, and we meet with the combination of extra-systoles and heart-block. 
 
 (4) These degenerative processes are more common in advanced years, 
 hence it is in the elderly we find extra-systole most frequent. So far as 
 Dr. Keith has examined the hearts of patients I have sent him who showed 
 extra-systoles during life, he has invariably found evidence of degeneration of 
 the a.-v. node and bundle. As, however, there was always present degene- 
 ration of the coronary artery and muscular fibres of the ventricle, it does 
 not exclude the possibility of ventricular degeneration giving rise to the 
 extra-stimulus, except for the a priori reason already given. 
 
 I give these reasons, not that I consider they are conclusive, but as 
 suggesting a possible explanation. The matter, however, awaits further 
 experimental work before it can be finally settled. The explanation given 
 seems to me to be more satisfactory than the one hitherto adopted. 
 
 § 150. Conditions inducing extra-systoles A condition necessary 
 
 to the production of an extra-systole is an undue excitabihty of the remains 
 of the primitive cardiac tube. It is not easy in all cases to understand 
 how this arises. In elderly people there are almost invariably sclerotic 
 changes in the coronary artery, and especially in the branch that supphes 
 the a.-v. node and bundle ; and secondary changes are usually present 
 in these structures. I have reasoned, therefore, that these secondary 
 changes increase the excitability of this tissue, so that the stimulus for 
 contraction arises quicker here than at the sinus. A great many facts 
 point to the reasonableness of this interpretation. A normal slow sinus 
 rhythm gives an opportunity for the stimulus to arise elsewhere, and it 
 is in the elderly with a slow pulse that one most often finds extra-systoles. 
 On the other hand, extra-systoles sometimes occur in rapidly-beating 
 hearts, perhaps because, although the sinus is discharging impulses more 
 rapidly than normal, these are not sufficient to exhaust the irritability of 
 some very sensitive point in the primitive tube. But not infrequently 
 when a heart which ordinarily exhibits extra-systoles is accelerated, as in 
 slight fever, the extra-systoles disappear, because the impulses arising from 
 the sinus are now sufficient to exhaust the irritability of the part which 
 ordinarily gives rise to the extra-systole. 
 
 Another condition that tends to increase the excitability of this structure 
 is the changes subsequent to rheumatic affections of the heart, for in these 
 cases extra-systoles are often present, and frequently the heart's contraction 
 
 m2
 
 164 DISEASES OF THE HEART 
 
 starts from the a. -v. node continuously. Digitalis may give rise to them 
 in rheumatic hearts. Dyspeptic and neurotic people are often liable. That 
 other conditions give rise to extra-systoles is also evident from the fact 
 that they may occur in young people in whom there is no rheumatic history 
 and no cardio-sclerosis, and whose after-history reveals no sign of heart 
 trouble. 
 
 § 151. Sensations produced by extra-systoles — Some patients are 
 conscious of a quiet transient fluttering in the chest when an extra- 
 systole occurs ; others are aware of the long pause * as if their heart had 
 stopped ' ; while others are conscious of the big beat that frequently 
 follows the long pause. So violent is the effect of this after-beat that 
 in neurotic persons it may cause a shock followed by a sense of great 
 exhaustion. Most patients are unconscious of the irregularity due to 
 the extra-systole until their attention is called to it by the medical 
 attendant. Both being ignorant of its origin, and it being characteristic 
 of human nature to associate the unknown with evil, patient and doctor 
 are too often unnecessarily alarmed. 
 
 § 152. Prognosis — The most serious thing about these cases is that 
 the consciousness of having an irregularity sometimes makes a patient 
 introspective and depressed. He keeps feeling his pulse, and communicates 
 his doleful tale whenever he finds a sympathetic ear. 
 
 As the process which gives rise to it in elderly people is the same as 
 that which produces the tortuous temporal arteries, no more significance 
 should be attached to the one symptom than to the other. I have followed 
 cases for many years, and watched them pass through seasons of sickness 
 and of stress, and have seen no reason to attach any serious import to this 
 symptom. In rare instances, the heart, from being occasionally irregular, 
 has after many years become continuously irregular for short or long periods, 
 and in a few the permanent establishment of the nodal rhythm has been the 
 means of hastening the end. But this is infrequent, and in cases of cardio- 
 sclerosis has only happened in advanced life, and the patient should on no 
 account be frightened by being warned of the possible occurrence of this 
 unlikely contingency. In younger and neurotic people I have never seen 
 it lead to any bad results. It may appear in serious affections of the heart, 
 as in febrile complaints, but it does not of itself add to the gravity of the 
 condition, though I am not sure that when due to an acute affection of the 
 heart, as in pneumonia and rheumatic fever, it may not be a sign of invasion 
 of the myocardium by the diseased process. 
 
 § 153' Treatment. — If the patient is aware of the irregularity he 
 should be assured that there is no cause for alarm. It is useless to attempt
 
 THE EXTRA-SYSTOLE 165 
 
 to treat the irregularity itself. If in other respects the patient is well, then 
 there is no need for any special treatment. If the patient be suffering 
 from conditions which seem to promote the irregularity, such as worry, 
 fatigue, dyspepsia, the treatment should be devoted to the removal of the 
 pre-disposing cause. In people with temporary high blood-pressure who 
 show extra-systoles, I find plenty of healthy exercise in the open air specially 
 beneficial, though until they get trained, the extra-systoles may at times 
 become more frequent by the exertion.
 
 CHAPTER XX 
 
 The Nodal Rhythm (Continuous Irregularity of the Heart — 
 
 Paroxysmal Tachycardia) 
 
 § 154. Meaning of the term ' nodal rhythm '. 
 
 155. Etiology. 
 
 156. Manner in which the nodal rhythm leads to heart failm-e. 
 
 157. Classification. 
 
 158. Cases in which the rate is not markedly increased. Symptoms. Prognosis. Treat- 
 
 ment. 
 
 159. Cases in which the rate is greatly increased. Symptoms. Prognosis. Treatment. 
 
 160. Cases in which the nodal rhythm is transient and recurrent (paroxysmal tachycardia). 
 
 Symptoms. Prognosis. Treatment. 
 
 § 154. Meaning of the term * nodal rhythm ' The term ' nodal 
 
 rhythm ' is apphed to that action of the heart where the auricles and ven- 
 tricles contract simultaneously — the ventricular contraction preceding the 
 auricular by about one-tenth of a second in the great majority of cases. 
 Prom this fact, proved by experimental as well as clinical evidence (§ 115), 
 it is reasoned that the starting-place is no longer at the remains of the sinus, 
 but in the remains of the primitive cardiac tube lower down. It has been 
 established that when the a.-v. bundle has been cut across after it has left 
 the a.-v. node (Fig. 2), the auricle and ventricle beat at independent rates — 
 the ventricular rate being slow (true ventricular rhythm, § 168). In the 
 vast majority of cases of nodal rhythm the heart beats more rapidly than 
 normal, and the auricle and ventricle contract together. Prom these 
 circumstances I have reasoned that here, as in the case of the nodal extra- 
 systole, the source of the heart's contraction starts at or about the a.-v. 
 node — hence the term ' nodal rhythm '. Whether this may ultimately be 
 found to be the real starting-point or not, the cases described under this 
 term have such well-marked characters that it is imperative that they 
 should be singled out for special recognition. The nodal rhythm is present 
 in the majority of cases of severe heart failure, and in a great many the 
 immediate breakdown is directly attributable to the inception by the heart of 
 this abnormal rhythm. When it occurs the heart is at once placed at 
 a great disadvantage in carrying on its work, and the extent of the impair- 
 ment of the circulation depends on the integrity of the heart muscle.
 
 THE NODAL RHYTHM 
 
 167 
 
 I have already drawn attention to the outstanding features of these 
 cases, where it was shown that the ventricular venous pulse indicated 
 a change in the starting-place of the heart's contraction, and that all sign 
 of the auricular contraction at the normal period of the cardiac cycle dis- 
 
 B^^^^^^^^^^^^^^^Hj^^^^^^^^B 
 
 lffl||n|^^H||^|H|^^M^ 
 
 Fig. 107. Tracing of the radial pulse showing the irregularity characteristic of the sudden 
 
 inception of the nodal rhythm, 
 
 appeared. Detailed proof of this is given in the record of illustrative cases 
 cited in Appendix II. 
 
 The most obvious sign which, in the great majority of cases, indicates 
 this abnormal rhythm, is the character of the heart's action. Except in 
 
 Fig. 108. Shows a type of irregular pulse with the nodal rhythm. 
 
 some cases of excessive rapidity, this rhythm is invariably irregular ; the 
 irregularity sometimes being extreme. It may be occasionally so slight 
 that it is apt to be overlooked, but if the heart's action be watched for a few 
 minutes, it will show variation in rhythm. The character of the irregularity 
 
 Fig. 109. Characteristic type of nodal irregularity occurring in the elderly. 
 
 will be better realized by looking at such tracings as Figs. 107, 108, 109, and 
 110, where the rhythm will be seen to be nondescript and disorderly (other 
 examples will be found in § 115, and in Appendix II). 
 
 § 155. Etiology. — The exact pathological details of these cases have not 
 been sufficiently worked out, but from an examination of a series of hearts 
 in which I was able to demonstrate all the features of this irregularity
 
 168 
 
 DISEASES OF THE HEART 
 
 during life, Dr. Keith has found evidence of pathological changes which, 
 with the well-authenticated clinical evidence, permits the following pro- 
 visional descriptive account : — 
 
 The great majority of cases of nodal rhythm are found among 
 those who have suffered from rheumatic affection of the heart, or cardio- 
 sclerosis. In rheumatic hearts there are often deposits of cells scattered 
 through the heart, which ultimately cicatrize. These deposits when on or 
 near the a. -v. bundle impair its function, and this is frequently recognized 
 in early cases by the delay which occurs between the contraction of the 
 auricle and ventricle, from the retarded transmission of the impulse through 
 the connecting fibres. A later result may be obtained when the cicatri- 
 zation irritates the bundle, and renders it more excitable than the sinus. 
 In accordance with the law that the contraction starts at the most excitable 
 part of the primitive tissue, the contraction of the heart then originates 
 in this more irritable part. Somewhat analogous changes follow in cardio- 
 
 Apex beat 
 
 Radial pulse 
 
 HMJM^Vn^/^, 
 
 Fig. 110. Simultaneous tracings of the apex beat and of the radial pulse, showing charac- 
 teristic type of nodal irregularity during a period of severe heart failure. 
 
 sclerosis and in degeneration of the coronary arteries. In certain typical 
 cases of this irregularity Keith has found the artery supplying the bundle 
 affected with marked arterio-sclerosis, and with an invasion of fibrous tissue 
 in and around the a. -v. node and bundle (see report of cases in Appendix II). 
 
 In these cases the increased irritability of the degenerated a. -v. node and 
 bundle seem to lead to the inception of the abnormal rhythm. Another 
 cause of nodal rhythm is suggested by some cases in which there has 
 been found such distension of the auricle that it appeared impossible that 
 the stimulus from the sinus could have been transmitted through the 
 attenuated muscle (see pathological report of Case 8 in Appendix II). In 
 my earlier investigations it seemed to me that the auricle must have been 
 paralysed during life, particularly as in these cases no evidence was afforded 
 of the auricular contraction. 
 
 § 156. Manner in which the nodal rhythm leads to heart failure. 
 — Mc William 129 has demonstrated experimentally that when a heart is 
 made to reverse its contraction, the ventricle contracting first, there is 
 at once a great embarrassment of the circulation. It is readily intelligible 
 that the heart being adapted to perform its work most efficiently in such
 
 THE NODAL RHYTHM 169 
 
 a manner that the auricles contract and then the ventricles, reversal of 
 this sequence must be against efficiency. When, therefore, the ventricle 
 starts the contraction the heart is at once embarrassed in its work. This 
 embarrassment is made evident by a diminution in the reserve force, and the 
 symptoms produced are simply those that imply an exhaustion of this 
 reserve force. 
 
 The degree to which the heart failure may proceed depends on the 
 integrity of the heart muscle. If this be good, then it is able to cope 
 with the embarrassment induced by the abnormal rhythm, and very little 
 change may take place. If it be much degenerated, and particularly if the 
 inception of the rhythm is accompanied by excessive rapidity and dilatation 
 of the heart, then the condition becomes speedily very grave. 
 
 § 157* Classification. — In the analysis of over 600 cases where this 
 abnormal rhythm has occurred, I have sought for the facts that would 
 be of use in treatment. With our imperfect knowledge of the cause of this 
 rhythm, it is not yet possible to give a scientific analysis, and I therefore 
 present the matter in the following classification, which will be found to be 
 one readily applied and very useful in practice. As the manner in which 
 the heart carries on its work after the inception of the nodal rhythm depends 
 a great deal upon the rate of its contraction, the cases can be classified as 
 follows : — 
 
 (a) Where the rate is not markedly increased. 
 
 (6) Where the rate is greatly increased. 
 
 (c) Where the nodal rhythm is transient and recurrent (one form of 
 
 paroxysmal tachycardia). 
 
 (d) Where the rate is markedly slower than normal (nodal bradycardia, 
 
 see p. 337). 
 
 § 158. Cases in which the rate is not markedly increased. 
 Symptoms. — In a great many people this continued irregular action of the 
 heart is found with the rate about normal or very slightly increased (under 90). 
 The change in the heart's action may take place so quietly that the patient 
 may be unconscious of it, and continue at his work, which may be laborious. 
 Usually there is a slight limitation of the field of cardiac response, and 
 many go about quietly for years with little further trouble, even though 
 the legs may become a little swollen. Sooner or later this tendency to 
 oedema increases, yielding at first to treatment but tending to recur, until 
 finally extreme heart failure sets in. This form in rheumatic hearts may 
 occur in early life ; in cardio-sclerosis, rarely before fifty, becoming more 
 frequent with increasing years. 
 
 Prognosis. — Many people may show this characteristic irregularity
 
 170 DISEASES OF THE HEART 
 
 and be engaged in arduous labour for many years. In such cases if it 
 occurs before fifty years of age, there is usually a past history of rheumatic 
 fever. When it occurs in later life, the extent to which the field of response 
 becomes Hmited is the best guide. If the field be fairly good patients may 
 go on quietly for many years, some living well over seventy. 
 
 Treatment. — Unless there is a distinct evidence of heart failure, no 
 treatment is necessary. If the heart-rate begins to increase in frequency 
 and dropsy sets in, then the treatment should follow the lines laid down 
 in the chapters on treatment. 
 
 § 159. Where the rate is greatly increased. Symptoms. — The 
 sensation felt by the patient when this rhythm is first started may be so 
 slight as to pass unnoticed. Usually he is conscious of' a curious fluttering 
 sensation inside the left chest. This sensation is very characteristic and 
 almost pathognomonic. It may be described variously according to the 
 literary gift of the sufferer, but the essential feature is the soft and gentle 
 movements, not rhythmical, but varying softly in intensity, in striking 
 contrast to the sensations that may arise from stimulation of the heart 
 during a normal rhythm, as in palpitation. Frequently this sensation is 
 so disquieting that the patient rests, or walks about cautiously and quietly. 
 About the same time the patient remarks a distinct hmitation in the field 
 of cardiac response, the exertion that he was wont to undertake with comfort 
 now inducing breathlessness. 
 
 The associated heart failure may be so extreme that in a few days, or 
 even in a few hours, evidences of imminent peril are shown. The patient 
 has to keep in bed, the dyspnoea being so great that he cannot lie on his 
 back, but_^must be propped up. If the patient survives, oedema of the legs 
 quickly supervenes, the hps become livid and the face swollen. The pulse is 
 small, rapid, and usually irregular, the beats varying remarkably in strength. 
 The character of the heart's action at this stage can be reahzed from such 
 tracings as Figs. 107, p. 167, and 110, p. 168. The veins of the neck are 
 often fuU and pulsate with great rapidity. The heart dilates in a few hours, 
 sometimes extending two inches in the transverse direction. The sounds 
 alter, becoming short and sharp, and if the heart's action is rapid, often 
 no murmur may be detected. If there has previously been a pre-systolic 
 mitral murmur, it disappears, and if the heart's action is fairly slow a dia- 
 stolic mitral murmur may be detected, but never a pre-systohc. The liver 
 becomes enlarged, and may be found pulsating two or three inches below 
 the ribs. The tissues covering the heart and the liver often become 
 extremely^tender on pressure. 
 
 If the heart does not slow down after this sudden inception of the
 
 THE NODAL RHYTHM 171 
 
 nodal rhythm, the patient drifts on to death, and many cases of rapid 
 and fatal breakdown, particularly in old people, are directly due to the 
 inception by the heart of this rhythm (Cases 11, 12, and 15, Appendix II). 
 Usually the heart does slow down and the circulation improves, and the 
 patient may so far recover as to be able to go about for years with more or 
 less comfort, but is always liable to relapses more or less severe. One often 
 comes across people who have had a continual irregularity of the heart's 
 action for many years, and they have learned to treat themselves with 
 remarkable success, and some of the more intelligent can give the physician 
 very important information as to the relative value of many heart drugs, 
 as digitalis and strophanthus. 
 
 Prognosis. — The prognosis depends on how the heart behaves, and 
 how well it maintains the circulation under the new rhythm. If the patient 
 feels little or no distress then he may be assured of many years of fairly 
 comfortable life. If there is some distress in breathing, or a tendency to 
 ' bronchitis ' and swelling of the legs, he may still live for many years, his 
 life chequered by attacks of heart failure more or less severe. If the condi- 
 tion be extreme with rapid heart and much dropsy and dyspnoea, the prog- 
 nosis depends on how he reacts to treatment. The young, or those with 
 a rheumatic history, usually rally from their breakdown, and may be for 
 many years free from attacks. The elderly also rally from their first attacks, 
 and may live for years a somewhat crippled existence. But, as I have 
 already indicated, the persistence of a rapid heart, and evidence of failure 
 of the heart to maintain the circulation, in spite of treatment, are evidences 
 of a very serious kind. 
 
 Further evidence will be found in estimating the size of the heart, as 
 dilatation in these cases is always an indication of the failure of tone, and 
 with the permanent failure of tone the work of the heart is further grievously 
 embarrassed (Chapter XXIII). 
 
 Treatment. — It should be borne in mind that the condition is the 
 outcome of a series of changes that have been going on for years, and that 
 it is foolish to suppose that by any means we possess we are able to remove 
 the diseased processes on which this arrhythmia depends. 
 
 Attempts, therefore, to ' cure ' the diseased condition are futile. What 
 we have to do is, not to waste time in the pursuit of a hopeless quest, but to 
 make the best of an irremediable condition, and in recognizing this we are 
 at once placed in a position to render real help. 
 
 When the change in rhythm is accompanied by little distress, no treat- 
 ment is necessary. When, however, there is evidence of distress, treatment 
 should follow in the main the principles laid down in the chapters on
 
 172 DISEASES OF THE HEART 
 
 treatment. If there be extreme difficulty in breathing and great restlessness, 
 it is of the first importance that rest should be secured, and that the patient 
 should sleep. For this purpose sedatives are necessary, and they should 
 be given on the lines laid down elsewhere. 
 
 A curious and instructive reaction to digitaUs will be found in these 
 cases. Most of those whose arrhythmia is of rheumatic origin show a remark- 
 able sensitiveness to digitalis, the heart sometimes responding to a very 
 few doses, and at the same time becoming much slower (see § 251 and 
 Appendix VI). On the other hand, in many cases in which the arrhythmia 
 arises secondarily to cardio-sclerosis, the digitaUs has no effect upon the heart. 
 
 § 1 60. Where the nodal rhythm is transient and recurrent 
 (paroxysmal tachycardia) . — In this class the heart suddenly takes on the 
 nodal rhythm, and this may last for a few beats, or it may go on for 
 minutes, hours, days, or weeks. The rate is usually greatly increased 
 (200 per minute and over), and is then recognized as ' paroxysmal tachy- 
 cardia '. Sometimes the rate is not markedly increased, and in rare cases 
 it may be slower than normal (Case 17, Appendix IV). An individual may 
 have but one attack, or the attacks may come on at frequent intervals 
 in the course of ten or twenty years, or they may be of great frequency, 
 occurring every few weeks or days ; or there may be several attacks in one 
 day. After one or two attacks the heart may settle down permanently 
 with the nodal rhythm. 
 
 The term ' paroxysmal tachycardia ' has been used to describe several 
 conditions that present a superficial resemblance, but are fundamentally 
 different in origin. While the nature of the rapid action was unknown 
 the term served a useful purpose ; now it should not be used without a clear 
 definition of what is meant. Though many cases with a normal rhythm 
 have been included under this term, the most striking instances described 
 as paroxysmal tachycardia in literature are undoubtedly due to the inception 
 of an abnormal rhythm ; so far I have been able to make out two forms 
 of paroxysmal tachycardia, the transient nodal rhythm referred to here, 
 and an auricular form described on p. 334. 
 
 Symptoms. — In extreme cases the sensation of the patient and the asso- 
 ciated heart failure are exactly those described in § 159. The rhythm in 
 such cases may be quite regular, and the rate may be over 200 beats per 
 minute. The changes described in § 159 may appear in a few hours. With 
 the sudden reversion of the rhythm to the normal, the change in the patient's 
 condition is even more remarkable than the rapid onset of the symptoms 
 of heart failure. At once the patient heaves a sigh of relief, and in a very 
 short time, within half an hour, all abnormal signs in the lips, face, and
 
 THE NODAL RHYTHM 173 
 
 enlarged liver disappear, while in a few hours the heart may be found beating 
 within its normal limits. 
 
 In others, the paroxysmal tachycardia may occur for a day or two, with 
 no marked change in the size of the heart. In these, the patient is generally 
 conscious of the heart's abnormal action, and instinctively avoids active 
 exertion, either keeping in bed or resting in a chair, or walking about very 
 quietly. The attack usually lasts for a few hours, but may occasionally 
 last for many hours, or even one or two days. At the end of this time 
 no increase in the size of the heart is detectable, and there is no sign of 
 dropsy or enlarged liver. This condition may be found at all ages over ten 
 years (Appendix II). 
 
 Prognosis. — The prognosis in these cases is one of considerable difficulty. 
 The symptoms during an attack may be so alarming that the inexperienced 
 are apt to look upon the patient as hopelessly stricken. I remember 
 being called one night to a woman eighty years of age, I found her heart 
 extremely rapid and irregular, her face swollen and livid, and she was 
 gasping for breath. I told the friends the end was approaching, and, calling 
 to see her next morning, I found her walking out in the street. After that 
 she had several attacks and finally died during one. Other patients I have 
 watched for years, when the symptoms have not been so extreme, sometimes 
 only giving rise to a slight uneasiness in the chest. In these the heart has 
 not dilated, though the rate may have reached nearly 200 per minute. Others 
 have had but one attack, and I have watched some of these for nearly twenty 
 years and they have had no other. 
 
 In some the change from being transient becomes permanent, and here 
 lies the danger. If the extreme form of heart failure persists and the 
 dilatation cannot be reduced, then the patient drifts to death (Cases 10, 
 11, 12, and 15, Appendix II). 
 
 The prognosis also depends on the degree of dilatation. If the heart 
 does not increase in size and the attacks are transient, then on the whole 
 the prognosis is good, though in many cases the patient's life is greatly 
 crippled because of the fact that the attacks recur in spite of treatment. 
 When there is dilatation with the accompanjdng symptoms of dropsy and 
 enlarged liver, then the outlook is bad. 
 
 Treatment. — Absolute quiet is needed during the attack — a sugges- 
 tion scarcely necessary, for the patient usually seeks rest, though he may 
 move about quietly with little distress. A great many suggestions as to 
 the arrest of these attacks may be found scattered through medical literature. 
 As the attacks are commonly but transient, some remedy employed oppor- 
 tunely seems to the inexperienced onlooker to restore the heart to its normal
 
 174 DISEASES OF THE HEART 
 
 action. Many patients themselves have a knack of doing something that 
 seems to change the rhythm. Sometimes attacks can be stopped by the 
 patient simply taking a series of deep breaths, by slapping the chest, by the 
 sudden application of cold water to the chest. Drugs of the most diverse 
 character have been cited as active agents in stopping attacks, such as 
 nitro-glycerine and adrenahn. In my early days I, too, thought I knew how 
 to stop attacks, but more extended experience has shown me that when they 
 stopped it was from some cause unknown to me, and VhichVas independent 
 of any means I employed. 
 
 When signs of heart failure appear the treatment should follow the 
 lines laid down in the chapters on treatment.
 
 CHAPTER XXI 
 
 Affections of the Conducting Functions of the Primitive Car- 
 diac Tissue (Heart-Block, Adams-Stokes Disease, Ventricular 
 Rhythm) 
 
 § 161. Definition. 
 
 162. Methods of recognizing depression of conductivity. 
 
 163. Intersystolic period (the a~c interval). 
 
 164. Depression of conductivity without arrhythmia. 
 
 165. Influence of rest upon conductivity. 
 
 166. Arrhythmia due to depression of conductivity. 
 
 167. Missed beats due to depression of conductivity. 
 
 168. Independent ventricular rhythm due to heart-block. 
 
 169. Effect of the auricular contraction on the radial pulse. 
 
 170. Etiology. 
 
 171. Significance of the milder forms of depression of conductivity. 
 
 172. Symptoms. 
 ' 173. Prognosis. 
 
 174. Treatment. 
 
 § i6l. Definition. — In the last two chapters the irregular action of 
 the heart was ascribed to the contraction of the heart starting lower down 
 in the primitive tissue than the sinus. In this chapter another important 
 function of this tissue is considered, namely, the conduction of the stimulus 
 from auricle to ventricle. The stimulus for contraction reaches the ventricle 
 from the auricle by passing along the bridge of primitive tissue that con- 
 nects the auricle and ventricle (Fig. 2, p. 15). This bridge may be so 
 affected that (1) the stimulus is delayed ; (2) the stimulus is at times pre- 
 vented from crossing over ; (3) the stimulus may be completely blocked 
 beyond the a.-v. node, and the ventricle then contracts in response to 
 a stimulus that arises in the uninjured remains of the a.-v. bundle (heart- 
 block, ventricular rhythm). 
 
 § 162. Methods of recognizing depression of conductivity Apart 
 
 from suitable tracings, the clinical evidence is limited to the recognition of 
 the fact that there is a slow radial pulse, or, better, a slow ventricular rate, 
 while the veins in the neck pulsate more frequently, owing to the normal 
 rate of the auricular contractions being maintained. If the ventricular 
 contractions are over thirty-six per minute, these may have a distinct 
 relationship to the auricular waves in the jugular pulse, the ventricle
 
 176 DISEASES OF THE HEART 
 
 responding to every second, third, or fourth auricular contraction. When 
 the ventricular contractions are about thirty or under, they are probably 
 independent of the auricle, and auricle and ventricle beat at independent 
 rates and in response to independent stimuli. 
 
 When there is a mere delay in the response of the ventricle to the stimulus 
 from the auricle, the evidence is very scanty, apart from graphic records. 
 I have, however, in cases of mitral stenosis been able to recognize this 
 delay by a slight separation of the presystolic murmur from the first sound 
 of the heart (represented diagrammatically by the shading in Figs. 112, 
 p. 177 ; 272, p. 365, and 265, Plate V). Occasionally ' missed beats ' or pulse 
 intermissions are due to the auricular stimulus failing to provoke a ventri- 
 cular contraction, and a strong suspicion of the nature of this irregularity 
 may be aroused by observing that during the pause the ventricular 
 sounds are absent ; this distinguishes it from most cases of extra- 
 systole, in which, as has already been described, there are usually 
 heard two short, sharp sounds, the result of the weak, short, premature 
 contraction of the ventricle. As, however, extra-systoles may occur with 
 no audible sound, this distinction is not reliable. In tracings of the radial 
 pulse alone, Wenckebach ^^^ was able to recognize the nature of the irregu- 
 larity by an ingenious method of measurement. No difficulty is presented, 
 as a general rule, when tracings of the radial pulse or apex beat are taken at 
 the same time as tracings of the jugular pulse. The slighter forms of this 
 affection are recognized by the delay that occurs between the auricular and 
 ventricular systoles. In the jugular tracings, as has already been shown, 
 there is usually present a wave due to the auricular systole, (a) followed 
 at a short interval by the carotid wave (c). This interval between a and c is 
 of great value in estimating the condition of the conductivity in the primitive 
 tissue. 
 
 §163. The intersystolic period (a-c interval) — This] interval]' is 
 occupied by three events, namely, (1) the systole of the auricle ; (2) the 
 transmission of the stimulus from auricle to ventricle ; (3) a minute portion 
 of time during which the ventricular pressure is rising before opening the 
 semilunar valves {Anspannungszeit, or presphygmic interval). As 3 is 
 practically constant, it may for the purpose of this inquiry be ignored, and 
 assuming that the stimulus for contraction starts on its way to the ventricle 
 at the beginning of auricular systole, any variation in the length of the 
 a-c interval is due to the variation of the rate of stimulus conduction. 
 
 In normal hearts I have found that the a-c interval is fairly constant, 
 lasting usually one-fifth of a second (as in Fig. 44). It is a little shorter in 
 frequent action of the heart.
 
 CONDUCTING FUNCTION OF PRIMITIVE CARDIAC TISSUE 177 
 
 § 164. Depression of conductivity without arrhythmia While 
 
 the a-c interval may be considered normal when it does not exceed one-fifth 
 of a second, considerable increase of this interval may take place with no 
 interference with the rhythm of the heart. 
 
 Fig. 111. Shows a great increase in the a-c interval (space A) due to a delay in the 
 stimulus passing from auricle to ventricle. (Case 17, Appendix IV, taken 1892.) 
 
 In Fig. Ill there is a tracing of the jugular pulse taken at the same 
 time as the radial pulse. The radial shows a perfectly regular rhythm, 
 while the neck tracing shows a great increase in the a~c interval (space A). 
 The heart may continue to beat perfectly regularly for years with the 
 
 Fig. 112. Shows an increased a-c interval, nearly two-fifths of a second in dura- 
 tion (space A). The shading shows the position of the murmurs — a short murmur 
 due to the auricular systole, the loudest part of which is separated from the first 
 sound by a brief interval, a murmur following the first sound, and another following 
 the second sound running up to the presystohc (or auricular systolic) murmur. 
 (Case 17, Appendix IV, taken 1903.) 
 
 conductivity afEected to this extent. Thus, Fig. 112 was taken in 1903 
 from the same patient from whom Fig. Ill was taken in 1892, and the 
 jugular tracing shows a hke increase of the a-c interval (space A). Except 
 for a short period in 1898, this patient's pulse was quite regular up to 1904. 
 § 165. Influence of rest upon conductivity. — With each contraction 
 
 MACKE.s'ZIU 
 
 N
 
 178 
 
 DISEASES OF THE HEART 
 
 all the functions of the muscle-fibres are for the time being abolished, to 
 be gradually restored during diastole. Normally, their recovery is simul- 
 taneous, so that when the rhythmical stimulus arises at the auricle or great 
 veins it passes over the whole heart, and the muscular fibres respond at 
 a uniform time. When one of these functions is depressed, its recovery 
 does not take place as speedily as the others, therefore the relationship of 
 the action of these functions is not uniform, and an interference with the 
 regular sequence of events results. Certain variations in the rate of con- 
 duction can frequently be detected, not only when conductivity is depressed^ 
 but also when it is presumably normal, such variations apparently depending 
 on the time required for recovery after the previous exhaustion. One has 
 little difficulty in illustrating this in a variety of ways in certain forms of 
 heart irregularity. In a patient aged 24, suffering from mitral disease, 
 
 Fig. 113. Shows the influence of rest when the conductivity of the a.-v. fibres is depressed. 
 The radial pulse shows a respiratory irregularity. The carotid and jugular tracings show 
 a shortening of the a-c interval (space A,^) after the long diastolic periods, and a lengthening 
 (space ^j) after the short diastolic period of the cardiac cycle. 
 
 and pregnant with her first child, I had noted an increase in the a-c interval 
 for some years. During labour it frequently happens that the pulse becomes 
 irregular, the irregularity often being of a respiratory type (sinus irregularity). 
 The radial tracing in Fig. 113 shows such an irregularity. The tracing of 
 the carotid and jugular shows a rise and a fall due to the movements of 
 respiration — the rise in the tracing corresponding with expiration, and the 
 fall with inspiration. It will be noted that the irregularity is due to a 
 lengthening of the diastole, and that the a-c interval during the short pulse 
 period (space A^) is nearly double the duration of the a-c interval during the 
 long pulse period (space A.^)- The reason for this variation in the a-c interval 
 is that the conductivity is continually depressed, but when the heart beats at 
 a slower rate the a.-v. fibres have time to recover during the longer diastolic 
 pause, so that the stimulus is conveyed from auricle to ventricle at about 
 the normal rate [A^). Here the arrhythmia is not due to the depressed 
 conductivity, but evidently originates in the sinus, for the auricular wave,
 
 CONDUCTING FUNCTION OF PRIMITIVE CARDIAC TISSUE 179 
 
 a, appears at irregular intervals. The modifying effect on the ventricular 
 rhythm of the variable condition of the conductivity can be illustrated in 
 a variety of ways. If we examine minutely the incidents where an occasional 
 premature or extra systole occurs, sometimes very curious variations in 
 conductivity can be detected (as in Fig. 106, Plate II; also Figs. 274, and 
 265 Plate V). 
 
 It may seem an unnecessary refinement to dwell upon such minute 
 changes, but I trust to show later that the recognition of these facts affords 
 the evidence for determining with certainty some changes of the utmost 
 significance in a large class of cases of heart disease. 
 
 § 1 66. Arrhythmia due to depression of conductivity Slight 
 
 arrhythmia may be due to variations of conductivity. Thus the short space 
 
 Fig. 114. Shows a gradual lengthening of the a-c interval tiU the 
 stimulus from the auricle at a' reaches the a. -v. bundle before the latter 
 has recovered from the previous stimulation, and finds it ' refractory '. 
 The ventricle, therefore, does not respond to this stimulus, but remains 
 quiescent till the next physiological stimulus comes from the auricle, and 
 the conductivity being restored the ventricular beat (c) follows the 
 auricular wave at a shorter interval. Note the increasing size of the 
 a wave before the intermission. This is due to the auricular systole 
 falling at the same time as the preceding ventricular systole, so that the 
 auricular contents cannot be sent into the ventricle, but a bigger wave is 
 sent back into the veins. 
 
 o in the radial in Fig. 98 is seen to be due to an increase of the preceding 
 a-c interval (space A^), that is, to a delay in the ventricular systole. 
 
 Arrhythmia of a more marked character arises when the conductivity 
 is so grievously depressed that the stimulus occasionally or frequently fails 
 to cross the auriculo-ventricular junction. How this occurs is well seen 
 in Fig. 114. There is a constant delay in the conduction of the stimulus 
 here, the a-c interval being unduly prolonged. Before the intermission 
 there is a slight but gradual increase of the a-c interval. After the auricular 
 wave a' there is no carotid wave (c) nor pulse beat in the radial. The reason 
 for this is manifestly that the auricular systole a' occurred so soon after the 
 previous ventricular systole (as evidenced by the carotid wave c immediately 
 before a') that there was not sufficient time for the recovery of the function 
 
 N 2
 
 180 
 
 DISEASES OF THE HEART 
 
 of stimulus conduction in the a. -v. bundle, and hence the stimulus failed to 
 reach the ventricle, and a beat dropped out. By this means a longer rest 
 was procured for these fibres, and when the next stimulus comes down from 
 
 Fig. 115. Regularly intermitting pulse due to depression of conductivity. 
 (Case 17, Appendix IV, 1898.) 
 
 the auricle the longer rest has so restored the function of conductivity 
 that the a-c interval following the pause is shorter than the average. This 
 dropping out of ventricular beats may occur at regular intervals. Fig. 115 
 was taken in 1898 from the patient from whom Figs. 1 1 1 and 112 were taken. 
 
 Fig. 116. Taken at the same visit as Fig. 115, and shows the venous pulse during the 
 arrhythmia. The wave a is quite regular in its appearance. For the interpretation of this 
 tracing see diagram Fig. 117. 
 
 For many years tracings from this patient showed constant depression of 
 the conductivity. For some reason, in 1898 the conductivity became 
 further depressed, so that at regular intervals a ventricular beat dropped out 
 (Fig. 115). The true nature of this arrhythmia is shown in the jugular tracing 
 
 Fig. 117. Diagram constructed to show that the irregularity in Figs. 115 
 and 116 is due to a blocking of the conductivity at the fibres joining auricle and 
 ventricle. Note the increased length of the a-c interval before the pause in 
 the Vs. 
 
 (Fig. 116), where the auricle is shown to contract regularly (wave a), while 
 the ventricle fails to respond to every third auricular systole. To demon- 
 strate this more clearly, I reconstruct Fig. 116 in the form of a diagram 
 (Fig. 117). The downstrokes in the upper division represent the auricular
 
 CONDUCTING FUNCTION OF PRIMITIVE CARDIAC TISSUE 181 
 
 systole {As), those in the lowest the ventricular systoles {Vs), and correspond 
 with the radial and carotid pulses in Figs. 115 and 116. The slanting lines 
 represent the a-c interval. It will be seen that a ventricular beat drops 
 out regularly after every third auricular systole. 
 
 § 167. Missed beats due to depression of conductivity. — Gaskelli-^ 
 states that on applying a screw clamp around the auriculo-ventricular 
 
 Fig. 
 
 118. The ventricle only responds to every alternate auricular systole 
 ventricular rate 48, auricular rate 96. 
 
 groove of a frog's heart, ' according to the tightness of the clamp the ventricle 
 can be made to beat synchronously with the auricles, to respond to every 
 second contraction of the auricle, to respond to every third, fourth, or 
 other contraction, or to remain quiescent.' Hering^^^ and Erlanger^'^ have 
 recently produced the same changes in the mammalian heart. All these 
 varying results can be demonstrated to occur in the human heart. 
 
 ac a 
 
 UM\ ^^ 
 
 
 -^ RaHidl 
 
 Fig. 119. Is from a slow, irregular pulse after influenza, and the jugular tracing shows 
 that the slow pulse is due to the ventricle failing to respond to the stimulus from the auricle. 
 Note that after the short pulse period in the radial the a-c interval is much longer than at the 
 other periods. This is because the fibres have had a short rest, and the conductivity has in 
 consequence not been completely restored. Note also at a; a slight depression in the radial 
 tracing due to the systole of the left auricle affecting the arterial column (see Fig. 120). 
 
 In Fig. 114 the ventricular systole is seen to drop out at rare intervals ; 
 in Fig. 116 the ventricular systole drops out after every third auricular 
 systole (3:2 rhythm) ; in Fig. 118, after every second (2:1 rhythm). In 
 Fig. 119 the ventricular systole usually drops out after every second auricular 
 systole ; but there is one short pulse period, and the a-c interval here is much 
 longer than the a-c period after the longer periods, the lengthening being 
 an evidence that the conducting power of the auriculo-ventricular fibres 
 has not had time to recover as effectually as after the longer pulse periods
 
 182 
 
 DISEASES OF THE HEART 
 
 (see diagram, Fig. 120). In Fig, 121 there are three auricular contractions 
 to one ventricular (3:1 rhythm), except during the last arterial pulse-period, 
 when there are but two auricular waves, and after the second of these the 
 a-c interval is longer than the other a-c intervals in this tracing. 
 
 In tracings published by G. Gibson ^, Hay ^^^, and Beards ^^^, there are 
 four auricular beats to one ventricular. This blocking may be so extreme 
 that the auricle may beat ten or twelve times and the ventricle stand stiU. 
 
 Fia. 120. Diagram of Fig. 119, showing the blocking of the stimulus after every second auricular 
 systole, except in one instance when it gets through, with a lengthened a-c interval. 
 
 § 1 68. Independent ventricular rhythm due to heart-block. — In 
 
 the tracings I have given so far, it could be shown that when the ventricle 
 does contract it is in response to a stimulus from the auricle. When a ligature 
 is applied in the auriculo-ventricular groove of the frog's heart, so that the 
 stimulus can be conveyed no longer from auricle to ventricle, the latter beats, 
 after a time, with a rhythm different from, and independent of, that of the 
 auricle (complete heart-block). Wooldridge and Tigerstedt produced 
 
 Fig. 121. Here the tracing from the neck shows sometimes three auricular waves (o) to 
 one carotid wave (c). In the last two periods there are but two auricular waves, and the 
 a-c interval is longer than in the periods when there are three auricular waves, because in the 
 former case the conductivity has not had so long a time to be restored. 
 
 complete independence of the auricular and ventricular rhythms by 
 physiologically separating the auricles from the ventricles, while a similar 
 result has been attained by His, jr., Hering and Erlanger through compres- 
 sion of the a.-v. bundle. Erlanger 2-2 has produced complete heart-block 
 experimentally in dogs, and the dogs have lived for many months, with 
 symptoms identical with those found in human subjects suffering from 
 heart-block. This independent rhythm can be demonstrated as the cause 
 of certain forms of a slow pulse-rate in the human subject. Fig. 122 is 
 a tracing of the radial taken at the same time as the pulsation in the neck
 
 CONDUCTING FUNCTION OF PRIMITIVE CARDIAC TISSUE 183 
 
 due to the jugular and carotid. The small waves, a, are due to the right 
 auricle, and there are two of these auricular waves to one carotid or radial 
 pulse beat. But when one carefuUy analyses their relationship, it is found 
 that the two auricular periods are less than one ventricular period, so that the 
 
 Fig. 122. Shows complete heart-block, the auricle pursuing one rhythm, and the ventricle 
 
 another and slower rhythm. 
 
 relationship of the auricular systole to the ventricular systole is a constantly 
 varying one, sometimes at a distance, and then gradually approaching till 
 they are synchronous. Whatever relationship the a has to c, no variation 
 takes place in the rate. The same thing is shown in Fig. 123, where the apex 
 
 Fig. 123. From the same case as Fig. 122. Shows the influence of the left auricle on the 
 apex tracing (wave a). In the radial tracing the dips ( x ) due to left auricle are found to occur 
 immediately after the auricular waves in the apex tracing. 
 
 beat is recorded at the same time as the radial. Here there is a small wave, 
 a, due to the systole of the left auricle, and the same maintenance of indepen- 
 dent rhythms is manifest here. One can infer with certainty that the auricle 
 contracted at the same time as the ventricular systole during the first four
 
 184 DISEASES OF THE HEART 
 
 or five of the ventricular apex beats, but that the evidence of this simul- 
 taneous contraction is obscured by the large ventricular wave, for we can 
 see in Fig. 122 how the wave a occurred at the same time as the carotid 
 wave. I have taken a large number of tracings from this patient at various • 
 times and under various circumstances, and I have invariably found the 
 independence of rhythm between the auricle and ventricle. 
 
 § 169. Effect of the auricular contraction on the radial pulse. 
 — The auricular systoles can sometimes be recognized in another way in 
 tracings of the radial pulse, where, during a long ventricular pause, a series 
 of notches can be seen occurring at regular intervals on the descending 
 line of the radial tracing, as in Fig. 124. If a jugular tracing be taken at 
 the same time, there wiU be found auricular beats occurring exactly at the 
 same time as these notches, as is shown in Figs. 119, 122, and 123. From 
 this I suggest that those notches in Fig. 124 are due to the movement of the 
 
 Fig. 124. From Webster's case of heart-block, showing in the falling line of the radial 
 tracing a series of interruptions (a) due to the left auricle. 
 
 left auricle, the systole of the left auricle pressing against the aortic valves 
 temporarily affecting the arterial column. The sudden cessation of this 
 pressure causes a slight but abrupt fall in the aortic pressure, giving rise 
 to the notches in the radial tracing. 
 
 § 170. Etiology. — Except in cases of complete heart-block, the ana- 
 tomical changes have not been fully worked out. In the majority of the 
 cases of heart-block examined post mortem, damage of the a.-v. bundle at 
 or beyond the a.-v. node has been found, due to acute inflammatory changes 
 or to sclerotic changes, or to the presence of gummata. In the milder cases 
 one can only infer the cause. From Gaskell's experiments we know that 
 if the bridge of muscle connecting the auricle and ventricle be narrowed, 
 the stimulus takes longer in passing. We know also that in rheumatic 
 affections of the heart numerous deposits of cells occur in the muscle sub- 
 stance. As it is in rheumatic heart cases and cardio-sclerosis that I have 
 found most of the milder forms of depressed conductivity, I infer that 
 when such deposits occur, or when a slight cicatrization takes place, the 
 bundle is injured, and so the function of conductivity is impaired. In 
 other acute affections of the heart we get evidence of the implication of this
 
 CONDUCTING FUNCTION OF PRIMITIVE CARDIAC TISSUE 185 
 
 bundle in the diseased process (see Chapter XXIV). Little is known as regards 
 complete heart-block as an acute condition, but I refer to its possibility in 
 febrile affections of the heart, and one case has been recorded by Jelhnek 
 and Cooper ^°i with confirmatory post-mortem details. In cardio-sclerosis we 
 may observe symptoms of impaired conductivity and even heart-block in 
 an individual who has shown extra-systoles and the nodal rhythm. 
 
 The sclerotic changes in the heart muscle associated with arterio-sclerosis 
 of the coronary arteries appear likely to be the most common cause of 
 heart-block. If one looks at Fig. 2, it will be seen how the a. -v. bundle passes 
 through the central fibrous body of the heart. This body is composed, of 
 fibrous tissue, and is the fixed point in which are inserted many of the muscular 
 fibres of the ventricle, and from this place sclerotic changes are apt to 
 spread. Further, Keith's researches into the hearts I have sent him have 
 shown that the sclerotic process is apt to extend from the base of the mitral 
 valve into the central fibrous body, and to involve the bundle. I have 
 suggested this as a probable cause for the production of extra-systoles and 
 the nodal rhythm, and, in certain advanced cases, of heart-block. 
 
 Several cases have been reported where the damage to the bundle was 
 due to gummata, and the recovery of other cases under anti-syphilitic 
 treatment indicate that syphilis may be an agent in the production of com- 
 plete heart-block. Bramwell^^^ has recently reported a case of complete 
 heart-block in a rheumatic heart, and I have found that sHght impairment 
 of the bundle in rheumatic hearts, especially with mitral stenosis, is not 
 infrequent. 
 
 In complete heart-block the a. -v. node may be either destroyed or sepa- 
 rated from the remainder of the a. -v. bundle. The remains of the bundle 
 in the ventricle beyond the a. -v. node have been found perfectly normal 
 in a case described by Keith in which there was a history of complete heart- 
 block for eighteen years. Seeing that the bundle was healthy, it must have 
 had some function during life, and as it did not convey stimuH from auricle 
 to ventricle, it must have had some other function, which I suggest was 
 stimulus production, and the maintenance of the slow ventricular rate. 
 
 There is a great defect in our knowledge of the condition leading up to 
 heart-block. Before the slow ventricular rhythm becomes permanent, in 
 many people there are periods in which, though the rhythm of the heart 
 is normal, there is frequently an increased a-c interval ; and at times ventri- 
 cular systoles drop out at intervals more or less regular and frequent. I am 
 convinced that in some cases there is a connexion between the conditions 
 producing the nodal rhythm and heart-block, I have reasoned that most 
 cases of nodal rhythm are due to degeneration or irritation of the a. -v. node,
 
 186 DISEASES OF THE HEART 
 
 while a few may be due to a break between the sinus remains and the a. -v. 
 node on account of the atrophy of the auricular wall from long-continued 
 distension. The mischief causing the nodal rhythm and the independent 
 ventricular rhythm of heart-block is thus seen to be very near. I cite fully 
 in the Appendix (IV) cases of nodal bradycardia having some affinity to 
 heart-block. In one there was for years an increased a-c interval, and at 
 one period a mild heart-block, and finally a nodal rhythm of a very slow 
 character (Case 17, Appendix IV). 
 
 The possibility of vagal stimulation taking part in the production of 
 heart-block must be borne in mind. Stimiilation of the vagus can produce 
 a similar action of the heart, as Chauveau 2^' pointed out. Roy and 
 Adami ^^^ give excellent tracings showing complete heart-block due to direct 
 stimulation of the vagus and to the administration of muscarin. I give 
 tracings where a mild form of heart-block was produced by a reflex stimula- 
 tion of the vagus by swallowing (Case 27, Appendix VI). Digitahs may 
 also produce it. But in these cases there is evidence of a defect of the a. -v. 
 bundle — in the permanent delay of conduction. In Webster's ^^e Q^^gg i\^q 
 arrest of the ventricle arose in two ways, as Wenckebach's ^^^ masterly 
 analysis brings out, and one of these ways points to vagus stimulation. 
 
 § 171. Significance of the milder forms of depression of con- 
 ductivity — It must not be thought that the foregoing data are merely 
 of academic interest. Their recognition and appreciation clear up many 
 obscurities surrounding heart affections, and are of practical importance in 
 treatment. As will be shown, in acute affections of the heart the presence of 
 the irregularity due to this cause indicates that the muscle is being invaded 
 by the disease. When it occurs without any irregularity, the increased 
 a-c interval is of importance in the administration of such drugs as digitaUs. 
 I have rarely failed in such cases in increasing the a-c interval and causing 
 the dropping out of ventricular systoles by the administration of digitalis, 
 and the recognition of this form of irregularity produced by digitafis is of 
 importance, for digitahs should never be pushed further. One reads of 
 accounts of sudden death during or after the digitalis had slowed the pulse, 
 and it has seemed to me that the immediate cause might be the production 
 of severe heart-block and consequent syncope. I have a few times seen 
 in consultation patients whose hearts were greatly slowed by excessive 
 doses of^digitahs, but at that time I had not acquired the means of recog- 
 nizing the cause. I always make it a rule to stop digitalis as soon as I find 
 the pulse dropping a beat (see § 252). The recognition of the cause of the 
 intermission, as in Fig. 115, should always be an indication against the use 
 of digitalis.
 
 CONDUCTING FUNCTION OF PRIMITIVE CARDIAC TISSUE 187 
 
 § 172. Symptoms associated with heart-block Apart from the 
 
 characteristic irregularity, and the slow ventricular rhythm with its asso- 
 ciated syncopal attacks, there are no characteristics. Patients with a 
 pulse-rate of thirty to forty beats per minute may go about their affairs, 
 but quietly — the field of response being distinctly hmited. The manner of 
 limitation is varied : in some it is a sense of weakness, in others exertion 
 induces attacks of dyspnoea — sometimes extremely violent on very slight 
 exertion. The picture given by the late Sir W. T. Gairdner, a sufferer 
 from heart-block, of his own experiences, is very characteristic of 
 some cases. ' I am wonderfully free ' — he wrote me four years after 
 the slow rhythm began, and two years before his death at the age of 
 eighty-two, his pulse-rate then being thirty per minute — ' from all the 
 symptoms that usually go along with organic heart-disease. My sleep is 
 almost always undisturbed, and I get abundance of it both by day and night, 
 nor is there the slightest trace of angina pectoris, severe dyspnoea, dropsy, 
 or any of the usual accidents of prolonged cardiac disease.' He wrote later : 
 * Although a little uncertain in my gait, I can go from one room to another 
 or even up a simple stair, taking plenty of time and assisted by the railing ; 
 but for the last two years at least, if not more, my position has been with 
 few exceptions recumbent, or at most sitting, and repeated attempts have 
 shown me that it is practically impossible to cross the street or to go into the 
 garden opposite the house except in a wheeled armchair ; and along with this 
 there is a feeling of perpetual weariness which never leaves me even after 
 the soundest sleep, and which is not explained by any pain or suffering, 
 though in itself it often tends to fits of yawning and even exclamations 
 which would sound to others as if I was suffering inwardly ' (see also Gibson 
 and Ritchie's 232 description of this case). 
 
 The syncopal and epileptiform attacks due to cerebral anaemia induced 
 by the slow action or temporary stoppage of the ventricles (Adams-Stokes 
 syndrome) have been described on p. 24. This tendency to infrequent 
 action may appear in affections of the bundle at two stages, namely, before 
 the permanent establishment of the independent ventricular rhythm and 
 after its establishment. While there are intermittent periods of temporary 
 heart-block, there is a certain hability to these syncopal attacks, and the 
 following appears to me to be the reason. After a Stannius' ligature is 
 applied between auricle and ventricle, the ventricle stands still for a longer or 
 shorter period before it starts on its own rhythm. In certain cases of heart- 
 block the stimulus to contraction passing from auricle to ventricle may sud- 
 denly stop, and the ventricle pause for a brief period before it starts its own 
 contraction. It is during this period that the syncopal attacks occur. Thus,
 
 188 DISEASES OF THE HEART 
 
 Sir W. T. Gairdner noticed that his attacks always came on with the sudden 
 dropping of his pulse-rate : ' These cardiac and cerebral attacks were at one 
 time so frequent that I think from twenty to thirty of them were numbered 
 in twenty-four hours.' His pulse-rate would be seventy per minute, and after 
 his syncopal attack he invariably found it at or below thirty per minute. 
 When the pulse subsided to a permanent rate of twenty to thirty per minute, 
 the cerebral attacks disappeared. My reading of this description is that 
 while the block was partial the stimulus at times got through from the 
 auricle and the rate of the pulse rose to seventy ; then the stimulus suddenly 
 failed to get through, and the ventricle paused for a brief period as it does 
 on first applying the Stannius' ligature, anaemia of the brain resulted, and 
 the patient fainted. On the ventricle starting its own rhythm the circula- 
 tion of the brain was restored, and the patient, recovering, found his pulse 
 at the rate of thirty per minute. When, however, the block became perma- 
 nent, the ventricle went on at its slow, independent rate, with no pauses 
 and therefore with no syncopal attacks. From tracings taken during 
 attacks of syncope, Wenckebach and Gossage have shown that the cerebral 
 anaemia may arise by the ventricle suddenly beating with great rapidity, 
 the individual contractions, however, being so small that the brain is not 
 sufficiently supplied with blood. 
 
 Syncopal attacks may appear when the rate is constant at thirty and 
 under. In such cases there is invariably a greater slowing of the heart's 
 action, the rate falUng sometimes as low as five beats per minute. This 
 point is well brought out in the tracings from patients during an attack 
 taken by Webster 3-^, Hay ^^^, and Barr ^^^^ The immediate cause of the 
 greater slowing is not understood. 
 
 I have only seen a patient recovering from an attack, and I take the 
 following description, which seems fairly representative, from Hay and 
 Moore's '^^^ description : — 
 
 ' He was sitting up in bed when suddenly another attack seized him ; no 
 sooner had he recovered and spoken a few words, than he was again attacked. 
 He made one or two hurried respirations, his head fell on his breast, and he 
 sank on to his piUow, breathing stertorously ; his cheeks and alae nasi flapped 
 in and out ; he ceased breathing, his eyes closed, but his pupils were widely 
 dilated, and his eyeballs were turned upwards and to the left. His face was 
 ashen grey, the malar flush had vanished, and he had all the appearance 
 of a corpse. In a little, however, the colour gradually returned to his face, 
 he sighed deeply and woke up. He raised himself a little, stared about, 
 and then sank back on the pillows exhausted and sweating. During the 
 seizure the radial pulse could not be felt until just before the return of 
 consciousness.' 
 
 In other descriptions epileptiform movements are also included.
 
 CONDUCTING FUNCTION OF PRIMITIVE CARDIAC TISSUE 189 
 
 From the patient's sensations of an attack, I quote the following 
 letter written by an old friend of mine who suffered from Adams-Stokes 
 syndrome due to nodal bradycardia, the pulse-rate usually being thirty per 
 minute: — ' 
 
 ' At your request I try to give you a description of an extraordinary 
 swoon I had whilst suffering under heart trouble. It happened in the middle 
 of the night. I awoke from a quiet sleep feeling a most curious creepy 
 sensation ; my functions all seemed to be stopping, and in front of me, about 
 two feet from the floor, appeared a circular light about two inches in diameter, 
 and brilliant beyond anything I had ever seen before. I thought the period 
 of my dissolution had arrived. I was perfectly calm, and I began to reason 
 with myself whether I should waken my wife (I don't know whether I should 
 have had strength ; I was turned from her at the time), in which case she 
 would be greatly alarmed, or leave things to take their course. Before my 
 mind]was made up what to do, the light began to contract, and when it was 
 reduced to about half its original size suddenly went out, but before entirely 
 losing consciousness I had such a feeling of peace and restfulness as I never 
 experienced before, and had just time to say to myself, " There is no after- 
 life anyway." 
 
 ' How long I lay in that condition of course I don't know, but when I did 
 come to, I felt it utterly impossible to move : I might have been a leaden 
 image, I felt such a weight. For a long time I persevered in trying to move 
 a limb. At last I got a little life in one of my feet, and then gradually the 
 use of all my limbs.' 
 
 Cheyne-Stokes respiration may appear in patients suffering from heart- 
 block, and Gibson and Ritchie ^^^ record falls of arterial pressure during the 
 apnoeic stage. 
 
 A curious feature in cases of heart-block is that circumstances 
 that usually excite the heart to rapid action have Uttle effect upon the 
 independent ventricular rhythm. Causes of excitement, and the ad- 
 ministration of alcohol or chloroform, have very slight or no effect on the 
 ventricle, though the auricular contractions may be rendered much more 
 frequent. 
 
 § 173. Prognosis In the milder cases where there is a delay in the 
 
 stimulus passing from auricle to ventricle, or where there may be occa- 
 sionally the characteristic irregularity caused by the dropping out of a 
 ventricular systole, no grave conditions arise. Its recognition, however, warns 
 us that myocardial changes are involved, and the susceptibility of the patient 
 to the digitalis group of remedies should be borne in mind. Patients with 
 mild forms of heart-block, even where the pulse is continuously about thirty, 
 may lead quiet, uneventful lives for ten or twenty years. When there is 
 a tendency to syncopal attacks, then the patient's life is uncertain, as such 
 patients usually die in one of these attacks, often being found dead in bed
 
 190 DISEASES OF THE HEART 
 
 or elsewhere. Death may arise from heart failure, preceded by symptoms 
 of oedema of the lungs and dropsy. 
 
 § 174' Treatment. — We occasionally meet with cases where, after 
 repeated attacks of syncope and long-continued slow pulse, the conducting 
 power is restored and the rate becomes normal. But considering the 
 pathological change producing these cases, it will be reaUzed how futile it 
 is, except in syphilitic cases, to attempt to give remedies to cure. Notwith- 
 standing this, many writers prescribe drugs of the most diverse character — 
 even digitalis, which is so demonstrably contra-indicated. Fortunately 
 for the patients most of the drugs are innocuous so far as the heart is con- 
 cerned. The management of these cases should be directed to seeing that 
 the patient leads a life according to his strength, avoiding anything that 
 induces over-exertion, limiting the amount of food to what is necessary for 
 his limited way of living. While the tendency to syncopal attacks is present, 
 extreme care should be taken that he should not expose himseK to the attack 
 occurring in dangerous situations. He can move quietly about with such 
 attendance as his means can afford. 
 
 In a few syphilitic cases, recoveries have been effected by the energetic 
 use of anti-syphilitic remedies.
 
 CHAPTER XXII 
 
 Exhaustion of Contractility 
 
 § 175. Necessity for recognizing exhaustion of contractility 
 
 176. The function of contractility. 
 
 177. Conditions inducing exhaustion of contractility. 
 
 178. Symptoms : (o) reflex, (b) changes in the heart's action. 
 
 179. The pulsus alternans. 
 
 180. Prognosis. 
 
 181. Treatment. 
 
 § 175. Necessity for recognizing exhaustion of contractility. — 
 
 Seeing that the cause of all forms of heart failure finally resolves itself 
 into the inabiUty of the contractile force to maintain efficiently the circulation, 
 it is necessary to describe in some detail the part played by the failure of 
 contraction alone. While it is true that heart failure may be induced by the 
 disturbance of other functions, and that the symptoms produced by these 
 commonly dominate the situation— excessive rapidity, irregularity, dilatation 
 — there are also signs evoked by the failure of contractility which are often 
 obscured and overlooked in the confusion created by more pronounced symp- 
 toms, but which nevertheless can be recognized and apportioned to their 
 appropriate cause. We sometimes see dyspnoea, enlargement of the liver, 
 and dropsy described as the cardinal symptoms of heart disease, but equally 
 serious conditions of heart disease and heart failure may be present with 
 none of these symptoms. With the exception of dyspnoea, the ' cardinal ' 
 symptoms are usually associated with dilatation of the heart, i. e. failure 
 of tonicity. Failure of contractility may occur with little or no increase 
 in the size of the heart, without dropsy and with no marked dyspnoea, 
 and this, if properly appreciated, will be found to throw much light on the 
 nature of the heart disease, and to indicate the line of treatment. 
 
 § 176. The function of contractility The circulation is carried on 
 
 by the force derived from this function of the heart muscle. It is from 
 this source that the arterial pressure is maintained. To understand the 
 results of failure or exhaustion of this function, it is necessary to bear in 
 mind certain of its physiological pecuharities. After each contraction 
 of the muscle-fibres the function is so exhausted that no further contraction 
 can occur until a brief period is allowed for recovery. If the stimulus to
 
 192 DISEASES OF THE HEART 
 
 contract is applied too soon, a short and feeble contraction results. If a 
 longer period of rest be allowed, the contraction will be longer in duration 
 and more powerful, so that, within certain limits, the longer the rest, the 
 longer and more powerful the subsequent contraction. 
 
 Another feature to keep in mind when considering this matter is that, 
 like aU the other functions, this possesses in a high degree the peculiar 
 property of ' reserve force '. It is, in a measure, the too easy exhaustion 
 of the reserve force which is the subject of this chapter. 
 
 § 177. Conditions inducing exhaustion of contractility These 
 
 may be summed up in the general statement that exhaustion of contractility 
 occurs when the heart muscle has been exposed to a resistance greater than 
 it can overcome without calling upon its reserve force. This may be brought 
 about by the healthy heart muscle having to meet abnormal resistance, 
 or by a weakened muscle opposing a normal resistance. The following 
 description includes the most striking of these conditions. 
 
 (a) Increased frequency. — A certain rate which we recognize as normal 
 is most favourable to the performance of the heart's work, this rate 
 being that which gives time for the functions exhausted by the contraction 
 to recover. An excessive rate prevents the due recovery of the function, 
 and a call is made upon the reserve force, which thus tends to become 
 exhausted. 
 
 (b) Dilatation of the heart. — A certain size of the heart is also 
 necessary for the perfect performance of contraction, and if the chambers 
 be dilated the contractile force is placed at a disadvantage, and exhaustion 
 results. 
 
 (c) Obstruction of the heart's work. — Exhaustion of this function may 
 arise from embarrassment of its work by valvular defects, or by increased 
 peripheral resistance, or by too great calls made upon it by over-exertion. 
 
 (d) Imperfect nutrition. — As each contraction depends on the supply 
 of appropriate nutriment, any interference with this leads to exhaustion. 
 This may arise from deficient supply, on account of the small output of 
 the heart (as in mitral stenosis), or from narrowing of the coronary arteries 
 from disease. It may be due to the blood containing insufficient nutriment 
 of the special kind required, or containing elements that have a deteriorating 
 effect on the muscle. 
 
 (e) Degeneration of the muscle-fibres. — Finally, there may be changes in the 
 heart muscle itself, fibrous or fatty, which may predispose to a depression 
 of contractility by diminishing the number of the fibres, or by impairing 
 the activity of those that are left. 
 
 § 178. Symptoms. — The failure of this function may occur while
 
 EXHAUSTION OF CONTRA^CTILITY 193 
 
 the other functions of the heart are intact. Thus it may be present with 
 the heart beating at a normal rate, with the ventricular systole following 
 normally on the auricular, and with the heart of a normal size. If we 
 analyse the symptoms present in such cases where the other functions are 
 intact, we can then refer the symptoms with a fair degree of certainty to 
 exhaustion of this function. 
 
 It might at first sight be supposed that failure of the force which keeps 
 up the arterial pressure would show itself first of all by a faU in arterial 
 pressure. This, however, is not the case. So readily does the heart respond 
 to the call from the tissues that the arterial pressure with exhausted con- 
 tractility may be kept up to an extreme height until the moment of death. 
 What happens first is an exhaustion of the reserve force. So great indeed 
 may the exhaustion be, that a patient may be scarcely able to turn over in 
 bed without distress, and yet the arterial pressure may be abnormally high, 
 and the size of the heart be not increased. The frequency of the pulse 
 and respiration may be normal before and after the effort. The classes of 
 patient where the failure of contractility with the integrity of other functions 
 is seen most strikingly are those of rheumatic hearts with valvular and 
 myocardial lesions, and those of cardio-sclerosis. In the former class are 
 the young and middle-aged who have had rheumatic fever some years 
 before, and have gone on doing the work that they were wont to do when 
 their hearts were healthy. Gradual symptoms of exhaustion appear until 
 they become so clamant that exertion has to be restricted. In hke manner, 
 those with cardio-sclerosis have continued their wonted exertion until pulled 
 up by some distressing symptoms. Exhausted contractility produces 
 symptoms in a twofold manner, {a) by reflexly caUing into play the protective 
 phenomena, and (&) by certain changes in the action of the heart. 
 
 (a) Reflex symytoms. — Concerning the first of these, they belong to 
 the class described in detail in Chapter VII, the most striking being the 
 attacks of angina pectoris. Though the group of symptoms included in 
 angina pectoris are more commonly found associated with exhausted con- 
 tractility in cardio-sclerosis, it may also appear in the young with mitral 
 stenosis. The symptom that usually arrests the patient when the reserve 
 contractile force is exhausted is a suffocating feeling coming on during exer- 
 tion, and referred to the throat and upper part of the chest, or breathless- 
 ness, or a sense of exhaustion. Sometimes it is a distressing consciousness 
 of the heart beat (palpitation), often with excessive rapidity of the heart. 
 In females there may be pain complained of in the chest and left arm, and 
 the tissues there may become extremely hyperalgesic. 
 
 In those of more advanced years with cardio-sclerosis, the symptoms 
 
 MACEENZIB Q
 
 194 DISEASES OF THE HEART 
 
 may be the same, though, as I have said, angina pectoris is far more frequent 
 (see Chapter XXVII). 
 
 (6) Changes in the heart's action. — This is shown by the pecuHar irregu- 
 larity — the pulsus alternans. 
 
 § 179' Pulsus alternans. — A very striking and characteristic sign of 
 exhausted contractility is sometimes seen in the size of the pulse beat. 
 I have repeatedly dwelt upon the fact that the duration and force of con- 
 traction depends in a measure on the length of the preceding period of rest. 
 In hearts with good contractility, recovery after a contraction is so rapid 
 that little or no difference can be detected in the size of the beat after pauses 
 of varying duration. In cases of exhausted contractility the matter is 
 very different, recovery being slow, so that the size of the beat has a distinct 
 relation to the length of the preceding diastolic pause. The application of 
 this law assists in the interpretation of many obscure conditions, and gives 
 in many cases a clue to what is going on in the heart. If we observe, for 
 instance, what happens after the long pause following on an extra-systole, 
 we find a different reaction in different hearts. In those with good con- 
 tractility, the succeeding beat may not be much increased in size, or it may 
 be big. The circumstances causing the increased size are complicated, 
 such as the greater filling of the heart during the long diastole, the lower 
 arterial pressure which the contraction has to overcome, and of course the 
 longer period of rest for the restoration of the contractility. One cannot, 
 therefore, draw any safe deduction from the character of the first beat after 
 the long pause. But the second and third beats may vary remarkably. 
 If the contractility be good the size of the beats after the first big beat are 
 uniform. Sometimes, however, the second beat is smaller than the third 
 and following beats (Fig. 125 a). This difference in the size of the beats is 
 a very important one, as it indicates a very grave exhaustion of contractility. 
 Fig. 125 is a tracing of the carotid pulse of a dog whose heart was dying 
 from exhaustion. An artificial stimulus applied to the ventricle produced 
 the extra-systole r'. The next beat is large, and is followed by a beat, x , 
 smaller than the succeeding beats. A very similar result is seen in 
 Figs. 125 a, 125 b, and 126 from patients with advanced cardio-sclerosis. 
 Not infrequently, the difference in the size of the beats persists for a shorter 
 or longer period, in such a manner that a large beat alternates with a smaller — 
 the pulsus alternans (Fig. 126). F. B. Hoffman ^^^ explained this alternating 
 size of beats in the frog's heart as due to an impairment of contractility, 
 and from among the groups of allorhythmia, where every second beat 
 rhythmically varied, Wenckebach -^^ distinguished one where a small beat 
 regularly followed a large beat, while the rate of the heart was perfectly
 
 EXHAUSTION OF CONTRACTILITY 195 
 
 regular. He, most appropriately, desires to limit the name pulsus alternans 
 to this form of aUorhythmia. Hitherto the name has been applied very 
 loosely to arrhythmias that we now recognize as due to extra-systoles. 
 The explanation of the cause of pulsus alternans is as follows : — 
 
 Fig. 125. Tracing from the carotid artery of a dog. The heart was exposed and the 
 ventricle directly stimulated to produce the extra-systole r'. The long pause after the extra- 
 systole is followed by a large beat and succeeded by one beat ( X ) smaller than the other beats. 
 Its small size is due to the shorter period of rest preceding it, and implies grave exhaustion of 
 the contractile power of the left ventricle. Compare with Fig. 125 a (Cushny). 
 
 When contractiUty is depressed, if time be allowed for a full and strong 
 contraction, the longer duration of contraction encroaches upon the period 
 of rest, so that by the time the next stimulus arrives the contractility has 
 not sufficiently recovered, and a smaller and shorter contraction results. 
 
 Fig. 125 a. The long pause after the extra-systole (r') is followed by a large beat ; this 
 in turn is followed by a small beat ( x ), and the succeeding beats are larger. The small beat ( X ) 
 is an evidence that the contractility of the heart was greatly exhausted. Compare with 
 Fig. 125. (From a case of advanced cardio-sclerosis.) 
 
 As this contraction is shorter in duration, the period of rest is thereby 
 lengthened before the next stimulus arrives, so that the contraction will 
 be stronger and longer ; being longer it wiU again encroach upon the period 
 of rest, and so the process of alternation goes on. 
 
 o 2
 
 196 DISEASES OF THE HEART 
 
 This variation in the duration of the systole can be seen in Fig. 125 a 
 by noting the distance between the up-stroke and the dicrotic notch of the 
 radial beats. 
 
 I have now collected a large number of cases in which this irregularity 
 occurs, and it is of far greater frequency than is usually suspected. The 
 
 Fig. 125 b. Shows the same variation as Figs. 125 and 125 A. (From a case of advanced 
 
 fatty and sclerotic heart.) 
 
 condition in which it is most frequent is cardio-sclerosis, where it is usually 
 associated with high blood-pressure, extra-systoles, and great limitation of 
 the field of cardiac response, and not infrequently with angina pectoris 
 (Cases 1 and 7, see Appendix I). After a period of rest and a fall of arterial 
 pressure, it may entirely disappear, and it is for this reason that it is so 
 infrequent in hospitals, where the rest in bed favours the restoration of 
 the contractility. In such cases I have frequently been able to bring it 
 back by making the patient hurry up and down a flight of stairs. When 
 it is associated with extra-systoles, an extreme form of irregularity may 
 be presented which seems at first to be hopelessly confused, but by careful 
 analysis we can detect the extra-systole, the long pause after it, and the 
 
 ^^^BBSB^^H^^^g2^^BSZ!B&&S8&8S&SS5S&&BHI 
 
 Fig. 120. The alternating character of the pulse is increased after the long pause following 
 the extra-systole (r') ; the second beat ( X ) following the pause appears at the normal interval, 
 but is greatly reduced in size. (From a case of advanced cardio-sclerosis.) 
 
 marked difference in the size of the following beats (see Appendix V). 
 In patients who have exerted themselves, a transient but extreme irregularity 
 may sometimes be detected in the pulse. Small beats and big beats may 
 follow one another in a bewildering fashion. But so brief is the duration 
 of the tumultuous action of the pulse, that before one can apply a sphygmo-
 
 EXHAUSTION OF CONTRACTILITY 197 
 
 graph the arrhythmia has to a great extent disappeared. I have, how- 
 ever, been able on several occasions to catch the irregularity before it had 
 subsided, as in Figs. 127 and 128, in which it may be seen how variable 
 
 Fig. 127. This tracing and the next were taken from a man with cardio-sclerosis, after 
 walking up a steep road. The pulse felt extremely irregular, and an analysis of the tracing 
 shows it to have been regular in rhythm, but the individual beats varied greatly in force. At x 
 the exhaustion is so great that only a small wave appears in the radial. 
 
 is the size of the beats ; one can probably infer that at a: a: in Fig. 128 the 
 beats were too weak to cause a movement in the radial, so that the pulse is 
 intermittent in character. 
 
 Fig. 128. Intermittent pulse due probably to extreme exhaustion of contractility, the 
 contraction of the ventricle being too weak to send a wave into the radial artery at x. Note 
 the increase of the alternating character of the pulse after the long pause. 
 
 It may appear in cases of cardio-sclerosis after an exhausting illness, as 
 bronchitis, when the patient is confined to bed (Fig. 129). 
 
 I have found this pulsus alternans during an attack of paroxysmal 
 
 Fig. 129. Pulsus alternans, male, 64, cardio-sclerosis and bronchitis. 
 
 tachycardia (Figs. 130, and 228, Appendix III), in a case of dilatation of the 
 heart from some obscure cause, in acute febrile affections of the heart (pneu- 
 monia and rheumatic fever), and after the administration of digitalis (Figs. 
 164 and 166).
 
 198 
 
 DISEASES OF THE HEART 
 
 This form of irregularity must be distinguished from that where an 
 extra-systole alternates with a normal beat (pulsus bigeminus). As has 
 already been described, the latter form of irregularity is caused by the too 
 
 Fig. 130. Pulsus alternans during an attack of paroxysmal tachycardia, sixty-six hours 
 from its commencement. (Case 11, Appendix II.) 
 
 early appearance of the smaller beat, which is followed by a long pause. On 
 the other hand, the rhythm in the pulsus alternans is quite regular (compare 
 Figs. 131 and 132), or the smaller beat occurs after a slightly lengthened 
 pause. Volhard ^-^ has pointed out that this slight delay is due to the fact 
 that the weak contraction takes a longer time to open the aortic valves. 
 
 Fig. 131. Pulsus bigemiuus, due to the regular occurrence of extra- 
 systoles. The numbers represent in tenths of seconds the duration of each 
 pulse period, and it is seen that the longest pauses occur after the small 
 beats. (Compare with Fig. 132.) 
 
 The pulsus alternans can sometimes be perceived by the finger, but it 
 is apt to be overlooked. The sounds of the heart often can be heard to 
 alternate, those accompanying the weaker being less loud. When there 
 
 Fig. 132. Pulsus alternans. The numbers show a slight prolongation of the pause before 
 the smaller beat, in contrast to what occurs in Fig. 131. 
 
 is a musical murmur the alternation in the strength of the sounds is very 
 marked (Case 24, Appendix V). 
 
 § i8o. Prognosis — The prognosis of exhausted contractility naturally 
 depends on the conditions that have induced it. These conditions are
 
 EXHAUSTION OF CONTRACTILITY 
 
 199 
 
 discussed under the different symptoms described elsewhere. It may, 
 however, be pointed out that the pulsus alternans is a very grave sign at all 
 times, and especially in febrile affections. In cardio-sclerosis it implies an 
 advanced degree of exhaustion, and one may confidently infer that the 
 muscular degeneration is fairly extensive, as I have found in a number of 
 post-mortem examinations. A patient may go quietly about for years 
 after the appearance of the pulsus alternans, but it is usually a sign of an 
 irrecoverable underlying condition. 
 
 Fig. 133. The extra-systole (?') occurs regularly after every third normal beat. The two 
 beats preceding the extra-systole are of equal size (22. 3. '94). 
 
