(Stvrn bg Radiograph of a Healthy Child's Chest. Digitized by the Internet Archive in 2010 with funding from Open Knowledge Commons http://www.archive.org/details/physicaldiagnosiOOcabo PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST BY RICHARD C. CABOT, M.D. PHYSICIAN TO OUT-PATIENTS, MASSACHUSETTS GENERAL HOSPITAL ; ASSISTANT IN CLINICAL MEDICINE, HABVABD MEDICAL SCHOOL WITH ONE HUNDRED AND FORTY-TWO ILLUSTRATIONS NEW YORK WILLIAM AVOOD AND COMPANY M DCCCCI Copyright, 1900, By WILLIAM WOOD AND COMPANY. TO FREDERICK C. SHATTUCK, M.D. Jackson Professor of Clinical Medicine in Harvard University IX EVIDEXCE OF MY APPRECIATION OF THE EXAMPLE OF SINCERITY, COMMON SENSE, AND ENTHUSIASM ESTABLISHED BY HIM IN THE TEACHING AND THE PRACTICE OF MEDICINE PREFACE. This book is intended for students and, so far as I am aware, contains nothing original. I have written it because I have not been able to find any small work upon the subject which does not contain glaring errors. The correct books are too large ; the small books are out of date and repeat such well-worn myths as that the aortic second sound is normally louder than the pulmonic second, that aortic regurgitant murmurs are usually best heard in the sec- ond right interspace, that a hypertrophied left auricle can produce dulness and pulsation near the left sternal border, that systolic re- traction at the cardiac apex means adherent pericardium, that epi- gastric pulsation denotes hypertrophy of the right ventricle, etc. Further, none of the smaller text-books contains any adequate ac- count of muscle sounds, of pulmonary atelectasis, or of adlierent pericardium. To record the well-known but often forgotten truth on such matters as these has seemed to me of importance in small books as well as in encyclopaedic treatises. The diagrams illustrating respiratory types are modifications of those used by Wylie and Sahli. I am indebted to Mr. Eliot Alden, of the Harvard Medical School, for his kind assistance in the preparation of the illustra- tions and to Drs. E. C. Bradford and R. W. Lovett for.jjermission to use three cuts from their well-known work on orthopedic sur- gery. I am also indebted to the editor of the Archives of the Rontrjen Eay for permission to use two radiographs from that journal. TABLE OF CONTENTS. PAGE . 1 ERRATA. Page 35, line 7, for "expiration" read "inspiration". Page 81, last line, first word, for "of" read "or". Page 120, in the legend underneath Fig. 78, for "pulmonic" read "aortic". Page 125, last line but one, for "found" read "sound". Page 261, line 11, for "aphonic" read "aphonia". Page 299, third paragraph, for "three" read "two". 2. Increased Expansion, (c) Dyspnoea, The Respiratory Rhythm, . (a) Asthmatic Breathing, (6) Cheyne-Stokes Breathing, (c) Restrained Breathing, (d) Shallow and Irregular Breathing, (e) Stridulous Breathing, 18 21 21 21 22 22 23 TABLE OF CONTENTS. Introduction, ....... I. Methods of Examining the Thoracic Organs, II. Regional Anatomy of the Chest, . PAGE . 1 1 . 2 I. II. III. IV. PAET I. TECHXIQUE AXD GEXEEAL DIAGNOSIS. CHAPTER I. INSPECTION. Size, .... Shape, .... (a) The Rachitic Chest, (b) The Paralytic Chest, (c) The Barrel Chest, . Deformitiks, («) Curvature of the Spine, {b) Flattening of One Side of the Chest, (c) Prominence of One Side of the Chest, (d) Local Pi'ominences, . Respiratory Movements, (a) Noi-mal Respiration, {b) Anomalies of Expansion, 1. Diminished Expansion, 2. Increased Expansion, (c) Dyspnoea, The RiispiRATORv Rhythm, (a) Asthmatic Breathing, (6) Cheyne-Stokes Bi-eathing, (c) Restrained Breathing, (d) Shallow and Irregular Breathing, (e) Stridulous Breathing, 5 6 7 8 9 12 12 U 14 15 16 16 16 17 18 18 21 21 21 22 22 23 vni TABLE OF CONTENTS. PAGE VI. Diaphragmatic Movements (Litten's Phenomenon), . . .23 VII. The Cakdiac Movements, 26 1. Normal Cardiac Impulse, ....... 26 2. Displacement of the Cardiac Impulse, 29 3. Apex Retraction, .... .... 31 4. Epigastric Pulsation, 32 5. Uncovering of the Heart, 32 VIII. Aneuuism and Other Causes of Abnormal Pulsations of the Chest Wall, .......... 