COLUMBIA LIBRARIES OFFSITE HEALTH SCIENCES STANDARD HX641 34210 RC681 .N391917 Clinical cardiology, v d* CHolUsf nf pi|gBirtattB anh &str$*anB $ urrtjaarti bg tttr \ ?V Digitized by the Internet Archive in 2010 with funding from Open Knowledge Commons http://www.archive.org/details/clinicalcardioloOOneuh CLINICAL CAKDIOLOGY •The THE MACMILLAN COMPANY NEW YORK • BOSTON • CHICAGO • DALLAS ATLANTA - SAN FRANCISCO MACMILLAN & CO., Limited LONDON • BOMBAY • CALCUTTA MELBOURNE THE MACMILLAN CO. OF CANADA, Ltd. TORONTO CLINICAL CARDIOLOGY BY SELIAN NEUHOF, B.S., M.D. VISITING PHYSICIAN, CENTRAL AND NEUROLOGICAL HOSPITAL ADJUNCT ATTENDING PHYSICIAN, LEBANON HOSPITAL THE MACMILLAN COMPANY 1917 All rights reserved Copyright, 1917, By THE MACMILLAN COMPANY. Set up and electrotyped. Published September, 1917. Nortaooo ^reas J. S. Cushing Co. — Berwick & Smith Co. Norwood, Mass., U.S.A. TO i MY PARENTS IN TRIBUTE TO THEIR CONSTANT SELF- SACRIFICE, THIS BOOK IS AFFECTIONATELY DEDICATED PREFACE In the many recent books on cardiac disease, dealing chiefly with polygraphy, electrocardiography, and orthodiascopy, there has been much confusion regarding the proportionate value of graphic methods, with the result that undue emphasis has been placed upon purely in- strumental and technical considerations. The author has, therefore, included in this book the graphic as well as the usual bedside methods, while writing from the clinician's, rather than from the cardiologist's standpoint, and he believes that this work will therefore supply a com- prehensive,, practical reference book for both practitioner and student. The opening chapters are devoted to a description of instrumental and graphic methods in the study and examination of normal and abnormal rhythms and of normal and abnormal silhouettes. From a study of these chapters, the physician is enabled to discern the rela- tion and application of instrumental methods to clinical cardiology and bedside examination. Without minimizing their importance, I have emphasized the fact that instrumental methods are not infrequently subsidiary. Indeed, as will be shown, graphic devices may sometimes be dispensed with if their fundamental significance is comprehended. Subsequent chapters are devoted to the purely clinical side of cardi- ology. Careful consideration is given to the important subjects of the pathology, etiology, diagnosis, prognosis, and therapy of endocarditis, myocarditis, and cardiosclerosis. Questions occurring in everyday practice with reference to diet, exercise, and general management of heart disease are fully dealt with. There are special chapters on pre- cordial pains, blood pressure, and the heart in pneumonia. I desire to express my sincere thanks to Dr. Alfred E. Cohn of the Rockefeller Institute for valuable aid and suggestions, especially on the chapters dealing with the arrhythmias ; to my publishers, The Mac- millan Company, for courteous cooperation ; and to my wife, without whose aid and stimulus this book could not have been written. Vll CONTENTS PAGE Chapter I. The Heart 1 Its Development — Position in the Chest — Anatomy and Physi- ology — Nerve, Lymphatic, and Arterial Supply. Chapter II. The Conduction System 7 Position and Structure of the Pacemaker — Nerve and Arterial Supply — Position, Distribution, Dissection, and Structure of the Auriculo-ventricular Conduction System — Course of the Normal Impulse — Neurogenic or Myogenic Impulse ? Chapter III. Polygraphic Tracings 12 Mackenzie Polygraph — Venous Pressure Curves — Schematic Curves — Phlebogram — Physiological Variations — Dicrotic Wave — Types of Pulse — Radial Palpation. Chapter IV. The Electrocardiogram 22 Fundamental Physiological Considerations — Electrocardiographic Apparatus — Methods of Taking the Electrocardiogram — The Three Leads — Normal Electrocardiogram — Its Interpretation — Normal and Abnormal Electrocardiograms — Variations Due to Change of the Ventricular Axis — Squatty, Vertical, and Drop Hearts — Shift of the Interventricular Septum — Ventricular Hypertrophy and Dilatation — Congenital Dextrocardia — Phasic Variation with Breathing — Different Positions of the Heart in the Chest — Intra- ventricular Block — Abnormally Wide R. Chapter V. Mathematical Considerations Underlying the Electrocardiogram . . . . . . • . . .39 " Manifest" Size — Angles Produced by the Leads with the Electri- cal Axis — Their Mathematical Measurement and Approximation. Chapter VI. Course of the Excitation Wave .... 44 Effect of Vagus and Accelerator Stimulation upon the Electro- cardiogram. T Wave : Its Variations and Clinical Significance. Chapter VII. The Arrhythmias — Their Polygraphic, Electro- cardiographic, and Clinical Recognition ..... 47 Tabulation — Auricular Arrhythmias — Ventricular Arrhythmias — True Bradycardia — Arrhythmias from Disturbances in the Sino- auricular and the Atrio-ventricular Nodes. Alternation — Pulsus Paradoxus. ix x CONTENTS PAGE Chapter VIII. The Arrhythmias, Their Etiology and Therapy . 96 General Considerations — Sinus Arrhythmia — Sino-auricular Block — Extras y stoles — True Bradycardia. Heart Block : Etiology — Cardiac Disease — Drugs — Asphyxia — Chemical Poisons — Interference with Cerebral Circulation — Abnormal Pressure on the Cardio-inhibitory Center — Abnormal Pressure on the Vagus — ■ Increased Vagal Inhibition by Digital Pressure, and by Reflex Peripheral Excitation. Prolonged Conduction Time — Shortened Conduction Time — Auricular Fibrillation — Simple Tachycardia — Paroxysmal Tachy- cardia — Auricular Flutter — Ventricular Escape. Chapter IX. Orthodiascopy and Fluoroscopy .... 110 Their Advantages — Description of the Orthodiascopic Apparatus — Its Use Combined with Fluoroscopy — Normal Orthodiascopic Tracing — Its Measurement — Objections to Measurement as a Standard — Abnormally Broad and Abnormally Slender Hearts — Orthodiagrams and Fluoroscopy in Mitral and Aortic Valvular Lesions — Aortitis Involving the First Portion, Arch and Descending Thoracic Aorta — Congenital Cardiac Malformations of the Aorta — Patent Ductus Arteriosus — Patent Interventricular Septum — Pat- ent Foramen Ovale. Chapter X. Physical Examination of the Heart . . . 129 Inspection — Palpation — Percussion — Rational Method for the Determination of the Cardiac Outline — Auscultation — Valvular Murmurs — Murmurs in Atherosclerosis — Non-organic " Func- tional" Murmurs of Intracardiac Origin — Third Heart Sound — Extracardiac Inorganic Murmurs — Cardio-respiratory and Cardio- pulmonary Murmurs — Reduplicated Sounds — Reduplicated Apical Impulse — Reduplicated First and Second Sounds. Chapter XI. Etiology of Endocarditis and of Cardiovascular Disease 149 Classification — Chemical Agents — Metallic Poisons — Lead — Alcohol — Tobacco : Experimental Observations, Neurotropic Ac- tion — Diabetes — Gout — Food Metabolism : Experimental and Clinical Evidence — Bacterial Toxins — Diphtheria : Myocardial Changes, Heart Block, Milder Toxemia, Arrhythmias, Unexpected Death — Pneumonia — Heart Block in Pneumonia, Effect of Pneu- monia on the Heart Muscle, Experimental Evidence, Cardiovascular Disease as a Late Sequela — Rheumatism and Tonsillitis — Relation between Rheumatism and Tonsillitis — Pyorrhea Alveolaris — Strepto- coccus Viridans in the Mouth — Pyogenic Abscesses — Bacterial Endo- carditis : Its Relation to Rheumatism — Classification of Organisms : Their Frequency — Frequency of Affections of the Various Valves — Streptococcus Viridans — Renal Infarction — Distinction between Acute and Chronic Streptococcus Viridans — Spirochetal Infection — Syphilis: Pathological Changes, Wassermann Reaction. CONTENTS xi Chapter XII. Pathology of the Endocardium and Myocardium — Pathology of Cardiosclerosis ....... 160 Chapter XIII. Symptomatology, Therapy, and Prognosis of Rheu- matic Endocarditis 165 Clinical Phenomena and Signs of Acute Rheumatic Endocarditis — Endocardial Exacerbations — Clinical Phenomena of Chronic Rheu- matic Endocarditis — Decompensation — Types of Dyspnoea — "Acidosis " — Cyanosis — Visceral Congestion — Special Signs and Symptoms of Decompensation in the Various Valvular Lesions — Paralysis of the Left Recurrent Laryngeal in Mitral Stenosis — - Therapy in Acute and Chronic Rheumatic Endocarditis — • Prognosis in Acute and Subacute, Quiescent, and Chronic Stages. Acute Bacterial Endocarditis 176 Symptomatology — Therapy. Subacute and Chronic Streptococcus Viridans Infection. Pathology — Clinical Course — Petechias — Heubner's Nodes — Skin Gangrene — Hematology — Renal Manifestations — Neuro- logical Manifestations — Cardiac Manifestations — Blood Culture — Bacteria-free Stage — ■ Therapy. Chapter XIV. Cardiac Syphilis ....... 184 The Heart in Secondary and Tertiary Syphilis — Myocarditis — Aortitis. Physical Signs of Aneurismal Dilatation of the First Portion and Arch of the Aorta — Diagnosis, Symptomatology, Prognosis, and Therapy of Dilatation Aneurisms of the Descending Thoracic Aorta. Chapter XV. Symptomatology, Physical Signs, Diagnosis and Prognosis of Myocarditis and Cardiosclerosis — Physical Signs and Diagnosis of Ventricular Hypertrophy . . . 194 Chapter XVI. Therapy in Circulatory Disease .... 