 The grave significance of this seemingly trivial sign is seen in the case 
 from whom Figs. 133 and 134 were taken. The patient was a female, aged 
 fifty, whom I had under treatment for a large thoracic aneurysm about ten 
 years. For some months before her death she showed extra-systoles (Figs. 83 
 and 84) ; on March 22, 1894, she had a feverish attack, the temperature 
 102°, and the pulse-rate 120, still showing the extra-systole after every third 
 normal beat. On the 24th, her pulse-rate and irregularity was the same 
 (Fig. 134), but now it is seen that the second beat ( x ) after the long pause 
 
 Fig. 134. Shows the same irregularity as Fig. 133, but here the second of the normal beats 
 is always smaller than the third, implying a grave exhaustion of the contractile power of the 
 left ventricle. (Taken 24. 3. '94. The patient died on 26. 3. '94.) 
 
 is smaller than the third. She died on March 26, 1894 (see also Case 7, 
 Appendix I, and Cases 23 and 24, Appendix V). 
 
 § 1 8 1 . Treatment. — While the treatment will depend on the conditions 
 causing the exhaustion, we can obtain from the pulsus alternans an idea 
 of the principle which should guide us in every case. Its production by 
 excessive work in degenerated hearts, or after a long period of tachycardia, 
 implies that over-exertion or want of rest is the immediate cause. The 
 occurrence of the larger beat in the alternating pulse shows what rest can 
 do to restore the contractility. Therefore relief from over-exertion, whether
 
 200 DISEASES OF THE HEART 
 
 from exercise, rapid action, or from too high blood-pressure, should be the 
 aim. This may be secured by bodily rest, or by the administration of 
 remedies that ensure rest — above all, sleep. When there is a high blood- 
 pressure, dyspnoea, and no dilatation of the heart, chloral has been of great 
 use in my hands. On the other hand, drugs of the digitalis group are not 
 only useless, but may be injurious. 
 
 In a few cases I have seen distinct relief from the associated symptoms 
 of pain and breathlessness obtained by large doses of oxygen (p. 278).
 
 CHAPTER XXIII 
 
 Dilatation of the Heart (Failure of Tonicity) 
 
 § 182. The cause of dilatation of the heart. 
 
 183. The function of tonicity. 
 
 184. The symptoms of depression of tonicity. 
 
 185. Dilatation of the heart. 
 
 186. The cause of functional murmurs. 
 
 187. The consequences of dilatation of the heart, and how they are brought about. 
 
 188. Dropsy. 
 
 189. Enlargement of the liver. 
 
 190. Oedema of the lungs. 
 
 191. Urinary symptoms. 
 
 192. Prognosis. 
 
 193. Ti-eatment. 
 
 Although the matter of the ' tone ' of the heart is frequently present 
 in the minds of physicians, nevertheless I venture to doubt if ever it is more 
 than a vague conception. Some writers have described certain conditions 
 associated with it, yet it has not received that consideration its importance 
 merits. The recognition of depression of tonicity will be found to be of 
 the greatest service in appreciating the nature of the heart failure and the 
 remedies appropriate for the restoration of the heart's power. For some 
 years now, I have been inquiring into this function, and although many 
 important features have been revealed, I am far from comprehending its 
 full significance. 
 
 § 182. The cause of dilatation of the heart. — Before considering 
 the symptoms produced by depression of tonicity, it is necessary to appre- 
 ciate the cause of the most prominent of these symptoms, namely, dilatation 
 of the heart, and one cannot fail to be struck with the inadequacy of the 
 explanation usually given for this condition. The prevalent idea seems to 
 be that it is due to an increasing pressure within the chambers forcing the 
 walls outwards. But if it be asked, Whence comes this distending force ? 
 the inadequacy of such an explanation is at once apparent. During systole 
 the increased pressure within the chamber is produced by the contraction 
 of the wall of the chamber itself, and one can scarcely assume that in the 
 process of contraction dilatation is produced. Dilatation of an auricle,
 
 202 DISEASES OF THE HEART 
 
 it is true, might be produced by the forcible regurgitation of blood from 
 a powerful ventricle, but such a thing can only happen when there is a lesion 
 of the auriculo-ventricular valves. Regurgitation, apart from valvular . 
 lesion, can only occur after the muscle-fibres surrounding the auriculo- 
 ventricular orifices have become relaxed — that is to say, dilatation of the 
 auricle from such a cause would be produced after dilatation of the ventricle. 
 
 That neither the resistance opposed to a chamber during the systole, 
 nor the distending force during its diastole, is the cause of dilatation becomes 
 evident when the conditions observed in certain hearts are carefully studied. 
 Thus hearts whose walls are thinned, and whose muscle-fibres are degenerated, 
 may continue to work against an abnormally high arterial pressure, and 
 never show any signs of dilatation. In fact, the wall of the left ventricle 
 may be so thinned that it actually bursts in its effort to overcome the aortic 
 pressure, yet the walls show no signs of dilatation. Professor Keith, who 
 has especially looked into this matter of ruptured hearts, informs me that 
 such hearts may show no sign of increase in the size of their cavities. In 
 a patient under my care the heart was so enfeebled that he could scarcely 
 walk fifty yards without an attack of angina pectoris coming on, but no 
 enlargement of the heart could be detected. He died suddenly from rupture 
 of the heart, and I found that part of the heart-wall was so thinned as to 
 be made up of little except the endocardium and pericardium, yet, notwith- 
 standing this enfeeblement of the heart-waU, there was no sign of dilatation 
 of the cavity. 
 
 Dilatation of the left ventricle may occur even when the diastolic force 
 filling the ventricle is greatly diminished, as in cases of pure mitral stenosis. 
 Here the quantity of blood reaching the ventricle and the force with which 
 it enters the ventricle are so greatly diminished that we must look for some 
 other cause for the dilatation of the left ventricle that is found in advanced 
 cases of mitral stenosis. 
 
 § 183. The function of tonicity — In default of this mechanical 
 explanation we turn naturally to the functions of the normal heart, to inquire 
 what maintains the fibres in health in a position short of their extreme 
 relaxation. In this way we may succeed in obtaining a more definite con- 
 ception of what occurs in dilatation, even if we fail to elucidate altogether 
 its etiology. 
 
 This function of maintaining a position short of extreme relaxation 
 is not peculiar to the cardiac muscle, but is also met with in the ordinary 
 skeletal fibres, and in both cases it is due to the possession by the fibres of 
 the function of tonicity. 
 
 § 184. The symptoms of depression of tonicity. — These symptoms
 
 DILATATION OF THE HEART 203 
 
 are threefold : (1) those due directly to the changes in the heart, viz. 
 increased size of the heart, alterations in the position and in the character 
 of the movements of the heart, and the presence of murmurs ; (2) those 
 associated symptoms due to the failure of the circulation in remote organs 
 and tissues, as dropsy, enlargement of the liver, and breathlessness ; 
 (3) certain reflex sensory symptoms mainly shown by regions of hyperalgesia 
 affecting the skin, breast, and muscles of the left chest and axillary fold, and 
 sometimes also the left sterno-mastoid and trapezius muscles. 
 
 § 185. Dilatation of the heart. — The evidence of dilatation of the 
 heart is made out by marking out the increased size of the heart. I need 
 not dwell upon how this is done, for the methods for percussing out the heart's 
 dullness are described in sufficient fullness in every handbook of physical 
 diagnosis. For practical purposes the transverse dullness at the level of 
 the fourth interspace gives on the whole the best estimate of the size of the 
 heart. In exceptional cases the whole area of deep dullness may be with 
 advantage mapped out, as when dullness is found extending to the left 
 above the third rib. In such cases the possibiHty of pericardial effusion 
 should be kept in mind. 
 
 It is very difficult to teU with certainty what share each chamber of the 
 heart takes in the production of the increased size, on account of the dis- 
 placement of the whole organ. The manner in which the heart is fixed 
 above, by the aorta, pulmonary artery and veins, and superior vena cava, 
 and below by the inferior vena cava, keeps fixed an axis on which the heart 
 to a certain extent rotates in the enlargement of its various cavities. The 
 tendency when the right ventricle dilates, is for it to push the left ventricle 
 to the left and behind, with the result that in the great majority of cases 
 we get evidence of an extension of the dullness to the left. When the right 
 auricle becomes greatly distended, it may push itself to the front of the 
 chest, and, as Keith's dissections show, compress the right ventricle to a 
 remarkable degree. When there is extension of the dullness beyond the 
 right border of the sternum, it may with certainty be put down to the right 
 auricle, except in aneurysm or other intra-thoracic tumour. 
 
 The manner in which the right heart pushes over to the left side is well 
 brought out in Figs. 135 and 136. These are typical of the dilatation 
 secondary to mitral stenosis. If a comparison be made with the position 
 of the chambers in the normal heart (Fig. 19), it will be observed that the 
 increase to the right side, notwithstanding the great dilatation of the right 
 heart, is very sHght, whereas the great increase in the size of the heart is 
 to the left — sometimes with only a slight depression of the apex (Fig. 135), 
 sometimes with considerable depression (Fig. 136). Note also how the
 
 204 
 
 DISEASES OF THE HEART 
 
 right auricle pushes into the second left interspace. So long as the lungs 
 cover a portion of the heart the perceptible movements will be entirely due 
 to the right ventricle ; but when the lung is pushed from the front of the 
 heart, then the real apex will be found at the extreme left (see § 83). 
 
 In seeking for the cause of the increased dullness, the character of the 
 impulse should always be studied, not only to determine the nature of the 
 
 Fig. 135. Position of the chambers of the heart in extreme dilatation, as in the late stage 
 of mitral stenosis. The portion of the heart on the right of the sternum shaded deeply- 
 together with that behind the sternum up to the dotted line represents the right auricle, while 
 the small strip to the left shaded deeply represents the left ventricle. The part between is 
 the right ventricle. (Harris). 
 
 heart's enlargement, but to distinguish it from pericardial effusions and 
 displacement of the heart by such conditions as aneurysm, pleural effusion, 
 and so forth. Another point to bear in mind is that, in the early stages of 
 enlargement of the heart, the lung may still cover a part of its left border, 
 but with persistence of the enlargement the lung is compressed, and if non- 
 adherent, recedes from the anterior surface of the heart, altering altogether 
 the character of the apex movements. 
 
 § 1 86. The cause of functional murmurs — Functional murmurs
 
 DILATATION OF THE HEART 205 
 
 have hitherto been looked upon as a consequence of simple dilatation of the 
 heart, but this explanation is far from being sufficient. Thus we may have 
 considerable dilatation of the heart without a murmur. Again, we may 
 have very little dilatation with marked systolic murmurs at apex and base, 
 and with a great regurgitant wave in the veins. The explanation of these 
 apparent anomalies seems to be in the condition of the muscles supporting 
 
 Fig. 136. Dilatation of the heart with the apex beat displaced downwards. The 
 shading is the same as in the preceding figure. 
 
 the auriculo-ventricular orifice. If their tonicity be depressed regurgitation 
 ensues, and gives rise to the functional murmurs. 
 
 § 187. The consequences of dilatation of the heart, and how they 
 are brought about — Before describing in detail the results that foUow 
 dilatation of the heart, it is necessary to consider the manner in which 
 these symptoms of heart failure are brought about. The maintenance 
 of the circulation is due to the contractile force of the heart, and normally 
 the factors concerned are so balanced that everything is done to facilitate
 
 206 DISEASES OF THE HEART 
 
 the work of the heart. It is reasonable to assume that the chambers of the 
 heart are normally of the size that enables them to contract with the greatest 
 efficiency. The dilatation of these chambers will therefore embarrass the 
 heart muscle, with the usual result, a limitation of the reserve force. At 
 first, this limitation may only call forth disagreeable symptoms when it is 
 exhausted, the exhaustion occurring much sooner than normal. The 
 degree of exhaustion depends on the integrity of the heart muscle. If the 
 contractile force is embarrassed by inherent defects of the muscular wall, 
 or by other causes, such as irregularity of action, or valvular defects, then 
 the heart failure corresponds to the degree of embarrassment and inability 
 of the muscle to overcome it. For this reason we find all degrees of heart 
 failure associated with dilatation. In the milder cases there may be only 
 the subjective symptoms of breathlessness, palpitation, and weakness. In 
 the more extreme cases, dropsy (more or less extensive), diminished secretion 
 of urine, effusion of fluid into the serous cavities, enlargement of the liver, 
 lividity of the face may be present. The rationale of the production of this 
 extreme heart failure seems to be as follows : So long as the contractile 
 force of the heart is able to maintain a degree of arterial pressure sufficient 
 to supply the organs and tissues, the heart failure will be limited to those 
 subjective symptoms involved in a great reduction of reserve force ; the 
 patient is comfortable at rest, for the heart is then able to maintain the 
 circulation, but is distressed by exertion, for the heart has so Httle reserve 
 force that it is unable to meet the extra demand. When the force of the heart 
 fails to maintain the arterial pressure at the height necessary for the tissues, 
 then we get the symptoms in the remote organs and tissues (dropsy, ascites, 
 enlarged liver, &c.). 
 
 I have endeavoured in a number of ways to demonstrate the relationship 
 between dilatation of the heart and these evidences of extreme heart failure, 
 and I give a few instances where the association of these symptoms with 
 dilatation of the heart is clearly marked. 
 
 In advanced cases of cardio-sclerosis with a blood-pressure continuously 
 high, between 180 mm. Hg. and 200 mm. Hg., the heart may be of normal 
 size, or only very slightly enlarged. There is great limitation of the field 
 of response, exertion readily inducing attacks of angina pectoris or breath- 
 lessness, Cheyne-Stokes respiration may occur also, and attacks of cardiac 
 asthma or severe dyspnoea at nights. There may be large pulsation in the 
 veins of the neck, but no dropsy. Patients may gradually weaken and die, 
 and the heart remain unchanged in size. On the other hand, in the course 
 of a day or two, one may be struck by a great change. The patient seems 
 easier ; the blood-pressure has fallen to 150 mm., or lower ; attacks of angina
 
 DILATATION OF THE HEART 207 
 
 pectoris, cardiac asthma, and Cheyne-Stokes respiration disappear. But 
 the legs begin to swell, the urine becomes scanty, the jugular pulse disappears, 
 the breathing is continuously hurried, and the patient has to be propped up 
 in bed. He may begin to expectorate blood-stained mucus, and there is 
 evidence of oedema of the base of the lung. If the heart be examined, it 
 will be found to extend one or two inches further to the left, and it may be 
 a mitral murmur has developed. 
 
 Even more striking, because more sudden and violent, are the changes 
 that take place in certain cases of paroxysmal tachycardia. In describing 
 this condition (Chapter XX), I pointed out that the symptoms varied in 
 patients according to the condition of tonicity, — if the heart remained 
 unaltered in size during an attack, the symptoms were less marked, and the 
 condition less grave than if the heart dilated. In the cases recorded in the 
 Appendix (Cases 11 and 12, Appendix II), the heart dilated, and in the course 
 of a few hours symptoms of extreme heart failure set in. I have seen these 
 cases on several occasions shortly before an attack, and watched the steady 
 progress of the change. The hearts were nearly normal in size, but in three 
 hours' time the transverse diameter had increased by two inches, the face 
 had become livid and the lips swollen. The veins of the neck, which had shown 
 little movement, now pulsated largely in the nodal rhythm. In the course 
 of twenty-four hours oedema of the legs appeared, and the liver became large, 
 and in one case pulsated. After some days the dropsy extended up the 
 legs, the abdomen became distended, and the urine scanty. With the 
 cessation of the attack of paroxysmal tachycardia, the patients at once 
 experienced relief, and in a few hours every vestige of heart failure had 
 disappeared, and the heart itself returned to a normal size and rhythm. 
 I give these instances because, owing to the sudden change of appearance, 
 one could account fairly satisfactorily for the symptoms. In various modi- 
 fications they will be found associated with extreme heart failure from all 
 forms of cardiac disease. I have seen many cases in which the inception 
 of the nodal rhythm was followed by these changes, and when it persisted 
 a partial recovery only followed, with reduction of the size of the heart. In 
 certain alcoholic hearts — especially in those of Graham Steell's group of 
 ' muscle failure ' — these phenomena can also be recognized, as well as in 
 other conditions. 
 
 This manner of looking at dilatation, and the cause of dropsy and other 
 symptoms, has a very practical bearing on the treatment of heart failure 
 associated with valvular disease, the nodal rhythm, and cardio-sclerosis. 
 
 § 1 88. Dropsy Oedema of the subcutaneous tissues is a common 
 
 feature in heart failure with dilatation. It is apart from my purpose to
 
 208 DISEASES OF THE HEART 
 
 discuss the various theories propounded to account for its occurrence, it being 
 sufficient here to note that its appearance is often a definite sign of heart 
 dilatation, and its disappearance an equally definite sign of restoration of 
 the heart's tone. It begins first in the most dependent parts : in people not 
 confined to bed it is found first about and above the ankles ; in people lying 
 in bed, across the sacrum. It may linger in the legs for years in some folks — 
 worse towards night, better in the morning. In extreme cases it invades the 
 thighs and abdominal waU. The loose cellular tissue of the scrotum and the 
 penis and vulva becomes infiltrated, and may attain an enormous size. Before 
 marked effusion takes place into the abdominal cavity, the bowels often 
 become greatly distended. It may finally invade the pleural cavities, 
 producing hydrothorax. The distended abdomen and the hydrothorax 
 add to the embarrassment of the breathing. If the patient leans more to 
 one side than to the other, in extreme cases, the arm and check of that side 
 may become greatly swollen. When an arm becomes swollen apart from 
 this, and where there is not extensive oedema, one may suspect a clot in 
 some of the larger veins in or near the chest. 
 
 Associated with dropsy there is usually a diminished urinary secretion, 
 and disappearance of the dropsy usually coincides with an increased flow 
 of urine. 
 
 The significance of oedema is extremely varied. Many elderly people, 
 especially if they are stout, may for years have their legs more or less swoUen 
 even if their hearts present no particular abnormahty beyond a shght dilata- 
 tion, though it is more common amongst those with the nodal rhythm. It may 
 be present in attacks of heart failure to an extreme degree, with ascites and 
 hydrothorax, and notwithstanding the patient may make a good and lasting 
 recovery. These are found more particularly in cases of rheumatic affection 
 of the heart of some duration, starting in some with the nodal rhythm. 
 If the heart reverts to its normal rhythm, the disappearance of the dropsy 
 is more speedy than its onset. If the heart reacts to digitalis, the disap- 
 pearance of the dropsy accompanies the other beneficial effects of the drug. 
 When all attempts to restore the heart fail, the dropsy increases, embarrasses 
 the heart and the respiration by effusion into the serous cavities, and adds 
 much to the suffering of the patient, who drifts to a fatal issue. 
 
 § 189. Enlargement of the liver Another result of the failure of 
 
 the circulation secondary to dilatation of the heart is sweUing of the hver 
 from passive congestion (Chapter XIV). It may not appear in the earher 
 stages in the first instance, but when a patient has once recovered from 
 an attack of heart failure with enlargement of the hver, every subsequent 
 attack induces this symptom, sometimes before any sign of dropsy sets in.
 
 DILATATION OF THE HEART 209 
 
 There may be associated with the enlargement a certain amount of 
 jaundice, and the combination of enlarged Uver and jaundice, with the wasting 
 that sometimes accompanies long-continued heart failure, may raise the 
 suspicion of mahgnant disease of the liver (§ 121). The dilatation or 
 irregular action of the heart should direct attention to the real nature of 
 the trouble. 
 
 There may be a considerable degree of pain and discomfort associated 
 with the enlargement of the liver, and the painful contracted muscles may 
 embarrass the respiration (described in § 117). 
 
 § 190. Oedema of the lungs. — A symptom of great value is found in 
 the careful auscultation of the bases of the lungs in cases threatened with 
 some forms of heart failure. I carried out for some years an extensive 
 observation on all kinds of people — healthy, and with failing hearts from 
 a great variety of causes — and I was able to anticipate attacks of heart 
 failure in a great number of cases. If one systematically examines the 
 bases of the lungs in elderly people who are perforce confined to bed, as in 
 consequence of an operation or a fractured leg, in a certain proportion the 
 earliest symptom of heart failure wdll be found in the appearance of fine 
 crepitations at the bases of the lung. The same experience will be met with 
 in patients confined to bed from any exhausting complaint, particularly if 
 the heart muscle be involved in the ailment, as in typhoid fever. Many 
 patients with mitral lesions have no dropsy, but suffer from severe attacks 
 of heart failure with great breathlessness. In such cases the bases of the 
 lungs will be found to show signs of oedema at the early stages of the break- 
 down. 
 
 It has been my habit in these cases to begin the examination of the patient 
 by asking him on which side he lies, then make him sit up, and while I auscul- 
 tate the base of that lung on the side he had lain, I ask him to take in one full 
 and deep inspiration. This opens up the alveoli at the base, and if there is 
 any abnormal moisture it is manifested by numerous fine crepitations. 
 Healthy people show no sign of this. Slightly weakened hearts may show 
 it with the first deep inspiration only ; if there is distinct cardiac enfeeblement 
 the crepitations do not disappear at first, but persist. I have seen cases 
 where the first sign was the crepitation during the first deep inspiration, and 
 gradually the crepitations became more persistent until the resonance of the 
 bases of the lung became impaired, even to complete dullness, with no breath 
 sounds, and at the post-mortem examination the lungs at the bases have 
 been sodden and airless. In some instances there have been patches of in- 
 flammation (catarrhal pneumonia — the hypostatic pneumonia of the feeble). 
 
 MACKENZIE p
 
 210 DISEASES OF THE HEART 
 
 I have also seen this hjrpostatic congestion disappear, and as the patient 
 improved the crepitations gradually disappeared, the last sign being the 
 crepitations with the first deep inspiration. 
 
 I have found this method of observation of the greatest practical use. 
 In the elderly it governs the position which the patient should occupy — 
 lying down or propped up. In typhoid fever it is a prognostic sign of the 
 very greatest value — the absence of oedema indicating that the heart has 
 escaped infection ; its presence and gradual increase, a sign of great gravity. 
 In heart disease it is likewise one indication of the heart's condition, and in 
 the compHcation of pregnancy and heart disease it is one of the most 
 important guides in the management of these cases. 
 
 It is of no less importance in treatment, as will be realized when the 
 reason for its appearance is appreciated. It invariably accompanies dila- 
 tation of the right heart, and the manner of its production is as follows : The 
 factors that move the blood through the lungs are twofold — first and most 
 important, the right ventricle ; and second, the movements of respiration. 
 In healthy hearts the first of these is so powerful that the second is scarcely 
 appreciated. When, however, the right ventricle is enfeebled, the assistance 
 of the respiratory movements becomes necessary. When the patient lies 
 in bed on one side, the pressure of the ribs on the mattress restrains their 
 movement, so that the flow of blood through this part of the lung is retarded, 
 and oedema results. This can be shown in the early stages, for when the 
 patient breathes deeply the whole of the crepitations may disappear. 
 
 From this account will be realized the part that can be played in suit- 
 able cases by placing the patient in a position to breathe freely, avoiding 
 the restraint exerted by pressure on the ribs, and by making the patient 
 deeply inspire. In addition, the importance of recognizing the nature of 
 the symptoms due to the enlargement of the liver is here apparent, where 
 not only the abdominal muscles, but the intercostals also, may be tender 
 and contracted. In thus ceasing to act as respiratory agents, while exer- 
 cising their primitive function of protection, these contracted muscles 
 further add to the embarrassment of the heart in its work. 
 
 § 191. Urinary symptoms — I doubt if ever we get the characteristic 
 urinary symptoms of heart failure in the absence of dilatation of the heart. 
 These symptoms are a scanty secretion and increased specific gravity, and 
 frequently the presence of albumen. A diminished supply of blood to the 
 kidneys may cause a large quantity of albumen to appear in the scanty 
 urine, as can be observed in heart-block and nodal bradycardia, when the 
 heart's rate becomes very infrequent. The diminution of the quantity 
 usually goes hand in hand with the dropsy. The cause in the main is
 
 DILATATION OF THE HEART 211 
 
 a fall in arterial pressure and a rise in the venous, with consequent venous 
 stasis in the kidneys. Other conditions may co-operate, such as the chemical 
 constitution of the fluid in the tissues and changes in the secreting cells of 
 the kidney. It is often a difficult point to determine whether the albu- 
 minuria has been pre-existent, or whether it is induced by the venous stasis 
 and subsequent inflammatory changes in the kidneys. The history of the 
 patient will help, and the presence of arterio-sclerosis and retinitis point to 
 a pre-existent Bright's disease. It may be necessary to suspend judgement 
 until a recovery of tonicity of the heart restores the circulation, as with the 
 increase in flow of urine the albuminuria may entirely disappear. 
 
 It is often useful to direct the patient's attention to the urinary secretion, 
 as its diminution may give the first warning of an impending breakdown, 
 and the increase in the flow is often the first sign of recovery of heart 
 power. 
 
 § 192. Prognosis. — While the degree of tone present is of first-class 
 importance in estimating the nature of the heart failure, we must use great 
 discretion in determining the value of dilatation as a prognostic factor. 
 Great dilatation may be compatible with a favourable prognosis, while 
 a much smaller degree of dilatation may be a sign of considerable gravity. 
 If we find the patient getting along comfortably and well with a dilated heart, 
 it means that the muscular tissue is otherwise sound, and that there is no 
 material obstacle to the work of the heart, and the muscle itself is able to 
 overcome the embarrassment induced by the dilatation. 
 
 Another element in the prognosis is the manner in which the heart 
 responds to treatment, especially to drugs of the digitalis group. As I shall 
 point out in Chapter XXXIV, tonicity is one of the functions of the heart 
 which digitalis readily affects in many cases, and it is probably because of 
 the effects of this drug on this function that it has often such a wonderfully 
 beneficial infiuence on the heart. The improvement produced by digitalis 
 is therefore a guide to the condition of the heart muscle, and to the suscepti- 
 bility of this function to its action. On the other hand, when dilatation 
 of the heart and the symptoms accompanying it described above are 
 unresponsive to digitahs, the outlook becomes grave. Especially is this 
 the case in the heart failure with dilatation in advanced arterio-sclerosis. 
 
 § 193. Treatment — As dilatation is invariably secondary to some 
 other condition of the heart, the treatment has to take into considera- 
 tion other factors. I may point out, however, that, unless in the acute 
 febrile stage, dilatation is an indication for the prescription of digitahs in 
 all rheumatic hearts. In other conditions it should be tried, especially if 
 
 there is dropsy and deficient secretion of urine. The treatment of such 
 
 p 2
 
 212 DISEASES OF THE HEART 
 
 associated symptoms as dropsy and diminution of urine should consist in the 
 attempt to restore the heart's strength. When dropsy becomes a distressing 
 symptom, special means have to be undertaken for its removal. As free 
 diuresis is the most effective way of getting rid of it, a great many agents are 
 recommended which effect this purpose. The virtues of many a prescription 
 can be estabhshed by the recital of illustrative cases in which its exhibition 
 was followed by an extraordinary discharge of urine and speedy disappear- 
 ance of all dropsy. These preparations will be found to vary from the 
 mixtures containing every conceivable drug that is supposed to have diuretic 
 properties, to some recent synthetical preparation. The fact of the matter 
 is, that in many of these cases the secretory activity of the kidneys seems 
 to be in temporary abeyance, and some sUght adventitious aid gives it the 
 necessary stimulus. This auspicious moment coinciding with the adminis- 
 tration of the drug, results in a profuse diuresis. This aid need not be a drug. 
 I have seen a patient, who had to sit up in a chair for three weeks on account 
 of his breathing, become extremely dropsical, passing very little urine. 
 The mere return to bed was followed at once by a profuse diuresis and the 
 rapid disappearance of the dropsy. It is, however, necessary in many cases 
 to try various agents, and happily here the digitalis group is most effective, 
 the combination of digitalis, squill, and calomel being particularly useful, 
 not only from its action on the heart and kidneys, but also from its effects 
 on the bowels. When these drugs fail others may be found to act, such as 
 theobrominae sodii saHcylas (Diuretin) or theocin-sodium acetate. In 
 some cases the elimination of common salt from the food helps to reduce 
 the dropsy. In all cases of dropsy the bowels should invariably be kept 
 well moved. 
 
 Special efforts to give relief are often necessary. In certain cases when 
 the patient can go about, an elastic bandage skilfully appUed is beneficial, 
 particularly in those hard, swollen legs when the skin threatens to give way. 
 Massage also is of assistance. When the legs or genitals become greatly 
 distended, deep pricks with a needle will often be followed by a free flow 
 of serum and a great diminution of the swelling. The utmost cleanliness 
 should be observed in carrying out this simple procedure. The employment 
 of Southey's tubes inserted into the legs or abdominal cavity will often 
 drain off a large quantity of fluid. The abdominal and thoracic cavities 
 may need to be tapped ; such tapping invariably gives temporary relief. 
 In some advanced cases where the penis is greatly swollen (ram's horn), 
 there may be inability to void urine. In using a catheter there may be 
 some trouble in finding the meatus, the glans penis being buried in the 
 scrotum under the swollen prepuce. If the swollen foreskin be gently but
 
 DILATATION OF THE HEART 213 
 
 firmly grasped in the hand and compressed, the fluid is driven out, and 
 the glans can then be exposed. 
 
 The employment of judicious breathing exercises in oedema of the lung 
 is often beneficial, the patient sitting up and breathing slowly and deeply. 
 In severe cases this is limited at first to a few movements. If the patient 
 bears the exercise, these deep respirations should be employed at regular 
 intervals every two or three hours when awake. In the intervals the 
 patient should be propped as high as he can bear with comfort.
 
 CHAPTER XXIV 
 
 Acute Febrile Affections of the Heart 
 
 § 194. INIanner in which the heart is affected in fever. 
 
 195. The febrile heart. 
 
 196. Acute febrile affections of the heart. 
 
 197. Symptoms in myocarditis : changes in rate, changes in rhythm due to depressed 
 
 conductivity of the a. -v. bundle, depressed contractility, extra-systole, nodal 
 rhythm, depressed tonicity (dilatation of the heart). 
 
 198. Symptoms in endocarditis. 
 
 199. Symptoms in pericarditis. 
 
 200. The heart in rheumatic fever : pathological changes, symptoms. 
 
 201. The heart in pneumonia. 
 
 202. The heart in diphtheria. 
 
 203. The heart in septic iijfections. 
 
 204. Treatment. • 
 
 § 194. Manner in which the heart is affected in fever. — In con- 
 sidering the state of the circulation in febrile conditions, it is necessary 
 to bear in mind three facts, viz. that the heart's action is modified by an 
 increase in temperature, that the heart reacts differently according to the 
 toxins produced by the agent causing the fever, and finally, that the heart 
 itself may be the seat of the conditions causing the fever. Recent researches 
 demonstrate conclusively the invasion of the heart by the specific organism in 
 rheumatic fever, pneumonia, typhoid fever, diphtheria, erysipelas, influenza, 
 and various septic infections. The results of such invasion are shown in 
 the occurrence of endocarditis, myocarditis, and pericarditis. The symp- 
 toms evoked in such invasions are not always distinctive, and may resemble 
 the symptoms induced in the heart by febrile conditions alone, or by toxins 
 produced from other sources in the body. I dwell upon this because an 
 attempt should always be made in febrile conditions to judge rightly the 
 effects on the heart. One cannot but be struck, for instance, by the fact 
 that people with previously seriously damaged hearts may pass scatheless 
 through severe attacks of pneumonia or typhoid fever, while the young 
 and vigorous may succumb after a few days' illness on account of the 
 implication of the heart in the disease. 
 
 Another point to bear in mind is that in the invasion of the heart the 
 specific organism rarely affects one tissue alone. In order to be exact and
 
 ACUTE FEBRILE AFFECTIONS OF THE HEART 215 
 
 methodical, writers usually describe separately the symptoms of endo- 
 carditis, myocarditis, and pericarditis. But if one reflects on the nature of 
 the symptoms, such as the condition of the pulse, its strength, rate, and 
 rhythm, the size of the heart, and the praecordial distress — symptoms which 
 are usually included in the description of endocarditis and pericarditis — it 
 will be realized that they are not really the manifestations of endocarditis 
 or pericarditis, but are the signs of a myocardial affection. One must 
 consider carefully the murmurs arising in the course of a febrile attack, 
 even in rheumatic fever, for the presence of a murmur may not neces- 
 sarily mean the invasion of the mitral valves by the inflammatory 
 process, but may be due to the tonicity of the poisoned heart muscle failing 
 and giving rise to incompetence of the mitral orifice — due, therefore, 
 not to an endocardial, but to a myocardial affection. Endocarditis and 
 pericarditis, both acute and chronic, bulk so largely in medical literature 
 only because an abnormal sound invariably impresses the mind more than 
 an abnormal sign perceptible by the other senses, and the easy recognition 
 of the valvular murmur and the friction sound has led to the associated 
 symptoms being ascribed to the same lesion. 
 
 § 195. The febrile heart — By this term I mean the changes induced 
 by the rise in temperature. The whole circulatory apparatus is remark- 
 ably sensitive to alterations in temperature, whether arising from external 
 sources or due to changes within the body. The most striking of these 
 is the change in rate — a rise in temperature increasing the rate, and 
 a fall diminishing it. In the more simple febrile affections there is 
 a certain correspondence between the height of the temperature and the 
 rate of the heart's contraction. Roughly speaking, there is an increase of 
 from eight to ten beats with a rise of temperature of one degree F. This 
 does not hold universally, but any considerable departure from this rule 
 should always arouse watchfulness and suggest the possibility of other 
 complications, such as the involvement of the heart in the infection. 
 
 In the simple febrile heart the radial artery enlarges and the pulse remains 
 of good strength, particularly during the diastolic phase of the cardiac cycle. 
 The heart itself shows little change at first, beyond having its rate abnor- 
 mally accelerated by exertion. The sounds are clear and distinct, and there 
 is no increase in size. With long continuation of the fever a certain amount 
 of dilatation may arise. This most readily occurs on the right side of the 
 heart, particularly if the pulmonary circulation is interfered with, as by 
 a pneumonia or a pleuritic effusion, or by lying a long time on the back, 
 as during the course of typhoid fever. The sounds may become feeble, or 
 systolic murmurs may develop at the tricuspid and mitral orifices, and the
 
 216 DISEASES OF THE HEART 
 
 characteristic pulsation of the right heart in the epigastrium become visible 
 (Figs. 29 and 30, pp. 84, 85). In many of the minor febrile attacks the course 
 is modified by the nature of the toxins generated. A rise of a few degrees of 
 temperature may provoke an undue frequency — 120-140, and with the 
 subsidence of the temperature the rate may speedily fall to normal, 
 leaving no ill effects. A slight rise of temperature may even be accompanied 
 by a fall in the pulse-rate — sometimes, if the patient's pulse is normally 
 a slow one, below fifty per minute. I have found remarkable variation in 
 rate with the same temperature at different times, in the same individual, 
 due probably to a difference in the agent producing the fever. The effects 
 produced by agents other than a rise in temperature cannot perhaps be 
 better illustrated than by those occurring during an attack of ague ; here in 
 the course of twenty-four hours, with a continuously high temperature, we 
 have a remarkable series of changes in the pulse. During the cold stage the 
 pulse becomes small and scarcely perceptible, on account of the contraction 
 of the peripheral arteries. The blood driven from the surface and from the 
 arterial system accumulates in the venous system and in the internal organs. 
 Then the lips and fingers become blue, and the congestion of internal organs 
 may reach such a degree that capillary haemorrhages occur within them. 
 Within a few hours, the temperature still being high, the arterioles relax, 
 the arteries become larger, and the pulse itself is of considerable force. 
 
 § 196. Acute febrile affections of the heart The lesion induced 
 
 by the invasion of the heart by specific organisms is rarely limited to one 
 structure or tissue, so that it would be better to use the term carditis 
 than to employ such misleading terms as endocarditis and pericarditis. 
 This will be brought out more clearly when an analysis is made of the symp- 
 toms present in any given case, and I shall endeavour briefly to summarize 
 the symptoms and try to apportion them to the particular tissues affected. 
 I do this here, because by the appreciation of the nature of the primary lesion 
 we are better able to understand" the conditions found many years after, 
 when the cicatrizing process has wrought other changes. 
 
 § 197. Symptoms in myocarditis — The rate and rhythm are the 
 most easily recognized. Seeing that a rise of temperature alone induces 
 an increased frequency, it is impossible to apportion the relative influences 
 of this and of the myocardial infection. But many cases of moderate 
 fever have a heart-rate greatly accelerated, and then we can infer there is 
 some other factor at work than the rise in temperature. It would be of 
 great interest to know the mechanism by which increased rate is brought 
 about by myocardial lesions, whether through nerve stimulation arising 
 reflexly from the inflamed tissue, or from the increased irritabihty of the
 
 ACUTE FEBRILE AFFECTIONS OF THE HEART 217 
 
 muscle, particularly of the tissue in which the stimulus for contraction 
 arises. But here such an inquiry would be purely speculative. 
 
 Changes in rhythm come under a different category, and in irregularity 
 we often get a clue to the changes that are going on in the muscle. The 
 arrhythmia due to purely nervous influences is generally abolished during 
 the excitation of the heart by the fever — the chief exception being the 
 arrhythmia due to vagus stimulation in affections of the brain (as in tuber- 
 cular meningitis). 
 
 The myocardial irregularities have not been as carefully worked out in 
 acute conditions as their importance demands, and the slight advance I have 
 made in the study of the subject shows it to be of the utmost importance 
 if we would understand the pathology of the living heart. 
 
 Degression of conductivity. — The most characteristic evidence of direct 
 damage done to the muscle of the heart is the irregularity or pulse inter- 
 mission due to the dropping out of ventricular systoles, because of the damage 
 done to the a. -v. bundle by the lesion. In carefully watching cases of rheu- 
 matic fever, I have detected the appearance of a mitral murmur, and found 
 a lengthening of the interval between the auricular and ventricular systoles, 
 followed later by the presence of an aortic diastolic murmur. The adminis- 
 tration of digitalis in such cases has produced a mild form of heart-block 
 (Case 27, Appendix VI). This affection of the a.-v. bundle, shown by slight 
 spontaneous heart-block, I have detected in rheumatic fever and in influenza 
 (Fig. 119), and it has been detected in otker acute affections. Professor 
 Hoist, of Christiania, has shown me tracings of mild heart-block from 
 a case of septic poisoning, and Dr. Grosh, of Toledo, U.S.A., similiar trac- 
 ings from a case of puerperal fever, while Dr. Cooper, of San Francisco, 
 has shown me tracings of complete heart-block from a case of septic 
 poisoning under the care of Dr. Jellinek. In this last case the patient died 
 within fourteen days of the onset of the heart-block, and an examination 
 of the heart by Dr. Ophuls showed an anaemic necrosis of the muscular 
 septum involving the a.-v. bundle, consequent on a recent thrombus of 
 the nutrient artery. 
 
 In acute affections of the heart, writers usually content themselves by 
 mentioning irregularity as one of several symptoms, but the instances cited 
 show that if graphic records were taken this condition would be found 
 fairly frequent. 
 
 Depression of contractility. — Towards the later stages of fatal pneu- 
 monias, I have frequently detected a missed beat or an irregularity. 
 Analysis of a number of these cases has shown that it has probably been 
 due to failure of the power of contraction. Thus a typical example is seen
 
 218 DISEASES OF THE HEART 
 
 in Fig. 137, where towards the end of the tracing there is shown a marked 
 pulsus alternans. The missed beats in the earlier part of the tracing I think 
 are due to the contraction having been so feeble that it failed to propagate 
 a wave into the arteries. Thus we see in Fig. 138, from another case of 
 
 Fig. 137. Irregular pulse in the course of a pneumonia, showing the pulsus alternans in the 
 latter half of the tracing. The intermissions may be due also to failure of contractility. 
 
 pneumonia, how the small beats s' arise at the normal interval, but the 
 exhaustion of the heart is so great that it only sends out a small quantity 
 of blood, and after the last small beat it fails altogether to send out a wave. 
 Such signs in pneumonia I have found always to be of the gravest signi- 
 
 FiG. 138. Tracmg of the respiratory curve and of the irregular pulse in the course of a fatal 
 case of pneumonia. The small beats s^ are probably due to exhausted contractility. 
 
 ficance. John Hay has shown a similar arrhythmia in a patient suffering 
 from septic poisoning. 
 
 Extra-systoles. — Extra-systoles are of rare occurrence in severe infec- 
 tious febrile hearts, but Fig. 139 shows the occurrence of extra-systoles 
 
 Fig. 139. Extra-systoles occurring in the course of a fatal attack of rheumatic fever. 
 
 in the course of a fatal attack of rheumatic fever. As there is no com- 
 pensatory pause, the premature beat is probably of auricular origin (§ 145). 
 Nodal rhythm. — I have seen in several instances the sudden inception 
 of this rhythm in pneumonia, and always with disastrous results. In one 
 patient whom I saw in consultation everything seemed to be progressing 
 favourably, but while talking to the doctor in attendance we were suddenly
 
 ACUTE FEBRILE AFFECTIONS OF THE HEART 219 
 
 summoned to the bedside of the patient, and found that the heart's action 
 had, in the interval since our seeing him, taken on this nodal rhythm, and 
 the pulse had become rapid and irregular. The patient died a few hours 
 after. In another case I was called to see, the doctor told me the patient 
 had passed well through an attack of pneumonia terminating by crisis. 
 The day following the fall of temperature the patient suddenly became 
 weak and ill, and the doctor being summoned found him collapsed. I saw 
 him shortly after and found the heart had taken on the nodal rhythm ; the 
 doctor assured me that he had gone through the pneumonia with a good and 
 regular pulse. He also died a few hours after. 
 
 Dilatation of the heart. — Evidences of myocardial affections can be 
 found in the changes in the size of the heart. The symptoms of dilata- 
 tion have been fully described in Chapter XXIII, but it is well to remember 
 that the size of the heart may very speedily become greatly increased in the 
 course of a febrile affection of the heart, as in rheumatic fever, diphtheria, 
 &c. In such cases the sounds often become very faint, and soft murmurs 
 may arise at the mitral and tricuspid orifices, and simulate valvular changes. 
 
 § 198. Symptoms in endocarditis. — The only direct evidence of acute 
 endocarditis is the presence of murmurs at one or other orifice of the 
 heart. For practical purposes there are only two murmurs which need 
 to be considered here, viz. a mitral systolic murmur and an aortic diastolic. 
 It is not always easy to tell whether the appearance of a murmur during 
 a febrile attack is due to involvement of the mitral valve in an endocarditic 
 process or to the relaxation of the muscle supporting the orifice. A 
 diastolic aortic murmur is, as a rule, diagnostic of the involvement of 
 the aortic valve in some destructive process. At first this murmur is so 
 faint that one is simply conscious of the fact that the sound does not 
 end with sufficient abruptness. Gradually, however, this passes into 
 a very soft short whiff at the end of the second sound, becoming day by 
 day more marked. 
 
 In the vast majority of cases the murmurs due to endocarditis are not 
 definitely recognized until some time after the subsidence of the fever — when 
 the sclerosis sets in. This is particularly the case with presystolic mitral 
 murmurs, which are never recognized during the acute condition that induces 
 the lesion, unless there is narrowing of the mitral orifice on account of vegeta- 
 tions. The formation of vegetations at the mitral and aortic orifices may 
 give rise to murmurs indistinguishable from those due to destruction of 
 the cusps. The presence of a musical murmur may generally be assumed, 
 particularly in acute cases, to be due to a vegetation. An attack of hemi- 
 plegia during an acute febrile condition may generally be ascribed to an
 
 220 DISEASES OF THE HEART 
 
 infarct from a valvular vegetation, and infarcts in any other organ may be 
 assumed to arise from the same cause. 
 
 § 199. Symptoms in pericarditis. — Until the introduction of auscul- 
 tation, dry pericarditis was a disease only discovered on the post-mortem 
 table. The only evidence we have of its presence is the characteristic 
 superficial to-and-fro murmur produced by the movements of the heart. 
 Its discovery is usually accidental, and made when the heart is examined 
 as a matter of routine. There is no other distinctive sign associated with it, 
 and, in marked contrast to dry pleurisy, it is essentially a painless complaint. 
 When pains are associated with its presence it will invariably be found that 
 there is evidence of a myocardial affection. This curious painlessness of 
 pericarditis compared with pleurisy is one that has long puzzled me, and 
 I have only a dim perception of how it may arise. I merely call attention 
 to this fact in passing. 
 
 Pericarditis may arise in the course of a number of chronic complaints, 
 as in diabetes and Bright 's disease, or in the course of an acute disease, as 
 pneumonia or rheumatic fever. Sometimes one comes across it quite acci- 
 dentally — the patient, not feehng quite well, consults his doctor, and in the 
 course of an examination this is detected. Such patients may go quietly 
 about their occupation for many weeks with a well-marked to-and-fro 
 murmur, and suffer no further trouble. 
 
 When effusion takes place into the pericardial sac there is an increase 
 in the area of the cardiac dullness, which assumes a somewhat characteristic 
 shape. It reaches up to or above the second rib, and if the area be mapped 
 out it will have a somewhat pear-shaped character. There is an absence 
 of the heart's movements at the lower point to the left, and this should 
 always arouse the suspicion of effusion where there is an increase in the heart's 
 dullness. Ewart describes a small area of dullness behind at the base of 
 the left lung. This is important to remember, for an increase in the size 
 of this area may cause an extensive pericardial effusion to simulate fluid in 
 the pleural cavity. I have tapped a pericardial purulent effusion in mistake 
 for an empyema, and my mistake arose from not ascertaining the position of 
 the heart's movements. Had the case been one of pleural effusion, I should 
 have found the heart beating to the right of the sternum ; but the whole left 
 chest was dull, so that the idea of it being pericardial never crossed my mind. 
 
 The question of pericardial effusion embarrassing the work of the heart 
 has arisen on account of the results of experimentally distending the sac 
 with fluid. I have never found any very serious embarrassment of the 
 heart from extensive pericardial effusion, the reason being probably that 
 while the normal pericardium is a more or less inelastic bag, with the
 
 ACUTE FEBRILE AFFECTIONS OF THE HEART 221 
 
 inflammatory invasion it becomes distensile, and therefore able to accom- 
 modate an enormous amount of fluid with httle embarrassment to the heart. 
 
 § 200. The heart in rheumatic fever — The real nature of the 
 changes that take place in acute affections of the heart are being gradually 
 revealed, and it is now possible to connect many of the obscure signs observed 
 during life with the disease process in the heart. Many workers have con- 
 tributed to our present knowledge, but the following description is taken 
 more particularly from the observations of Cowan ^^^ and of Poynton and 
 Paine ^22, as they have sought with some degree of success to correlate their 
 pathological findings with chnical and experimental data. These observa- 
 tions have been worked out more particularly in rheumatic affections of the 
 heart ; but similar changes have been found in other acute affections, as 
 in pneumonia, diphtheria, influenza, septic poisoning. 
 
 According to Po3niton and Paine, the heart trouble starts with the inva- 
 sion of the heart by the specific organism of rheumatic fever — the Diplococcus 
 rheumaticus. (Many later investigators have failed to isolate this organism.) 
 They reckon to have isolated this organism from vegetations found on 
 the valves of the heart and pericardium in acute rheumatism, have cultivated 
 it, and produced changes in animals identical with rheumatic endocarditis, 
 myocarditis, and pericarditis. The invasion of the endocardium usually 
 affects first the base of the valves, and produces sweUing and infiltration of 
 the margins. The swollen edges may break down and ulcerate, or vege- 
 tations may form. The course of the disease varies greatly, from the simple 
 endocarditis which recovers, to extensive ulceration of the valves, associated 
 with the severe symptoms characteristic of malignant endocarditis. 
 
 The myocardium rarely escapes, and the changes in it are of great 
 importance, both for the acute condition and for the subsequent integrity 
 of the heart muscle. Fatty degeneration and breaking down of the 
 muscle-fibres are fairly common, while the specific organism has been 
 found accompanied by cellular infiltration. There may be congestion of 
 the blood-vessels, exudation of the leucocytes, and swelling of the connective 
 tissues. Aschoff ^^^ describes the occurrence of numerous cellular foci. 
 
 During the acute attack extreme dilatation may occur, due probably to 
 a toxaemic poisoning of the heart muscle, as no microscopic change may 
 be present. This poisoning is probably also the cause of the extreme weak- 
 ness and irritability of the heart, which persists for some time after the subsi- 
 dence of the fever. The pericardium is also liable to invasion, and here the 
 changes may vary from a shght transient pericarditis to an extreme inflam- 
 mation, which does not entirely subside, but lingers on, forming adhesions, 
 to the tissue outside the pericardium and penetrating to the heart itself.
 
 222 DISEASES OF THE HEART 
 
 A process of slow cicatrization often follows, producing changes in the 
 valves, heart muscle, and pericardium that seriously embarrass the heart 
 in its work in after years. 
 
 Symptoms. — x4ttacks of rheumatic fever may complete their course 
 with no affection of the heart. In some instances the heart may be affected 
 and give rise to no positive sign, and it may be only after months or years 
 that a murmur or irregular action indicates that there must have been 
 some affection of the heart which the symptoms of the subsequent sclerosing 
 process has revealed. 
 
 Generally, however, we can recognize certain changes in the heart's 
 condition, chiefly in an increase in the size and the presence of a murmur. 
 These cardiac changes may go on with very little increase of temperature 
 and little or no evidence of joint trouble. Sometimes in these milder cases 
 I have detected evidence of involvement of the a.-v. bundle by signs of 
 interference with its power of conveying the stimulus from auricle to ventricle. 
 
 With more serious involvement the dilatation of the heart may be 
 extreme, and Lees and Poynton 1^° particularly have called attention to the 
 enlargement, and the ease with which it may be mistaken for pericardial 
 effusion. At first, the full extent of the enlargement may not be realized, 
 because it is partly masked by the lung. When the lung is pushed aside, 
 the greatly enlarged heart can then be readily recognized. The rate of the 
 heart is usually greatly increased beyond what might be expected from 
 a mere rise in temperature. The pulse becomes soft and compressible, and 
 sometimes shows irregularities whose nature in all cases I have not been 
 able to make out. With subsidence of the fever, the patient enters on 
 a long and slow convalescence. Other cases do not terminate so favour- 
 ably, especially if the heart has been damaged by a previous attack. Com- 
 plications, as pneumonia, are apt to arise. In severe cases there may 
 be a considerable amount of praecordial distress. The breathing becomes 
 shallow and rapid. The patient feels easiest with his shoulders well raised. 
 The face becomes dusky, the lips dark red, sleep is broken and fitful, and 
 the patient is continuously altering his position. The mind wanders and 
 mental delusions arise. 
 
 From such a state as this the young during their first attack may recover, 
 but in the middle-aged the condition is very serious. Attacks of syncope 
 may appear, and the patient may die in one. Frequently they gradually 
 sink in spite of all treatment and die. 
 
 In the recurring attacks of rheumatic fever this question of previous 
 damage to the heart is a very important one. Patients with damaged 
 aortic and mitral valves may pass scatheless through serious attacks of
 
 ACUTE FEBRILE AFFECTIONS OF THE HEART 223 
 
 rheumatic fever, presumably where the heart is not involved in these later 
 attacks. When, however, the process lays hold on the heart, the patient's 
 life is in great danger, and after a period of extreme suffering the struggle 
 frequently ends in death. 
 
 While the foregoing description gives briefly the main points of the heart 
 affection in rheumatic fever, it also holds good for the condition in other 
 infectious diseases, apart from the recurrent attacks. As, however, the 
 presence of other lesions has a modifying effect upon the course of the 
 disease, it is necessary to refer to them. Unfortunately, the reference can 
 only be brief and in the main unsatisfactory, the analysis of the symptoms 
 in these cases having been very imperfectly carried out. 
 
 § 201. The heart in pneumonia — The invading organism may assail 
 the heart as well as the lungs, and the course of the illness be rapid and 
 severe. It is difficult to distinguish between the changes due to invasion 
 
 Fig. 140. Febrile pulse of low arterial pressure, T. 103°, P. 116, R. 36. This was taken 
 eight hours after the rigor at the beginning of a pneumonia. This and the four following 
 tracings show a type of asthenic pulse. 
 
 of the heart from those due to the general infection. In severe cases the 
 evidence of the heart affection is very prominent. Within a few hours 
 of the initial rigor, and before there is any pulmonary sign, the evidence of 
 the heart affection is all too apparent. The patient may be young and, 
 prior to the attack, a perfect specimen of youthful health and vigour. A few 
 hours after the rigor, the temperature may be over 102° F. The condition 
 of the pulse is the best guide to the state of the heart at this stage, and shows 
 ominous signs of what is to follow. It is greatly increased in rate, 115-130 
 per minute. It is soft and compressible, and offers no resistance between 
 the beats. The peculiar manner in which it impinges against the finger — 
 sharp and short, then quickly subsiding, indicating an absence of sustained 
 pressure — is always to me a serious sign. It is usually associated with greatly 
 relaxed arteries, and a sphygmogram shows little or no sign of a dicrotic 
 wave (Figs. 140-4), indicating great lowering of the pressure during the 
 diastole of the heart. The heart itself shows little definite sign. The sounds 
 are short and sharp at first, becoming later somewhat muffled, A certain 
 amount of dilatation occurs, detected more particularly to the right of the 
 sternum. Usually in these cases the end comes with tragic suddenness ; 
 the rate of the pulse increases, irregularities appear, and the patient succumbs
 
 224 
 
 DISEASES OF THE HEART 
 
 within three or four days of the initial rigor. Figs. 140-4 show the charac- 
 teristic features of the pulse in acute fatal pneumonia in a young previously 
 strong and healthy adult. 
 
 There are two conditions I have come to look upon as signs of grave 
 comphcations in pneumonia — the occurrence of an occasional irregularity 
 before the crisis, and a pulse-rate over 140 per minute. Neither of these is 
 
 Fig. 141. T. 101-5°, P. 96, R. 28— second day. 
 
 Fig. 142. Asthenic type of pulse with well-marked systoUc wave s, and only a faint indi- 
 cation of the dicrotic wave d — third day. 
 
 Fig. 143. T. 103°, P. 124, R. 48— fourth day. 
 
 Fig. 144. T. 102°, P. 148, R. 52. The irregularity and rapidity of the pulse heralded the 
 
 fatal end on the fifth day. 
 
 necessarily a fatal symptom. I had pointed this out in my book on the pulse, 
 and John Hay*"^^ analysing 200 cases of pneumonia, found a small number 
 recover who had shown an irregularity preceding the crisis. I therefore 
 went into the matter more carefully, and found that the occasional irregu- 
 larity might be due to more conditions than one, and in all my fatal cases 
 the irregularity was due to exhaustion of the contractiUty, as shown in Figs. 
 137 and 138 ; but this subject needs further elucidation. 
 
 § 202. The heart in diphtheria — The comphcations here are so
 
 ACUTE FEBRILE AFFECTIONS OF THE HEART 
 
 225 
 
 varied that danger may arise in several quarters. The heart muscle itself 
 may be the seat of profound changes, the symptoms somewhat resembUng 
 those in rheumatic fever. But in diphtheria more than in any other acute 
 disease there is a tendency to fatal syncope, and I do not understand how 
 this is brought about. 
 
 § 203. Septic infections. — There are a great many septic infections 
 that injure the heart either from toxaemia or by a specific organism invading 
 the heart. In the latter case the endocardium is frequently attacked, and 
 the disease is then described as septic endocarditis. In these cases there 
 is also invasion of the myocardium, and it is the profound depression of the 
 heart muscle which is often the grave element. 
 
 In an account of 150 cases of infective endocarditis, Horder*''^ states that 
 in 90 per cent, of cases a culture of a pathogenic organism can be obtained. 
 The following table gives the analysis of forty positive results of blood 
 culture during hfe : — 
 
 Number of Cases. 
 26 
 5 
 5 
 2 
 1 
 I 
 
 Micro-organism isolated. 
 
 Streptococcus 
 Bacillus influenzae 
 Pneumococcus 
 Gonococcus 
 Staphylococcus albus 
 Unclassified. 
 
 The illness in these cases usually begins insidiously, and at first may be 
 mistaken for some trivial febrile complaint, or for influenza. Soon, however, 
 the extreme prostration of the patient, the recurrence of rigors, and the 
 patient's own sensation of illness, show that the condition is of a more 
 serious nature. Usually also there is excessive perspiration. If the heart be 
 watched it will be found to dilate and a systolic murmur appear. The true 
 nature of the condition may not be revealed until the detachment of a vege- 
 tation produces hemiplegia, or an infarct in the spleen or kidney or elsewhere, 
 and death may speedily supervene (malignant endocarditis). 
 
 Other cases may Hnger on with indefinite febrile attacks, the patient 
 sick, pale, and ill, and the real nature of the illness be a mystery. In some 
 of these cases very little change takes place in the heart. I have seen a case 
 after confinement have slight fever for nine weeks with no change in the 
 size of the heart, the rate generally about eighty per minute, a rough systolic 
 mitral murmur the only abnormal sign, until an attack of hemiplegia led 
 to the recognition that the rough mitral murmur was due to vegetations on 
 the valves. Osier ^^^ has recently published an account of ten cases of chronic 
 
 MACKEXZIE
 
 226 DISEASES OF THE HEART 
 
 infectious endocarditis. In addition to the irregular fever he gives the 
 following as the most suggestive features which help to identify the nature 
 of the disease. (1) A knowledge of the existence of an old valve trouble; 
 (2) the occurrence of embolic features, sudden swelhng of the spleen, sudden 
 attack of haematuria, embohsm of the retinal arteries, hemiplegia, or the 
 blocking of a vessel in one of the limbs ; (3) the onset of special skin symptoms, 
 purpura, and more particularly the painful erythematous nodules, in aU 
 probabihty due to minute emboli ; (4) the progressive cardiac changes, 
 the gradual increase in the dilatation of the heart, the marked change in the 
 character of the mitral murmur, the onset of a loud rasping tricuspid murmur, 
 or the development under observation of an aortic diastolic bruit. 
 
 In pyaemia and puerperal septicaemia we get conditions of profound 
 gravity caused by certain organisms. The pulse in these cases gives the 
 most trustworthy information. It is small, soft, and easily compressed, 
 not necessarily very rapid, and the temperature need not be high (101-2°). 
 The heart shows little change except that the sounds are feeble, the patient 
 is lethargic, the face is slightly sallow or pale and sunken. The aspect of 
 the patient, taken with the rate of the pulse, affords assistance in recognizing 
 the condition. I dwell upon this because, happily, some of the younger 
 members of the profession have Uttle experience of dangerous forms of 
 puerperal fever, but, having heard of the terrors surrounding them, are not 
 infrequently unnecessarily frightened at the occurrence of a post-partum 
 rise of temperature of trivial significance, while others do not recognize the 
 significance of the heart symptoms when danger actually arises. 
 
 § 204. Treatment. — When the real nature of the trouble is appreciated 
 in acute affections of the h^rt, it will be realized how powerless we are 
 directly to modify the diseased process. In vaccine or serum therapy there is 
 a promise of a specific remedy in each case to meet the special organism 
 causing the mischief. But so far our efforts have been attended with httle 
 success. Horder *°^ states that of thirty-nine cases treated in this way only 
 one recovered, and unfortunately in this case no micro-organism was demon- 
 strated in the blood. He says, ' I have given the treatment most thorough 
 trial in several cases, and occasionally seen temporary improvement result, 
 but never any permanent good. Conder^^^ has recently described a case 
 where the recovery seemed directly due to the vaccine injection. 
 
 In rheumatic fever the sahcylates seem to have an undoubted action on 
 the course of the disease, and it may be that the drug can modify the heart 
 affection. Their employment is so frequently of use that it should always 
 be tried, even pushing it at times as Lees advocates. I have not given the 
 large doses of the salicylates recommended by Lees in a sufficient number
 
 ACUTE FEBRILE AFFECTIONS OF THE HEART 227 
 
 of cases to be able to dogmatize, but as the few in which I have followed 
 his directions seemed to get benefit, I have included in Chapter XXXIII 
 a short account by Dr. Lees of the method he pursues. 
 
 Apart from the probably specific action of salicylate in rheumatic cases, 
 the employment of cardiac or other drugs is of httle avail.* The heart is 
 already in possession of a poison far more powerful than the drugs at our 
 command, and these in medicinal doses are without effect. But on this 
 account it must not be supposed that all treatment is useless ; rather should 
 it direct our attention to the consideration of other means of treatment. The 
 man who puts his faith in drugs exclusively neglects too often the most 
 useful methods. Recognizing that the heart muscle is greatly embarrassed 
 in its work, the endeavour should be n^^ade to give it as little work to do as 
 possible, and to save it from all sources of irritation ; in fact, to place it in 
 a condition of rest, as far as rest is possible for such an active organ as the 
 heart. To this end the general condition of the patient should be carefully 
 studied, the position he assumes should be one that gives the heart least work 
 to do, the food should be so administered that while nourishing him it does 
 not lead to abdominal distension, his bowels should be so regulated as to 
 act freely without straining. As fidgeting and restlessness keep the heart 
 irritable and variable in its action, everything should be done for his bodily 
 comfort — sponging, and arranging his piUows and the bedclothes, and the 
 many Httle things that a deft and intelligent nurse can suggest. Above 
 all, sleeplessness, which is so often present, or the sleep that is broken and 
 disturbed, should have most careful consideration, and suitable hypnotics 
 be given as described in Chapter XXXIII. 
 
 AVhen there is reason to suspect that the heart muscle has been affected 
 by the illness, great care should be taken during the convalescence to give 
 the heart muscle time to recover. Any cause, effort or excitement, that 
 accelerates the heart's action, should be avoided, and exertion only per- 
 mitted when the dilatation has subsided, and effort ceases to call forth 
 any disagreeable sensation. It may be weeks or months after the fever 
 before the heart muscle recovers. 
 
 * Hordei' says : ' " Blood antiseptics " seem doomed to failure in dealing with pyogenic blood 
 infections, because it is not possible to get the drugs into the blood in a nascent or active 
 condition. Combination with the proteids of the blood-cells or the plasma takes place before 
 the drug comes into contact with the micro-organism. Quinine, mercury, arsenic, carbolic 
 acid, formalin, and many other reputed remedies, all fail, whether administered by the mouth, 
 subcutaneously , or intravenously. The sulpho-carbolates which have had a special vogue are 
 equally disappointing ; I have used them in very large doses in several cases without any 
 results. Silver salts in combination with nuclein have been highly spoken of in the treatment 
 of septicaemia, but here again I have never seen any good results in infective endocarditis. 
 The same remarks apply to yeast and its active principle.' 
 
 Q 2
 
 CHAPTER XXV 
 
 Valvular Defects 
 
 § 205. The manner of heart failure with vali^ular defects. 
 
 Mitral stenosis. 
 
 206. Conditions inducing heart failure in mitral stenosis. 
 
 207. Murmurs present in mitral stenosis (presystolic, diastolic, disappearance of the pre- 
 
 systolic murmur, presystolic murmur of ventricular origin, systolic murmur due 
 to mitral stenosis). 
 
 208. Progress and s3Tnptoms in mitral stenosis. 
 
 209. Occasional symptoms : paroxysmal tachycardia, haemoptysis, cerebral embolism, 
 
 angina pectoris. 
 
 Mitral regurgitation. 
 
 210. Murmurs due to mitral regurgitation. 
 
 211. Conditions inducing heart failure in mitral regurgitation. 
 
 § 205. The manner of heart failure with valvular defects It is 
 
 manifest that valvular defects can embarrass the work of the heart in two 
 ways : first, by narrowing the orifice and thereby impeding the outflow ; 
 second, by imperfect closure so that leakage occurs. 
 
 The defects are recognized clinically mainly by the presence of murmurs, 
 but it must not be assumed that absence of murmurs implies an intact 
 valvular apparatus, for great widening of an orifice and large regurgitation 
 may take place when no murmur can be detected. As valvular lesions are 
 produced by a variety of conditions, it might have been more logical to discuss 
 them under the heading of these conditions. As, however, they are pre- 
 sented to us at a stage when all immediate symptoms of their causal con- 
 dition are in abeyance, it is more convenient to describe them at the time 
 that the heart-changes evoke symptoms of exhaustion. Years may elapse 
 after the mischief has been done to the valves before symptoms arise that 
 call attention to the heart trouble. In the acute condition producing the 
 valvular lesion, the matter is presented in an entirely different aspect, for 
 the febrile state and the symptoms associated with the cause of the fever 
 predominate. In chronic valvular affection the symptoms only arise where 
 exhaustion of the heart muscle sets in. The symptoms due to exhaustion 
 appear at varying periods after the damage has been done to the valves, 
 and the time of the appearance of these symptoms depends on the degree of 
 embarrassment offered to the heart's work by the damaged valve, on the
 
 VALVULAR DEFECTS 229 
 
 condition of the muscle-wall, and on such accessory factors as tend to 
 exhaustion, as over-exertion, excessive food, drink, and so forth. 
 
 In organic lesions of the valves it must always be borne in mind that the 
 sclerotic process causing the lesions may be progressive, and that there 
 may also be present advancing changes in the heart muscle. 
 
 Generally speaking, the symptoms of heart failure show little that is 
 distinctive of the particular valves affected. In the aortic cases the reflex 
 sensory phenomena are more prominent, and the ashen colour of the face 
 is sometimes characteristic. Where there is a mitral lesion, the pulmonary 
 symptoms are usually more prominent, and the face may be ruddy with 
 a dark tinge. Apart from such differences there is a great similarity in the 
 symptoms of heart failure produced by all kinds of lesions. 
 
 Mitral Stenosis 
 
 § 206. Conditions inducing heart failure in mitral stenosis. — 
 
 This is perhaps the most common of valvular defects with which heart 
 failure is associated. It arises generally in consequence of rheumatic endo- 
 carditis, though it may be found in people with no rheumatic history, and 
 a previous history of erysipelas, or some other febrile complaint, may give 
 a possible clue to its origin. 
 
 The condition is never recognized during the acute process which induces 
 it, for the reason that its presence can only be detected when the cicatrizing 
 process following the inflammation narrows the orifice, and on account of 
 its origin in scar-formation it is often a progressive lesion. Once the stenosis 
 is present it may remain moderate in amount, and offer so little embarrass- 
 ment to the heart that patients may reach extreme old age with no heart 
 failure. As a rule, however, the cicatrizing process goes on with varying 
 rapidity until in some cases the mitral orifice is reduced to a mere slit, and 
 the valves resemble a thickened calcareous diaphragm. It is important to 
 bear in mind the progressive nature of the lesion, for it accounts for the 
 varying changes in the symptoms. It should also be borne in mind that the 
 cicatrizing process may be going on in the muscle, causing contraction of 
 the chordae tendineae, impairing at other places the functional activity of 
 the heart muscle, and affecting the a. -v. bundle, depressing the conductivity 
 or producing the nodal rhythm, thereby profoundly modifying the nature 
 of the rhythm of the heart. 
 
 From this it can readily be understood that the manner in which heart 
 failure is brought about in many cases is somewhat complicated. In some, 
 embarrassment may not ensue until the narrowing of the orifice has become 
 extreme. In others there may be a fatal issue while the harrowing is yet
 
 230 DISEASES OF THE HEART 
 
 moderate. In the latter cases the muscle-wall will inevitably be found to have 
 been damaged. In a third class of case the cicatrizing process has extended to 
 the a.-v. bundle, and encroaching on it has induced the nodal rhythm, charac- 
 terized sometimes by greatly increased frequency of the heart's action, 
 and usually by a continuous irregularity (see Chapter XX). This irregular 
 action further embarrasses the heart muscle in carrying on its work, as 
 alread}^ described. The mechanical embarrassment may not only lead to 
 increasing back-pressure involving in succession the left auricle, pulmonary 
 circulation, and right heart, but the smaU quantity of blood passing into 
 the left ventricle leads to the tissues generally being poorly nourished. The 
 left ventricle, suffering hkewise from an impoverished supply of blood, may 
 offer independent symptoms of exhaustion, as for instance by dilating 
 (exhaustion of tonicity), and possibly by reflex phenomena, as in the rare 
 instance of an attack of angina pectoris in mitral stenosis. 
 
 § 207. The murmurs present in mitral stenosis. The presystolic 
 murmur. — The presystolic murmur — the auricular systohc murmur of 
 Gairdner^^^ — is due to the contraction of the left auricle forcing blood 
 through the narrowed mitral orifice. With the varying changes in advancing 
 cicatrization the murmurs of mitral stenosis alter, and present pecuharities 
 that have hitherto not been sufficiently appreciated. In the very early 
 stages, — some years before the appearance of a murmur, — I have detected 
 a slight presystolic thrill. The first murmur to appear precedes or runs up 
 to and seems to terminate in the first sound, and is audible over a small area 
 around the apex. Tliis murmur may vary in duration, being usually short 
 and abrupt, but it sometimes begins earlier and is somewhat prolonged. It 
 is of a crescendo character, rising in pitch till it ends in the first sound. 
 Now although this is the usual position in the cardiac cycle of the pre- 
 systolic murmur, I have found a few cases in which it did not terminate 
 abruptly in the first sound, but was separated from it by a very brief 
 interval. In some of my cases I asked a number of my colleagues to mark 
 out on a tracing of the radial pulse the exact position of the murmur in 
 the cardiac cycle, and every one without hesitation indicated the position 
 as represented in Fig. 112, where the loudest part of the murmur is separated 
 by a minute interval from the first sound. When a jugular or an apex 
 tracing was taken it was seen that the position was identical with that of 
 the auricular systole. In other words, there was a delay in the transmission 
 of the stimulus for contraction between auricle and ventricle. This delay 
 can sometimes be increased by digitalis, and the position of this murmur 
 in its relation to the first sound moves in the same way. 
 
 I mention this not only to enforce the evidence of changes in the a.-v.
 
 VALVULAR DEFECTS 231 
 
 bundle in mitral stenosis, but because some clinicians deny that the auricular 
 systole causes the presystohc murmur in mitral stenosis. I have long been 
 puzzled to account for their denial of what seems so obvious, but I have 
 found what seems to be the explanation, and will deal with it after describing 
 the murmurs with the nodal rhythm. 
 
 The diastolic murmur. — With advancing stenosis of the orifice another 
 murmur makes its appearance, namely, one occurring immediately after 
 the second sound, heard only in the immediate neighbourhood of the apex 
 beat. At first it is very faint, and not very constant, but it usually increases 
 in duration until the whole diastolic period may be filled up by it. This 
 diastolic mitral murmur diminishes in intensity from the beginning — 
 differing thus in its diminuendo character from that of the presystolic. 
 Frequently we can detect a continuous murmur during the diastole of the 
 heart, beginning loudly, falling away, then increasing in intensity. The 
 fkst or diminuendo portion of such a murmur is the diastoHc mitral murmur, 
 while the terminal crescendo portion is the presystohc. The cause of the 
 diminuendo diastolic mitral murmur is the flow of the blood that has been 
 accumulated in the auricle during the ventricular systole through the 
 narrowed mitral orifice ; this begins as soon as the mitral valves open, that 
 is, when the pressure in the ventricle falls below that in the auricle. 
 
 The disappearance of the presystolic murmur. — The next change in 
 the character of these murmurs is the sudden disappearance of the pre- 
 systolic crescendo murmur, while the diastolic murmur persists. Usually 
 this change occurs with the onset of grave symptoms of heart failure, the 
 heart's action becoming rapid and irregular. At other times the change 
 takes place with no serious symptom, but the heart invariably becomes 
 irregular. I have explained this fully in Chapter XX and in the Appendix 
 (II), as being due to the fact that the rhythm of the heart starts no longer at 
 the normal place but lower down, perhaps at the a. -v. node, and that in 
 consequence the auricular contraction no longer precedes the ventricular, 
 but the auricles and ventricles contract together. Clinicians hitherto have 
 not recognized the fact that in mitral stenosis the presystolic murmur 
 disappears with the onset of the continuous irregularity of the heart. 
 
 When the heart's action is slow there is no difficulty in recognizing the 
 diastohc murmur, and the absence of the presystolic. The diastolic murmur 
 is sometimes of great length, starting immediately after the first sound, and 
 slowly dying away, as in Fig. 57. When the heart's action is rapid, this 
 diastohc murmur may fill up the whole diastohc pause, and it might hastily 
 be assumed that the murmur was presystolic. But if it be carefully auscul- 
 tated, it will be found that it is not crescendo in character ; when a longer
 
 232 DISEASES OF THE HEART 
 
 pause occurs it will be found that the murmur stops short before the first 
 sound, so that there is a silence between the end of the murmur and the 
 first sound (see shading in Fig. 57), In these cases the jugular and liver 
 pulses are invariably of the ventricular form. 
 
 The presystolic murmur of ventricular origin. — In the careful examination 
 of a large number of these cases of nodal rhythm we find that the first sound 
 has not the sonorous rumble of the normal first sound, but is represented 
 by a sharp, short snap of very brief duration. Preceding this snap, in a 
 very few cases I have heard a brief crescendo murmur, but a venous tracing 
 showed that there was no auricular systole at the normal time. From this 
 I suggest that the disputants in the matter have hitherto been confusing 
 two separate conditions. As I have already pointed out, the evidences of 
 auricular systole producing a presystolic murmur are indisputable. While 
 the auricular systole is one cause, it is obvious there must be another 
 cause in these cases of nodal rhythm, and I therefore accept the view that 
 a slight regurgitation through the mitral orifice at the beginning of ven- 
 tricular systole may produce the brief presystohc murmur. (As a matter 
 of fact such a murmur does not precede the ventricular systole, but only 
 precedes that portion of the first sound represented by the terminal snap). 
 
 Systolic murmur due to mitral stenosis. — There is another form of 
 murmur associated with mitral stenosis, systolic in time, and heard best 
 at the apex. It is peculiar in the respect that it begins a minute interval 
 after the first sound, and rises in intensity until it terminates in the second — 
 a systolic crescendo murmur, in marked contrast to the usual form of mitral 
 systolic murmur. I have watched for years a number of cases who had 
 this peculiar murmur, and have noted that the majority had a history of 
 rheumatism in their youth, but I had no case that came to a post-mortem 
 examination. In conversation with Dr. David Drummond, he told me 
 he was acquainted with the murmur, and that it was usually associated with 
 mitral stenosis. 
 
 All the murmurs due to mitral stenosis have usually a very limited area 
 of propagation, being heard over a small space immediately surrounding 
 the apex beat. Occasionally we meet with presystolic murmurs heard over 
 the whole heart. 
 
 § 208. Progress and symptoms in mitral stenosis From the pro- 
 gressive nature of the lesions in the valves and in the heart muscle, it will 
 be realized that the symptoms are not constant. 
 
 The patient comes first into consideration mostly in early or middle 
 adult life. The complaints then are shortness of breath, a sense of suffoca- 
 tion, and palpitation on exertion. In some the face is ruddy, with a hue
 
 VALVULAR DEFECTS 233 
 
 a shade darker than is compatible with the ruddy countenance of robust 
 health. At this stage there is little or no increase in the size of the heart 
 and no dropsy. A presystolic murmur can usually be detected. The 
 patient's complaints may be the only evidence we have of the heart failure, 
 and these point to an exhaustion of the reserve contractile force. After 
 a period of rest this exhaustion may disappear and the patient may go on 
 for years with but little further trouble. After a time, however, some 
 again break down, and the symptoms complained of may be of the same 
 nature. Frequently, however, a change is found in the character of the 
 murmurs — a diastolic murmur usually being perceived, and there is some- 
 times a longer duration of the thrill, these signs implying an increased narrow- 
 ing of the orifice. On the other hand, in those in whom no further narrowing 
 takes place, the murmur does not change, and the patient may go on for 
 many years, and, if a female, may bear children, with no breakdown. In 
 these cases we can infer that there is no progressive muscular or valvular 
 sclerosis. With the increased narrowing of the orifice, as indicated by the 
 appearance of the diastolic mitral murmur, the heart becomes much embar- 
 rassed, the symptoms become much more distressing, and finally dilatation 
 of the heart (failure of tonicity) may set in. But even without the progres- 
 sive narrowing, dilatation may appear early, and then it may be inferred 
 with certainty that the rheumatic process has permanently injured the 
 heart muscle. 
 