33 IX. The Peripheral Vessels, ........ 34 (a) Venous Phenomena, 35 (6) Arterial Phenomena, 36 (c) Capillary Phenomena 38 X. The Skin and Mucous Membranes, 39 1. Cyanosis, ,39 2. CEdema 40' 3. Pallor, 40 4. Jaimdice, 40 5. Scars and Eruptions 41 XI. Enlarged Glands, . 41 CHAPTER II. PALPATION AND THE STUDY OF THE PULSE. I. Palpation, 42 1. The Cardiac Impulf^o 42 2. Thrills, 43 3. Tactile Fremitus, 44 4. Friction, Pleural or Pericardial, 46 5. Palpable Rales 47 6. Tender Points, 48 7. Abnormal Pulsatior..s 48 8. Tumors 48 0. Temperature and Quality of the Skin. 49 II. The Pulse, 49 1. The Rate 61 2. Rhythm, 51 3. Compressibility, 52 4. Size and Shape of Pul.se Wave 52 6. Tension, ........... 53 6. Size and Position of Arteiy. 55 7. Condition of Artery Walls, 55 TABLE OF CONTENTS. CHAPTER III. PERCUSSION. I. Technique, ( Mediate Percussion, . ^ ' ( Immediate Percussion, (6) Auscultatory Percussion, (c) Palpatory Percussion, . II. Percussion-Resonance of ti (a) Vesicular Resonance, . (6) Dulness and Flatness, . (c) Tympanitic Resonance, (d) Cracked-pot Resonance, (e) Amphoric Resonance. . (/) The Lung Reflex, III. Sense of Resistance, Normal Chest IX PAGE 58 58 58 65 67 67 68 68 70 74 75 76 76 CHAPTER IV. AUSCULTATION. 1. Mediate and Immediatk Auscultation, 2. Selection of a Stethoscope, 3. The Use of the Stethoscope, A. Selective Attention and What to Disregard, B. Muscle Sounds, C. Other Sources of Error, . 4. Auscultation of the Lungs, I. Respiratory Types, (rt) Vesicular Breathing, . ip) Tubular Breathing, (c) Broncho-vesicular Breathing {d) Emphysematous Breathing, (e) Asthmatic Breathing, . (/) Cog-wheel Breathing. . ((/) Amphoric Breathing, . (/i) Metamorphosing Breathing, Differences between the Right and the Left Chest, Pathological Modifications of Vesicular Breathing (rt) Exaggerated Vesicular Breathing, (6) Diminished Vesicular Breathing, Bronchial Breathing in Disease, . . . . II. III. IV. 83 84 86 88 91 92 93 95 96 97 97 99 99 99 100 102 t TABLE OF CONTENTS PAGE V. Amphoric Breathing, 103 VI. Kales, 103 (rt) Moist, 103 (b) Dry, 104 (c) Musical, 106 VII. Cough. Effects on Respiratory Sounds, 107 VIII. Pleural Friction, 107 IX. Auscultation of the Voice Sound, 109 (a) The Whispered Voice, 109 (b) The Spoken Voice, 110 (c) Egophony, Ill X. Phenomena Peculiar to Pneumo-Hydrothorax, .... Ill (a) Succussion, Ill (6) Metallic Tinkle, . . . " 112 (c) The Lung Fistula Sound 112 CHAPTER V. AUSCULTATION OF THE HEART. 1. The Valve Areas, 113 2. Normal Heart Sounds, ......... 114 3. Modifications in the Intensity of the Heart Sounds, . . . 116 (a) Mitral First Sound, 117 1. Shortening, 117 2. Doubling, 118 (6) The Second Sounds at the Base of the Heart, .... 118 1. Physiological Variations, 118 2. Pathological Variations, 120 (a) Accentuation of Pulmonic Second Sound, . . . 120 (6) AVeakening of Pulmonic Second Sound, . . . 121 (c) Accentuation of the Aortic Second Sound, . . . 121 ((/) Weakening of the Aortic Second Sound, . . . 121 (e) Accentuation of Both Second Simnds, .... 122 (/) Summary, . . . . . . . .122 (c) Modifications in Rhythm of Cardiac Sounds and Doubling of Sec- ond Sounds, 123 (d) Metallic Quality of the Heart Sounds, ...... 124 (e) "Muffled" Heart Sounds 124 4. SOI.NDS Al'DIBLE OvER THE PeKIPHEKAL VeSSEI.S, .... 124 (a) Arterial Sounds, 124 (b) Venous Sounds, 125 TABLE OF CONTENTS. XI II. III. IV. V. CHAPTER YI. (Auscultation of the Heart Continued.) CARDIAC MURMURS. Terminology, .... 1. Mode of Production, 2. Place of Murmurs in the Cardiac 3. Point of Maximum Intensity, 4. Area of Transmission, . 5. Effects of Respiration, Exertion, 0. Intensity, Quality, and Length, 7. Relation to Heart Sounds,. 8. Metamorphosis of Murmurs, Functional Murmurs, Cardiorespiratory Murmurs, Venous Murmurs, Arterial Murmurs, ... Cycle and Position, PAGE . 126 . 126 . 128 . 129 . 1.30 . 1.35 132-1.35 . 135 . 136 . 1.36 . 1.38 . 139 . 140 PAKT II. DISEASES OF THE HEAKT. CHAPTER YII. VALVULAR LESIONS. 1. Valvular and Parietal Disease, . . . . 