206 Digitalis : General Considerations, Use in Auricular Fibrillation and Other Arrhythmias, Arrhythmias Produced by Digitalis, Cause of Digitalis Vomiting and Its Prevention — Preparations and Dosage, Coupled Rhythm and Digitalis, Use of Digitalis in Decompensation with Regular Pulse, Cumulative Effect, Continuance of the Effect of the Drug, Possible Dangers, Other Therapeutic Indications, Sum- mary and Conclusions. Tincture Strophanthus : Strophanthin — Squills — Apocynum — Caffeine and Its Derivatives : Theobromin Sodium Salicylate. Karrell Diet : Its Use, Indications, and Modification — Strych- nine — Nitrite Group — Camphor — Alcohol — Aconite — Spartein — Adrenalin — Sedatives — Acetate of Potash and Sodium — Purging Salts — Calomel — Venesection — Vaccines — Sera — Silver Prepa- rations — Massage — Passive Motion — Calisthenics — Medical Gym- nastics — Resistance Exercises — Walking — Hydrotherapy — Baths : Carbonated and Oxygenated Baths — Tonsillectomy — Extraction of Teeth. xii CONTENTS PAGE Chapter XVII. Diet, Renal and Blood Tests in Cardiac Disease 229 General Considerations — Diet in Compensated Endocarditis — In Obese Individuals — In Myocardial Insufficiency with and without Edema — Tests for Renal Insufficiency : Phenolsulphophthalein Test : Method of Administration, Conclusions — Nephritic Test Diets — Estimation of Water, Salt, and Urea Output in the Urine — Chemi- cal Examination of the Blood : Non-protein Nitrogen — Diet in Cardiosclerosis and Nephritis — Sugar Solution and Bicarbonate of Soda in Nephritis. Chapter XVIII. Management of Cardiac Disease . . . 235 Fundamental Considerations — Types of Exercise and Occupation — Functional Efficiency Tests — Indications for Drug Therapy. Marriage in Women with Valvular Lesions .... 237 General Considerations. Cardiac Symptoms during Gestation — Prognostic Consideration of the Various Valvular Lesions, Indications for Terminating Pregnancy. Chapter XIX. Blood Pressure 242 Physiological Considerations ; Factors Involved, Cardiac Energy, Peripheral Resistance, Elasticity of Arterial Walls, Volume of Cir- culating Blood, Viscosity of Blood — Clinical Estimation of Blood Pressure — Types of Instruments — Methods of Blood Pressure Estimation : Auscultatory Method and Its " Phases " — Normal Blood Pressure : Physiological Variations — Effect of Alcohol, Excitement, Cyanosis, Smoking — Increased Intracranial Pressure — Hypertonus — Clinical Classification for Study of Blood Pressure — Hypertensive Cardiovascular Disease with Myocarditis — Hyper- tension and Myocardial Insufficiency with Labile Vasomotor Mecha- nism — Uremic Group — Myocardial Disease and Insufficiency without Hypertension — Valvular Disease and Myocardial Insuffi- ciency with and without Hypertension — Hypotension — Blood Pressure in Cardiac Arrhythmias — Therapeutics of Hypertension : Vasodilators, Venesection, Hydrotherapy, Diathermy, Diet, Exercise. Chapter XX. "Weak" Heart 255 Clinical Symptoms — Illustrative Cases — Therapy. Chapter XXI. Precordial Pains of Cardiovascular and Extra- cardiac Origin — Angina Pectoris 258 Historical — Confusion of Terms — Cardiovascular Nerve Sup- ply — Epigastric Pains and Heart Disease — Intra- and Extra-cardiac Disease — Classification of Common Causes of Precordial Pain — Organic Cardiovascular Disease : Illustrative Cases — Extracar- diac Disease : Illustrative Cases. Chapter XXII. Therapy of Pneumonia from the Circulatory Standpoint 273 LIST OF PLATES Plate I Plate II Plate III Plate IV Plate V — Plate VI Plate VII — Plate VIII — Plate IX Fig. 7 Fig. 32 Fig. 33 Fig. 36 Fig. 39 Fig. 40 Fig. 41 Fig. 42 Fig. 45 Fig. 47 Fig. 48 Fig. 49 Fig. 50 Fig. 51 Fig. 52 Fig. 53 Fig. 54 Fig. 55 Fig. 56 Fig. 59 Fig. 60 Fig. 61 Fig. 62 Fig. 63 Fig. 65 Fig. 66 Fig. 67 Fig. 68 Fig. 69 Fig. 73 Fig. 74 Fig. 75 Fig. 76 Fig. 95 Fig. 96 Fig. 97 Fig. 98 opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite opposite page page page page page page page page page page page page page page page page page page page page page page page page page page page page page page page page page page page page page 12 23 24 2S 2S 2^ 28 30 30 30 30 30 33 33 33 33 33 33 35 35 35 35 35 35 35 35 37 37 37 52 52 XIV Plate X Plate XI Plate XII Plate XIII Plate XIV — LIST OF PLATES Plate XV Plate XVI Plate XVII Plate XVIII Plate XIX Plate XX Fig. 99 Fig. 130 Fig. 131 Fig. 132 Fig. 134 Fig. 135 Fig. 137 Fig. 140 Fig. 144 Fig. 163 Fig. 177 Fig. 162 Fig. 169 Fig. 183 Fig. 179 Fig. 197 Fig. 198 Fig. 202 Fig. 203 Fig. 233 Fig. 234 opposite page 62 opposite page 62 opposite page 62 opposite page 63 opposite page 63 opposite page 63 opposite page 63 opposite page 64 opposite page 66 opposite page 66 opposite page 66 opposite page 74 opposite page 74 opposite page 74 opposite page 82 opposite page 82 opposite page 91 opposite page 110 opposite page 111 opposite page 122 opposite page 123 COMPLETE LIST OF ILLUSTRATIONS Fig. 1 — Heart of the human embryo. 2 — Diagrammatic position of the cardiac valves. 3 — Schematic view of sino-aucurilar node of dog. 4 — Detail of the S-A node of dog. 5 — Right ventricle of ox heart, showing the auriculo-ventricular node (A-V node) and the main stem. 6 — Left ventricle of ox heart, showing conduction system. 7 — Plate I — Mackenzie Ink Polygraph. 8 — Schematic view of the a-c-v waves and of the jugular bulb. 9 — Diagrammatic representation of the normal polygraphia curve. 10 — Normal venous and radial tracing. 11-13 — Split c(c-c) waves in the venous tracing. 14 — Combined venous and arterial tracing in the jugular. 15-16 — h wave in the jugular tracing. 17 — Normal phlebogram in aortic regurgitation. 18-19 — Normal jugular tracing in aortic stenosis and double mitral lesion. 20 — Normal a and other peaks in mitral stenosis. 21 — Normal a wave in mitral regurgitation. 22-25 — Normal jugular tracings in exophthalmic goiter. 26 — Normal radial pulse tracing. 27 — Low dicrotic notch in aortic regurgitation. 28 — Low dicrotic notch in aortic aneurism. 29 — Scheme of monophasic action current. 30 — Scheme of diphasic action current. 31 — Scheme of rheostat and connection with the galvanometer. 32 — Plate II — Photograph of the Electrocardiographic Apparatus in Position. 33 — Plate III — Photograph of patient with electrodes cbnnected with the galvanometer. 34 — Diagram illustrating the three leads. 35 — Schematic representation of a typical electrocardiogram. 36 — Plate IV — Electrocardiogram showing the deflection time of the string. 37 — Normal electrocardiogram. 38 — Scheme showing the angles made by the leads with the varying ven- tricular axes. 39 — Plate IV — Electrocardiogram of normal patient ; negative R in L III. 40 — Plate IV — Electrocardiogram of normal patient ; negative R in L III. 41 — Plate IV — Electrocardiogram of normal patient ; negative R in L III. XV xvi COMPLETE LIST OF ILLUSTRATIONS Fig. 42 — Plate V — Electrocardiogram of patient with narrow heart. 43 — Orthodiascope tracing of heart of normal child lying on its back (A), left (B) and right (C) sides. 44 — Orthodiascopic tracing of heart of normal child lying on its back (A), left (B) and right (C) sides. 45 — Plate V — Electrocardiogram of a child whose orthodiascopic tracing is Fig. 148. 46 — Electrocardiogram of congenital dextrocardia. 47 — Plate V — Electrocardiogram of acquired dextrocardia. 48-49 — Plate V — Electrocardiogram showing slight respiratory phasic varia- tion. 50 — Plate VI — Electrocardiogram of marked respiratory phasic variation. 51 — Plate VI — Electrocardiogram of aneurismal dilatation of the aorta and left ventricular hypertrophy. 52 — Plate VI — Electrocardiogram of aortic stenosis and left ventricular hypertrophy. 53 — Plate VI — Electrocardiogram of left ventricular hypertrophy. 54 — Plate VI — Electrocardiogram of aortic regurgitation and left ventric- ular hypertrophy. 55 — Plate VI — Electrocardiogram of congenital ductus arteriosus. 56 — Plate VII — Electrocardiogram showing an interpolated extrasystole and an abnormally wide R. 57 — Electrocardiogram of advanced mitral stenosis and auricular fibrillation. 58 — Electrocardiogram of advanced mitral stenosis and auricular fibrillation. 59 — Plate VII — Electrocardiogram of thickened R summit. 60 — Plate VII — Electrocardiogram of notched R summit. 61 — Plate VII — Electrocardiogram of split R (M complex). 62 — Plate VII — Electrocardiogram of split R {W complex). 63 — Plate VII — Electrocardiogram of split R (W complex). 64 — Electrocardiogram of notched P wave in mitral stenosis. 65 — Plate VII — Electrocardiogram of intraventricular block. 66 — Plate VII — Electrocardiogram of ventricular complexes of abnormal width and normal form. 67-69 — Plate VIII — Electrocardiograms of ventricular complexes of abnor- mal width and normal form. 70-71 — Diagrams of relation of the ventricular axis to the leads. 72 — Diagram of the direction of the leads to the electrical axes. 73 — Plate VIII -^ Electrocardiogram showing tall T II. 74 — Plate VIII — Electrocardiogram showing T taller than R. 75 — Plate VIII — Electrocardiogram showing negative T III. 76 — Plate IX — Electrocardiogram showing diphasic T II and negative T II and T III. 77-82 — Diagrams showing the origin of physiological and pathological con- tractions. 83-87 — Polygrams of ventricular extrasystoles. COMPLETE LIST OF ILLUSTRATIONS xvii Fio. 88-92 — Polygrams of auricular extrasystoles. 93-94 — Polygrams of multiple auricular extrasystoles. 95-98 — Plate IX — Electrocardiograms of auricular extrasystoles. 99 — Plate X — Electrocardiogram of auricular extrasystoles coming from two ectopic foci. 100-101 — Polygrams of varying ventricular rates in exophthalmic goiter. 102 — Polygram of paroxysmal tachycardia. 103-106 — Polygrams of exophthalmic goiter. 107-120 — Polygrams of various types of auricular fibrillation. 121 — Polygram of auricular fibrillation with anacrotic radial pulse. 122 — Polygram of auricular fibrillation and fibrillary (/) waves. 123 — Polygram of auricular fibrillation. 124 — Polygram of auricular fibrillation with rhythmical radial pulse. 125-129 — Arteriograms of auricular fibrillation illustrating pulse irregularities. 130 — Plate X — Electrocardiogram showing small, fairly regular fibrillation waves. 131 — Plate X — Electrocardiogram showing very fine fibrillation waves. 