 The rhythm of the heart may become continuously irregular, from the 
 cicatrizing process affecting the a. -v. bundle, and with the onset of this nodal 
 rhythm further embarrassment arises as described in Chapter XX. If 
 there be no change in the size of the heart with this nodal rhythm, and no 
 great acceleration of rate, the heart failure may be very slight in degree, but 
 if the heart dilates, especially if the rate is accelerated, then all the extreme 
 symptoms of heart failure follow (dropsy, enlargement of the liver, &c. 
 See Chapter XX). 
 
 In the vast majority of cases the heart recovers from its first break- 
 down and usually from many subsequent attacks. Indeed, after one attack, 
 I have known patients go on for twenty years and more with no further 
 trouble beyond a slight limitation of the field of response to effort. 
 
 After repeated attacks, the patient's life becomes one of great limitation. 
 The future depends often on the rapidity of the advance of the sclerotic 
 process of the valves and the heart muscle. If the rate of advance be slow, 
 and the heart muscle capable of responding to treatment, the patient may 
 go on for many years with a crippled existence. Sometimes we find in the 
 young, about twenty years of age, at the post-mortem examination, the
 
 234 DISEASES OF THE HEART 
 
 orifice narrowed to a mere slit. In others we find the mitral orifice not much 
 contracted but the heart-wall greatly dilated, and evidence of fibrosis of the 
 muscle. Hence it will be seen that the progress of these cases is largely- 
 dependent on the rate of change in the muscle as well as in the valve. The 
 final issue is usually by great extension of the dropsy and exhaustion. 
 
 There are several complications which may arise. 
 
 § 209. Occasional symptoms. Paroxysmal tachycardia. — In place 
 of the nodal rhythm being permanently estabHshed, it may appear inter- 
 mittently as attacks of paroxysmal tachycardia. These attacks are of 
 varying importance. Some patients may have them for more than twenty 
 years and seem httle the worse. Others may have them occasionally, and 
 then the heart settles down with the rhythm permanently altered. In such 
 cases the future depends on whether the heart slows down or remains 
 at a greatly increased rate, as already described (§ 160, also Case 11, 
 Appendix II). 
 
 Haemoptysis. — At various stages patients may be seized with great 
 bleeding from the lungs. Here doubtless the cause is the back-pressure in 
 the pulmonary circulation and rupture of the blood-vessels. As a rule this 
 is a grave sign, the patient dying sometimes shortly after an attack. 
 
 Cerebral embolism. — Vegetations may exist at the mitral valves, with 
 no certain sign of their presence until a small portion is detached and 
 impacted in some vessel, giving rise to a hemiplegic attack, or an attack of 
 aphasia. Usually recovery takes place speedily, and may be permanent, 
 but cases have been recorded in which the aphasia or hemiplegia has remained 
 complete for many years. 
 
 Attacks of angina pectoris. — Although very rare, these may occur in 
 mitral stenosis. In the few cases I have observed they were all secondary 
 to some excessive exertion, and the patients had only one or two attacks, 
 remaining perfectly free from them for years afterwards. 
 
 Mitral Regurgitation 
 
 Mitral regurgitation may be the result of a damaged valve or of dilatation 
 of the orifice from depression of the tonicity of the muscles supporting 
 the valves. 
 
 § 210. Murmurs due to mitral regurgitation — The murmur of 
 mitral regurgitation is systohc in time, heard loudest at the apex. It may 
 be soft and blowing, of little intensity, and heard over a very limited area, or 
 propagated into the axilla. Or it may be rough and loud, and heard over 
 the whole heart and round to the back of the chest. It is not always 
 possible to tell whether it is due to dilatation of the orifice or to damage
 
 VALVULAR DEFECTS 235 
 
 of the valves. The rough loud murmur with an accompanying thrill is 
 always a sign of damaged valves. 
 
 §211. Conditions inducing heart failure in mitral regurgitation. 
 — When the muscle is unimpaired, little or no bad effect may follow damage 
 to the mitral valves. Even where the regurgitation is due to ' functional ' 
 dilatation of the orifice from depressed tonicity, the contractile power of 
 the muscle may maintain a good and efficient circulation. The really 
 serious trouble in connexion with mitral regurgitation arises when the 
 muscle is impaired and the regurgitation is due to a complication of the 
 dilated orifice and diseased valve. The subsequent results depend on the 
 degree of the exhaustion of the muscle of the heart. The backward pressure 
 resulting from the regurgitation embarrasses the left auricle, pulmonary 
 circulation, and right heart. The degree to which this may extend depends 
 in a great measure on the tone of the heart muscle. While back-pressure is 
 a factor of importance and may be a predisposing cause, yet it produces 
 comparatively few symptoms until the tonicity gives way, which is mani- 
 fested by dilatation of the heart. The dilatation is generally looked upon 
 as the result of the regurgitation, the back-pressure ultimately producing 
 yielding of the walls of the right heart. This is not quite correct, for long 
 before there is any back-pressure we may find evidence of a dilated right 
 heart. If we examine carefully the condition of the heart when the valves 
 have been damaged by rheumatic endocarditis, during one of the shght 
 attacks of heart failure which are liable to occur after over-exertion, we may 
 find the heart shghtly dilated, the right ventricle being in front so that 
 the left ventricle is pushed to the left behind the lung ; the apex beat is 
 then due to the right ventricle, which gives a negative cardiogram (Fig. 33). 
 After a few days' rest and treatment, the right heart may retreat and the 
 apex beat is then due to the left ventricle, the cardiogram now presents the 
 normal characters, rising during systole. In such cases there is no evidence 
 whatever of pulmonary engorgement and back-pressure. In fact, in the 
 majority of cases, as Graham Steell^^° says, the change in the 'valves is alto- 
 gether inadequate to explain the evidently free regurgitation that occurred 
 during life, and the disastrous dilatation of the heart. The muscle-failure 
 factor, it may be presumed, was the essential one '. 
 
 The damage to the valves is most commonly the result of rheumatic 
 endocarditis, and, as we have seen, the process is rarely limited to the 
 endocardium, but invades the myocardium. Septic endocarditis may also 
 damage the valves. In all cases of mitral stenosis there is mitral regurgita- 
 tion, but the amount of the regurgitation is never so marked as to be the 
 serious factor in the case.
 
 236 DISEASES OF THE HEART 
 
 Serious regurgitation occurs through the mitral orifice with the valves 
 uninjured in the latter stages of many affections, but more particularly in 
 renal disease and cardio-sclerosis. Here the condition is brought about 
 by the failure of the muscle to support the orifice, and this is too often the 
 sign of a final and fatal exhaustion of the heart muscle (see Chapter XXVII). 
 
 It will thus be seen that the symptoms produced by mitral incompetence 
 are only of gravity when there is also muscle failure, and this is dealt 
 with in sufficient detail in the chapter on Dilatation of the Heart 
 (Chapter XXIII).
 
 CHAPTER XXVI 
 
 Valvular Defects (continued) 
 
 § 212. Tricuspid incompetence. 
 
 213. Tricuspid stenosis. 
 
 214. Disease of the aortic valves. Etiology. 
 
 215. Aortic stenosis. 
 
 216. Aortic incompetence. 
 
 217. Prognosis in valvular affections. 
 
 218. Treatment. 
 
 Affections of the Tricuspid Valves 
 
 Lesions of the tricuspid valves are rare, and are nearly always 
 associated with similar lesions in the mitral and aortic valves. The heart 
 failure associated with these lesions is never due to the tricuspid lesion 
 alone. 
 
 § 212. Tricuspid incompetence — Although actual disease of the valves 
 is rare, incompetence of the tricuspid orifice is extremely common — so com- 
 mon, indeed, that I am inclined to look upon the valves as being barely able 
 to close the orifice perfectly. This view is based upon the observation of 
 many patients, in whom I have been able to detect a tricuspid systolic 
 murmur with no appreciable increase in the size of the heart. The murmur 
 in many cases is very fugitive, being present in the first few minutes of an 
 examination, and disappearing when the heart becomes quieter. A con- 
 sideration of the size of the orifice and the size of the valves led John 
 Hunter ^^^ to doubt their competency, while Mayo ^^ declared that the 
 tricuspid valves never perfectly close the orifice. Experimentally it has 
 been found impossible to raise the pressure in the right ventricle, on account 
 of the ease with which regurgitation takes place through the tricuspid orifice. 
 
 The slighter forms of tricuspid murmurs are limited to a small area 
 over the middle of the sternum. With increase in the size of the right 
 heart they may be heard over the whole anterior surface of the heart. They 
 are often associated with mitral systolic murmurs, but one can usually detect 
 a difference in quality in the mitral murmur heard beyond the left nipple 
 line and in the axilla from the tricuspid murmur heard over the middle of 
 the sternum. 
 
 It should never be concluded that no tricuspid regurgitation occurs
 
 238 DISEASES OF THE HEART 
 
 because of the absence of a murmur, for it is of frequent occurrence to find 
 evidence of tricuspid incompetence in the character of the jugular and liver 
 pulsation (ventricular form), and in the greatly widened orifice post mortem, 
 while during life there was no systolic tricuspid murmur. A weak muscular 
 waU and a wide orifice may give rise to no murmur. 
 
 I dwell at some length on these points, not because the tricuspid regurgita- 
 tion is of much practical value, but because misunderstanding of its symp- 
 toms has led to a wrong construction being put on the effects of tricuspid 
 regurgitation, and to the real significance of the ventricular form of the 
 venous and liver pulse being missed. I have already pointed out that 
 slight regurgitation in a normal heart would add to the accumulating blood 
 in the right auricle during ventricular systole, and would therefore be a factor 
 in the production of wave v in the jugular pulse. Now most writers overlook 
 the fact that a dilating auricle is interposed between ventricle and jugular, 
 and have assumed that as soon as tricuspid regurgitation takes place a wave 
 appears in the jugular at the beginning of ventricular systole. They have 
 therefore regarded the ventricular form of the venous pulse as only a sign 
 of tricuspid regurgitation, and have missed the real significance of this 
 very important symptom. • That it is a sign of tricuspid regurgitation there 
 is no doubt, but it is a sign of far greater significance, namely, that the 
 auricle does not precede the ventricle in the cardiac cycle. This is illustrated 
 in Chapter XX and Appendix II. 
 
 § 213. Tricuspid stenosis. — In the majority of cases tricuspid 
 stenosis is not recognized during life, as the symptoms produced are not 
 always distinctive. It is only rarely that a presystoUc tricuspid murmur 
 is heard ; I have only heard it in three cases, in which it was present in 
 a very limited area over the middle of the sternum. There is usually present 
 also a mitral presystoHc murmur at the apex, but as each murmur is con- 
 fined to such limited regions I have had no difficulty in distinguishing them. 
 In one case the auricle had become so greatly hypertrophied that it sent 
 back a large wave into the jugular, and that with such force that it 
 caused the valves in the jugular and subclavian veins to close with 
 a snap, which I could hear over these veins as a clear, sharp sound 
 preceding the first sound. 
 
 As a result of the stenosis of the tricuspid orifice, the right auricle hyper- 
 trophies, and on this account sends a wave back into the vein Avith such force 
 that it distends the liver, and I therefore look upon pulsation of the fiver 
 with a marked wave due to the auricle as an evidence of possible tricuspid 
 stenosis (§ 120). 
 
 § 214. Disease of the aortic valves. Etiology. — By far the greater
 
 VALVULAR DEFECTS 239 
 
 number of cases of affection of the aortic valves owe the lesions primarily 
 to one of two conditions — rheumatic endocarditis and the sclerotic process 
 accompanying arterial degeneration. Under rare circumstances the valves 
 may rupture, but here there is usually some antecedent disease of the valve. 
 Congenital defects may in rare cases give rise to great embarrassment of the 
 heart. 
 
 It is the lesions induced by the two first-named conditions that require 
 most consideration. In both instances the condition is usually well estab- 
 lished before it is found out. In many cases the presence of aortic changes 
 is discovered accidentally, when a systematic examination is being made 
 for other ailments, or for insurance or a health certificate. 
 
 The heart failure in aortic valvular disease is rarely due to this lesion 
 alone. In the majority of cases changes impairing the power of the muscle 
 have been proceeding at the same time as those that induced the valvular 
 changes. 
 
 In the rheumatic cases there is frequently present a comphcating lesion 
 of the mitral valve. 
 
 When the valvular disease embarrasses the heart's work by the extent of 
 the lesion, as by great incompetence, and the heart muscle is healthy, the 
 latter responds to the obstruction to its work by hypertrophy, and this may 
 proceed to an enormous extent, giving rise to one of the largest of human 
 hearts — the Cor Bovinum. 
 
 § 215. Aortic stenosis — Aortic stenosis is often associated with aortic 
 regurgitation, and the symptoms of the latter usually dominate the situation. 
 When there is little or no regurgitation, the symptoms of aortic stenosis, 
 being less prominent, are often only detected accidentally in the routine 
 examination of the patient. 
 
 The sign most characteristic of aortic stenosis is a murmur systohc in 
 time, heard loudest over the second right costal cartilage, and propagated 
 into the carotids. It may be faint — a mere whiff, or it may be pro- 
 longed, and accompanied by a thrill perceptible over the upper part 
 of the chest- wall. The heart's rate is often slow, between fifty and sixty 
 beats per minute. The radial pulse is sometimes very characteristic. It 
 impinges against the finger in a slow, leisurely fashion, and a sphygmo- 
 graphic tracing may show a slanting up-stroke with a shght interruption 
 near the summit (anacrotic pulse, Fig 145), or even a double wave at the 
 top (pulsus bisferiens. Fig. 146). Graham SteelP^^ and Lewis ^^^ state that 
 they have been able to detect this double beat by the finger, and Graham 
 Steell says he has perceived it on one side only. Its real nature is yet 
 obscure.
 
 240 
 
 DISEASES OF THE HEART 
 
 Beyond these signs there is Httle that is characteristic in aortic stenosis. 
 There may be symptoms of angina pectoris, but these are due to associated 
 changes in the heart muscle, and other evidences of heart faihire can be 
 referred to the same cause. 
 
 § 2i6. Aortic incompetence — The aortic valves being contracted are 
 no longer able to support efficiently the column of arterial blood during the 
 diastole, but permit a backward flow into the heart, and as a result we find 
 certain alterations in the character of the second sound and of the arterial 
 
 Fig. 145. Anacrotic pulse, from a case of aortic stenosis. 
 
 pulse. The closure of the valves no longer gives to the second sound the 
 characteristic snap, but the sound ends in a murmur sometimes long drawn 
 out, sometimes so brief as to be scarcely perceptible — as if the second sound 
 terminated not abruptly but with a faint sigh. The diastolic murmur is 
 usually propagated down the sternum, but sometimes it is heard loudest at 
 the apex. Foster has suggested that this variation in the propagation of 
 the murmur depends on the direction given to the backward flow by the 
 
 Fig. 146. Pulsus bisferiens, from a case of aortic stenosis. 
 
 position of the retracted valve. This seems plausible, but I have not been 
 able to verify it, and the explanation is ignored in recent textbooks. 
 
 The regurgitant murmur is usually associated with the murmur of 
 aortic stenosis, and we get the characteristic double aortic murmur (bellows 
 murmur). There is frequently dilatation of the smaller arteries, and this, 
 combined with the effect of the regurgitation on the arterial pulse, causes the 
 artery to become emptier than usual towards the end of diastole. This means 
 a fall of pressure, and in order to maintain a normal mean pressure the 
 heart increases the force of its contractions raising the pressure during 
 systole, so that there is a great increase in the systolic pressure and a great 
 fall during diastole, thus giving rise to the characteristic collapsing pulse 
 (Corrigan's pulse, the water-hammer pulse. Figs. 147, 148, 149). The 
 collapsing character of the radial pulse may be intensified by raising the
 
 VALVULAR DEFECTS 241 
 
 arm above the head. At times the arterial pulse is conveyed through the 
 capillaries into the veins, and G. Gibson has obtained a graphic record of 
 such pulsation of the veins on the back of the hand. If the forehead be 
 rubbed so as to produce redness, the flush is seen to wax and wane with 
 each beat of the heart (capillary pulsation). 
 
 Fig. 147. Pulse of slight aortic regurgitation with good heart muscle. 
 
 The double aortic murmur may be detected without any history of a 
 heart affection. In many cases there may be little or no dilatation, and the 
 individual may be able to indulge in games and in occupations requiring 
 considerable exertion with no discomfort. In such cases it may safely be 
 
 Fig. 148. Pulse of slight aortic regurgitation with gi-eat cardiac failure. 
 
 assumed that the damage to the valves has been slight, and that the heart 
 muscle has escaped serious injury. 
 
 In other cases the heart is greatly enlarged and the apex beat is diffuse 
 and forcible. The systole and diastole of the heart may cause movements 
 
 Fig. 149. Pulse of extreme aortic regurgitation with great cardiac failure. 
 
 of the liver that simulate pulsation of that organ, but analysis of its graphic 
 records show it to be merely the dragging up and pushing down of the liver 
 by the changes in the size of the heart (Figs. 27, 28). Even under these 
 circumstances the individual may for years pursue an active vocation, but 
 he is always liable to attacks of heart failure. The condition is often 
 associated with affection of the mitral valves, and this is one of the factors 
 
 MACKENZIE
 
 242 DISEASES OF THE HEART 
 
 participating in the production of the heart failure that finally terminates 
 these cases. 
 
 The most frequent sufferers from aortic valvular disease are the middle- 
 aged. In them the sclerotic process has been gradually advancing, and the 
 early symptoms of exhausted reserve force have been neglected until symp- 
 toms of distress command attention. There may have been a history of 
 rheumatism, of excessive drinking, of hard bodily exertion, of syphihs, but, 
 on the other hand, no definite causal condition may be discovered. The 
 facial aspect is frequently pale grey (earthy countenance), though in others 
 it may be full-blooded and ruddy. The complaints are varied. Shortness 
 of breath on exertion, violent throbbing in the neck, attacks of pain over 
 the chest on exertion, are amongst the most common symptoms of which 
 the patient complains in the first instance. For a varying period, under 
 suitable treatment, a certain store of reserve force is gained, and he may go 
 on for months or years, sometimes in fair comfort, but his existence is usually 
 more or less crippled. 
 
 The end of these patients is frequently dilatation of the heart, dropsy, 
 and exhaustion. Sometimes this is due to the inception of the nodal rhythm. 
 Those who suffer from angina pectoris may die suddenly. I have seen a few 
 cases die during a sudden attack of dyspnoea of the greatest severity. 
 
 § 217. Prognosis in valvular affections — The heart failure depends 
 upon so many and so varied conditions — as the extent of the valvular lesion, 
 its progressive nature depending on the cicatrizing process affecting the 
 valves, the coincident changes in the muscle and in the a. -v. bundle, the 
 conditions of life of the individual — that no rule applicable to aU cases can 
 be made. If, however, an attempt be made to appreciate the value of the 
 symptoms present, on the lines I have laid down, an approach to a true 
 prognosis may be made in each case. There is just one point I again wish 
 to insist upon : let no single symptom be the ground for forming a prognosis. 
 In this respect the presence of a murmur has so oppressed the profession that 
 a vast amount of positive harm is continually being done to patients by 
 taking too seriously the prognostic significance of this sign. The field of 
 cardiac response is the only true and safe guide in these cases. Even if for 
 the time being it is limited, judgement should be suspended until an oppor- 
 tunity has been obtained for ascertaining to what extent the heart muscle 
 can regain a store of reserve force (see Chapter XXXII). 
 
 § 218. Treatment. — As heart failure with valvular defects touches 
 every phase of the subject, the matter of treatment must be discussed from 
 a very wide aspect. The special chapters on treatment therefore include 
 the full consideration of this subject.
 
 CHAPTER XXVII 
 
 Cardio-Sclerosis (Arterial Degeneration, The Senile Heart) 
 
 § 219. Conditions producing cardio-sclerosis. 
 
 220. Conditions inducing degenerative changes in the arterial system. 
 
 221. Obliteration of the capillaries. 
 
 222. Symptoms of cardio-sclerosis. 
 
 223. Prognosis. 
 
 224. Treatment. 
 
 225. Aneurysm. 
 
 § 219. Conditions producing cardio-sclerosis. There are certain 
 changes which we recognize as accompanying and giving rise to the features 
 characteristic of advancing years. These changes may be detected in every 
 tissue and organ of the body, and they can be recognized in the bald scalp, 
 white hair, or tortuous artery. The changes in the arteries and capillaries 
 may modify the structure and functions of the various organs, but not all 
 organs equally. Arterial degeneration may in one person be more advanced 
 in the brain, in another in the kidneys, in another in the limbs, in another 
 in the heart. In many these changes are merely those associated with 
 advancing years, and give rise to what we understand by senile changes. 
 When affecting the heart they are usually accompanied by some fibrous or 
 fatty changes in the heart muscle. If these changes are considerable in 
 extent, then we get a train of symptoms which we recognize as due to 
 ' cardio-sclerosis '. 
 
 There are two main circumstances that induce degenerative changes 
 (fatty and fibrous) in the heart, namely, the cicatricial changes that follow 
 acute affections, as after rheumatic fever, and the changes that accompany 
 arterial degeneration. Both these conditions affect the muscular structure 
 as well as the valves, and the resulting heart failure is often the outcome 
 of the invasion of both tissues by the sclerotic process. Although it may be 
 convenient to follow conventional lines and describe separately the valvular 
 affections, it must be borne in mind always that in the serious cases there 
 is a widespread condition of which the valvular lesion is but a part. 
 
 The changes in cardio-sclerosis due to rheumatic fever have a certain 
 resemblance to those due to arterial degeneration. In both instances there 
 is a replacement of the muscular fibres by fibrous tissue, and a shrinking 
 
 R 2
 
 244 DISEASES OF THE HEART 
 
 of the valvular apparatus, and as a consequence both conditions present 
 identical symptoms. Though there is this resemblance in progress and 
 symptoms, there are other differences which have an important bearing on 
 prognosis and treatment. 
 
 The consideration of the rheumatic and other inflammatory forms of 
 sclerosis is included in the chapters on valvular disease. Here I wish to 
 draw particular attention to the changes in the heart that are associated 
 with arterial degeneration and senile changes. The causes of arterial 
 degeneration are still not clear, and it is difficult to say, of the complications 
 in any given case showing arterial degeneration, which are the cause and 
 which the consequence. Clifford Allbutt ^^ rightly protests against arterio- 
 sclerosis being considered a disease ; it is the outcome of processes which 
 we imperfectly understand, and may arise as the result of high blood-pressure, 
 toxic conditions, or senile changes. I do not enter into the, at present, 
 hopeless task of distinguishing the causes of the changes in the arterial 
 system. A little of the truth may be present in each of the many competing 
 theories at present holding the field, but no one of them can be considered 
 wholly satisfactory and convincing. 
 
 In the meantime, an appreciation of the changes as they affect the heart 
 gives us great assistance in the treatment of our patients. 
 
 § 220. Conditions inducing degenerative changes in the arterial 
 system. — It is usual to attribute the changes to some earlier process that 
 has affected the blood or the arteries, of which kidney disease, sj^hilis, over- 
 exertion, are the most striking examples. But it wiU be found frequently 
 that extensive arterial degeneration may be present for which one can 
 find no definite cause. 
 
 There can be no doubt that affections of the kidneys tend to induce these 
 changes. But in many people the kidney lesions are undoubtedly secondary, 
 and patients may show well-marked and extensive arterial degeneration 
 many years before there is the slightest evidence of kidney ailment. In 
 such instances it is but reasonable to assume that the renal degeneration, 
 like the cardiac and cerebral, is secondary to the arterial degeneration. 
 
 § 221. Obliteration of the capillaries One of the most striking 
 
 changes that take place in the progress of arterial degeneration is the 
 diminution of the capillary field. This obliteration of the capillaries is 
 likely to be found of the greatest importance not only in the production of 
 the degenerative changes that occur in the heart itself, but by narrowing 
 the communication between the arterial and the venous system it entails 
 more work on the heart in forcing the blood through the constricted area. 
 
 If one notes the changes in the skin that occur with advancing years.
 
 CARDIO-SCLEROSIS 246 
 
 how it loses its velvety thickness, becomes shrivelled and attenuated, so 
 that in advanced conditions the scalp may be found denuded of hair and 
 plastered to the underlying bones, the extent of the diminution of the capil- 
 lary field may, to a certain extent, be appreciated. A still more striking 
 evidence of the diminished capillary field in the old is the absence of free 
 bleeding in a freshly-made wound. In the young the abundant oozing of 
 bright red blood is a source of satisfaction to the surgeon, for it is a testimony 
 to the healthiness of the subject and to the recuperative power, and is in 
 striking contrast to the bleeding from a wound in the aged, where the bleeding 
 is mostly from some cut vein or from the persistent spouting of a degenerated 
 artery, indicating an impoverished blood-supply rendering the healing 
 process less satisfactory. 
 
 This diminution of the capillary field, so easily recognized in the external 
 body-wall, also occurs in the heart, and the results are shown in a variety 
 of ways. It leads to malnutrition of the tissues and degeneration of the 
 heart muscle. The character of the degeneration varies according to the 
 structure affected, but in all it leads to impairment of function. The first 
 structures to show evidence of the capillary obliteration are those that have 
 the smallest blood-supply, and it may be partly for this reason that it is 
 early marked in the cornea (arcus senilis), the valves of the heart, and the 
 arterial walls. 
 
 In the heart muscle the effect of these changes in the arteries and 
 capillaries is a degeneration, fibrous or fatty. In the production of this 
 myocardial degeneration we get the diminished capillary field complicating the 
 consequences of the degenerated artery — a degeneration at times so extreme 
 that little blood can penetrate the coronary arteries or their branches. If it 
 be borne in mind how dependent the muscular structure of the heart is upon 
 an abundant supply of blood, it will be easy to recognize the fact that such 
 changes must have a profound effect upon the efficiency of the organ. 
 
 Accompanying the arterial degeneration, Savill*^^ and Russell *^^ have 
 shown a great increase in the muscular coat of the smaller arteries. This 
 hypertrophy implies during life abnormal contraction (hypertonus of Russell). 
 This is bound to raise the blood-pressure and embarrass the heart. 
 
 The diminished capillary field has also probably a further complicating 
 effect in so far as it introduces an obstruction to the heart's contraction. 
 The narrowing of the outflow necessitates a greater force to send the blood 
 through the tissues ; consequently the ventricle has to contract more strongly 
 to raise the arterial pressure, and thus produces a further embarrassment to 
 the degenerated heart. 
 
 § 222. Symptoms of cardio-sclerosis. — The symptoms arising from
 
 246 DISEASES OF THE HEART 
 
 such changes are extremely varied, ^nd at first sight hopelessly confused, but 
 there is good reason to expect that with a better knowledge of the functions 
 of the different parts of the heart a more satisfactory appreciation of all 
 the symptoms may be obtained, and, in turn, a more accurate under- 
 standing of the symptoms during life will guide the pathologist in his post- 
 mortem examination. I have submitted to Professor Keith a large number 
 of hearts afEected by the changes associated with arterio-sclerosis from 
 patients ranging from forty-two to seventy-seven years of age, and in all the 
 post-mortem appearance had such a close resemblance that it might have 
 been assumed that during Ufe the sjnmptoms would have been identical. 
 A study of these symptoms showed, however, a wide diversity, soine patients 
 suffering from angina pectoris, others with no pain ; some with severe 
 cardiac asthma, others with no respiratory trouble ; some had very irregular 
 hearts, others frequent or infrequent extra-systole, while some had marked 
 pulsus alternans, and in others the heart was perfectly regular till the end. 
 Some patients had extensive dropsy, other patients showed no sign of 
 oedema. Some had aortic or mitral murmurs, others had no murmurs. It 
 will thus be seen that the symptoms of well-authenticated cardio-sclerosis 
 exhibit every phase of cardiac symptoms, and the superficial observer might 
 think that each case presented a different form of heart disease. Instead 
 of this, while the organic or fundamental lesion is the same, the variety 
 of symptoms is due to the different parts or functions particularly affected. 
 The earhest result of cardio-sclerosis is a diminution of the reserve force 
 of the heart, manifested by a hmitation of the field of cardiac response. The 
 patient rarely presents himself before the physician until this exhaustion of 
 the reserve force has produced some distressing symptom, it may be breath- 
 lessness, cardiac asthma, angina pectoris, or ' bronchitis '. In every case 
 it will be found to be preceded by a history of an ever-diminishing area of 
 cardiac response. At the beginning the individual will not acknowledge 
 that his powers are being curtailed — indeed the patient may be proud of his 
 virility — but it may be taken as a certain sign that when a middle-aged man 
 boasts of his strength he is trying to hide from others his own consciousness 
 of a limitation of his powers. Continuing to work as hard as he did before 
 these degenerative changes made their appearance, the exliaustion of the 
 reserve force, though slight at first and scarcely perceptible, in the long run 
 reaches a stage when the suffering or discomfort entailed compels the patient 
 to consult his physician. When this occurs the changes in heart and blood- 
 vessels are well estabfished. The skin of the hand has already lost its velvety 
 thickness, and the arteries show a varying degree of change, as tortuosity, 
 slight or considerable thickening of the radial ; sometimes one can detect
 
 CARDIO-SCfiEROSIS 247 
 
 pieces of peculiar hardness, fine and granular, or patches Uke small beads, 
 or the artery may be thickened Uke the characteristic pipe-stem, the surface 
 being shghtly nodulated. 
 
 Even in the absence of any of these signs in the superficial arteries, it 
 must not be inferred that the degenerative process is absent in the visceral 
 arteries. Arterial degeneration is often very irregularly distributed, affecting 
 different regions in different patients. It is for this reason that in this affec- 
 tion the symptoms of its progress may be more marked, now in the cerebral 
 arteries, giving rise to cerebral apoplexy, now in the arteries of the leg, giving 
 rise to gangrene, now in the arteries of the heart, giving rise to the symptoms 
 here described. 
 
 The blood-pressure measurements show, in many cases, a great rise. In 
 the earlier stages, when the patients are first seen, there is seldom much 
 enlargement of the heart unless there has been long-standing Bright 's disease. 
 Usually the heart's dullness does not extend beyond the nipple fine. The 
 sounds of the heart may be clear and well struck, often with some accentua- 
 tion of the second sound. In some an aortic murmur may be present, most 
 frequently systoHc in time, though occasionally there may also be a diastohc 
 murmur, usually of very short duration. The heart's action, though fre- 
 quently perfectly regular until the end, may show irregularities, the most 
 common being of the nature of extra-systole. In advanced cases we may 
 find good examples of the pulsus alternans. The heart may be continuously 
 irregular (nodal rhythm), and sometimes of great rapidity. Not infrequently 
 this continuous irregularity, with or without excessive rapidity, comes on in 
 intermittent attacks lasting for a few minutes, a few hours, or a few days 
 (paroxysmal tachycardia). In rare cases the degenerative process may 
 affect the a. -v. bundle and give rise to heart-block. 
 
 The subjective phenomena vary. In the early stages there may be no 
 symptom beyond a limitation of the field of cardiac response, shown by 
 breathlessness on moderate exertion. In more advanced cases there may be 
 a shght tightness across the chest on exertion or on going into the cold air, 
 as on going from a warm room into a cold bedroom, or going into the open 
 air on a winter's morning. This sensation is usually ignored until it is accom- 
 panied by pain, sometimes of such severity as to be recognized as an attack 
 of angina pectoris. In rare cases the pain may never arise, but the gripping 
 sensation felt in the chest may be so severe that the patient feels his chest 
 fixed, and has to stop and draw several deep breaths to reheve the spasm. 
 
 In many cases it is only breathlessness on exertion that arrests the patient, 
 the breathing being short and hurried on such exertion as he used to under- 
 take in comifort. In extreme cases the mere turning over in bed induces
 
 248 DISEASES OF THE HEART 
 
 the hurried respiration. The breathlessness may seize him in the night — 
 in attacks of cardiac asthma, or Cheyne-Stokes respiration may appear. 
 
 The symptoms described so far arise from the heart while the tonicity 
 is still good. In a great many of these cases a stage is reached when the 
 heart dilates. In addition to the increased size of the heart, a number of 
 symptoms disappear, while others come into prominence ; the arterial 
 pressure falls, the attacks of angina pectoris, cardiac asthma, and Cheyne- 
 Stokes respiration usually disappear, while a mitral systolic murmur may 
 be heard ; dropsy sets in, and oedema of the lungs, sometimes with the 
 expectoration of blood, or blood-stained sputa — in short, all the symptoms 
 already described under failure of tonicity (Chapter XXIII). 
 
 If the cause of the symptoms in cardio-sclerosis is appreciated, it helps 
 one to understand the reason of the great variety of phenomena present in 
 this affection. The variations in symptoms are in all likelihood due to the 
 parts invaded by the degenerative process. As the presence or absence of 
 aortic murmurs depends on whether the disease affects the aortic valves, so 
 the presence or absence of the various irregularities (with the exception of 
 the pulsus altemans) depends on the invasion of the primitive cardiac 
 tissue. The extent of the invasion determines whether the irregularity is 
 limited to an occasional extra-systole, or whether it terminates in the nodal 
 rhythm or in heart-block. In like manner the degree of exhaustion of 
 the function of contractiUty determines the nature of the subjective pheno- 
 mena, the breathlessness, anginal symptoms, and the cardiac asthma. On 
 the other hand, with exhaustion of the tonicity we get the transformation 
 in the character of the symptoms resulting in the dilatation of the heart, 
 dropsy, oedema of the lungs, and so forth. 
 
 § 223. Prognosis — The prognosis depends to a great extent on the 
 nature of the symptoms, and the manner in which the heart responds to treat- 
 ment. If, for instance, a patient has an irregular pulse due to extra-systole, 
 while in other respects the response of the heart to effort is such as woidd be 
 expected under normal conditions at his time of life, then the prognosis, in 
 the absence of other evidences of disease, is very favourable. When graver 
 symptoms are present, as the tightness across the chest, slight or severe 
 attacks of pain, then, if the previous history of the patient points to worry, 
 sleeplessness, and overwork, a prognosis should be deferred to see how he 
 responds to treatment. If these signs speedily disappear under treatment, 
 the prognosis is favourable ; on the other hand, the prognosis becomes the 
 more unfavourable the more the symptoms refuse to yield. But even here 
 comparative freedom from suffering may be enjoyed by a patient who pursues 
 a life that exposes him to little effort, and many patients may live a useful
 
 CARDIO-SCLEROSIS 249 
 
 though crippled life for years. Where there are attacks of cardiac asthma 
 occurring in the night, or attacks of Cheyne-Stokes respiration, or when the 
 pulsus alternans is present, the condition may be considered far advanced, 
 and though the patient may live for months or a few years, it is with very 
 limited powers, and he is liable to a serious breakdown at any time. When 
 the pulse is continually irregular, the prognosis depends on how well the heart 
 maintains the circulation. If dropsy supervenes and steadily increases, it is 
 not very susceptible to treatment in contrast to the parallel condition due 
 to rheumatic sclerosis. But apart from this, many patients may lead a 
 fairly active existence with the nodal rhythm for many years, though 
 exposed to frequent attacks of ' bronchitis '. 
 
 It must be borne in mind that the sudden inception of the nodal rhythm 
 is not infrequently the direct cause of death in elderly cardio-sclerotics. 
 
 The rather rapid dilatation of the heart, with accompanying dropsy, is 
 usually a sign of approaching dissolution. 
 
 I doubt if the blood-pressure measurements prove of much use as a guide 
 in prognosis. I have watched for a number of years individuals glide past 
 seventy years of age with a blood-pressure from 180 to 200 mm. Hg., and 
 I could not see that their condition was materially worse in consequence. 
 
 § 224. Treatment. — In treating cardio-sclerosis it should always be 
 borne in mind that the condition is progressive, and we cannot stay it, 
 because the changes are those which are inseparable from advancing years. 
 It usually proceeds very slowly, so that a man may show signs of arterial 
 degeneration and irregularity of the heart from the age of fifty to sixty years, 
 but may live in fair health for twenty years afterwards, ending his days 
 without any marked failure of the heart. The early stages are generally 
 recognized in the examination of the patient for some other condition, when 
 the distinctive signs may be found in the tortuous arteries, raised blood- 
 pressure, and the occasional occurrence of an extra-systole. Medical men 
 often attempt to combat these signs by some treatment more or less energetic, 
 and as many people are frightened by the evidences of advancing years they 
 readily comply with the proposals that are supposed to put back the hands 
 of time ; hence the great variety of drugs, methods, and modes of life we 
 find current. 
 
 It is rare that one has occasion to treat the milder symptoms in the 
 working-man — not that they are not frequently present, but because he has 
 not the time to consider his complaints, and he seems in no way to suffer 
 from the neglect. It is the well-to-do who are most concerned about some 
 trifling symptom incidental to these changes, and when their attention is 
 called to such a symptom as an extra-systole, either by their own sensations
 
 250 DISEASES OF THE HEART 
 
 or by their medical attendant, they beHeve that some calamity is impending, 
 and readily submit to any suggestion that promises to stave off the evil day. 
 
 When the patient is aware of the irregular action of his heart, and when 
 we find by examination that there are no changes beyond what would be 
 expected at his time of life, he should be strongly reassured that the irregu- 
 larity is a trivial symptom and of no vital importance. When the symptoms 
 are unpleasant and are aggravated by his mode of life — for example, by too 
 close application to a sedentary occupation — certain rational suggestions 
 as to the manner of living are obligatory. 
 
 In cases presenting these milder signs no further treatment is necessary, 
 beyond insisting that the patient should lead a well-regulated life, avoiding 
 over-feeding, over-drinking, and taking as much exercise in the open air as 
 can be reasonably obtained. Some of the symptoms, as extra-systole, come 
 on for periods and disappear for longer and shorter intervals. In these cases 
 I have frequently seen the patient get much benefit from a hohday with 
 healthy open-air exercise. Several of my patients, for instance, were conscious 
 of the occurrence of extra-systoles, and when they felt them they indulged 
 in a game of goK two or three afternoons a week, or took a short golfing 
 holiday, and invariably experienced relief. In fike manner, judicious hill- 
 climbing and walking are of benefit. In some cases the bodily exertion may 
 in the first instance increase the frequency of these extra-systoles, but the 
 exercise should not be given up on that account ; rather should it be continued 
 with moderation till a recovery of the reserve force takes place by training, 
 when the irregularities wiU become less frequent or disappear. 
 
 The amount of recovery depends on the stage which the degeneration 
 of the heart muscle has reached. We know of no method which can restore 
 a better blood-supply by removing the arterial degeneration, and without 
 this it is impossible to arrive at any process that would restore the degenerated 
 muscle of the heart ; so that when a considerable degree of recovery has taken 
 place, it is foolish to imagine that the favourable result has come to pass 
 because the treatment has restored the degenerated muscle-fibres. All we 
 can say in such cases is that the treatment has increased the reserve force of 
 the muscle-fibres. Recovery means the retention of a certain amount of 
 active muscle-fibre, and the greater the recoveryj^the less the degeneration, 
 and the less serious the prospect for the patient. 
 
 Another most important factor in treatment in all these cases is sleep. 
 Many suffer from troubled and broken sleep, and when they begin to suffer 
 from attacks of heart failure the occurrence of sleepless nights almost invari- 
 ably precipitates the exhaustion. Attacks of angina pectoris may be directly 
 induced by this want of refreshing sleep, and may be stopped by measures
 
 CARDIO-SCLEROSIS 251 
 
 taken to induce sleep. The means best adapted to this object varies with 
 different individuals. In some it may be found that their former habits in 
 the matter of their food are no longer suitable for their condition ; it is some- 
 times enough for them to take some light nourishment, as milk or biscuit, on 
 going to bed or during the night, to induce a restful sleep. Most require some 
 form of hypnotic, and the bromides — 20 grains thrice daily, for instance — 
 may induce a degree of drowsiness that is very beneficial. Again, the safer 
 hypnotics, as veronal or sulphonal, prove very useful in the milder cases. 
 When, however, the nights are disturbed by attacks of distressful breathing, 
 oxygen is of great service in some cases, and in others opiates or chloral must 
 be resorted to. On the whole, I find chloral the more useful drug. But 
 the cases are so variable that sometimes one drug is more efficacious than 
 the other, so that it may be necessary to try each of them, or a combination 
 of both. As regards contra-indications, I do not prescribe opiates when 
 there is exudation in the bronchial tubes with duskiness of the face, as I have 
 seen serious results follow, probably from the secretion not being got rid of 
 and thus inducing a certain amount of suffocation, which further impairs 
 the enfeebled heart. 
 
 Iodide of potassium is now generally recognized as of service in the 
 relief of many of the milder symptoms associated with arterial degenera- 
 tion. In many people the symptoms are not constant, but are manifested 
 occasionally in attacks of dizziness, dull headaches, inabihty to walk as far 
 as usual on account of breathlessness, sHght attacks of angina pectoris, and 
 even more violent attacks ; these all seem to benefit by the use of iodide 
 of potassium. In the attacks of ' bronchitis ' so common in the winter and 
 spring months in certain classes I have found distinct benefits from the use 
 of the iodide. I am not at all sure that the good results attributed to the 
 iodide may not have been due to the accompanying change in the food and 
 mode of Hfe. The action of iodide of potassium is not understood. 
 
 When dilatation of the heart sets in, with dropsy and scanty urine, the 
 treatment should follow the lines laid down in Chapter XXXIII. I may 
 remark here that drugs of the digitahs group are frequently of Httle avail in 
 these cases. They may increase the fiow of urine, but the heart does not 
 readily respond to them. 
 
 § 225. Aneurysm — It is not my purpose to enter into the discussion of 
 aneurysm, as it comes within the province of arterial disease, with which 
 I do not propose to deal. As, however, aneurysm is a frequent comphcation 
 of cardio-sclerosis and adds to the embarrassment of the heart in its work, 
 I wish to point out that many of the symptoms present in aneurysm really 
 arise from the heart, which has become affected by the processes that have
 
 252 DISEASES OF THE HEART 
 
 led to the production of the aneurysm. The aneurysm itself is such a patent 
 abnormality, while the heart affection (cardio-sclerosis) may give rise to no 
 distinctive sign, that the cardiac symptoms are usually attributed to the 
 aneurysm. Thus the pain in aneurysm is very often cardiac in origin, 
 especially when it occupies the region illustrated in Fig. 12. There are, 
 however, other pains in aneurysm whose origin it is difficult to indicate, 
 such as the persistent boring pain felt at the back over the left scapula, or on 
 the top of the shoulder. Whether they are the direct result of the pressure 
 on sensitive structures, or are of the nature of referred pain, I cannot decide. 
 The majority of cases of aneurysm do not die from rupture of the 
 aneurysm, but from exhaustion of the heart. This is important to remember, 
 for the treatment is often directed to the aneurysm, whereas it is the heart 
 that needs to be looked after.
 
 CHAPTER XXVIII 
 
 Adhesive Mediastino-Pericarditis 
 
 § 226. Etiology. 
 
 227. Symptoms. 
 
 228. Prognosis. Treatment. 
 
 § 226. Etiology — The adherent pericardium secondary to rheumatic 
 pericarditis rarely gives rise to any sign. In these cases the pericardium 
 is not adherent to structures outside the heart. On the other hand, 
 certain obscure inflammatory affections, probably of a tubercular nature, 
 such as occur in ' polyserositis ', give rise to very marked phenomena. 
 There is an extension of an inflammatory process which affects all the struc- 
 tures in the mediastinum, welding together the heart and pericardium, and 
 firmly binding these to all the surrounding structures. The heart becomes 
 anchored to the spinal column behind and to the chest-wall in front. As the 
 spinal column is unyielding, the contracting heart puUs on the ribs in front, 
 and as they yield to a greater or less extent we find the ribs drawn in during 
 systole and springing back during diastole. This embarrassment of the 
 heart leads to great enlargement in its size, and some of the biggest hearts 
 met with are due to this disease. 
 
 § 227. Symptoms. — The patients are always very short of breath, and 
 usually have to be propped up when in bed. As a rule, little or no pain is 
 complained of, but in one case I found that attacks of angina pectoris of 
 the most severe form were easily provoked. A slight effort would bring 
 on an attack, especially if the patient laughed. Attacks could sometimes 
 be induced by pinching the skin under the left nipple, or by applying the 
 stethoscope. 
 
 The adhesion of the heart to the lungs, blood-vessels, and other surround- 
 ing structures produces a great variety of symptoms, the cause of many of 
 which is obscure. The chief symptoms are great enlargement of the heart — 
 so great sometimes as to cause a marked difference between the two sides 
 of the chest — and retraction of the structures surrounding the heart during 
 ventricular systole. The systolic retraction alone is not distinctive, as 
 I have shown that it occurs when the anterior surface of the heart is made
 
 254 
 
 DISEASES OF THE HEART 
 
 up of the right ventricle (Fig. 33). During the ventricular systole there is 
 often an indrawing of the lower intercostal space on the left side behind 
 (Broadbent's sign, Fig. 150). Tallant and Cooper have shown that this 
 may arise in enlargement of the heart (with compression of the lungs) without 
 pericardial adhesion. In such cases, however, the interspaces affected 
 vary with respiration, and Cooper suggests that when they do not vary 
 
 Fig. 150. The upper tracing was taken from the 9th left 
 intercostal space behind from a case of adhesive mediastinitis, and 
 shows ' Broadbent's sign ', which is seen to be an indrawing of the 
 intercostal space during ventricular systole (space E). 
 
 with respiration the sign is, as Broadbent states, an evidence of pericardial 
 adhesion. When the chest-wall is thin and the heart is not covered by lung, 
 the systolic retraction of the different interspaces can be seen in a peculiar 
 wave-like rhythm. 
 
 Though various murmurs and modified sounds are often heard, no 
 distinctive sign can be found on auscultation. The veins of the neck may 
 sometimes be seen to swell up during inspiration. A very curious symptom 
 
 Fig. 151. Simultaneous tracings of the radial and jugular pulses, showing a great depression 
 (z) occurring during the ventricular diastole. (From a case of adhesive mediastinitis.) 
 
 is a sudden collapse of these veins at the beginning of diastole, which 
 Friedreich has explained as due to the springing back of the ribs after the 
 ventricular systole has dragged them down, the cavity of the thorax being 
 thus suddenly enlarged and expediting the flow from the overfilled veins. 
 This is well seen in the jugular tracing. Fig. 151, where the fall z is due to 
 the diastolic expansion of the chest. 
 
 The radial pulse may show a diminution in size during inspiration — the 
 pulsus paradoxus. It is now recognized that a respiratory variation of the
 
 ADHESIVE MEDIASTINO-PERICARDITIS 255 
 
 pulse may occur in a great variety of conditions, but I think that in adhesive 
 mediastinitis presents certain distinctive features. Curiously enough, no 
 tracings have been given, so far as I know, showing the pulsus paradoxus 
 in adhesive mediastinitis along with the respiratory curve, except in two 
 instances taken by Nicholson from Gibson's ^^^ cases. The study of these 
 tracings, compared with some I have taken, leads me to think that the 
 variations point to very different causes. As, however, my observations 
 are few in number, I do not enter into the subject, but call attention to 
 a field that needs exploring. 
 
 There is usually associated with these signs enlargement and sometimes 
 pulsation of the liver, which in Wenckebach's *^' case was of the auricular 
 type. The spleen also may be greatly enlarged, and there may be con- 
 siderable dropsy. 
 
 § 228. Prognosis. — The future of these cases is bad, though they 
 sometimes show periods during which they make remarkable progress 
 towards recovery from serious symptoms. But these are only temporary, 
 and they gradually drift to a fatal issue. 
 
 Treatment. — The treatment of these cases has so far been unsatisfac- 
 tory, and one can only advise the principles usual in extreme heart failure. 
 Attempts have been made, following the suggestion of Brauer, to free the 
 heart by resecting the ribs. This has been done in several cases, and 
 Wenckebach*'^' describes marked improvement in a case in which the 
 operation was performed.
 
 CHAPTER XXIX 
 
 Congenital Affections of the Heart 
 
 § 229. Etiology. 
 
 230. Symptoms. 
 
 231. Prognosis. 
 
 232. Treatment. 
 
 § 229. Etiology — Congenital heart affections are due to the persistence 
 of certain foetal forms of the circulation, such as persistent patency of the 
 foramen ovale or ductus arteriosus, or to some interference with development 
 leading to deformation of the valves or narrowing and obliteration of the 
 large arterial trunks. They may also arise in consequence of foetal endo- 
 carditis. The conditions are incompatible with life in many cases. 
 
 It is only in exceptional instances that the symptoms permit of a recogni- 
 tion of the nature of the cardiac defect. 
 
 § 230. Symptoms. — The most characteristic symptom is cyanosis, 
 which is present in a great number of patients. Clubbing of the fingers 
 is a common accompaniment of the cyanosis. The size of the heart is often 
 greatly increased. This may be due to hypertrophy of the left ventricle 
 when there is an obstruction to the outflow of the blood through the aorta, 
 or to dilatation of the right heart when there is interference with the pul- 
 monary circulation or a patent foramen ovale. Murmurs are usually present, 
 almost invariably systolic in time, but it is difficult to detect their origin 
 except in the case of the patent ductus. Here the communication between 
 the aorta and pulmonary artery persists, and as the pressure is much higher 
 in the aorta a continuous stream passes during the whole cardiac cycle 
 from the aorta to the pulmonary artery, and, as Gibson ^^' has pointed out, 
 this leads to a murmur which, beginning with great intensity at ventri- 
 cular systole, extends over ventricular systole into diastole, fading away 
 towards the end of diastole. This murmur is loudest over the second and 
 third left interspaces, and here also a well-marked thrill synchronous with 
 the murmur can be felt.
 
 CONGENITAL AFFECTIONS OF THE HEART 257 
 
 § 231. Prognosis — If there be no cyanosis, little or no enlargement of 
 the heart, and the development of the child good, with a fair field of cardiac 
 response, then the prognosis is good ; otherwise the outlook is bad, though 
 the child may lead a crippled existence for many years. 
 
 § 232. Treatment — If the heart maintains the circulation well, no 
 treatment is required. In more serious cases, beyond attending to the 
 child's comfort and nourishment, special treatment for the heart is of little 
 benefit, digitalis being rarely of value unless there is dropsy. 
 
 MACKENZIE
 
 CHAPTER XXX 
 
 Heart Disease and Pregnancy 
 
 § 233. Importance of the subject. 
 
 234. Standards for guidance. 
 
 235. Management of the labour. 
 
 § 233. Importance of the subject. — It is almost certain to be the 
 experience of every practitioner who has a midwifery practice to be met 
 by the question of pregnancy in women with some affection of the heart, 
 and this question is of supreme importance, for life and death depend upon 
 the views held by the doctor. If the gravity of the question is not sufficiently 
 appreciated, the consequences in certain cases may be ruined health or even 
 the death of the woman, while a too serious view of other cases may unjustly 
 entail upon the woman an uncalled-for restraint. Hitherto the guide in 
 the diagnosis has been in the main the presence of a valvular murmur, and 
 some doctors, having seen patients with valvular lesions pass scatheless 
 through repeated pregnancies, treat the subject too lightly, while others, 
 who have witnessed the disastrous results of pregnancy, are oppressed by 
 the gravity of the condition. 
 
 The treatise on The Bearings of Chronic Diseases of the Heart upon 
 Pregnancy, Parturition, and Childbed, by Angus Macdonald, in 1878, is stiU 
 the best work on the subject, and long experience and observation lead me 
 to agree with him in most points. The researches on this subject have too 
 often been directed to the somewhat barren and academic question as to 
 whether the heart hypertrophies during pregnancy, and the bearing of this 
 on prognosis. If, however, it be borne in mind that heart failure is essentially 
 a question of the integrity of the heart muscle, a better standpoint will be 
 obtained for judging these cases. The valve lesion in the great majority 
 is at the most only an embarrassment to the heart in its work, and one 
 which it may easily overcome. The presence of the lesion is important, 
 however, in another respect, namely, in that it calls attention to the heart 
 and serves to remind us that the disease that injured the valve may at the 
 same time "have injured the muscle : our object in examining these cases 
 is to find out the extent of the lesion in the muscle, and how far the valve 
 lesion embarrasses the muscle.
 
 HEART DISEASE AND PREGNANCY 259 
 
 § 234. Standards for guidance — The essential question in cases of 
 valve disease is the condition of the muscle, and this is determined by the 
 manner in which the heart responds to effort. Additional help will be 
 obtained by noting the size of the heart, its rate and rhythm, and the 
 tendency to oedema of the legs and lungs. Given a fair field of cardiac 
 response with little or no enlargement of the heart, then pregnancy need 
 have no terrors. If the field of cardiac response is distinctly limited, 
 particularly if palpitation is readily induced by exertion, with no oedema, 
 then the opinion should be suspended till the result of treatment is ascer- 
 tained. If the condition does not improve, then the outlook is not hopeful, 
 and pregnancy should be forbidden. 
 
 With the appearance of dilatation and its accompanying symptoms — 
 oedema of the legs and lungs — pregnancy should be forbidden. In doubtful 
 cases, with some dilatation and no swelling of the legs, I have been accus- 
 tomed to be guided by the tendency to oedema of the lungs. This is readily 
 ascertained by examining the patient after a night's rest, before she gets up. 
 If she be instructed to lie on one side as much as possible, and not to sit up 
 until she is examined, numerous fine crepitations will be found on the first 
 deep inspiration, if there be any tendency to oedema. The auscultation 
 of the lung base should be the first procedure adopted in the examination. 
 If the crepitations are dispelled with the first few deep inspirations, then it 
 may be taken for granted that there is only a slight tendency to oedema, 
 and the case requires care and watchfulness before finally deciding. If the 
 crepitations persist, then the tendency to oedema is so great that pregnancy 
 should be forbidden (see also § 190). 
 
 It must be kept in mind that patients with valvular lesion may suffer 
 from most severe heart failure (dilatation, and extensive dropsy), and make 
 such good recoveries that repeated pregnancies may be undertaken with 
 impunity. Here, however, the degree of recovery gives the standard for the 
 judgment, and I mention this lest the knowledge of a bygone heart failure 
 be considered a bar to marriage and pregnancy. 
 
 One of the most difficult problems I have had to face has been where 
 a pregnant woman has shown evidence of heart failure, and the question 
 has arisen whether interference is necessary. For one thing, a natural 
 labour entails less strain upon the heart than one artificially induced. In 
 the former case the preliminary preparation and softening of the tissue 
 render the expulsion of the child much easier, even though the head is larger. 
 But, on the other hand, the dropsy may increase to such an extreme degree 
 that no aid can be rendered. 
 
 One of my most painful experiences was in the case of a woman of 
 
 s 2
 
 260 DISEASES OF THE HEART 
 
 thirty-five years of age with mitral stenosis, who became pregnant with her 
 first child ; when labour set in the dropsy had become so extensive, and the 
 breathlessness so great, that she could not lie down, but had to sit up in bed. 
 It was impossible to make a vaginal examination, as she could not turn to 
 one side without great suffering. She could not take chloroform, as the 
 inhalation intensified the dyspnoea, and we were helpless, and had to see 
 her die after thirty-six hours of suffering, relieved slightly by opium. In 
 other cases where the dropsy and breathlessness were threatening to become 
 extreme, I have successfully induced premature labour. Fortunately, 
 many women with advanced heart failure abort. Ii others abundant 
 bleeding from a varicose vein gives great relief, and suggests venesection 
 when there is much evidence of over-filling of the venous system. 
 
 The nodal rhythm should be a bar to pregnancy in aU cases. 
 
 Although the valvular lesion by itself is not a contra-indication, yet the 
 particular valvular lesion influences the decision when it is combined with 
 indications of muscle failure. Thus aortic lesions are very serious unless 
 there be a good intact heart muscle. Mitral stenosis, when there is only 
 a presystolic murmur and good effective muscle, is no bar ; but if there is 
 also a diastolic murmur, then, unless the muscle is very good, pregnancy 
 should not be permitted, as the diastolic murmur points to a progressive 
 narrowing of the orifice. 
 
 § 235. Management of the labour — In regard to the management 
 of labour in these patients with heart affections, if there is the slightest 
 sign of heart failure the patient should be instructed not to bear down, 
 and chloroform should be administered very early, the anaesthesia being 
 gradually deepened. As soon as it is feasible, forceps should be appHed, 
 and gentle, firm traction intermittently maintained until delivery is effected 
 — even if the forceps have to be on for a considerable time. 
 
 I have never seen the slightest risk from chloroform in these cases. 
 
 After the delivery is over the patient is not out of danger, for symptoms 
 of severe heart failure may supervene any time within the next three weeks. 
 In view of this, care should^be taken to ease the heart's work, by rendering 
 the patient comfortable and inducing refreshing sleep. In severe cases 
 nursing the child is out of the question, nor should the child be allowed to 
 disturb the mother. The judicious administration of digitalis is of service, 
 following the lines laid down in Chapter XXXIV.
 
 CHAPTER XXXI 
 
 Chloroform in Heart Affections 
 
 § 236. Conditions contra-indicating its use : respiratory embarrassment, cardio-sclerosis, 
 status lymphaticus. 
 237. Estimation of the fitness of the patient. 
 
 § 236. Conditions contra-indicating its use — For a number of years 
 I made numerous careful observations on patients to see if I could detect 
 any special action of chloroform on the heart. I got various alterations 
 in the pulse-rate, and in the degree of venous engorgement, but these 
 were in the main due to the patient being excited or struggling, or holding 
 his breath, so that I could detect no sign of any direct influence of the 
 chloroform on the heart. It must be borne in mind that a great many of 
 the physiological experiments have been carried out with very large doses, 
 and with the animal's heart in a very unnatural condition, so that the results 
 cannot be compared with those of the small doses given to a human being. 
 
 The question whether a patient can take chloroform has often to be 
 met, and the indications against its administration have never been clearly 
 given. The stethoscopic examination of the patient just before administra- 
 tion is useless ; the decision must be made independently of any results 
 obtained by it, for no form of murmur, irregularity, or rate is a bar to the 
 administration of chloroform. I am not aware of a single form of heart 
 ailment discoverable by auscultation that would render the administration 
 of chloroform dangerous. The dangers do not lie in the action of chloroform 
 upon the heart alone, but on other considerations. Thus, there is often 
 trouble and even danger in giving chloroform to emphysematous people 
 with great liability to bronchitis, and to elderly people with a tendency to 
 bronchitis and with wheezing rales accompanying respiration, and also in 
 cases of embarrassment of the lungs from oedema, abundant pleural 
 effusion, or tumours pressing on the windpipe — in fact, all cases with 
 imperfect oxygenation of the blood. 
 
 Elderly people with a suspicion of cardio-sclerosis are also bad subjects, 
 not because of the chloroform, but because their hearts are unable to with- 
 stand even sHght strains. Thus one typical cardio-sclerotic who was to 
 be operated upon for piles, and who had suffered from intense irritation 
 about the anus, and was most anxious to be relieved, had shown signs
 
 262 DISEASES OF THE HEART 
 
 of slight attacks of angina pectoris. He was greatly excited on entering 
 the operating room, and when laid down preparatory to receiving the chloro- 
 form his pulse was very rapid. The towel had just been placed over his 
 face when his pulse stopped. The towel was at once removed, and he con- 
 tinued to respu-e with considerable force for a few minutes and then stopped, 
 and he was dead. Manifestly it was not the chloroform that killed, but the 
 strain on the enfeebled heart. 
 
 The Status Lymphaticus. — Of late years, a number of deaths have 
 occurred in a condition described as the status lymphaticus. I have no 
 experience of this condition myself, but it is described as a state in which 
 the sufferer may die from any trivial cause, and which is marked by enlarged 
 thymus and spleen, hypertrophied lymphatic glands in various regions, 
 with swelling of the tonsils, and of the solitary follicles and Peyer's patches 
 in the intestine, and flaccid cardiac muscle. The condition may be recognized 
 during life from the pale thin skin and pasty complexion and fairly abundant 
 subcutaneous fat, along with frequent signs of rickets or scrofula, enlarge- 
 ment of the tonsils and of the superficial glands, especially in the axilla 
 and neck, adenoid growths, a palpable spleen, and often enlargement of 
 the thyroid (McCardie). 
 
 § 237. Estimation of the fitness of the patient — It will be seen that 
 the examination of the patient should be made prior to his reaching the 
 table, and if there is a doubt, even a day or two before the operation. 
 Apart from the status lymphaticus, the best test is the patient's field of 
 cardiac response. But even when the field is greatly limited from some 
 exhausting disease, with or without valvular affection, the patient may take 
 chloroform with safety. In these circumstances, the operation is sometimes 
 delayed for days or weeks in order that the heart may be strengthened by 
 drugs like strychnine and digitalis. Now this is very bad practice, for it 
 may be taken for granted that no patient's heart will gain strength while 
 an operation is hanging over his head, more particularly if he or she knows 
 that the operation is delayed for the heart to be strengthened. I can 
 conceive of nothing better calculated to weaken the heart than such 
 a procedure, for the anxiety is bound to react upon the heart and make 
 it more irritable. When a patient with a weak heart is to be operated on, 
 the sooner it is done the better. 
 
 Under the influence of excitement and fear, the patient's heart may 
 appear worse than it is, and one should always keep that in mind when the 
 heart is behaving strangely before an operation, as the following illustration 
 shows. I proposed to remove a large ovarian cyst from a very intelligent 
 patient ; all arrangements were made, and when I arrived in the morning
 
 CHLOROFORM IN HEART AFFECTIONS 263 
 
 to do the operation I was informed that the patient had gone out of her 
 mind, and that her heart was very bad. When I saw her she was muttering 
 incessantly, and took no notice of any question I put to her. Her pulse 
 was extremely small and very rapid, 160 beats per minute. After reflecting 
 over the case I concluded that the condition was in all likelihood due to 
 apprehensive fear, and that chloroform would be likely to soothe the brain 
 and relieve the heart, so that to delay the operation would but add to the 
 terror of the patient when she recovered. I therefore asked the anaesthetist 
 to proceed, but he refused, and I started the chloroform myself. She went 
 under very quickly, and the pulse speedily fell to seventy beats per minute, 
 at which rate it remained during the operation, and when she came out of 
 the chloroform she was perfectly rational, and made a good recovery. 
 
 I have administered chloroform repeatedly in cases of extreme heart 
 failure with valvular lesions — for example, during labour, and in one case 
 where the patient appeared to be dying from a severe attack of pneumonia — 
 and I have never seen the slightest bad effect from the chloroform. Cases 
 with extreme irregularity of the heart can take chloroform without danger. 
 I watched for a whole hour a case of complete heart-block under full 
 anaesthesia. 
 
 The cause of death under chloroform anaesthesia — apart from over- 
 dose and imperfect aeration of the blood — has so far escaped recognitiqn. 
 It is probable that the secret lies in the fact that certain changes, as yet 
 unknown, render some hearts abnormally susceptible to the action of 
 chloroform. One can infer this from the effect of digitalis, which is shown 
 in Chapter XXXIV to have a varied action depending on the nature of the 
 heart lesion. At all events, no satisfactory conclusion will ever be reached 
 until graphic records of the movements of the circulation and respiration 
 are made during the whole time of anaesthesia. As death occurs quite 
 unexpectedly, it would be necessary to make observations consecutively 
 on many thousands of cases.
 
 CHAPTER XXXII 
 Prognosis 
 
 § 238. Responsibility of the medical profession. 
 239. Basis for prognosis. 
 
 § 238. Responsibility of the medical profession In addition to 
 
 recognizing the meaning of any abnormal sign or symptom, we should 
 endeavour to acquire a knowledge of what bearing it has upon the future 
 history of the patient. This knowledge can only be obtained by watching 
 how patients exhibiting the abnormality meet the storm and stress of life. 
 This has been a special object of my work on the heart for over a quarter 
 of a century, and in the following observations I am culling from my own 
 personal experience, and in each deduction I give I have in my mind 
 a number of cases from which it has been drawn. 
 
 I am rather afraid that our profession as a body does not recognize 
 sufficiently its responsibility in regard to prognosis. When an individual 
 submits himself for an opinion, he does so with such implicit confidence 
 that the verdict given may alter the whole tenor of his life. He may be, 
 for instance, seeking to enter some profession, when a preliminary medical 
 examination reveals what the medical man takes to be an abnormality. 
 An imperfect knowledge of its nature may, and unfortunately often does, 
 lead to its being regarded as presaging possibly grave consequences, and the 
 candidate is rejected. He is thus shut off from the prospect of his chosen 
 calling, and, knowing the reason of his rejection, passes through life uneasily 
 conscious that some disaster is always impending, while aU the time the 
 supposed abnormality may be a sign of little or no consequence. 
 
 If we look at an insurance paper we realize the hardships to which an 
 applicant is exposed. Is the pulse regular ? Are the sounds pure ? If 
 either question is answered in the negative, the applicant is either rejected 
 or is penalized for life by having to pay a higher premium, and, in addition, 
 is burdened with the painful consciousness of infirmity. 
 
 I dwell on this matter with some insistence, because I have known of 
 so many instances in which gross injustice has been done to individuals, 
 not only in the pecuniary aspect, but in having imposed upon them great 
 expense, unnecessary treatment, and mental disquiet, because the meaning
 
 PROGNOSIS 265 
 
 and prognostic significance of some simple symptom, as a murmur or an 
 extra-systole, have not hitherto been recognized. I sometimes wonder 
 whether the use of auscultation has not been the means of doing more harm 
 than good. That it is not an unalloyed blessing is too painfully evident, 
 for not only have totally incorrect conclusions been drawn as to the bearing 
 of murmurs on the future of the patient, but so much time has been spent 
 in investigating the physics of their production that more important matters 
 have been lost sight of. It is so easy to recognize a murmur, that other less 
 obvious but more significant signs have too often been neglected. 
 
 A serious responsibility is thrown upon every practitioner at times in 
 advising upon other questions. Should a man give up his business ? is a 
 question on which advice is constantly sought, and whether the individual be 
 a statesman or a labourer the greatest care is necessary in formulating the 
 answer. Should a woman with some heart affection marry, or, if she is 
 pregnant, should the pregnancy be allowed to proceed ? are problems that 
 every general practitioner at one time or another will have to meet ; and 
 if he seeks for guidance in the textbooks he finds merely general views 
 which he cannot apply to the individual case. This fact alone should arrest 
 the attention of the profession, and make it conscious how inefficient the 
 teaching of heart affections has been. 
 
 § 239. Basis for prognosis — A rational prognosis must be based on 
 a clear idea of the manner in which any given symptom is produced. 
 Knowledge never dispelled the terrors of darkness with more effect than in 
 showing the true meaning of the symptoms in affections of the heart. So 
 impressed are the public and profession with the suddenness with which 
 death may take place, that an unnecessary fear lays hold of them when the 
 heart shows any sign out of the common, lest this should be the thing that 
 slays. It is because of this that I have entered with such fuUness into the 
 explanation of so many symptoms. I confess there are still many which 
 I do not understand, but I have endeavoured to find out their value by 
 watching individuals who exhibited them, and to find a basis on which their 
 value can be estimated. 
 
 In estimating the value of any abnormal sign, or in determining the 
 condition of a heart, the most reliable guide is the manner in which the heart 
 responds to exertion. This, again, is but an attempt to estimate the amount 
 of reserve force. If the individual can with comfort make such exertions as 
 we would expect at his time of life, then the abnormaUty may with certainty 
 be assumed to be of little real significance. 
 
 If there be a complete breakdown, the decision should not be made until 
 time has shown to what extent recovery takes place. The amount of
 
 266 DISEASES OF THE HEART 
 
 recovery enables us to judge the condition of the muscle of the heart, for 
 it is on its capability to renew its reserve force that the future of the patient 
 depends. To illustrate this I cite the history of a man whose case is also 
 described in the Appendix for other reasons (Case 17, Appendix IV). 
 
 In 1883, at the age of thirty-two, the patient had a severe attack of 
 rheumatic fever, and was left with a mitral lesion. In 1897 he lay for weeks 
 unconscious and swollen with dropsy. From this he recovered with a well- 
 marked presystolic and diastolic mitral murmur and a slightly enlarged heart. 
 In 1904 his heart became continuously irregular, and has remained so ever 
 since. It now extends two inches beyond the nipple line, and he has a 
 systolic and long diastolic mitral murmur. Notwithstanding all this, for the 
 past four years he has followed his trade as a mechanical engineer, doing 
 the very hardest work of this laborious trade, and from 1904 to 1906 he 
 worked overtime almost daily. Beyond being somewhat short-winded 
 going uphill, especially in cold weather, he feels as fit for work as ever 
 he did. 
 
 Even cases that never show so complete restoration of function as this, 
 and in which attacks of extreme failure are frequent, may go on for many 
 years and lead sometimes fairly useful lives, though in time the progressive 
 changes become so great, or the muscle so exhausted, that the possibility of 
 even temporary recovery is precluded. 
 
 In individuals in whom there is a distinct limitation of the field of cardiac 
 response, a close scrutiny should be made into the cause. It should be 
 borne in mind that if a heart is not properly exercised its field of response 
 becomes more and more restricted. Thus a man who for a long time leads 
 a sedentary life is often startled by the fact that he is rendered extremely 
 breathless by undertaking some exertion that he was wont to make with 
 ease a few years previously. But with moderate training there is soon 
 restored sufficient reserve force to enable him to perform his task without 
 distress. Therefore in all cases, even when there is an abnormal symptom — 
 as a murmur or an irregularity — this question of the nature of the exhaustion 
 should be borne in mind. It must not be forgotten also that the supposed 
 abnormaUty may have nothing to do with the symptoms of exhaustion. 
 This is particularly the case in the young, in whom syncopal attacks are 
 not infrequent. I have repeatedly seen grave alarm aroused because a boy 
 or girl has fainted, and has had an irregular pulse when quiet in bed. This 
 irregularity has been of the youthful type (sinus irregularity), and if it had 
 any connexion with the syncopal attacks it was merely incidental, and in 
 no sense added any gravity to a trivial affection. 
 
 While the lines on which prognosis is based can be fairly well recognized
 
 PROGNOSIS 267 
 
 in regard to the more common affections of the heart, we often meet with 
 patients who show symptoms whose nature is too obscure for us to identify. 
 A prognosis in these cases is often required and difficult to give. The plan 
 I have adopted is to exclude the possibility of degenerated muscle by an 
 analysis of the condition of the separate functions of the heart muscle, 
 and consider how far the complaints may be nervous in origin ; having 
 satisfied myself that the muscle is sound, I give a favourable prognosis, 
 at the same time indicating the obscurity of the case. I do this because, 
 as a matter of experience, I have found that these exceptional cases, particu- 
 larly in young adults, always tend to recovery to a greater or less degree. 
 This unfortunately is not the usual plan, for some signs are too often 
 taken to be more serious the more obscure they are. In many cases the 
 physician must be prepared to back up his opinion by taking a grave amount 
 of responsibility. For instance, I have on several occasions seen patients 
 kept in bed and put through elaborate forms of treatment after some such 
 affection as influenza. The patients have complained of obscure signs, to 
 them alarming, and a certain amount of abnormality has been present, as 
 frequent pulse or extra-systoles. Having satisfied myself that there was no 
 serious mischief, I have had no hesitation in making the patients get up and 
 resume their ordinary life, even when the medical attendant has shrunk 
 from the responsibility. I have never yet had cause to regret such a pro- 
 cedure, and it is better to run a little risk in a rare case than to have a 
 patient drifting on to invalidism because of our ignorance and fear of 
 responsibility.
 
 CHAPTER XXXIII 
 
 Treatment 
 
 § 240. Tlie essential principle in treatment. 
 
 241. Rest. 
 
 242. Sleep. 
 
 243. Bodily comfort. 
 
 244. Diet. 
 
 245. Condition of the bowels. 
 
 246. The mental factor. 
 
 247. Drugs. 
 
 248. Oxygen. 
 
 § 240. The essential principle in treatment In order to treat 
 
 failure of the heart intelligently it is necessary to find out some principle 
 which will serve as a guide. So far as the heart is concerned we get a safer 
 guide than is possible for any other viscus, as the nature of its failure can be 
 more easily ascertained. As in all forms of heart affections exhaustion of 
 the reserve force is the essential factor in the failure, so the restoration of 
 this reserve force is the aim and object of treatment. But in the first place 
 an accurate diagnosis should be made, and if we detect some change which 
 alarms the patient, but is really of Httle significance, as certain murmurs or 
 irregularities, then the reassurance of the patient as to the innocent nature 
 of his trouble brings relief ; or if we detect some permanent change it is 
 useless to waste time and energy in the haphazard prescription of supposed 
 remedies. It is futile to imagine that we can restore a cicatrized valve, 
 a sclerotic myocardium, or a calcareous artery to their pristine condition. 
 We must recognize facts, and, with the knowledge of the presence of such 
 irremediable conditions, endeavour to make the best of the heart muscle 
 that is left. 
 
 Whatever may be the nature of the organic lesion, the immediate heart 
 failure in any given case is due to the heart having to undertake work which 
 makes a call upon the reserve force, while the period of rest is not suffi- 
 ciently long to permit it to recuperate. Step by step the exhaustion pro- 
 ceeds till some striking evidence of this heart failure finally compels the 
 patient's attention. If this conception of the cause of the heart failure 
 be grasped, we are at once placed in a position to undertake a rational treat-
 
 TREATMENT 269 
 
 ment ; the principle of such treatment is so simple that it seems almost 
 unnecessary to dwell upon it, namely, the placing of the heart in a position 
 to regain its reserve force. This principle is so obvious that it is apt to be 
 ignored, but when any successful form of special treatment is investigated, 
 it will be found that its success is due to the unconscious adoption of this 
 principle. 
 
 The next step to be taken after recognizing the principle is to find out 
 what functions of the heart muscle are exhausted. This, as a rule, can 
 be ascertained by methodical inquiry into all the symptoms after the 
 manner I have detailed in the text. The adoption of special measures 
 when necessary will follow the result of this examination into the nature 
 of the failure, and these I have indicated under the description of the 
 different symptoms. Here I will dwell more on the general appUcation 
 of principles suitable to the treatment of the great majority of cases of 
 heart failure. 
 
 § 241. Rest. — On examination we may find evidence of some organic 
 change in the heart, as a valvular murmur, persistent irregularity, or dilata- 
 tion, and then we recognize that the heart has not only been doing the work 
 incumbent on a healthy heart, but it has been doing so hampered byjts 
 own inherent defect. As we cannot modify the latter condition we must 
 seek to ease the load in the other direction, and it is here that the physician 
 has to exercise a very wise discretion. He should enter into the patient's 
 daily life and find out the circumstances that are likely to induce heart 
 exhaustion. To give up the work by which the patient earns his Uvelihood 
 may be too serious a matter, but the physician may be able to suggest the 
 omission of certain kinds of work that may relieve the strain without inter- 
 fering too seriously with the patient's employment. Or it may be that 
 some habit, as over-indulgence in alcohol or tobacco, or some dietetic error, 
 can be corrected with benefit. Besides relieving the heart from over- 
 work, it must be placed in a position to do its work as free from irritation 
 as possible. The great influence which the nervous system has on the heart 
 must always be borne in mind. A worried and anxious mind invariably 
 reacts on the heart, rendering it unstable or excitable. This factor is of 
 such importance that when the question of work arises, if it is found that 
 the cessation of work results in mental worry and disquiet, it is far safer 
 to allow the patient to follow his occupation Avith discretion, and with 
 due regard to the nature of the work. In severe heart failure, it is scarcely 
 necessary to say, rest in bed is imperative. 
 