2. The Establishment and Failure of Compensation, 3. Hypertrophy and Dilatation, 4. Valvular Disease, I. Mitral Regurgitation, (o) Pre-compensatory Stage, (b) Stage of Compensation. . (c) Stage of Failing Compen.sation, (cZ) Differential Diagnosis, . II. Mitral Stenosis, 1. First Stage, 2. Second Stage, . 3. Third Stage, . 4. Differential Diagnosis, . III. Aortic Regurgitation, 1. Inspection, 141 144 146 151 151 1.53 154 158 159 161 163 165 166 167 170 171 Xll TABLE OF CONTE^'TS. IV. (a) Arterial Jerking, . (6) Capillary Pulsation 2. Palpation, .... 3. Percussion, .... 4. Auscultation, .... 5. Summary and Differential Diaguos (). Prognosis 7. Complications, Aortic Stenosis, .... 1. {a) The Murmur. (b) The Pulse, .... (c) The Thrill, (d) Feeble Aortic Second Sound, 2. Differential Diagnosis, . V. Tricuspid Regurgitation, 1. (rt) The Murnuir, (b) Venous Pulsation, (f) Cardiac Dilatation, {(l) Feeble Pulmonic Second Sound 2. Differential Diagnosis, . VI. Tricuspid Stenosis, VII. Pulmonary Regurgitation. VIII. Pulmonary Stenosis, IX. Combined Valvular Lesion?. . (rt) Double Mitral Disease, . (b) Aortic and Mitral Regurgitation. (c) Aortic Stenosis and Regurgitaiion, CHAPTER YIII. PARIETAL DISEASE AND CARDIAC NEUROSES I. Acute Myocarditis, 1 Acute Moycarditis. 2. Chronic Myocarditis, . 3. Fatty Overgrowth, 4. Fatty Degeneratior, II. Cardiac Neuroses, 1. Tachycardia, 2. Bradycardia, 3. Arrhythmia, 4. Palpitation, . 5. Congenital Heart Disease, TABLE OF CONTENTS. XUl CHAPTER IX. DISEASES OF THE PERICARDIUM. PAGE I. Pericarditis, 209 (a) Dry or Fibrinous, 209 (6) Pericardial Effusion, 212 1. The Area of Dulness, 213 2. The Cardiac Impulse and the Pulse, ..... 214 8. Pressure Signs, 215 (c) Adherent Pericardium, ........ 216 1. Retraction of Interspaces, 217 2. Limitation of Respiratory Movements, .... 217 3. Absence of Cardiac Displacement with Change of Position, 217 4. Hypertrophy and Dilatation not otherwise Explained, . 217 5. Capsular Cirrhosis of the Liver, 218 II. Hydropericardium and Pneumopericahi>ium, ..... 219 CHAPTER X. THORACIC ANEURISM. 1. Abnormal Pulsation, 220 2. Tumor, ... . 221 3. Thrill, 222 4. Diastolic Shock, 222 6. Tracheal Tug, 223 6. Pressui'e Signs, 224 7. Percussion Dulness, 224 8. Auscultation, 225 (a) Murmurs, 225 (b) Diastolic Shock Sound, . ...... . 226 9. Radioscopy, 227 10. Summary . 227 11. Diagnosis, , 229 PART III. DISEASES OF THE LUNGS AND PLEURA. CHAPTER XL BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 1. Tracheitis, 233 2. Bronchitis, 233 TABLE OF CONTENTS. 4. (a) Physical Signs, (6) Differential Diagnosis, Croupous Pneumonia, (a) Inspection, (b) Palpation, (c) Percussion, (d) Auscultation, (e) Summary, (/) Differential Diagnosis, Broncho-Pneumonia, Pulmonary Tuberculosis, (a) Incipient Tuberculosis, (b) Moderately Advanced Cases, (c) Advanced Phthisis, (d) Anomalous Forms of Pulmonary Tuberculosis, PAGE . 284 . 235 . 237 . 237 . 238 . 238 . 230 . 242 . 242 . 244 . 245 . 245 , 249 . 252 . 256 CHAPTER XII. (Diseases of the Lungs, Continued.) 1. Emphysema, ............ 258 (a) Small-Lunged Emphysema, 258 (6) Large-Lunged Emphysema ........ 258 (c) Emi^hysema with Bronchitis and Asthma 261 (d) Interstitial Emphysema, ........ 262 (e) Complementary Emphysema, ....... 262 (/) Acute Pulmonary Tympanites, 262 2. Bronchial Asthma, .......... 263 3. Syphilis of thk Lung, ......... 264 4. Bronchiectasis, 264 5. Cirrhosis of the Lung, ......... 265 CHAPTER XIII. DISEASES AFFECTING THE PLEURAL CAVITY. I. Hydrothorax, 266 II. Pneumothorax 266 III. Pneumohydrothorax and Pneuniopyothorax 268 Differential Diagnosis of Pneumothorax and Pneumohydrothorax, . 270 IV. Pleurisy 271 1. Dry Pleurisy, 271 TABLE OF CONTENTS. XV 2. Pleuritic Effusion, .... (a) Percussion, ..... {b) Auscultation, .... (c) Inspection and Palpation, . .3. Pleural Thickening, .... 4. Encapsulated Pleural Effusions, . 5. Pulsating Pleurisy and Empyema Necessitatis, 0. Differential Diagnosis of Pleural Effusions, PAGE . 273 . 273 . 279 . 281 . 283 . 283 . 284 . 284 CHAPTER XIV. ABSCESS, GANGRENE AND CANCER OF THE LUNG, PULMONARY ATELECTASIS, CEDEMA AND HYPOSTATIC CONGESTION. 