132 — Plate XI — Electrocardiogram showing fairly regular fibrillation waves resembling flutter. • 133 — Electrocardiogram with fine fibrillation waves. 134 — Plate XI — Electrocardiogram with various types of fibrillation waves. 135 — Plate XI — Electrocardiogram with very fine fibrillation waves. 136 — Electrocardiogram with fairly regular fibrillation waves. 137 — Electrocardiogram of auricular fibrillation showing tachycardia. 138 — Electrocardiogram of auricular fibrillation with ectopic beats. 139 — Electrocardiogram of auricular fibrillation with coarse waves. 140 — Electrocardiogram of auricular and ventricular extrasystoles, and auric- ular fibrillation. 141-143 — Polygrams of auricular flutter. 144 — Plate XIII — Electrocardiogram of auricular flutter ; incomplete heart block (4:1). 145 — Electrocardiogram of paroxysmal auricular tachycardia and auricular fibrillation. 146 — Electrocardiogram of nodal extrasystole. 147-148 — Polygrams of nodal extrasystoles. 149-150 — Polygrams of ventricular extrasystoles with compensatory pauses. 151 — Polygram of ventricular extrasystole with decreased compensatory pause. 152-153 — Polygrams of ventricular extrasystoles without compensatory pauses. 154 — Schematic view of types of ventricular extrasystole showing the direc- tion of the corresponding R deviations. 155 — Electrocardiogram of ventricular extrasystole from right ventricle near the base. 156 — Electrocardiogram of ventricular extrasystole from left ventricle near the base. 157 — Electrocardiogram of ventricular extrasystole from wall of left ventricle. xviii COMPLETE LIST OF ILLUSTRATIONS Fig. 158 — Electrocardiogram of extrasystoles arising from various ventricular foci, with complete heart block. 159 — Electrocardiogram of coupled rhythm (pulsus bigeminus). 159 A-159 B — Polygram of frustrate ventricular extrasystoles (coupled rhythm) . 160 — Electrocardiogram of paroxysmal tachycardia of ventricular origin. 161 — Polygram of ventricular escape. 162 — Plate XIV — Electrocardiogram of ventricular escape. 163 — Plate XIII — Electrocardiogram of lesion of the left branch of the con- duction system. 164 — Electrocardiogram of lesion of the right branch of the conduction system. 165-168 — Polygrams of true bradycardia. 169 — Plate XIV — Electrocardiogram of true bradycardia. 170-171 — Arteriograms of sinus arrhythmia. 172 — Arteriogram of sinus slowing. 173 — Arteriogram of slight sinus arrhythmia. 174-175 — Polygrams of sinus arrhythmia. 176 — Polygram of sinus arrhythmia, non-respiratory type. 177 — Electrocardiogram of sinus arrhythmia of respiratory origin. 178 — Electrocardiogram of sino-auricular block due to smoking. 179 — Plate XV — Electrocardiogram of sino-auricular block. 180 — Diagram showing the effect of nicotine upon the vagus and accelerators. 181 — Electrocardiogram of blocked auricular beat. 182 — Electrocardiogram showing very slow ventricular rate and .prolonged P-R time. 183 — Plate XIV — Electrocardiogram of prolonged conduction time. 184 — Electrocardiogram of backward conduction from ventricle to auricle. 185 — Polygram of incomplete block. 186 — Polygram of incomplete block and ventricular extrasystole. 187-192 — Polygrams of complete heart block. 193 — Polygram of complete heart block and irregular ventricular action. 194 — Polygram of complete heart block and ventricular extrasystole. 195 A and B : — Polygrams of heart block, ectopic beats and auricular fibrillation. 196 A and B — Polygrams of prolonged conduction time and heart block. 197 — Electrocardiogram of complete heart block. 198 — Electrocardiogram of incomplete and complete heart block. 199 — Arteriogram showing slight alternation. 200-201 — Arteriograms of alternation following extrasystoles. 202 — Plate XVII — Groedel Apparatus. 203 — Plate XVIII — Details of marking mechanism of Groedel apparatus. 204 — Orthodiascopic tracing of normal heart. 205 — Orthodiascopic tracing of long and slender heart. 206 — Copy of an orthodiascopic tracing of a broad heart. 207-208 — Orthodiascopic tracings of abnormally slender hearts ('drop' hearts) . 209 — Orthodiascopic tracing of compensated mitral regurgitant lesion. COMPLETE LIST OF ILLUSTRATIONS xix Fig. 210 — Orthodiagram of compensated double mitral lesion. 211-213 — Orthodiagrams of globular hearts of cases of decompensated double mitral lesions with auricular fibrillation. 214 — Orthodiagram of globular heart of extreme size. 215-216 — Orthodiascope tracings of slightly globular hearts with moderate enlargement. 217 — Orthodiagram of extreme, rounded right-sided enlargement. 218 — Orthodiascope tracing of double mitral lesion. 219 — Orthodiascope tracing of recent mitral regurgitant lesion. 220 — Orthodiagram of mitral regurgitant lesion showing a somewhat ovoid contour. 221 — Orthodiagram of old rheumatic double aortic lesion. 222 — Orthodiagram of aortic regurgitation. 223-224 — Orthodiagrams of double mitral and aortic lesions. 225 — Orthodiagram of dilatation of aortic arch with left ventricular hyper- trophy. 226 — Orthodiagram of aortitis. 227 — Orthodiagram of dilatation of aortic arch and left ventricular hyper- trophy. 228 — Orthodiagram of aortitis of first portion and arch of the aorta, and extreme left ventricular hypertrophy. 229 — Orthodiagram of luetic aortitis and left ventricular hypertrophy. 230 — Orthodiagram of enlargement and low implantation of the first portion of the aorta, and moderate enlargement of the left ventricle. 231 — Orthodiagram of luetic aortitis and left ventricular hypertrophy. 232 — Orthodiagram of diffuse aneurismal dilatation of the descending thoracic aorta. 233 — Plate XIX — Photograph from X-ray plate, showing aneurismal dila- tation of the descending thoracic aorta. 234 — Plate XX — Photograph from Roentgenogram of aneurismal dilatation of the descending thoracic aorta. 235 — Orthodiagram of aneurismal dilatation of the arch and descending thoracic aorta. 236 — Orthodiagram of aneurism of the first portion of the aorta due to con- genital aortic stenosis. 237 — Orthodiagram of double mitral lesion and aortic aneurism. 238 — Orthodiagram of patent ductus arteriosus. 239 — Orthodiagram of congenital dextrocardia and patent interventricular septum. 240 — Diagram of probable cardiac circulation in patent interventricular septum. 241 — Outline of heart with dilated right auricle. 242-246 — Diagrams of difference in percussion and orthodiascope outlines of normal and abnormal hearts. 247 — Orthodiascope tracing from a case of mitral stenosis and left recurrent laryngeal paralysis. \L£FT CLINICAL CARDIOLOGY CHAPTER I THE HEART Development of the Heart. — In very early fetal life the heart is represented by a simple tube, the cardiac tube. It consists of two dis- tinct strata : an inner, thinner layer, derived from the hypoblast, which later becomes the endocardium ; and an outer, thicker layer, derived from the visceral mesoblast, which finally develops into the musculature. Later, the cardiac tube elongates and becomes bent upon itself so as to form an S-shaped loop, with an anterior right, and a posterior left angle. Slight constrictions soon appear, which serve to divide the loop into four parts (Fig. 1) : (1) the sinus venosus (sinus reuniens of His), (2) the common auricle, (3) the common ven- tricle, (4) the aortic bulb. The sinus venosus is at first situated transversely behind the com- mon auricle and connects with the latter by a median aperture ; it afterwards becomes oblique and divides into two projections or horns: the ev ' right forms part of the right auricle, the line of FiG 1> _ Heartc f thehu- union being marked in the adult heart by a ver- man embryo 5 mm. long. tical crest, the crista terminalis of His; the left (Modified from His.) horn persists as the coronary sinus. The com- mon auricle (C.A) becomes partitioned off into right and left auricles by the gradual formation of a septal wall, the septum superius ; the foramen ovale results from a perforation of this wall. Another sep- tal structure, the septum inferius, similarly forms, and separates^ the common ventricle {C.V) into right and left chambers. For some time, however, it does not quite reach the auricular canal, thus leaving a foramen between the auricles and ventricles, the common auric- ulo-ventricular orifice. The formation of a septum is also responsible for the division of the aortic bulb (A.B) into the two great vessels, — the aorta and the pulmonary artery. Position of the Fetal Heart. — In early fetal life, the heart lies im- mediately under the head and is of relatively large size. Later, it be- comes a thoracic organ, lying at first vertically, then gradually assuming B 1 CLINICAL CARDIOLOGY a more oblique position. The auricular portion with its intercommunica- tion (the foramen ovale) is at first larger than the ventricle. By means of the ductus arteriosus (ductus Botalli), the blood from the right ventricle and pulmonary artery passes mainly to the aorta instead of to the lungs. To carry on this circulation, the wall of the right ventricle is correspondingly muscular and as thick as that of the left. Toward the end of fetal life, the left ventricle becomes thicker and heavier than the right. Weight of the Adult Heart and Position of the Valves. — The aver- age normal adult heart weighs, in the male, from 280 to 360 grams (9i to 12 oz.), in the female, from 240 to 330 grams (8 to 11 oz.) ; its proportion to body weight ranges approxi- mately from 1 : 160 to 1 : 170. Though hearts vary considerably in size within normal limits, the average length of the adult heart on its longest axis is from twelve to fifteen centimeters, its greatest breadth, nine to eleven centimeters. The adult heart lies behind the lower two thirds of the sternum. The methods for deter- mining