 § 242. Sleep — Whatever the form the heart failure may assume, sleep 
 is essential. It may be taken as an axiom that if the patient does not get
 
 270 DISEASES OF THE HEART 
 
 sufficient sleep he will never get well. Inquiries should be made of every 
 patient in regard to his sleep ; if it is not good and cannot be attained by 
 removing all forms of bodily discomfort, then resort must be had to soporifics. 
 If an individual has been accustomed to some alcohol — beer, stout, or 
 whisky — at bedtime, and the want of it results in sleeplessness, then he should 
 be allowed to have it. The milder hjrpnotics may be tried, as antifebrin, 
 veronal, or sulphonal, but if these fail resort must be had to chloral and 
 opium. In great restlessness from breathlessness, cardiac asthma, Cheyne- 
 Stokes respiration, these drugs must be carefuUy pushed until the desired 
 effect has been obtained. As to the selection of the drug, in serious cases 
 I have found chloral the safer and more useful when there is little or no 
 dilatation of the heart, when the blood-pressure is high, as in cardio-sclerosis, 
 and when there is a tendency to ' bronchitis ', opium being contra-indicated 
 in the latter class because of its tendency to prevent the free expulsion 
 of the phlegm. 
 
 Among more neurotic patients I have found bromide of ammonium 
 of inestimable service, not only in inducing sleep, but in keeping the mind 
 from worrying, and in inducing a lethargy that is beneficial to the heart. 
 Even in severe cases of angina pectoris I have found it of great value. Thus, 
 a lady with aortic valvular disease, between the age of fifty and sixty, 
 became liable to attacks of angina pectoris. At times these were so severe 
 that she was forced to lie in bed. The exhaustion of the heart was so great 
 that the sounds were sometimes scarcely perceptible. After a period of 
 rest the heart regained strength and she was able to go about, collapsing, 
 however, again and again after a few months. On making minute inquiry 
 into the cause of these attacks, I found that she suffered from sleeplessness 
 for a week or two prior to a breakdown. I therefore prescribed bromide 
 of ammonium, 20 grains three times a day, during one of her attacks of 
 heart failure. In a few days she got quiet sleep and speedily recovered. 
 When she began to experience a restless night she resorted to the bromide, 
 and it never failed to give her sleep, and no doubt warded off the attack, 
 for on several occasions she neglected the medicine and after a few sleepless 
 nights the attack of angina pectoris returned. 
 
 The good effects of the bromide in nervous cases have been referred to in 
 Chapter VIII. The dose of the various hypnotics varies with each patient. 
 Small doses should be used at first, and the drug pushed carefully and 
 steadily till some effect is produced. Repeated doses every one or two hours 
 should be tried at first. 
 
 § 243. Bodily comfort — In cases of severe heart failure much can be 
 done by removing all sources of discomfort. Detailed instructions regarding
 
 TREATMENT 271 
 
 sponging the body and arranging the bed so that the patient lies com- 
 fortably with light and warm bedclothes should be given ; too great 
 warmth should be avoided. The patient often wishes to assume some 
 position that the attendant may fancy to be harmful, but his inclination 
 should be complied with and everything done to keep him comfortable in 
 the position assumed, as with the shoulders raised, sitting upright, or bending 
 forward with the head supported. He may prefer sitting in a chair with 
 his arms on a table and his head resting on them. In all these positions he 
 is instinctively assuming a position that helps the heart in its work. In all 
 cases, mild or severe, every source of discomfort from other parts of the 
 body should be attended to, such as an irritating skin affection, piles, 
 frequent micturition. 
 
 § 244. Diet. — In calculating the results obtained by any mechanical 
 process it is necessary to understand all the factors concerned. The neglect 
 of one factor necessarily vitiates the calculation. Because of the slight 
 advance in biochemistry many attempts have been made to find a scientific 
 dietary. But as the factors concerned in metabolism are as yet imperfectly 
 understood, it is manifestly hopeless to base a dietary on knowledge that 
 does not include all the factors concerned. Notwithstanding the confident 
 assertion of many dietetic authorities, the perfect dietary has yet to be 
 evolved, and in the meantime we must be content to be guided by common 
 sense and experience. 
 
 In cases of heart failure a good deal of harm can be done by injudicious 
 feeding. It must be kept in mind that in extreme heart failure and in febrile 
 cases the digestive functions are themselves greatly weakened, and that to 
 pour food into a weakened stomach is not only to add to the discomfort of 
 the patient, but may produce flatulent distension of the stomach and bowels, 
 which, pressing on the diaphragm, embarrasses the heart and respiration. The 
 manifest weakness of the patient is often taken as an indication for more 
 food to restore the strength, and satisfaction is felt so long as fluid is seen to 
 disappear into the patient's interior. It is very curious how prevalent the 
 custom is, when the stomach is weak, to give it more work to do. The food 
 is prepared in such a manner that the assistance of the mouth is dispensed 
 with, and more work is therefore thrown upon the stomach. Bread and 
 milk, a favourite food, is so prepared that no mastication is needed, and the 
 stomach is burdened with the duty of getting rid of the load. The great 
 importance of oral digestion is not sufficiently appreciated. Not only does 
 the process of mastication in several subtle ways stimulate the digestive 
 glands of other organs, but the juices from the mouth that are mixed with 
 the food not only assist digestion but prevent the flatulence which is so often
 
 272 DISEASES OF THE HEART 
 
 such a troublesome feature in the weakened digestion of heart failure. I wish 
 to insist upon this all the more as it is becoming more and more the vogue 
 to give patients partially digested foods, or foods supposed to be prepared to 
 make digestion easier, and, relying upon the notion that digestion is being 
 assisted, the physician is apt to ignore the natural and infinitely better 
 methods provided by nature. These short cuts to treatment are invariably 
 in the end bad for patient and physician — leading the latter to a rule-of- 
 thumb practice, neglecting thereby to make of each individual a special 
 study. 
 
 In cases of extreme heart failure, with dropsy, the food should be very 
 limited in quantity — as a rule, small quantities of milk given at frequent 
 intervals, in extreme cases not more than one pint per day. The patient 
 should be encouraged to take a small portion of biscuit, or a dainty sandwich 
 with fresh potted meat, chewed very thoroughly. In febrile cases, or when 
 the mouth tends to become dirty, it should be washed or sponged out, and 
 immediately afterwards a smaU piece of solid food should be given to chew. 
 The quantities should always be smaU, so that the patient is not nauseated 
 by the spectacle of an untempting quantity of food. 
 
 With less severe cases the food should be more varied, but it should 
 never be forced on the patient. The quantity he can chew is often a very 
 good guide, because if he cannot be tempted to chew much it is manifest 
 his digestive functions are at fault, and it is a very bad practice in such cases 
 to pour in beef-tea and other easily eliminated fluids. The guiding principle 
 should be food, tempting, needing mastication, with Kttle fluid, and that 
 chiefly milk, given smaU in quantity and at fairly frequent intervals — the 
 intervals depending on the quantity he is able to take. The kind of food 
 should be that which the patient hkes, so long as it does not disagree with 
 him. The doctor must be on his guard not to prescribe a dietary suitable 
 to himself, but must bear in mind that what disagrees with him may agree 
 with his patient. In selecting a dietary the resources of an inteUigent 
 housewife wiU often be found to be of much service. 
 
 Individuals with heart trouble, but able to get about, should lead a hfe of 
 abstemiousness, avoiding aU excesses. The meals should be small in quantity, 
 and of such frequency that faintness is avoided. It often happens that they 
 become faint in the night, or early in the morning, as they have not broken 
 their fast since the evening meal. A dry biscuit and a smaU cup of milk 
 at bedtime or in the early morning wiU often prevent the occurrence of 
 disagreeable sensations. 
 
 A class of people for whom many dietaries have been evolved are those 
 who with advancing years show some signs of wear and tear. It may be that
 
 TREATMENT 273 
 
 in their vigorous manliood they enjoyed and gratified excellent appetites, 
 but as the years begin to tell the pleasures of the table no longer appeal 
 to them. Signs of the heart faihng may manifest themselves, and the 
 individual begins to take thought and seeks advice. Such a one readily 
 becomes the victim of a dietetic craze. A course of life that seems to put 
 back the hand of time appeals to him. As one who has watched many of 
 these patients over periods of many years, I have seen no evidence which 
 convinces me that the various abstemious dietaries that I have tried and 
 seen others try arrest the progress of senility. With advance of years the 
 appetite diminishes as a rule, and this is good, as the process of assimilation 
 also becomes enfeebled. While moderation in all things is good, it is difficult 
 to tell what are its hmits. 
 
 In some of my cardio-sclerotic patients the appetite has been maintained 
 with remarkable keenness. I have seen such patients becoming seriously 
 crippled through failure of the heart, with the nodal rhythm, very high 
 blood-pressure, and sweUing in the legs. I have endeavoured to restrain their 
 appetite and to restrict their diet, but have only succeeded in increasing their 
 weakness and making them miserable. With the resumption of their old 
 dietary I have seen them improve, and glide gently past the threescore years 
 and ten and well on to the fourscore years before they passed away with 
 little suffering. To the dyspeptic, asceticism may appear an ennobling 
 creed, but, as a practical physician doing my best for my patients, I think 
 I would rather see my patients passing the declining years in comfort, even 
 though their chief pleasures were those of the table, than having their lives 
 made tedious and uninteresting through depriving them of that which gives 
 them pleasure in the hope of adding a few months to their existence. 
 
 I must also add a warning to those who may imagine they can modify 
 changes in the heart and blood-vessels by the elimination of certain 
 constituents of food, as common salt. I have seen patients made neurotic 
 and apprehensive because a physician had warned them of the evils of 
 common salt, so that they were made conscious of their ailment at each 
 meal, and were filled with dread lest their food should contain salt. The 
 domestic comfort of a whole household may be jeopardized by having to 
 cook the food free from salt, and all the members are made to suffer because 
 of this foohsh restriction. This does not apply to patients seriously ill, 
 when, for the removal of dropsy, a special invahd dietary, salt-free, may 
 be tried. The same foohsh notion exists in regard to lime, the notion 
 being that hme salts can be removed from the tissues by decalcifying agents, 
 or prevented from being deposited by restricting the Hme contents of the 
 food. Calcium given by the mouth is absorbed very slowly and only to 
 
 MACKENZIE m
 
 274 DISEASES OF THE HEART 
 
 a slight extent, and is as rapidly excreted, while decalcifying agents like 
 citric acid have no appreciable effect. 
 
 § 245. The condition of the bowels — The condition of the bowels 
 should be attended to in every case. Constipation and straining at stool 
 may produce great exhaustion. In the less severe cases of heart affections 
 the habit of going regularly to the closet and patiently waiting wiU sometimes 
 be effectual. When the bowels are more stubborn, aperients are necessary. 
 The various mineral waters are beneficial, but where the expense is a con- 
 sideration simpler remedies can be usefuUy substituted, as a smaU quantity 
 of Epsom salts in a tumbler of hot water every morning, or a teaspoonful of 
 compound Hquorice powder in a tumbler of water at bedtime. A pill 
 containing | grain each of extract of belladonna, extract of nux vomica, and 
 aloin, taken three times a day, is in many cases extremely useful. In more 
 stubborn cases enemata may have to be resorted to — a pint of soap and 
 water given at night. 
 
 Treatment by purgatives is often helpful in cases where there is much 
 congestion of the Uver and abdominal stasis, and scanty flow of urine. A free 
 evacuation can be obtained by any of the purgatives, such as the coloc3mth 
 and hyoscyamus piU, calomel, or blue pills. After the free evacuation of the 
 bowels, they should be kept open by some milder aperient. 
 
 In all these cases care must be observed that the patient is not too greatly 
 exhausted by the movement of the bowels, for it is sometimes surprising how 
 prostrate some patients become after the bowels are moved. An enema 
 may prevent straining, but if the exhaustion is too extreme, the bowels had 
 better be left alone. 
 
 § 246. The mental factor — The consciousness of heart trouble has 
 often a depressing effect upon people, whether the trouble be shght or serious. 
 When such people become convinced that the trouble is curable or not serious, 
 their condition at once becomes greatly improved. Cures by faith, whether 
 in drugs, baths, elaborate methods, or religion, act by playing upon the 
 mental condition. I have already said that we should always study the 
 mental condition of the patient, and its bearing upon his complaint, and 
 we should utilize its peculiar features in treatment. But our employment of 
 this element in treatment should not be the outcome of blind unreasoning 
 faith in some rite or ceremony, bath or drug, but in the intelligent 
 perception of the nature of the symptom. The reassurance of the patient 
 of the harmless nature of the complaint goes a great way in curing him. 
 When there is some affection that cripples him, the reassurance that with 
 reasonable care no danger need be feared is extremely helpful. Even in 
 serious cases, when there is reasonable hope of recovery, or a certain
 
 TREATMENT 275 
 
 degree of recovery, the encouragement of the patient may and does help 
 forward his improvement. 
 
 This mental factor should, on the other hand, make us extremely chary 
 of giving the patient a gloomy prognosis. There is nothing in my ex- 
 perience so surprising as the manner in which the heart can recover from 
 the seemingly most hopeless condition of exhaustion. And we must bear in 
 mind that a gloomy view may in itself nullify the best attempts at treatment. 
 We should aim at getting the patient into a placid, contented, hopeful frame 
 of mind, so that the heart is not disturbed by emotional reflexes. 
 
 § 247. Drugs. — The influence of drugs upon the heart is one to which 
 I have given a good deal of attention, and I have carried out a long series 
 of observations with many of those most commonly employed in practice. 
 The subject is one that needs a great deal more elucidation, and I give here 
 the results of my observations so far. 
 
 Many drugs have a reputation for the good effect they have upon the 
 heart, but I found very little evidence of their beneficial action. An exception 
 to this, however, was found in the case of the digitalis group, but even here 
 the manner of action and the cases suitable for treatment have never been 
 clearly described, so that a great portion of my observations were devoted 
 to finding out how the drug acts and how it should be used. The results 
 obtained are so important that I give an outline of them in Chapter XXXIV, 
 with a fuller illustration of some particular instances in the Appendix (VI). 
 
 The class of drugs, apart from digitalis, that I found having a more or less 
 demonstrable effect upon the heart were the vaso-dilators. Every one 
 knows and appreciates the effect that the inhalation of the nitrite of amyl 
 has upon the peripheral circulation. But although its evidence is so demon- 
 strable, I am not at all sure how it acts beneficially upon the heart. The 
 most obvious explanation is not necessarily the true one. I have already 
 expressed my doubts as to the correctness of the explanation of its action 
 in angina pectoris (§ 58). The usual explanation is that there is an arterial 
 spasm which offers great resistance to the heart, and the amyl nitrite relieves 
 the spasm. There can be no doubt but that the rehef obtained by many 
 people during attacks of angina pectoris where there is high blood-pressure 
 by means of amyl nitrite or trinitrin, may be due to lowering of the blood- 
 pressure, but there are other cases in which the drugs give relief where 
 there is no arterial spasm, and if the arterial pressure be taken as the measure 
 of the spasm, it will be found that a few minutes after the effect of the amyl 
 nitrite has passed off the arterial pressure may be greatly raised. 
 
 The employment of other nitrites, as nitro-glycerine, to reduce per- 
 manently high arterial pressure, has been in my hands of very Uttle avail, 
 
 t2
 
 27& DISEASES OF THE HEART 
 
 though I have persevered with the drug for considerable periods. The 
 action of the nitrites is, as a rule, transient, and they seem to have little 
 lasting effect. I am now of opinion that in high pressures, with degenerated 
 arteries and a diminished capillary field, they are useless. Even if they 
 acted as permanent vaso-dilators, I doubt if their use would be justified 
 in cases of high arterial pressure. Besides, one often notices that when by 
 any means the high pressure is reduced, the patient is certainly no better, 
 but often weaker. 
 
 In cases of high arterial pressure, with a good deal of discomfort, as 
 pain and tightness across the chest, iodide of potassium has a great reputa- 
 tion, which has been justified in my experience. I have also used it with 
 seemingly good results in elderly patients with recurrent attacks of bronchitis. 
 At one time I thought it acted by lowering the pressure, but I found the good 
 results occur with no alteration in the pressure. I have not used the large 
 doses sometimes recommended, but 5 grains three or four times a day. 
 These doses rarely produce iodism. 
 
 I have been struck with the good effects of chloral in some of these cases 
 of high blood-pressure, given in small doses (5 grains) two or three times 
 a day, as well as in larger doses to induce sleep. Many of my patients who 
 suffered from severe attacks of angina pectoris found chloral gave them the 
 greatest relief, and some used to carry it when liable to these attacks. The 
 attacks did not come on with sudden violence, but gradually after exertion, 
 and the chloral often gave complete relief in about ten minutes. 
 
 The vaso-constrictors have been of little use in my hands. I have 
 repeatedly used adrenalin in cases of low arterial pressure, but it never pro- 
 duced any effect that led me to look upon it as of much value. A number of 
 drugs apart from the digitalis group have a reputation as ' cardiac tonics ', 
 but I could never find any evidence of their effect upon the heart, beyond 
 that indefinite beneficial tonic effect that follows the administration of such 
 drugs as quinine. The most popular remedy of this class is strychnine, or 
 some preparation of nux vomica. I have carefully sought for its special 
 i effect on the heart and found none. When I inquired into the evidence for 
 jits supposed good effect, I found that it was practically all clinical, and 
 clinical evidence endows the drug with the most diverse properties. It is 
 recommended as a cardiac stimulant in slow-acting hearts, and even in 
 heart-block it is said to quicken the beat. It is also recommended in the 
 too-excitable heart, as when there are extra-systoles, and in the rapid heart 
 of acute myocardial affections. It is said to be beneficial in cases of low 
 blood-pressure, and equally beneficial in cases of high tension, and even in 
 angina pectoris. The evidence that can show a drug to possess the property
 
 TREATMENT 
 
 277 
 
 of exciting the sluggish and of soothing the excited, of raising the low 
 pressure and reUeving the high, speaks more for unreasoning faith in the 
 drug than for the beneficial properties of the drug itself. 
 
 Since this was written, Professor W. E. Dixon 392, in an address before the 
 — ' ' ""' ■ " 'e British Medical Association, 
 
 e) are still employed on the 
 ^ased activity. The effect of 
 e doses it tends to depress 
 never excites. Strychnine 
 art ; by exciting the vaso- 
 )-motor activity indirectly, 
 jry with digitalis, lead, and 
 
 Inst placing trust in drugs to 
 nt. There is a very common 
 heart, not to the rest that it 
 thod employed. This is hke 
 who is restored by a plate of 
 '«soup is flavoured, 
 'n is invaded by some organism, 
 pe of effective treatment, but of 
 (leumatic affection of the heart, 
 ^ oy great benefit. These should, 
 ' 3 not used them frequently in 
 tiave seen such good results that 
 trial. He has kindly written out 
 employs in giving large doses of 
 
 N OF SODIUM SALICYLATE 
 
 ie and subacute rheumatism and of 
 te are often necessary. In spite of 
 jleasant symptoms, such as vomitmg, 
 ile to give large doses, if the following 
 
 cylate, twice as much Sodium Bicar- 
 
 -^■^^ given every two hours during the day 
 night : ten doses in twenty-four hours. 
 GREATEST PLEASURE symptoms are produced two ^J ^^ree dose^ 
 n XT T- H T7 \T7 T7 G T- the administration should be recommencea, 
 UN IHbVVEST one-half, or two-thirds of the previous dose.
 
 276 
 
 DISEASES OF THE HEART 
 
 though I have persevered with the drug for considerable periods. The 
 action of the nitrites is, as a rule, transient, and they seem to have little 
 lasting effect. I am now of opinion that in high pressures, with degenerated 
 arteries and a diminished capillary field, they are useless. Even if they 
 acted as permanent vaso-dil 
 
 in cases of high arterial pres^ 
 
 any means the high pressure 
 but often weaker. 
 
 In cases of high arteri 
 pain and tightness across t 
 
 VEXICE 
 
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 WESTERN AND FRANKLIN 
 AVE. LINE 
 
 Los Angeles — Via Sanborn, 
 Santa Monica Blvd., Western 
 and Franldin Ave., to Vine 
 St., HoUy^vood 
 
 LOS ANGELES ! 
 
 HOLLYWOOD 
 
 Hill St. 
 
 Station 
 
 Vine 
 
 Street 
 
 U 40 
 
 12 46 
 
 6 05 
 
 12 05 
 
 7 16 
 
 1 16 
 
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 11 16 
 
 5 16 
 
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 11 46 
 
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 12 16 
 
 6 16 
 
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 5 35 
 
 Connects with Brush Canyon Line. 
 All trains daily. 
 
 COLEGROVE, CRESCENT 
 
 JCT. AND SHERMAN 
 
 LINE 
 
 LOS ANGELES (Hill St. Sta- 
 tion) to Colegrove, Crescent 
 Jet. and Sherman 
 
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 SHERMAN, Crescent Jet. and 
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 litll 58 
 
 ♦4 II 
 
 t9 16 
 
 ♦7 41 
 
 ♦12 II 
 
 lit4 28 
 
 t9 36 
 
 llt7 58 
 
 lit 12 28 
 
 ♦4 41 
 
 t9 56 
 
 ♦8 11 
 
 ♦12 41 
 
 i:t4 58 
 
 tlO 16 
 
 HtS 28 
 
 lltl2 58 
 
 ♦5 11 
 
 tlO 36 
 
 ♦8 41 
 
 ♦1 II 
 
 llt5 28 
 
 tlO 56 
 
 HtS 58 
 
 Htl 28 
 
 ♦5 41 
 
 til 16 
 
 ♦9 11 
 
 ♦1 41 
 
 HtS 58 
 
 til 36 
 
 UtO 28 
 
 fitl 58 
 
 t6 16 
 
 ♦II 56 
 
 ♦9 41 
 
 ♦2 II 
 
 t6 36 
 
 
 Htn 58 
 
 llt2 28 
 
 ta 56 
 
 
 ♦10 11 
 
 
 
 
 
 ■jiXaioi^^as SxVoixvaoitK033V
 
 TREATMENT 277 
 
 of exciting the sluggish and of soothing the excited, of raising the low 
 pressure and reheving the high, speaks more for unreasoning faith in the 
 drug than for the beneficial properties of the drug itself. 
 
 Since this was written. Professor W. E. Dixon ^^^^ [^ an address before the 
 section of Pharmacology and Therapeutics of the British Medical Association, 
 said: 'Both these drugs (ether and strychnine) are still employed on the 
 supposition that they excite the heart to increased activity. The effect of 
 ether is to depress nerve-tissues ; in very large doses it tends to depress 
 muscle-tissue, including cardiac muscle, but it never excites. Strychnine 
 likewise has no direct stimulant action on the heart ; by exciting the vaso- 
 motor centre it may sUghtly increase the vaso-motor activity indirectly, 
 but it should never be put in the same category with digitahs, lead, and 
 other cardiac drugs.' 
 
 The reason I dwell upon this is to warn against placing trust in drugs to 
 the neglect of the essential requisite in treatment. There is a very common 
 tendency to attribute the improvement in the heart, not to the rest that it 
 has obtained, but to the special drug or method employed. This is hke 
 attributing the recovery of a famishing man who is restored by a plate of 
 nourishing soup to the garhc with which the soup is flavoured. 
 
 In acute febrile conditions, when the heart is invaded by some organism, 
 vaccine or serum therapy holds out some hope of effective treatment, but of 
 this I have had no experience. In acute rheumatic affection of the heart, 
 the use of the salicylates is often attended by great benefit. These should, 
 however, be pushed, and, though I have not used them frequently in 
 the manner recommended by Lees, yet I have seen such good results that 
 I think Lees's method should be given a trial. He has kindly written out 
 for me the directions and precautions he employs in giving large doses of 
 salicylate of soda : — 
 
 NOTE ON THE ADMINISTRATION OF SODIUM SALICYLATE 
 
 For the effective treatment of acute and subacute rheumatism and of 
 chorea, large doses of Sodium SaUcylate are often necessary. In spite of 
 the tendency of this drug to produce unpleasant symptoms, such as vomiting, 
 deafness, &c., it is almost always possible to give large doses, if the following 
 method of administration be adopted : — 
 
 (1) To every dose of Sodium Sahcylate, twice as much Sodium Bicar- 
 bonate must be added. 
 
 (2) The combined drugs must be given every two hours during the day 
 and every four hours during the night : ten doses in twenty-four hours. 
 
 (3) When any unpleasant symptoms are produced, two or three doses 
 should be omitted. Then the administration should be recommenced, 
 using smaller amounts ; one-half, or two-thirds of the previous dose,
 
 278 DISEASES OF THE HEART 
 
 according to circumstances, but given as before ten times daily. The 
 amount should then be increased as rapidly as possible. 
 
 (4) The initial dose may be 15 grains for an adult, 10 grains for a child 
 of 8-12 years, 5 grains for a younger child. This amounts to — 
 
 150 grains Sod. Sal. with 300 grains Sod. Bicarb, daily 
 
 lUU ,, ,, ,, ,, ^\J\j ,, ,, ,, ,, 
 
 "'-' )) 5 5 5 5 5 5 iUU ,, ,, ,, ,, 
 
 (5) The amount of these drugs should be increased every day, or every 
 second day, by 5 grains of Sod. Sal. and 10 grains of Sod. Bicarb, in each 
 dose, or daily 50 and 100 grains respectively. 
 
 (6) The administration should be temporarily suspended if vomiting, 
 deafness, tinnitus, or any tendency to delirium be produced. But the 
 period of suspension should be short — rarely more than 12 hours — often 
 a shorter period suffices if the amount given be reduced. 
 
 (7) The amount of Sodium Salicylate required in ordinary acute rheu- 
 matism is from 100 to 250 grains daily ; in chorea from 200 to 350 grains ; 
 in chronic subacute rheumatism the dose may require to be raised to 450 
 grains or even 500 grains. 
 
 (8) Children require nearly as large doses as adults, for in them the 
 rheumatic infection is specially virulent. 
 
 (9) Enough Sodium Bicarbonate must be employed to render the urine 
 alkaline. If this be secured, and constipation be prevented, the Salicylate 
 may be given freely without apprehension. But if a rheumatic child be 
 costive and too little bicarbonate be given, it is possible to bring about a 
 condition of poisoning by Salicylate — drowsiness, and deep breathing, in- 
 creasing to air hunger and coma, with acetonuria and the odour of acetone 
 in the breath. This is the real danger from Salicylate ; it may also be pro- 
 duced by aspirin. But it can always be avoided by attention to the direc- 
 tions given above. The existence of this danger should make the physician 
 watchful, but it should not lead him to deprive the patient of the great benefit 
 to be obtained from large doses of the drug. 
 
 § 248. Oxygen. — Although oxygen has been employed for many 
 years in affections of the heart and lungs, it must be confessed that its 
 employment has not been followed by the good results which were hoped 
 for. Every one who has used it to any extent in affections of the heart 
 has found it of distinct advantage in exceptional cases, but on the whole 
 the results have been disappointing. In a measure it may be that this 
 disappointment was due to two things, (1) that there are only certain cases 
 suitable for this oxygen treatment, (2) that it has not been given in sufficient 
 amount. 
 
 To take the second of these suggestions first, I was impressed with the 
 observations of Hill and Flack *°2, whose experimental work demonstrated 
 that oxygen relieved the strain on the athlete's heart, and that by the 
 somewhat open method usually employed there was not sufficient con- 
 centration of the oxygen inhaled. Thus Hill and Flack found that the
 
 TREATMENT 279 
 
 percentage of oxygen inhaled in the ordinary open method by a funnel 
 was 19-27 per cent, in the alveolar air, whereas by the method described 
 below there was over 70 per cent, of oxygen in the alveolar air. 
 
 In regard to the cases suitable for oxygen, slight temporary relief is 
 obtained by all cases that are more or less cyanotic. I had hoped, however, 
 that it would have proved useful in another class of case where the suffering 
 from breathlessness and pain is often very distressing, such as in cardio- 
 sclerosis with cardiac asthma, Cheyne-Stokes respiration, and angina pectoris. 
 In these cases I reasoned that the exhaustion of the heart muscle that 
 induced these distressing symptoms was due to deficient nourishment. 
 As, however, the tissues were bathed in the lymph which contained the 
 salts necessary for the nourishment of the heart, it might be the deficiency 
 of oxygen that was the main cause of exhaustion. I therefore employed 
 HiU's method of giving concentrated oxygen, and in the first few cases 
 I met with most gratifying success : patients who had suffered for months 
 from restless and disturbed nights due to dyspnoea and pain obtained 
 great and, in some cases, immediate relief. Further experience, however, 
 showed that apparently similar cases in which 'prima facie I would have 
 expected the same satisfactory results, little or no relief was obtained. 
 The matter therefore requires further consideration in order to recognize 
 more accurately the class of patient that should benefit by oxygen, and 
 I give here a short description of HiU's method, which I have used. 
 
 I have found that in attempting to give oxygen in a concentrated form, 
 a mask like a chloroform mask conveys to the patient a sense of suffocation. 
 HiU employs a mask of a very simple kind. A piece of light macintosh 
 cloth about two feet square is taken, and near one side a hole is cut in the 
 middle over which is glued a piece of transparent celluloid six inches square. 
 An elastic band is attached around this border of the macintosh, so narrow 
 that it will grasp the head lightly in such a position that the celluloid covers 
 the face while the remainder of the macintosh is lightly packed around the 
 neck. The oxygen direct from the cylinder is introduced by a tube through 
 a hole below the celluloid. The cool cmrent of oxygen is felt as refreshing, 
 and is greatly appreciated by the patient. I generally give a fair stream 
 of oxygen for 15-20 minutes — using in that time 10-12 feet of oxygen. 
 
 When this mask is not available (it can be had from Siebe, Gorman & Co., 
 187 Westminster Bridge Road, London) I have employed a lady's hat-box, 
 cutting out of the side a space for the patient's neck, so that the patient's 
 head goes comfortably into the box. I then put on the lid, and pass the 
 tube from the cylinder through a small hole in the side of the box. 
 
 This method of giving the oxygen is rather wasteful, and for economy
 
 280 DISEASES OF THE HEART 
 
 another method may be tried where the oxygen is given by means of a bag, 
 and the patient inspires and expires through a tube, where by a valvular 
 arrangement the expired air passes through a tin containing sticks of caustic 
 soda, which takes up the CO^ while the oxygen is led back to the bag to 
 be respired again. This apparatus is also made according to Hill's design 
 by Siebe, Gorman & Co. 
 
 Leonard Hill has also devised a simple apparatus by which a patient 
 can make a small quantity of oxygen and use it as desired. It consists 
 of a small metal box — the generator — connected with a vulcanized rubber 
 breathing-bag. The bag holds about 15 litres of gas, and ends in a mouth- 
 piece. The bottom of the generator is formed by a screw-lid fitted with 
 asbestos washer. A piece of wire gauze is interposed between the generator 
 and the bag. A screw-clip closes the mouth-piece during the generation 
 of the gas. The oxygen is generated out of oxylithe (NagOg) by contact 
 with water, and a solution of caustic soda results which is used to absorb 
 the exhaled carbonic acid. Na^Og + H^O = ^^aOH -I- Og. The oxylithe is 
 sold in flat tins containing ten blocks to the pound, and three blocks make 
 a charge sufficient for fifteen minutes' inhalation. 
 
 The bag is laid flat on the table and emptied of air. The oxyUthe is 
 then put into the generator, and water introduced into the bag through the 
 mouth-piece. The screw-clip is then closed, and the bag raised. Some 
 of the water then enters the generator, and the bag becomes fuU of oxygen. 
 The patient puts the mouth-piece into his mouth and a soft chp on his 
 nose, and, opening the screw-clip, breathes in and out of the bag, shaking 
 the solution round the bottom of the bag meanwhile to absorb the carbonic 
 acid exhaled. When about two-thirds of the bag of gas has been used up, 
 the instrument is washed out and hung up to dry.
 
 CHAPTER XXXIV 
 
 Treatment {continued) 
 
 § 249. The action of digitalis on the human heart. 
 
 250. Action on dilatation of the heart. 
 
 251. Action on rate and on the nodal rhythm. 
 
 252. Action on conductivity (heart-block). 
 
 253. Action on contractility. 
 
 254. Action on blood- pressure. 
 
 255. Digitalis in practice. 
 
 256. Other drugs of the digitalis group (strophanthus, squills, helleborein). 
 
 § 249. The action of digitalis on the human heart — In inquiring 
 into the therapeutic action of digitahs, I found that the result of clinical 
 experience was that digitalis was undoubtedly beneficial, but that it was 
 uncertain in its action, and that the various preparations varied much 
 in their potency. A wide divergence of opinion existed in regard to what 
 cases were suitable for its administration. 
 
 On starting this inquiry I was at first lost in confusion, unable to find 
 any sure line to follow. I systematically gathered a great number of cases 
 where I had given digitalis, and, on classifying the results obtained, certain 
 clear issues came out, which gave very definite lines for me to follow in 
 the subsequent investigation. A summary of these results I give here, 
 dealing somewhat fully with a few illustrative cases in Appendix VI. 
 
 In regard to the question of preparation, I limited myself to three different 
 forms — viz. B.P. Tincture of Digitalis, Nativelle's Digitalin Granules, and 
 the pills containing Digitalis, Squills, and Calomel (R. Digitalis pulv. gr. |, 
 Scillae pulv. gr. |, Hyd. subchlor. gr. 1). I did not extend my observations 
 to other forms, as it seemed better, with my limited field, to get a definite 
 result from these very diverse preparations, than to arrive at an indefinite 
 result with a multiplicity of preparations. The results of this investigation 
 showed that all three forms were equally potent in certain cases and equally 
 impotent in other cases. As a rule, when in one patient a certain definite 
 reaction was obtained by one preparation it was also obtained by the 
 exhibition of the others. I drew the conclusion that variability in the 
 action of the drug did not depend so much on the preparation as on the 
 nature of the lesion with which the heart was affected.
 
 282 DISEASES OF THE HEART 
 
 § 250. Action on dilatation of the heart. — ^When I came to inquire 
 into all the symptoms in these cases where digitalis had a beneficial action, 
 I found them limited to those in which there was dilatation of the heart- 
 But it was not equally effective in all cases of dilatation. In cases of 
 old-standing rheumatic affection with dilatation it was generally very 
 effective, and in many cases with no history of rheumatism ; while in 
 others of similar origin and with heart failure, but without dilatation (e.g. 
 mitral stenosis), digitalis had no beneficial effect. In fact, I failed to see any 
 evidences of a good result in any patient where the heart was not dilated. 
 
 The good results obtained by the use of digitalis are doubtless due to 
 the specific action of the drug on the function of tonicity. 
 
 In acute dilatation of the heart, as in febrile affections, I could never find 
 any improvement under it ; nor was there much benefit in cases of dilatation 
 secondary to advanced cardio-sclerosis. In a few cases some shght improve- 
 ment might take place, especially if there was dropsy — a slight increase in 
 the quantity of urine. But as a rule no appreciable benefit resulted. 
 
 § 251. Action on rate and on the nodal rhythm ^When the 
 
 rhythm was normal, i. e. when the ventricular contractions followed the 
 auricular, digitaUs did not often have much effect beyond slowing the rate 
 to a slight extent. In a few cases of dilated heart with frequent action, 
 due to old-standing rheumatic affection, the heart slowed under digitaUs, 
 but it never feU below the normal. In rapid hearts in febrile affections 
 it never had any influence, nor in the quick heart of exhausting disease, 
 as in tuberculosis, the reason probably being that a far more powerful 
 poison was already in the possession of the heart. 
 
 In cases of nodal rhythm the action of digitalis is sometimes Httle short 
 of miraculous. It is really to its action in these cases that the digitahs 
 group of remedies owe their great reputation. I have endeavoured to find 
 out in the literature of the subject the nature of the cases which have 
 led authors to eulogize digitalis, but I have found the greatest difficulty. 
 Most writers deal in such general terms that it is evident they have not 
 reahzed the nature of the heart's lesion in which they found digitaUs 
 effective. Where particulars have been given, I could infer with fair cer- 
 tainty that the cases were those of rheumatic hearts with the nodal rhythm. 
 
 In Figs. 152, 153, and 154 are given tracings which show the action very 
 typicaUy. In Fig. 152 the heart is irregular in its action, 80 beats per 
 minute. The jugular pulse is of the ventricular form (nodal rhythm), 
 and is typical of the condition so common in advanced rheumatic hearts. 
 The heart was dilated ; there was a systolic and long diastolic murmur at 
 the apex (see shading under Fig. 153), the urine was scanty, and there was
 
 TREATMENT 
 
 283 
 
 much dropsy. The patient was put upon the digitalis, squills, and calomel 
 pill three times a day. In ten days' time the heart became much slower, 
 and took on the rhythm shown in Figs. 153 and 154, The curious doubling 
 
 J ^ i UJ 1 i £ / 
 
 lAA^XAiLM M An 
 
 
 
 Fig. 152. Tracings from an old rheumatic case witli the nodal rhythm, showing the charac- 
 teristic irregularity and ventricular venous pulse. At the post-mortem examination there was 
 both mitral and tricuspid stenosis. Before digitalis. (Figs. 153 and 154 are from the same 
 patient.) 
 
 Fig. 153. Shows the characteristic effect of digitalis in old rheumatic hearts with the nodal 
 rhythm. The figures 1, 2, represent the first and second sounds of the heart, and the shading 
 represents the murmurs present. 
 
 Fig, 154. Shows a digitaUs effect with coupled beats and slow single beats, 
 
 of the beat shown in these tracings is a very common result of digitaHs in 
 this class of case. With the slowing of the pulse the patient's condition 
 improved ; the urine became more abundant, and the dropsy to a great 
 extent disappeared.
 
 284 
 
 DISEASES OF THE HEART 
 
 The curious coupling of the beats in Fig. 153 requires consideration as 
 a matter of practical importance and scientific interest. If cases were 
 judged by the pulse alone the nature of the change would be entirely lost. 
 
 Fig. 155. Tracings of the radial and liver pulses before administration of digitalis from 
 an old rheumatic heart, with great dilatation, and where the mitral valves were shrunken at 
 the post-mortem examination. Figs. 153 and 154 were taken from the patient after the 
 administration of digitalis. 
 
 Thus, Fig. 155 is from a patient with great dilatation of the heart and 
 mitral incompetence — the valves damaged by an old rheumatic affection 
 of the heart. Under digitalis the heart became slow, the radial pulse 
 
 Fig. 156. Tracing of the radial pulse (28 per m.) after digitalis. The real nature of the 
 
 slowing is shown in Fig. 157. 
 
 being at the rate of 28 per minute (Fig. 156). Tracing Fig. 157, taken 
 simultaneously from the apex and liver, showed that both ventricles con- 
 tracted together, the apex giving the characteristic cardiogram of the left 
 
 Fig. 157. Simultaneous tracings of the liver pulse and apex beat, showing complete 
 harmony in the rhythm of both ventricles, Tlie sounds and murmurs present are diagram- 
 ma tically represented. After digitalis. 
 
 ventricle, while the liver pulse was produced by the right ventricle. The 
 curious coupling of the beats is shown here, and the slow radial pulse (Fig. 156) 
 is seen to be due to the fact that the smaller beats did not reach the radial.
 
 TREATMENT 
 
 285 
 
 The same features are brought out in the tracings from another patient. 
 Fig. 158 shows the jugular and radial pulses when the patient was not 
 under the influence of digitalis. Figs. 159 and 160 show the action of the 
 
 Fig. 158. Simultaneous tracings of the jugular and radial pulses. The jugular pulse is of 
 the ventricular type, and the tracing shows complete agreement in rhythm between the right 
 and left ventricles. From an old rheumatic heart, in which, at the post-mortem examination, 
 there was found great stenosis of the mitral orifice. Before digitalis. Figs. 159 and 160 are 
 from the same patient. 
 
 heart due to digitaUs, In these tracings, the one of the apex and radial and 
 the other of the liver and radial, the characteristic coupling of the beats seen 
 in the apex and liver is not observed in the radial because the smaller 
 
 Fig. 159. Simultaneous tracings of the apex beat and of the radial pulse from a case of 
 mitral stenosis. The coupled beats are well marked in the apex tracing. The shading under- 
 neath shows the time of the murmurs. After digitalis. 
 
 beats did not affect the radial pulse. In this case there was a long diastoUc 
 murmur, as shown by the shading, and the post-mortem examination showed 
 extreme stenosis of the mitral orifice. 
 
 Fig. 160. The coupled beats are well marked in the liver 
 tracing. After digitalis. 
 
 I have a large collection of tracings showing the same results, and every 
 one of them came from patients with the nodal rhythm, and with a past 
 history of rheumatism. The practical importance of this reaction lies in the 
 fact that the appearance of these coupled beats is at once the signal to lessen
 
 286 DISEASES OF THE HEART 
 
 the dose of digitalis. No good is to be obtained by pushing it further, 
 and when one can just manage to keep the patient at the stage where 
 this tendency occurs the best results from digitaUs will be obtained — the 
 patient feels easier, makes more urine, and the dropsy is kept under 
 control. 
 
 The scientific interest lies in the fact that no other form of heart ailment 
 produces this reaction. It has never been produced experimentally, and 
 cannot occur while the auricles are active and occupying their normal 
 place in the cardiac cycle ; in other words, it is a reaction limited to patients 
 with the nodal rhythm. I have thought much on the nature of this rhythm, 
 but my conclusions are of too speculative a nature to be of any real value. 
 I wish, however, to point out that the second of the linked beats are not 
 extra-systoles. In § 141 I defined an extra-systole as the premature occur- 
 rence of an auricular or ventricular systole while the fundamental or sinus 
 rhythm of the heart was maintained — the retention of that rhythm 
 accounting for the character of the irregularity. Here there is no sinus or 
 fundamental rhythm, and as a consequence the pauses between the beats 
 are continuously liable to variation. 
 
 In cases with the auricles active, the production of extra-systoles by 
 digitalis does occur in a small proportion of cases, but usually only after 
 the drug has been pushed rather far. In Case 25, Appendix VI, this 
 coupling of the beats occurred while the patient had the nodal rhythm. 
 After a time the normal rhythm was restored, and when digitalis was 
 pushed extra-systoles occurred, but the whole character of the heart's 
 action was very different, as a study of the tracings given from this case 
 wiU show. This coupUng of the beats has been noticed by other observers. 
 Thus Broadbent ^ describes the coupled beats as a result of digitalis, but he 
 and others have failed to appreciate the class of case in which it occurred, 
 and did not reaUze it was a reaction peculiar to this kind of heart. 
 
 The manner in which the heart-rate can be played upon by digitalis in 
 these cases of nodal rhythm is very remarkable. I have frequently seen the 
 heart increase in frequency, sometimes very greatly (up to 120-130 beats 
 per minute) when the digitalis was withheld, and in the course of a few 
 days digitalis often soon slowed it down to between 60 and 70 beats per 
 minute. (See Case 25, Appendix VI.) 
 
 But the effect is not only upon the rate of the heart : the size of the 
 heart diminishes, the urine increases, and the dropsy disappears. If there 
 be much liver enlargement, the digitalis at the same time diminishes the 
 size. Fig. 66, p. 127, was taken from a pulsating liver at the level of the 
 umbilicus. The patient was at the time extremely breathless, and had to
 
 TREATMENT 287 . 
 
 be propped up in bed. Tincture digitalis, 15 Q) three times a day, was 
 prescribed, and in three days' time he was up and about, and no sign of 
 the liver could be detected below the ribs. 
 
 I am convinced that it is the striking effect of digitaUs in these cases 
 that has led cUnicians to form such a high opinion of this drug. FaiUng 
 to recognize that the action depended on the nature of the lesion, they have 
 sought to find a similar benefit in cases not so susceptible to it, and from 
 this have arisen the confusion and contradictory statements in regard to. 
 the action of digitalis. 
 
 No such reaction as that shown in Figs. 152-160 can be obtained, unless 
 where the nodal rhythm is present. And even amongst cases of nodal 
 rhythm a further differentiation has to be made, for I never get this result 
 in cases of nodal rhythm secondary to cardio-sclerosis associated with 
 arterial degeneration. In these cases I have sometimes seen a little im- 
 provement — an increase in the flow of urine and a diminution of the dropsy, 
 and it may be a slight slowing of the heart's rate — but never anything 
 approaching the slowing in old rheumatic cases. In many cases, though 
 I have pushed the drug till the patient was sick and had diarrhoea, I have 
 seen no alteration in the heart's condition. This difference is probably due 
 to the greater extent of the degeneration of the heart muscle. 
 
 § 252. Action on conductivity (heart-block) — In a great many 
 cases I have been able to produce a mild form of heart-block by the adminis- 
 tration of digitaHs, and I can now recognize the class of case in which this 
 occurs. I have already pointed out that the interval between the auricular 
 systole and the ventricular can be determined by the length of the a-c 
 interval in tracings from the jugular pulse (§ 163). If this interval be 
 above one-fifth of a second (unless in a very slow heart) it is due to a depres- 
 sion of the function of conductivity of the a. -v. bundle. When the heart's 
 action is over 100, with the interval one-fifth of a second, a depression of 
 conductivity may be suspected. By the administration of digitaHs in 
 a great number of my patients I have been able to increase this depression 
 of conductivity, so that ventricular systoles have dropped out because the 
 stimulus from the auricle did not reach the ventricle. 
 
 In Fig. 161 there is a wide a-c interval (two-fifths of a second). I gave 
 the patient from whom this tracing was taken three drachms of tincture 
 of digitalis in the course of four days, and her pulse became irregular, due to 
 the dropping out of ventricular systoles (Fig. 162). Some years previously 
 I had produced a similar effect in this patient by digitaHs, when every 
 second ventricular systole dropped out (Fig. 163). 
 
 When digitalis is prescribed for a patient with a regular pulse and the
 
 288 
 
 DISEASES OF THE HEART 
 
 heart becomes irregular, it is probably due to this cause. The nature of 
 the irregularity can be inferred with fair certainty by auscultation when 
 the heart sounds are found to be absent during the pause. Extra-systoles 
 sometimes follow the administration of digitalis, and the irregularity of the 
 pulse may resemble the dropping out of beats due to heart-block, but with 
 
 Ro^d'\a\ 
 
 Fig. 161. The a-c interval is twice the normal period (two-fifths of a second in place of 
 one-fifth), indicating a delay in the stimulus passing from the auricle to the ventricle. (This 
 and the next two tracings are from a female, aged 24 years, suffering from mitral stenosis.) 
 
 extra-systoles the short, sharp sounds of the heart during the pause in the 
 radial pulse will usually be detected (Fig. 87). In many cases where there 
 is dilatation of the heart, as soon as the irregularity appears the patient 
 experiences a good deal of relief, though sometimes the throb after the 
 pause is distressing. (See also Cases 26 and 27, Appendix VI.) 
 
 Fig. 162 shows the missing of a ventricular systole at frequent intervals on account of the 
 delay in the stimulus passing from the auricle. It will be noticed that the wave a is perfectly 
 regular in its appearance, and that its relationship to the carotid and radial is variable 
 (digitalis effect). Note the gradual increase of the size of the auricular wave, a, before the 
 intermission. Tliis is due to the gradual increase in the width of the a-c interval until the 
 auricular contraction occurs before the preceding ventricular systole is completed (see also 
 Fig. 114). 
 
 In most of the cases in which I have been able to produce this condition 
 of mild heart-block there has been a previous history of rheumatic fever. 
 
 § 253. Action on contractility If tracings be taken systematically 
 
 of patients under the influence of digitalis, evidence of a depression of 
 contractility may occasionally be detected in the form of the pulsus
 
 TREATMENT 
 
 289 
 
 alternans. It is generally so slight as to escape detection unless a tracing 
 be taken. 
 
 In Figs. 164 and 166 are tracings of the pulsus alternans, due in the one 
 
 Fig. 163. Slowing of the pulse due to digitalis depressing the conductivity, so that the 
 ventricle responds only to every second stimulus. Wliile the ventricle contracted forty-eight 
 times per minute the auricle contracted ninety-six times. 
 
 case to digitalis, squiU, and calomel piU, and in the other to the tincture 
 of digitalis. Curiously enough, the appearance of this change in the rhythm 
 of the pulse was accompanied by an improvement in the patient's con- 
 
 FiG. 164.' Typical pulsus alternans due to digitalis. (Case 9, Appendix 11.) 
 
 dition. The reason for the improved condition when the conductivity of 
 the a.-v. bundle and the contractihty of the heart muscle was depressed, 
 is in all probabihty a coincident improvement in the tonicity. This view 
 
 Fig. 165. Taken at the same visit as 164, and from the same patient, to show that the 
 conductivity was not affected — the a-c interval being normal (one-fifth of a second). 
 
 is confirmed by some observations Gossage has shown me. That the function 
 of conductivity was unaffected in these two cases is shown by the normal 
 a-c interval in the jugular tracings (Figs. 165 and 167). 
 
 § 254. Action on blood-pressure — Contrary to expectation, I found 
 that it is only in exceptional cases that the administration of digitalis 
 
 Mackenzie: 
 
 U
 
 290 
 
 DISEASES OF THE HEART 
 
 raises the blood-pressure. I have repeatedly pushed it until distinct evidence 
 of its physiological action was produced on the stomach or on the heart, 
 without any apparent rise in the blood-pressure. Even when the patient 
 was greatly benefited by the drug, I have frequently seen httle or no evidence 
 of an increase in the blood-pressure. The only cases where I did find 
 increase in the blood-pressure were in extreme dilatation of the heart with 
 
 mummimmmmmmmmmmmmmmmfmmm^i;si^i^^r^ 
 
 Fig. 166. Typical pulsus alternans due to digitalis. 
 
 considerable dropsy. In these cases a slight rise in the blood-pressure 
 accompanies the improved condition under digitalis. 
 
 § 255. Digitalis in practice — In the following summary of the con- 
 ditions in which digitalis wiU be found to act beneficially it may seem that 
 its field of usefulness is far too restricted. While I do not think so, I wish 
 to insist upon the limitations of its usefulness for a very important reason, 
 
 Fig. 167. Taken at the same visit as 166, and from the same patient, to show 
 there was no affection of the conductivity, the a-c interval being normal. 
 
 namely, because the reliance placed upon this drug has led to the belief 
 that it should be tried in all forms of heart affection, with the result that 
 valuable time which should have been spent in putting the heart under 
 favourable conditions has been wasted. 
 
 The condition of heart failure where it acts best is where there is dilata- 
 tion of the heart with healthy muscle-fibres that have been exhausted in 
 the endeavour to overcome abnormal resistance. This effect is best seen 
 in old rheumatic affections of the heart, but it may also be observed in 
 other cases with a fair amount of healthy muscle. It is of very little use
 
 TREATMENT 291 
 
 when the dilatation of the heart is due to extensive degeneration of the 
 muscle-fibres, as in cardio-sclerosis. In a sense the degree of reaction gives 
 a measure of the extent of the degeneration — the greater the extent of the 
 degeneration the less the reaction. It will be found to be of little value 
 when the heart is already in the grip of some poison, whether it be the 
 specific organism of such disease as rheumatic fever, pneumonia, or the 
 toxins of such diseases, or such poisons as alcohol and arsenic. 
 
 This conclusion, drawn from the careful study of individual patients, is 
 in striking accordance with the conclusions drawTi by Cushny ^* from experi- 
 ment : ' In cases of dilatation of the heart with a weak and insufficient 
 systole its action is almost specific. This is true whether one or both 
 ventricular chambers are affected, so long as the cardiac muscle has not 
 undergone degeneration.' 
 
 When the heart becomes continuously irregular (nodal rhythm) in old 
 rheumatic cases, digitalis usually acts with great promptness and certainty. 
 In these cases the administration should be kept up for considerable periods, 
 just sufficient of the drug being given to keep the rate between 60 and 
 70 beats per minute, or until the characteristic coupled beats appear. Some- 
 times good results are obtained when the rate cannot be reduced so low. 
 Under such circumstances the condition of the patient in other respects 
 should be the guide, the dose being modified according to the degree of 
 improvement. 
 
 In cases of nodal rhythm due to other conditions the heart is not so 
 susceptible, and great caution should be exercised in the prescription of 
 digitaHs here. Occasionally we read of precautions in the use of digitalis, 
 and of its tendency to cause a fatal stoppage of the heart, but I have been 
 unable to determine the form of heart disease in which these sudden deaths 
 are liable to occur. The only cases of sudden death I have seen during 
 the administration of digitalis were unyielding cases of nodal rhythm. In 
 one patient with cardio-sclerosis I was carefully pushing it, when the 
 patient died suddenly in the night. In another case of rheumatic origin, 
 digitalis had little effect, and the patient had taken only an occasional 
 dose when she died suddenly while dressing one morning. But I am not 
 clear in my mind that the digitalis had any part in the sudden end of these 
 cases, and there was no preliminary slowing of the heart's action. 
 
 § 256. Other drugs of the digitalis group (strophanthus, squills, 
 helleborein) — I have used other drugs of this group (strophanthus, squills, 
 heUeborein), but only to a limited extent. So far as my observations 
 extended, I found that if digitalis failed to act they also failed. I tried 
 strophanthus on several cases that were susceptible to digitahs and got 
 
 U 2
 
 292 DISEASES OF THE HEART 
 
 the same reaction, but only after a much longer time. This result was in 
 striking agreement with the experience of a very intelligent man whom 
 I saw in consultation. He had had rheumatic fever, and his heart had 
 acquired the nodal rhythm. For many years he had been hable to fre- 
 quent breakdowns, but could pull himself together with digitalis, and 
 he always knew the exact quantity to take. He told me he had tried 
 strophanthus, but that, while it restored him, it took a much longer time 
 to do so than digitaHs. 
 
 Some observers have found that cases have responded to strophanthus 
 after digitahs had bi^en tried and been found ineffective. We must be on 
 our guard against the conclusion drawn from such an observation, for it 
 is possible that the digitahs had in a measure prepared the way for the 
 strophanthus, for it often happens that no effect is obtained from the 
 digitahs until it has been pushed for some time.
 
 CHAPTER XXXV 
 
 Treatment (continued) 
 
 § 257. 
 
 Venesection. 
 
 258. 
 
 Exercises. 
 
 259. 
 
 Massage. 
 
 260. 
 
 Special movements and exercises. 
 
 261. 
 
 Baths. 
 
 262. 
 
 Spa treatment. 
 
 263. 
 
 Nauheim baths. 
 
 264. 
 
 Cause of efficacy of the spa treatment. 
 
 There are a great number of other methods that are useful in relieving 
 the patient or in assisting in restoring the reserve force of the heart, and 
 I deal here with the most important of them. 
 
 § 257. Venesection — In a number of cases the abstraction of blood 
 from the patient affords very considerable relief. Unfortunately the rehef 
 is only temporary, and in extreme cases only delays the end. Although 
 I have practised venesection in a great variety of cases, I cannot say 
 I have seen it do any lasting good. The indications for its use that have 
 been my guide have been distress in breathing, on account of great distension 
 of the right heart. In cases of mitral disease this has generally been recog- 
 nized by the increase of the heart's dullness to the right. In cases of high 
 blood-pressure (cardio-sclerosis) it has sometimes been difficult to detect 
 much enlargement of the right heart, and the tense filHng of the veins of the 
 arm has been the indication. I have always bled at the usual place — at the 
 bend of the elbow — and abstracted from twenty to thirty ounces of blood. 
 The immediate relief given to the patient is often very striking. 
 
 § 258. Exercises — The heart, like every other organ, becomes more 
 efficient with reasonable exercise of its functions, while with a too limited 
 exercise the store of reserve force gradually dwindles, so that most people 
 who pursue sedentary occupations have a Limited field of cardiac response. 
 When such people exhibit some cardiac abnormality, such as an irregularity, 
 a murmur, or a fainting attack, the easily exhausted store of reserve force 
 shown by the shortness of breath and palpitation on exertion is too often 
 taken as an evidence of serious affection of the heart. Tliis is more
 
 294 DISEASES OF THE HEART 
 
 particularly the case in the young with sinus arrhythmia (youthful form 
 of irregularity) and in chlorotic females. Improvement in all these cases is 
 best obtained by the gradual increase in the daily amount of bodily exercise. 
 In the great majority of cases of serious heart-failure, even after recovery 
 has set in, the judicious employment of muscular exertion is beneficial. It 
 may be a matter of difficulty to determine whether more serious cases are 
 fit for exertion, and if so to what extent. There is a very simple rule that 
 I have been accustomed to follow for many years with the greatest satis- 
 faction : let the patient employ that form of muscular exercise which he 
 can best do without cardiac discomfort, and never indulge in it after the 
 first sign of discomfort. By discomfort I mean the various signs which are 
 given by the heart when its reserve force is exhausted — as breathlessness, 
 palpitation, sense of exhaustion, pain. Discomfort may be experienced 
 first in the muscles exercised, when some particular group of muscles is 
 more particularly employed, as certain thigh muscles in climbing, and certain 
 arm muscles in plajdng golf — indications more of want of training of these 
 muscles than of heart exhaustion. This form of discomfort need not prevent 
 further exercise. 
 
 If the rule, that exercise should stop short of exhaustion, be followed, 
 it is surprising what an amount of effort can ultimately be endured by 
 patients who may once have suffered from extreme heart failure. This 
 will be appreciated by those who practise among the classes employed in 
 hard manual labour. They may have continually irregular hearts (nodal 
 rhythm), with aortic and mitral murmurs, and may have suffered at times 
 from the most extreme failure of the heart with extensive dropsy, yet they 
 can undertake the most severe form of manual labour with no discomfort. 
 In such cases the heart muscle is healthy and capable of acquiring a con- 
 siderable store of reserve, and it is from observing such patients that I base 
 the prognosis of heart cases so much on the power of the heart to regain 
 its reserve force. 
 
 AVlien patients can go out, their exercise should be in the open air, even 
 though it is limited to certain gymnastic movements. If they can walk 
 quietly, that in itself may be sufficient, and if the walk be taken system- 
 atically a great amount of reserve force may ultimately be acquired. As 
 a rule, people benefit more by exercise when it has an object beyond the 
 medical needs. Hence the added interest of a game or the study of objects 
 of interest, as architecture, botany, &c., will add materially to the efficiency 
 of the exercise. The particular taste of each patient has therefore to be 
 studied, and the form of exercise prescribed that is likely to combine the 
 therapeutic with personal interest.
 
 TREATMENT 295 
 
 When patients are confined to the house, or to bed, moderate 
 exercise of the muscles proves useful, so long as it does not embarrass 
 the heart. To this end the various movements and gymnastics may be 
 of use. 
 
 The good results of exercise are obtained by a variety of obscure pro- 
 cesses. The increased functional activity of the heart assists in accelerating 
 its own circulation and in restoring its strength, but there are also changes 
 in the circulation of the muscles exercised which lead to a freer flow of blood 
 through the system. The contraction of a muscle expels blood from its 
 capillaries, and is at once followed by a dilatation of the capillaries. This is 
 well seen when the hand and arm are placed in a plethysmograph, and the 
 variation in their bulk registered. After a single closing of the fist, the bulk 
 of the arm at once increases from the dilatation of the capillaries of the used 
 muscles. 
 
 § 259. Massage — A benefit similar to that of exercise can, in a 
 measure, be attained by massage. It is not necessary that a skilled 
 person should apply it, for that would exclude its use among the majority 
 of sufferers. The gentle but firm intermittent pressure upon the muscles 
 in the body is quite sufficient. In dropsical cases the gentle but firm 
 massage of the legs may prevent the dropsy reaching the extreme degree 
 where the skin becomes thin and glistening and liable at any moment to 
 ulcerate. In some extreme forms of the condition I have referred to as 
 the X disease, when there is a persistent contraction of the smaller blood- 
 vessels of the extremities, massage has been attended with benefit. 
 
 § 260. Special movements and exercises There is a number of 
 
 methods employed involving muscular exercises that have gained con- 
 siderable repute. Such methods may have a limited usefulness when 
 patients cannot take natural exercise. Their chief recommendation seems 
 to be in reheving the tedium of convalescence, and in giving mental 
 satisfaction to the patient that something is being done. I have made 
 a careful inquiry into the effects of passive resistance movements and 
 voluntary contractions of the muscles, and could find no appreciable effect 
 upon the heart. In certain people, especially those of a slightly neurotic 
 habit, the slowing of the pulse at the end of the seance was sometimes 
 very marked, but I found I could produce exactly the same result by 
 employing, with equal solemnity, indifferent acts, such as stroking the 
 finger nails and the shin bones. No effect was produced on hearts acting 
 at a frequent rate in consequence of serious heart failure or the nodal 
 rhythm. On no occasion could I detect any decrease in the size of the 
 heart as a result of the movements. That certain hearts may become
 
 296 DISEASES OF THE HEART 
 
 slow and diminish in size after a month's restful treatment every one will 
 acknowledge, but it is assuming too much to say that such results were 
 due to the special method employed. 
 
 § 261. Baths. — A very powerful influence can be exercised on the 
 circulation by the immersion of the body in water ; this may act in several 
 ways, perhaps mainly depending on the temperature. Great thera- 
 peutic efficacy is claimed for certain waters, but it is very doubtful if the 
 ingredients in these waters have any effect upon the heart, beyond their 
 effect in stimulating the skin. My personal experience has been limited 
 to observing the results in patients who have returned from the various 
 spas, and I have seen nothing of their good effects to lead me to place 
 hydrotherapy very high as a means of treating affections of the heart. The 
 best results I have seen have been in patients who have bathed in the open 
 sea. When I have had patients with heart trouble who were fond of sea- 
 bathing, I have allowed them to indulge in it, warning them to be honest 
 with themselves, and refrain if it brought on any sense of discomfort. In 
 many cases the result has been extremely satisfactory, the whole system of 
 the patients has been braced up, and they have returned from the hoHday 
 greatly benefited. 
 
 § 262. Spa treatment — Sea-bathing has, after all, only a limited 
 sphere of usefulness, and many patients obtain great benefits from visiting 
 spas, and the supporters of each claim for its waters some special virtue. 
 In order to assess the value of these claims, it is well to bear in mind by 
 what process benefit is obtained at the various spas. The vast majority of 
 patients go there as much for a hohday as for treatment, and when a patient 
 is sent there, it is often because the individual, in addition to his complaint, 
 has been busy with his affairs, and his heart complaint has been thereby 
 aggravated ; or a patient is convalescent, and a change of air, scene, and 
 mode of fife is often found beneficial. As the various spas cater for the more 
 enjoyable side of existence, they attract large numbers of invahds who 
 naturally desire the reputed benefits of the waters, and drink them enthu- 
 siastically, or, if they cannot drink them, at the least bathe in them. 
 It will thus be seen that the benefits gained at such places arise from 
 a variety of sources, and it is but human nature to attribute what benefit 
 has accrued to the factors that most appeal to the imagination, such as 
 hot gaseous waters from the bowels of the earth. Every practitioner of 
 experience wiU agree with me that a large proportion of heart cases return 
 from their holiday greatly improved, and this improvement is not limited 
 to those who went to some particular spa, but includes aU sorts of places — 
 spas, seaside and mountain resorts, sailing on sea and lake. It is evident
 
 TREATMENT 297 
 
 that results thus obtained cannot be due to the peculiar constituents or 
 the waters of any single place. 
 
 § 263. The Nauheim baths — When I began to write this book the 
 purpose was to give a faithful account of my own experience. It was no 
 part of my project to enter into controversial matters, and in matters of 
 dispute I have simply expressed my own views. But I feel it would be 
 misleading if I passed in silence a method of treatment that has obtained 
 s, world-wide reputation which I consider out of proportion to its merits. 
 Though I enter into this matter reluctantly, I conceive it none the less a duty 
 to give my views on it, particularly as I am impressed with the injury done 
 to individual patients through the unmerited reputation of the Nauheim 
 baths among the medical profession. Institutes have been started for the 
 financial exploitation of the Nauheim waters, and I must confess to a feeling 
 of shame for my profession, when I consider the manner in which it has been 
 imposed upon. One reads in sober Enghsh medical journals accounts of 
 cures effected that seem like the puffs of an empiric remedy. One writer 
 will teU how a patient obtained no benefit from his treatment, but was cured 
 by a visit to Nauheim. Another describes how he watched the patients 
 enter into the bath-room feeble, tottering, and Hvid, and how they came 
 out upright and brisk, with a glow of health on their countenances. It is 
 little wonder that the stay-at-home practitioner is impressed by all this 
 dithyrambic praise. The following painful experience resulted directly 
 from this indiscriminate exaltation of the virtues of the Nauheim waters. 
 I saw a man in consultation whose history was this : He was seized 
 with symptoms of heart failure, and not improving as he liked, his 
 doctor advised him to go to Nauheim. An eminent physician was con- 
 sulted later who also strongly recommended Nauheim. Visiting another 
 part of the country, he was taken iU, and the doctor who saw him there 
 also told him to go to Nauheim. He was so impressed with the advice given 
 independently by three doctors, that he made up his mind to follow it and go 
 to Nauheim. His circumstances were such that he had to stop all his pro- 
 fessional work and to expend a sum of money that he could ill afford. He 
 was only able to travel to Nauheim by easy stages, and took three days on 
 the journey, arriving there spent and exhausted. He was put through the 
 routine treatment of the baths, and had digitahs prescribed in addition. 
 He returned to England worse than when he set out, though bearing with 
 him a letter from the Nauheim physician saying that he had greatly improved 
 by his visit. The patient himself shrewdly remarked that, seeing that 
 he arrived there dead beat from his journey, it would have been surprising 
 if he had not picked up a httle by the rest, but as to his condition he had
 
 298 DISEASES OF THE HEART 
 
 gained no benefit, but the reverse, from his trip. When I saw him after his 
 return, his was an undoubted case of advanced cardio-sclerosis, with extreme 
 exhaustion of the heart muscle. The organic changes were irremediable, 
 but the exertion of going to and from Nauheim had injuriously exhausted 
 the heart, and no doubt hastened the end of the patient, in addition to 
 exhausting his financial resources, for which those dependent on him had 
 to suffer. 
 
 This is b}' no means an exceptional instance, and one physician of 
 experience tells me that every year he is called upon to treat a number of 
 the ' Nauheim wrecks ', as he calls them, on their return. But I do not wish 
 to seem to condemn a method without reason, and shall briefly recount my 
 experiences in an attempt to appreciate the curative virtues of the Nauheim 
 methods. 
 
 On arriving at Nauheim and interviewing several doctors as to how the 
 efficacy of the cure was to be investigated, I discovered that in serious cases 
 no practising physician believed the waters to possess sufficient curative 
 properties, but that accessory means had to be taken if a good result was 
 to be obtained. Nor could I find among those practising there any agree- 
 ment in regard to what was the best accessory means. One said the waters 
 were good when assisted by the additional movements attained by the 
 machinery of the Zander Institute ; another derided the use of the Zander 
 machinery, and said the best effects were obtained from the baths combined 
 with his specially invented method of exercise ; while a third said the methods 
 of the other two were of little avail, and that the best results were obtained 
 when to the baths something extra was added — such as an electric current. 
 When all these methods and baths were of little avail, every doctor prescribed 
 in addition drugs of the digitalis group. It was hopeless for me to attempt 
 to find out the efficacy of any given bath or method when such complications 
 were introduced, so I did what httle I could to understand the influence of 
 the baths. 
 
 I found that ten to twenty years ago, when the notion was prevalent 
 that to have a good heart you must have a strong pulse, these baths had 
 a remarkable effect in strengthening the pulse, raising the arterial pressure 
 20, 30, and 40 mm. Hg. But now^adays the fashion being to soften a strong 
 pulse, these waters are discovered to have a remarkable effect in lowering 
 the arterial pressure. So remarkable are these waters that it is claimed 
 that they can increase the pressure when it is low, and lower the pressure 
 when it is high. 
 
 I found that these baths were so modified as to be of different strengths, 
 and it was stated that the different baths were given according to the nature
 
 TREATMENT 299 
 
 of the complaint. But I could find no evidence of any rule being followed. 
 I found that people with nothing the matter with their hearts were having 
 the same baths as those who were suffering from severe heart affection. 
 I also found patients with a weak frequent pulse having the same baths as 
 others with a slow hard pulse. 
 
 I saw nothing which, by the greatest stretch of imagination, could confirm 
 the statement that patients are to be seen entering these baths bent and ill 
 and coming out of them straight and strong. In the patients I watched in 
 the baths, I could discover no improvement from the single immersion. 
 Certain effects on the heart, such as slowing of its action, did occur in several 
 cases, notably in healthy hearts, as in my own case and in that of a friend 
 whom I watched. This was in the strong sprudel bath, when the tem- 
 perature of the water was 89° F. But it seemed to me merely a temperature 
 effect, and this was confirmed by the fact that when I returned home I found 
 my pulse-rate and that of my friend slowed in exactly the same manner 
 when we lay in a bath of ordinary tap-water at the same temperature. 
 I found this experience corroborated in a series of careful observations by 
 Reissner and Grote, who compared the effects of the waters from these 
 springs with those of plain water at the same temperature, and found the 
 slowing of the heart entirely dependent on the temperature. This effect 
 of temperature is practically never referred to, but is attributed to some 
 specific effect of the waters on the skin. Thus in lying in the bath, the water 
 being charged with carbonic acid, this gas comes off in innumerable small 
 bubbles which can be seen adhering to the skin. At the same time the skin 
 becomes red. These very simple phenomena are pointed out as in some way 
 bringing about a reflex stimulation of the heart. 
 
 § 264. Cause of the efficacy of the spa treatment — It may be 
 said, and truthfully, that large numbers of people flock to Nauheim 
 and many of them derive great benefit from the treatment. I recognize 
 this, and have carefully endeavoured to find out the reason for the success 
 of the Nauheim methods. When the cases that are cured and the cause of 
 then- cure are strictly analysed, it will be found that at Nauheim what I call 
 the essentials of treatment are carried out in an excellent manner. Every- 
 thing is conducive to the restfulness of the patient. It is a pleasant place, 
 sunny and weU shaded, with beautiful gardens and an excellent band. 
 People jaded with their cares and duties find here that repose which is 
 essential to the recovery of the heart. A very large proportion of them 
 are somewhat neurotic, and there is consequently a very susceptible 
 mental element that can be influenced. The patient comes to Nauheim 
 buoyed up mth the reputation of the place. When he consults a doctor,
 
 300 DISEASES OF THE HEART 
 
 he is confidently told that the treatment will do him good — at once half 
 the cm'e is effected in a great proportion of the cases. 
 
 Of wonderful cm:es I saw none. Pursuing my work in a remote manu- 
 facturing town, when I read of the wonderful cures performed at places like 
 Nauheim, I imagined that these would be the class of cases that I failed 
 to benefit. What was my surprise to find at Nauheim that the so-called 
 wonderful cures that were being effected were identical with those that 
 practitioners achieve at home. 
 
 I found at Nauheim that which I had also found at other spas, that the 
 practitioners there were scarcely aware of what the human heart was capable. 
 Those who, like myseff, have practised largely among the better working 
 class know what enormous capacity for recovery it possesses. Many of the 
 ailments I saw at Nauheim would not keep a working man or woman from 
 their work, and here they were going through elaborate methods of cure. 
 I may frankly confess that I saw no patient get benefit at Nauheim who 
 would not have done equally well elsewhere. 
 
 The argument is used that cases that have been treated elsewhere without 
 success have obtained benefit at Nauheim. What doctor of experience has 
 not the same to tell ? I have repeatedly had patients place themselves 
 under my care who had been treated by other doctors, and they have bene- 
 fited. But I trust I am not so foolish as to fancy the recovery was due to 
 my skill. In many heart cases the early stages of recovery are very pro- 
 tracted, and marked improvement often takes place with some shght change 
 in the treatment, and the conclusion is often too hastily drawn that the 
 recent change effected the cure, whereas the heart's power was being slowly 
 restored by the treatment previously employed. 
 
 I have gone into the subject of the Nauheim treatment at length, so that 
 the reader may appreciate the strength or weakness of the position I take 
 up, and I want each practitioner seriously to consider his responsibihty in 
 every case before recommending an elaborate and expensive treatment. If 
 the individual is well to do, and there is not much the matter with him — weU, 
 Nauheim is as good a place to send him to as any other. But when it means 
 crippHng a man's resources either by the outlay or by stopping his work, 
 a grave responsibility rests upon his adviser. 
 
 In the case of growing boys and girls, I think Nauheim and the various 
 methods are distinctly detrimental when the heart's weakness is purely 
 functional and the symptoms consist in occasional fainting and some 
 enlargement and irregularity of the heart. This class of patient is often 
 sent there, and, in consequence of the elaborate ritual, they get the notion 
 there must be something serious, and go through Ufe under the impression
 
 TREATMENT 301 
 
 that they have a weak heart, with the consequences seen in the malade 
 imaginaire. I have seen numbers of these going through these elaborate 
 methods whom I would have sent out to the play-fields. 
 
 The assembling in crowds of neurotic people is a bad feature. 
 They are so fond of detailing their symptoms to one another that they 
 cultivate the habit of self -analysis. If this were done sanely, good might 
 result, but it often ends in making the individual too self-conscious of 
 what little infirmity he suffers from, so that I prefer to send my heart 
 cases with a . nervous element where they will associate as much as pos- 
 sible with healthy people, whose pursuits and tastes do not lean towards 
 introspection.
 
 APPENDIX I 
 
 The Pulse in Angina Pectoris 
 
 The condition of the arterial system immediately before and during an 
 attack of angina pectoris has been the subject of a good deal of speculation, 
 and a good many h3rpotheses in regard to diagnosis and treatment have been 
 based upon the conditions that are supposed to exist. Unfortunately, very 
 few observations have been made to determine the actual condition, and 
 those that have been published do not bear a very critical examination. It 
 is only at unexpected times that one has the opportunity for making the 
 observation, and the circumstances are rarely suited for making these suffi- 
 ciently accurate. I have been somewhat fortunately circumstanced for 
 this purpose. For many years while I was in Burnley I had been consulted 
 by large numbers of people with affections of the heart. Three of the four 
 roads that led past my house were steep, and the patients suffered in climbing 
 the hill. Not infrequently in my consulting room, or in my waiting room, 
 patients would be seized with attacks of angina pectoris, and I have had 
 many times to administer amyl nitrite for their relief. As I always had 
 my sphygmograph ready, I frequently obtained very good tracings. I may 
 say that in not a single case did I ever find any evidence of vascular spasm, 
 recognizable by the finger, nor had I any difficulty in getting tracings on 
 account of the smallness of the pulse. While one cannot always infer 
 from the size of the tracing that the radial artery was large, yet it does offer 
 confirmatory evidence. A small deformed tracing may easily be got from 
 a large radial pulse, by hasty and inaccurate adjustment of the instrument, 
 but it is rare to get a large tracing from a small contracted artery, and 
 I give the following tracings merely as corroborating the sensations imparted 
 to my finger. 
 
 In tracings taken before and after the administration of amyl nitrite, 
 the size of the artery and the character of the tracing showed very little 
 difference. During the administration there was always the characteristic 
 changes — increased rapidity and lowering of the dicrotic notch, as in Fig. 
 169. It may be said that the attacks in the cases cited were after bodily 
 exertion had exhausted the heart, and that the attacks that come on when
 
 THE PULSE IN ANGINA PECTORIS 
 
 303 
 
 the patient is at rest may be due to arterial spasm. I have also had occasion 
 to see a good number of cases who suffered from attacks while in bed, and 
 here likewise I detected no arterial spasm. In a few cases I have found the 
 arterial pulse small during an attack, and in one case imperceptible ; but 
 these were cases of extreme exhaustion of the heart, with very feeble heart 
 sounds, and the administration of amyl nitrite had no effect. Two of 
 these patients died a few hours after my examination. 
 
 Fig. 168. Large alternating pulse during an attack of angina pectoris. B.P. 190. (Case 1. 
 Figs. 169 and 170 are from the same patient.) 
 
 I have a large amount of material to select from, but I limit myself to 
 a few cases of the most severe type. 
 