1. Abscess and Gangrene of the Lung, 290 2. Cancer of the Lung, 291 3. Atelectasis, 292 4. CEdema and Hypostatic Congestion, . , 293 APPENDICES. Appendix A. — Diseases of the Mediastinum 293 1. Mediastinal Tumors . . . 293 2. Mediastinitis, 295 3. Tuberculosis of Mediastinal Glands, 296 Appendix B. — Acutk Endocarditis, ....... 296 Appendix C. — Examination of Infant's Chests, 297 Appendix D. — Radioscopy of thk Chest, 298 Appendix E. — The Sphygmograph. 305 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. INTRODUCTION. I. Methods of Examining the Thoracic Organs. To carry out a thorougli examination of the chest we do five things: 1. We look at it; technically called "inspection." 2. We feel of it; technically called "palpation." 3. We listen to the sounds produced by striking it; technically called "percussion." 4. We listen to the sounds produced withm it by physiological or pathological processes; technically called "auscultation." 5. We study pictures thrown on the fluoroscopic screen or on a photo- graphic plate by the Roentgen rays as they traverse the chest; technically called "radioscopy." Measuring the dimensions or the movements of the chest ("men- suration ") is often mentioned as co-ordinate with the above meth- ods, but it yields very little information of practical value, and is at present very little used. The data obtained by examining the sputa, blood, and urine are frequently of great value in helping us to interpret the signs re- vealed by examination of the chest, but do not fall within the scope of this book. Accordingly, I shall confine myself in the first part of this book to a description of the methods of inspect- ing, palpating, percussing, and auscultating the chest, with a brief account of the physical signs which we have learned to appreciate by the use of these methods. (For radioscopy, see Appendix.) 1 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. "Without some knowledge of the regional anatomy of the chest no intelligent investigation of the condition of the thoracic organs can be carried on. Accordingly, I shall begin by recalling very briefly some of the most essential anatomical relations. II. Eegioxal Axatomy of the Chest. It seems to me a mistake to divide the chest into arbitrary por- tions and to describe physical signs with reference to such division. The seat of any lesion can best be described by giving its relation to the clavicle, ster- num, or ribs on the front and sides of the chest, and to the scapulae and ribs behind. Thus we may speak of rales as heard " above the left clavicle in front," "below the right scapula behind, " " between the seventh and ninth ril)s in the axilla," and so on. When we want to state more exactly what part of the axilla anteroposterioiiy is affected, we may refer to the " mid-axillary line " (see Fig. 1) ; or better, we niay place the lesion by measuring the number of centimetres or inches from the median line of the sternum. In a similar way the place of the sqyex im- pulse of the heart (whether in the normal situation or farther toward the axilla) can be determined by measuring from the median line of the sternum. Measurements refer- ring to tlie ni}»i)le are entirely useless in women and not very reliable in men. It is better to measure as above. If, then, we confine ourselves chiefly to the bones of the chest as landmarks, and fix, with reference to them, the position of any portion of the in- ternal organs which Ave desire to study, it becomes unnecessarj' to memorize any technical terms or to learn the ]K)sition of any arbi- trary lines and divisions such as are frequently forced upon the Fig. 1.— The Mid-Axillary Line. INTRODUCTION. 3 student. The only points which it is necessary to memorize once for all are : 1. The position of the heart, lungs, liver, and spleen with ref- erence to the bones of the chest. 