the position of the valves with the heart in situ by frozen sections, and also by coating the valvular surface with lead and subse- quently taking radiographs, have not given uniform results. Accord- ing to Piersol, the aortic valves lie behind the left half of the sternum, a little below and to the right of the pulmonary valves ; the latter are situated behind the sternal end of the third left costal cartilage. The tricuspids are situated behind the midsternum, opposite the fourth interspace and the fifth chondro-sternal articulation ; the mitral valves are opposite the sternal end of the third left interspace (Fig. 2). Anatomy and Physiology of the Heart. — The heart consists of three layers : the endocardium, pericardium, and myocardium. The endo- cardium is a connective tissue membrane containing smooth muscle and numerous elastic fibers. Its free endocardial surface consists of a single layer of irregularly shaped polygonal endothelial cells. The epi- cardium is a connective tissue structure containing fat cells and elastic fibers; its outer surface is covered with a single layer of squamous Fig. 2. — Diagrammatic position of the cardiac valves. P.V = pulmonary valves ; T.V — tricuspid valves ; A.V = aortic valves ; M.V = mitral valves. THE HEART 3 epithelium. The muscle fibers of the heart although transversely striated, must be regarded, developmentally and histologically, as modifications of smooth muscle. The undifferentiated protoplasm of the heart muscle fiber — the sarcoplasm — is found chiefly in its axial part. The oval nucleus, which frequently contains oil droplets or pig- ment granules, is embedded in the sarcoplasm. The muscle cells anas- tomose by means of short, oblique, or transverse processes into various complexes and layers. In the auricular musculature there is a super- ficial muscular layer which runs transversely and encircles both auricles. Each auricle also possesses a relatively independent system of fibers which runs at right angles to the superficial layers. The course of the ventricular fibers and layers is quite complex and as yet a matter of uncertainty. According to the most reliable studies, the fibers on the ventricular surface arise from tendinous rings and membranes at the base of the heart ; here they form a vortex, pass into the interior of the left ventricle to the septum, and connect with the papillary muscles ; they thus turn on themselves toward the base and form spiral loops, which when contracting, approximate base and apex, and at the same time rotate the apex clockwise from left to right. Mall divides these " super- ficial fibers " into two groups : the Superficial Bulbo-spiral and Super- ficial Sino-spiral. The former belong chiefly to the left ventricle. They arise from the conus to the left of the aorta and left ostium venosum, proceed spirally, penetrate to the interior of the left ventricle and end in the septum and posterior aspect of the ventricle ; at that point they connect with the posterior papillary muscles. Some of the deeper fibers of this layer encircle the lower part of the ventricle and pass upward, to end at the base of the heart. The superficial sino-spiral fibers arise mainly from the posterior aspect of the heart in the neighborhood of the right ostium venosum, proceed spirally (though more transversely than the first group) to the apex over the anterior surface of the right ventricle. They penetrate the interior of the left ventricle and terminate on its anterior surface and in the papillary muscles, especially the anterior. Beneath the superficial layers of the bulbo- and sino-spiral systems lie similar deep layers which run more transversely or circularly. The deep bulbo-spiral layer encircles the left ventricle and ends by way of the septum on the dorsal side of the aorta. Some fibers make a circular loop around the conus at the base of the pulmonary artery. The entire layer makes a strong circular system whose contraction tends to diminish the lumen of the left ventricle. The deep sino-spiral layer originates from the posterior aspect of the left ostium venosum, passes transversely to enter the interior of the right ventricle, and then turns upward toward the base. Here some strands pass circularly around the base of the heart and left ostium. The arterial supply of the heart is derived from the right and left coronaries. Though often so regarded, they are not end arteries, for anastomoses have been clearly demonstrated by Spalteholz's method. 4 CLINICAL CARDIOLOGY Furthermore, blood is sometimes found beyond an old, complete obstruc- tion of the coronary artery. The veins accompany the arteries and empty in the right auricle. The lymph vessels are very abundant; they are formed from radicals derived from the lymph spaces in the clefts between the muscle fibers; they accompany the blood vessels in their course and terminate in the thoracic and right lymphatic ducts. Attributes of the Cardiac Musculature. — Engelmann and Gaskell, by careful experimentation some thirty-five years ago, established certain attributes of the cardiac musculature, namely : irritability, contractility, rhythmicity, and conductivity. These have been respectively desig- nated by Engelmann as bathmotropic, inotropic, chronotropic, and dromo- tropic functions ; he has qualified them as positive or negative, depending upon influences which act favorably or unfavorably upon the individual functions. This nomenclature, however, has not found its way in general clinical use. To the four attributes mentioned, Gaskell has added a fifth — tonicity. This property is similar to that found in ordinary skeletal musculature, which, in the case of the heart, keeps it in a slight state of contracture even during diastole. Tonicity is a term which is perhaps used too loosely and indiscriminately and is often confused with the contractile power of the heart; it is the attribute about which few clinical or experimental facts are known. It is necessary to emphasize not alone the differentiation of the various cardiac properties, but the fact that certain parts of the heart are endowed with these properties in varying degrees ; for example, the sinus region with rhythmic attributes. Regarding our present knowledge of these various functions, it may be stated that though much is known about disturbances of rhythm and conductivity, many details of the other properties are still wanting. Besides the cardiac properties mentioned, another is that each systole is of maximum intensity. This property — the so-called all- or none-re- action — means that the heart muscle answers any stimulus sufficient to cause response by a maximal contraction. The latter is probably due to the intricate intertwined cardiac muscular system already described. Cardiac contractility therefore does not depend upon the strength of the impulse ; it varies, however, considerably with the state of irrita- bility, one of the heart muscle functions. Regarding this function, during systole the heart is not irritable, it is refractory to all other im- pulses and therefore cannot be tetanized like skeletal musculature. There is an experimental exception to this law ; hearts that have been poisoned by muscarine, alcohol, chloral, etc., may have a shortened refractory phase and hence may be brought into tetanic contraction by proper stimuli. Nerve Supply. — Situated at the base of the heart are the intercom- municating superficial and deep cardiac plexuses, from which the ex- trinsic cardiac nerves are derived. The superficial plexus lies in the THE HEART 5 concavity of the aortal arch ; the deep, between the trachea and aorta. The latter plexus is composed of nerves derived from the sympathetic cervical ganglia and the cardiac branches of the recurrent laryngeal and vagus. The branches from the right side of the plexus go to form parts of the anterior and posterior coronary plexuses, besides sending a few filaments to the right auricle. The branches from the left side are distributed to the left auricle and compose a large part of the pos- terior coronary plexus. The superficial cardiac plexus forms the chief part of the anterior coronary plexus. The posterior and anterior coronary plexuses surround and accom- pany the branches of the right and left coronary arteries, respectively, and distribute filaments to the ventricular musculature. The coronary plexuses as well as their muscular filaments are richly supplied with ganglia. Intracardiac ganglia have been found in the auricular wall, at the entrance of the superior and inferior vena cava and at the mouth of the coronary sinus. They have also been found at the level of the auriculo- ventricular junction, especially about the aorta and the pulmonary artery. Scattered ganglia have likewise been observed in the upper part of the ventricles. One observer claims to have discovered ganglion cells along the entire ventricular chamber. The nerves of the conduction system are described in the next chapter. The extrinsic nerves to the heart are derived from the cardiac plexuses. The heart is often profoundly influenced by impulses which reach it from these nerves. The vagi contain the inhibitory fibers. If, in the experimental animal, the vagi be cut in the neck, the cardiac rate is increased. If the peripheral ends of the cut vagi be stimulated, there is slowing or stoppage of the heart, or a condition in which the auricles beat more rapidly than the ventricles with no rhythmic relationship between the two (Complete Heart Block, Chapter VII). In warm-blooded animals there is not only a diminution of cardiac rate, but also of the strength of auricular and ventricular contraction, until the heart finally stops in diastole. On the other hand, stimulation of the cut end