 Case 1. — Male, aged 52 (whose case is described more fully later — Case 23, 
 Appendix V). Had suffered two years from breathlessness. As he had 
 a well-marked pulsus alternans I have made a large number of observa- 
 tions on him. His condition fluctuated very much. During a period when 
 he was worse than usual he called to see me, walking up a steep hill on 
 
 Fig. 169. Under amyl nitrite. (Case 1.) 
 
 the way. He began to feel a tightness across his chest which developed 
 into a severe pain. I examined him and took a tracing of his pulse 
 (Fig. 168). I took his blood-pressure and found it 190 mm, Hg. His 
 pulse did not alter in character during his suffering, and the height of the 
 waves showed that there was no contraction of the artery, nor did it differ 
 in character from the pulse tracing taken when he was free from pain. 
 I gave him amyl nitrite to inhale, the pulse quickened (Fig. 169), and the 
 amyl nitrite gave him instant relief. Fifteen minutes after he was quite 
 free from pain, his blood-pressure had risen to 200 mm. Hg., and the
 
 304 
 
 DISEASES OF THE HEART 
 
 alternating character of the rhythm became more marked (Fig. 170). In 
 the post-mortem account of the patient it will be shown that there was 
 extensive fibrosis of the heart muscle, and disease of the coronary artery. 
 
 Case 2. — Female, aged 60 ; complained of pain in her chest, radiating 
 into the left arm, and persisting in the left fore-arm with great severity. It 
 was easily 'induced by exertion, and one day when coming to see me she 
 had hurried. While I was examining her the pain seized her with great 
 violence. I took tracings of her radial and jugular pulses. The heart's rate- 
 
 Fig. 170. Fifteen minutes after the inhalation of amyl nitrite and after cessation of the 
 anginal symptoms the alternating character of the pulse became more marked, and the blood- 
 pressure of the larger beats had risen to 200 mm. Hg. (Case 1.) 
 
 was increased but the radial pulse was of a good size (Fig. 171). I gave her 
 amyl nitrite and it relieved the pain at once. The patient died three months 
 after from heart failure, and Dr. R. T. Williamson examined the heart for 
 me and found marked atheroma and calcification of the coronary arteries 
 and extensive fibrous changes in the muscle of the left ventricle. 
 
 Case 3. — Male, 52. Mechanical engineer ; was going to his work on 
 March 14, 1903, when he was seized with a severe pain across his chest and 
 
 Fig. 171. Taken during an attack of angina pectoris — the radial pulse is seen to be of good 
 
 size. (Case 2.) 
 
 called on me. I found him suffering great agony ; his face ashen in colour, 
 his pulse full and regular (Fig. 172). I gave him first amyl nitrite with no 
 effect on the pain, then a hypodermic injection of | grain of morphia. This 
 gave him relief. The heart's dullness was normal, but the sounds were soft 
 and there was a murmur after the first sound. After a week's rest the 
 patient improved and resumed his work, but on January 15, 1905, he was 
 again seized with a severe attack of angina pectoris. For some months after- 
 wards the pain came on with little provocation, and I saw him in one attack
 
 THE PULSE IN ANGINA PECTORIS 
 
 305 
 
 and the pulse was not affected. The pains diminished in severity as the 
 heart dilated and became weaker, dropsy and oedema of the lungs super- 
 vened and he died on June 1, 1905. Dr. Keith's report of the heart stated 
 that the coronary arteries showed a slight thickening of the intima, but 
 the muscle coat was hypertrophied ; thickening of the mitral cusps but no 
 stenosis ; the foramen ovale was slightly patent ; the right ventricle was 
 hypertrophied and dilated, while the left was dilated and atrophied with 
 a considerable degree of fatty degeneration and a shght degree of fibrosis. 
 
 Fig. 172. During an attack of angina pectoris. (Case 3.) 
 
 Case 4. — Male, aged 52 at his death ; had been under my care for four 
 years. His complaint at first was pain induced by exertion, starting across 
 his chest and radiating into the left arm. At times the pain was so 
 easily excited that he had to keep in bed for a few days. On February 8, 
 1894, he complained, in addition, of a pain and soreness in the head, which 
 developed into severe attacks of headache. I saw him in an attack of 
 angina pectoris, which came on while he was in bed on March 19, 1894 ; 
 his pulse was full and regular, and there was no sign of contracted arteries 
 
 Fig. 173. During an attack of angina pectoris. (Case 4.) 
 
 (Fig. 173). I gave him amyl nitrite without effect on the pain, and he was 
 only eased by chloral. He died in an attack of angina on March 27, 1894. 
 Dr. Williamson reported that the ventricles were soft and friable ; well- 
 marked atheroma of the coronary arteries ; in many places the arteries and 
 their branches were calcified. Microscopic examination of the left ventricle 
 showed fatty degeneration. 
 
 Case 5. — Male, aged 68 at his death. Consulted me on November 17, 
 1899, because of pain over his chest on exertion. He was a millwright by 
 trade — a big powerful fellow. As he was in comfortable circumstances 
 I advised him to give up hard manual work. He followed this advice, and 
 
 MACKENZIE -V"
 
 306 
 
 DISEASES OF THE HEART 
 
 was free from pain until July 8, 1902, when he was seized with violent pains 
 on going up a hill. He came home and went to bed, when the pain returned, 
 and I saw him during an attack of agonizing severity which lasted over ten 
 minutes. While amyl nitrite was being fetched, I took tracings of his 
 pulse (Figs. 174 and 175). The amyl nitrite gave him a little ease, and the 
 pain gradually subsided. During the attack the character of the pulse did 
 not alter, and there was no sign of contracted arteries. The heart was 
 
 Fig. 174. Large irregular pulse during an attack of angina pectoris. (Case 5.) 
 
 irregular, due mainly to extra-systoles, sometimes interpolated as in Figs. 174 
 and 175. He had repeated attacks and died in one on July 10, 1902. 
 
 I have found in a good number of cases that the rate became more 
 frequent during attacks of angina pectoris. In one case of aortic disease 
 the attack of angina coincided with a sudden increase in the rate, of which I 
 got a tracing, but unfortunately it is lost. There is often a tendency to 
 the production of extra-systole induced at the same time, as shown in the 
 
 Fig. 175. The same as Fig. 174. (Case 5.) 
 
 two last tracings (Figs. 174 and 175). The following case illustrates this 
 tendency : — 
 
 Case 6. — Male, 43 years of age : consulted me on September 13, 1900. 
 Had good health until a year ago, when he began to be short of breath on 
 exertion. Shortly after this he suffered from a pain that shot into his 
 left arm when he exerted himself. Four days before coming to me the pain 
 struck with great severity into his chest and down the inside of the left arm, 
 and lasted for half an hour. He has been a heavy drinker. On the 19th
 
 THE PULSE IN ANGINA PECTORIS 
 
 307 
 
 he called again upon me ; was seized with the pain, which held him for some 
 minutes, and I got tracings of the jugular and radial pulses while the pain 
 was present. The pulse increased in rate and became irregular (Figs. 176 and 
 
 .V^vA^V^A^iVtvlA/lAAM 
 
 Fig. 176. Shows extra-systoles occurring during an attack of angina pectoris. (Case 6.) 
 
 177). These irregularities are due to ventricular extra-systoles ; in Fig. 177 
 the extra-systole is interpolated between two normal beats. 
 
 The patient improved under treatment, and I did not see him again after 
 
 Fig. 177. Shows an interpolated extra-systole during an attack of angina pectoris. (Case 6.) 
 
 the end of September. He dropped dead in January, 1901, while watching 
 a football match. 
 
 Irregularities of a more obscure kind may appear during an attack of 
 angina pectoris, and the pulse may become slow. 
 
 Fig. 178. Pulse of high arterial pressure from a case of chronic albuminuria. (Case 7.) 
 
 Case 7. — Female, aged 68. Had been under my care for five years, 
 suffering from cirrhotic kidney. Her pulse was always hard and regular 
 (Fig. 178). On February 28, 1900. she was seized with an attack of angina 
 
 Fig. 179. Irregular pulse during an attack of angina pectoris. (Case 7.) 
 
 pectoris. These attacks kept recurring, though she lay in bed. I saw her 
 in an attack on the 25th ; her face was blanched and shrunk, and damp 
 with perspiration. The pulse became very irregular, as in Figs. 179 and 180. 
 
 x2
 
 308 DISEASES OF THE HEART 
 
 Relief was only obtained by large doses of opium, vaso-dilators having no 
 effect (amyl nitrite, whisky and hot water). Next day she was better and 
 
 Fig. 180. Tracing of radial pulse showing the appearance of the 
 pulsus alternans after a long pause during an attack of angina pectoris. 
 (Case 7.) 
 
 her pulse quite regular (Fig. 181). She died in the following week during 
 an attack of angina pectoris. 
 
 The nature of the irregularity in Fig. 180 is easy to understand. An 
 
 Fig. 181. Pulse of the same patient after the subsidence of an attack of angina pectoris. 
 The pulse is here regular. (Case 7.) ' 
 
 extra-systole occurred during the long pause, and this was followed by 
 the pulsus alternans — an indication of profound exhaustion of contractility. 
 I am not able to account satisfactorily for the nature of the irregularity in 
 Fig. 179.
 
 APPENDIX II 
 
 The Nodat, Rhythm 
 
 The starting of the contraction of the heart at a place other than the 
 normal is a conception so novel in the physiology of the heart's action, 
 and has such a profound bearing upon the diagnosis and treatment of heart 
 failure, that it is necessary to give the evidence for this conception in some 
 detail. Already experimental evidence is accumulating in favour of this 
 idea, as shown by the observations of Cushny^^' (Figs. 58 and 59) and 
 Lewis 207. Further, the most accurate of all methods of cUnical observation, 
 viz. by means of the electro-cardiogram, has amply confirmed the con- 
 clusions I have drawn from the study of the heart murmur and graphic 
 records of the circulatory movements (see Appendix VII). Clinical and 
 pathological evidences are given in this Appendix, the former full and 
 complete, the latter confirmatory, and awaiting further work. 
 
 The cUnical evidence consists in the disappearance of all signs of the 
 auricular systole occurring at the normal period in the cardiac cycle. Such 
 signs of normal auricular activity are : — 
 
 (1) A wave in the jugular pulse tracing due to a contraction of the right 
 auricle. 
 
 (2) A wave in the apex tracing due to a contraction of the left auricle. 
 
 (3) A wave in the liver pulse due to a contraction of the right auricle. 
 
 (4) A presystolic mitral murmur due to a contraction of the left auricle. 
 
 (5) A presystolic tricuspid murmur due to a contraction of the right 
 auricle. 
 
 The most important evidence is found in the character of the jugular 
 pulse. As has been already pointed out, there is normally a wave preceding 
 the carotid and radial pulse, as in Fig. 183, where the wave, a, from its 
 position in the cardiac cycle, is recognized as being due to the auricular 
 systole. When the nodal rhythm arises the character of the venous pulse 
 at once changes, and we get a form of venous pulse in which there is no 
 evidence of an auricular contraction in the normal period ; in other words, 
 the jugular pulse changes from one of the auricular type to one of the ven- 
 tricular type (§ 115), and the heart's action becomes irregular. PresystoHc
 
 310 DISEASES OF THE HEART 
 
 murmurs due to the auricle, as well as auricular waves in liver and apex 
 tracings, disappear. 
 
 In the clinical history of the cases cited I will only refer to the evidence 
 bearing upon the matter in hand. These cases are selected to show that 
 every one of the above-mentioned signs of auricular activity disappear. 
 
 I have now collected records of nearly 600 cases of nodal rhythm, and a 
 careful analysis of these leads me to conclude that there are a number of dis- 
 tinct varieties. Most of these I am unable yet to classify with sufficient pre- 
 cision, but I entertain no doubt that with extended experience and improved 
 methods this classification will be ultimately attained. One small class 
 stands out from the others very clearly. In the majority of cases of nodal 
 rhythm the rate of the heart-beat is increased, sometimes extremely so. 
 In a few cases it is found slower than normal, sometimes markedly so. 
 These cases of infrequent rate I place in a separate class and describe them 
 under the term Nodal Bradycardia (Appendix IV). 
 
 I had hoped to have been able to give a fairly full account of the patho- 
 logical condition in cases of the nodal rhythm, but I find there is a vast 
 amount of pioneer work still to be done, and the pathological results given 
 here are put forward with all reserve and are suggestive rather than con- 
 clusive. Monckeberg ^i- has recently published a book on the pathology of 
 the auriculo-ventricular bundle, but the clinical records are so scanty that 
 no clear perception can be obtained of the symptoms during life, but, so 
 far as I can see, his observations seem to confirm those of Keith given here. 
 For some years I have sent to Professor Keith hearts affected with many 
 forms of disease. He has examined these without knowing the clinical 
 histories. On comparing his descriptions with the clinical notes, I found, 
 with one exception, that all cases that had the nodal rhythm during life 
 presented some evidence of change in the primitive cardiac tissue, or in the 
 artery supplying it. There were also found such changes in the auricular 
 wall in a few cases as to suggest an interruption of the means of com- 
 munication between the sino-auricular and auriculo-ventricular nodes 
 (Fig. 2). The exceptional case I have subsequently found to belong to 
 a different category (nodal bradycardia. Case 22). 
 
 I would particularly draw attention to Cases 11 and 12, which repre- 
 sent typical instances of paroxysmal tachycardia, the one secondary to 
 rheumatic sclerosis, and the other associated with arterial degeneration. 
 The pathological conditions found in these cases afford support for the view 
 put forth that the a.-v. node or bundle, by the invasion of the diseased 
 processes, is rendered more irritable than the sinus remains, and on account 
 of its excessive irritability starts the rhythm of the heart.
 
 THE NODAL RHYTHM 
 
 311 
 
 Before entering into a detailed account of the cases, there are two points 
 to which it may be useful to refer for the help of those who may follow this 
 line of inquiry. In many cases it will be found that when the radial pulse- 
 beats are very small or occasionally absent, the jugular or liver pulse may 
 be large, as in Figs. 66, 158, 160, and 209. The reason for this is that the 
 force opposing the contraction of the left ventricle (the aortic pressure) is so 
 great that the ventricular contraction is barely able to overcome it. On the 
 other hand, the force opposing the backward flow through the incompetent 
 tricuspid orifice is so sHght (the pressure in the great veins) that the right 
 ventricle has no difficulty in overcoming this pressure even with a feeble 
 contraction. 
 
 2, a 3 3 V 
 Jugular ^ 
 
 3 3 3 1 
 
 ^. 1 1 
 
 ^^^"^""^ r "^^-^-^ / ^ — ~-,^ / ' 'fc-,^/'^- — , -"^^^ J "'^s.-.^^ Lf—- *^^ _ X "'*'*^.^ y'"" ■»» 1 
 
 ^rorid ' 1 
 
 Fig. 182. At x and x ' a series of waves is shown which were produced by partial com- 
 pression of the vein by the receiver. The stream of blood passing through the narrowed 
 lumen caused a perceptible thrill in tlie surrounding structures, and produced vibrations of the 
 tambour wMch are registered as waves in the tracing. With care the tracing can be obtained 
 free from these artificial waves, as in Fig. 53, which was taken from the same patient. 
 
 I have in a few cases of nodal rhythm found in the tracings during 
 ventricular diastole a series of small waves. In the first few cases I sought 
 carefully to see that there was not some error in the method, and failing to 
 find any fault I inferred that these waves were due to fibrillation of the 
 auricle, and I have so described them in one or two published articles. 
 From one patient with a large, full, jugular vein I obtained sometimes very 
 large waves during a long pause, as at x in Fig. 182. When I carefully 
 inspected this vein I found that when I partially compressed the vein with 
 my finger perceptible thrills in the surrounding structures were produced, 
 because the blood was flowing through the constricted vein. From this 
 observation, I now recognize that what I had taken for waves due to fibril- 
 lation of the auricle may in some instances have been due to a fault in the 
 method of registration, wherein by compressing the vein with the receiver 
 I had artificially produced thrills which appeared as waves in the tracing.
 
 312 
 
 DISEASES OF THE HEART 
 
 Other waves due to the same cause are apt to appear, and if the cause be 
 not recognized it might be assumed that the waves were due to the auricle, 
 as at x' in Fig. 182. 
 
 Case 7. — Sudden inception of the nodal rhythm shown by the disappear- 
 ance of the auricular wave from the jugular pulse, and of the presystolic mitral 
 murmur, with the appearance of permanent irregularity in the heart's action, and 
 
 Fig. 183. Simultaneous tracings of the jugular and radial pulses in the first part, of the 
 carotid and radial in the latter part. The jugular tracing shows the form characteristic of the 
 auricular venous pulse where the wave, a, due to the auricle precedes the carotid wave, c (down- 
 stroke 3). The shading underneath represents the time of the presystolic murmur. (Case 7, 
 November 5, 1895). 
 
 ventricular form of the venous pulse. Post-mortem evidence of disease affecting 
 the remains of the primitive cardiac tissue. 
 
 Female, born 1864. I first saw this patient in 1895, she being then 
 thirty-one years of age. There was a history of acute rheumatism in her 
 youth, and she had marked mitral stenosis. She became pregnant in 1896, 
 
 Fig. 184. The jugular pulse is now of the ventricular form — no auricular wave precedes 
 the downstroke 3, and the rhythm is irregular. (Case 7, March 19, 1904.) 
 
 and I watched her during the pregnancy and puerperium. She had a long 
 illness from gastric ulcer in 1899. During these years I made frequent 
 observations on her heart. It was invariably regular, and the jugular pulse 
 always showed a well-marked wave due to the systole of the right auricle. 
 There was at first a presystolic mitral murmur of the crescendo type, and 
 latterly a long murmur following the second sound and running up to the 
 crescendo presystolic murmur. The position of the presystoUc murmur in 
 the cardiac cycle is diagrammatically represented in the shading under the 
 radial tracing in Fig. 183. This perfect regularity of the heart's action
 
 THE NODAL RHYTHM 
 
 313 
 
 continued until she suffered from an attack of heart failure in 1900. 
 Coincident with this failure the heart's action became irregular, and the 
 jugular pulse showed no sign of a wave due to the auricular systole at the 
 normal period of the cardiac cycle (Fig. 184). The crescendo presystolic 
 
 Fig. 185. The jugular pulse is of the ventricular form, and a' is probably due to the auricular 
 systole occurring at the same time as the ventricular. (Case 7, December, 1906.) 
 
 murmur had disappeared, while the diastoUc portion persisted, as shown by 
 the shading under the apex tracing in Fig. 186. 
 
 From this date until she died in February, 1907, these altered conditions 
 persisted. Fig. 185 being a simultaneous tracing of the jugular pulse and 
 
 Fig. 186. The jugular pulse shows the same features as in Fig. 185. (Case 7, 
 
 February, 1907.) 
 
 radial taken in December, 1906, and Fig. 186 of the jugular and apex beat 
 taken February, 1907, shortly before she died. 
 
 Concerning the jugular pulse, it will be seen that in Figs. 184, 185, and 
 186, there is not the slightest sign of the auricular wave, a, at its normal 
 period in the cardiac cycle, which is so marked a feature in Fig. 183. The
 
 314 DISEASES OF THE HEART 
 
 rhythm of the heart was sometimes fairly regular, but invariably after a few 
 beats the diastolic period showed distinct variations in length ; among 
 a large number of tracings which have been taken from this patient since 
 1900, I have never found one that was regular. 
 
 The following is an abbreviated report on the post-mortem examination 
 of the heart : 
 
 Valves : Great stenosis of the mitral valves ; tricuspid valves shallow 
 and incompetent ; pulmonary and aortic valves normal. Coronary arteries 
 healthy ; coronary veins dilated to twice their normal diameter. Superior 
 and inferior vena cavae much dilated. The sino-auricular node is normal, 
 but the auricular wall below it is atrophied and fibrous. The taenia 
 terminalis is h3rpertrophied. The auriculo-ventricular bundle has partly 
 assumed the characters of the ordinary muscular fibres, and has been 
 stretched, and the a. -v. node is flattened by the great inter-auricular 
 pressure. The central fibrous body is marked (fibrous and contracted), 
 and the artery perforating it is atheromatous. The apical half or two- 
 thirds of the left ventricle shows extensive fibrosis. The fibrotic process 
 approaches and incorporates the musculature along a sharply defined 
 line. In the fibrotic tissue are nodules characteristic of rheumatic con- 
 ditions. Since the fibrotic process is most marked at the base of the 
 musculi papillares, it is possible that it may have spread from the mitral 
 valves. 
 
 Case 8. — Sudden inception of the nodal rhythm, shown by the disappear- 
 ance of the auricular wave from the liver pulse, and of the presystolic mitral 
 murmur, with the appearance of permanent irregularity in the heart's action 
 and ventricular form of the liver pulse. Post-mortem evidence of the invasion 
 of the primitive cardiac tissue by the diseased process. 
 
 Female, born 1851, came under my care in 1880. She had had rheumatic 
 fever in childhood, and had suffered from mitral stenosis, there being a well- 
 marked presystolic murmur. In 1880 and 1882 I attended her for attacks 
 of rheumatic fever. In 1892 there was considerable enlargement of the 
 liver, which pulsated (Fig. 187). 
 
 The character of the pulsation being of the auricular type, I concluded 
 that there was also tricuspid stenosis, a diagnosis which was afterwards 
 verified at the post-mortem examination. Occasionally I detected an 
 extra-systole. Fig. 189, which Fig. 190 shows to be due to premature con- 
 traction of the ventricle. Tliis characteristic pulsation of the liver continued 
 until 1898 (Fig. 188, for instance, being taken in 1897), when she had an 
 attack of heart failure, during which time her pulse was rapid and irregular 
 (Fig. 191).
 
 THE NODAL RHYTHM 
 
 315 
 
 When the heart had quieted down the tracing showed a complete absence 
 of the wave due to the auricular systole (Fig. 192), and the' presystolic 
 murmur had disappeared. 
 
 Fig. 187. The liver pulse shows a well-marked wave (a) due to the 
 auricle. (Case 8. 1892.) 
 
 Fig. 188. There is still a well-marked wave in the auricle. (Case 8. 1897. ) 
 
 Fig. 189. Shows an extra-systole. (Case 8.) 
 
 Fig. 190. Simultaneous tracings of the apex beat and 
 of the liver pulse, showing the rhytlimical contraction of 
 the auricle, a', while there is a premature beat in the apex 
 (ventricular extra-systole). (Case 8.) 
 
 This patient lived until 1899, and in the numerous tracings taken up 
 to her death the rhythm was never again found regular, nor was there 
 present either the presystolic murmur or the wave in the liver pulse due to
 
 316 DISEASES OF THE HEART 
 
 the auricle. Here, again, the irregularity in the action of the heart was 
 coincident with the disappearance of all signs of auricular systole, namely, 
 the disappearance of the auricular wave from the liver pulse, showing the 
 cessation of the action of the right auricle, and the disappearance of the pre- 
 systoHc murmur, showing the cessation of the action of the left auricle. 
 
 The report of the post-mortem examination of the heart is as foUows : — 
 Extreme stenosis of mitral and tricuspid orifices ; great dilatation of auricles, 
 
 Fig. 191. Sudden inception of the nodal rhythm, showing 
 increased frequency of the heart's action, irregularity and dis- 
 appearance of the auricular wave from the liver pulse. (Case 8. 
 1898.) 
 
 with atrophy of the musculature. There is a large nodular mass of endo- 
 cardial thickening showing calcareous masses in its centre, and active 
 inflammatory proliferation at its periphery, on the endocardium, under the 
 aortic orifice, and situated in the pars membranacei septi right over the a.-v 
 bundle. At one point the inflammatory extension has invaded and involved 
 a great part of the bundle. The stretching of the bundle is extreme, and 
 
 Fig. 192. When the heart became slower the nodal rhythm persisted. When compared 
 with Figs. 187 and 188, it will be seen tliat there is no auricular wave in the liver pulse, and 
 the heart's action is irregular. (Case 8. 1898.) 
 
 there is cell proHferation which Professor Keith regards as due to changes 
 in the walls of the small vessels. 
 
 There is extreme atrophy of the upper part of the inter-ventricular 
 septum. It measures only 4 mm. instead of 14-18. The sub-endocardial 
 tissue is thickened, and in parts the Pur kin je system is fibrosed and atrophied. 
 
 Case 9. — Disappearance of large auricular waves from the venous pulse with 
 the onset of continued irregular action of the heart. Fibrosis of the a.-v. bundle. 
 
 Female, born 1850 ; enjoyed good health till 1900, when she began to 
 be short of breath. I saw her first in November, 1902. She was then
 
 THE NODAL RHYTHM 317 
 
 very weak, and had to lie in bed propped up ; the legs and abdomen were 
 swollen and the urine scanty ; the pulse was small, weak, and regular, and 
 there was a large pulsation in the veins of the neck (Fig. 193). The heart's 
 dullness extended two inches to the right of the mid-sternal line, and one 
 inch to the left of the nipple line. The sounds were clear and free from 
 murmur. 
 
 Fig. 193. Shows a well-marked auricular wave in the jugular tracing during an attack 
 of extreme heart failure. (Case 9. 1902.) 
 
 Under treatment she improved very much, the pulse becoming slower 
 (Fig. 194), but she had several relapses, until the final breakdown in November, 
 1904, Figs. 193 and 194 are tracings of the radial pulse and jugular pulse 
 taken in 1902. The jugular pulse is of the auricular form, and the rhythm 
 there is perfectly regular. I took a large number of tracings at different 
 times up till November, 1904, and the rhythm was invariably regular, 
 
 Fig. 194. .Shows a well-marked auricular wave (a) in the jugular tracing. (Case 9. 1902). 
 
 and the jugular pulse of the auricular type. On one occasion after digitalis 
 she developed a pulsus alternans (Figs. 164 and 165). The breakdown 
 at the last-mentioned date was the most severe she ever had, the legs and 
 abdomen being enormously swollen and the pleural cavities containing 
 a large quantity of fluid. The pulse was now continuously irregular, and 
 the venous pulse had completely changed its character, being of the ventri- 
 cular form (Fig. 195). She died in December, 1904, two months after I had 
 detected the presence of the nodal rhythm.
 
 318 
 
 DISEASES OF THE HEART 
 
 The report on the post-mortem examination of the heart is as follows : — 
 
 Greater part of auricle has been left behind in subject. 
 
 The right ventricle is of quite average length and atrophied ; left ven- 
 tricle is of quite average length and dilated and atrophied. 
 
 Arteries. — Show patches of thickening and dilatation, but nowhere is 
 lumen so reduced as to greatly impede circulation. Aorta shows patches 
 of atheroma. 
 
 Fig. 195. Simultaneous tracings of the radial and jugular pulses taken on November 9, 
 1904. The jugular pulse is now of the ventricular type, and the rise in the jugular during the 
 ventricular systole (space E) is in marked contrast to the fall during tliis period in Fig. 194. 
 There is no wave due to the auricle, and the rhythm is continuously irregular (nodal rhythm). 
 (Case 9. 1904.) 
 
 Orifices and Valves. — Valves healthy; mitral orifice 29 mm. diam., 
 tricuspid 30 mm., both dilated. 
 
 Musculature. — There is atrophy and perivascular fibrosis ; this is 
 extensive in basal part of left ventricle, especially at upper border of inter- 
 ventricular septum, but elsewhere fibrotic changes not marked. 
 
 Fig. 196. Radial tracing showing small beats due to the premature contraction of the 
 ventricle (extra-systoles). (Case 10. 1892.) 
 
 A.-v. system. — The network at beginning of bundle is normal in size and 
 form, although certain cells which seem inflammatory in nature are present. 
 The bundle, on the other hand, is stretched and small, the fibres show no 
 reticular structure, and in parts show fibrosis. The Purkinje system is 
 overlaid by a very thick fibrous endocardium. There is a marked degree 
 of stretching of the apical half of the left ventricle, and the trabeculae are 
 thin and atrophied ; on section, some of the Purkinje fibres are seen to be 
 undergoing fibrous changes.
 
 THE NODAL RHYTHM 
 
 319 
 
 Case 10. — Frequent extra-systoles from 1892 till 1906. Signs of contrac- 
 tion of the left auricle in the apex tracings and of the right auricle in the 
 jugular. Sudden disappearance of these signs of auricular activity on the 
 inception of the nodal rhythm in 1906. 
 
 Female, born 1840 ; came under my care on May 1, 1892, complaining 
 of weakness, shortness of breath, and depression. The radial pulse was 
 
 Fig. 197. Shows premature contractions of tlie ventricle, o (extra-systoles), in the apex 
 tracing, wliile in the jugular tracing are sIiowti waves, a', due to the auricular systole occurring 
 at the same time as the premature ventricular contractions. (Case 10. 1892.) 
 
 large and sHghtly collapsing ; there was capillary pulsation on rubbing 
 the forehead, and pulsation in the jugular vein. The heart rhythm was 
 frequently interrupted by extra-systoles, Fig. 196, and during the occurrence 
 of an extra-systole a big wave appeared in the vein. Simultaneous tracings 
 of the jugular pulse and of the apex showed these extra-systoles to be due 
 to the premature contraction of the ventricle. (Fig. 197). 
 
 
 B^BP^^^^^^^^^^^^^^^^^^^^^^^^^^^^B^^^^^^^^^^^^^^^^^^^^^^B 
 
 Fig. 198. Shows well-marked auricular waves (a) in the jugular and apex tracings. (Case 10). 
 
 The heart was only slightly enlarged, and there was a faint systolic and 
 a well-marked diastolic murmur in the aortic area. 
 
 This patient's condition varied very much during the later years of 
 her life. She suffered greatly at times from severe attacks of angina 
 pectoris, but no change could be detected in the rhythm of the heart. 
 At other periods the extra-systoles, like those in Figs. 196 and 197, were
 
 320 
 
 DISEASES OF THE HEART 
 
 very frequent. The jugular pulse was invariably of the auricular type 
 as shown in Fig. 198. In the apex tracings Figs. 197 and 198 there are 
 shown well-marked auricular waves {a), due to contraction of the left 
 auricle. 
 
 In July of 1906 she was seized with breathlessness and great prostration. 
 I found the heart extremely rapid and irregular in its action (Figs. 199, 
 205, Plate II, and 206, Plate III). She regained a certain amoimt of strength 
 when the heart slowed down, which it did after a couple of months, and 
 Fig. 200 is a tracing of the apex and jugular taken in November, 1906, and 
 Fig. 208, Plate III, is a tracing of the radial and jugular taken at the same 
 time. The heart never dilated very much, and there was never any dropsy, 
 but she died from exhaustion in February, 1907. Figs. 198 and 200 are 
 simultaneous tracings of apex beat and jugular pulse, and the contrast in 
 
 Fig. 199. Rapid irregular pulse due to the sudden inception of the nodal rhythm. 
 
 July, 1906.) 
 
 (Case 10, 
 
 the two tracings is very marked. In Fig. 198 the rhythm is regular and 
 there is a wave, due to the left auricle, in the apex tracing, and a wave, 
 due to the right auricle, in the jugular tracing. In Fig. 200 there is no 
 sign of the movement of auricle either in apex or jugular tracing and the 
 rhythm is irregular. Figs. 199, 205 Plate II, and 206 Plate III are 
 characteristic examples of the heart rhythm and rate on the sudden inception 
 of the nodal rhythm in many cases. 
 
 Case 11. — Transient attacks of nodal rhythm {paroxysmal tachycardia), 
 slight at first, but becoming permanent and causing death. Post-mortem 
 examination showed involvement of the a.-v. bundle in the disease process. 
 
 Male, born 1860. This patient first consulted me in January, 1900. He 
 had an attack of rheumatic fever at fourteen years of age. In 1896, after 
 walking for twenty minutes at a rapid pace, he felt extremely weak and 
 exhausted. After this he was always short of breath on exertion. A year 
 later, immediately after throwing a cricket baU, he felt the heart flutter for 
 a few seconds. Ten minutes after this the heart ' fluttered and beat quickly 
 for six or seven hours '. He has had an attack of this kind every two or
 
 THE NODAL RHYTHM 
 
 321 
 
 three weeks since. These attacks last from a few minutes to thirty hom-s. 
 At first he could sometimes stop the attack by bending down and taking 
 a deep breath, but this does not act now. Sometimes he passes a large 
 quantity of clear urine in the course of an attack. During an attack, if in 
 bed, he feels exhausted and limp, if walking he is easily tired, and if he has 
 to work for some hours he feels swollen round the waist and very sore over 
 the upper part of his abdomen, and feels pain sometimes very severe across 
 the back under the shoulder-blades. During the night the sleep is disturbed. 
 The pulse during these attacks has varied under my observation from 
 one hundred and seventy to two hundred and twenty beats per minute. 
 When the heart is acting quietly a short presystoUc murmur at the apex 
 and also a soft diastolic murmur over the middle of the sternum can 
 occasionally be detected. It often happens that these murmurs cannot be 
 
 Fig. 200. Here there is no sign of an auricular wave in either jugular or apex tracing. 
 Compare the jugular and apex tracings with Figs. 197 and 198. (Case 10, November, 1906.) 
 
 perceived. On producing shght redness by rubbing the forehead, the capillary 
 pulsation can be readily seen. Occasionally the pulse-rate falls to forty- 
 eight beats per minute. Towards the end of an attack, irregularity of the 
 pulse has been detected, due to exhausted contractility (pulsus alternans) 
 (Fig. 130). The patient (who was a very intelligent man) stated that some- 
 times when the attack of rapid heart-action ceased the heart gave three 
 or four violent beats at intervals longer than the usual pulse-rate. The 
 patient died on November 21, 1900. During the last four months the 
 pulse-rate continued rapid for days together, during which time he would 
 lie prostrate and exhausted. Sleep could only be got by large doses of 
 morphia. During the last two weeks of his Ufe the heart acted slowly only 
 at rare and brief intervals. Signs of heart failure quickly supervened — the 
 face swollen and livid, and general oedema. 
 
 It is only necessary here to call attention to the pulsation in the liver and 
 in the veins. I have made many observations on this patient during numerous 
 
 MACKENZIE Y
 
 322 
 
 DISEASES OP THE HEART 
 
 attacks of paroxysmal tachycardia. When he was free from the attack 
 only the faintest movement could be detected in the jugular bulb, and, as 
 Fig. 201 shows, there is only a slight wave preceding the carotid pulse. I was 
 fortunate enough one day to see him \\dthin five minutes after an attack began. 
 The pulse at first was not excessively rapid, and the carotid pulsation was 
 fairly evident, and I took a tracing (Fig. 202) of the carotid immediately above 
 the clavicle, from the situation from which the jugular pulse in Figs. 201 
 and 204 was afterwards obtained. In Fig. 202 it will be noted that no sign 
 
 Fig. 201. Tracings of a slight movement in the jugular vein taken at the same time as the 
 radial jDulse. The wave a is due to the systole of the right auricle. (Case 11.) 
 
 of the jugular pulse is present. This would imply that at first the increased 
 action of the heart diminishes the venous pressure, as usually happens when 
 the heart is quickened from other causes. The radial tracing is not so 
 good as I could have wished ; still it shows its time relation to the carotid 
 pulse. When I saw him again eighteen hours later the condition of affairs 
 had greatly altered. He had slept little aU night ; he felt Avretched, and 
 
 Fig. 202. Simultaneous tracings of the carotid (ujiper tracing) and radial 
 pulses at the beginning of an attack of paroxysmal tachycardia. The carotid 
 pulse was obtained immediately above the clavicle, from the same place that 
 the jugular pulses in Figs. 201, 203, and 204 were obtained. (Case 11.) 
 
 complained of great pain in the upper part of the abdomen and behind 
 about the level of the eighth dorsal vertebra. His face had a wan and weary 
 look, and was of a greyish colour. Above the inner end of the clavicles on 
 both sides there was now visible a large and distinct pulsation. If one care- 
 fully palpated this part a distinct pulsating tumour could be felt. It did not 
 extend up the neck, and was quite distinct from the carotid artery. It was 
 evidently the jugular bulb distended by regurgitating waves of blood, and the 
 valves in the jugular and subclavian veins were evidently competent. On 
 auscultating either of these pulsating tumours or under the middle of the
 
 THE NODAL RHYTHM 
 
 323 
 
 clavicle, one very loud sound was heard, synchronous with each pulse beat. 
 These sounds were evidently originated by the sudden and forcible stretching 
 of the jugular and subclavian valves. When I applied the receiver connected 
 with the tambour over this movement, the lever was jerked up with great 
 violence, and the tracing got had a totally different character from that 
 taken at the beginning of the attack. After taking a few beats from the 
 pulsating jugular bulb, I applied the receiver over the carotid in the middle 
 of the neck, and got the tracing of the carotid pulse (Fig. 203). The wave 
 
 Fig. 203. Simultaneous tracings of the pulsation in the jugular bulb and in the radial, 
 and of the carotid and radial pulses, during an attack of paroxysmal tachycardia, taken 
 eighteen hours from the beginning of t!ie attack. (Case 11.) 
 
 obtained from the jugular bulb occurs at the same time as the radial pulse, 
 and must therefore be due to the ventricular systole. I have taken a large 
 number of tracings during many attacks, and they have all presented a similar 
 character. The tracing Fig. 204 was taken after an attack had lasted 
 twenty-four hours. It will be noted that the wave here occurs at the same 
 
 Fig. 204. Simultaneous tracings of the radial and jugular pulses twenty-four hours 
 from the beginning of an attack of paroxysmal tachycardia. (Case 11.) 
 
 period as the venous tracing in Fig. 203. That this wave is not due to the 
 carotid can be seen by comparing its character with that of the carotid pulse 
 in Figs. 202 and 203. One could convince oneself that it was not the carotid 
 by examination, the movement being so distinctly limited to the root of 
 the neck, while the carotid above the pulsation could only be found with 
 difficulty. Six months before he died I was able to detect slight enlargement 
 and pulsation of the liver after an attack of tachycardia had lasted fifteen 
 to twenty hours. During the last few weeks of his life he was seldom free 
 from the rapid action of the heart, and the liver extended three inches below 
 
 Y 2
 
 324 DISEASES OF THE HEART 
 
 the ribs and pulsated very largely (Fig. 207). As the heart became exhausted 
 the pulse did not acquire so great a rapidity as it did in the earlier stages of 
 the disease, so that we can recognize with certainty the occurrence of the 
 liver pulse during the ventricular systole. 
 
 Report of post-mortem examination of the heart : — 
 
 Coronary artery healthy ; coronary sinus and veins dilated, but not 
 markedly so. 
 
 Left auricle greatly dilated and inter-auricular septum greatly stretched. 
 
 IVIitral orifice = a linear chink 18 x 3 mm. Anterior cusp of mitral valve 
 and chordae tendineae are the site of a warty hard vegetation, the size of 
 a hazel-nut. 
 
 Tricuspid valves healthy, but orifice dilated. 
 
 Myocardium = partial fibrosis in areas. Everywhere the small vessels 
 and capillaries are dilated and the nuclei in their walls dividing, and in the 
 
 Fig. 207. Simultaneous tracings of the radial and liver pulses during an 
 attack of paroxysmal tachycardia towards the end of life. (Case 11.) 
 
 neighbourhood of capillaries are plasma cells. This is markedly the case 
 with the upper part of the a. -v. bundle and lower part of node. 
 
 The sino-auricular node is very well marked, but appears in parts to be 
 more fibrous than usual, and the vessels show the proliferation of cells seen 
 elsewhere in the heart. 
 
 The pathological process which has affected the mitral valves spread 
 up to the central fibrous body, and where the bundle perforates this there 
 are signs of cellular changes in the margin of the bundle. In some sections 
 of the a.-v. bundle lower down, nearer the ventricles, there are seen in it 
 smaU areas from which the muscular tissue seems to have disappeared. 
 There are thus distinct evidences of cellular changes in the bundle. 
 
 Case 12. — History of many years of extra-systoles, sometimes becoming 
 very frequent. Transient attacks of the nodal rhythm, slight at first, becoming 
 more prolonged till it became permanent. Died five months after permanent 
 establishment of the nodal rhythm. Post-mortem : obliteration of lumen of 
 artery supplying the a.-v. bundle, and probable disease of the a.-v. bundle. 
 
 Female, born 1846. I have known and attended her for slight ailments 
 at intervals since 1880. In 1892 I obtained tracings of her pulse, which
 
 THE NODAL RHYTHM 325 
 
 showed extra-systoles. These occurred sometimes at rare, sometimes at 
 frequent intervals (Figs. 99, 103 and 104, Plate II). They were usually 
 ventricular in origin, but occasionally nodal and auricular. I also noted 
 in 1892 that there was a gallop rhythm of the heart when it was regular. 
 In 1900 she began to have attacks of ' palpitation ' of short duration, and 
 I obtained tracings of the radial and jugular during one of these attacks, 
 and they showed a transition of the venous pulse to the ventricular form 
 during the attack. On October 13, 1903, she felt weak and exhausted, and 
 had a distressing fluttering sensation within her chest, and I found the 
 heart's action extremely irregular. The attack lasted four or five hours. 
 The tracings taken during the attack were of the same character as Fig. 209. 
 On October 19 she was again seized with a similar attack, which lasted 
 
 Fig. 209. Characteristic irregularity on the sudden inception of the nodal rhythm — 
 the jugular pulse is of the ventricular form. (Case 12.) 
 
 a whole day, and the tracings in Fig. 209 convey a very good idea of the 
 character of the heart's irregularity. The next day the heart was quite 
 regular and the jugular pulse a typical example of the auricular form. 
 
 On October 27 the heart again became very irregular. This attack 
 continued without intermission until November 1. On October 29 the 
 heart's action became much slower, but the irregularity still persisted, and 
 the character of the jugular pulse showed a curious change (Figs. 210 and 
 211), viz., during the ventricular systole (the period between the perpendi- 
 cular lines 3 and 6) there are two waves a' and v, while there is no wave 
 at the normal time of the auricular wave. The heart suddenly reverted 
 to the normal rhythm, and became regular with a typical auricular venous 
 pulse (Fig. 212). 
 
 The attacks gradually lessened in frequency and duration until June 12, 
 1904, when, after a long walk in the country, she was seized with an attack 
 which lasted for a fortnight. A few days before the attack finally subsided 
 the heart became normal in its rhythm for a few hours. On October 16, 
 1904, this nodal rhythm again started, and continued, with great dilatation 
 of the heart, dropsy, ascites, and hydrothorax, until her death on 
 March 17, 1905.
 
 326 
 
 DISEASES OF THE HEART 
 
 In this patient the remarkable changes described in § 159 were seen 
 most typically. A few hours after an attack the heart dilated, the liver 
 enlarged, the face became swollen and livid. Immediately the normal 
 rhythm was restored, the patient at once felt relief, and in a few hours all 
 the abnormal symptoms disappeared. 
 
 f 
 
 Tubular g 
 
 i' a! CL' <^' ^ a.' ^, 3S-6 
 
 xwna^msa^mB. 
 
 ^^ ^^'^^^ ^^ "^"^ ^'^^^ '""^ 
 
 Fig. 210. The rhythm is still irregular and the jugular pulse is of the ventricular type, 
 the auricular wave a' occurring during the ventricular systole. (Case 12.) 
 
 As this patient Uved close to my house I saw her very frequently, and 
 had the opportunity of watching the attacks begin and finish. Once when 
 taking a tracing the attack started, and on several occasions the attacks 
 ceased while I was watching her. I have accumulated a great number of 
 tracings taken at all stages. 
 
 Fig. 211. Shows the same as Fig. 210 except that during the long pause of the ventricle an 
 independent auricular wave {a') appears, not followed by a v wave. (Case 12.) 
 
 The character of the jugular tracing showed invariably the typical 
 ventricular venous pulse during the attack, and the return to the auricular 
 jugular pulse with the cessation of the attack. There are a few instructive 
 features in the character of the jugular pulse. The heart's rate varied very 
 much during the attack. At the beginning it was usually very rapid, then 
 it began to get slower in an irregular way ; at first an occasional long diastolic 
 pause would occur, followed by a large ventricular contraction. Then longer 
 pauses sometimes became more frequent, till finally the heart's rate was 
 not much above the normal, though it was irregular in rhythm (Figs. 210 
 and 211). "V^Tien the rate was rapid, sometimes there was scarcely any 
 evidence in the radial pulse of the ventricular contraction, while the jugular
 
 THE NODAL RHYTHM 
 
 327 
 
 pulse showed well-marked waves during the intermission (Fig. 209) in the 
 radial pulse. When the heart was rapid, the wave v in the jugular tracing 
 was full during the whole of the ventricular systole ; but during slow action 
 of the heart — whether the slow beat was occasional, as in Fig. 209, or con- 
 tinuous, as in Fig. 210 — the wave v was divided into two portions (a' and v) 
 
 Fig. 212. With the sudden reversion to the normal rhythm the heart becomes regular 
 and the jugular pulse of the normal auricular type. Compare this tracing with the three 
 preceding. (Case 12.) 
 
 by a deep depression. The explanation I suggest is that the auricular contrac- 
 tion occurred during the ventricular systole, but, being short, it finished before 
 the ventricular systole (as in Cushny's tracing, Fig. 58), and that the wave 
 a' in these tracings is due to the auricular systole, and the fall x is due to 
 the auricular diastole (probably the other factors mentioned in § 108 assist 
 
 Fig. 213. Sometimes when the heart reverted to the normal rhythm ventricular extra- 
 systoles (r') would appear. (Case 12.) 
 
 in deepening this fall). When the heart beats rapidly the engorgement 
 of the right side is so great that it obliterates the effect of the auricular 
 diastole. This explanation of a' is supported by the fact that sometimes 
 during a long pause, when the heart was acting slowly and irregularly, 
 a wave, presumably auricular in origin, would appear as in Fig. 211. 
 When the heart suddenly reverted to the normal rhythm, then it was 
 sometimes quite regular, as in Fig. 212, or there was an occasional
 
 328 
 
 DISEASES OF THE HEART 
 
 extra-systole, sometimes of auricular origin, as in Fig. 99, sometimes 
 ventricular, as in Fig. 213. During the last three months of her life the 
 rate was continuously rapid, and though I pushed such drugs as digitalis and 
 strophanthus no change was produced. Fig. 214 was taken a month before 
 she died. 
 
 Report of the post-mortem examination of the heart : — 
 
 Arteries. — Left coronary chiefly affected ; lumen narrowed. Anterior 
 interseptal artery which supplies the a. -v. bundle closed completely ; right 
 coronary affected, but to a less degree. 
 
 Orifices and Valves. — Valves not diseased. Mitral orifice dilated, tricuspid 
 dilated, inferior caval dilated, aortic normal. 
 
 Musculature. — Taenia terminalis hypertrophied. A.-v. node and bundle 
 large ; the fibres have the appearance of being stretched, having lost their 
 stellate reticular form : applied closely, and rather longer than usual. The 
 
 IB^^^^BIIWIHiBll 
 
 Fig. 214. Shows tlie character of the persistent nodal rhythm one month before death. 
 
 (Case 12.) 
 
 right and left septal divisions are normal in appearance. The inter- 
 auricular septum is stretched. The apical two-thirds of the left ventricle 
 shows large patches of fibrosis, and the trabeculae with the Purkinje system 
 are stretched, and certainly not healthy — fibrosis and atrophy — result of 
 endarteritis. 
 
 Case 13. — Frequent attacks of the nodal rhythm, with no serious ejects, in 
 old age. 
 
 Male, born 1827. Has suffered from frequent attacks of rapid action 
 of the heart, accompanied by a feehng of great prostration since he was 
 seventy-six years of age. During the attacks he feels very exhausted, 
 and lies in bed ; they last from half an hour to twelve hours. He may 
 be free from them for weeks, at other times he has several in one week. 
 I have seen him in consultation during these attacks and also when quite 
 free from them. In the latter condition he is a hale man, considering his 
 years, and takes an active part in his business ; his heart shows no abnor- 
 mality, and his pulse is slow and regular (Fig. 215). During the attack he 
 lies very still in bed ; his face is pale and slightly drawn. He does not care
 
 THE NODAL RHYTHM 
 
 329 
 
 to make much exertion, but has no actual suffering. The pulse sometimes 
 attains a rate of 200 per minute at the beginning of the attack. It was 
 always several hours after an attack had begun before I saw him, and the 
 pulse was usually between 150 and 170 beats per minute. Fig. 215 is 
 a tracing of his jugular and radial pulses while free from the attack ; there 
 was very slight pulsation in the neck, and I had some difficulty in getting 
 
 Fig. 215. Tracings from a man aged 78, when free from an attack of paroxysmal 
 
 tachycardia. (Case 13.) 
 
 a tracing. Its character, however, clearly shows it to be of the auricular 
 form. Fig. 216 shows the radial and jugular pulses during an attack. 
 I had considerable difficulty in getting satisfactory tracings, as the patient 
 was in bed in a position not conducive to taking a good tracing, but in 
 all those I took the characters were the same as in Fig. 216. Here the 
 
 boranstasiisifHil 
 
 IffiBBBBBml 
 
 
 JH 
 
 Fig. 216. From the same patient that gave Fig. 215, during an attack of paroxysmal 
 tachycardia. Note slight pulsus alternans in the radial tracing. (Case 13.) 
 
 jugular pulse is manifestly of the ventricular type. In the radial pulse there 
 is seen a tendency to the alternans form. 
 
 When last I heard of him (1908), at the age of eighty-one, he was in fair 
 health, and still liable to these attacks. 
 
 Case 14. — Attacks of paroxysmal tachycardia. 
 
 Male, aged thirty. Came under my care suffering from a hydatid cyst of 
 the liver. There was no history of any heart trouble, except that for the 
 last two years he had been conscious of a rapid ' fluttering ' action of the
 
 330 
 
 DISEASES OF THE HEART 
 
 heart. I was about to operate on him when I felt his pulse — it was beating 
 at the rate of about 200 beats per minute. He was conscious of this rapid 
 action, and said that it had come on two hours previously when at the 
 closet. The attack ceased quite suddenly two hours afterwards. I lost 
 sight of him some months afterwards, but he seemed in no way impaired 
 by these attacks. 
 
 Fig. 217 is a tracing of the jugular pulse when he was at rest. It is 
 a typical instance of the auricular form of the venous pulse. Fig. 218 shows 
 the character of the jugular and radial pulses during the attack. The 
 jugular pulse is now of the ventricular t3rpe. 
 
 Fig. 217. Simultaneous tracings of the jugular ani radial pulses from a case of paroxysmal 
 tachycardia during the quiet period of the heart's action. There is a well-marked auricular 
 wave, a, in the jugular pulse. (Case 14.) 
 
 Fig. 218. Simultaneous tracings of the radial and jugular pulses during an attack of 
 paroxysmal tachycardia. The jugular pulse is due to the ventricular systole, there being now 
 no trace of the amicular waves. (From the same patient as Fig. 217. Case 14.) 
 
 Case 15. — Sudden inceptioyi of the nodal rhythm, with 'persistent rapid 
 heart action, dilatation of the heart, dropsy, death in three weeks. 
 
 Female, aged sixty-five. I had attended her for various ailments 
 (rheumatism, bronchitis, &c.) during a period of over twenty years, and her 
 heart had invariably been quite regular. On June 20, 1904, she returned 
 from the seaside to her home and sent for me. She had been taken ill 
 a few days before, her chief complaint being shortness of breath. When 
 I saw her she was propped up in bed, and breathing rapidly and laboriously. 
 Her pulse was extremely rapid and irregular, but I did not have my poly- 
 graph with me. Next day when I called to see her, I found her greatly 
 improved, out of bed, and free from distress. Her pulse was full, regular,
 
 THE NODAL RHYTHM 
 
 331 
 
 and not rapid (Fig. 219). The following day, however, she was again very 
 bad, and Fig. 220, taken on June 23, gives a good idea of her pulse. She was 
 very stout and short-necked, and I had difficulty in getting a jugular tracing ; 
 her breatliing was laboured and, the sterno-mastoid being in action, I could 
 only get an imperfect tracing from the jugular, as in Fig. 220. Imperfect 
 as it is, it shows clearly that the venous pulse is of the ventricular form. 
 I tried all sorts of remedies to slow the heart — digitahs and opium, adi'enaUn, 
 trinitrin, &c., but all without avail. The heart dilated, di'opsy set in and 
 became very extensive, and she died three weeks after the permanent 
 establishment of the nodal rhythm. 
 
 Fig. 219. Regular pulse between attacks of nodal rhythm. (Case 15.) 
 
 Fig. 220. Permanent inception of nodal rhythm, leading to a fatal issue in three weeks. 
 
 (Case 15.) 
 
 Case 16. — Frequent attacks of paroxysinal tachycardia without serious 
 symptoms. 
 
 Female, aged thirty-five, eight months pregnant with her second child. 
 For several years she suffered from breathlessness, and was conscious that 
 her heart beat ' very queerly '. She was under my care for only a few weeks, 
 and I saw her during several attacks of paroxysmal tachycardia. After she 
 left me I heard that she had had an easy confinement, and some years later 
 was in fair health, though still at times prostrate on account of her heart. 
 The periods of nodal rhythm were of varying duration, the attacks not being 
 continuous, but interrupted frequently by normal beats. At other times 
 the heart would only show frequent extra-systoles. When the heart was 
 irregular the venous pulse was always large, while when the heart was regular
 
 332 
 
 DISEASES OF THE HEART 
 
 it was scarcely perceptible, and it was with difficulty that I got the faint 
 tracing of it in Fig. 221. The waves in the jugular, though slight, are recog- 
 nizable, and the jugular pulse is of the auricular type. In Fig. 222 the heart 
 is acting irregularly. The radial pulse shows three long pauses at x x X . 
 The auricular waves, a and a\ in the venous pulse occur at regular intervals. 
 During each long pause in the radial there is a large wave, a', due to the 
 auricle, and larger than the other auricular waves, for the reason already 
 given, p. 153, namely, because at the period at which the auricle contracted 
 
 \^i Jugular «,, 
 
 i 
 
 RctdxcLl ' 
 
 Fig. 221. Simultaneous tracings of the jugular and radial pulses. The jugular pulse 
 is of the auricular form. These and the following four tracings are from the same patient. 
 (Case 16.) 
 
 Fig. 222, Simultaneous tracings of the jugular and radial pulses during irregular action 
 of the heart. The auricle preserves its rhythm, there being a large wave, a', during the pre- 
 mature contraction of the ventricles. (Case 16.) 
 
 Fig. 223. Shows the same as Fig. 222. (Case Iti.) 
 
 the ventricle was in systole, and hence a larger wave was sent back into 
 the veins. It wiU be noted that after the large auricular wave, a', there 
 is never a ventricular wave. This tracing exemplifies the form of irregu- 
 larity due to premature stimulation of the ventricles alone .(ventricular 
 extra-systole). 
 
 In Fig. 223 a very similar irregular condition is present, the difference 
 being that every third arterial beat here is missed, and is represented in 
 the radial tracing by the notch n' . In these three tracings (Figs. 221, 
 222, and 223) the period E, representing the time when the semilunar valves
 
 THE NODAL RHYTHM 
 
 333 
 
 are open, shows in the jugular pulse a great fall. In Fig. 224 the radial 
 tracing shows two normal beats in the centre of the tracing, all the others 
 being nodal in origin. The beat preceding the full beats shows only a 
 notch, n', as in Fig. 222. The venous pulse at the time of the normal 
 radial beats shows the same features as are present with the normal radial 
 beats in the three preceding tracings, namely, a small auricular wave, a, 
 the carotid wave c, the auricular depression during the period E, and the 
 ventricular wave v. But when the venous pulse corresponding to the 
 
 Fig. 224. Simultaneous tracings of the jugular and radial pulses, showing two norma 
 radial beats in the centre of the tracing. Coriespondirg to the ventiicular systole, E, there is 
 a fall in the jugular pulse when the radial beat is normal, and a rise, E', when it is of nodal 
 origin. (Case 16.) 
 
 Fig. 225. Shows an alternation of the normal and nodal rhythms. (Case 16.) 
 
 E 
 
 
 e' Rad. 
 
 
 ^"^■-^wv^ 
 
 ^^r^ -^V.JV-'V-AyJV.A.-JVvA^-^^^' 
 
 AAx— ih^ 
 
 ^\r- 
 
 v^VvvwvvVaa./- 
 
 E 
 
 
 e' -^^ff- 
 
 Fig. 226. There is only one normal beat {E), all the other beats being of noda 
 
 origin. (Case 16.) 
 
 nodal beats is considered, a remarkable change is found. There is 
 but one large wave and one large fall, and the period when this wave occurs is 
 during the ventricular systole E', in striking contrast to the large depression at 
 the time with the normal radial beats showTi in the preceding three tracings. 
 A similar condition is seen in Fig. 225, where there is a continuous variation 
 from the normal rhythm to the nodal. In Fig. 226, with the exception of 
 one normal beat preceded by a long pause, the jugular pulse is of the ven- 
 tricular form. The transition from one form of jugular pulse to the other 
 is well brought out in Fig. 225.
 
 APPENDIX III 
 
 Paroxysmal Tachycardia of Auricular Origin 
 
 In reflecting upon the causes of abnormal rhythms of the hearty it seemed 
 reasonable to expect that at the place where an occasional stimulus arose 
 giving rise to an extra-systole it would be probable that the same place 
 might start off the heart's action continuously. This view has been con- 
 firmed in the instances of ventricular and nodal extra-systoles being the 
 precursors of the nodal rhythm. I had considered that inasmuch as auricular 
 extra-systoles were of frequent occurrence, it would be but reasonable to 
 expect that the heart's action might in some cases start continuously from 
 the place at which the auricular extra-systoles arose. In preparing the 
 first edition of this book I had examined my records for such a condition 
 and found a number of cases that seemed to fulfil this prediction. In four 
 instances the patients were suddenly seized with great rapidity of the 
 heart's action, and they all died from heart failure after a period varying 
 from one to four weeks. The tracings taken from these patients present 
 considerable difficulty in their interpretation, but I could only conclude 
 that they were cases of auricular tachycardia. In two other cases there 
 seemed distinct evidence of a paroxysmal tachycardia of auricular origin. 
 As the tracings were not altogether convincing I did not allude to the 
 matter, but resolved to wait for further experience. Within the past year 
 cases of undoubted paroxysmal tachycardia have been published by 
 Cowan, Macdonald and Binning ^^s^ and Lewis ^^i, while a case of continuous 
 auricular tachycardia has been published by Hertz and Goodhart ^43^ and 
 Dr. W. T. Ritchie has shown me another. 
 
 I have at present under observation a very instructive case of this 
 auricular form of paroxysmal tachycardia. The patient, a man aged 41, 
 a carpenter by trade, complains of weakness, palpitation, and attacks of 
 giddiness. The radial pulse is soft and compressible, and shows a varied 
 irregularity. At times there may be an occasional intermission, or these 
 intermissions may be very frequent. At irregular intervals the rate becomes 
 suddenly very rapid, and as suddenly becomes slow. These periods of
 
 PAROXYSMAL TACHYCARDIA OF AURICULAR ORIGIN 335 
 
 rapid action may last for a few seconds or for ten minutes. Tracings 
 taken of the radial and jugular pulses show the intermission to be due, 
 as a rule, to auricular extra-systoles, when the ventricle failed to respond 
 
 Fig. 227. Simultaneous tracings of the jugular and radial pulses during one attack of 
 paroxysmal tachycardia. The first cardiac cycle in the jugular tracing shows the normal 
 events {a, c, v). The second cycle shows the normal waves a and c, but the wave following 
 marked a' occurs earlier than the wave v in the previous cycle, and is due to a premature 
 or auricular extra-systole, but is not followed by a c wave or by a radial pulse beat. The 
 next two normal a, c, waves are each followed by an auricular extra-systole (a') with no 
 ventricular response, as shown by the absence of the c wave and the radial pulse beat. These 
 are all ' interpolated auricular extra-systoles '. After these there follows a series of auricular 
 premature beats (a') to which the ventricle responds as shown by the c waves and the small 
 radial puis 3 beats. 
 
 The onset of the paroxysm always coincides with great distension of the jugular veins, 
 which is shown in the tracing by the greater amplitude of the auricular waves a'. 
 
 r r Q. a' A k a ^. ^ a' ^' 9' a' 
 
 
 Fig. 228. From the same patient as Fig. 227, taken at the end of a long paroxysm. It 
 shows the same features as Fig. 227, but here there is a well-marked alternation of the radial 
 pulse beats during the paroxysm. 
 
 to the auricular extra-stimulus, or responded so weakly that the pulse beat 
 did not reach the radial (Figs. 227 and 228). 
 
 The rapid pulse beats in the radial are seen to be in response to a 
 rapid series of auricular contractions — the waves a' in Figs. 227 and 228
 
 336 DISEASES OF THE HEART 
 
 being due to the abnormal series of auricular contractions. In Fig. 227 
 one of these short paroxysms is shown, while in Fig. 228 there is shown 
 the end portion of a long attack. The radial pulse shows a well- 
 marked pulsus alternans, a feature not infrequently^ found after a long 
 paroxysm in the more common form of nodal paroxysmal tachycardia 
 (see Fig. 130, p. 198).
 
 APPENDIX IV 
 
 Nodal Bradycardia 
 
 I HAVE already remarked that in the vast majority of cases, where the 
 nodal rhythm is present, the heart's action is at first more rapid than normal, 
 but there is a class of case where, so far from the rate of the contraction 
 being more rapid than the normal, it becomes slower, and sometimes very 
 markedly so. In most other respects the character of the heart's action 
 corresponds to the more common forms of nodal rhythm, but if, as seems 
 probable, these commoner forms owe their inception to disease rendering 
 some part of the heart, such as the node, more excitable, this cannot hold 
 good when the rate is much slower than that of the normal rhythmic area. 
 Hence a search has to be made for some other cause. Facts pointing to 
 a definite cause may appear when all the features connected with these 
 cases are studied, and are compared with the results of experiment. There 
 is probably more than one form of this nodal bradycardia, for, in the cases 
 I have collected, in some the pulse though slow is quite regular, while in others 
 it is continuously irregular. 
 
 In some of these cases the heart's action becomes so slow that cerebral 
 anaemia results, with all the phenomena characteristic of the Adams-Stokes 
 syndrome, so that they may easily be mistaken for heart-block. The 
 differential diagnosis between cases of nodal rhythm and heart-block lies in 
 this — in heart-block the auricle is active and independent of the ventricular 
 systole, so that there is never a jugular pulse of the ventricular form ; the 
 ventricular form of the venous pulse, on the other hand, is characteristic of 
 the nodal bradycardia. 
 
 Case 17. — Old rheumatic affection of the heart, with long-continued impair- 
 ment of the a.-v. bundle, with a delay between the As and Vs. Sudden inception 
 of a slow and irregular action of the heart, with disappearance of all evidences 
 of auricular contraction, at first transient, later permanent. 
 
 Male, born in 1851. I attended him for an attack of rheumatic fever in 
 1883. He was left with a damaged mitral valve, but remained in fair health 
 till 1897, when he had serious heart failure. From this also he made a good 
 recovery, and his heart remained perfectly regular till 1904. I have taken 
 tracings of his apex, radial pulse, and jugular pulse at frequent intervals 
 
 MACKENZIE •/,
 
 338 
 
 DISEASES OF THE HEART 
 
 since 1892, His heart was invariably regular except for a short period in 
 1897, the irregularity being due to dropping out of ventricular systoles 
 <mild heart-block, see Fig. 115). His jugular pulse was always of the 
 auricular form, a peculiarity in this case being a persistent increase in the 
 a-c interval. Tracings of the jugular and radial pulses, taken in 1892, are 
 given in Fig. 229 ; in 1903 in Fig. 230. Jugular and apex tracings are 
 
 i 
 
 A « } 
 
 
 h/V 
 
 mmmmum 
 
 /Radial 
 
 2,Ur 
 
 r^''^ -w -— ^ 
 
 Fig. 229. Shows a regular rhythm and an auricular venous pulse and wdde a-c interval 
 (space A). Taken 1892. (Case 17.) 
 
 represented in Fig. 231. The rhythm is regular, and the auricular wave, 
 a, is well marked in both apex and jugular tracings. There was a long 
 diminuendo murmur after the second sound, and a well-marked presystolic 
 murmur separated by a brief interval from the first sound (shading in 
 
 Fig. 230. Shows a regular rhythm and an auricular venous pulse and wide a-c interval 
 (space A). Taken 1903. (Case 17.) (Figs. 229 and 230 are also discussed in § 164.) 
 
 Fig. 230). In the numerous tracings of the apex beat I have taken up to 
 April 19, 1904, there was always a well-marked auricular wave, a, preceding 
 the large wave. When he visited me on the last-named date I found his 
 heart continuously irregular, and on taking tracings of the jugular pulse 
 I found it of the ventricular type (Figs. 232 and 233), the presystolic murmur 
 had gone, and there was at the time only a diastolic murmur as shaded in 
 Fig. 232. The wave due to the auricular systole had disappeared from the
 
 NODAL BRADYCARDIA 
 
 339 
 
 apex tracing. Here, again, with the appearance of the ventricular venous 
 pulse and continuous irregularity all evidences of the contraction of the 
 right and left auricles had disappeared. When this patient called to see me 
 
 Fig. 231. Shows the auricular wave (a) in jugular and apex tracings. There is an increase 
 in the time from the beginning of the auricular wave (a) to the large wave due to the ventricle 
 in the apex tracing, and a corresponding increase in tlie a-c interval in the jugular tracing. 
 Taken 1903. (Case 17.) 
 
 Fig. 232. With the inception of the nodal rhythm the heart is irregular, the auricular 
 wave is gone from jugular and apex tracings (compare with Fig. 231), and the shading 
 underneath shows a disappearance of the presystoUc murmur. (Case 17, April 19, 1904.) 
 
 in the following week I found his heart perfectly regular, the auricular wave 
 present in the venous pulse, the presystolic murmur, and the auricular wave 
 in the apex tracing also present (Fig. 234). These conditions continued 
 
 z 2
 
 340 DISEASES OF THE HEART 
 
 until November, 1904, when his heart again became irregular, and all 
 evidence of auricular systole again disappeared. From that date up to the 
 present (1908) the heart has remained in this state, and on the numerous 
 occasions when I have taken long tracings I have never yet found the heart 
 regular for one moment (Fig. 238, Plate III). 
 
 Fig. 233. Shows a slow irregular rhythm with the ventricular form of the venous pulse. 
 
 (Case 17, April 19, 1904.) 
 
 
 Fig. 234. Shows a regular rhythm and the presence of the auricular wave in the apex and 
 jugular tracings. (Case 17, April 26, 1904.) 
 
 Case 18. — Sudden inceptio?i of nodal bradycardia, lasting for about three 
 weeks. 
 
 Male, born 1852, a stout, healthy-looking individual. I had known him 
 for about twenty-eight years, and had attended him at various times for 
 trivial complaints, and in 1903 for an attack of erysipelas of the face. He 
 had enjoyed good health, was getting fat and somewhat short of breath. 
 On November 9, he was hurrying from the train to a football match, a mile 
 distant from the station. As he approached the football field he was seized 
 with pain across the middle of the chest, but as it was not severe he pushed 
 on tiU he arrived at the field. He sat down, but the pain increased, striking 
 into both arms, and his hands went white and cold. He felt as if he wanted 
 to breathe deeply but could not. He endured the suffering for twenty 
 minutes, and as it became worse, and he felt as if he would die, he was 
 assisted 'off the field, put into a cab and driven to the station. He was
 
 NODAL BRADYCARDIA 
 
 341 
 
 given some brandy, which made him sick. The pain gradually diminished, 
 and he returned home by train ; as he was better he walked home (about 
 a quarter of a mile), but felt sick and short of breath. He went to bed, 
 and one of my colleagues saw him and found his pulse between 30 and 
 40 beats per minute. I saw him next morning. He felt very weak ; the 
 pain was nearly gone, though it had kept recurring through the night. He 
 had some pain if he took a deep breath. The pulse rate was 52, the heart's 
 dullness extended from mid-sternum to 2 inches beyond the nipple line ; 
 apex beat faint in the fifth interspace ; sounds clear and free from murmur. 
 The superficial jugular vein was very full, but did not pulsate. The deep 
 jugular was large, filling up during ventricular systole, and collapsing 
 suddenly at the beginning of ventricular diastole. There was no sign of 
 an auricular wave preceding the ventricular systole. The patient was kept in 
 
 fn-y^t. /y^fj-- 
 
 FiG. 235. Simultaneous tracings of the jugular and radial pulses. The jugular pulse is 
 of the ventricular form, and shows the wave a' preceding by a short interval the time of the 
 carotid pulse (perpendicular line 3). Pulse-rate, 40 per minute. (T.A., November 24, 1907.) 
 
 bed, and his condition did not undergo much change for the next fortnight, 
 except that the pain gradually grew less till it finally disappeared and 
 he was able to sit up. The pulse-rate varied, sometimes falling as low 
 as 30, but never rising above 52. On November 24 a long tracing was 
 taken with the ink polygraph, and the rate showed great uniformity ; the 
 rhythm was also quite regular. Fig. 235 is a small portion of the tracing 
 taken on that day, and represents the same features as were present on 
 November 10 ; the rate was 40 per minute, the rhythm regular, and the 
 venous pulse of the ventricular form. When I next examined him on 
 November 29, his pulse had increased in rate, with occasional intermissions. 
 I had the greatest difficulty in getting a tracing of the jugular pulse ; he 
 had a very short fat neck. But imperfect as the tracings were, they showed 
 a return of the auricular wave a to its normal period before c. From this 
 date he gradually improved, and has been able to get about, though he is 
 perhaps a little shorter of breath than before his attack. Tracings were 
 taken from him in December, 1908, and on May 11, 1909. The venous
 
 342 DISEASES OF THE HEART 
 
 pulse was the same on both occasions, and showed an auricular wave, a, 
 preceding the carotid wave, c, while the rate was 68 per minute ; the 
 rhythm was regular. 
 
 Case 19. — Inceptioii of the nodal rhythm, the heart's rate at first not 
 infrequent, but becoming slow with attacks of unconsciousness and epileptic 
 fits. Recovery from these attacks with an increase in the heart's rate. 
 
 Male, born 1838. I have known this patient intimately since 1894. 
 He was a healthy, vigorous man up till 1907. He was a very heavy smoker, 
 and for a great many years he smoked two ounces of tobacco and half 
 a dozen cigars a day. I had occasion to examine him in 1906, and found 
 his heart normal in rate and rhythm, though for some years he had been 
 rather short of breath. I again examined him in February, 1907, and 
 found that his heart was continuously irregular mth the disorderly rhythm 
 characteristic of the nodal rhythm. He was not conscious of the change, 
 but there was a further increase in his breathlessness. He was still able 
 to attend to business, and to play a game of goH. He Uved some distance 
 from me, and I did not see him again until October 11, 1907, when I was 
 asked to see him with his medical attendant, Dr. O'Connor, to whom I am 
 indebted for an excellent account of his many seizures. The history given 
 was that his pulse had become very slow for some months, and that latterly 
 he had been seized at times with attacks of unconsciousness. The pulse- 
 rate on such occasions was found below 30 beats per minute. He was very 
 weak and faint when I saw him, the pulse varying in rate from 30 to 40 
 beats per minute, and irregular with long pauses at times. During the 
 long pauses there was often a small premature beat in the jugular (see 
 v' , Fig. 236). The heart's dullness extended 1| inches beyond the left nipple, 
 and there was a soft blowing murmur at the apex. There was a small 
 amount of albumen in the urine. The attacks of unconsciousness continued, 
 and I saw him again in November, when the heart's condition was much 
 the same. After this the pulse-rate increased, the attacks disappeared, 
 and he went to Torquay in June, 1908, where he had a slight recurrence 
 of his attacks of loss of consciousness. From this he recovered, and con- 
 tinued well till August 4, when after some effort he was seized with great 
 breathlessness, and the attacks of unconsciousness recurred. These increased 
 in number and severity, and for two whole days he was unconscious and 
 deeply cyanosed. ^ For some hours he passed from one epileptic seizure to 
 another as if affected with uraemic convulsions. He also developed Cheyne- 
 Stokes respiration. The pulse during these convulsive attacks was not 
 perceptible. The severity of the attacks gradually lessened, and in the 
 month of September his pulse-rate rose to 50 or 60 beats per minute. In
 
 NODAL BRADYCARDIA 343 
 
 October he had a number of very transient fainting attacks. Dr. O'Connor 
 described the attacks as resembling petit mal. Thus, while the doctor 
 was talking to him, the patient's face would suddenly become pale, and 
 consciousness would be lost for a brief period. During these attacks no 
 pidse could be felt at the radial. 
 
 I saw him again on December 18, 1908. He was able to go about, 
 and had been free from attacks for a few weeks. The pulse was rather 
 slow, about 60 per minute, and irregular. The heart's dullness extended 
 1| inches beyond the left nipple, the sounds were clear, with a faint doubling 
 of the first sound. There was no dropsy, and the urine was free from 
 albumen. 
 
 On May 5, 1909, he was seen by Dr. John Hay, who took a long tracing 
 with the ink polygraph. The rhythm was of the disorderly kind, charac- 
 
 FiG. 236. Simultaneous tracings of the jugular and radial pulses. The jugular pulse is 
 of the ventricular form. During the long pauses in the radial pulse, there are small premature 
 beats, v', in the jugular. The pulse-rate varied from 25 to 30 beats per minute. The patient 
 was just recovering from a series of syncopal and epileptic attacks. (W.N., October 11, 1907.) 
 
 teristic of the nodal rhythm, and the jugular pulse was of the ventricular 
 form. In August, 1909, the heart's action became very infrequent, and he 
 was seized with attacks of loss of consciousness and epileptic convulsions, and 
 he died in one of these attacks. 
 
 I had looked upon this case, at first, as an instance of Adams-Stokes 
 syndrome, due to heart-block, but at the time I was puzzled to account for 
 the fact that he had nodal rhythm prior to the onset of the attacks of uncon- 
 sciousness and slow heart-rate, and also because of the nature of the jugular 
 pulse, which was of the ventricular type. The tracing of the jugular has never 
 been shown to be of this type in cases of heart-block. Case 18, which came 
 under my observation in December, 1907, also puzzled me, and it was only 
 when I began to analyse the tracings more carefully that the nature of the 
 tracings from this patient dawned upon me, and that it became obvious that 
 here we had an instance not of blocking of the stimulus between auricle and 
 ventricle, but one of slow nodal rhythm producing anaemia of the brain.
 
 344 DISEASES OF THE HEART 
 
 Case 20. — Permanent nodal rhythm, bradycardia associated ivith mitral 
 stenosis. Occasional attacks of syncope and convulsions {Adams-Stokes 
 syndrome). 
 
 Male, born 1865. When a soldier in India he had dysentery at the age 
 of 20, syphilis at the age of 22. He had malarial fever in America at the 
 age of 27. In 1894 he had the first attack of syncope. After lying up 
 a week he went out, and in hurrying to avoid a cab he fell unconscious 
 on the pavement, but quickly recovered. He consulted a doctor, who said 
 his heart was affected. Two years later he was laid up with shortness of 
 breath and swelling of the legs, and was treated for ' mitral disease '. He 
 partially recovered, and had frequent attacks of weakness until the final 
 
 Fig. 237. Simultaneous tracings of the jugular and radial pulses. The jugular pulse is of 
 the ventricular form, and the rate about 28 per minute. (M.M., November 9, 1908.) 
 
 breakdown occurred in 1905. He had been feeling ill for some years, but 
 had worked hard, and had kept himself going on brandy, bovril, eggs, &c. 
 He says his pulse was slow four years ago, and that it has remained so ever 
 since. 
 
 In 1904 he began to have mild * fits ' in which he lost consciousness 
 and was slightly convulsed. From November, 1905, to April, 1906, he had 
 a great number of fits, some severe with convulsions and cyanosis, others 
 slight without convulsions. He had no attacks for a year, but he had 
 a very severe one in April, 1907, and since then only three mild attacks. 
 He had lived a life of hard work with frequent bouts of drinking. 
 
 The patient is taU, spare, and intelligent looking. The face is usually 
 ruddy, with a faint duskiness. He walks slowly and carefully, and his 
 gait is slightly ataxic ; if he hurries or gets excited he becomes giddy. 
 He has a somewhat violent temper, and when in a passion his face becomes 
 dusky and cyanosed. When lying down there is a large pulsation, seen 
 in the deep jugular on both sides, heaving in the lower part of the neck, 
 as in Fig. 237. It is very slow and synchronous with the apex beat. 
 