of the sympathetic produces a varying degree of cardiac acceleration. De- pending upon the degree of stimulation of vagus and sympathetic, the one or other nerve has a predominating influence upon the cardiac rate. Though antagonistic, this antagonism cannot be measured purely arithmetically ; if vagus influence predominates during the course of the experiment, after cessation of stimulation, a typical accelerator influence results. This fact in itself indicates that a certain amount of tone is present in both nerves. Nerves of sensation have not been discovered in the heart. Since the lower cervical and upper dorsal nerves, which supply the integument of the neck, chest, and upper ex- tremity, also send filaments to the deep and superficial cardiac plexuses, painful skin areas of varying degrees of intensity and extent are found 6 CLINICAL CARDIOLOGY as the result of reflex excitation originating in the heart itself from some pathological process or function (Chapter XXI). REFERENCES Chapter I Einthoven, W. : Neuere Ergebnisse auf dem Gebiete der thierischen Elek- tricitaet ; Gesellsehaf t deutscher Naturforscher und Aertzte ; Verhandlung, 1911. Engelmann, T. : Bijdrage tot de Kermis von den negatief-inotropen invloed . . . vagus op net hart. Gaskell, W. H. : On the Tonicity of the Heart and Blood Vessels ; Journal of Physiology, 1880, III, 48. Gray's Anatomy ; Edition 1901. His, W. : Beitraege zur Anatomie des menschliehen Herzens. Howell's Physiology, 5th Edition. Lewis, T. : Pathology of the Heart Functions ; Lancet, October 10, 1914. Mackenzie, J. : Diseases of the Heart, 3d Edition. McCallum, J. B. : On the Histogenesis of the Striated Muscle Fibre and the Growth of the Human Sartorius Muscle; Johns Hopkins' Bulletin, 1898, IX, 208. Mall, F. P. : Muscular Architecture of the Human Heart ; American Journal of Anatomy, 1910-1911, XI, 211. Norris, G. H., and Fetterolf, G. : The Topography of the Cardiac Valves as revealed by the X-Ray ; American Journal of the Medical Sciences, 1913, CXLV, 225. Stohr, P. : Text Book of Histology ; Edition 1901. Tigerstedt, R. : Lehrbuch der Physiologie des Menschens; Edition 1911, I. CHAPTER II THE CONDUCTION SYSTEM N.f. Fig. 3. — Schematic view of sino- auricular node of dog, showing gen- eral form of the node and differential structure. A = artery ; N.T = nodal tissue ; M.A = auricular musculature. Position and Structure of the Pacemaker. — Thorough experimental electrocardiographic investigations in mammals, and histological and pathological studies in man and ani- mals, have proven that the primum movens — the normal impulse center in the human being — ■ exists in a bit of specialized cardiac tissue situated in the sinus region immediately beneath the epicardium and in the groove be- tween the right auricle and superior vena cava. This rhythm center is variously known as the pacemaker, the sino-auricular node (S-A node), or the node of Keith-Flack. Its shape is irregularly pyriform (Fig. 3) with a larger upper, and a somewhat tapering lower end. The node is surrounded by branches of the vagus and sympathetic ; it contains a plexus of moniliform nerve fibrils and a few ganglionic cells ; it is therefore, histologically considered, a neuro-muscular structure. Its blood supply is derived from a special artery. The structure, arrangement, and composition of the node differ materially from the remainder of the cardiac musculature. The cells are smaller, stain more delicately, and are paler; the cross striations are indistinct or may be absent, the nucleus is pale, and there is a relative richness of perinuclear sarcoplasm. The cells contain more glycogen than those of the non-specialized muscle. They do not follow any orderly layer-like arrangement, but are placed irregularly in a rich stroma of fine connective tissue (Fig. 4). A small specialized muscle band con- 7 NX... A.M. Fig. 4. — Detail of the S-A node of dog (high power), showing the cells. N.T = nodal tissue ; A.M. = auricular musculature. 8 CLINICAL CARDIOLOGY Fig. 5. — Right ventricle of ox heart, showing the auriculo- ventricular node (A-V node) and the main stem. The right branch is seen running along the " Moderator Band." (Modified from Tawara — "Das Reitzleitungssystem des Saugethierherzens. ") necting the sino-auricular node with the remainder of the conduction system has been described by Thorel, but its presence has not been corroborated by other observers. Position and Distribution of the Auxiculo-ventricular Conduction System. — Similar in structure to the sino-auricular node is the larger mass of specialized tissue, known as the atrio- or auriculo- ventricular conduc- tion system, or junc- tional tissue. For purposes of anatomi- cal identification, its various parts are dif- ferently named, but they together form one continuous strand. The node of Tawara — the be- ginning of the junc- tional tissue — and the bundle of His constitute the major part of the conduction system before its division. They lie imme- diately beneath the endocardium in the lower part of the right auricle, slightly above the level of the ventricle, and about midway between the opening of the coronary sinus and the fibrous tissue beneath the aortal cusps (the aortic vestibule or "undefended space")- The con- duction system is then continued into the main stem, which soon makes a hairpin-like division into its two main branches — the right (Fig. 5) and left (Fig. 6). Both FlG . 6 .. branches course on either side of the in- terventricular septum in a direction roughly parallel to the axes of the respective ventricular cavities, and are contained in their own sheaths. The right branch is thin and spreads out in a somewhat fan-shaped fashion; the left is more compact, thicker, and club-like. In their POST A.CITTA1. GUtf> RT. ACUTA'- CUSP ■ Left ventricle of ox heart, showing conduction sys- tem. (Modified from Tawara.) THE CONDUCTION SYSTEM 9 upper portions, both branches are superficial and subendocardial. They split into secondary and minor branches as they spread toward the apex (Figs. 5, 6). In the ox heart, the left branch has three main divisions — to the anterior and posterior papillary muscles, respectively, and to the apex. The right branch has one division that goes to the large papillary muscle and venous base, the other forms the " moderator band " which supplies the septal papillary muscle and the arterial base (conus arteriosis) ; from both of these, a division to the apex is formed from separate heads. The branches in human and mammalian hearts finally divide into terminal aborizations (known as Purkinje fibers in the mam- mal) , which ramify through the papillary muscles and probably through- out the entire ventricular musculature. Some of these terminal aboriza- tions run free across the apical portion of the ventricular cavities ; they were formerly regarded as aberrant tendinous strands. They are macroscopically distinguished from the latter by their paler and finer structure and non-glistening appearance. The main stem and branches of the conduction system are sometimes dimly distinguished through the shimmering endocardium as paler, non-glistening structures. Dissection and Demonstration of the Conduction System. — In order to dissect out the conduction system, the endocardium over the site of the auriculo-ventricular (A-V) conduction system is gently teased off with forceps after the heart has been washed in water and hardened in a formaldehyde solution. The conduction system is most readily dissected in the ox or calf heart, less readily in the human. The heart is first incised with a scalpel near the margin of the inter- ventricular septum. The ventricles are then cut parallel to the latter. In this manner they can be turned back, and the septal walls of the auricle and the interventricular septum exposed without injury to the con- duction system. In oxen the main branch on the right side exists as a separate strand — the moderator band. After exposure by teasing in the manner described, the structure of the A-V conduction system will be found paler, softer, and more delicate than that of the surrounding musculature. Another method of gross demonstration of the conduction system is by subendocardial injection of the main branches with a fine hypodermic needle and syringe containing a 50 per cent solution of India ink. If carefully performed, not only the main branches but the subsidiary divisions stand out prominently as darker strands. In this manner, also, corroborative evidence is derived that ventricular contraction begins at the papillary muscles, for the ink may be seen to reach the latter first and then the base and apex of the heart. The cellular structure of the main junctional tissue is similar to that of the S-A node. The aborizations consist of larger, paler cells with large nuclei and with protoplasm containing faint striations at the periphery. Arterial and Nerve Supply of the A-V System. —The main arterial supply of the A-V system is derived from a special branch of the right 10 CLINICAL CARDIOLOGY coronary. The junctional tissue is supplied and intertwined with niedullated nerve fibrils and ganglia. There are numerous ganglion cells, — mono-, bi-, and multipolar, — whose processes pass to adjacent ganglion cells, to nerve fibers in the bundle, or through the A-V system, some of which end in ganglia cells of the bundle or in the muscle plexus. There is an intricate plexus of varicose fibrils around and in close relation to the muscle fibers of the bundle. Thus the A-V system, like the sino-auricular node, is a neuro-muscular spindle. Though the exact distribution to the nodes of the extrinsic cardiac nerves is not known, it appears probable that, regarding the vagus distribution, the S-A node is supplied chiefly by branches of the right, and the A-V by those of the left vagus. There appears to be a similar distribution to the S-A and A-V nodes by the right and left accelerators, respec- tively. Course of the Normal Impulse. — From a study of the physiological and anatomical distribution of the specialized tissues, it is evident that the normal impulse arises in the S-A node ; it spreads thence through the auricle, following, as far as known, no especially differentiated path in the latter. It then reaches the junctional tissue, and by way of the right and left branches and terminal aborizations, it finally spreads to the papillary muscles and throughout the ventricular musculature. Myogenic or Neurogenic Impulse ? — The question whether the original impulse is of myogenic or neurogenic origin has been for years a matter of dispute, and has not yet been decided. The intimate and intricate relationship existing between the muscle and nerve structures in the nodal regions demonstrates how difficult must be the final deter- mination of this question. It is known clinically that the rhythm center is readily influenced by purely neurogenic impulses ; these can indeed upset the normal cardiac control and give rise to abnormal rhythms (Chapter VIII). How far such clinical observations can be applied to the question of the normal control of the rhythm center it is impos- sible to state. All in all, it seems probable that the sino-auricular node is activated by both neurogenic and myogenic influences, though we have at present no means of discovering under what circumstances either becomes the controlling factor. REFERENCES Chaptek II Aschoff, L. : Referate ueber die Herzstoerungen der specifischen Muskelsystems des Herzens ; Verhandlungen der deutschen pathologischen Gesellschaf t, 1910. Cohn, A. E. : Observations on Injection Specimens of the Conduction System in Ox Hearts ; Heart, 1912-1913, IV, 225. Cohn, A. E., Kessel, L., and Mason, H. H. : Observations on the Functions of the Sino-auricular Node in the Dog; Heart, 1911-1912, III, 311. THE CONDUCTION SYSTEM 11 Cohn, A. E., and Lewis, T. : The Predominant Influence of the Left Vagus on Conduction between Auricle and Ventricle in the Dog ; Journal of Ex- perimental Medicine, 1913, XVIII, 739. Engel, I. : Beitraege zur normalen und pathologischen Histologic des atrio- ventrikularen Buendels ; Ziegler's Beitrage zur pathologischen Anatomie, 1910, XLVIII, 499. Keith, A., and Flack, M. : The Form and Nature of the Muscular Connections between the Primary Divisions of the Vertebrate Heart ; Journal of Anat- omy and Physiology, 1907, XLI, 172. Lewis, T. : Lectures on the Heart. Lewis, T., Oppenheimer, B. S., and Oppenheimer, A. : The Site of Origin of the Mammalian Heart Beat ; The Pacemaker in the Dog ; Heart, 1910- 1911, II, 147. Lhamon, R. M. : The Sheath of the Sino- ventricular Bundle ; American Journal of Anatomy, 1912, XIII, 55. Oppenheimer, B. S. : A Routine Method of Opening the Heart with Conserva- tion of the Bundle of His and the Sino-aurieular Node ; Journal of American Medical Association, 1912, LIX, 937. Oppenheimer, B. S., and Oppenheimer, A. : Nerve Fibrils in the Sino-aurieular Node; Journal of Experimental Medicine, 1912, XVI, 613. Tawara, S. : Das Reitzleitungssystem des Saeugethierherzens. Thorel, C. : Vorlaeufige Mittheilung ueber eine besondere Muskelverbindung zwischen der Cava Superior und dem Hissischen Buendel ; Muenchener Med. Wochenschrift, 1909, LVI, 2159. Wilson, J. G. : The Nerves of the Atrio-ventricular Bundle ; Proceedings of the Royal Society, 1909, B, LXXXI, 151. CHAPTER III POLYGRAPHIC TRACINGS Mackenzie Ink Polygraph. — For purposes of exact study of arterial and venous pulsations, mechanical methods, instruments, and graphic representation (sphygmograms) are necessary. Instruments that simultaneously transcribe arterial and jugular pulsations are called polygraphs. For clinical use I have found the Mackenzie Ink Polygraph perfectly satisfactory. Its compact size, the comparative simplicity and ease of operation, the fact that if neces- sary very long records can be taken, and the use of ink and a paper roll instead of smoked paper, make it suitable for clinical work. The Mackenzie polygraph (Fig. 7, Plate I) consists essentially of a clockwork (CI) incased in a metal container. The clock is fitted with a time-marker ( Ti) which ticks and marks fifth seconds by means of a small pen. The speed of the time-marker may be regulated by a small screw (S) . There are two separate keys (S.B 1, S.B 2) for winding the driving gear and the time-marker. There is also a small lever (Le) which starts and stops the driving mechanism. Attached to one side of the case is a slot (ST) into which is fitted a support for a paper roll (Pr). On the opposite side is a smaller slot, which acts as a rest for a long, narrow arm (Ar) for the support of two transmitting tambours (T.T) ; the latter are so arranged that they can move in any direction. To the tambours are attached long writing pens (P) ; the pressure of the points upon the paper may be regulated by manipulating the tambours. Each tambour is also separately connected with the receiving apparatus applied to the venous and arterial pulse by means of elastic tubing (E. T). The receiver for the venous pulsations is a small circular metal cup (Cu), which may also be used for registering cardiac pulsations by plac- ing it over the apex. For transmitting radial pulsations, a perforated leather strap (L.S) is buckled about the wrist and so adjusted that the button (Bit) or pelotte rests upon the most prominently pulsating part of the radial ; the pressure of the pelotte upon the latter is regulated by a small flat spring (Sp). There is a broad wrist tambour (W.T) which rests upon the button and transmits radial pulsations to the writing pens through the transmitting tambour. 12 PLATE I Fig. 7. — Mackenzie Ink Polygraph. CI = Clockwork ; Ti = Time-marker ; aS = Screw which regulates speed of time-marker; S.B 1,2= Keys for winding the driving gear and time-marker; Le = Lever for starting and stopping the driving mechanism ; SI = Slot for support of the paper roll (P.R) ; At = Arm for the support of the two transmitting tambours (T.T) ; P = Writing pens ; E.T = Elastic tubing connecting the transmitting tambours to the receiving apparatus ; Cu = Cup for receiving venous or cardiac pulsations ; L.S = Leather strap for buckling over the radial artery ; Bu = Button for receiving the radial pulsations ; Sp = Screw for regulating the pressure of the button upon the radial ; W.T = Wrist tambour. POLYGRAPHIC TRACINGS 13 Poi-yeRAPti RcceiVen- Method of Use of the Mackenzie Polygraph. — The polygraph is used as follows : the driving mechanism and time-marker are wound up, the paper roll set in place, the pens thoroughly inked and lightly adjusted upon the paper. After palpating the radial, its most pul- satile point is marked by an ink spot, or preferably by two rectangular lines ( |~)> one along the radial, the other across the wrist; these serve as guides for the proper position of the pelotte and wrist strap. The best position of the wrist is with the hand in moderate extension or hyperextension, because this tends to make the radial artery more super- ficial. This position can be conveniently maintained by firmly pressing the extended hand against the physician's thigh. The upper strap of the wrist attachment is put on loosely so as not to obliterate the artery ; the lower is buckled on firmly. The spring regulating the pressure of the pelotte is then pressed down sufficiently to make the latter bob vigorously with the radial pulsations. The wrist tambour is slipped in position with its screw sup- port loose, so that the ^—^ c metal tip on the under sur- face of the tambour rests full upon the bobbing but- ton; it is then screwed and held in this position. Thus through the receiv- ing and transmitting air system of tambours and their connecting elastic tubing, the radial pulsa- tions are transmitted to the writing pens. To transmit and tran- scribe venous pulsations the metal cup is placed over the jugular bulb (Fig. 8), preferably on the right side, because the vein is usually more prominent on that side. The neck of the cup is grasped between the fore and middle fingers, the rim by the thumb, and the cup slid along the outer border of the sterno-mastoid muscle until it touches the clavicle. It thus rests over the triangular area formed by the jugular vein (with its bulb), the inner end of the clavicle, and the sterno-mastoid muscle. The patient is made to lie as flat as possible ; he should breathe quietly, for stertorous breathing interferes with proper registration. Rigidity of the neck muscles also mars pulsations. Superabundance of fat and respiratory dyspnoea are other factors which may interfere with or vitiate accurate registration. After the wrist tambour and venous cup have been satisfactorily adjusted, the pens are separately slid across the paper, so as to establish coincident ordinates for measurement of the curves. These lines need Fig. 8. — Schematic view of the a-c-v waves and of the jugular bulb. 14 CLINICAL CARDIOLOGY not necessarily be continuous, for simultaneous venous and arterial pulsations may be measured off and standardized by means of calipers. The driving mechanism is now released and arterial and venous pulsa- tions simultaneously registered. Correlation between Experimental Auricular Pressure Curves and the Human Jugular Pulse. — Early experimenters gained information regarding auricular pressure curves by inserting sounds directly into the auricles of dogs and horses ; they found that auricular contractions were accompanied by increased auricular pressure, that