 The radial pulse is slow and deliberate, usually about 30 per minute, 
 and usually quite regular. At times two beats are close together, and are
 
 NODAL BRADYCARDIA 345 
 
 followed by a long pause. These coupled beats may appear at rare intervals 
 or alternate with a single beat, or they may appear continuously for a short 
 period. The apex beat is large and diffuse in the sixth interspace, and in 
 the anterior axillary line. The heart dullness extends 1 inch to the right 
 of the middle hne and 8 inches to the left. 
 
 There is a rough blowing systolic murmur heard best at the apex and 
 propagated towards the axilla. The second sound is clear and well struck 
 and followed by a soft murmur. This diastohc murmur is heard only over 
 a limited space at the apex, and is not always perceptible. It is, as a rule, 
 faint and fades away. 
 
 A large number of tracings have been taken from this patient at different 
 times and they always present the same features, the only difference being 
 that sometimes the coupled beats are more frequent or are entirely absent. 
 The jugular tracing shows one large wave occupying the whole time of 
 ventricular systole. 
 
 The Tendency to Standstill of the Heart in Nodal 
 Rhythm, with Notes of Two Cases 
 
 The tendency for long pauses in the heart's action in cases of nodal 
 rhythm, such as those seen in Cases 17 and 19, has been a matter of interest 
 to me for many years. These pauses may not produce any symptoms, but 
 they may last long enough to produce anaemia of the brain with transient 
 loss of consciousness, and even the more prominent phenomena of Adams- 
 Stokes syndrome (Cases 19 and 20). The symptoms then resemble those 
 of the more common condition, auriculo-ventricular block. I have been 
 impressed by the fact that not a few cases of nodal rhythm die suddenly, 
 and it seems that this tendency to long pauses shown in the figures may 
 be the immediate cause of death, as in the following case. The proof of 
 this view is not complete, but the following cases are also very suggestive. 
 
 Case 21. — Nodal rhythm, with long pauses in the heart's action, producing 
 attacks of unconsciousness and 'probably the death of the patient. 
 
 Female, born 1854. I had known this lady for many years. She had 
 a large goitre, and for the last few years of her life her heart was con- 
 tinuously irregular. She was not robust, but was able to attend to her 
 household duties ; she was liable to attacks of palpitation, and had frequent 
 attacks of syncope, which I could not account for at that time. On July 2, 
 1902, I was summoned to see her, and on my arrival I found her recovering 
 from an attack of unconsciousness during which she had been convulsed. 
 Her face had a deathly ex-sanguine appearance. She gradually recovered,
 
 346 DISEASES OF THE HEART 
 
 and her colour improved in the course of half an hour. On inquiry, I found 
 that she was talking to her sister when she fell down in a faint and became 
 convulsed for a few minutes. 
 
 When I examined her, the heart was acting irregularly but with fair 
 strength. During the next few days her heart was irregular with long 
 pauses, as shown in Fig. 239, taken on July 3, 1902. She sometimes lost 
 
 Fig. 239. Simultaneous tracings of the apex beat, and of the radial pulse. The rhythm 
 is disorderly and characteristic of the nodal rhythm, with frequent long pauses. It was 
 probably in consequence of these long pauses that the patient suffered from attacks of 
 unconsciousness and convulsions. (M.B., July 7, 1902.) 
 
 consciousness for a few seconds, but I did not see her at those times. On 
 July 7 I was again summoned to see her, but when I arrived she was dead. 
 I was informed that she had again fainted, become convulsed, and then 
 lay quite quiet. 
 
 ■■MM^^l^HH^HMHHM^^l^^BHIH^H^I^HHail^^^^^ia^^lMHBHI^HBIi^HBHHa 
 
 Fig. 240. The jugular pulse shows a large auricular wave and an increased a-c interval 
 
 (space A). (Case 22. 1892.) 
 
 Case 22. — Large auricular waves in the jugular and liver pulsation. Pre- 
 systolic mitral and tricuspid murmurs. Auricular sound over the valves in the 
 large veins. Sudden disappearance of all signs of auricular contraction, with 
 the appearance of continuous irregularity in the heart's action. Sudden death. 
 
 Female, born 1862 ; came under my care in 1891. She suffered from 
 shortness of breath on exertion, and for some months before her death 
 from severe attacks of pain striking from the front of the left chest down 
 the inside of the left arm to the Httle finger, with great tenderness of skin 
 over the area of pain after the attack had subsided. She had erysipelas in the
 
 NODAL BRADYCARDIA 
 
 347 
 
 face in 1883 and 1885, and since then she has been short of breath, and 
 with a tendency to sweUing in the legs. The pulse was small, quick, and 
 usually regular, but I occasionally detected an extra-systole, which Fig. 246 
 shows to be auricular in origin. There was a large pulsating sweUing on 
 
 Fig. 241. Simultaneous tracings of jugular and carotid pulses. (Case 22. 1892.) 
 
 Fig. 245. Simultaneous tracings of jugular and liver pulses ; a, auricular wave ; 
 V, ventricular wave; .r, auricular depression. (Case 22.) 
 
 Fig. 246. 
 
 Simultaneous tracings of tlie jugular and radial pulses, showing a large wave (a') 
 due to an extra-systole of the auricle. (Case 22.) 
 
 either side of the neck near the sternal end of the clavicle, Figs. 240 and 
 241, but no distinct pulsation in the veins above these swellings. When 
 compared with the carotid pulse there were seen to be two distinct move- 
 ments, the one larger than the other, to each carotid pulse, and the larger 
 movement could be observed to precede that of the carotid pulse (Fig. 241).
 
 348 DISEASES OF THE HEART 
 
 The liver could be felt pulsating just below the ribs, and the liver pulse 
 was of the same character as the jugular (Fig. 245). 
 
 The area of cardiac dullness was increased, extending transversely one 
 and a half inches to the right beyond the middle line. There was always 
 present a long murmur, presystolic in time, heard best at the apex ; another, 
 shorter and rougher, of a different character, but corresponding in time, 
 was heard best over the middle of the sternum. The latter murmur was 
 occasionally absent at first, but ultimately became a constant pheno- 
 menon. There was also a murmur, systolic in time, heard at the apex. 
 At the base the second sound was reduplicated. No murmur was heard 
 in the carotids, but there was a distinct sound heard over the pulsating 
 swelling in the neck synchronous with the pulsation and preceding the 
 
 Fig. 247. Simultaneous tracings of a slight movement in the neck and of the radial pulse. 
 The rhythm is now continuously irregular, with a tendency to long pauses. The tracing 
 from the neck was taken from the same situation which gave the jugular pulse in the four 
 preceding figures, and demonstrates the absence of any wave due to the auricle. (Case 22. 
 1895.) 
 
 first sound of the heart. This sound could also be heard under the clavicle 
 and over Poupart's ligament — i.e. over the valves of the subclavian and 
 femoral veins. The jugular and subclavian valves being competent, the 
 jugular bulb became distended into a ball-like protrusion over the inner 
 end of the clavicles, and the pulsation was conspicuous at the distance of 
 ten yards. 
 
 These symptoms persisted, though the patient became gradually weaker 
 and had severe attacks of angina pectoris on the shghtest exertion. (Figs. 1 1 
 and 12 are drawn from her.) At 3 a.m., October 9, 1895, she awoke and 
 was conscious that the beating in her neck had ceased. She called my 
 attention to this next morning, and on examination I found that there 
 was now no pulsation in the jugular bulb. Thus Fig. 247 was taken from 
 her on October 9, 1895, and the receiver was held over the place where the 
 jugular tracings Figs. 240 and 241 were obtained, and it will be observed 
 that there is a complete absence of the auricular wave which is so marked 
 in these tracings. In Fig. 247 there is only a faint movement due to the 
 carotid, and possibly at the beginning of this tracing a sUght ventricular 
 venous pulse can be detected. Careful examination showed that the liver
 
 NODAL BRADYCARDIA 349 
 
 pulse had entirely disappeared, as well as the mitral and tricuspid presystohc 
 murmurs. 
 
 On October 13, 1895, on getting out of bed, she fell and died. 
 
 Before removing the heart at the post-mortem examination I injected 
 water forcibly into the superior vena cava, and the water could not pass 
 beyond the jugular valves, but distended greatly the jugular bulb. The 
 report on post-mortem examination of the heart is as follows : — Marked 
 tricuspid and mitral stenosis. There is dilatation of the apex of the left 
 ventricle, pre-mortem clot in apex of right auricle. The series of sections 
 of a.-v. biuidle is good, and shows that in this heart the node at the com- 
 mencement of the main bundle and the septal divisions were uncommonly 
 well developed. Main bundle healthy. There are signs of great venous 
 back-pressure in the capillaries and veins. The arteries in the neighbour- 
 hood of the bundle are not thickened. 
 
 I have dealt with this subject of nodal bradycardia more fully else- 
 where ^^^.
 
 APPENDIX V 
 
 Irregularities in Cardio-Sclerosis 
 
 The cause of the variations in the size of the pulse-wave is a subject that 
 needs elucidation. There are different ways in which it may arise. The 
 amount of blood in the heart at the time of the systole has little bearing in 
 the cases to which I refer, inasmuch as there is usually plenty, the heart 
 being somewhat dilated. Apart from this, the difference in the size of the 
 pulse-wave depends on the strength of the ventricular contraction, which is 
 determined by the contractile force of the heart muscle and the number of 
 the fibres participating in the contraction. In a case of sinus irregularity, 
 especially one of those occurring in young subjects, we find that, no matter 
 how long or short the rest preceding the contraction, the beats themselves 
 are of great miiformity (Figs. 73, 74, 79). On the other hand, in the irregu- 
 larities of the nodal rhythm we find the size of the beat varies with the length 
 of the preceding pause — the longer the rest, the bigger the beat. This 
 implies that the recovery of contractile force is not so rapid as in the young 
 with a sinus irregularity. This is the explanation adopted in § 179 to 
 explain the pulsus alternans. But this explanation is not the only possible 
 one. Muskens maintains that the smaller size of the beat is due to the 
 fact that aU the fibres do not contract, that there is a block preventing the 
 stimulus for contraction from reaching all the fibres. He states that he 
 has been able to produce the block experimentally in the frog's heart. On 
 consideration, I have, however, adopted the view of Hoffmann and Wencke- 
 bach in regard to the pulsus alternans, though Muskens' views are appHcable 
 to other conditions of irregularity, and I have arrived independently at 
 a similar conclusion. I refer to those instances in which there are varying 
 sizes in the pulse-wave, and in which big waves may occur after a short 
 period of rest, while very small waves may occur with a period of rest of the 
 same duration. Here the smaller beats may be caused by some fibres of 
 the ventricle faihng to contract along with the general mass, or, as recent 
 electro-cardiograms seem to show, the variation in the size of the beats may 
 be due to the starting of the ventricular contractions from different places. 
 
 I have not been able to work out the matter to a satisfactory conclusion, 
 but I have used it as a means of forming a prognosis, and I am inclined to
 
 IRREGULARITIES IN CARDIO-SCLEROSIS 351 
 
 think this point will be of some value. The matter needs further considera- 
 tion, and the different factors will be better appreciated by the study of 
 typical irregularities, whose nature can be analysed with a greater degree of 
 certainty. A good deal of preliminary work will have to be done to under- 
 stand the different causes of variations in the strength of the beats. To that 
 end, I quote here two cases that showed during life a somewhat bewildering 
 variety of irregularities, and I demonstrate how these can be referred 
 to their various causes with certainty. The citation of these cases also 
 brings out certain important features due to cardio-sclerosis which must not 
 be looked upon as exceptional, for I have seen a great many cases exhibiting 
 the same features and due to the same causes. Briefly, these features are 
 variations in the strength of the contraction, the size of the beat depending 
 on the period of rest and the occurrence of extra-systoles. 
 
 Case 23. — Male, aged fifty-seven. Consulted me on May 1, 1905, com- 
 plaining of weakness on exertion, a sense of great exhaustion and trembHng 
 of the legs. He first noticed the breathlfessness three years ago on hurrying 
 up a hiU, when he had a severe attack. He felt fairly well until six months 
 after, since which time the breathlessness is very easily provoked. 
 
 He is a life-long abstainer, and has led a steady, regular life. In his 
 younger days his work entailed severe bodily effort, but for the last twenty 
 years his occupation as mill manager has not demanded much exertion. 
 Twenty years ago he had an attack of ' inflammation of the kidneys '. He 
 is a powerfully built man ; face greyish in colour, pulse rapid (86 per minute) 
 and hard, the artery large and leathery in consistence. Heart is enlarged, 
 dull to the nipple line. The sounds are clear and distinct ; the urine con- 
 tains a large quantity of albumen. Blood-pressm-e, 210 mm. Hg. He was 
 directed to take his food in small quantities, and to chew it thoroughly ; to 
 have his bowels freely opened ; and he was put upon iodide of potassium. 
 He improved wonderfully for a time, aU the albumen disappearing from the 
 urine, but he began to relapse. Abstinence from meat was tried and seemed 
 to do him good for a short time, but he relapsed. The blood-pressure records 
 were very confusing, sometimes falling to 145 and rising to 210, and this 
 independent of drug or diet. There was no corresponding improvement in 
 his condition with the fall of blood-pressure. When it was low he felt 
 depressed, and sometimes felt very well when it was high. His pulse 
 was usually alternating in rhythm, and the pecuharity was more marked 
 when the pressure was high. When the irregularity had disappeared with 
 lowered blood-pressure, it could easUy be brought back by running up a flight 
 of stairs. The difference in pressure between the beats was about 20 mm. Hg. 
 — that is to say, if the radial pulse was obliterated by raising the pressure
 
 352 
 
 DISEASES OF THE HEART 
 
 in the cuff to 200 mm. Hg., and the air allowed to escape from the cuff, the 
 large beats would be felt coming through at 190 mm. Hg., while the smaller 
 would not be felt till the pressure in the cuff had fallen to 170 mm. Hg. (see 
 Fig. 248). 
 
 Fig. 248. Tracing taken from the radial artery after tlie air bag connected with the mano- 
 meter had obUterated the pulse at a pressure of 190 mm. Hg. The air was allowed to escape 
 gradually, and when the pressure fell to 180 mm. Hg. the sphygmograph received the stronger 
 beats, and the smaller beats came tlu-ough when the pressure fell to 170 mm. Hg. When the 
 pressure in the air-bag was exhausted the pulse tracing showed rhythmical variation in the 
 size of the waves — that is, the pulsus alternans. 
 
 Notwithstanding the alternating rhythm, the pulse rate was practically 
 regular (Figs. 249, 250, also Figs. 168-170). In May, 1906, extra-systoles 
 began to appear, and they gave a peculiar character to the tracing. Thus, in 
 Fig. 249 the tracing shows a perfectly regular rate with a smaU and large 
 
 RctdiaL 
 
 JAiiiAMtWIMiiiAlIiABlll 
 
 Fig. 249. Typical pulsus alternans with ventricular extra-systole r'. In the diagram 
 it is shown to occur prematurely (downstroke x ) and independently of the auricular stimulus. 
 After the extra-systole there is a longer pause, and the alternating character of the pulse 
 becomes more marked. (Case 23.) 
 
 beat alternating, except in the centre, where there are two small beats in 
 succession. On measuring the tracing it wiU be found that the second of 
 the two smaller beats (r') occurs a little too early. The jugular tracing shows 
 that the auricular wave (a) is perfectly regular, therefore r' is a ventricular 
 extra-systole and after it there is a longer pause than normal, so that the 
 beat after the pause is large, and the succeeding beat smaller than the other
 
 IRREGULARITIES IN CARDIO-SCLEROSIS 353 
 
 beats for the reason explained in § 179. This increase of the alternating 
 character of the rhythm is seen in Fig. 250. Here there are two extra- 
 systoles, one as in Fig. 249 after the small beat, and the other after a large 
 beat, and here also the character of the alternating rhythm is more marked 
 after the extra-systole. 
 
 The patient also began to have attacks of angina pectoris, which I have 
 described (Case 1, Appendix I). He became restless and disturbed at night, 
 and the attacks of pain became more frequent, until he was put upon bromide 
 of ammonium, when he began to sleep better, and the angina disappeared. 
 Towards the end of 1906, Che3nie-Stokes respiration appeared (Fig. 6, Plate I), 
 his nights became very restless, and he could only be reheved by opium and 
 chloral. In January dropsy set in, the heart dilated, and his blood-pressure 
 fell permanently to 150 mm. Hg. and under. The virine became scanty. 
 
 Fig. 250. Here there are two extra-systoles (r' r'), one after the small beat and the-other 
 after the large beat of the alternating rhythm. (Case 23.) 
 
 Various preparations of digitalis and other drugs were tried with little good 
 results, and the patient died in March, 1907. Permission was only given to 
 examine the heart, and the following is the report of the post-mortem 
 appearance : — 
 
 Musculature of ventricles. — Hypertrophied, but the apical half of ventricle 
 is fibrosed and dilated ; large pre-mortem clot adherent to the anterior wall 
 of the left ventricle. Thickness of wall at base, 18-22 mm. ; over the fibrosed 
 area, 6-8 mm. The musculature at the mouth of the superior vena cava is 
 hypertrophied. Taenia terminahs is hj^ertrophied, and under the microscope 
 shows many fibres atrophied and fibrosed. 
 
 Valves and orifices. — Mitral cusps thickened ; tricuspid, pulmonary, and 
 aortic healthy. Auriculo-ventricular orifices smaller than normal, due to 
 tonus or contraction of the musculature of the base. 
 
 Arteries. — Patches of atheroma in aorta, especially at orifices of coronary 
 arteries. Intense endarteritis of left coronary artery, diameter 6 mm., 
 
 MACKENEIE r ^ g^
 
 354 DISEASES OF THE HEART 
 
 lumen 2-5 mm. ; the interior is especially thickened. The right coronary 
 artery is not so much affected. All the arteries of the heart above 1-5 mm. 
 in diameter are affected if they lie outside the musculature of the heart ; if 
 surrounded and supported by the musculature, less affected. The anterior 
 inter-ventricular artery was most affected, while the artery to the a.-v. bundle 
 from the right coronary was more like a needle-prick. 
 
 Remains of 'primitive cardiac tissue. — Sino-auricular node, less muscu- 
 lature (more fibrosed) than in health, still not marked. The a.-v. bundle is 
 normal in size, and its fibres and ceUs are normal. 
 
 Case 24. — Male, aged seventy-two. I have known the patient for over 
 twenty-five years as a steady, sober, and industrious man. He worked at his 
 occupation as an engineer up to within a year of his death — though in later 
 years he did not do much laborious work. He had a slight attack of hemi- 
 plegia in December, 1906. He consulted me in June, 1907, because he passed 
 blood in his urine. Except for being rather short of breath, he felt fairly well. 
 He looked a hale old man. His radial arteries were large and tortuous, pulse 
 full, seemingly regular. His heart's dullness extended to the nipple Une. 
 The sounds of the heart were clear except for a musical murmur, systolic in 
 time, heard over the whole heart region, but loudest in the aortic area. It 
 varied distinctly in loudness, a loud murmur alternating with one less loud. 
 When I took a radial tracing it showed a well-marked pulsus alternans. He 
 visited me several times. The urine became quite clear, but the heart's 
 condition continued, and extra-systoles were sometimes very frequent, 
 and gave to the pulse the appearance of extreme irregularity (Figs. 243, 
 Plate III, 244, Plate IV). 
 
 Early in August he complained greatly of attacks of bad breathing in the 
 night. He would go to sleep quite quietly and then awake suddenly with 
 a sense of suffocation, and sit up in bed breathing heavily. After half an 
 hour he would feel easier, but could not lie down, and had to be propped up 
 in bed. These attacks occurred on several occasions, until they disappeared 
 in September, when his legs began to swell, and he expectorated quantities of 
 blood-stained mucus and small clots of blood. His heart's dullness extended 
 two inches beyond the nipple fine ; the veins of the arm became full. Vene- 
 section was tried, but with little good result, and he died in October. 
 
 An analysis of the tracings taken shows that the irregularity which looked 
 80 hopelessly confused was due to the mixture of the pulsus alternans with 
 extra-systoles. Thus, Fig. 242, Plate III, shows exactly the features described 
 in Fig, 250, where there are several extra-systoles {r') after the large beat 
 and one after the small, with an increase in the alternating character of 
 the rhythm after the extra-systole. Sometimes the extra-systole appears
 
 IRREGULARITIES IN CARDIO-SCLEROSIS 355 
 
 regularly after each smaU beat, and the pulse has the appearance of what 
 used to be called a trigeminal pulse, but this is simply due to a big beat after 
 the long pause followed by a small normal beat, which is in turn followed by 
 a ventricular extra-systole (Figs. 243, Plate III, 244, Plate IV). The jugular 
 tracing is due to the auricle and varies at times in rhythm, so as to give rise 
 to the suspicion of auricular extra-systoles at ax. The patient being unable to 
 hold his breath, the jugular pulse varies in size with the respiratory move- 
 ments. These movements are recorded in Fig. 244, Plate IV. The respiratory 
 movements render it somewhat difficult to be sure of the beginning of the 
 auricular systole, and I have endeavoured in the intercalated diagrams to 
 show the relative time of the auricular and ventricular systoles, and the time 
 the stimulus took to pass from auricle to ventricle. Except in Fig. 243, the 
 slanting line in the middle space represents the a-c interval ; in Fig. 243 it 
 represents the interval between the auricular systole and radial pulse. It 
 will be seen that the duration of the interval varies, suggesting that the 
 cardio-sclerosis from which the patient suffered also affected the a. -v. 
 bundle — a suggestion which receives some support from the post-mortem 
 examination. 
 
 Report of the post-mortem examination of the heart : — 
 The mitral and tricuspid valves show no pathological changes. The 
 auricles are not markedly dilated ; the coronary sinus is filled with post- 
 mortem clot. The ventricles are not dilated, except at the apical part 
 of the left. Both coronary arteries show a thickening of their coats, with 
 dilatation, the left more than the right, and the anterior interventricular 
 branch of the left most affected. At the apex of the left ventricle is an area 
 showing intense fibrosis with deposits of premature clot, but microscopic 
 sections show the Purkinje and inner muscle-layer healthy. 
 
 The a.-v. node and bundle show a fibrosis, not intense, and also a stretching 
 of the bundle, as if the pars membranacea had been stretched. There is no 
 sign of cellular change in the bundle or node, except the predominance of 
 the fibrous tissue over the muscle tissue — the muscle-fibres, instead of reticu- 
 lating, being stretched and parallel. 
 
 Aa 2
 
 APPENDIX VI 
 
 The Effects of Digitalis on the Human Heart 
 
 In Chapter XXXIV I dealt with this subject, and here I cite a few 
 cases to illustrate further the importance of this line of investigation, and 
 to call attention to the varying ejBfects of digitalis on different heart-lesions. 
 I wish also to impress upon hospital physicians, by these illustrative cases, 
 the great opportunities they have of demonstrating by such observations 
 the efifects of remedies. The experiences I detail here were obtained in the 
 course of my daily work as a general practitioner, and from among my 
 private patients. The difficulties of sufficiently precise observation were 
 insuperable, so that of necessity my work lacks the precision of a physio- 
 logical experiment — a precision, however, that could easily be attained 
 were the patients under continual observation in a hospital ward. 
 
 This Une of investigation has, I am glad to say, been adopted by several 
 physicians, and John Hay ^^, A. G. Gibson ^^, Hewlett i°^, Gossage^^, Lewis i^^, 
 and Guilleaume ^^ have demonstrated equally striking results from the 
 administration of digitaUs. 
 
 In the interpretation of the phenomena given here, I have been greatly 
 assisted by Professor Gushny, whose knowledge of the physiological action 
 of digitaUs is unrivalled. 
 
 The following case is important, as it shows the rhythm of the heart 
 changing from the normal to the nodal rhyi:hm, and back again to the 
 normal, and the difference in the behaviour of the heart to digitalis under 
 the two rhythms. 
 
 Case 25. — Female, aged sixteen. Seen first on March 21, 1903. Has had 
 rheumatic fever, and for some years has suffered from breathlessness and 
 palpitation on exertion. This has increased lately, and there is shght 
 oedema of the legs. There is marked pulsation of the veins of the neck 
 of the auricular type (Fig. 251). The pulse is small, regular, 86 per minute. 
 There is great heaving of the left chest with the movements of the greatly 
 enlarged heart. The apex beat is large and diffuse, and felt in the sixth 
 interspace and in the anterior axillary line. There is a loud, rough systolic 
 murmur heard over the whole heart and round to the back, but loudest 
 at the apex. With rest and digitalis she rapidly improved. She broke
 
 THE EFFECTS OF DIGITALIS ON THE HUMAN HEART 357 
 
 down again, and a note on January 9, 1904, states that the abdomen is 
 greatly swollen, the liver enlarged, the legs oedematous, and the urine 
 scant. The radial pulse is small, soft, and rapid, 126 per minute, while 
 the Jugular pulse is of the ventricular type. Under digitalin granules she 
 again improved, but in February the granules were stopped, and she speedily 
 
 Fig. 251. This and the following seven tracings are from the same 
 patient. Here tlie pulse is regular, and the jugular pulse is of the auricular 
 type. (Case 25, March. 190.3.) 
 
 
 Fig. 252. The jugular pulse is now of the ventricular type. (Case 25, March 10, 1904.) 
 
 Fig. 253. The jugular pulse is still of the ventricular type, but under the action of digitalis 
 the radial has become slow and irregular. (Case 25, March 18, 1904.) 
 
 broke down again. On March 10, 1904, the condition was similar to that 
 described on January 9, the radial and jugular pulse-tracings being shown 
 in_Fig. 251. 
 
 She was prescribed digitalin granules, one per day. They speedily 
 took effect, and on March 18 the pulse had become slow and irregular 
 (Fig. 253). The urine had greatly increased in quantity, the abdomen and
 
 358 
 
 DISEASES OF THE HEART 
 
 liver had diminished in size, and all signs of dropsy had gone. The digitalis 
 was continued till March 28, one granule being taken every second day, 
 and she continued in fair health, the pulse still slow and irregular, as shown 
 by Fig. 254, which was taken on March 26. 
 
 The digitahn was stopped on March 28. Four days after stopping it 
 the pulse had increased to 85 per minute, though she felt stiU fairly weU. 
 
 Fig. 254. Shows the characteristic effect of digitalis being maintained. (March 26, 1904.) 
 The jugular tracing shows the nature of the arrhythmia, and the coupled beats resemble the 
 tracings in Figs. 153, 157, 159, and 160. (Case 25.) 
 
 On April 5 — that is, eight days after stopping the digitalin — the rate of 
 the heart had increased to 120 beats per minute, the pulse had become 
 small and weak, and the jugular distension had increased (Fig. 255), The 
 other signs of heart failure were beginning to show themselves. She was 
 again put on digitalin, one granule per day. On April 9 the pulse was still 
 
 Fig. 255. Eight days after stopping the digitalin, failure of compensation again set in, 
 the pulse here being 120 per minute, and the jugular pulse being still of the ventricular type. 
 (Case 25, April 5, 1904.) 
 
 120 per minute. On April 11 it was 130, on April 14 it had again become 
 slow and irregular (Fig. 256). 
 
 The digitaUn was again stopped, but as the pulse began to increase in 
 rate, on April 17, one granule per day was prescribed. The patient con- 
 tinued in fair health, but as the pulse did not slow down satisfactorily, on 
 May 1 I doubled the dose. I did not take any further tracings tiU May 14, 
 contenting myself with watching for the slowing of the pulse. Finding it 
 did not yield as before to the increased doses of digitahn, I took tracings
 
 THE EFFECTS OF DIGITALIS ON THE HUMAN HEART 359 
 
 on this day, and found a perfectly regular radial pulse, while the jugular 
 pulse had completely changed its character, being now of the auricular 
 
 Fig. 256. Nine days after beginning the digitalis the characteristic effect is 
 reproduced. (Case 25, April 14, 1904.) 
 
 Fig. 257. With continued use of digitalis the auricles resume the inception of 
 the rhythm of the heart, as shown by the fact that here the jugular pulse is of the 
 auricular type. (Case 25, May 15, 1904.) 
 
 Fig. 260. Shows a jugular pulse of the auricular type with the 
 occasional occurrence of a ventricular extra-systole. The auricular 
 waves {a and a') occur at regular intervals, while the small waves ( x ) 
 in the radial occur prematurely. The larger size of a' is due to the fact 
 that when the auricle contracts the ventricle is already in systole, and 
 therefore cannot receive the auricular contents, which are thus sent back 
 into the veins, producing tills larger wave. (Case 25, January 2, 1905.) 
 
 type that is, the auricle had again resumed its normal action and the 
 
 heart chambers contracted in their normal sequence. Occasionally, for 
 a short period, it would show a shght alternating rhythm, as in Fig. 257.
 
 360 DISEASES OF THE HEART 
 
 The digitalin was stopped, and the patient continued in fair health for 
 some ^months. The jugular pulse continued of the auricular type, and the 
 pulse was quite regular until her death in December, 1905, except during 
 a short period shortly to be described. On December 18, 1904, she was 
 again beginning to get oedema of the legs, and the abdomen began to swell, 
 and she was very breathless. The pulse was small, soft, and rapid, 110 per 
 minute, and the jugular pulse was still of the auricular type. She was 
 prescribed one granule of the digitalis per day. No improvement had taken 
 place by December 27, when she was ordered to take two granules per day. 
 By January 2, 1905, the rate had fallen to 80, as a rule quite regular, but 
 occasionally an extra-systole of ventricular origin would occur (Fig. 260), 
 Sometimes for a short period these ventricular extra-systoles would appear 
 after every second beat. The digitaHs was stopped, and the arrhythmia 
 disappeared. 
 
 Fig. 262. Simultaneous tracings of the jugular and radial pulses. The jugular pulse is of the 
 auricular type and the distension of the veins obscured the carotid. (Case 26, April 22, 1907.) 
 
 Case 26. — Male, aged eleven, seen by me on April 26, 1907 ; complained 
 of weakness, shortness of breath, and palpitation. He had rheumatic fever 
 at the age of seven. His pulse was rapid (110 per minute), small, and regular 
 (Fig. 259). The heart was enlarged, the apex beat diffuse, extending one inch 
 beyond the nipple line. There was a long, loud systolic mitral murmur. 
 There was only a faint pulse in the distended jugular, and I had some 
 difficulty in getting a tracing (Fig. 262). It was of the auricular form, 
 and the a-c interval (space A) was rather greater than would normally 
 appear with so rapid a heart-rate. I prescribed digitalin granules, one 
 granule per day, and after taking ten granules he became very sick and 
 vomited, and his pulse became slow and irregular. The granules were 
 at once stopped, and after the sickness subsided the boy felt much better 
 and remained in a fair state of health up to the last time I saw him, in 
 November, 1907. I took a large number of observations when the heart 
 was slow from the effects of digitalis, and the irregularities were all 
 due to the same cause — the di'opping out of ventricular systoles as shown
 
 THE EFFECTS OF DIGITALIS ON THE HUMAN HEART 361 
 
 in Fig. 264. I have constructed a diagram showing the character of the 
 irregularity, and it can be seen that the auricle pursues a regular course ; 
 that the a-c interval varies, being shorter after a pause and lengthening 
 until a beat drops out (Fig. 269). 
 
 Fig. 264. The auricular wave, a and a', is regular. .The long pauses in the radial tracing 
 are due to dropping out of the ventricular contractions — the stimulus from the auricle being 
 blocked at tlie a-v bundle (see diagram, Fig. 269). Note the variation in the a-c interval 
 (spaces .4). (Case 26, April 26, 1907. After 10 digitalin granules.) 
 
 Fig. 269. Diagram showing the auricular and ventricular systoles from Fig. 264. Note 
 the lengthened a-c interval before and the shortened a-c interval after the dropping out of 
 the ventricular contraction. (Case 26.) 
 
 Fia. 270. The jugular tracing shows a wide a-c interval (space A ). (Case 27. Before digitalis.) 
 
 Case 27. — Male, aged twenty-five, consulted me for a stiffness and 
 swelling in sundry joints, wrists, ankle, and knee, on May 4, 1906. The heart 
 was rapid in its action, 120 per minute ; slightly enlarged with systolic 
 mitral and tricuspid murmurs. There was marked pulsation in the neck, 
 of which Fig. 270 is a tracing. The movement due to the carotid was 
 always large, and forms a marked feature (wave c in aU the tracings). In 
 the course of the next fortnight there gradually developed double aortic
 
 362 
 
 DISEASES OF THE HEART 
 
 murmurs. By May 23, under treatment, he had gradually improved, the 
 rate of the heart falling to 90 beats per minute. 
 
 As the a-c interval, space A, in Fig. 270, showed a delay in the function 
 of conductivity, I reasoned that the carditis had probably affected the 
 a.-v. fibres, and had depressed the function of conductivity. I administered 
 digitalin granules, one to be taken three times a day. 
 
 I kept him under observation, but could detect no change in the heart's 
 action until May 30, after he had taken nineteen granules. On this date 
 I found the pulse at times very irregular. Fig. 271 is a tracing, showing 
 the nature of the irregularity. Between the jugular and radial pulses 
 I have intercalated a diagram illustrating the events in the tracing from 
 the neck. It will be noticed that before a ventricular beat drops out 
 
 maam^mmam 
 
 Fig. 271. After taking nineteen digitalin granules the pulse became irregular, wliich the 
 intercalated diagram shows to be due to dropping out of the ventricular systoles — a mild form 
 of heart-block. (Case 27.) 
 
 there is a gradual lengthening of the a-c interval, and that the dropping 
 out of the ventricular systole is manifestly due to an increased depression 
 of the conductivity of the fibres joining a and v — that is to say, the 
 stimulus from the auricle is blocked before it reaches the ventricle. 
 I stopped the digitalin, and a few days later all signs of irregularity had 
 disappeared. The patient himself was conscious when his heart was irregu- 
 lar, and I remarked to him that the irregularity had gone ; he repUed, 
 * I can bring it back.' I asked him how he could do so, and he said, ' By 
 swallowing.' I asked him to swallow, and he did so, and immediately 
 I detected long pauses in his pulse, while, on auscultation of the heart, 
 no sounds were heard during the pauses. I took a large number of tracings 
 for an hour and a half, during which time he swallowed forty or fifty times, 
 and the alteration in the pulse-rate never failed to appear. The character- 
 istic changes are seen in Figs. 258, Plate IV, and 259, Plate IV. After 
 swallowing there are each time three regular beats, then the pulse slows 
 in the manner shown in the tracings. After two or three slow beats the
 
 THE EFFECTS OF DIGITALIS ON THE HTOIAN HEART 363 
 
 rate of the heart increased for six or seven beats, then gradually slowed in 
 the manner shown in the latter part of the tracings. Occasionally during 
 the secondary slowing one ventricular systole would drop out, as is shown 
 in Fig. 259, Plate IV. In Fig. 259, Plate IV, I have intercalated a diagram 
 which shows the nature of the arrhythmia, and it can there be seen that 
 the long pauses in these tracings are preceded by an increase of the a-c 
 interval, just as happened when the patient was under the influence of 
 digitalis (Fig. 271), and that the dropping of the ventricular systole was 
 due to a block of the stimulus from auricle to ventricle. The numbers 
 given under the radial tracings in Fig. 259, Plate IV, represent tenths of 
 seconds, and from these numbers the manner in which the rate of the pulse 
 varies can better be realized. 
 
 The susceptibihty of the heart to the act of swallowing continued for 
 a week, then entirely disappeared. There is no doubt it arose through 
 reflex stimulation of the vagus induced by the act of swallowing. The 
 analogy between the effects of digitahs and of reflex stimulation of the 
 inhibition by swallowing appears worthy of note, as it indicates that the 
 action of the drug here is exerted through its effects on the inhibitory centre, 
 and not through the changes it induces in the heart muscle directly. Digi- 
 talis, as is generally known, affects the vagus centre and also the myocardium, 
 and it is often difficult to determine which is the factor in its therapeutic 
 effects. This case, taken along with Case 28, seems to give valuable data 
 on this question. 
 
 The cases I have quoted here and in Chapter XXXIV present the more 
 common effect of digitahs on diseased hearts. Other cases crop up that 
 show different changes, some of which are capable of being analysed, so 
 that one can teU with fair certainty what is happening, though the manner 
 in which the phenomena are produced remains obscure. These cases are 
 nearly all due to rheumatic affection of the heart. The following case 
 showed a series of pecuUar symptoms, and I select the most significant 
 of these. It is impossible here to give fully the whole of the observations 
 in this case, for verbal description is of httle use, the tracings alone demon- 
 strating the changes, and I have taken as many observations on this patient 
 as would fill a goodly volume. I am also unfortunately unable to give 
 minute particulars as to the quantity of the drug that produced the symp- 
 toms, for the patient was not confined to bed, and, hving some distance 
 from me, visited me at irregular intervals. Being the wife of a working 
 man she had her household duties to perform, and when feeling better 
 did not trouble to come to see me. As the improvement in her condition 
 always coincided with the changes in the heart's rhythm, I was not able
 
 364 DISEASES OF THE HEART 
 
 to note the beginning of the changes and the quantity of the drug that 
 induced them. 
 
 The drugs used in this case were the digitalis, squill, and calomel pills, 
 digitaHn granules, and the tincture of strophanthus. So far as the heart's 
 irregularities were concerned, each form of medicine produced the same 
 result. The patient preferred the digitaUs, squill, and calomel piU, as it 
 was the speediest in diminishing the dropsy by inducing an increased flow 
 of urine, and a little diarrhoea, and the appearance of the diarrhoea was 
 always accompanied by improvement in the breathing. 
 
 When not taking any drug the heart was quite regular in its rhjrthm 
 until the last month of these observations, when the nodal rhythm became 
 established. Under the influence of the digitalis or strophanthus the 
 . following irregularities appeared : — 
 
 (1) Nodal rhjrthm (transient). 
 
 (2) Slowing of the auricles and ventricles, the whole heart participating 
 in the slow action. 
 
 (3) After a long pause the heart's contraction started feebly, and 
 increased in strength with each succeeding beat (staircase phenomenon). 
 
 (4) Extra-systoles. 
 
 The a-c interval when the heart was not under the influence of the drug 
 was always greatly increased, and the digitalis did not increase the delay, 
 as in the cases already quoted. During the long pauses the a~c intervals 
 became greatly shortened. As there was in this case a marked presystolic 
 murmur, the relationship of this murmur to the first sound varied with 
 the length of the a-c interval, sometimes being separated from the first 
 sound, sometimes running up into it, and sometimes not being distinguish- 
 able from it (see Fig. 265, Plate V). During the nodal rhythm the 
 presystolic murmur disappeared. 
 
 Case 28. — Female, aged twenty-eight. Consulted me April 24, 1907, 
 complaining of swelling of the abdomen, shortness of breath, and palpitation. 
 She began to feel ill in November of the previous year ; she had rheumatic 
 fever fifteen years previously. The face is dusky, the breathing laboured, 
 the legs and abdomen swollen. She passes little urine. There is rapid pulsa- 
 tion in the veins of the neck — two to each radial pulse (Fig. 272) — the pulse 
 is small and regular, blood-pressure 100 mm. Hg. A thrill systohc in time can 
 be felt over the upper part of the chest. The movement of the heart farthest 
 to the left is three inches beyond the nipple, and shows an indrawing during 
 ventricular systole (giving rise to an inverted cardiogram). The heart's 
 dullness extends half an inch to the right of the sternum. At the apex 
 there is heard a presystolic murmur, a diastolic murmur, and a reduplicated
 
 THE EFFECTS OF DIGITALIS ON THE HUIVIAN HEART 365 
 
 second sound. At the base there is a loud, rough murmur systolic in time, 
 heard also over the carotid. There is also a sHght diastohc murmur at the 
 aortic area. Over the heart's dullness inside the nipple there is another 
 murmur systohc in time, and while hstening one could imagine that two 
 hearts were working, a series of sounds being heard immediately under the 
 stethoscope, while another series of sounds could be heard faintly and 
 seemingly at a distance. 
 
 Sometimes when the heart was regular but slow, a confusing change 
 took place. During the diastole of the heart there was a sudden increase 
 in the intensity of the diastoUc murmur, in fact a mid-diastohc murmur 
 followed after a pause by the first sound. When I drew the position of 
 
 Fig. 272. Shows two pulsations in the jugular tracing (a and v) to one radial pulse. The 
 a-c interval (space A) is increased. The shading shows the sounds of the heart and the 
 murmiurs present at the apex, viz. a presystoUc murmur separated by a brief interval from 
 the first sound, a reduplicated second sound followed by a diastohc murmur. These features 
 of the jugular pulse and sounds and murmurs were always present when the patient was 
 not under the influence of digitahs until the final establishment of the nodal rhythm as shown 
 in Fig. 268, Plate V. (Case 28.) 
 
 the murmur under a tracing I found it corresponded to the position of the 
 auricular wave in the jugular tracing (Fig. 272), and no doubt it was due 
 to the auricular systole. When the heart became very slow, because of 
 the digitalis, the longer rest gave the a. -v. fibres time to recover and the 
 murmur was heard nearer and nearer the first sound, and sometimes it 
 ceased to be heard. This only happened when the heart became very slow 
 and the auricular wave in the jugular approached quite close to the carotid. 
 These changes in the sounds and position of the auricular wave are seen in 
 Fig. 265, Plate V. I am aware that this explanation may appear fanciful, 
 but it is the outcome of long and patient study on the part of myself and 
 some of my colleagues. My colleague. Dr. Crump, who is a very skilled 
 auscultator, verified, after a long examination, these changes in the position 
 of this auricular systole, and when shown the tracings which were taken
 
 366 DISEASES OF THE HEART 
 
 while he was Ustening, agreed to the place of the murmur indicated by 
 the shading in Fig. 265, Plate V. I dwell at length upon this on account 
 of the views that are held by some able clinicians that the presystoUc 
 murmur in mitral stenosis is not due to the auricular systole. 
 
 The patient was put on the digitaUs, squill, and calomel pill, one taken 
 three times a day. On May 1, after taking eighteen pills, she was passing 
 more urine. She felt much better on the 8th — the swelUng had gone from 
 the abdomen and the legs were less in size. On the 15th the swelling had 
 all gone, she had a little diarrhoea and felt sickly, but breathed easier and 
 was able to walk better. The heart was slow and irregular. On examina- 
 tion there was only one wave visible in the jugular, and when recorded 
 it was found synchronous with the carotid pulse (Fig. 261, Plate IV). 
 There was no presystolic murmur, but only a long diastoUc murmur at the 
 apex, diagrammaticaUy represented in Fig. 261, Plate IV. The tracing 
 shows the jugular pulse to be of the ventricular type, i. e. the heart has 
 taken on the nodal rhythm. The pills were stopped, but the heart was 
 still irregular on the 19th. On the 26th it was regular and the jugular 
 pulse double waved as in Fig. 272. She felt better, but the legs and abdo- 
 men were swelhng again. Digitalin granules were prescribed, one three 
 times a day. On the 31st the pulse became irregular and tracings taken 
 on this day and on June 2 showed that it was due to the slowing of the 
 whole heart (Figs. 273, and 263 Plate IV). On June 4 the heart had again 
 taken on the nodal rhythm (Fig. 261, Plate IV), which persisted until the 
 17th, when the auricular contractions appeared and the heart showed 
 frequent pauses. She was taking one granule of digitalin per day until 
 the 23rd, when it was stopped, and on the 28th the heart was found rapid 
 and regular and the pulsation in the veins double waved, as in Fig. 272. 
 Up till November 4 these reactions due to digitalis continued to appear ; 
 sometimes the nodal rhythm would appear and sometimes the long pauses 
 as in Figs. 273, and 263 Plate IV, and occasionally extra-systoles as in 
 Figs. 266 and 267, Plate V. A few days after stopping the digitalis the 
 heart invariably became regular. On November 6, after digitalis treat- 
 ment had ceased, the heart assumed the nodal rhythm (Fig. 268, Plate V) 
 continuously, beating rapidly, but it could be slowed by digitalis or 
 strophanthus. 
 
 Interpretation of tracings. — The tracings showing the nodal rhythm 
 (Figs. 261, Plate IV, and 268, Plate V) call for no special description, 
 as they resemble the tracings of the ventricular venous pulse so fully 
 described elsewhere. The only point which seems novel is that when it 
 began under the influence of digitalis (Fig. 261, Plate IV) it was a slow
 
 THE EFFECTS OF DIGITALIS ON THE HUMAN HEART 367 
 
 rhythm resembling in some respects the cases of nodal bradycardia 
 (Appendix IV). On the other hand, when it started independently of 
 digitalis the heart's action was rapid, as is usually the case. 
 
 In Fig. 273 there is a long pause in which the whole heart stands still ; 
 during these pauses no sound could be heard and the tracings show the 
 auricles arrested as weU as the ventricle — differing thus from heart-block. 
 I observed that after the long pause the radial beats were at first small, 
 then gradually increased in size, but as the pulse was small and soft the ink 
 polygraph did not show the beats well ; I therefore took several tracings 
 with the Dudgeon sphygmograph, of which Fig. 263, Plate IV, is a good 
 instance. Here the gradual increase of the radial pulse after the long pause 
 is very evident. The pauses lasted sometimes from three to four seconds. 
 Thus in Fig. 263, Plate IV, one pause lasts fifteen-fifths of a second, while 
 
 Fig. 273. Shows the temporary arrest of the whole heart from digitalis. (Case 28.) 
 
 the other lasts nineteen-fifths of a second. This standstill of the whole 
 heart is probably due to vagus stimulation. The staircase phenomenon 
 after the pause has been shown experimentally to occur after a vagus 
 standstill of the whole heart, and, according to Gaskell, arises in two ways : 
 
 (1) From exhaustion of contractiUty — the vagus stimulation depresses aU 
 the functions and their restoration is gradual, that of restoration of con- 
 tractihty being showTi by a gradUal increase in the strength of the beat. 
 
 (2) From depression of conductivity, the stimulus for contraction not 
 spreading throughout the whole heart, but reaching at fii'st a limited 
 number of fibres, and gradually reaching more and more until they all 
 respond. 
 
 The pauses were not always so long as in Fig. 263, Plate IV, and the 
 heart would beat slowly for a short period. When this happened, the relation 
 of the auricular systole to the ventricular underwent an interesting change. 
 As I have already remarked, the a-c interval was always increased in this 
 patient, but digitahs did not interfere with the conduction of the stimulus
 
 368 DISEASES OF THE HEART 
 
 from auricle to ventricle. When the heart acted slowly the a.-v. fibres 
 obtained a long rest, with the result that the a-c interval gradually dimin- 
 ished until it was scarcely perceptible. Fig. 274 shows the carotid and 
 radial pulses. The carotid is taken from luider the right jaw, but the 
 wave (a) due to the auricular systole is present in the tracing. When the 
 heart was beating at the more rapid rate, the a-c interval (spaces A) was 
 nearly two-fifths in duration, whereas when beating at the slower rate it 
 became less than one-fifth in duration. This is brought out particularly 
 well in Fig. 265, Plate V, where the auricular wave, a, gradually approaches 
 the carotid and ventricular wave tiU it is not discernible as a distinct wave. 
 It was during periods such as this that Dr. Crump and I made out the 
 
 Fig. 274. The upper tracing was taken high up in the neck and shows a slight auricular 
 wave (a) preceding the carotid pulse (c). After a long pause the a-c interval (space A) is 
 much diminished. (Case 28.) 
 
 change in the relation of the presystohc murmur to the first sound and 
 its apparent cessation — as shown by the shading underneath the jugular 
 tracing. 
 
 It may be taken as certain that in this patient the marked slowing and 
 long pauses were inhibitory in origin. But the inhibition appeared not to 
 involve the a.-v. fibres, for their conductivity was not reduced, this proving 
 that the drug acts on the a.-v. fibres through its action on the inhibitory 
 function and not through its direct effects on the heart muscle. (Compare 
 Case 27.) 
 
 Another phase that occasionally occurred during the irregular period 
 was the appearance of extra-systoles. Figs. 266 and 267, Plate V (Fig. 267 
 is a continuation of Fig. 266), are characteristic examples, and show that 
 the extra-systoles are probably of ventricular origin, though the pauses 
 following the extra-systoles are of varying duration, due to the influence 
 of the digitaUs on the sinus. 
 
 This case, as I have said, is an exception to the general rule that when 
 there is a delayed a-c interval digitalis increases it and produces blocking
 
 THE EFFECTS OF DIGITALIS ON THE HUMAN HEART 369 
 
 of the systoles between auricle and ventricle. I have carefuUy considered 
 whether there may not have been blocking between the sinus and auricle, 
 as has been shown to occur by Wenckebach ^-^ and Hewlett 202. i can find 
 no reason for suspecting such a thing here, particularly as the slow periods 
 have no such regularity as to lead one to infer that the sinus was beating 
 at regular intervals. In this case the whole heart seemed affected by the 
 digitahs, but on exceptional occasions the ventricles escaped and produced 
 extra-systoles. 
 
 Records of blood-pressure showed generally a faU (100 mm. Hg.) when 
 there was much dropsy, and a rise with slowing of the heart to 135 or 
 140 mm. Hg. Sometimes, however, the pressure was 130 with dropsy, 
 and no increase occurred with its disappearance and the coincident 
 improvement of the patient's condition after taking digitalis. 
 
 MACKENZIE 3 |)
 
 APPENDIX VII 
 
 The Electro-cardiogram * 
 By Thomas Lewis, M.D., M.R.C.P. 
 
 1. The relation of contraction to electric changes in muscular tissue. 
 
 For many years it has been known that muscular activity is accompanied 
 by electric changes. When a strip of somatic musculature is stimulated 
 at one end, and contraction is induced at the point of stimulation, this point 
 becomes electro-negative to the resting or inactive end. If, as a result of 
 the excitation, a wave of contraction is propagated in the muscle, then, as 
 each successive segment enters upon the contractile state, each segment 
 becomes relatively electro-negative. The change in potential, or the varia- 
 tion in the current produced by it, may be registered by connecting the two 
 ends of the strip to suitable recording apparatus. In the instance of a wave 
 of contraction which passes from end to end of a single strip, the changes 
 registered are diphasic ; for at first the excited end is negative to the distal 
 end, and eventually, as the distal end becomes negative, the excited end is 
 relatively positive. 
 
 Now precisely analogous changes in electric state occur in visceral 
 musculature, such as cardiac muscle, contracting under the influence of 
 physiological impulses, and these may be similarly recorded. Activity is 
 always associated with the development of negativity, and if leads are made 
 from base and apex of the ventricle and the electric state of one relative to the 
 other is recorded, it will be obvious that a very definite idea of the direction 
 which the contraction-wave takes in the ventricle may be formed. And, further, 
 an important clue to the point at which contraction starts will be at our disposal. 
 These conclusions are of great importance, and should form the basis of all 
 electro-cardiographic studies. 
 
 2. Electric changes as a residt of the heart beat. 
 
 In the frog, electric changes as a result of the heart beat were described 
 by Kolliker and Miiller^^^ in 1855 ; their observations were followed by those 
 of many other workers. The mammalian heart was the subject of special 
 investigation at the hands of Waller *^'' '*^^' *°^ and others. It was found that 
 the type of curve yielded by leads from base and apex, is approximately dupH- 
 cated by leads from other parts of the body. Stated in a simple form, it 
 
 * The expenses of the work, upon which this appendix is based, have been defrayed by 
 the British Medical Association.
 
 THE ELECTRO-CARDIOGRAM 
 
 371 
 
 was showTi that the body can be mapped out by a plane crossing the base 
 of the heart, into two parts, one abutting upon the base, the other including 
 the apex of the ventricle ; and that leads from these tivo divisions of the body 
 are equivalent to leads from base and apex of the ventricle. Thus the possibihty 
 of registering the electric changes produced by the heart beat in the intact 
 animal was demonstrated, and in. man they were first studied by Waller. 
 In the human subject, the dividing-Une already referred to passes, according 
 to the last-named writer, from the left shoulder to the right loin. The right 
 arm may therefore be utihzed as a basal lead, while the left arm, or either 
 leg,* serves as an apical lead. Leading off from the human body, through 
 
 Fig. 275, for which we are indebted to Professor Einthoven, shows a portion of a carotid 
 curve and a single beat of an electric curve. The abscissae are divided at intervals of 
 0-01 sec. ; the ordinates are divided at intervals of 10~* volt. The lead, as in all figures 
 shown, was from right hand and left foot. In this, as in all figures also, corresponding points 
 of time are directly vertical to each other, p represents the auricular and r, s, and t the 
 ventricular contraction. 
 
 the unbroken skin, records of the electric change as a result of systole of 
 the ventricle may therefore be obtained, and they correspond very closely to 
 records yielded experimentally by direct leads from base and apex of the 
 mammalian heart. In addition, distinct changes as a result of auricular 
 contraction are registered. 
 
 The method employed clinically. 
 
 The galvanometer which is employed chnically is that invented by 
 Einthoven **^' ^^, to whose papers the reader is referred for a detailed 
 account of its construction and working. 
 
 It consists of a heavy magnet, permanent or in circuit, the poles of which 
 are close together. Between the poles a fine platinum or silvered quartz 
 thread is suspended. When the instrument (string galvanometer) f is 
 
 * The changes registered necessarily vary to some extent with the ' lead '. 
 t Sold by the Cambridge Scientific Instrument Co., and by Dr. Th. Edelmann of Miinich. 
 
 B b 2
 
 372 
 
 DISEASES OF THE HEART 
 
 working, the thread Hes in a powerful magnetic field, and deviates whenever 
 a current is led through it. The shadow of the string and its movements are 
 magnified and projected, by means of a system of lenses and an arc light, on 
 to a photographic apparatus. The delicacy of the instrument depends 
 upon the strength of the magnetic field, and the fineness of the conducting 
 thread. The body-current which it is desired to register is led from the 
 limbs (right arm and left leg, or right arm and left arm) by immersing them 
 in electrolytic solutions which are in connexion with the ends of the suspended 
 thread. 
 
 S S S S ^/ect. s 
 
 Fig. 276. Simultaneous records of time, in ^ sec, venous and electro-cardiographic 
 curves. The delay in the venous curve is due to the aii* transmission employed, to the 
 delay in transmission from auricle to neck, and to the fact that the electric change slightly 
 precedes the contraction. From a patient in which the p-r and a-c intervals show sUght 
 prolongation, but in which the curve is otherwise normal. 
 
 3. The normal electro-cardiogram and its significance. 
 
 The normal electro-cardiographic curve consists of three negative and 
 usually one positive wave (directed upward and downward respectively in 
 the accompanjdng figures). They are designated by the letters p, r, and t 
 (negative peaks) and s (positive depression), p is a result of auricular 
 contraction, r, s, and t are due to systole of the ventricle. 
 
 The ventricular portion of the curve (r, s, and t) is thus triphasic* It 
 
 * Not infrequently the curve shows four phases, q, r, s, and t (Fig. 275). The depression 
 Q, which is distinct in Fig. 275, is usually less marked than the depression s, but may be 
 more prominent than the latter. In brief, the opening events of the ventricular electro- 
 cardiogram are subject to variations, and it is possible that these variations depend on slight 
 differences in the direction of the contraction- wave when it starts in the ventricular muscula- 
 ture. It will simplify the description if further reference to tliis depression q is omitted, for 
 it is not certain that it is ventriaular in origin. Nevertheless, its frequent presence should 
 not be forgotten.
 
 THE ELECTRO-CARDIOGRAM 373 
 
 shows two displacements, r and t, in a direction indicating negativity of 
 the base of the heart, and one displacement, s, indicating negativity of 
 the apex (or positivity of the base). The curve is of such a nature as to 
 suggest that the contraction of the heart originates at its base, travels to the 
 apex, and returns to the base (Gotch**") (cf. § 1). 
 
 4. Variations in the individual electro-cardiographic curve. 
 
 Both auricular and ventricular portions of the galvanometer curve are 
 subject to considerable variation in form, a variation seen more especially 
 in pathological conditions. Thus in mitral stenosis an increase in the size 
 of P accompanies hypertrophy of the auricle, and in the later stages of the 
 affection, p shows a division into two parts (p^ and P2 of Fig. 277), and may 
 be prolonged as a whole. (The normal p-r interval varies from •12-- 16 
 seconds ; the p-r interval in the accompanying figure. Fig. 277, is -2 second ; 
 in the normal curve, Fig. 275, it is -15 second). 
 
 Fig. 277. From a case of mitral stenosis and aortic regurgitation. Showing tlie prolonga- 
 tion of P-R interval, a splitting of p, and an increase in s. 
 
 Similarly, variations are met with in the ventricular portion of the curve. 
 Thus hypertrophy of the left ventricle, especially hypertrophy of its apical 
 portions, such as is met with in aortic regurgitation, is commonly accom- 
 panied by an increase in the magnitude of the variation s. This fact, which 
 is in accordance with the interpretation of the normal curve, is well illus- 
 trated in Fig. 277, and in the patient from which this curve was obtained 
 left ventricular hypertrophy was a notable feature. 
 
 5. Analysis of the sequence of contraction in the cardiac chambers. 
 
 In the last paragraph examples were given illustrative of information 
 to be obtained from individual auricular or ventricular curves, where the 
 heart beat shows the usual sequence of chamber contraction. The method 
 is of still greater service in the analysis of disordered sequence, and in this 
 direction forms a valuable adjunct to venous pulse work. 
 
 For the time being two examples will suffice. Fig. 278 is taken from 
 a case of complete heart-block. The photograph, as a whole, is composed
 
 374 
 
 DISEASES OF THE HEART 
 
 of frequent auricular and infrequent ventricular curves, accurately super- 
 imposed upon each other. The ventricular curve is identified by the peak R, 
 its most constant feature. The variation t is anomalous and inverted (a by 
 no means uncommon occurrence in pathological conditions). The peak p 
 occurs at regular intervals in the figure, and whenever it falls with a ven- 
 tricular curve it is superimposed upon it. 
 
 The second example is shown in Fig. 279, and is taken from a patient 
 with the disorderly action of the heart, termed ' Nodal rhythm ' in this book. 
 It shows no sign of the normal auricular contraction during the diastole of 
 the heart. Further, it shows marked tremulousness of the line joining the 
 
 Fig. 278. From a case of complete heart-block, showing the dissocixtion of auricle and 
 
 ventricle. 
 
 Fig. 279. From a case of ' nodal rhythm ', showing the absence of the normal wave p, and 
 the presence of irregular waves having fixed relationsliip to other events. 
 
 peaks R. This tremulousness has been found in association with myocardial 
 degeneration* (Einthoven, Kraus and Nicolai *^2» *^ ). 
 
 6. The point in the musculature at which a contraction arises. 
 
 In the preceding paragraphs the importance of electro-cardiographic 
 curves have been shown from two separate aspects. First, they give infor- 
 mation of the nature of a contraction in auricle or ventricle respectively. 
 Secondly, they serve in the analysis of disordered rhythm and in the elucida- 
 tion of disturbed sequence of systole. Information of the first and second 
 
 * The explanation of the tremulousness will be fully dealt with in an early article to 
 Heart.
 
 THE ELECTRO-CARDIOGRAM 
 
 375 
 
 order is also obtained by other methods ; by direct inspection, palpation or 
 percussion, &c., and by means of graphic records from pulsating areas. The 
 electro-cardiogram may consequently be said to yield, as a rule, evidence 
 which is but confirmatory of that obtained by other means, when regarded 
 from these special points of view. But on this account its importance should 
 not be underrated, for it frequently happens that the remaining physical 
 signs are obscure or difficult to obtain. 
 
 Finally, the galvanometer yields evidence of a distinctive nature. It 
 allows recognition of contractions arising in the separate chambers of the 
 heart, which start in areas of the musculature other than the normal. 
 It is in this direction that galvanometric observations promise the richest 
 harvest of fact. We have seen that the normal electro-cardiogram of the 
 
 fl^F^^^^^^^^^^^'^^f^l^^P^lf^^f^^fP^IP^P^^fi^^ 
 
 y^sec 
 
 Fig. 280. The curve shows tliree beats in which the normal p-r sequence is observed, 
 and four extra-systoles of the ventricle. The p waves which are regular are superimposed 
 upon the extra-systoUc curves in three places (dotted Unes). 
 
 ventricle commences with a taU and sharply-pointed peak, e, and it has 
 been stated that in the presence of this peak we have presumptive evidence 
 of the origin of ventricular contraction in the morphological base of the 
 ventricle. In examples of complete heart-block (Fig. 278), the ventricular 
 curve commences in the same way, and we may conclude with a fair degree 
 of certainty that the beats of the ventricle in this condition are propagated 
 from a point in its musculature, corresponding to that from which they start 
 in the normal beat. A similar observation applies to the curves of * nodal 
 rhythm ' (Fig. 279). In this instance, as in that of complete heart-block also, 
 it may be asserted that all the beats start in the ventricle from a single focus. 
 In Fig. 280 an example of ventricular extra-systoles is portrayed. The 
 normal beats (of which three are present) are represented by p, R 
 variations. The extra-systohc curves (of which four are present) are highly 
 atypical. Each is manifested by a primary positive and a secondary
 
 376 DISEASES OF THE HEART 
 
 negative displacement. They are all of the same nature, and therefore arise 
 from a single focus in the ventricular musculature. The actual point of 
 origin is undecided, but there is evidence to show that they proceed from 
 the left ventricle and rather from its apical than from its basal portion.* 
 *rhe ultimate elucidation of the birth-place of anomalous beats of a nature 
 similar to those shown is a matter of experiment and time. It will be 
 obvious from the remarks in § 1 that when a systole of the ventricle starts 
 at a point other than the normal, such atjrpical curves must result, and that 
 many forms of atypical curve are to be anticipated. Such is found to be 
 the case, but at present a fuU description of these curves would not be 
 profitable. Again, just as beats, arising in areas of the ventricular muscula- 
 ture other than the normal starting-points, produce atypical electrical 
 curves, so also do those beats which arise out of place in the auricle. For 
 example, when a beat of the auricle is started by a beat of the ventricle 
 (retrograde contraction) the peak p disappears and is replaced by a curve 
 of a highly atypical character. 
 
 The importance of this aspect of the electro-cardiogram will now be 
 clear, for in all probability it will eventually be possible to accurately 
 determine the focus in which the impulses of all such abnormal contractions 
 are developed. 
 
 It occasionally happens that extra-systolic contractions of the ventricle 
 fall at such points in the auricular cycles that it is impossible to determine 
 by venous pulse methods whether such ventricular beats are the result of 
 transmitted auricular impulses or not. In such cases the nature of the 
 electro-cardiographic curve of these beats may be very helpful. In Fig. 280 
 the second auricular curve falls upon the first extra-systolic curve (it is 
 indicated by a dotted outUne). It is succeeded by a contraction of the 
 ventricle, which in the absence of the galvanometric curve, might have been 
 readily mistaken for a response to auricle. With the evidence of the electric 
 curve before us, its origin in an auricular impulse can be definitely denied, 
 and it is recognized as an extra-systole of precisely the same nature as those 
 which precede and succeed it. 
 
 *' Curves identical with those shown in the figure may be obtained by electrical stimulation 
 of the heart apex.
 
 Fio. 4. Respiratory 
 
 Fig, 5. Respiratory e 
 
 from B case of Cbeyne-Stokea respiration (see page 29). 
 
 s from a caae of Cheyne-Stokes respiration (see page 29) 
 
 1 and the radial pulse from 
 le in the radial tracing rises 
 during the respiratory phase and the irregularity of the pulse (due to depression of 
 contractility) becomes more marked. The blood pressure also rose at the same time. 
 (Case 23, Appendix V ; see page 29.) 
 
 Fia. 7. Tnicing of the respiratory movements and of the 
 during Cheyne-Stokea respiration (see page 30). 
 
 due to Hiccough (H) 
 
 75. Sinus irregularity produced by reflex stimulation o£ the vagus by the act of 
 swalloH-ing. The numbers re'er to the duration of each cardiac cycle in tenths of 
 seconds, and they show that the heart quickened its rate for a few beate after 
 gwallowiog, then gradually slowed ; then again increased slightly io rate, followed 
 by another short period ol slowing (9i & 94). The respiratory curve shows that tlie 
 irregularity was independent of respiration. Compare with Figs. 258 and 259, 
 Plate IV (see page 144). 
 
 IS) shown by a temporary
 
 o 
 
 Fin. "7. The respiratory mov< 
 
 I. luc respiratory movomenM vttre «t tho rale of 7 or 8 per minute There Is 
 
 i patient that gave Figs. 90 and ] 
 
 Fiu. IM is from tUe t 
 
 periods during which the large bro 
 
 was due. They are probably tlie result of pn 
 o( auriele and ventricle— being therefore nodal i 
 
 appear before the a 
 
 ira-systoles during A and D (see page 159), 
 
 Flc. too. The extra-syatolos [a', r') arc of nodol origin, and the a-e interval after the 
 pauses IS ahortened and gradually inoroases in length (epacea A,. ,1,, A^ A,) 
 
 . Simultaneous tracings of Uio apex beat and the radial to show 
 e page 320.) 
 
 > iiuuuigs ui uiB apex oeat ana tue radial to show the irregularity 
 the Budden inception of the nodal rhythm. (Case Hi, July. 1900 ; 
 
 C)
 
 I 
 
 IlG. 
 
 Fig. 
 
 Fig. 
 
 Fig.
 
 Fio. 200. Shows the charnclcristic change in the jugular pulso (venlrtcular form of jugi 
 
 pulse) with " ■'■''- ' " - -' ■' ..... 
 
 page 320). 
 
 pulse) with the sudden iacoption of the noi^ rhythm. (Case 10. July. 
 
 slower, the irreguJarity and jugular pulse 
 
 Ro. 238. Continued iiTC^arily which has porabted fiom 1004 to IU08. The jugulai 
 pulse ia ol the vcnUiDuIar form. {Case 17, 190S ; sec page 340.) 
 
 ■8 tl)e pulsus ^iltcrnanH in the radial tracings with tlic frequent occurrence c 
 ,r cxtra-syslolcs (r'). In the jugular tracing there is only one large wave, . 
 . „....;„i» rru ^ impairment of conductivity ol the a-v biuidlo. i 
 
 ludle, and of deptc&scd conlractiUty 
 
 o
 
 Fio. 244. The respirnto 
 
 of the pulsus altenmna. (Case 24 
 
 Shovrs a reflex effect of the vagus d 
 e diagram in Pig. 2o9). After this tl 
 
 hcort'a irregularity 
 ince of the ra<"' ' 
 
 lystoles (r") and ai 
 
 radial pulae 
 page 354.) 
 
 1 be independent of the 
 I, after the smaller 
 
 §walloning. After the act of avallotring 
 dropping out uf the ventricular syatoles 
 art's rate increased slightly, then became 
 
 Piti, iW. ShowR the same na Fig. 2S8, except that during the second period of stoning aftej 
 nivalloH-ing there is n long paiue due to the dropping out of a ' ' ' " ' 
 
 Fio, 201. Shan's the inocptJon of the nodal rhythm aft«r digitalis. Compare 
 pulse and the niurmuiB with Fig. 212. page 305. (Case OS ; see page 360, 
 
 Fio. 203, Shows the arrest of the whole heart for 1 
 
 Fig. 273. page 307- Digila Us effect. tCa«e28; seepage 360.) 
 
 ^KJVJ\rJVJVJ\/^-^^ 
 
 o
 
 w 
 
 205. Slowing of the 
 of the 0-1. bundle 
 approached t 
 
 shown by tbe eboding. (d'os 
 
 Rq. 200, Extra-ayatoles, r'. probably of 
 
 are due to the extra- systole. Tliere ore occi 
 occurred, followed by a shortening of tbe a-e 
 
 bole heart due to digitalis. During tbe pauses the conductivity 
 
 "" -" "-■ -' incular wave a griidunlly 
 
 The murmur due to the 
 med to become lost in the tirst sound, as 
 
 gin. due to digitalis. The waves v' 
 I long pauses when no extra-eystole 
 
 Q of Fig. 200 and shows the same kinda of irregularity. (Coae 28 ; 
 
 • irregularity und ventricular form of ■ 
 which linally became pennaDcnt i 
 
 t 
 
 
 
 c
 
 BIBLIOGEAPHY 
 
 The bibliography given here deals mainly with articles bearing on the more recent inquiries 
 into cardiac symptoms. As my own views are sufficiently expressed in the text I have given 
 references to only a few of my own articles, except in the case of those dealing •with the sensory 
 or reflex phenomena of visceral disease, and on this subject fairly full references are given, 
 as I am deeply impressed with the importance of this subject in its relation not only to cUnical 
 medicine, but also to clinical surgery, and consider that the profession in general, and clinical 
 teachers in particular, have not fully realized the significance of this class of symptom. 
 
 I. ANGINA PECTORIS AND SENSORY SY:MPT0MS ASSOCIATED WITH 
 
 VISCERAL DISEASE 
 
 1. Allbtttt. On Visceral Neuroses. The Gulstonian Lectures for 1884. London, 1884, p. 31. 
 
 2. Broadbent. Heart Disease, 4th Edition. 
 
 3. Brodie. Recent Work on Visceral and allied Nerves. Science Progress, 1896, No. 1. 
 
 4. Brtjnton. Nitrite of amyl in Angina Pectoris. Chnic. Soc. Rep., vol. iii, 1870. 
 
 5. Charante. De Hyperalgetische Zonen van Head. Leiden, 1900. 
 
 6. Garrod. Angina Pectoris due to plugging of the coronary artery. Proc. Roy. Soc. of 
 
 Med., April, 1908. 
 
 7. Gaskell. On the structure, distribution, and functions of the nerves which innervate 
 
 the viscera and vascular system. Jom-n. of Physiol., vol. vii, 1886, p. 1. 
 
 8. Gibson. Nervous Affections of the Heart, 1904. 
 
 9. Some hitherto undescribed symptoms in Angina Pectoris. Brain, 1905, part cix. 
 
 10. Haller. ' De partibus c.h. sensibiUbus et irritabiUbus.' Gottingen, 1752. 
 
 11. Hare. The Food Factor in Disease. 1905. 
 
 12. Harvey, The Works of. Sydenham Society translations, 1846, p. 382. 
 
 13. Head. On disturbances of sensation with especial reference to the pain of visceral disease. 
 
 Brain, vol. xvi, p. 1. 
 14. Ibid. Part II : Head and Neck, vol. xvii, p. 339. 
 
 15. Ibid. Part III : Heart and Lungs, vol. xix, p. 153. 
 
 16. The afferent nervous system from a new point. Brain, vol. xxvii, p. 99. 
 
 17. Head and Sherren. The consequences of injury to the peripheral nerves in man. 
 
 Brain, vol. xxviii, p. 116. 
 
 18. Head and Thompson. The grouping of afferent impulses witliin the spinal cord. 
 
 Brain, vol. xxix, p. 537. 
 
 19. Head and Campbell. The pathology of herpes zoster and its bearing on sensory localisa- 
 
 tion. Brain, vol. xxiii, p. 353. 
 
 20. Heitz, Les Nerfs du Coeur chez les Tabetiques. Paris, 1903. 
 
 21. Herringham. The minute anatomy of the brachial plexus. Proc. of the Roy. Soc, 
 
 vol. xU, 1887, p. 423. 
 
 22. Hertz, Cook and Schlesinger. The sensibility of the stomach and intestines in man. 
 
 Journ. of Phys., vol. xxxvii, December, 1908. 
 
 23. Hoffmann. Pathologie und Therapie der Herzneurosen. Wiesbaden, 1901.
 
 378 DISEASES OF THE HEART 
 
 24. loTEYKO. Le sens de la Douleur. Journal de Neurologie, October, 1905. 
 
 25. Kart and Meltzer. Die Sensibilitat der Bauchorgane. Mitteilungen aus den Grenz- 
 
 gebieten der Med. u. Chir., vol, xix, p. 586. 
 
 26. Langley. The autonomic nervous system. Brain, Part I, 1903, 
 
 27. Lennander, Observations on the Sensibility of the Abdominal Cavity, Barker's 
 
 translation, 1903. 
 
 28. JIackenzie. Symptoms and their interpretation. London, 1909. 
 
 29. Contribution to the study of sensory symptoms associated with visceral disease. 
 
 Medical Chronicle, August, 1892. 
 30. Some points bearing on the association of sensory disorders and visceral disease. 
 
 Brain, Ixiii, 1893. 
 
 31. The ' pilomotor ' or ' goose-skin reflex '. Brain, Ixiv, 1893, 
 
 32. Heart pain, and sensory disorders associated with heart failure. Lancet, January 5, 
 
 1895. 
 
 33. Pain. Brain, xcix, 1902. 
 
 34, Article, ' Visceral Pain.' Encycl. Medic. Edinburgh, 1902. 
 
 35, A suggestion for the observation of new paths in the spinal cord. Caledonian 
 
 Medical Journ., April, 1905. 
 36. The meaning and mechanism of visceral pain. Brit. Med. Journ., June, 1906. 
 
 37. An inquiry into the cause of Angina Pectoris. Brit. Med. Journ., October 7, 
 
 1905. 
 
 38. Murray. Diagnosis and treatment based on visceral reflexes. Univ. Penn. Med. Bull., 
 
 May, 1908, p. 71. 
 
 39. Nothnaqel. Angina Pectoris vaso-motoria. Deutsches Archiv f. khn. Med. Leipzig, 1867. 
 
 40. Schmerzhafte Empfindungen bei Herzerkrankungen, Zeitsch, f. klin, Med. 
 
 Berhn, 1891. 
 
 41. OsLER. The Principle and Practice of Medicine, 6th Edition. 
 
 42. Paterson, The limb plexus of mammals, Journ. of Anat. and Phys., vol. xxi, p. 611, 
 
 43. Ramstrom. Anatomische und experimentelle Untersuchungen iiber die lamellosen Nerven- 
 
 korperchen im Peritoneum parietale des Menschen. Anatomische Hefte. Heft 109, 
 1908. 
 
 44. RiCHERAND. Elements of Physiology (Note on insensitiveness of heart in operation), 
 
 p. 613. 
 
 45. Ross. On the segmental distribution of sensory disorders. Brain, Jan., 1888. 
 
 46. Russell, W. Relation of Angina Pectoris and alUed conditions to an arterio-cardiac reflex 
 
 having its origin in the Abdomen. Brit. Med. Journ., February 10, 1906. 
 
 47. ScHMOLL. Ueber motorische, sensorische und vaso-motorische Symptome diu'ch Koronar- 
 
 sklerose und sonstige Erkrankungen der linksseitigen Herzhalfte. Miinchener Med. 
 Wochenschrift, No. 41, 1907. 
 
 48. Sherrington, Article, ' Cutaneous sensations,' Schaefer's Text Book of Physiology. 
 
 49. The Integrative Action of the Nervous System. London, 1906. 
 
 50. Peripheral distribution of the fibres of the posterior roots of some spinal nerves. 
 
 Phil. Trans. Roy. Soc, London, vol. cxc, p. 45. 
 
 51. Steell. Textbook on Diseases of the Heart, 1906. 
 
 52. Sturge. The phenomena of Angina Pectoris and their bearing upon the theory of 
 
 counter-irritation. Brain, vol. v, 1883, p. 492. 
 
 53. Trotter and Davies. The exact determination of areas of altered sensibility. Rev. of 
 
 Neurol, and Psychiat., October, 1907. 
 54. Experimental studies in the innervation of the skin. Journ. of Physiol., vol. xxxviii, 
 
 February, 1909. 
 55. Weber. Case of Angina Pectoris with Aortitis. Proc. Roy. Soc. of Med., April, 1908.
 
 BIBLIOGRAPHY 379 
 
 56. WiLLOUGHBY. Site of referred pain in visceral disease from an embryological standpoint. 
 
 Lancet, April 16, 1904. 
 
 57. Wilson. The onset of fear and the onset of pain in cardiac disturbance. Trans. Med. 
 
 Ch. Soc. of Edinburgh, 1905. 
 