is, by positive pres- sure waves. While there is a general correspondence between such pressure curves and human jugular tracings obtained by the polygraph, it must be remembered that the latter primarily depend upon difference in volume created in the confined air space of the cup resting over the jugular bulb. These volumetric differences are transmitted to the tambour, and the pen is then correspondingly deflected. Hence dif- ferences in auricular pressure are not necessarily transmitted and tran- scribed as volumetric waves ; and as a corollary, one can rarely predicate and estimate auricular pressure by the excursion and direction of the " venous " poly graphic waves. The Waves of the Normal Jugular Pulse, — the Normal Phlebo- gram. — Frequent observations have shown that, corresponding to the j_„ first auricular pressure curve coincident with auricular systole, there exists normally a venous pulse best seen in the venous trunks at the root of the neck. In man, for each radial beat, there are in the normal jugular tracing three waves or elevations; each elevation is accompanied by a corresponding depres- sion (Fig. 9). We shall fol- low the simple nomenclature usually adopted in the litera- ture and call the elevations the a-c-v waves. The a refers to the auricular, c to the carotid, and v to the ventricular filling wave. The rise (Figs. 8-9) and fall (Figs. 8-9, 1) of the first wave a are caused by the reflux wave produced in the veins of the neck by auricular systole. In rhythmically beating hearts, the a wave comes before the advent of ventricular systole (c wave). The absence of the a elevation in those types of arrhythmia in which experimental and electrocardiographic evidence shows absence of normal rhythmic au- ricular contractions (Auricular Fibrillation, Chapter VII), and its abnormal position in arrhythmias affecting relationship between auricu- lar and ventricular contractions (Heart Block, Chapter VII), are con- 30CUi.AR Fig. 9. — Diagrammatic representation of the nor- mal polygraphic curve. a — auricular wave ; c = carotid wave ; v = ventricular filling wave. (See text.) POLYGRAPHIC TRACINGS 15 firmatory evidence that the a wave is in the main, if not entirety, due to auricular systole. If the jugular tracings were quite similar to the experimental auricular pressure curves, following auricular systole (a wave) there should be a continuous fall (Fig. 9, 1-2) and two eleva- tions (a-v) and depressions (2-3) in the venous tracing. The post- auricular fall is interrupted by the advent of an elevation, the c wave. For the present disregarding the latter, the chief cause of the postauric- ular fall of pressure (Figs. 8-9, 1-2) is undoubtedly auricular relaxation following systole ; ventricular systole acts as a contributory cause in increasing this relaxation, mainly by dragging down the interventricular septum, and to a lesser degree, by producing diminished intrathoracic pressure. The physiological limit of the duration of the a wave is one fifth of a second. The cause of the carotid wave is still a matter of dispute. Its oc- casional appearance one twentieth of a second before the onset of ca- rotid pulsation, and its presence after experimental ligation have been offered as evidence that the c wave is not due to carotid pulsation. How- ever, those who have worked with the cup receiver over the jugular bulb will have observed how the venous tracing is often vitiated by placing the receiver too close to the carotid, in consequence of which the c wave will often obtrude itself upon the venous tracing. Although there exists some dispute as to its cause, the practical importance of the incidence of the c wave in the study of the "*/§P* — »— W V »■•«•• ^hymAJ human phlebogram rests upon the fact that its foot point is coincident with the onset of carotid pulsation. The determination of the foot point, therefore, be- comes an important land- mark in the study of the polygram. Since the pulse wave reaches the wrist ap- proximately one tenth of a second after its arrival at the carotid artery, and the onset of the individual radial beats is readily discernible in the arteriogram, the foot point of the c wave may be determined and distinguished from the a and v waves by measuring with calipers from coincident ordinates in the radial and venous tracings. These ordinates are derived by stopping the driving mechanism for a moment and sliding both pens across the paper (Fig. 10) ; when measuring in the direction of the physiological progression of the waves, one tenth of a second (the difference in time between carotid and radial pulsations) is added ; in this manner the foot point of the c wave is derived. With the latter determined, it becomes a simple matter in good curves to determine the Fig. 10. — Normal venous and radial tracing show- ing rhythmical a-c-v waves in the jugular trac- ing, and regular radial beats. The points S-S are coincident ordinates derived by sliding the pens when the driving mechanism is at rest. The method of derivation of the foot point of the c wave is also shown. 16 CLINICAL CARDIOLOGY a and v waves when the pulse beats rhythmically : the precarotid is the a, and the postcarotid, the v wave. The third positive (Fig. 9, v), the ventricular wave which follows the second depression, is due to ventricular systole ; it results almost entirely from reflux of the stored auricular blood which is forced into the venous system with ventricular systole while the auriculo-ventricular valves are still closed. Another factor in its production is the sudden release of the base of the ventricle at the commencement of ventricu- lar diastole. The slightly variable beginning of the v wave depends upon the varying amount of blood stored up during auricular diastole ; its termination is coincident with the opening of the tricuspid valves. The third fall or depression (Fig. 9, 3) is caused by the rapid drop of pressure in the auricle and in the venous trunks at the root of the neck, which follows the beginning of ventricular diastole and the opening of the auriculo-ventricular valves. Translating the knowledge gained from the graphic orderly sequence of auricular and carotid pulsations (the a and c waves) into terms of auricular and ventricular systoles, we have the means of studying rhythmical sequential cardiac cycles — the normal pulse — as well as the numerous disturbances of rhythm affecting auricle and ventricle. Variations in the Normal Phlebogram. — There are certain varia- tions in the normal phlebogram which require consideration. The a » p w * Tte* W * • ■ » r »» » ■ t t* Fig. 20. — Normal sized a and other peaks from a case of mitral stenosis. Fig. 21. — Normal a wave from a case of mitral regurgitation. 18 CLINICAL CARDIOLOGY cardial lesions, and after comparison with normal tracings, I have been unable to discover any distinction between them. Figures 17-24 taken from patients with various diseases illustrate this fact. Figs. 22, 23, 24. — Normal jugular tracing from cases of exophthalmic goiter. The Radial Pulse. — Because of the method of instrumental ap- plication — a spring and pelotte pressing upon the radial artery — the arterial sphygmogram represents differences of arterial pressure. The amount of spring tension required to sufficiently occlude the artery for the purposes of tracing is quite variable, hence the resultant curve is in many instances no accurate or even approximate measure of the amount of arterial pressure. In addition to these mechanical draw- backs, extraneous factors, e.g. the position of the radial, its accessi- bility, the pliability of its walls, etc., are considerations which profoundly modify inferences drawn from the pulse tracing. The special value derived from the radial tracing in the polygram rests upon knowledge gained regarding cardiac rate and rhythm, and the aid in fixing the time relation of events in the cardiac cycle ; the foot point of the radial serves as a standard for determining the incidence of the c wave in the venous tracing. The first wave of the radial (Figs. 25, 26, 1-2), usually called the primary or percussion wave, is generally steep, its fall sharp. It is due Figs. 25, 2G. — Normal radial pulse tracings. 1-2 = abrupt rise probably due to instrumental fling of the lever (also called primary or percussion wave) ; 1-3 = time of ventricular systole — the aortic valves are open ; D.N = dicrotic notch ; D.W = dicrotic wave ; S.W = systolic wave (also called tidal and predicrotic wave). to the sudden instrumental fling given to the pelotte and lever by the sharp impact of the onrushing blood. It occurs in, and is part of, the POLYGRAPHIC TRACINGS 19 wave produced by systolic arterial distention, and may be regarded as an initial artificial peak superimposed upon the arterial wave during systole. It is immediately followed by the systolic wave, sometimes called the secondary tidal or predicrotic wave (Figs. 25, 26, SAY, 2-3). The termination of the systolic and the beginning of the dicrotic wave (Figs. 25, 26, DAY) is marked by the dicrotic notch (Fig. 25, D.N). This notch corresponds to certain events in the cardiac cycle : the end of the ventricular systole and the foot point of the v wave in the venous tracing (Fig. 26). Other small waves are sometimes found in the radial tracing ; their cause and significance are not known. The cause of the dicrotic wave is still in dispute. Mackenzie re- gards it as due to sudden relaxation of the ventricular wall, including that portion supporting the aorta : according to him there is thus de- veloped a tendency to the production of a negative aortic wave, which is checked by the sudden stretching of the membranous aortic valves, thereby causing a second positive, the dicrotic