 II. BLOOD PRESSURE 
 
 58. Allbutt. Clinical remarks on Arterio-sclerosis. Brit. Med. Journ., October 20, 1906. 
 
 59. The senile cardio-vascular system. The Hospital, November 16, 1907. 
 
 60. Basch. Ueber die Messung des Blutdrucks am Menschen. Zeits. f. klin. Med., 1881. 
 
 61. Broadbent. Clinical significances and therapeutical indications of variations in the 
 
 blood pressure. Brit. Med. Journ., October 20, 1906. 
 
 62. Dawson. The lateral blood pressure at different points of the arterial tree. Amer. 
 
 Journ. of Phys., 1906, vol. xv. 
 
 63. The systohc output and work of the heart and their relation to the blood pressure 
 
 in man. Brit. Med. Journ., October 20, 1906. 
 
 64. Eblanger. a new instrument for determining the minimum and maximum blood pressure 
 
 in man. Johns Hopkins Hosp. Rep., 1904, vol. xii, p. 53. 
 
 65. Erlanger and Hooker. An experimental study of blood pressure and pulse pressure 
 
 in man. Johns Hopkins Hosp. Rep., 1904, vol. xii, p. 145. 
 
 66. Edgecombe. Blood pressure in spa practice. Journ. of Balneology and Climatology, 
 
 April, 1908. 
 
 67. Gaertner. Ueber einen neuen Blutdruckmesser (Tonometer). Wien. KHn. Woch., 1899, 
 
 No. 25. 
 
 68. Gibson. A clinical spliygmomanometer yielding absolute records of the arterial pressure. 
 
 The Quarterly Journal of Medicine, October, 1907. 
 
 69. Hill. Article, ' The mechanism of the circulation of the blood,' in Schaefer's Text Book of 
 
 Physiology. 
 70. The measurement of systolic blood-pressure in man. Heart, vol. i, 1909. 
 
 71. Hill and Flack. The accuracy of the obHteration method of measuring arterial pressure 
 
 in man. Journ. of Physiol., vol. xxxviii. No. 4. 
 
 72. HiRSCHFELDER. Some observations upon blood pressure and pulse form. Johns Hopkins 
 
 Bull., June, 1907. 
 
 73. Janeway. Observations on the estimation of blood pressure in man. New York Bull. 
 
 of Med. Sc, 1901, vol. i, p. 105. 
 74. The Chnical Study of Blood Pressure, 1904. 
 
 75. Janowski. Ueber Blutdruck, wahre Pulsgrosse und Pulszeleritat in verschiedenen 
 
 pathologischen Zustanden. Wiener Klin. Woch., 1907, No. 50. 
 
 76. Lewis. Note on the estimation of blood pressure. Brit. Med. Journ., October 27, 1906. 
 
 77. Matthew. Vaso-dilators in High Blood Pressure. Quart. Journ. of Med., vol. ii, p. 261. 
 
 78. Mummery. Comparison of blood pressure readings obtained simultaneously with a 
 
 manometer and with a sphygmomanometer. Proc. Physiol. Soc, Journ. of Physiol., 
 1905, vol. xxxii, p. 23. 
 
 79. MiJNZER. Apparat zur objektiven Blutdruckmessung ; gleichzeitig auch ein Beitrag zur 
 
 Sphygmo-Turgographie. Miinch. Med. Woch., No. 37, 1907. 
 80. Zur graphischen Blutdruckbestimmung und Sphygmobolometrie nebst Beitragen 
 
 zur klinischen Bewertung dieser Untersuchungsmethoden. Mediz. Khnik, 1908, 
 
 Nos. 14, 15, and 16. 
 81. Oliver. Haemomanometry in man. Lancet, July 22, 1905. 
 82. Studies in Blood Pressure. 2nd Ed., London, 1908.
 
 380 DISEASES OF THE HEART 
 
 83. PoTAiN. Determination experimentale de la valeur du sphygmomanometre. Arch, de 
 
 Physiol, 1890, fifth series, vol. ii, p. 300. 
 
 84. Recklinghausen. Ueber Blutdiuckmessung beim Menschen. Arch. f. exp. Path. u. 
 
 Pharmak., 1901, vol. xlvi. 
 
 85. Sahli. Ueber das absolute Sphygmogramm und seine klinische Bedeutung. Deuts. Arch. 
 
 f. klin. Med., 1904, vol. Ixxxi, p. 493. 
 
 86. Sewall. Experiments on venous blood pressure and its relation to arterial pressure in 
 
 man. Journ. Amer. Med. Assoc, October 20, 1906. 
 
 87. Stabling. Observations on the arterial blood pressure in heart disease. Lancet, 
 
 September 29, 1906. 
 
 88. Stbassberger. Ueber Blutdruck, Gefasstonus und Herzarbeit bei Wasserbadern ver- 
 
 schiedener Tempera turen. Deuts. Arch. f. klin. Med., 1905, vol. Ixxxii, p. 459. 
 
 89. Vaquez. Eclampsie puerperale et tension arteriale. Semaine Medicale, 13 mars 1907. 
 
 90. Williams. The practical value of blood pressure estimation. The CUnical Journal, 
 
 January 8, 1908. 
 
 III. DIGITALIS 
 
 91. Brunton. Case of poisoning by infusion of digitaUs. Collected papers on circulation 
 
 and respiration, p. 99. London, 1907. 
 
 92. Christison. A Dispensatory. 1848, p. 401. 
 
 93. CusHNY. On the action of substances of the digitalis series on the circulation of mam- 
 
 mals. Journ. Exp. Med., vol. ii. 
 
 94. Text Book of Pharmacology and Therapeutics, 4th Ed. 
 
 95. Fatjconnet. Ueber Herzbigeminie nach DigitaUsgebrauch. Miinch. Med. Woch., 1904, 
 
 vol. U, p. 2277. 
 
 96. Gibson, A. A contribution to the knowledge of the action of digitalis on the human 
 
 heart. Quart. Journ. Med., January, 1908. 
 
 97. Gossage. The tone of cardiac muscle. Proc. Roy. Soc. Med., 1908. 
 
 98. GtriLLEAUME. Un cas de Pouls alternant provoque par la digitale. Arch, des Malad. 
 
 du Cceur, No. 6, juin 1909. 
 Hay. Some points in the treatment of diseases of the heart. Practitioner, October, 1907. 
 
 100. Hewlett, DigitaUs heart-block. Joiirn. Amer. Med. Assoc, January 5, 1907. 
 
 101. Lewis. Irregular action of the Heart in mitral stenosis ; the inception of the ventricular 
 
 rhythm. Quart. Journ. of Medicine, vol. ii, July, 1909, p. 356. 
 "102. MoRisoN. The treatment of the muscular, haemic and mechanical factors in heart disease. 
 Edin. Med. Jomn., 1904, p. 322. 
 
 103. Pletnew. Ueber das Verhalten der Anspruchsfiihigkeit des unter Digitaliseinfiuss 
 
 stehenden Saugethierherzens. Zeitsch. f. exp. Path, und Therapie, 1. Bd. 
 
 104. Tabora. Ueber die experimentelle Erzeugung von Kammersystolenausfall und Disso- 
 
 ciation durch DigitaUs, Zeitsch. f. exp. Path, und Therapie, BerUn, 1906. 
 
 IV. DILATATION OF THE HEART AND TONICITY 
 
 105. Allbutt. Hypertrophy and dilatation of the heart. Practitioner, January, 1902. 
 
 106. CoLBECK. Dilatation of the heart. Lancet, April 9, 1904. 
 
 107. Gaskell. Tonicity. Schaefer's Text Book of Physiology, vol. u. 
 
 108. Gossage, On some aspects of dilatation of the heart, Med. Chir. Trans., vol. xc. 
 
 109. The tone of cardiac muscle. Proc. Roy. Soc. of Med., 1908. 
 
 110. Lees and Poynton. Acute dilatation of the heart in the rheumatism and chorea of 
 
 childhood. Med. Chir. Trans., vol. Ixxxi.
 
 BIBLIOGRAPHY 381 
 
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 December, 1888. 
 
 115. Steell. Heart failure as a result of chronic alcoholism. Medical Chronicle, April, 1893. 
 
 116. DiastoUc murmur in dilatation of the heart, without arterial imcompetence or 
 
 am-iculo-ventricular constriction. Edin. Med. Journ., 1895. 
 
 V. HEART BEAT 
 
 117. Adam. Experimentelle Untersuchungen iiber den Ausgangspunkt der automatischen 
 
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 118. Carlson. Co-ordination and conduction in the heart with special reference to the heart 
 
 of Limulus. Amer. Journ. Phys., vol. xv, p. 99. See also pp. 207 and 257. 
 
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 120. Cyon. Les Nerfs du Cceur. 1905. 
 
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 1903. 
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 p. 167. 
 
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 1876, vol. clxvi, p. 269, also 1877, vol. clxvii, p. 659, and 1880, vol. clxxi, p. 161. 
 
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 VI. ;_ MOVEMENTS OF THE HEART AND ARTERIES 
 
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 136. Broadbent. The pulse. London, 1890. 
 
 137. Brunton. On rhythmic contraction of the capillaries in man. Jom-n of Phys., vol. v> 
 
 No. 1.
 
 382 DISEASES OF THE HEART 
 
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 February 16, 1901. 
 
 139. Chauveau. Vue d'ensemble sm* le mecanisme du oceur. Association frangaise pour 
 
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 gen., Mai 1899. 
 
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 1899. 
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 mecanisme du coeur. Journ. de Phys. et de Path, gen., Juillet 1899. 
 
 143. H. Etude cardiographique sur le mecanisme du bruit de galop. Paris, 1902. 
 
 144. Clarke and Douglas. Some cardiographic tracings from the base of the human heart. 
 
 Journ. Anat. and Phys., vol. xxxvii. 
 
 145. Dabney. The Pulse ; its diagnostic and prognostic value. Journ. of the Amer. Med. 
 
 Assoc, November 12, 1898. 
 
 146. Elnthoven. Le Telecardiogramme. Arch. Internationales de Phys., septembre 1906. 
 
 147. L'enregistrement des bruits du cceiir de I'homme a I'aide du galvanometre 
 
 a corde. Arch. Neerland. des Sc. Exactes et Naturelles, Serie II, Tome xii, p. 401. 
 
 148. Fredericq. Sur I'existence d'un plateau systolique dans le sphygmogramme du pouls 
 
 senile. Arch. Internationales de Phys., 15 juin 1907. 
 
 149. Historisch-kritische Bemerkunger iiber die von klinischer Seite neuerdings aner- 
 
 kannte Identitat der Venen- und Oesophaguspulsbilder mit Vorkammerdruck- 
 kurven. Zentralbl. f. Physiol., Bd. xxii. No. 10. 
 
 150. Prey. Die Untersuchung des Pulses. Berhn, 1892. 
 
 151. Gerhardt. Ueber einige pathologische Formen des Spitzenstosses. Arch. f. exp. Path. 
 
 und Pharmak., Bd. xxxiv. 
 
 152. Hoy. Graphic Records in Heart Disease. London, 1909. 
 
 153. Janowski. Ueber die Dikrotie bei Aorteninsuffizienz. Zeits. f. klin. Med., Bd. Ixi. 
 154. Coeffizient der Pulszeleritat in normalen und pathologischen Zustanden. 
 
 Zeits. f. klin. Med., Bd. Ixv. 
 
 155. Keith. The evolution and action of certain muscular structures of the heart. Lancet, 
 
 February 27, 1904. 
 
 156. The anatomy of the valvular mechanism round the venous orifices of the right 
 
 and left auricles, &c. Proc. of the Anat. Soc. of Great Britain and Ireland, November, 
 1902. 
 
 157. Keyt. Sphygmography and Cardiography, Physiological and Clinical. New York and 
 
 London, 1887. 
 
 158. Lewis. The pulse in aortic disease. Lancet, September 15, 1906. 
 
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 October 29, 1906. 
 
 160. The factors influencing the prominence of the dicrotic wave. Journ. of Phys., 
 
 October 29, 1906. 
 
 161. The interpretation of sphygmograph tracings, &c. The Practitioner, February, 
 
 1907. 
 162. The interpretation of the primary and first secondary waves in sphygmograph 
 
 tracings. Journ. of Anat. and Phys., vol. xli. 
 
 163. McCalltjm. On the muscular arcliitecture and growth of the ventricles of the heart. 
 
 Johns Hopkins Hospital Reports, 1900, vol. ix, p. 307. 
 
 164. Mackenzie. The study of the Pulse, arterial, venous and hepatic, and of the movements 
 
 of the Heart. Edinburgh, 1902. 
 
 165. Marey. La Circulation du Sang. Paris, 1881.
 
 BIBLIOGRAPHY 383 
 
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 VII. IRREGULAR ACTION OF THE HEART 
 
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 3 fevrier 1909. 
 
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 ventricle in the various stages of block. Amer. Journ. of Phys., 1906, vol. xvi, p. 160. 
 
 193. Irregularities of the heart resulting from disturbed conductivity. Amer. Jom-n. 
 
 Med. Sc, June, 1908.
 
 384 DISEASES OF THE HEART 
 
 194. Gerhardt. Beitrag zur Lehre von den Exirasystolen. Deut. Ai'ch. f. klin. Med., 
 
 Bd. Ixxxii. 
 
 195. tJber Unregelmassigkeiten des Herzschlags. Sonderabdruck aus den Sitzungs- 
 
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 196. Harris. Indurative Mediastino-Pericarditis. London, 1895. 
 
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 203. Hoffmann, A. Neue graphische Methoden nebst Beobachtvmgen von kiinstlich erzeugter 
 
 Arhjrthmie am freiliegenden Menschenherzen. Congress f. innere Med., 1904. 
 
 204. Hoffmann, F. tJber die Anderung des Kontraktionsablaufes am Ventrikel und Vorhof 
 
 des Froschherzens bei Frequenzanderung und im hypodynamen Zustande. Pfliigers 
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 205. Laslett. Note on the Pulsus Bigeminus. Brit. Med. Journ., April 24, 1909. 
 
 206. Lewis. Single and successive Extra-systoles. Lancet, February 6, 1909. 
 
 207. The experimental production of paroxysmal tachycardia and the effect of ligation 
 
 of the coronary arteries. Heart, vol. i, 1909, p. 98. 
 208. Mackenzie. Nodal Bradycardia. Heart, vol. i, 1909, p. 23. 
 
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 210. Die Bedeutung der ventrikularen Form des Venenpulses. Medizinische Klinik, 
 
 1907, No. 46. 
 211. The inception of the rhythm of the heart by the ventricle as the cause of the 
 
 continuous irregularity of the Heart. Brit. Med. Journ., March 5, 1904. 
 
 212. MacWilliam. On the influence exercised by the central nervous system on the cardiac 
 
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 213. MusKENS. An analysis of the action of the vagus nerve on the heart. Amer. Jom-n. 
 
 Phys., 1898. 
 
 214. Nicholson. Article, ' The pulse,' Encycl. Med. Edin., 1902. 
 
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 Unregelmassigkeiten des menschhchen Herzens. Zeitsch. f. exp. Path, und Ther., 
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 222. Ueber Herzalternanz beim Menschen. Zeitsch. f. exp. Path, und Ther., Bd. iii.
 
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 VIII. PAROXYSMAL TACHYCARDIA 
 
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 232. Balfour. The Senile Heart, 1894. 
 
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 MACKEKZIE Q Q
 
 386 DISEASES OF THE HEART 
 
 IX. PRIMITIVE CARDIAC TISSUE, HEART-BLOCK, AND ADA3IS-ST0KES 
 
 SYNDROME 
 
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 266. CoHN. The auriculo-nodal junction. Heart, vol. i, 1909. 
 
 267. Deneke. Die Uberleitungsstorungen zwischen Vorhof und Kammer des Herzens. 
 
 Jahrbiicher der Hamb. Staatskrankenanstalten, xi, 2. 
 268. Zur Rontgendiagnostik seltener Herzleiden. Deutsch. Arch. f. klin. Med., 
 
 Bd. Ixxxiv. 
 269. Erlanger. Physiology of heart-block in mammals with especial refei'ence to the 
 
 causation of Stokes- Adams disease. Journ. Exp. Med., 1906, vol. viii, p. 8. 
 270. Fiuther studies in the physiology of heart-block. Amer. Jotu-n. of Phys., 
 
 Slay 1, 1906. 
 27L A review of the physiology of heart-block in mammals. Brit. Med. Journ., 
 
 October 27, 1906. 
 
 272. Experimental Heart-block. Heart, vol. i, 1909. 
 
 273. Erlanger and Hirschfelder. Further studies on the physiology of heart-block in 
 
 mammals. Amer. Joru-n. of Phys., 1903, vol. xv, p. 153. 
 274. Eine vorlaufige JNIitteilung iiber weitere Studien in bezug auf den Herzblock in 
 
 Saugetieren. Zentralblatt fiir Physiologic, Bd. xix. No. 9. 
 
 275. Finny. Bradycardia with Arrhythmia and epileptiform seizures. Dublin Jom-n. 
 
 Med. Sc, May, 1906. 
 
 276. Galabin. On the interpretation of cardiographic tracings, &c. Guy's Hospital 
 
 Reports, 1875, vol. xx, p. 261. 
 
 277. Gibson, A. The heart in a case of Stokes-Adams disease. Quart. Journ. Med., January, 
 
 1908. 
 
 278. Gibson, G. Bradycardia. Edin. Med. Journ., July, 1905. 
 
 279. The electromotive changes in heart-block. Brit. Med. Jomn., July 7, 1906. 
 
 280. Heart-block. Brit. Med. Journ., October 7, 1906.
 
 BIBLIOGRAPHY 387 
 
 281. Gibson and Ritchie. Further observations on heart-block. Practitioner, May, 1907. 
 
 282. A historic instance of the Adams-Stokes Syndrome due to Heart-block. Edin. 
 
 Med. Journ., June, 1909. 
 
 283. Gillies. A case of Bradycardia. AustraHan Med. Gaz., January 20, 1906. 
 
 284. GossAGE. Cases of Stokes- Adams disease. CHn. Soc. Trans., vol. xxxviii. 
 285. — Some cases of partial heart-block. Clin. Soc. Trans., vol. xl. 
 
 286. Handfobd. Remarks on a case of Gummata of the heart. Death from heart-block ; 
 
 rhythmical contraction of the auricles during the long pauses. Brit. Med. Journ., 
 vol. ii, 1904. 
 
 287. Hay. The pathology of Bradycardia. Brit. Med. Journ., October 21, 1905. 
 288. Bradycardia and cardiac arrythmia. Lancet, January 20, 1906. 
 
 289. Heart-block in its relationship to Stokes- Adams disease. Med. Chron., September, 
 
 1906. 
 290. Stokes- Adams disease. Report of a case. Liverpool Medico-Chir. Journ., 
 
 July, 1906. 
 
 291. Hay and Moore. Stokes- Adams disease and cardiac arrythmia. Lancet, November 10, 
 
 1906. 
 
 292. Hering. Ueber die Erregungsleitung zwischen Vorkammer und Kammer des Saugethier- 
 
 herzens, &c. Arch. f. die ges. Phys., Bd. cvii. 
 293. Nachvveis dass das His'sche Uebergangsbiindel Vorhof und Kammer des Sauge- 
 
 thierherzens functionell verbindet. Arch. f. die ges. Phys., Bd. cviii. 
 294. Ueber die unmittelbare Wirkung des Accelerans und Vagus auf automatisch 
 
 schlagende Abschnitte des Saugethierherzens. Pfliig. Arch., 1905, vol. cviii, p. 281. 
 295. ijberleitungsstorungen am Saugethierherzen mit zeitweiligem Vorhof systolenaus- 
 
 fall. Zeitschrift flir exper. Path, und Therapie, Berlin, 1906. 
 296. His, Jr. Dritter intern. Physiol. Congress in Bern. Centbl. f. Physiol., 1895, vol. ix, 
 
 p. 469. 
 297. Ein Fail von Adams-Stokes'scher Klrankheit mit ungleichzeitigem Schlagen 
 
 der Vorhofe und Herzkammern (Herzblock). Deutsch. Arch. f. klin. Med., 1899, 
 
 Ixiv, p. 316. 
 
 298. HoLST. Om Stokes- Adams sygdom og ' Heart-block ' hos menneskit. Kristiania, 1908- 
 
 299. HuMBLET. Le faisceau interauriculo-ventriculaire constitue le lien physiologique entre 
 
 les oreillettes et les ventricules du coeur du chien. Arch, inter, d. Phys., 1904, 
 vol. i, p. 278. 
 300. Allorhythme cardiaque par section du faisceau de His. Ibid., 1906, vol. iii, p. 330. 
 
 301. Jellinek and Cooper. Report, with comment, on six cases of heart-block with tracings 
 
 and one post-mortem examination of the heart. Brit. Med. Journ., Apr. 4, 1908. 
 
 302. Keith. The auriculo-ventricular bundle. London Hosp. Gaz., June, 1906. 
 
 303. Keith and Flack. The auriculo-ventricular bundle of the human heart. Lancet, 
 
 August 11, 1906. 
 
 304. Keith and Miller. Description of a heart showing gummatous infiltration of the 
 
 auriculo-ventricular bundle. Lancet, 1906, vol. ii. 
 
 305. Kent. Researches on the structure and function of the mammalian heart. Journ. of 
 
 Phys., 1893, vol. xiv, p. 233. 
 
 306. Kraus. Einiges iiber functionelle Herzdiagnose. Deutsch. Med. Woch., 1905, pp. 1 
 
 and 53. 
 
 307. Laslett. a case exhibiting the Adams-Stokes syndrome. Lancet, June 4, 1904. 
 
 308. Syncopal attacks associated with prolonged arrest of the whole heart. Quart. 
 
 Journ. of Medicine, vol. ii, p. 347, 1909. 
 309. Lewis. The occurrence of heart-block in man and its causation. Brit. Med. Journ., 
 
 vol. ii, 1908, p. 1798. 
 
 C c 2
 
 388 DISEASES OF THE HEART 
 
 310. LoHMANN. Zur Automatie der Briickenfasern und der Ventrikel des Herzens. Physiol. 
 
 Abtlieilung des Arch. f. Anat. und Physiol., Leipzig, 1904. Bd. i und ii. 
 
 311. Mackenzie. Nodal Bradycardia. Heart, vol. i, p. 23. 
 
 312. MONCKEBERG. Untersuchungen iiber das Atrioventricularbiindel im menschlichen 
 
 Herzen. Jena, 1908. 
 
 313. Morrow. Heart-block. Brit. Med. Journ., October 27, 1906. 
 
 314. Nagayo. Pathologisch-anatomische Beitrage zum Adams-Stokes" schen Symptom- 
 
 complex. Zeitsch. f. klin. Medizin, 67. Bd., Hefte 5-6. 
 316. OsLER. On the so-called Stokes- Adams disease. Lancet, August 22, 1903. 
 
 316. Retzer. Ueber die musculose Verbindung zwischen Vorhof und Ventrikel des 
 
 Saugethierherzens. Arch. f. Anat., 1904, p. 1. 
 
 317. RiHL. Analyse von fiinf Fallen von Ueberleitungsstorungen. Zeits. f. exp. Path. u. 
 
 Therap., 1905-6, vol. ii, p. 82. 
 
 318. Ritchie. Complete heart-block Avith dissociation of the action of the amides and 
 
 ventricles. Proc. Roy. Soc. of Edinbm-gh, vol. xxv. Part xii, 
 
 319. ScHMOLL. Zwei Falle von Adams-Stokes'scher I^o-ankheit mit Dissociation von Vorhof 
 
 und Kammerrhythmus und LJision des His'schen Biindels. Deuts. Arch. f. klin. Med., 
 Band Ixxxvii. 
 320. Adams-Stokes disease. Journ. Amer. Med. Assoc, vol. xlvi, p. 361. 
 
 321. Stengel. Fatal case of Stokes-Adams disease with autopsy. Amer. Journ. Med. Sc, 
 
 1905, vol. cxxx, p. 1083. 
 
 322. Stokes. Observations on some cases of permanently slow pulse. Dublin Quart. Journ. 
 
 Med. Sc, 1846. 
 
 323. Tawara. Das Reizleitungssystem des Saugethierherzens. Jena, 1906. 
 
 324. Tigerstedt. Ueber die Bedeutung der Vorhofe fiir die Rhythmik der Ventrikel des 
 
 Saugethierherzens. Arch. f. Physiol., 1884, p. 497. 
 
 325. Vaquez et Esmein. Pouls lent d'origine myocarditique (Herzblock). Bulletins et 
 
 Memoires de la Societe medicale des Hopitaux de Paris (Seance du 25 janv. 1907). 
 
 326. Webster. Cardiac Arrhythmia in relation to cerebral anaemia and epileptiform crises. 
 
 Glasgow Hospital Reports, 1901. 
 
 327. Wenckebach. Beitrage zui- Kenntniss der menschlichen Herztatigkeit. Arch. f. 
 
 Anatomic und Physiol., 1906 and 1907. 
 328. Arrythmia of the Heart (Snowball's Translation). 
 
 329. Wilson. The nerves of the atrio-ventricular bundle. Proc. Roy. Soc, B, vol. Ixxxi, 1909. 
 
 330. WooLDRiDGE. Ueber die Function der Kammernerven des Saugethierherzens. Arch. 
 
 f. Physiol., 1883, p. 522. 
 
 X. TRICUSPID REGURGITATION 
 
 331. Adams. Dublin Hospital Reports, 1827, vol. iv, p. 437. 
 
 332. Bramwell. Diseases of the Heart, p. 531. 
 
 333. Fran(^ois-Franck. Note sur la reproduction experimentale des insuffisances valvulaires 
 
 du coeur. Memoires et Bulletins de la Societe de Medecine de Bordeaux, (1882) 1883. 
 
 334. Gairdner. On the action of the auriculo-ventricular valves of the heart. Dublin 
 
 Hospital Gazette, October, 1857, p. 295. 
 
 335. Gibson, G. Jugular reflux and tricuspid regurgitation. Edin. Med. Journ., May, 1880, 
 
 vol. xxv. 
 336. Our debt to Ireland in the study of the circulation. Dublin Journ. of Medical 
 
 Science, 1907. 
 337. Hebing. Zur experimentellen Analyse der Um-egelmassigkeiten des Herzschlages. 
 
 Separatabdruck aus dem Archiv fiir die ges. Physiol., Bd. Ixxxii, Seite 8.
 
 BIBLIOGRAPHY 389 
 
 338. Hu>'TER. Works, Palmer's Edition, 1835, vol. iii. 
 
 339. King. The safety-valve function in the right ventricle of the human heart. Guy's 
 
 Hospital Reports, 1837, vol. ii, p. 132. 
 
 340. Luton. Article ' Circulation ' in the Nouveau Dictionnaire de Medecine et Chirurgie 
 
 pratiques, tome vii, p. 715. 
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 344. RiEGEL. Zur Diagnose der Tricuspidainsufficenz. Berlin. KHn. Woch., 1886, No. 38, 
 
 p. 621. 
 
 345. Stokes. The Diseases of the Heart and Aorta. Dublin, 1854, p. 234. 
 
 346. Walshe. Diseases of the Heart. Third Edition, p. 376. 
 
 XI. VENOUS AND LIVER PULSATION 
 
 A full bibliography of tlus section up to 1893 will be found in a paper I wrote on ' The 
 venous and liver pulses and the arrhythmic contraction of the cardiac cavities ' in the 
 Journ. of Path, and BacterioL, 1894, vol. ii, p. 84. 
 
 347. Babd. De Tem-egistrement graphique du pouls veineux des jugulaires chez I'homme, 
 
 &c. Journ. de Phys. et de Path, gen., mai 1906. 
 
 348. Bonniger. Ueber den aiirikularen Lebervenenpuls. Charite-Annalen, xxix. Jahrgang. 
 
 349. CuSHNY AND Grosh. The venous pulse. Joui-n. Amer. Med. Assoc, October 12, 1907. 
 
 350. Deane. Respiratory pulse curves and venous pulse in healthy people. Jom-n. Royal 
 
 Army Med. Corps, June, 1907. 
 
 351. Deutsch. Ueber eine neue Methode zur Untersuchung des Venenpulses. Congress f. 
 
 innere Medizin, 1904. 
 
 352. DoTOiA. De Analyse van het Phlebogram. Groningen, 1906. 
 
 353. Fredebicq. La seconde ondulation positive (premiere ondulation systolique) du pouls 
 
 veineux physiologique chez le chien. Archives Internat. de Physiologie, 15 juin 
 1907, pp. 1-25. 
 
 354. Gerhardt. KHnische Untersuchungen iiber Venenpulsationen. Leipzig, 1894. 
 
 355. Beitrag zur Lehre von den Extrasystolen. Deut. Arch. f. kUn. Med., Bd. Ixxxii, 
 
 356. Gibson, A. The significance of a hitherto undescribed wave in the jugular pulse. Lancet, 
 
 November 16, 1907. 
 
 357. GuiLLEAUME. De I'importance du pouls veineux dans la semeiologie du cceur. Soc. Med. 
 
 et Chii'urg. de Liege, seance du 4 mars 1909. 
 
 358. Hering. Die Verzeichnung des Venenpulses am isolirten kiinstlich durchstromten 
 
 Saugetierherzen. Arch. f. die ges. Phys., Bd. cvi. 
 
 359. Hewlett. The interpretation of the positive venous pulse. Journ. Med. Research, 
 
 October, 1907. 
 
 360. Hirschfelder. Graphic records in the study of cardiac diseases. Amer. Journ. Med. 
 
 Sc, September, 1906. 
 
 361. Inspection of the jugular vein, &c. Jom-n. Amer. Med. Assoc, March 30, 1907. 
 
 362. Some variations in the form of the venous pulse. Johns Hopkins Bull., June- 
 July, 1907. 
 
 363. Lewis. Pulse records in their relation to the events of the human cardiac cycle. Hill's 
 ' Recent advances in Physiology and Biochemistry', 1908. 
 
 364. The normal venous pulse. Brit. Med. Journ., November 14, 1908. 
 
 365. Mackenzie. Die Bedeutung der ventrikularen Form des Venenpulses. Medizin. Klinik, 
 1907, No. 46.
 
 390 DISEASES OF THE HEART 
 
 366. Morrow. Forms of negative venous pulse. Brit. Med. Journ., December 22, 1906. 
 
 367. Nicholson. Article ' The pulse ', Encyclopaedia Medica, Edin., 1902. 
 
 368. PiERSOL. An observation on the jugular pulse of man. Amer. Journ. Med. Science, 
 
 June, 1908. 
 
 369. Rautenberg. Ueber Synergie und Asynergie der Vorhofe des menschlichen Herzens. 
 
 Miinch. Med. Wochensch., No. 8, 1909. 
 
 370. RiHL. Ueber das Verhalten des Venenpulses unter normalen und pathologischen Be- 
 
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 371. VoLHARD. Ueber Venenpulse. Congress fiir innere Medicin, 1902. 
 
 372. Ueber Leberpulse und iiber die Compensation der Klappenfehler. Berliner Klin. 
 
 Woch., 1904, No. 20. 
 373. Wenckebach. Beitrage zur Kenntnis der menschlichen Herztatigkeit. Arch. f. 
 
 Anat. u. Phys., phys. Abteilung, 1906. 
 
 XII. GENERAL 
 
 374. Allbutt. On the hypodermic use of morphia in diseases of the heart and great vessels. 
 
 The Practitioner, vol. iv, 1869. 
 
 375. Bard. Les insuffisances aortiques sans souffle. Semaine Medicale, 2 juin 1909. 
 
 376. Bolton. Experimental production of uncompensated heart disease with especial 
 
 reference to the pathology of dropsy. Journ. of Path, and Bact., 1903. 
 
 377. On the pathology of dropsy produced by obstruction of the superior and inferior 
 
 venae cavae and the portal vein. Proc. Roy. Society, B, vol. Ixxix, 1907. 
 
 378. Brockbank, The Murmurs of Mitral Disease. 1899. 
 
 379. Brtjnton. On breathlessness, especially in relation to cardiac disease. Practitioner, 
 
 June, 1905. 
 
 380. Buchanan. The frequency of the heart-beat and the form of the electro- cardiogram in 
 
 birds. Journ. Physiology, vol. xxxviii. 
 
 381. CoNDER. A case of acute infective endocarditis treated with a vaccine prepared from 
 
 the patient's own blood and ending in recovery. The Practitioner, August, 1909. 
 
 382. Conner. Chnical study of heart cases. Amer. Journ. Med. Science, June, 1908. 
 
 383. Coombs. Rheumatic Carditis in childhood. Bristol Med. Ch. Journ., September, 1907. 
 384. Rheumatic Myocarditis. Quart. Journ. Med., vol. ii, 1908. 
 
 384a. Cowan. Current theories regarding the causation of arterio-sclerosis. Practitioner, 
 August, 1905, and March, 1906. 
 
 ^385. The heart in acute disease. Journ. Path, and Bact., August, 1903. 
 
 -386. The fibroses of the heart. Journ. Path, and Bact., December, 1903. 
 
 387. On obstruction of the coronary arteries. Trans. Glasgow Path, and Clinical 
 
 Society, vol. ix. 
 
 388. Croom. Remarks on certain points in tricuspid obstruction. Edin. Med. Journ., Sep- 
 
 tember, 1905. 
 
 389. Cushny. Two cases of Cheyne-Stokes respiration. Journ. Phys., vol. xxxvi. 
 
 390. Deane. The irritable heart of soldiers ; its causation and prevention. Journ. Pre- 
 
 ventive Medicine, May, 1906. 
 
 391. Delepine. Meaning of cardio-pneumatic impulses, &c. Brit. Med. Journ., July 25, 1891. 
 
 392. Dixon. Facts and Fancies in Pliarraacology. Brit. Med. Jom-n., August, 1909, p. 539. 
 
 393. Douglas and Haldane. The cause of periodic or Cheyne-Stokes breathing. Journ. 
 
 Phys., vol. xxxviii, June, 1909. 
 
 394. Dreysil. Ueber Herzhypertrophie bei Schwangeren und Wcichnerinnen. Miinch. 
 
 med. Abhand., Heft iv.
 
 BIBLIOGRAPHY 391 
 
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 396. Gairdner. Clinical Medicine. Edinburgh, 1862. 
 
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 398. , BuLLMORE AND CoNDER. Adhesive Mediastino-pericarditis. Practitioner, 
 
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 401. Harris. Some clinical and post-mortem observations on the cardiac dullness in cases 
 
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 403. Hill and Flack. The influence of oxygen on athletes. Journ. of Physiol., vol. xxxviii, 
 
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 404. HiRSCHFELDER. The rapid formation of endocarditis vegetation. Johns Hopkins 
 
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 405. HoRDER. Infective Endocarditis. With an analysis of 150 cases and with special 
 
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 406. Janowski. Le diagnostic fonctionnel du coem-. Etude critique des methodes modernes 
 
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 407. JosuE ET Paillard. Symphyse cardiaque, syndrome surreno-vasculaire, anevrisme 
 
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 408. Klotz. Studies upon calcareous degeneration. Journ. Exp. Med., March and August, 
 
 1906. 
 
 409. Kraus. Ueber Kropfherz. Deutsch. Med. Woch., November 22, 1906. 
 
 410. Landouzy et Heitz. Effets obtenus par la balneation carbogazeuse. Paris, 1906. 
 
 411. Letulle. Recherches sur I'etat du coeur des femmes enceintes, &c. Paris. 
 
 412. Mantle. The influence of the nervous system and external temperature upon circu- 
 
 latory changes, &c. Lancet, April 14, 1906. 
 
 413. McPhedran and Mackenzie. A case of massive haemorrhagic infarction of the lung 
 
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 414. MacWilliam. On the properties of the arterial and venous walls. Proc. Royal Soc, 
 
 vol. Ixx. 
 
 415. Merklen. LcQons sur les troubles fonctionnels du coeur. Paris, 1908. 
 
 416. Merklen et Heitz. Examen et semeiotique du coeur. 3rd Edition, Paris. 
 
 417. MoRisoN. On Thoracostomy in heart disease. Lancet, July 4, 1908. 
 
 418. OsLER. Chronic Infectious Endocarditis. Quart. Journ. of Med., vol. ii, p. 219. 
 
 419. Paterson. The influence of the auricle on the percussion of the heart. Bristol Med. 
 
 Chir. Journ., June, 1903. 
 
 420. Pembrey, Beddard and French. Observations on two cases of Cheyne-Stokes 
 
 respiration. Proc. Phys. Soc, Journ. of Phys., 1906, vol. xxxiv, p. 6. 
 
 421. PoYNTON. Clinical lectures on rheumatic fever. International Clinics, thirteenth 
 
 series, vols, ii, iii, iv. 
 
 422. PoYNTON AND Paine. A Contribution to the study of malignant endocarditis. Med. 
 
 Ch. Trans., vol. Ixxxv. 
 
 423. Pratt. On the causes of cardiac insufficiency. Johns Hopkins Hosp. Bull., October, 
 
 1904. 
 
 424. On the development of scientific hydrotherapy. Boston Med. and Surg. Journ., 
 
 January 25, 1906.
 
 392 DISEASES OF THE HEART 
 
 425. Russell, A. Cessation of the pulse during the onset of epileptic fits with remarks on the 
 
 mechanism of the fits. Lancet, vol. ii, 1906. 
 426. The pathology of epilepsy. Proc. Royal Soc. of Med., December, 1907. 
 
 427. Russell, W. Arterial hypertonus, sclerosis, and blood pressure. Edinbmgh, 1907. 
 
 428. Salaman. The pathology of the liver in cardiac disease, &c. Lancet, January 6, 1907. 
 
 429. Savill. On arterial sclerosis especially in regard to arterial hypermyotrophy, &c. 
 
 Trans. Path. Soc. of London, vol. Iv. 
 
 430. Sewall. a common modification of the first sound of the heart simulating that heard 
 
 with Mtral Stenosis. Amer. Joui-n. Med. Sci., July, 1909. 
 431. Safeguard of the Heart-beat. Amer. Journ. Med. Sci., 1908. 
 
 432. Steell. The auscultatory signs, &c., of mitral stenosis. A statistical inquiry. Med. 
 
 Chronicle, September, 1895. 
 
 433. Stockman. Contribution to the study of heart disease in tlie Horse. Journ. Compar. 
 
 Path, and Therap., 1895. 
 
 434. Thayer. On the early diastolic Heart Sound (the so-called Third Heart Sound). Boston 
 
 Med. and Surg. Journ., May 7, 1908. 
 
 435. Thomson. Clinical examination and treatment of sick children. 2nd Edition, Edin- 
 
 burgh, 1908. 
 
 436. Thomson and Drummond. Nine cases of congenital heart disease. Edinburgh Hos- 
 
 pital Reports, vol. vi. 
 
 437. Wenckebach. Some points in the pathology and treatment of adherent pericardium. 
 
 Brit. Med. Journ., January 12, 1907. 
 
 438. Ueber pathologische Beziehungen zwischen Atmung und Kreislauf beim Menschen. 
 
 Innere Medizin, Nr. 140, 1907. 
 
 439. White, Hale. On Disease of the Heart due to over-indulgence in alcoholic diinks. 
 
 Guy's Hospital Reports, vol. Iviii. 
 
 440. Williams, L. Acute pulmonary oedema. Lancet, December 7, 1907. 
 
 441. Wyllib. On gastric flatulence. Edin. Hosp. Reports, vol. iii. 
 
 THE ELECTRO-CARDIOGRAM 
 
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 Internat. Monatsschr. f. Anat. u. Physiol., 1892, ix. 256-81. 
 
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 444. EiNTHOVEN. Le Telecardiogramme. Archiv. Internat. d. Physiol., 1906, iv. 132-64. 
 
 445. Weiteres iiber das Elektrokardiogramm. Archiv f. d. ges. Physiol., 1908, 
 
 cxxii. 517-84. 
 
 446. Engelmann. Uber das elektrische Verhalten des thatigen Herzens. Archiv f. d. ges. 
 
 Physiol., 1878, xvii. 68-99. 
 
 447. GoTCH. Proc. Roy. Soc, 1907, Ixxix, March 14; 'Heart,' KOd, i. 
 
 448. Hering. Das Elektrocardiogramm des Irregularis perpetuus. Deutsch. Archiv f. kUn. 
 
 Med., 1908, xciv. 205-8. 
 
 449. Experimentelle Studien an Saugethieren iiber das Elektrokardiogramm. Arcliiv 
 
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 1909, cxxvi. 197-224. 
 
 451. KoLUKER AND MuLLER. Nachweis der negativen Schwankung des Muskelstroms am 
 
 natiirlich sich contrahirenden Muskel. Verhandl. d. phys.-med. Gesell. i. Wiirzburg, 
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 169-94.
 
 INDEX 
 
 PAGE 
 
 ABDOMINAL AORTA 
 
 tracings of . . . . 85, 86 
 
 pulse of, compared with the liver 
 pulse ..... 126 
 ABDOMINAL VEINS 
 
 stasis in . . . . .62 
 
 ACCELERATOR NERVES, ^ee Nerves. 
 A-C INTERVAL 
 
 cases showing great increase of 
 
 337, 361, 364 
 
 definition of . . . xviii, 161, 176 
 
 increased .... 177, 179 
 
 in cases of extra-systole . . 160 
 
 significance of . . .160 
 
 variations in duration of . 160 
 
 ADAMS-STOKES SYNDROME . . 24 
 
 in nodal bradycardia . 343, 344, 345 
 
 See also Heart-Block. 
 ADHERENT PERICARDITOI . 
 
 liver pulse in ... 
 
 inverted cardiogram in 
 
 ADRENALIN .... 
 AFFERENT NERVES 
 
 See Nerves of the Heart. 
 
 AGUE 
 
 the heart in . 
 
 AIR, BELCHING OF 
 
 after an attack of angina pectoris 
 
 AIR HUNGER . 
 
 AIR SUCTION . 
 
 in angina pectoris . 
 
 ALBUMINURIA 
 
 in dilatation of the heart 
 
 ALCOHOLIC HEART 
 
 dilatation of . 
 
 rate in . 
 AMYL NITRITE 
 
 action of . . . 
 in angina pectoris . 
 
 ANACROTIC PULSE 
 
 in aortic stenosis . 
 
 ANATOMY OF THE HEART 
 
 ANEURYSM 
 
 cardio-sclerosis with 
 mode of death in . 
 pain in ... 
 
 253 
 125 
 
 87 
 276 
 
 216 
 
 . 50 
 
 26 
 
 59 
 50,60 
 
 . 211 
 
 207 
 132 
 
 276 
 303 
 
 240 
 16 
 
 251 
 252 
 
 252 
 
 ANGINA PECTORIS 
 
 air suction in .... 60 
 
 amyl nitrite in ... . 303 
 aortic aneurysm with ... 42 
 aortic regurgitation with . . 242 
 aortic stenosis with . . . 240 
 aortic valvular disease with . . 42 
 arterial pressm-e in ... 42 
 
 arterial pressure during attacks of 49, 303 
 atheroma of coronary arteries \nih 42 
 belching of air during an attack of 50 
 bodily exertion causing . . 42, 46 
 cardio-sclerosis with. . . 42, 304 
 case of death due to . . .50 
 cessation of, with dilatation of 
 
 heart 47 
 
 cessation of, with onset of mitral 
 
 regurgitation .... 47 
 character of the attacks . . 47 
 
 cold air causing . . . 42, 47 
 
 conditions inducing an attack of 42, 47 
 conditions predisposing to an attack 
 
 of 42,45 
 
 conductivity in cases of . . .43 
 constriction ot chest in . . 47, 48 
 dilatation absent in severe . . 202 
 disease of the coronary arteries 
 
 with .... 46,304,305 
 danger in slight attacks of . .50 
 death during an attack of . . 48 
 definition of term . 
 duration of the attacks of 
 effect of dilatation in 
 excitability in cases of . 
 excitement causing 
 exhaustion of contractility causing 
 exhausted heart muscle and ex 
 
 hausted nervous system with 
 exhaustion of left ventricle causing 
 extra-systoles dmdng an attack of 
 
 50, 306, 307 
 herpes zoster compared with . 57 
 
 hyperalgesia after an attack of 50, 51 
 hyperalgesic areas in . . .40 
 impaired nourishment of the heart 
 
 muscle causing .... 
 increase of urine in atack of . 
 in mediastino-pericarditis 
 mental excitement causing 
 micturition after an attack of 
 mitral regurgitation prevents 
 
 57 
 47 
 206 
 43 
 42 
 43,193 
 
 57 
 46 
 
 42 
 24 
 253 
 47 
 50 
 47
 
 396 
 
 INDEX 
 
 PAGE 
 
 ANGINA PECTORIS (continued)— 
 
 in mitral stenosis . . . 230, 234 
 over-exertion causing . . . 103 
 pain in, a viscero-sensory reflex . 40 
 persistence of pain after an attack 
 
 of 50 
 
 pathology of heart vnth 304, 305, 353 
 increased peripheral resistance caus- 
 ing ...... 43 
 
 perspiration during an attack of . 48 
 position assumed during an attack 
 
 of 48 
 
 prognosis in . . . . .50 
 pulsus alternans with 43, 50, 196, 303, 308 
 the pulse in (illustrative cases) 302-308 
 iiTitable focus in spinal cord causing 
 
 i-ecuiTcnce of . . . .45 
 a reflex protective phenomenon . 45 
 region of pain in ... 40 
 
 resemblance of, to intermittent 
 
 claudication .... 46 
 saliva increased in ... 42 
 
 sense of impending death during 
 
 an attack of . . . .49 
 a sign of impaired contractility . 43 
 site of pain during an attack of . 48 
 sleeplessness causing . . 250, 270 
 state of arteries during an attack 
 
 of 49,302 
 
 state of heart during an attack of . 49 
 stimulus-production with . . 43 
 symptoms after an attack of . 50 
 
 symptoms during an attack of . 48 
 a symptom of exhausted con- 
 tractility . . . .43, 193 
 a symptom of exhausted heart 
 
 muscle ..... 42 
 suction of air during an attack of . 50 
 summation of stimuli causing . 43 
 
 tendency to recurrent attacks of . 50 
 tonicity with .... 43 
 
 treatment by ammonium bromide 270 
 treatment by chloral . . . 270 
 treatment during an attack of . 53 
 treatment of condition inducing 52, 270 
 unconsciousness during ... 48 
 valvular disease with ... 57 
 vasomotor .... .49, 62 
 viscero-motor reflex in . . .41 
 
 ANIMALS 
 
 insensitiveness of viscera in 
 
 ANTIARIN 
 
 action on tonicity . 
 
 ANTIFEBRIN . 
 
 34 
 
 9 
 270 
 
 AORTIC REGURGITATION 
 angina pectoris in . 
 arteries visible in . 
 capillary pulsation in 
 murmur characteristic of 
 in endocarditis 
 pulse in ... 
 
 facial aspect in 
 movement of liver in 
 
 PAGE 
 
 240 
 242 
 92 
 241 
 240 
 219 
 241 
 242 
 241 
 
 AORTA 
 
 in the fixation of the heart . . 16 
 tracings of abdominal . . .85, 86 
 aneurysm of, with angina pectoris . 42 
 
 symptoms of heart failure due to . 242 
 
 AORTIC STENOSIS . . . .239 
 angina pectoris witli . . . 240 
 mm-mur characteristic of . . 239 
 pulse in ..... 239 
 
 AORTIC VALVE DISEASE . . 238 
 angina pectoris in . . . .42 
 congenital ..... 239 
 liypertrophy of the left ventricle in 239 
 nose bleeding in . . . .23 
 and pregnancy .... 260 
 after rheumatism .... 239 
 from sclerotic changes . . . 239 
 
 AORTIC VALVES 
 
 rupture of 239 
 
 APERIENTS 274 
 
 APEX BEAT 
 
 in aortic regurgitation . . . 241 
 auricular wave in . . 81,86,183,339 
 definition of . . . . .77 
 due to extra-systoles . . . 154 
 in heart-block .... 183 
 how to record . . . .71 
 
 in nodal rhythm . . 81,321,339 
 period of contraction ... 78 
 period of filling .... 81 
 period of relaxation ... 80 
 and the retraction of the lung . 88 
 
 due to right ventricle . . 85, 88 
 
 interpretation of a tracing of . . 78 
 showing coupled beats . . 284, 285 
 systolic plateau in tracings of 78, 80, 82 
 time of opening of a.-v. valves 80, 110 
 
 APEX OF HEART 
 
 arrangement of muscle- fibres at 
 movement of . 
 
 17 
 17 
 
 31 
 
 20 
 
 APOPLEXY 
 
 pulmonary ..... 
 
 APPEARANCE OF THE PATIENT 
 
 ARM 
 
 pain in, during an attack of angina 
 pectoris ..... 
 development of . 
 nerve-supply of ... . 
 reason for heart pain felt in . 
 
 ARTERIAL DEGENERATION 
 
 and high blood-pressure . . 101 
 
 and cardio-sclerosis . 243, 245, 247 
 
 48 
 39 
 39 
 40
 
 INDEX 
 
 397 
 
 ARTERIAL DEGENERATION {con- 
 tiniied) — 
 definition of . 
 and extra-systoles 
 and heart failure . 
 and the nodal rliythm . 
 and obliteration of the capillaries 
 recognition of ... 
 
 superficial arteries in 
 
 XVUl 
 
 103 
 103 
 104 
 244 
 93 
 93 
 
 ARTERIAL PRESSURE 
 
 in angina pectoris . . . .42 
 during attacks of angina pectoris 49, 303 
 in cardiac asthma .... 29 
 effect of capillary obliteration on . 245 
 cause of ..... 98 
 in Cheyne-Stokes respiration 29, 30, 189 
 wath exhaustion of contractility . 193 
 difficulties in obtaining ... 98 
 digital examination of . . . 93 
 effect of digitalis on . . 289,369 
 diminished ..... 104 
 effect of dilatation of the heart on 49, 206 
 graphic records of . . . . 100 
 heart failure with increased . . 102 
 causes of increased . . . 101 
 method of measuring ... 98 
 increased by diminution of capil- 
 lary field 102 
 
 action of nitrites on . . .276 
 with the pulsus alternans . 196, 303 
 resistance of arterial walls in 
 
 estimating ..... 100 
 significance of a fall of . . . 104 
 
 y»— treatment of high . . . .103 
 in valvular disease . . . 103 
 
 ARTERIAL PULSE 
 
 natiu-e of movements of . . .91 
 
 ARTERIAL WALLS 
 
 condition of . . . . .93 
 in estimating arterial pressure . 100 
 
 ARTERIES 
 
 digital examination of . . .93 
 function of elastic coats of . . 1 
 hypertrophy of muscular coat of . 245 
 inspection of . . . . .92 
 in surgical operations how recog- 
 nized ..... 91 
 state of, during an attack of angina 
 
 pectoris . . . 49,302-308 
 visible movements of . . .92 
 
 ARTERIOLES 
 
 dilatation of, in exophthalmic 
 
 goitre ..... 133 
 
 dilatation of, in aortic regurgitation 240 
 
 ARTERIO-SCLEROSIS 
 
 causation of . . . . - 243 
 
 ARTERY 92 
 
 nature of movements of tortuous 91, 92 
 size of the , .... 93 
 
 PAGE 
 
 ARTERY {continued)— 
 
 supplying a. -v. bundle, condition 
 
 of in nodal rhythm . . . 168 
 changes in radial due to fever . 216 
 
 ARTIFICIAL WAVES 
 
 in tracings . . . . . ."U 1 
 
 ASTHMA, CARDIAC 
 
 arterial pressure with ... 29 
 associated sj'mptoms . . .28 
 in cardio-sclerosis .... 246 
 conditions giving rise to . . 29 
 
 pulse in ..... 29 
 
 sleep with ..... 28 
 signs of ..... 28 
 
 treatment of . . . . . 270 
 
 ATHEROMA OF CORONARY ARTERIES 
 angina pectoris in . . . .42 
 
 ATROPHY OF AURICULAR MUSCLE 118 
 
 AUDITORY NERVE 
 
 stimulation of . . . .35 
 
 AURICLE 
 
 electro- cardiogram of . . . 373 
 hypertrophy of right, in tricuspid 
 
 stenosis ..... 238 
 starting-place of the heart's con- 
 traction ..... 140 
 
 AURICULAR DEPRESSION 
 
 in a jugular pulse .... 109 
 
 AURICULAR DIASTOLE 
 
 effect of, on the jugular pulse . 109 
 
 AURICULAR EXTRA-SYSTOLES . 154 
 
 AURICULAR HYPERTROPHY 
 
 with ventricular jugular pulse, 
 significance of . . . .118 
 
 AURICULAR LIVER PULSE . . 123 
 cases of . . . . . 314, 347 
 
 AURICULAR MOVEMENTS . . 77 
 
 AURICULAR JilUSCLE 
 
 atrophy of . . . . .118 
 
 AURICULAR PARALYSIS 
 
 evidence of . . . . .118 
 and the nodal rhythm . . . 168 
 
 AURICULAR PAROXYSMAL TACHY- 
 CARDIA 334 
 
 AURICULAR PRESSURE CURVE . 108 
 
 AURICULAR SYSTOLE 
 
 disappearance from normal place 
 
 in cardiac cycle . . 117,166,309 
 effect of, on radial pulse . . .184 
 murmur due to . . 177, 232, 365 
 
 AURICULAR VENOUS PULSE 
 
 See JUGULAB PCLSE. 
 
 AURICULAR WAVES 
 
 in apex tracing, cause of . . 81,87 
 in apex tracings, time of . 81, 82, 183 
 in apex tracings in heart-block 183, 339 
 in a jugular pulse, cause of . . 108 
 in the ventricular jugular pulse 118, 326
 
 398 
 
 INDEX 
 
 PAGE 
 
 AURICULO-VENTRICULAR BUNDLE 
 arterial supply of . . . .14 
 in cardio-sclerosis . . . 184, 248 
 relation of, to central fibrous body 185 
 impaired in cases with extra- 
 systole .... 151,160 
 function of fibres of . . 14, 185 
 healthy in heart-block . . .185 
 affected in influenza . . . 217 
 lesions of . . . . .184 
 involved in mitral stenosis 
 
 229, 233, 312, 315, 320, 324 
 
 position of 13 
 
 isolation of . . . . .13 
 condition of, in nodal rhythm 168, 310 
 in paroxysmal tachycardia 310, 320, 324 
 pathology of, illustrative cases 
 
 310, 312, 315, 320, 324 
 in puerperal fever . . . . 217 
 in rheumatic fever .... 217 
 in septic poisoning .... 217 
 starting-place of heart's contraction 140 
 
 AURICULO-VENTRICULAR NODE 
 
 constitution of . . . .13 
 function of . . . . .14 
 
 position of 13 
 
 in cases of nodal rhythm . .310 
 
 in paroxysmal tachycardia 310, 320, 324 
 starting the heart's contraction . 140 
 
 AUTONOMIC NERVOUS SYSTEM 
 insensitiveness of structures sup- 
 plied by . . . . .34 
 
 A.-V. BUNDLE 
 
 See Aurictjlo-Ventkicular Bundle. 
 
 A.-V. NODE 
 
 See AuRicuLO- Ventricular Node. 
 
 A.-V. SEPTUM 
 
 action of muscles on . . .17 
 
 A.-V. VALVES 
 
 opening of . . . . .80 
 
 296 
 296 
 
 BATHS 
 
 in treatment .... 
 Nauheim .... 
 
 BED 
 
 lying in, effect of on heart . 27, 209 
 
 BELLOWS MURMUR . . .240 
 BILIARY COLIC. See Colic. 
 
 BLEEDING 
 
 character of, in capillary oblitera- 
 tion 
 
 in pregnancy with heart disease 
 
 BLOOD-PRESSURE 
 
 See Arterial Pressure. 
 
 BOWEL 
 
 insensitiveness of . . . .34 
 resection of, in conscious subject . 34 
 
 245 
 260 
 
 BODILY COMFORT 
 
 in treatment . 
 BODILY EXERTION 
 
 a cause of angina pectoris 
 
 BRADYCARDIA 
 
 definition of . 
 
 loose employment of term 
 
 nodal .... 
 
 true .... 
 
 due to vagus stimulation 
 BRAIN 
 
 diagram showing relation to sen- 
 sory nerve ..... 
 BRANDY 
 
 during an attack of angina pectoris 
 BROADBENT'S SIGN 
 
 in mediastino-pericarditis 
 
 BROMIDE OF AMMONIUM 
 in angina pectoris . 
 in exophthalmic goitre . 
 
 BROMIDES 
 
 in cardio-sclerosis . 
 
 BREASTS 
 
 hyperalgesia of 
 
 BREATHING 
 
 inability to stop 
 
 laboured, with dilatation of the 
 
 heart 
 laboured, on exertion . 
 laboiired, in heart failure 
 laboured, a sign of exhaustion of 
 
 the heart 
 laboured, with the nodal rhythm 
 
 270 
 
 42,47 
 
 , 138 
 56 
 . 337 
 . 138 
 . 139 
 
 36 
 53 
 
 254 
 
 66 
 270 
 134 
 
 251 
 
 56 
 
 27 
 
 27 
 
 28 
 
 27 
 
 28 
 28 
 
 exercises in oedema of the lungs 210, 213 
 
 rapid, a sign of pulmonary stasis 
 rapid, a sign of heart failure 
 
 BREATHLESSNESS . 
 
 attacks of ... . 
 sudden attack of, in aortic regm-gi 
 
 tation .... 
 
 cause of .... 
 
 due to infarct in lungs . 
 a symptom of exhausted con 
 
 ti'actility .... 
 treatment of . 
 ■ See also Asthma, Cardiac. 
 BRIGHT'S DISEASE 
 
 mitral regurgitation in . 
 pericarditis in 
 
 27 
 27 
 
 26 
 
 28 
 
 242 
 26 
 32 
 
 193 
 270 
 
 236 
 220 
 
 274 
 
 CALOMEL 
 
 CAPILLARY FIELD, DIMINUTION OF 46 
 
 a factor in raising arterial pressure 102 
 etiect of, on the heart . . . 244 
 
 in cardio-sclerosis 
 effects of 
 
 effect of, on blood-pressure 
 evidences of . 
 
 244 
 244 
 245 
 244
 
 INDEX 
 
 399 
 
 CAPILLARY PULSATION 
 
 in aortic regurgitation 
 
 CARDIAC ASPIRATION 
 due to ventricular systole 
 causing movements of the liver 
 
 CARDIAC ASTHMA. See Asthma. 
 
 CARDIAC CYCLE 
 
 diagram of events in a . 
 
 CARDIAC NEURASTHENIA . 
 
 CARDIAC NEUROSIS 
 
 241,321,324 
 
 82 
 82 
 
 108 
 56 
 56 
 
 CARDIAC RESPONSE 
 
 in cardio-sclerosis .... 246 
 
 limitation of, a sign of heart failure 4 
 
 and prognosis .... 266 
 
 CARDIOGRAM 
 
 nature of a . . . . .18 
 inverted .... 83,84,87 
 
 CARDIO-MOTOR CENTRES . . 15 
 
 CARDIO-SCLEROSIS 
 
 and aneui-ysm .... 251 
 and angina pectoris . . 42, 304 
 and arterial degeneration . . 243 
 a.-v. bundle in ... . 184 
 blood-pressm-e in . . . . 247 
 cardiac asthma in . . . 28, 246 
 change in symptoms with dilatation 246 
 and chloroform .... 261 
 condition of arteries in . . . 245 
 Cheyne-Stokes respiration in . 29, 248 
 exhaustion of conductivity in , 184 
 
 exhaustion of contractility in . . 193 
 definition of . . . . xviii, 243 
 
 diet in 273 
 
 dilatation of the heart in . 206, 248 
 disease of the kidneys with . . 244 
 effect of digitalis in . . . 286 
 etiology ..... 243 
 
 extra- systQles in . . . . 246 
 extreme, without dilatation , . 202 
 heart-block due to . . .184, 246 
 illustrative cases . .• . 351, 354 
 irregularities in . . . 246, 352 
 mitral regurgitation in . . . 236 
 murmurs in . . . . . 247 
 nodal rhythm in . . 142, 168, 247 
 with the nodal rhythm, effect of 
 
 digitalis in 172 
 
 paroxysmal tachycardia in 247, 324 
 
 pathology of . . 245,328,353,355 
 primitive cardiac tissue in . . 248 
 
 prognosis in 248 
 
 progress of .... . 243 
 pulsus alternans with 
 
 196, 197, 248, 352, 354 
 reason for variety of symptoms in . 248 
 reserve force in ... . 247 
 of rheumatic origin . . . 243 
 
 sensory phenomena in . . .58 
 
 248 
 245 
 245 
 244 
 249 
 41 
 
 216 
 
 107 
 
 91 
 
 75 
 
 113 
 
 270 
 
 CARDIO-SCLEROSIS {continued)— 
 significance of cardiac asthma in 
 symptoms of 
 diversity of symptoms in 
 and syphilis . 
 treatment of . 
 viscero-motor reflex in . 
 
 CARDITIS 
 
 produced by febrile affections 
 
 CAROTID ARTERY 
 
 relation of, to jugular vein 
 CAROTID PULSE 
 
 movement due to . 
 
 as a standard .... 
 
 CAROTID WAVE 
 
 in the jugular pulse 
 
 CASES ILLUSTRATING 
 
 effect of ammonium bromide in 
 angina pectoris .... 
 
 pathology of cardio-sclerosis 338, 353, 355 
 
 chloroform and cardio-sclerosis . 261 
 
 effect of digitalis on the heart 
 
 356, 360, 361, 364 
 
 effect of fear on the heart . . 262 
 
 heart-block .... 187, 188 
 
 relation of heart-block to the nodal 
 rhythm 364 
 
 danger of heart disease and preg- 
 nancy ..... 259 
 
 heart's power of recovery . . 266 
 
 effects of digitalis on the nodal 
 rhythm .... 283,284 
 
 the inception of the 
 rhythm 
 
 nodal bradycardia . 
 
 the pathology of the 
 
 rhythm . . 312,316,320,324 
 
 paroxysmal tachycardia 
 
 320, 324, 328, 329 
 
 significance of the pulsus alternans 199 
 
 character of pulse in angina pectoris 
 
 302-308 
 
 severe heart affection in pneumonia 223 
 
 CELLULAR FOCI 
 
 in heart muscle, in rheumatic fever 
 
 CENTRAL FIBROUS BODY 
 
 function of .... . 
 position of .... . 
 relation of, to a.-v. bundle 
 
 CEREBRAL ANAEMIA . 
 
 in heart-block .... 
 
 CEREBRAL EMBOLISM 
 
 in mitral stenosis .... 
 CEREBRO-SPINAL NERVOUS SYS- 
 TEM 
 
 CERVICAL FASCIA 
 
 in the fixation of the heart 
 
 CERVICAL NERVES. See Nerves. 
 
 nodal 
 . 309-333 
 . 337-349 
 nodal 
 
 221 
 
 16 
 16 
 
 185 
 
 23 
 
 187 
 
 234 
 34 
 16
 
 400 
 
 INDEX 
 
 PAGE 
 
 CHEST, CONSTRICTION OF . 22, 130 
 in angina pectoris . . . 41, 48 
 during an attack of angina pectoris 49 
 a viscero-motor reflex . . .41 
 
 CHEST-WALL 
 
 hyperalgesia of, in dilatation of the 
 heart 47,203 
 
 CHEYNE-STOKES RESPIRATION . 29 
 
 artificial production of . . .30 
 arterial pressure in . . 29, 189 
 
 with Bright' s disease ... 30 
 in cardio-sclerosis . . 29, 206, 248 
 condition of heart in . . .29 
 conditions simulating ... 30 
 consciousness dui'ing apnoeic stage 31 
 effect of dilatation of the heart on . 206 
 in heart-block .... 189 
 
 hiccough in . . . . .29 
 John Hunter's description of . 31 
 
 mental condition in . . .31 
 prognosis in . . . . .30 
 significance of, in cardio-sclerosis . 248 
 dming sleep ..... 29 
 suffering due to . . . .30 
 talking dm'ing apnoeic stage . . 31 
 treatment of . . . . 30, 270 
 twitching of muscles in . . .29 
 
 CHILDREN 
 
 periodic respiration in . . .30 
 heart uregularity in . 140, 142, 146 
 
 CHLORAL 270 
 
 in angina pectoris .... 54 
 in cardio-sclerosis .... 251 
 
 CHLOROFORM 
 
 in cardio-sclerosis .... 261 
 
 fitness of tlie patient to take . . 262 
 
 and heart affections . . . 261 
 
 and heart-block .... 263 
 and imperfect oxygenation of the 
 
 blood. . . . . 261 
 
 and irregular heart-action . . 263 
 
 and pregnancy .... 260 
 
 and the status lymphaticus . . 262 
 
 and valvular disease . . . 261 
 
 CICATRIZATION 
 
 after rheumatic fever . . . 222 
 
 CIRCULATION 
 
 object of the ..... 1 
 
 CLASSIFICATION OF SYAEPTOMS 
 
 in visceral disease .... 33 
 
 CLINICAL EVIDENCE 
 
 of the nodal rhythm . . . 309 
 
 COLD 
 
 effect of, on the heart's rate . . 139 
 
 COLD AIR 
 
 exposure to, a cause of angina 
 pectoris .... 42, 47 
 
 PAGE 
 
 COLD BATHS 
 
 in exophthalmic goitre . . .134 
 
 COLD HANDS 
 
 in the X disease .... 60 
 
 COLIC, BILIARY 
 
 hyperalgesia in . , . .37 
 situation of pain in ... 38 
 
 COLIC, RENAL 
 
 situation of pain in ... 39 
 
 COMPARISON OF AURICULAR PRES- 
 SURE 
 
 with the jugular pulse . . . 107 
 
 COMPENSATORY PAUSE 
 cause of ... 
 
 COMPLAINTS, CHIEF 
 
 COMPRESSION OF CHEST 
 
 sense of . 
 
 xviii, 162 
 . 21 
 
 22, 130 
 
 CONDUCTIVITY .... 8 
 
 aftections of 175 
 
 and angina pectoris ... 43 
 cause of depressed . . .185 
 
 depression of, in febrile affections 
 
 of the heart . . . .217 
 depressed in rheumatic hearts . 184 
 depressed in cardio-sclerosis . . 184 
 depression of, increased by digitalis 
 
 186, 288, 361, 362 
 method of recognizing depression of 175 
 significance of depression of . .186 
 prognosis in depression of . . 189 
 influence of rest upon . . . 177 
 irregularity due to depression of 142, 179 
 manner in which depression of is 
 
 produced in mitral stenosis . 229 
 
 CONGENITAL AFFECTIONS OF THE 
 HEART 
 
 etiology ..... 256 
 
 prognosis ..... 257 
 symptoms ..... 256 
 treatment ..... 257 
 
 CONGENITAL DEFECTS OF AORTIC 
 VALVES 239 
 
 CONSCIOUSNESS 
 
 loss of 23 
 
 dvu-ing apnoeic stage of Cheyne- 
 Stokes respiration ... 31 
 
 CONSCIOUS SUBJECT 
 
 resection of bowel in . . .34 
 
 CONSTIPATION 
 
 in heart failure .... 274 
 
 CONSTRICTION OF CHEST. See Chest. 
 
 CONTRACTILITY ... 8, 191 
 
 angina pectoris due to exhaustion 
 of 43, 193
 
 INDEX 
 
 401 
 
 PAGE 
 
 CONTRACTILITY {continued)— 
 
 arterial pressure with exhaustion of 193 
 effect of digitaHs on . . . 287 
 conditions inducing exhaustion of . 192 
 exhaustion of, due to degeneration 
 
 of muscle . . . . .192 
 exhaustion of, due to dilatation , 192 
 exhaustion of, due to imperfect 
 
 nutrition ..... 192 
 exhaustion of, due to increased rate 192 
 exhaustion of, due to obstruction to 
 
 the heart's work . . . 192 
 
 effect of rest on exhausted . . 199 
 exhaustion of, in pneumonia . . 218 
 exhaustion of, the cause of angina 
 
 pectoris ..... 43 
 necessity for recognizing exliaus- 
 
 tionof 190 
 
 prognosis of exhaustion of . . 198 
 pulsus alternans, a symptom of 
 
 exhaustion of . . . .194 
 reserve force of . . . .192 
 reflex symptoms of exhaustion of . 193 
 symptoms of exhaustion of, in 
 
 rheumatic hearts . . . 193 
 
 symptoms of exliaustion of, in 
 
 cardio-sclerosis . . . .193 
 symptoms of exhaustion of . . 192 
 
 CONVALESCENCE 
 
 after febrile affections of the heart 227 
 
 COR BOVINUM . 
 
 239 
 
 CORRIGAN'S PULSE 
 
 CORONARY ARTERIES 
 
 in cases of angina pectoris 
 
 42, 46, 304, 305 
 
 heart-block in sclerosis of . . 185 
 
 CORONARY SINUS 
 
 heart's contraction starting at . 13 
 how regurgitation into is prevented 16 
 
 240 
 
 COUPLED BEATS 
 
 due to digitalis, significance of 
 
 283, 284, 288 
 of the nodal rhythm distinct from 
 extra-systoles .... 286 
 
 CYANOSIS 
 
 in congenital heart affections . . 256 
 oxygen in .... . 279 
 
 DEATH 
 
 dm-ing an attack of angina pectoris 48 
 
 due to digitalis . . . 186,291 
 
 due to heart-block . . .189 
 
 sense of impending, during an 
 
 attack of angina pectoris . . 49 
 
 sense of impending, during an 
 
 attack of palpitation . . .135 
 
 PAGE 
 
 DEFINITIONS 
 
 apex beat 77 
 
 a-c interval .... xviii, 176 
 auricular venous pulse . . . xviii 
 auriculo-ventricular node . . xviii 
 auriculo-ventricular bundle . . xviii 
 cardiac asthma .... 28 
 cardio-sclerosis .... xviii 
 
 carditis 216 
 
 conductivity .... xviii, 175 
 
 contractility xviii 
 
 extra-systole xviii 
 
 heart-block .... xix, 175 
 hyperalgesia ..... xix 
 myogenic theory .... xix 
 nodal rliythm . . . xix, .309 
 
 palpitation .... xix 
 
 paroxysmal tachycardia . xix, 172 
 
 primitive cardiac tissue . . . xix 
 pulsus alternans .... xix 
 pulsus bigeminus .... xix 
 sino-auricular node . . . xix 
 
 sphygmogram .... 95 
 tonicity ..... xix 
 
 ventricular rhythm . . . 175 
 
 ventricular venous pulse . . xx 
 
 viscero- motor reflex . . . xx 
 viscero-sensory reflex . . . xx 
 
 DEGENERATION OF HEART MUSCLE 
 
 See Cardio-Sclerosis. 
 
 DELUSIONS 25 
 
 DEPRESSOR NERVE 
 
 See Nerves of the Heart. 
 
 DESIRE TO BREATHE ... 26 
 
 DEVELOPMENT 
 
 of arms ..... 39 
 of the heart 11 
 
 DIABETES 
 
 pericarditis in .... 220 
 
 DIAGNOSES 
 
 mistaken, how they arise . .215 
 
 DIAGRAM 
 
 showing relation of brain, spinal 
 cord and skin to a sensory nerve 36 
 
 DIAPHRAGM 
 
 in the fixation of the heart . . 16 
 
 DIASTOLIC MITRAL MURMUR 
 
 ^ee Murmurs. 
 
 DIASTOLIC NOTCH 
 
 in a sphygmogram ... 96 
 
 DIASTOLIC PERIOD 
 
 in a sphygmogram ... 95 
 
 DIASTOLIC WAVE 
 
 in the jugular pulse . . . 113 
 
 MACKENZIE 
 
 D d
 
 402 
 
 INDEX 
 
 DICROTIC WAVE 
 
 cause of 
 
 DIET 
 
 in cardio-sclerosis 
 in treatment . 
 
 PAGE 
 
 96 
 
 273 
 271 
 
 DIGESTIVE TUBE 
 
 nature of symptoms produced by , 34 
 
 DIGITAL EXAMINATION 
 
 of the arteries .... 93 
 
 of the arterial pressure ... 93 
 
 of the arterial pulse ... 90 
 
 DIGITALIS 
 
 and blood-pressme . . 289, 369 
 in cardio-sclerosis .... 251 
 causing heart-block . 287, 360, 365 
 causing intermittent pulse . .186 
 causing pulsus alternans . 197, 288 
 
 conditions in which it is useful . 290 
 conditions in which it is useless . 291 
 effect on conductivity . . 287, 365 
 increasing depression of conduc- 
 tivity . . . 186,360,365 
 effect on contractility . . . 288 
 effect on dilatation of the heart . 282 
 action of different preparations . 281 
 effect on dropsy .... 208 
 effect on enlargement of the liver . 286 
 action of, on the human heart 281, 356 
 illustrative cases, showing effects of 
 
 356, 360, 361, 364 
 
 effect on the nodal rhythm . 172, 282 
 
 susceptibility of nodal rhythm to . 286 
 
 effect on nodal rhythm due to 
 
 cardio-sclerosis .... 287 
 
 in practice 290 
 
 use of, in prognosis . . .211 
 effect on rate ..... 282 
 reason for uncertain action of . 281 
 reason for contradictory effects of . 286 
 significance of coupled beats pro- 
 duced by 285 
 
 and slow respiration . . .31 
 sudden death due to . . 186,291 
 action on tonicity ... 9, 282 
 
 in the treatment of dilatation . 211 
 
 DIGITALIS, SQUILL AND CALOMEL 
 in cardiac dropsy . . . .212 
 
 DILATATION OF THE HEART 
 
 in febrile affections . . , 219 
 
 albuminuria in . . . .211 
 
 alcoholic 207 
 
 effect on angina pectoris . . 206 
 
 effect on arterial pressure . . 206 
 laboured breathing in ' . . . 27 
 effect on cardiac asthma . . 206 
 
 in cardio-sclerosis . . . 206, 248 
 cause of . . . . . . 201 
 
 effect on Cheyne-Stokes respiration 206 
 
 DILATATION OF THE HEART (con- 
 ♦ tinned) — 
 
 consequences of . 
 exhaustion of contractility due to 
 effect of digitalis on . . . 
 displacement of lung due to . 
 causing epigastric pulsation 
 due to fever ..... 
 effect of, on the jugular pulse 
 enlarged liver in . 
 manner of production of 
 manner in which symptoms ai'e 
 produced . . . . . 
 and mitral regurgitation 
 and mitral stenosis 
 with the nodal rhythm . 
 its significance in the nodal rhythm 
 oedema of the lungs in . 
 in paroxysmal tachycardia 
 significance of, in paroxysmal 
 tachycardia . . . . 
 the position of the heart in 
 and pregnancy .... 
 prognosis in . 
 
 I'eflex symptoms produced bj' 
 in rheumatic fever 
 signs of . 
 
 bearing of, on treatment 
 urinary symptoms in 
 
 205 
 192 
 
 282 
 206 
 83,84 
 215 
 205 
 208 
 203 
 
 205 
 235 
 233 
 170 
 171 
 208 
 207 
 
 172 
 . 204 
 . 258 
 . 211 
 . 203 
 . 222 
 . 203 
 207,211 
 . 210 
 
 DILATATION OF LEFT VENTRICLE 
 in mitral stenosis . . . 203, 229 
 
 DIPHTHERIA 
 
 the condition of the heart in 214, 224 
 fatal syncope in . . . . 225 
 
 DIPLOCOCCUS RHEUMATICUS . 221 
 
 DISAPPEARANCE OF PRESYSTOLIC 
 MURMUR 223 
 
 DISEASE, NATURE OF 
 
 shown by irregularities . . . 217 
 
 DISPLACEMENT OF THE CHAMBERS 
 OF THE HEART 
 in dilatation 203 
 
 DISSOCIATION OF PLACES 
 
 in starting the heart's contraction 13 
 
 DIURESIS IN HEART FAILURE 
 
 cause of profuse .... 212 
 
 DIURETIN 212 
 
 DIZZINESS 23 
 
 DOG 
 
 irregular heart-action in . . 144 
 
 DORSAL NERVES 
 
 peculiar field supplied by upper . 40 
 
 DROPSY 
 
 in arms and face .... 207 
 effect of digitalis in . . . 208
 
 INDEX 
 
 403 
 
 DROPSY (continued)— 
 
 dilatation of the heart causing 
 a sign of dilatation of the heart 
 manner of onset of 
 in cases of nodal rhythm . 1 
 
 in paroxysmal tachycardia . 1 
 in rheumatic heart cases 
 the secretion of urine witli 
 significance of 
 treatment of . 
 
 DRUGS 
 
 in treatment 
 
 DYSPNOEA. See Breathlessxess. 
 
 47, 200 
 . 206 
 . 206 
 70, 208 
 73, 207 
 . 207 
 . 207 
 . 207 
 . 211 
 
 . 275 
 
 OF REFLEX 
 
 E 
 
 meaning of period 
 
 ELECTRO-CARDIOGRAM 
 
 of the auricle . 
 of the ventricle 
 the normal 
 of heart-block 
 of the nodal rhythm 
 of extra-systoles 
 
 75, 112 
 
 . 370 
 
 . 373 
 
 . 373 
 
 . 372 
 
 . 373 
 
 . 374 
 
 . 375 
 
 ELECTRIC CHANGES 
 due to heart beat . 
 in muscular tissue . 
 
 . 370 
 . 370 
 
 EMBRYOCARDIA 
 
 loose employment of term 
 
 . 56 
 
 ENDOCARDITIS 
 in acute fevers 
 malignant 
 misleading term 
 symptoms of . 
 
 . 214 
 . 221 
 . 215 
 
 219, "226 
 
 ENEMATA 
 
 . 274 
 
 ENLARGEMENT OF THE LIVER . 122 
 
 EPIGASTRIC PULSATION 
 
 causes of . . . 
 in fevers 
 
 83,85 
 . 216 
 
 in pernicious anaemia . 
 
 in typhoid fever 
 
 and the shock of ventr 
 
 systole 
 time of . 
 
 . 85 
 . 84 
 icular 
 
 . 89 
 . 84 
 
 EPILEPTIC ATTACKS . 
 due to heart-block 
 
 24, 342 
 
 . 187 
 
 ERECTOR-SPINAE MUSCLES 
 
 tenderness of, in liver enlargement 123 
 
 ERYSIPELAS 
 
 a cause of mitral stenosis . . 229 
 the heart in . . . . . 214 
 
 FACTOR IN HEART 
 
 ESSENTIAL 
 FAILURE 
 
 ESSENTIAL PRINCIPLE IN TREAT- 
 MENT 
 
 2,268 
 
 268 
 
 EXAGGERATION 
 SYMPTOMS 
 
 in nervous people .... 
 
 EXCITABILITY OF THE HEART . 
 
 and angina pectoris 
 
 EXCITEMENT 
 
 a cause of angina pectoris 
 
 EXERCISES 
 
 rules for employment of 
 
 special ...... 
 
 value of different forms of 
 breatliing ..... 
 
 EXHAUSTED HEART MUSCLE 
 the cause of angina pectoris . 
 
 EXHAUSTING DISEASES 
 heart-rate increased in . 
 
 EXHAUSTION 
 
 sense of . 
 
 EXOPHTHALMIC GOITRE 
 arteries visible in . 
 peripheral circulation in 
 treatment of . 
 
 EXPECTORATION 
 
 blood-stained, in dilatation of the 
 heart ...... 
 
 PAGE 
 
 EXPERIMENTAL EVIDENCE 
 THE NODAL RHYTHM 
 
 OF 
 
 EXPERIMENTAL STIMULATION 
 OF VAGUS NERVE 
 
 55 
 
 8 
 43 
 
 42 
 
 293 
 295 
 294 
 213 
 
 42 
 
 132 
 
 OO 
 
 92 
 133 
 134 
 
 206 
 
 120 
 
 145 
 
 EXTRA-SYSTOLES 
 
 electro-cardiogram of . . . 375 
 extra-systoles, definition of . xviii, 148 
 extra-systoles, classification of . 151 
 extra-systoles, in angina pectoris 
 
 50, 306, 307 
 extra-systoles and variations of the 
 
 a-c interval .... 161 
 extra-systoles in acute affections . 218 
 extra-systoles in arterial degenera- 
 tion 103 
 
 extra-systoles, am'icular . .154 
 
 extra-systoles and the a.-v. bundle 160 
 extra-systoles distinct from coupled 
 
 beats of nodal rhythm . . 286 
 extra-systole evidence of impair- 
 ment of a.-v. bundle . . . 151 
 extra-systole with cardiac asthma 29 
 extra-systole with cardio-sclerosis . 248 
 extra-systole cause of compensa- 
 tory pause ..... 161 
 extra-systole, character of the 
 
 irregularity . . . .148 
 
 extra-systoles, conditions inducing 163 
 
 extra-systole due to digitalis 
 extra-systoles, etiology 
 
 359, 368 
 150, 163 
 
 D d 2
 
 404 
 
 INDEX 
 
 lEXTRA-SYSTOLES (continued)— 
 
 extra-systole, relationship to heart- 
 block 185 
 
 extra-systole, nodal . . . 157 
 
 extra-systole, effect on mind . 55 
 
 extra-systoles and the nodal rhythm 164 
 
 place of origin of ventricular . 151 
 extra-systoles and the primitive car- 
 diac tube . . . . .162 
 
 extra-systole prognosis of . . 164 
 
 extra-systoles and pulsus alternans 195 
 extra-systoles distinct from the 
 
 pulsus alternans . . .198 
 
 extra-systoles, sensations produced 
 
 by 164 
 
 extra-systoles, sounds due to . 150 
 extra-systoles, treatment of 65, 164, 250 
 extra-systole, ventricular inter- 
 polated ..... 151 
 extra-systoles, varieties of . . 141 
 extra-systoles in the X disease . 62 
 
 FACIAL ASPECT .... 20 
 in aortic regm-gitation . . . 242 
 during an attack of angina pectoris 48 
 
 FAINTING 23 
 
 FATTY DEGENERATION OF THE 
 HEART 243,245 
 
 in acute febrile affection . . 216 
 
 pulsus alternans in . . .196 
 
 FEBRILE AFFECTIONS OF THE 
 HEART 
 
 convalescence after 
 symptoms in . 
 treatment of . 
 a.-v. bundle affected in . 
 
 FEVER 
 
 dilatation of the heart in 
 effect of, on the heart 
 heart symptoms in 
 pulse-rate in . 
 varying reaction on heart of . 
 
 FINGERS 
 
 clubbing of . 
 
 FIXATION OF THE HEART . 
 
 FOCUS, IRRITABLE, IN THE 
 SPINAL CORD .... 
 due to angina pectoris . 
 a cause of the tendency to recurrent 
 
 attacks of angina pectoris . 
 symptoms of . 
 
 FRACTURED TIBIA 
 
 pulmonary infarct from 
 
 FUNCTIONS OF THE HEART 
 MUSCLE-FIBRES .... 7 
 
 FUNCTIONS OF THE PRIMITIVE 
 CARDIAC TUBE . . . 11,141 
 
 227 
 216 
 226 
 217 
 
 219 
 214 
 215 
 215 
 216 
 
 256 
 203 
 
 37 
 45 
 
 50 
 37 
 
 32 
 
 GANGLION CELLS .... 14 
 their function .... 19 
 
 GALVANOMETER . . . .371 
 
 GANGRENE OF LEG 
 
 after intermittent claudication . 46 
 
 GASKELL'S BRIDGE, ^ee Auriculo- 
 Ventricular Bundle. 
 
 GASTRIC ULCER. See Ulcer. 
 
 GIDDINESS 23 
 
 GRAPHIC RECORDS 
 
 of arterial pressure . . .'100 
 of heart movements ... 77 
 of the jugular pulse . . . 106 
 use of 67 
 
 GRAVE CONDITIONS 
 
 due to the nodal rhythm . . 170 
 
 GRIPPING OF CHEST 
 
 in angina pectoris . . . .41 
 
 HALLUCINATIONS .... 25 
 
 HAEMOPTYSIS 
 
 in mitral stenosis .... 234 
 
 HAEMORRHAGES .... 23 
 
 HALLER'S OBSERVATION 
 
 of the insensitiveness of the viscera 35 
 
 HARVEY'S OBSERVATION 
 
 on the insensitiveness of the heart 34 
 
 HEALTHY PEOPLE 
 
 sinus irregularity in . . . 146 
 
 HEART 
 
 acute febrile affections of the 
 
 in ague ...... 
 
 in an attack of angina pectoris 
 apex, arrangement of muscle fibres 
 
 at ..... . 
 
 a.-v. bundle in rheumatic affections 
 
 of 
 
 a.-v. bundle in acute affections of . 
 
 4,216 
 
 , 216 
 
 49 
 
 17 
 
 184 
 184 
 
 HEART ABNORMALITIES 
 
 mental state induced by . . 56 
 
 HEART'S ACTION WITH THE NODAL 
 RHYTHM. See Nodal Rhythm. 
 
 HEART-BLOCK 24 
 
 in acute affections . . . 185 
 
 apex beat in . . . . . 183 
 auricular waves in apex tracings in 
 
 cases of . . . . .81 
 a.-v. bundle healthy in . . . 185 
 due to cardio-sclerosis . . . 247 
 produced by swallowing . . 365 
 
 cases illustrating relation of, to the 
 
 nodal rhythm . . . 337,364
 
 INDEX 
 
 405 
 
 HEART-BLOCK (continued)— 
 
 
 
 Cheyne-Stokes respiration in 
 
 
 189 
 
 and chloroform 
 
 
 263 
 
 definition of . 
 
 xix 
 
 175 
 
 due to digitalis 
 
 186 
 
 287 
 
 cases of, produced by digitalis 
 
 360 
 
 361 
 
 electro-cardiogram of 
 
 
 373 
 
 and epileptiform attacks 
 
 
 187 
 
 etiology 
 
 
 184 
 
 relationship to extra-systole 
 
 
 185 
 
 inexcitability of ventricle in 
 
 
 189 
 
 relationship to nodal rliythm 
 
 
 185 
 
 prognosis in . 
 
 
 189 
 
 due to septic poisoning . 
 
 
 218 
 
 symptoms in a case of . 
 
 
 187 
 
 symptoms associated with 
 
 
 187 
 
 and syncopal attacks 
 
 
 187 
 
 producing slow pulse-rate 
 
 . 138 
 
 142 
 
 vagus stimulation producing 
 
 
 186 
 
 treatment of . 
 
 
 190 
 
 HEART CHANGES 
 
 with increased rate . . .135 
 
 HEART, CONDITION OF 
 
 in Cheyne-Stokes respiration . . 29 
 
 HEART, CONGENITAL AFFECTION 
 OF 256 
 
 HEART'S CONTRACTION 
 
 electrical changes due to . . 370 
 
 normal starting-point of . 12, 15 
 
 starting in the primitive cardiac 
 
 tube 
 
 starting-places of . 
 starting in the auricle 
 starting in the a. -v. bundle 
 starting in the a. -v. node 
 starting in the sinus-venosus 
 
 11, 
 
 141 
 141 
 141 
 141 
 141 
 141 
 
 HEART, DEVELOPMENT OF THE . 11 
 
 HEART DILATATION 
 
 in acute febrile affections . . 219 
 and blood- pressure ... 47 
 
 and cessation of angina pectoris . 47 
 and dropsy ..... 47 
 and epigastric pulsation . 83, 84 
 
 laboured breathing in . . .27 
 and mitral regm'gitation . . 47 
 
 HEART IN DIPHTHERIA . 214, 224 
 
 HEART, EMBARRASSMENT OF . 3 
 by pericardial effusion . . . 220 
 
 HEART IN ERYSIPELAS . . 214 
 
 HEART EXHAUSTION 
 
 labom-ed breathing in . . . 28 
 from obstruction to its work . .251 
 from want of exercise . . . 293 
 from want of rest .... 47 
 
 PAGE 
 
 HEART FAILURE 
 
 and arterial degeneration . . 103 
 
 with increased arterial pressure . 102 
 
 constipation in ... . 274 
 
 essential factor in . . . 3, 268 
 
 with a fractured leg . . . 209 
 
 jaundice in . . . . . 125 
 
 means exhaustion of reserv'e force 2, 3 
 
 mitral stenosis induces . . . 229 
 
 muscle exhaustion in . . . 235 
 
 nature of symptoms in . . . 3 
 
 and the nodal rhythm . .168 
 
 cause of recovery from ... 3 
 
 due to valve defects . . . 228 
 
 w^asting in .... . 209 
 
 HEART, FEBRILE . . . .215 
 
 HEART, FEBRILE AFFECTIONS 
 OF THE 216 
 
 HEART, FIXATION OF . 
 
 17, 204 
 
 HEART, FUNCTIONAL ANATOMY 
 OF 16 
 
 HEART IN INFLUENZA . . .214 
 
 HEART, INSENSITIVENESS OF 
 THE 34 
 
 HEART IRREGULARITY 
 
 classification .... 
 
 significance of . . . 
 
 during attacks of angina pectoris 
 
 due to failm-e of conduction . 
 
 due to depression of conductivity 
 
 consciousness of . 
 
 meaning of term ' nodal rhj'^thm ' 
 
 in myocarditis 
 
 significance of in pneumonia . 
 
 due to respii-ation 
 
 during slow respiration 
 
 reveals the pathology of the heart 
 
 140, 
 sensation produced by 
 arising at the sinus 
 arising at the sinus, character of 
 arising at the sinus, etiology of 
 arising at the sinus, prognosis of 
 arising at the sinus, symptoms of 
 arising at the sinus, symptoms asso 
 
 ciated ^^^th 
 arising at tlie sinus, due to vagus 
 
 stimulation 
 in X disease .... 
 
 141 
 140 
 
 50 
 142 
 179 
 
 22 
 166 
 217 
 223 
 144 
 
 31 
 
 217 
 22 
 141 
 143 
 144 
 146 
 145 
 
 145 
 
 145 
 62 
 
 HEART MOVEMENTS 
 
 graphic records of . . .77 
 
 HEART MUSCLE 
 
 angina pectoris in exhaustion of 42, 58 
 angina pectoris in degeneration of 42 
 characteristics of function of fibres 
 of 9
 
 406 
 
 INDEX 
 
 HEART IVrUSCLE (continued)— 
 
 classification of functions of fibres of 
 conditions exhausting reserve force 
 
 of 
 
 co-ordination of functions of . 
 development of . . . 
 estimation of reserve force of 
 function*cf conductivity 
 function of contractility 
 function of excitability 
 function of stimulus production 
 function of tonicity 
 unequal endowment of functions of 
 
 fibres .... 
 
 unequal exhaustion of functions of 
 
 fibres .... 
 
 impaired nourishment of, a cause 
 
 of angina pectoris 
 importance of . . • 
 involved in mitral stenosis 
 reserve force of . . . 
 sclerotic changes in 
 
 HEART, NATURE OF SYAIPTOMS 
 PRODUCED BY . . . 
 
 HEART OVERSTRAIN . 
 
 HEART, PERCEPTIBLE MOVE 
 MENTS OF ... . 
 
 PAGE 
 
 3 
 
 9 
 
 7 
 20 
 
 10 
 
 42 
 2 
 
 230 
 2 
 
 229 
 
 32 
 132 
 
 HEART IN PNEUMONIA 
 
 76,77 
 214, 223 
 
 HEART IN RHEUMATIC FEVER 
 
 HEART, RUPTURE OF 
 
 214, 221 
 103, 202 
 
 heart; POSITION OF, IN THE 
 CHEST 76 
 
 HEART IN PREGNANCY . . 258 
 
 See Pkegnancy. 
 
 HEART- RATE 
 
 in alcoholics . . . .132 
 
 cause of increased . . . .136 
 effect of cold on ... . 139 
 continuously increased . . . 131 
 exhaustion of contractility due to 
 
 increased ..... 192 
 difficulties in reckoning increased . 134 
 effect of digitalis on . . . 282 
 increased on exertion . . . 129 
 increased in exhausting diseases . 132 
 in exophthalmic goitre . . .133 
 increased frequency of . . . 128 
 meaning of increased . . .130 
 in myocardial affections . . 131 
 
 increased in neurotic people . . 132 
 
 the normal 129 
 
 in palpitation .... 134 
 
 in pregnancy 132 
 
 in tuberculosis . . . .132 
 in valvular disease . . . 131 
 
 HEART REACTION 
 
 to the nature of the fever . . 214 
 
 HEART, RELATIONSHIP TO SEN- 
 SORY NERVES .... 39 
 
 HEART IN SEPTIC INFECTION 214, 225 
 
 HEART, THE SOLDIER'S . . 132 
 
 HEART SOUNDS 
 
 diu'ing an attack of angina pec- 
 toris 50,270 
 
 uith alternating rhythm . . 198 
 
 in depressed conductivity . . 176 
 
 due to extra-systoles . . 142, 150 
 
 with pulsus bigeminus . . .151 
 
 \\ith sinus irregularity . . . 145 
 
 HEART, SPASM OF, IMPOSSIBLE . 44 
 
 HEART'S STRENGTH 
 
 standard of measurement of . . 4 
 
 HEART IN TYPHOID FEVER 209, 214 
 
 HEART, VENTRICULAR RHYTHM 182 
 
 HELLEBOREIN . . . .291 
 
 HEMIPLEGIA 
 
 in acute febrile affections . . 219 
 
 HERPES ZOSTER 
 
 eruption of, in arm ... 40 
 
 pain of simulating angina pectoris . 57 
 
 HIBERNATING ANIMAL 
 
 and periodic respiration . . 30 
 
 HICCOUGH IN CHEYNE-STOKES 
 RESPIRATION .... 29 
 
 HIS' BUNDLE. See Aueiculo-Ventki- 
 CULAR Bundle. 
 
 HOLLOW MUSCULAR ORGANS 
 
 resemblance of symptoms in . .33 
 
 HOT DRINKS 
 
 during an attack of angina pectoris 53 
 
 HUNTER, JOHN 
 
 his description of a curious attack 26 
 his description of Cheyne-Stokes 
 respiration . . . .31 
 
 HYDROTHERAPY . . . 65,296 
 
 HYPERALGESIA 
 
 after an attack of angina pectoris 50, 51 
 
 40 
 
 56 
 
 xix 
 
 193 
 
 203 
 
 123 
 
 66 
 
 170 
 
 38 
 
 57 
 
 55 
 
 102 
 
 in angina pectoris 
 
 of breasts .... 
 
 definition of . 
 
 due to exhausted contractility 
 
 due to dilatation of the heart . 
 
 in enlargement of the liver 
 
 extensive in neurotic people . 
 
 with the nodal rhythm . 
 
 of skin and muscles in gastric ulcer 
 
 with valvular disease 
 
 in visceral disease . 
 
 HYPERPIESIS .
 
 INDEX 
 
 407 
 
 IR 
 
 HYPERTROPHY 
 
 of muscular coat of arteries . 
 of left ventricle in aortic valve 
 disease . .... 
 
 of right aui'icle in tricuspid stenosis 
 
 HYSTERIA 
 
 heart pain in . 
 
 INCREASED PERIPHERAL RE 
 SISTANCE 
 
 a cause of angina pectoris 
 
 INFANTS AND THE SINUS 
 REGULARITY 
 
 INFARCT, PULMONARY . 
 
 INFARCTS DURING ACUTE AFFEC 
 TIONS OF THE HEART 
 
 INFECTIVE ENDOCARDITIS . 
 treatment of . 
 
 INFLUENZA, A.-V. BUNDLE AF 
 FECTED IN . 
 
 INQUIRY INTO NAUHEIM TREAT 
 MENT 
 
 INSENSITIVENESS OF THE VIS 
 CERA 
 
 INSPECTION OF THE ARTERIES 
 
 INSPECTION OF THE JUGULAR 
 PULSE .... 
 
 INSPIRATION, EFFECT OF, ON 
 ABDOMINAL VEINS . 
 
 INSPIRATORY SWELLING OF 
 JUGULAR VEINS . 
 
 INTERCOSTAL MUSCLES 
 See Muscles. 
 
 INTERMITTENT CLAUDICATION . 
 
 INTERMITTENT PULSE 
 
 due to depression of conduc- 
 tivity ..... 176, 
 due to depressed conductivity in 
 
 febrile affections 
 due to exhausted contractility 
 produced by digitalis . . 186, 
 due to extra-systoles . 141, 149, 
 in pneumonia .... 
 
 sensations with .... 
 
 INTERPOLATED EXTRA-SYSTOLE 
 
 INTERPRETATION OF THE JUGU- 
 LAR PULSE .... 106, 
 
 INTERPRETATION OF A SPHYG- 
 MOGRMI 
 
 INTERPRETATION OF A TRACING 
 OF THE APEX BEAT . 
 
 INTERSYSTOLIC PERIOD 
 
 {a-c interval) . . . • 
 
 245 
 
 240 
 238 
 
 57 
 
 43 
 
 146 
 31 
 
 219 
 
 225 
 227 
 
 217 
 
 297 
 
 34 
 92 
 
 105 
 
 62 
 
 62 
 
 46 
 
 179 
 
 217 
 197 
 338 
 162 
 218 
 22 
 
 152 
 
 111 
 
 95 
 
 176 
 
 FAOB 
 
 . 78 
 . 82,86,88 
 
 91, 92 
 . 251, 276 
 THE 
 
 INTERVAL, PRE-SPHYGMIC 
 
 INVERTED CARDIOGRAMS 
 
 INVERTED SPHYGMOGRAM 
 
 IODIDE OF POTASSIUM . 
 
 IRREGULAR ACTION OF 
 HEART 
 
 classification of ... . 141 
 
 IRREGULAR HEART 
 
 and chloroform .... 263 
 
 IRREGULARITY 
 
 nature of disease shown by . .217 
 See also Heart Irregulakity. 
 
 IRREGULARITY CHARACTERISTIC 
 OF THE NODAL RHYTHM . 118 
 
 FOCUS IN SPINAL 
 
 IRRITABLE 
 
 CORD 37,45 
 
 IRRITABLE HEART AFTER RHEU- 
 MATIC FEVER 
 
 221 
 
 JAUNDICE 
 
 with dilatation of the heart . 
 with heart failui'e . . . . 
 the pulse-rate with 
 
 JUGULAR PULSE 
 
 airricular wave in the 
 aiuicular depression in the 
 ventricular wave in the 
 ventricular depression in the . 
 the carotid wave in the . 
 compared with auricular pressure . 
 conditions giving rise to a 
 a diastolic wave in the . 
 effect of dilatation of the heart on 
 
 the 
 
 effect of opening of tricuspid valves 
 
 on the . . . . . 
 with extra-systoles 
 factors producing the 
 graphic records of the 
 how to record the . 
 inspection of the 
 
 209 
 125 
 139 
 
 109 
 109 
 110 
 111 
 112 
 107 
 121 
 113 
 
 205 
 
 110 
 150-159 
 . 108 
 . 106 
 . 68 
 . 105 
 interpretation of the . . 106,111 
 meaning of the ventricular form of 
 
 the 116 
 
 in mediastino- pericarditis . . 245 
 period of stasis in the . . 11,114 
 with the nodal rhythm . 1 16, 167, 308 
 significance of ventricular form of 
 
 the 117,238 
 
 standard for interpreting a . 108,111 
 time of opening of tricuspid valves 
 
 in the 80 
 
 in tricuspid disease . . ,110 
 
 with tricuspid regurgitation . 1 10, 238 
 what it shows .... 105 
 
 variations of, due to heart's rate . 115 
 ventricular form of the . . .116
 
 408 
 
 INDEX 
 
 PAGE 
 
 JUGULAR VALVE SOUND 238, 322, 348 
 
 JUGULAR VEINS 
 
 inspiratory swelling of . . . 62 
 relation of, to carotid and sub- 
 clavian arteries . . . .107 
 thrills produced by compression of 311 
 
 KIDNEY DISEASE AND CARDIO- 
 SCLEROSIS 243 
 
 KNOTEN OF TAWARA 
 
 See Aueiculo-Ventriculab Node. 
 
 LACTIC ACID 
 
 action on tonicity ... 9 
 
 LEG, FRACTURE OF 
 
 and heart failure . . 27,32,209 
 
 LEG, DEGENERATION OF ARTERIES 
 
 OF 
 
 46 
 46 
 
 LEG, GANGRENE OF 
 
 LIFE INSURANCE 
 
 and the prognosis of symptoms . 264 
 
 LIVER 
 
 pain due to the .... 22 
 
 LIVER ENLARGEMENT 
 
 a cardinal symptom of heart failure 122 
 
 effect of digitalis on . . . 286 
 in dilatation of the heart . 207, 208 
 
 with nodal rhythm . . . 170 
 pain and tenderness in . . 122, 209 
 
 with paroxysmal tachycardia . 207 
 
 signs of ..... 123 
 
 treatment ..... 128 
 
 LIVER MOVEMENTS 
 
 in aortic regurgitation . 
 
 241 
 
 due to cardiac aspiration 
 
 83 
 
 ER PULSATION 
 
 123 
 
 in adherent pericardium 
 
 125 
 
 coupled beats in . 
 
 284 
 
 differential diagnosis of . 
 
 126 
 
 distinct from liver movement 
 
 83 
 
 forms of .... 
 
 123 
 
 how to record 
 
 69 
 
 with the nodal rhythm . 
 
 123 
 
 prognosis of . 
 
 126 
 
 with paroxysmal tachycardia 
 
 324 
 
 in tricuspid stenosis . 125, 238, 314, 347 
 
 LUNG, RETRACTION OF . . 88 
 
 LUNGS 
 
 acute suffocative oedema of . . 32 
 apoplexy of . . . . .32 
 bleeding from . . . .31 
 
 displacement of, with dilatation of 
 
 the heart 204 
 
 infarct into ..... 32 
 in the fixation of the heart . . 16 
 
 PAGE 
 
 LUNGS, OEDEMA OF . . . 208 
 
 in the elderly .... 27 
 
 factors in the production of . . 210 
 
 first sign of . . . . . 209 
 
 how produced .... 27 
 
 method of examining for . . 210 
 
 in mitral stenosis .... 27 
 prognostic significance of . .210 
 
 symptoms of .... 210 
 
 in typhoid fever .... 27 
 
 MALIGNANT ENDOCARDITIS . 225 
 
 MASSAGE 
 
 in treatment .... 295 
 
 MECHANISM OF THE PRODUC- 
 TION OF PAIN .... 35 
 
 MEDIASTINO-PERICARDITIS 
 
 angina pectoris in . . . . 253 
 
 etiology of 253 
 
 jugular pulse in ... . 254 
 
 liver pulse in .... 255 
 
 prognosis in . . . . . 255 
 
 symptoms of .... 254 
 
 treatment of .... 255 
 
 MEMORY 25 
 
 MENSTRUATION 
 
 nose bleeding during ... .23 
 
 MENTAL EXCITEMENT 
 
 a cause of angina pectoris . . 47 
 
 MENTAL FACTOR 
 
 in treatment .... 274 
 
 MENTAL STATE 
 
 in Cheyne-Stokes respiration . . 31 
 
 induced by heart abnormalities . 56 
 
 in the X disease .... 61 
 
 induced by physician's warnings . 56 
 
 induced by visceral disease . . 55 
 
 MESENTERY, INSENSITIVENESS OF 34 
 
 METHOD OF DESCRIBING HEART 
 
 AFFECTIONS .... 4 
 
 MICTURITION 
 
 after an attack of angina pectoris . 50 
 
 MITRAL MURMURS 
 
 due to acute endocarditis . . 219 
 
 due to dilatation .... 204 
 See also Murmurs. 
 
 MITRAL REGURGITATION 
 
 absence of angina pectoris in . . 47 
 cessation of angina pectoris with 
 
 onset of . . . . .47 
 
 in cardio-sclerosis .... 235 
 
 causes of .... . 235 
 
 conditions inducing heart failure in 235 
 with dilatation of the heart . 47, 235 
 
 murmurs due to . . . . 234
 
 INDEX 
 
 409 
 
 MITRAL STENOSIS 
 
 
 
 angina pectoris in . 
 
 230 
 
 ,234 
 
 causes of ... . 
 
 
 229 
 
 cerebral embolism in 
 
 
 234 
 
 conditions inducing heart failu 
 
 e in 
 
 229 
 
 dilatation of left ventricle in . 
 
 204 
 
 ,230 
 
 delayed conductivity with 
 
 
 229 
 
 haemoptysis in . . . 
 
 
 234 
 
 involvement of a. -v. bundle in 
 
 
 229 
 
 heart failure in . . . 
 
 
 229 
 
 moderate .... 
 
 
 229 
 
 murmurs due to . 
 
 
 230 
 
 meaning of disappearance of 
 
 pre- 
 
 
 systolic murmur of 
 
 
 231 
 
 not an acute condition . 
 
 
 229 
 
 nodal rhythm in . . . 
 
 229 
 
 ,233 
 
 paroxysmal tachycardia in 
 
 
 234 
 
 pregnancy with 
 
 
 251 
 
 post-mortem changes in 
 
 
 233 
 
 progress of . 
 
 
 232 
 
 a progressive lesion 
 
 
 229 
 
 sclerosis of muscle with . 
 
 
 233 
 
 symptoms in ... 
 
 
 232 
 
 systolic miu-mur due to 
 
 
 232 
 
 MOUTH 
 
 becoming dry in angina pectoris 
 
 MOVEMENTS DUE TO CAROTID 
 PULSE ...... 
 
 MOVEMENTS OF THE HEART . 
 
 MOVEMENTS OF RESPIRATION 
 
 effect of, on the pulmonary circula- 
 tion 
 
 MOVEMENTS IN TREATMENT, 
 SPECIAL 
 
 MURMURS 
 
 due to aortic incompetence . 
 
 due to aortic stenosis 
 
 amicular systolic .... 
 
 cause of functional 
 
 in cardio-sclerosis .... 
 
 diastolic mitral, cause of 
 
 diastolic, due to mitral stenosis 
 
 due to endocarditis 
 
 meaning of, in acute conditions 
 
 due to mitral stenosis 
 
 due to patent ductus arteriosus 
 
 due to pericarditis 
 
 presystolic, character of 
 
 presystolic, disappeai'ance of, in 
 nodal rhythm .... 
 
 presystolic, how produced 
 
 presystolic, meaning of disappear- 
 ance of .... . 
 
 presystolic, position of in cardiac 
 cycle ..... 
 
 presystolic, separation of, from first 
 sound ..... 
 
 presystolic tricuspid 
 
 59 
 
 91 
 76 
 
 210 
 
 295 
 
 240 
 239 
 230 
 204 
 246 
 231 
 231 
 219 
 215 
 230 
 256 
 220 
 230 
 
 170 
 230 
 
 231 
 
 230 
 
 176 
 
 238 
 
 MURMURS {continued)— 
 
 presystolic, varying relation to first 
 
 sound 
 
 presystolic ventricular . 
 significance of musical . 
 systolic, due to mitral regurgitation 
 systolic, due to mitral stenosis 
 tricuspid svstolic . 
 
 MUSCARIN 
 
 action on tonicity 
 
 MUSCLES, ABDOMINAL 
 reflex stimulation of 
 
 MUSCLES, CONTRACTED IN GAS- 
 TRIC ULCER 
 
 MUSCLE EXHAUSTION 
 a factor in heart failure 
 
 MUSCLE FAILURE 
 symptoms in 
 
 MUSCLES, INTERCOSTAL 
 
 contraction of, in angina pectoris . 
 
 MUSCLES, THEIR PRIMITIVE 
 FUNCTION 
 
 MUSCLES, SPASM OF, A CAUSE OF 
 PAIN 
 
 MUSCLE, STERNO-MASTOID 
 
 hyperalgesia of . 
 
 MUSCLE STIMULATION 
 in visceral disease 
 
 :\IUSCLES, TONICITY OF 
 
 MUSCLE, TRAPEZIUS 
 
 hyperalgesia of ... . 
 
 MUSCLES, TWITCHING OF 
 
 in Cheyne-Stokes respiration . 
 
 MUSCULAR HYPERALGESIA 
 
 consequence of, in liver enlarge- 
 ment ..... 
 
 MUSCULAR ORGANS 
 
 resemblance of symptoms in liollow 
 
 MUSCULAR RHEUMATISM. 
 See Rheumatism. 
 
 MUSICAL MURxMURS 
 
 significance of ... . 
 
 MYOCARDITIS 
 
 heart-rate in ... 
 
 in acute fevers 
 in rheumatic fever 
 irregular action of the heart in 
 symptoms of ... 
 
 MYOGENIC DOCTRINE . 
 
 368 
 232 
 219 
 234 
 232 
 237 
 
 9 
 
 37 
 
 38 
 
 235 
 
 207 
 
 41 
 
 38 
 
 4+ 
 
 41 
 
 37 
 202 
 
 41 
 
 29 
 
 123 
 33 
 
 219 
 
 131 
 216 
 221 
 217 
 216 
 
 6
 
 410 
 
 INDEX 
 
 NAUHEIM BATHS 
 
 PAGE 
 
 297 
 
 NECK 
 
 pain in, during an attack of angina 
 pectoris . . . . 41,48 
 
 NERVES OF THE HEART 
 
 accelerator ..... 19 
 afferent . . . . .19 
 depressor . . . . .19 
 effect of, on the functions of muscle- 
 fibres 10 
 
 effects of, on the heart muscle . 18 
 in a.-v. bundle .... 14 
 influence on the heart's rhythm . 141 
 inhibitory . . . . .18 
 action of sympathetic ... 18 
 origin of sympathetic . . .19 
 action of vagus . . . .41 
 vagus, effect of stimulation of, on 
 
 depressed functions . . .19 
 See also Vagus. 
 
 NERVES 
 
 diagram showing stimulation of, 
 
 in visceral disease 
 optic, stimulation of 
 peculiar field supplied by upper 
 
 dorsal .... 
 
 sensory stimulation of . 
 sensory, relationship of to heart 
 stimulation of trunk of . 
 sympathetic, diagram showing rela 
 
 tion to viscera and sensory nerve 
 
 NERVOUS SYSTEM 
 
 reaction of visceral disease on 
 hypersensitiveness of . 
 valvular disease with exhausted 
 
 NEURASTHENIA 
 
 cardiac ..... 
 
 and sinus irregularity 
 
 NEUROGENY 
 
 NEUROSES, CARDIAC . 
 
 NEUROTIC PATIENTS 
 
 treatment of . 
 
 36 
 34 
 
 40 
 36 
 40 
 35 
 
 36 
 
 55 
 55 
 
 57 
 
 56 
 146 
 
 56 
 
 . 270 
 
 NITRITE OF Al^IYL 
 
 dm-ing an attack of angina pectoris 53 
 
 NITRITES AND HIGH BLOOD-PRES- 
 SURE 275 
 
 NODAL BRADYCARDIA . . 337 
 
 NODAL EXTRA-SYSTOLES . . 157 
 
 NODAL RHYTHM 
 
 in acute affections . . . 218 
 analysis of symptoms of . . 309 
 with arterial degeneration . . 103 
 artificial waves in tracings of . .311 
 auricular wave absent in apex trac- 
 ings in . . . . .81 
 
 NODAL RHYTHM {continued)— 
 
 due to cardio-sclerosis . . 142, 247 
 significance of, in cardio-sclerosis . 248 
 illustrative cases of the . . 312, 333 
 character of irregularity in . . 142 
 characteristics of . . . .117 
 classification of cases of . . . 169 
 clinical evidence of . . . 309 
 
 definition of . . . . xix, 166 
 caused by digitalis . . . 364 
 
 effect of digitalis in . 172, 282, 357 
 difference when due to rheumatism 
 and cardio-sclerosis . . . 286 
 
 with dropsy 208 
 
 effect of, on the heart's strength . 142 
 
 electro- cardiogram of . . 297 
 
 ,374 
 
 etiology of .... . 
 
 167 
 
 and extra-systoles 
 experimental evidence of 
 relation to heart-block . 
 
 164 
 120 
 185 
 
 cases illustrating relation of to 
 
 
 heart-block . . .336 
 
 ,364 
 
 laboured breathing in . 
 
 27 
 
 and liver pulsation 
 
 in mitral stenosis . . . 230 
 
 127 
 ,233 
 
 causing paroxysmal tachycardia . 
 pathology of .... 
 
 172 
 310 
 
 in pneumonia .... 
 and pregnancy .... 
 pulsation of the liver with the 
 character of pulse in . . . 
 
 218 
 260 
 123 
 167 
 
 due to advanced rheumatic disease 
 
 142 
 
 signs of danger in . 
 starting-place of . 
 
 172 
 142 
 
 susceptibility of, to digitalis . 
 transient ..... 
 
 282 
 172 
 
 ventricular form of venous pulse 
 
 
 in 
 
 118 
 
 See also Heakt Irregularity. 
 
 
 NORMAL VENOUS PULSE. 
 
 See Jugular Pulse. 
 
 NOSE BLEEDING 
 
 at menstrual period ... 23 
 in aortic disease .... 23 
 
 NOURISHMENT OF HEART MUSCLE 
 
 angina pectoris due to impaired . 43 
 
 NUTRITION 
 
 exhaustion of contractility due to 
 imperfect . . . . .192 
 
 OBSCURE CASES 
 
 prognosis in . . . . . 267 
 
 OEDEMA. See Dropsy. 
 
 OEDEMA OF THE LUNGS 
 See Lungs. 
 
 OEDEMA, PULMONARY. See Lungs. 
 
 OLD AGE 
 
 viscero-motor reflex in . . .41
 
 INDEX 
 
 411 
 
 OPIUM 
 
 PAGE 
 
 . 270 
 
 in angina pectoris 
 in cardio-sclerosis . 
 
 . 54 
 . 251 
 
 OPPRESSION OF THE CHEST 
 
 
 in the elderly 
 
 . 130 
 
 OPTIC NERVE 
 
 
 stimulation of . . . 
 
 . 35 
 
 ORIGIN OF MISTAKEN DIAGNOSES 215 
 
 OVER-EXERTION 
 
 causing angina pectoris ... 42 
 
 OVERSTRAINED HEART . . 132 
 
 OXYGEN 
 
 in angina pectoris 
 in cardiac asthma 
 in treatment 
 
 54, 279 
 29, 279 
 
 . 278 
 
 PAIN 
 
 absence of, in pericarditis . . 220 
 in aneurysm .... 252 
 
 in angina pectoris, region of . 40, 48 
 persisting after an attack of angina 
 
 pectoris ..... 
 of biUary colic, situation of . 
 due to exhausted contractility 
 function of . 
 
 in gastric ulcer .... 
 of heart affections, reasons for in 
 
 arm ...... 
 
 of heart aflfections, situation of 
 
 of herpes zoster, simulating angina 
 
 pectoris 
 
 over the liver .... 
 
 in enlargement of the liver 
 
 mechanism of its production 
 
 due to peristalsis of the bowel 
 
 radiation of . 
 
 of renal colic, situation of 
 
 significance of ... . 
 
 situation of . 
 
 caused by spasm of hollow muscles 
 
 vague notion of position of 
 
 why it is referred .... 
 
 50 
 38 
 193 
 38 
 38 
 
 39 
 39 
 
 57 
 
 22 
 
 122, 209 
 
 . 35 
 
 . 34 
 
 22 
 
 '. 39 
 
 . 22 
 
 . 22 
 
 44 
 
 21 
 
 38 
 
 PALPITATION 22 
 
 definition of . . . . xix, 134 
 heart-rate in . . . . .134 
 and paroxysmal tachycardia, dis- 
 tinction between . . . 134 
 sensation during . . . .135 
 sign of exhausted contractility . 193 
 
 PARALYSIS OF THE AURICLE 
 
 evidences of . . . • .117 
 
 PAROXYSMAL TACHYCARDIA 
 
 of auricular origin . . • 334 
 
 a.-v. node affected in cases of . 324, 328 
 in cardio-sclerosis .... 247 
 
 PAROXYSMAL TACHYCARDIA 
 
 (continued) — 
 cases illustrating . 
 definition of . 
 
 dilatation of the heart with . 
 liver enlargement in 
 liver pulsation during . 
 meaning of the term 
 in mitral stenosis . 
 and palpitation, distinction betw 
 pathology of . . 310, 
 
 primitive cardiac tissue in 
 prognosis in . 
 pulsus alternans due to . 
 symptoms of ... 
 
 sudden relief on cessation of . 
 sudden changes due to . 
 treatment of ... 
 
 PATENT DUCTUS ARTERIOSUS 
 murmm's of . 
 
 PATENT FORAMEN OVALE . 
 
 320-336 
 
 xix, 134 
 
 . 207 
 
 127, 208 
 
 . 324 
 
 134, 172 
 
 . 234 
 
 een 134 
 
 324, 328 
 
 324, 328 
 
 . 173 
 
 198, 335 
 
 . 172 
 
 . 207 
 
 . 207 
 
 . 173 
 
 256 
 
 156 
 
 PATHOLOGY OF HEART 
 
 in angina pectoris . . 304, 305, 353 
 in cardio-sclerosis 245. 328, 353, 355 
 
 in nodal rhythm . . ' . 168,310 
 in paroxysmal tachycardia 310, 324, 328 
 shown by irregularity . . 140, 217 
 
 PATHOLOGICAL VENOUS PULSE. 
 See Ventricular Jugvlar Pulse. 
 
 PATIENT 
 
 position assumed by . . .20 
 preliminary examination of . . 20 
 respiration of .... 20 
 
 sensations of . . . . .20 
 sensations of a guide to condition 
 
 of reserve force . . . .21 
 necessity for precision in state- 
 ments of . . . . .21 
 
 PATIENT'S APPEARANCE . . 20 
 
 PATIENT'S GAIT .... 20 
 
 PATIENT'S HISTORY . . .20 
 
 PECTINATE FIBRES OF AURICLES 
 
 their function and position . . 16 
 
 PENIS 
 
 ram's horn 212 
 
 PERICARDIAL ADHESIONS 
 
 after rheumatic fever . . .221 
 
 PERICARDIAL EFFUSION 
 
 embarrassing the heart . . . 220 
 simulating dilatation . . 203, 204 
 symptoms of .... 220 
 
 PERICARDIAL SAC 
 
 in the fixation of the heart . . 16
 
 412 
 
 INDEX 
 
 PERICARDITIS 
 
 in acute fevers . . . .214 
 a misleading term . . . 215 
 
 a painless affection . . . 220 
 
 symptoms of .... 220 
 
 See also Mediastino-Pericarditis. 
 
 PERICARDIUM 
 
 adlierent ..... 252 
 insensitiveness of . . . .34 
 in rheumatic fever . . .221 
 
 PERIODIC RESPIRATION . . 31 
 
 PERIPHERAL RESISTANCE 
 
 effect of increased . . . 102 
 
 PERISTALSIS 
 
 of the bowel, pain caused by . . 34 
 
 PERITONEAL ADHESIONS 
 
 insensitiveness of . . . ,34 
 
 PERNICIOUS ANAEMIA 
 
 epigastric pulsation in . . .85 
 
 jugular pulse in ... . 121 
 
 laeart-rate in . . . .130 
 
 PERSPIRATION 
 
 during an attack of angina pectoris 48 
 
 PETIT MAL . . .24, 25, 343 
 
 PHYSIOLOGICAL VENOUS PULSE 
 
 See Auricular Jugular Pulse. 
 
 PLATEAU, SYSTOLIC 
 
 in apex tracing . . . 78, 80, 82 
 
 PNEUMONIA 
 
 case illustrating severe heart affec- 
 
 tion in 
 
 
 
 . 223 
 
 the heart in . 
 
 
 
 214, 223 
 
 hypostatic 
 
 
 
 . 209 
 
 irregular heart in 
 
 
 
 . 224 
 
 nodal rhythm in 
 
 
 
 . 218 
 
 pericarditis in 
 
 
 
 . 221 
 
 the pulse in . 
 
 
 
 . 223 
 
 pulsus alternans in 
 
 
 
 197,218 
 
 POLYGRAPH 
 
 
 the clinical 
 
 . 68 
 
 the ink . 
 
 . 72 
 
 POLYSEROSITIS 
 
 . 252 
 
 POSITION OF THE 
 
 HEART IN 
 
 DILATATION . 
 
 
 
 . 204 
 
 POST-MORTEM RECORDS OF CASES 
 
 of angina pectoris . . 304, 305, 353 
 of cardio-sclerosis . . 328, 353, 355 
 of nodal rhythm . 314,316,318,349, 
 
 [324, 328 
 of paroxysmal tachycardia . 324, 328 
 of pulsus alternans . . 353, 355 
 
 POWER OF RECOVERY 
 
 a basis for prognosis . . . 265 
 
 PREGNANCY 
 
 jugular pulse in 
 heart-rate increased in . 
 slow pulse-rate in . 
 and oedema of the lungs 
 
 121 
 132 
 139 
 
 209 
 
 PREGNANCY AND HEART DISEASE 
 
 importance of the subject . . 258 
 
 management of the labovir . . 260 
 
 standards for guidance . . . 258 
 
 signs of danger in mitral disease . 259 
 
 signs of danger in aortic disease . 259 
 
 signs of danger in dilatation . . 259 
 signs of danger with the nodal 
 
 rhythm 260 
 
 PRESPHYGMIC INTERVAL . 
 PRESSURE. See Arterial Pressure. 
 
 78 
 
 PRESYSTOLIC MURMUR 
 
 varying position of in cardiac cycle 231 
 varying relation to first sound . 368 
 See also Murmurs. 
 
 PRESYSTOLIC THRILL 
 
 the first sign of mitral stenosis 
 
 PRIMARY WAVE 
 
 in a sphygmogram 
 
 PRIMITIVE CARDIAC TISSUE 
 in cardio-sclerosis 
 cases illustrating pathology of 
 and extra-systoles 
 functions of . 
 in the mammalian heart 
 affected in the nodal rhythm . 
 the starting-place of the heart's 
 contraction in the 
 
 . 230 
 
 . 96 
 
 . 248 
 
 312,315 
 
 162 
 
 151 
 
 13 
 
 311 
 
 PRIMITIVE CARDIAC TUBE . 
 function of . 
 
 11, 141 
 
 11 
 141 
 
 PROGNOSIS 264 
 
 in angina pectoris .... 50 
 basis for .... 265,294 
 
 in cardio-sclerosis . . . 248 
 
 in cases with exaggerated sensory 
 
 symptoms ..... 63 
 in Cheyne-Stokes respiration . . 30 
 in depression of conductivity . .189 
 in congenital affection of the lieart 257 
 in exhaustion of contractility . 198 
 
 dangers of ignorance in giving a . 264 
 in dilatation of the heart . .211 
 use of digitalis in . . . . 212 
 of extra-systoles .... 164 
 effect of a gloomy . . 264, 275 
 
 the field of cardiac response in . 265 
 in heart-block . . . .189 
 and life insurance . . . 264 
 
 in liver enlargement . . . 126 
 importance of ... . 264 
 
 in increased heart-rate . . . 136
 
 INDEX 
 
 413 
 
 PAGE 
 
 PROGNOSIS {rontinued)— 
 
 in mediastino-pericarditis . . 255 
 in the nodal rhythm with increased 
 
 rate 169, 171 
 
 in obscure cases .... 267 
 
 in paroxysmal tacliycardia . . 173 
 of the pulsus alter nans . . .198 
 
 the reserve force in . . . 266 
 
 responsibility of giving a . . 264 
 
 of sinus irregularities . . . 146 
 
 in syncope ..... 266 
 
 in typhoid fever .... 210 
 
 in valvular affections . . . 242 
 
 PROGRESSIVE NATURE 
 
 of valvular sclerosis . . . 229 
 
 PROTECTION 
 
 the function of contracted muscles 37 
 the function of pain ... 37 
 
 PROTECTIVE MECHANISM 
 
 angina pectoris a . . . .45 
 in gastric ulcer .... 38 
 in joint disease .... 38 
 reflex ...... 33 
 
 PSEUDO-ANGINA PECTORIS 
 
 a useless and misleading term . 56 
 
 PSOAS ABSCESS 
 
 and the heart- rate . . .133 
 
 PUERPERAL FEVER 
 
 a.-v. bundle affected in . . . 217 
 the heart in 226 
 
 PULMONARY ARTERY 
 
 tracings from .... 78, 79 
 
 PULMONARY CIRCULATION 
 
 effect of respiratory movements on 210 
 
 PULMONARY STASIS, ^ee Lungs. 
 
 PULMONARY VEINS 
 
 heart's contraction starting at . 13 
 
 PULSATION 
 
 causes of epigastric . . . 83, 85 
 
 PULSATION, CAPILLARY 
 
 in aortic regurgitation . . .241 
 
 PULSE 
 
 anacrotic ..... 240 
 
 in aortic incompetence . . . 240 
 
 in aortic stenosis .... 239 
 
 in angina pectoris .... 302 
 character of irregularity in nodal 
 
 rhythm ..... 167 
 
 causes of unequal radial . . 94 
 
 Corrigan's ..... 240 
 
 digital examination of arterial . 90 
 effect of auricular contraction on 
 
 radial 184 
 
 liver ...... 123 
 
 how to record liver ... 69 
 
 PULSE {continued)— 
 
 intermission due to depressed con- 
 ductivity .... 176, 179 
 intermission due to extra-systoles 
 
 141, 149 
 nature of movements of arterial . 91 
 not due to expansion of the artery 91 
 in palpitation .... 
 
 in pneumonia .... 
 
 rate, classification of diminished 
 rate, slow, due to heart- block 
 rate, slow, due to true bradycardia 
 rate, reckoning of the 
 rate during syncope 
 rhythm of the .... 
 
 slow, due to feeble contraction of 
 ventricle ..... 
 water-hammer .... 
 wave, impact of the 
 wave, size of .... 
 
 what is it ? 
 
 135 
 223 
 
 138 
 138 
 139 
 
 93 
 187 
 
 94 
 
 138 
 
 . 240 
 
 94 
 
 94 
 
 90, 92 
 
 PULSE, VENOUS. -See Jugular Pulse. 
 
 PULSUS ALTERNANS . 
 
 in acute affections of the heart 
 
 43, 50, 196, 
 
 194, 196, 
 . 194, 
 
 xix, 
 . 197, 
 
 196, 
 
 in angina pectoris 
 and arterial pressure 
 with cardiac asthma 
 in cardio-sclerosis . 
 causation of . 
 
 conditions giving rise to tlie . 
 definition of . 
 due to digitalis 
 
 distinct from extra-systoles . 
 distinct from pulsus bigeminus 
 with extra-systoles 
 field of response with 
 frequency of ... 
 
 heart sounds with . 
 how produced 
 
 with paroxysmal tachycardia 
 in pneumonia . . . . 
 
 prognosis of . 
 
 significance of ... . 
 significance of, in cardio-sclerosis . 
 a symptom of exhausted con- 
 tractility , . . . . 
 
 198, 
 
 142 
 197 
 303 
 196 
 29 
 248 
 350 
 197 
 194 
 288 
 198 
 198 
 350 
 196 
 196 
 198 
 194 
 335 
 197 
 198 
 194 
 248 
 
 194 
 
 PULSUS BIGEMINUS 
 
 definition of . 
 
 heart sounds in . . • 
 distinct from pulsus alternans 
 due to extra-systoles 
 
 PULSUS BISFERIENS 
 in aortic stenosis . 
 
 PULSUS CELER 
 
 PULSUS PARADOXUS 
 
 in mediastino-pericarditis 
 
 PULSUS TARDUS . 
 
 xix, 149 
 . 150 
 . 198 
 . 141 
 
 240 
 94 
 
 254 
 94
 
 414 
 
 INDEX 
 
 PAGE 
 
 PURKINJE FIBRES ... 14 
 
 PURPOSE OF VISCERAL REFLEXES 37 
 
 PYAEmA 
 
 heart in 
 
 RADIAL PULSE 
 
 as a standard 
 causes of unequal 
 
 226 
 
 75 
 94 
 
 RECURRENT ATTACKS 
 
 of angina pectoris ... 50 
 
 REFLEX PROTECTIVE PHENOMENA 
 
 in visceral disease ... 33 
 
 REFLEX SYMPTOMS 
 
 dui'ing an attack of angina pectoris 48 
 cause of exaltation of . . .38 
 
 in dilatation of the heart . . 202 
 
 due to exhaustion of contractility . 193 
 in enlargement of the liver . .122 
 
 exaggerated in neurotic people . - 55 
 
 REFLEX, VISCERO-MOTOR . . 37 
 
 REFLEX, VISCERO-SENSORY . 35 
 
 in angina pectoris ... 40 
 
 REFLEXES, VISCERAL, PURPOSE 
 
 OF 37 
 
 REGURGITATION 
 
 into coronary sinus, how prevented 16 
 
 into veins, how prevented . . 16 
 
 RENAL COLIC. See Colic. 
 
 RESECTION OF BOWEL 
 
 in conscious subject ... 34 
 
 RESERVE FORCE .... 2 
 
 conditions exhausting the . . 3 
 
 of the function of contractility . 192 
 
 in prognosis ..... 266 
 
 restored by training . . . 266 
 increased heart-rate with exhaustion 
 
 of 130 
 
 See also Heart Muscle. t 
 
 RESPIRATION 
 
 effect of movements of, in the pul- 
 monary circulation . . . 210 
 causing irregular heart-action . 143 
 slow, due to digitalis . . .31 
 slow, inducing irregular action of 
 
 the heart . . . . .31 
 
 slow and vagus stimulation . . 31 
 
 RESPIRATORY SYMPTOMS . . 26 
 
 RESPONSE, FIELD OF 
 
 in heart-block .... 187 
 
 the standard of heart's strength . 4 
 
 PAGE 
 
 REST 
 
 effect of, on depressed conductivity 
 
 177, 180 
 
 importance of, in exhausted con- 
 tractility ..... 
 
 in treatment .... 
 
 want of, a cause of exhaustion of 
 the heart ..... 
 
 want of, a cause of angina pectoris 
 
 RESTLESSNESS 
 
 treatment of .... 
 
 199 
 269 
 
 46 
 46 
 
 270 
 
 RETRACTION OF STRUCTURES 
 
 due to ventricular systole 
 
 
 . 81 
 
 RETROGRADE EXTRA-SYSTOLE . 160 
 
 RHEUMATIC FE\T:R 
 
 
 affection of a. -v. bundle in 
 
 185, 217 
 
 cellular foci in heart muscle in 
 
 . 221 
 
 dilatation of the heart in 
 
 . 222 
 
 extra-systoles in 
 heart in . 
 
 
 . 218 
 214, 221 
 
 heart symptoms in 
 irritable heart after 
 
 
 . 222 
 . 221 
 
 mitral stenosis due to 
 
 
 . 229 
 
 pericardial adhesions after 
 pericarditis in . . . 
 slow cicatrization in heart after 
 
 . 221 
 . 220 
 . 221 
 
 RHEUMATIC HEART 
 
 exhaustion of contractility in 
 
 193 
 
 RHEUMATIC HEART CASES 
 
 dropsy in 209 
 
 RHEUMATIC AFFECTION OF THE 
 HEART ♦ 
 
 causing the nodal rhythm . 1-12, 168 
 
 RHEUMATIC HEART ^^^TH THE 
 NODAL RHYTHM 
 
 effect of digitalis on . . . 172 
 
 RHEUMATISM, MUSCULAR 
 
 contraction of intercostal muscles in 41 
 
 RHYTHmCAL CONTRACTION OF 
 THE HEART 
 
 cause of ..... 8 
 
 RIBS 
 
 resection of, in adhesive medias- 
 tinitis 255 
 
 RIGHT VENTRICLE 
 
 and epigastric pulsation • . . 85 
 
 RIGHT VENTRICLE CAUSING THE 
 APEX BEAT 85 
 
 RUPTURE OF AORTIC VALVES . 239 
 
 RUPTURE OF THE HEART . . 202 
 with arterial degeneration . . 103
 
 INDEX 
 
 415 
 
 S.-A. NODE. 
 
 See SiNO-AuRicuLAR Node. 
 
 SALICYLATE OF SODA 
 in rheumatic fever . 
 
 PAGE 
 
 223, 277 
 
 SALIVA, INCREASED SECRETION OF 
 in angina pectoris . . . 42, 48 
 
 SALT 
 
 in angina pectoris . . . .53 
 in dropsy ..... 212 
 
 SCHOOLBOYS 
 
 and the sinus irregularitj^ . . 146 
 
 SCLEROSIS OF MUSCLE 
 
 with mitral stenosis . . . 233 
 
 SCLEROSIS OF VALVES AND 
 HEART MUSCLE 
 
 association of .... 229 
 
 SCLEROTIC CHANGES 
 
 progressive nature of . . . 229 
 
 SEA-BATHING .... 65,296 
 
 SEGMENTATION OF THE BODY 
 
 cause of ..... 38 
 
 SENILE HEART ... 243 
 
 oedema of the lungs with . . 209 
 symptoms caused by the . .130 
 
 SENSATIONS OF PATIENTS 
 
 during an attack of heart-block 
 syncope ..... 188 
 
 SENSE OF EXHAUSTION . . 22 
 
 SENSE OF niPENDING DEATH 
 
 in angina pectoris ... 49 
 
 in palpitation .... 135 
 
 SENSORY NERVE. See Nerve. 
 
 SENSORY PHENOMENA 
 
 in cardio-sclerosis .... 58 
 in nervous people .... 59 
 
 SEPTIC INFECTIONS 
 
 a.-v. bundle affected in . 
 the heart in . 
 heart-block in 
 
 SEPTUM, A.-V. 
 
 action' of muscles on 
 
 SHOCK DUE TO VENTRICULAR 
 SYSTOLE . . . . 87,89 
 
 SINO-AURICULAR NODE 
 
 constitution of . . . .14 
 
 definition of term xix 
 
 position of . . . . .14 
 the starting-place of the heart's 
 contraction .... 141 
 
 PAGE 
 
 SINUS IRREGULARITIES . 141, 143 
 character of . . . . . 140 
 in healthy people .... 146 
 and the X disease . . . .146 
 See also Heart Irregularity. 
 
 SINUS VENOSUS .... 14 
 formation of . . . . .13 
 in the mammalian heart . . 13 
 
 starting-place of the heart's con- 
 traction ..... 140 
 
 SKIN, ATTENUATION OF 
 
 due to obliteration of capillaries 
 
 SKIN, HYPERALGESIC 
 
 after an attack of angina pectoris 
 
 . 217 
 
 214, 225 
 
 . 217 
 
 . 16 
 
 SLEEP 
 
 angina pectoris induced by want o 
 with cardiac asthma 
 Cheyne-Stokes respiration during 
 importance of, in treatment . 
 necessity for, in cardio-sclerosis 
 necessity for inquiry into 
 
 SLEEPLESSNESS 
 
 inducing angina pectoris 
 
 SLOW BREATHING . 
 
 244 
 
 51 
 
 250 
 
 28 
 
 29 
 
 269 
 
 250 
 
 21 
 
 , 270 
 31,62 
 
 SLOWING OF THE WTIOLE HEART 
 by digitalis ..... 367 
 
 SLOW PULSES 
 
 classification of ... . 138 
 
 SODIUM SALICYLATE 
 
 Lee's method of using . . . 277 
 
 SOLDIER'S HEART . . . .131 
 
 SOLDIERS 
 
 sinus irregularity in healthy . • . 146 
 
 SOUND CAUSED BY VENOUS 
 
 VALVES 
 
 SOUNDS OF THE HEART 
 
 in cardio-sclerosis . 
 due to extra-systoles 
 in nodal rhythm 
 in sinus irregularity 
 
 SOUTHEY'S TUBES 
 
 in the treatment of dropsy 
 
 SPAS 
 
 treatment at ... 
 
 cause of efficacy of treatment at 
 
 SPASM OF THE HEART 
 
 impossible .... 
 
 SPASM OF HOLLOW MUSCLES 
 a cause of pain 
 
 SPHYGM0GRA3I 
 
 definition of . 
 diastolic notch in a 
 diastolic period in a 
 
 322, 348 
 
 142 
 
 246 
 150 
 232 
 145 
 
 212 
 
 296 
 299 
 
 44 
 
 44 
 
 95 
 96 
 96
 
 416 
 
 INDEX 
 
 PAGE 
 
 SPHYG:\I0GRA^I (continued)— 
 
 diastolic wave in a . . .96 
 
 instrumental defects in a . .97 
 
 interpretation of a . . .95 
 
 inverted . . . . 91, 92 
 
 the primary wave in a . . . 96 
 
 systolic period in a . . .95 
 
 tidal wave in a . . . .96 
 
 the value of a . . . .94 
 
 SPHYGMOGRAPH, THE ... 67 
 
 SPINAL CORD 
 
 diagram showing relation to sensory 
 
 nerve ..... 36 
 
 effect of reflex stimulation on . 45 
 
 irritable focus in . . . 37, 45 
 
 irritable, in visceral disease . . 37 
 
 SQUILLS 281,291 
 
 STAIRCASE PHENOMENON 
 
 produced by digitalis . . . 367 
 
 STANDARDS 
 
 for recognizing events in a cardiac 
 revolution ..... 55 
 
 STANDPOINT 
 
 from which this book is written . 5 
 
 STANDSTILL OF HEART 
 
 due to digitalis .... 367 
 
 in nodal rhythm .... 345 
 
 in sinus irregularity . . . 146 
 
 in vagus stimulation . . . 145 
 
 STANNIUS LIGATURES . . 13, 141 
 
 resemblance of, to heart-block . 187 
 
 STARTING-PLACE 
 
 of heart's contraction 
 of the nodal rhythm 
 
 STASIS, PULMONARY. See Lungs 
 
 STATUS LYJ^IPHATICUS 
 and chloroform 
 
 STERNO-MASTOID. See Muscles. 
 
 STIMULANTS 
 
 danger in the use of 
 
 STIMULI, SUMMATION OF 
 and angina pectoris 
 
 STIMULUS PRODUCTION 
 and angina pectoris 
 
 STROPHANTHUS . 
 
 13 
 142 
 
 262 
 
 66 
 
 43 
 
 7 
 43 
 
 291 
 
 STRYCHNINE . 
 
 of little use in treatment v~:i ^^. 
 
 SUFFOCATION, SENSATION OF . 
 
 in Cheyne-Stokes respiration . 
 a symptom of exhausted con- 
 tractility ..... 
 
 SUFFOCATIVE OEDEMA OF LUNGS 
 
 PAGE 
 
 SUGGESTION IN TREATMENT . 64 
 
 SULPHONAL .... 251,270 
 
 STOIMATION OF STIMULI 
 
 a cause of angina pectoris . . 43 
 
 SURGICAL OPERATIONS 
 
 how arteries recognized in . .91 
 
 SWALLOWING 
 
 effect of, on conductivity . . 362 
 
 stimulates the vagus . . .186 
 
 effect of, on the heart . . .144 
 
 SYMPATHETIC FIBRES 
 
 in s.-a. node ..... 13 
 
 SYMPATHETIC NERVES. 
 
 See Nerves of the Heart. 
 
 sy:\iptoms 
 
 classification of, in visceral disease 33 
 
 due to changes in organs . . 33 
 nature of, produced by hollow 
 
 muscular organs ... 33 
 of heart affection, confusing and 
 
 contradictory .... 5 
 
 due to impaired function of organs 33 
 
 due to nerve reflexes ... 33 
 
 . 23 
 
 . 186 
 
 . 225 
 
 . 187 
 
 . 188 
 
 . 266 
 
 . 146 
 
 277 
 
 27 
 30 
 
 193 
 32 
 
 SYNCOPE 
 
 due to digitalis 
 
 fatal in diphtheria 
 
 due to heart-block 
 
 pulse- rate during . 
 
 prognosis in . 
 
 with sinus irregularity . ' . 
 
 SYPHILIS AND CARDIO-SCLER- 
 OSIS 244 
 
 SYPHILITIC GUMMATA 
 
 causing heart-block . . . 185 
 
 SYSTOLIC PERIOD 
 
 in a cardiogram .... 78 
 in a phlebogram . . . .110 
 in a sphygmogram ... 95 
 
 TACHYCARDIA 
 
 loose employment of term . . 56 
 
 See Heart-Rate. 
 
 See Paroxysmal Tachycardia. 
 
 TAENIA TERMINALIS 
 
 contraction of, prevents regurgita- 
 tion into veins . . . .16 
 in ventricular jugular pulse . . 118 
 
 TEMPERATURE 
 
 relation of, to pulse-rate . . 215 
 
 TENDERNESS 
 
 in enlargement of the liver . . 122 
 
 THEOBROMINAE SODII SALICYLAS 212 
 THEOCIN-SODIUM ACETATE . 212
 
 INDEX 
 
 417 
 
 PAGE 
 
 THRILL 
 
 due to aortic stenosis . . . 
 due to compression of jugular vein . 
 due to mitral stenosis . • 
 due to patent ductus arteriosus 
 
 TIDAL WAVE 
 
 in a sphygmogram 
 
 TONICITY . . 
 
 function of . 
 and angina pectoris 
 effect of digitalis on 
 effects of drugs on . 
 functional murmur caused by de- 
 pression of ■ • • ■ 
 importance of, in the nodal rhythm 
 symptoms of depression of 
 
 TORTUOUS ARTERY 
 
 nature of movements of . 'JI 
 
 TRACINGS 
 
 how to take 
 
 239 
 311 
 •230 
 256 
 
 95 
 
 70 
 
 TRAINING 
 
 reserve force restored by 
 
 TRANSIENT NODAL RHYTHM. 
 See Paroxysmal Tachycardia. 
 
 TRAPEZIUS. See Muscle. 
 
 TREATMENT . • • • j^ 
 
 of angina pectoris . . ' . Z^'" 
 of acute febrile conditions of the 
 
 heart ..••■• 
 of cardio-sclerosis . . • • 
 of cases with exaggerated sensory 
 
 symptoms . . ■ • • 
 of Cheyne-Stokes respiration . 
 of congenital affections of the heart 
 of exhausted contractility 
 
 of dropsy 
 
 bearing of dilatation on . 
 of dilatation of the heart 
 of extra-systoles . 
 of exophthalmic goitre . 
 of heart failure with dropsy . 
 of high arterial pressure 
 of heart-block . • • 
 
 with enlargement of the liver . 
 of mediastino-pericarditis 
 of neui-otic patients . • • 
 of nodal rhythm with no increase in 
 rate .••••• 
 of the nodal rhythm with increased 
 
 rate ..•■•■ 
 of oedema of the lungs . 
 of paroxysmal tachycardia . 
 of cases sho^ving the pulsus alter- 
 
 266 
 
 65, 
 
 nans . 
 of valvular affections 
 aperients in . 
 ammonium bromide in 
 
 JIACKENZIE 
 
 06, 134 
 
 226 
 
 249 [ 
 
 64 
 
 30 
 257 
 199 
 211 
 207 
 211 
 164 
 134 
 272 
 103 
 190 
 128 
 255 
 270 
 
 170 
 
 171 
 213 
 173 
 
 199 
 242 
 273 
 
 .270 
 
 in 
 
 TREATMENT (continued)— 
 
 baths in .... 
 
 bodily comfort in . 
 
 deep breathing in . • . ■ ' 
 
 the condition of the bowels in 
 
 essential principle in 
 
 digitalis in ... • 
 
 drugs in .... 
 
 diet in .... 
 
 enemata in . 
 
 rules for employment of exercise 
 
 food in . 
 
 hypnotics in . . . ■ 
 
 harm of injudicious feeding in 
 
 massage in . . • ■ 
 
 importance of mastication in . 
 
 milk in 
 
 the mental factor in 
 
 Nauheim . ■ • ■ 
 
 oxygen in 
 
 position assumed by patient in 
 
 by position . • • • 
 
 rest in . 
 
 sea-bathing in . . • 
 
 I sleep in . 
 
 I at spas . . . • • 
 
 j cause of efficacy of spa . 
 
 by special exercises 
 by special movements . 
 
 I by suggestion 
 
 vaso-clilators in . 
 venesection in . • • 
 
 TRICUSPID REGURGITATION 
 
 I effect on the jugular pulse 
 
 a normal condition 
 j without a murmur 
 
 I and the venous pulse 
 
 TRICUSPID STENOSIS 
 
 cases of . . • 
 pulsation of liver in 
 sound of jugular valves in 
 symptoms of . 
 
 TRICUSPID SYSTOLIC MURMUR 
 position of . • • • • 
 
 TRICUSPID VALVE DISEASE 
 
 jugular pulse in . • • • 
 
 TRICUSPID VALVES 
 
 effect of opening of, on the jugular 
 pulse • • • • • 
 
 TUBE 
 
 primitive cardiac . • • • 
 
 TUBERCULAR MENINGITIS 
 periodic respiration in . 
 sinus irregularity in 
 
 TUBERCULOSIS 
 
 heart-rate increased in . 
 
 PAGE 
 
 . 296 
 . 270 
 210, 213 
 . 274 
 . 268 
 . 212 
 . 274 
 . 271 
 . 274 
 293 
 . 66 
 . 270 
 . 271 
 . 295 
 . 271 
 . 271 
 . 274 
 . 297 
 . 278 
 . 271 
 . 212 
 . 269 
 65, 296 
 . 269 
 . 296 
 . 299 
 . 295 
 . 295 
 64, 274 
 . 275 
 . 293 
 
 110 
 237 
 237 
 238 
 
 315, 
 125, 
 
 346 
 238 
 238 
 
 238 
 
 237 
 110 
 
 110 
 11 
 
 31 
 
 146 
 
 132 
 
 E e
 
 418 
 
 INDEX 
 
 TYPHOID FEVER 
 
 epigastric pulsation in 
 the heart in . 
 heart failure in 
 heart- rate in . 
 
 84 
 214 
 •210 
 130 
 
 prognostic sign of oedema of tlie 
 
 lungs in 210 
 
 rapid breatliing in . . . .27 
 
 ULCER, GASTRIC 
 
 contracted muscles in 
 hyperalgesia in . . . 
 meaning and pui'pose of symptoms 
 
 in .... . 
 pain in 
 
 ULCERATION OP MITRAL VALVES 
 
 38 
 38 
 
 38 
 38 
 
 221 
 
 UMBILICAL REGION 
 
 cause of pain in . . . 
 
 UNCONSCIOUSNESS 
 
 due to angina pectoris . 
 
 URETER 
 
 nature of symptoms produced by 
 
 URINE 
 
 increased secretion of, during an 
 
 attack of angina pectoris . 42, 48 
 secretion of, in dilatation of the 
 
 heart ..... 
 
 diminished secretion of, with dropsy 
 significance of diminished secretion 
 
 of 210 
 
 secretion of, in dilatation of the 
 
 heart 210 
 
 UTERUS 
 
 natui'e of symptoms produced by . 
 
 VAGUS NERVE 
 
 in s.-a. node ..... 
 
 VAGUS SENSORY REFLEX . 
 
 VAGUS STIMULATION 
 causing slow respiration 
 by deep breatliing 
 in experiment .... 
 in heart-block .... 
 
 34 
 
 49 
 
 33 
 
 206 
 
 208 
 
 33 
 
 13 
 
 41 
 
 31 
 144 
 145 
 
 186 
 
 by swallowing, producing heart- 
 block 362 
 
 by swallowing . , . 140, 186 
 producing sinus ii'regularities . 146 
 
 VALVE DEFECTS 
 
 associated with sclerosis of heart 
 
 muscle 229 
 
 the manner of heart failure due to 228 
 
 VALVES 
 
 opening of auriculo- ventricular , 81 
 
 VALVULAR DISEASES 
 
 and angina pectoris ... 57 
 and arterial pressure . . . 103 
 
 PAGE 
 
 VALVULAR DISEASES (continued)— 
 
 and chloroform .... 261 
 
 with hyperalgesia .... 57 
 
 and exhausted nervous system . 57 
 
 heart-rate increased in . . . 131 
 
 prognosis in . . . . . 242 
 
 reflex symptoms exaggerated in . 57 
 
 treatment of . . . . . 242 
 
 VALVULAR SCLEROSIS 
 progressive natirre of 
 
 VASO-CONSTRICTORS 
 in treatment 
 
 VASO-DILATING DRUGS 
 in angina pectoris . 
 in high arterial pressui-e 
 
 229 
 
 276 
 
 54 
 104 
 275 
 
 in treatment 
 
 VASOMOTOR ANGINA PECTORIS 49, 62 
 
 VEGETATIONS IN ACUTE RHEU- 
 MATISM 221 
 
 VEGETATIONS ON VALVES 
 
 after confinement .... 225 
 symptoms of .... 219 
 
 VEINS 
 
 heart's contraction starting at the 
 
 mouths of . . . . .16 
 how regmgitation into is prevented 16 
 in the fixation of the heart . . 16 
 
 VENESECTION 
 
 indications for .... 292 
 
 VENOUS PULSE. See Jugular Pulse. 
 
 ^^NTRICLE 
 
 action of pectinate fibres on . . 16 
 coui'se of dilatation of left, in mitral 
 
 stenosis ..... 203 
 exhaustion of the left, a cause of 
 angina pectoris .... 46 
 
 filling of 81 
 
 fixation of the .... 16 
 perception of contraction of . .76 
 period of contraction of . . .78 
 period of filling of . . . .81 
 period of relaxation of . . .80 
 
 VENTRICULAR CONTRACTION 
 
 electro-carcUogram of . . . 373 
 
 \TENTRICULAR FALL 
 
 in a jugular pulse . . . 109,111 
 
 VENTRICULAR EXTRA-SYSTOLE . 151 
 
 VENTRICULAR HYPERTROPHY 
 in aortic valve disease . 
 
 239 
 
 VENTRICULAR JUGULAR PULSE 116 
 
 auricular hypertrophy in . .118 
 
 auricular wave in . . . .118 
 
 significance of . . . 117,238 
 
 VENTRICULAR LIVER PULSE . 124
 
 INDEX 
 
 419 
 
 VENTRICULAR MUSCLE 
 action on a. -v. septum . 
 insertion of . 
 relaxation of 
 
 PAGE 
 
 16 
 
 16 
 
 80 
 
 \^ENTRICULAR OUTFLOW . . 80 
 
 VENTRICULAR PRESSURE-CURVE 108 
 
 VENTRICULAR RHYTHM 
 
 definition of ... xx, 175 
 
 due to heart-block . . .182 
 
 inexcitability of the ventricle in . 189 
 
 starting-place of . . . . 143 
 
 symptoms associated with . .187 
 
 VENTRICULAR SYSTOLE 
 
 action of, on auricle ... 16 
 retraction of structures due to . 81 
 shock due to . . . . 86,88 
 
 VENTRICULAR VENOUS PULSE 
 
 different forms of . . . .116 
 
 VENTRICULAR WAVE 
 
 in a jugular pulse .... 110 
 
 VERATRIN 
 
 action on tonicity 
 
 VERONAL 
 
 VISCERA 
 
 insensitiveness of . 
 
 9 
 
 251,270 
 
 VISCERAL DISEASES 
 
 classification of symptoms in . 
 diagram showing mechanism of re- 
 flexes in .... . 
 effect of, on spinal cord . 
 
 34 
 
 33 
 
 36 
 37 
 
 VISCERAL DISEASES {continuci)— 
 
 hyperalgesia in ... . 55 
 mental state in . . . .55 
 reaction of, on central nervous 
 
 system 55 
 
 VISCERAL REFLEXES 
 
 purpose of 37 
 
 VISCEROMOTOR REFLEX 
 
 in angina pectoris ... 41 
 
 in cardio-sclerosis ... 41 
 
 in old age ..... 41 
 
 VISCEROSENSORY REFLEX . 35 
 
 in angina pectoris .... 40 
 
 WARMTH 
 
 feeling of, in exophthalmic goitre . 133 
 
 WASTING 
 
 in heart failure .... 209 
 
 WATER-HAMMER PULSE . . 240 
 
 WHISKY 
 
 during an attack of angina pectoris .53 
 
 WHORL 
 
 muscle- fibres constituting . . 16 
 
 WORRY 
 
 effect of on heart 
 
 X DISEASE 
 
 and the sinus irregularity 
 slow pulse-rate in . 
 symptoms of the . 
 
 . 270 
 
 146 
 139 
 
 60
 
 ^ Y?'' MAY i U 133D 
 
 ^T^-'-r^