wave. It has been experimentally demonstrated in a circulatory model in which the arterial system is represented by elastic tubing, that sudden check of the inflow produces a suction or negative pressure behind the column of fluid, and with it, resultant waves. Indeed, " dicrotic " waves have been produced in an " arterial system " in which the pumping mechanism was a syringe not comparable to the heart, a fact showing that these waves may be entirely the result of pressure effects in elastic arteries. With the influx of fluid, the tube expands ; with the sudden cessation of the flow, the resultant negative pressure in a rigid tube would lead only to a reflux of fluid. In elastic tubing, however, represented in the human being by the aorta, there is the additional force of elastic recoil. Both forces — suction and elastic recoil — produce shrinkage be- yond the natural caliber of the tube (aorta), the elastic constricted caliber causing secondary expansion and with it the secondary pul- satile " dicrotic " wave. Similar physical facts present in the arterial system seem to me sufficient to cause dicrotic waves. It is known, for example, that when the ventricles relax, the pressure in those chambers falls rapidly and the semilunar valves close ; there is in consequence a negative pressure at the mouth of the aorta, " accom- panied by an actual though slight movement of the blood current " (Wiggers). The element of elasticity in the human aorta has already been mentioned. It has also been held that the dicrotic wave is reflected from the periphery. Under such circumstances, the distance between dicrotic and primary crests ought to diminish as the arteries recede in distance from the heart, and there should be no dicrotism in the proximal part of the compressed artery. Both of these suppositions are dis- proved by sphygmographic tracings. In addition the manifold ar- terial division at the periphery would seem to make one large reflected wave impossible. 20 CLINICAL CARDIOLOGY The height of the dicrotic notch is ordinarily about one half of the arterial curve. In some cases, with sharp fall of arterial pressure fol- lowing ventricular systole, the notch is abnormally low. This happens frequently in aortic regurgitation with cardiac failure (Fig. 27), but it Mml Fig. 27. — Low dicrotic notch (d) Fig. 28. — Low dicrotic notch (d) from a case from a case of aortic regurgitation of aortic aneurism with cardiac failure, with decompensation. is also found in other decompensated heart lesions, valvular or myo- cardial in origin (Fig. 28). Types of Pulse. — From what has preceded, it is evident that only exceptionally can definite conclusions regarding the " strength " or " weakness " of the circulation be drawn from graphic records. In fact, the terms " weak " and " strong " pulse are usually misapplied to what should properly be called " soft " and " hard," respectively. The old terms previously in use have the advantage of describing the physical impression given to the examining finger. When thus descriptively applied and no deductions regarding the state of circulation are drawn, they serve a useful purpose. These terms and their definitions are as follows : a sudden fall of the pulse wave produces what is known as the " collapsing " pulse ; if extreme, it becomes the typical " water hammer " or Corrigan pulse. The radial pulse can also be described as large and expansile (pulsus magnus), small or compressible (p. mollis), or hard and incompressible (p. durus). The rise of the pulse wave may be quick (p. celer) or slow (p. tardus). If dicrotism becomes palpable, the pulse is known as dicrotic ; if the dicrotic notch breaks low and the dicrotic wave is marked, it is called hyperdicrotic. Occasionally, the pulse wave feels unduly sustained at the point of its maximal pulsation and falls slowly, — the anacrotic pulse. The bisferiens gives the sensation of a double pulsatile impact; it is produced by the rather equal split of the systolic plateau by the predicrotic or instrumental wave. Its assumed significance as evidence of aortic stenosis is not borne out by clinical experience. Important information of the state of the radial artery is sometimes gained by careful palpation. Marked nodosity, thickening, and tor- tuosity are immediately apparent. The opposite information — that of a normal elastic arterial wall — is not so readily derived. If the artery is emptied by compression and the collapsed vessel palpated, the radial, if normal, is barely definable as a separate strand ; if the radial is thick- ened and its walls stiff, the emptied artery is palpable below the point of compression. POLYGRAPHIC TRACINGS 21 REFERENCES Chapter III Foster's Physiology, Edition 1888, Part I. Gibson, G. A. : Further Observations on Heart Block ; British Medical Journal, 1906, II, 1113. Hirschfelder, A. D. : Diseases of the Heart and Aorta, Edition 1910. Lewis, T. : Mechanism of the Heart Beat. Mackenzie, T. : Diseases of the Heart, Edition 1913. Marey, B. J. : Circulation du Sang. Morrow, W. S. : Various Forms of the Negative or Physiological Venous Pulse ; British Medical Journal, 1906, II, 1807. Ohm, R. : Venen Puis und Herzschallregistrirung. Wiggers, C. J. : Circulation in Health and Disease, 64. CHAPTER IV THE ELECTROCARDIOGRAM Fundamental Physiological Considerations. — The electrocardio- gram is based upon the fundamental physiological fact that any muscle upon contracting produces a definite, though minute amount of elec- tricity. The current thus produced, if al- lowed to pass through a sensitive galvanom- eter, causes deflection of the needle. For ex- ample, a muscle con- sisting of parallel fibers (Fig. 29, M) is stimu- lated at the point S, the surface at that area is connected by means of a non-polarizable electrode (Ei) to the galvanometer (G), and the other electrode (E2) is grounded so that it remains constant (equi- potential) ; then the muscle at S in contracting becomes electrically negative relative to the remainder of the musculature. As the current passes, the stimulated end becomes quiescent ; the electropotential falls and reaches zero ; meanwhile the needle of the galvanometer is deflected and then comes to rest. If recorded, such deflection would be a monophasic curve (Fig. 29). If, instead of being grounded, the electrode is connected with the other end of a parallel fibered muscle (Fig. 30, E 2 ) and the latter is stimulated at the point S (Fig. 30), the stimulated area in contract- ing becomes electronegative, the other areas relatively positive. The current flows from — Ex to + E 2 (Fig. 30) and produces a current 22 Fig. 29. — Scheme of monophasic action current. (Modi- fied from Kraus and Nicolai — "Das Elecktrokardio- gramm.") M = muscle consisting of parallel fibers ; S = point of stimulation ; Ei = non-polarizable electrode ; E 2 = earthed electrode ; G = galvanometer ; C = resultant monophasic curve. •- gco © CX! . O — « M H b£ g .2 • — _g O DC ^ O 3 t-*" 2 o ■211 I J; m x g c S«^ «o -5 .2 * * ^ — - < — .2 as: "s*3 x -3*2 C 2 - O C^" S ft! o ■-.. A^ © o C :-r § "I -2 x '".- i «C x o-gfi O O S Z..Z -~ M u ii ii e "* o THE ELECTROCARDIOGRAM 23 in the galvanometric circuit. When the contraction wave arrives at the center of the muscle, no current is induced because this zone draws negative ions in equal amounts from both sides. The two latter being positive, there is no difference in po- tential and the needle is not deflected. With the passage of the contraction wave toward E 2 , the latter becomes elec- tronegative (the negative pole) ; the current now flows from — E 2 to + Ei and the needle is deflected in the op- posite direction. In other words, with change in electrical signs the needle is again deflected and a diphasic curve results. In view of later electrocardiographic considerations, it is important to em- phasize that the resultant curve depends upon the direction of the contraction wave in the muscle and upon the point at which the contraction arises. It further depends upon the axis of the muscle mass in relation to the electrical wave. It is also evident that the course of the contraction wave, of the galva- nometric deflections, and of areas of relative negativity are intimately corre- lated. These simple considerations regarding the action of a contract- ing muscle upon a galvanometric needle will serve to clarify the principles underlying the electrocardiographic apparatus. The latter as first constructed by Einthoven consists essentially of a fine conduct- ing fiber lying in a narrow space between two approximated poles of a powerful electromagnet. The fiber or string is deflected by cur- rents induced in it. The string is so sensitive and delicate that it is deflected by very weak currents drawn from the surface of the body. It is usually made of an exceedingly fine quartz fiber coated with silver. Its thickness varies from .002 mm. to .005 mm., its resistance from 1500 to 7000 ohms. The electrocardiographic apparatus which I use — a standard type — is schematically shown and described in Fig. 31. Figure 32 (Plate II) shows the apparatus set in position. Method of taking an Electrocardiogram — the Three Leads or Derivations. — There are various methods of employing non-polariz- able electrodes to conduct the potential produced by cardiac activity to the galvanometer. One method consists in wrapping flannel bandages, each about 6 inches wide and 9 feet long, thoroughly soaked in a strong warm salt solution (6 oz. of salt to one pint of water), around each fore- arm and around the left leg of the patient. After these extremities have Fig. 30. — Scheme of diphasic ac- tion current. (Considerably mod- ified from Kraus and Nikolai.) M u = parallel fibered muscle ; C = center point ;