2. The position of certain points which experience has taught us have a certain value in j^hysical diagnosis. I mean («) the so-called "valve areas" of the heart, which do not correspond to the actual position of the valves, for reasons to be explained later Upper lobe of left lung. Right lung Right auricle. — J- Liver. — Left ventricle. Lower lobe of left lung. ~ Stomacli. Fig. 2.— Position of the Heart, Lungs, Liver, and Stomach. The dotted lines correspond to the outlines of the lung ; the heavy continuous line represents the heart ; while the position of the liver and of the lower border of the stomach is indicated by light continuous lines. The ribs are numbered. on, and ih) the percussion outlines of the heart, liver, and spleen. These outlines do not correspond in size with the actual duuensions of the organs withm, yet there is a definite relation between the two which remains relatively constant, so that we can infer the size of the organ itself from the outlines which we determine by percus- sion. The position of the organs themselves is shown in Figs. '2, 3, and 4. It will be noticed in Fig. 2 that the lungs extend up above the clavicles and overlap the liver and the heart — facts of considerable importance in the physical examination of these or- gans, as will be later seen. It is also to be noticed how small 4 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. a portion of the stomach is directly accessible to physical examina- tion, the larger part of it lying behmd the ribs and covered by the ,k Upper lobe. ^ - Lower lobe. Spleen. Lower lobe. '' Upper lobe. Middle lobe. _ Liver Fig. 3.— Position of the Left Lung from the Fig, 4.— Position of the Right Lung from the Sides and of the Spleen. Side, and of the Liver. liver. The normal i)ancreas and kidneys are practically inacces- sible to physical examination. The percussion outlines — corresponding to those portions of the heart, liver, and spleen which lie immediately beneath the chest walls — will be illustrated in the section on Percussion (see page 58). PART I. TECHNIQUE AND GENERAL DIAGNOSIS. INSPECTION. Much may be learned by a careful inspection of all parts of the cliest, but only in case the clothes are wholly removed. A good light is essential, and this does not always mean a direct light ; for example, when examining the front of the chest it is often better to have the patient stand with his side to the window so that the light strikes obliquely across the chest, accenting every depression and making every pulsation a movmg shadow. In searching for abnormal pulsations, this oblique light is especially important. In examining the thorax we look for the following points : 1. The size. 2. The general shape and nutrition. 3. Local deformities or tumors. 4. The respiratory movements of the chest walls. 5. The respiratory movements of the diaphragm. 6. The normal cardiac movements. 7. Abnormal pulsations (arterial, venous, or capillary). 8. The peripheral vessels. 9. The color and condition of the skin and mucous membranes. 10. The presence or absence of glandular enlargement. I. Size. Small chests are seen in patients who have been long in bed from whatever cause ; also in those who have suffered in infancy from rickets, adenoid growths in the naso-pharynx, or a combma- tion of the two diseases. Abnormally large chests are seen chiefly in emphysema. Of course the chests of healthy individuals vary 6 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. a great deal iu size at any given age, and I have been referring in the last sentences only to variations greater than those normally found. II. Shape. There are marked differences in shape between the cliild's and the adult's chest in health. A child's trunk, as compared Avith FiU. 5.— Funnel Breast. that of an adult, is far more nearly cylindrical; that is, the antero- posterior diameter is nearly as great as the lateral. The adult's chest is distinctly flattened from before backAvard, although indi- vidual variations in this respect are considerable, as Woods Hutch- inson has shown. In childliood the commonest i)athological modifications are due INSPECTION. 7 to rickets ; in middle aud later life to emphysema, phthisis, or old jjleuritic disease. {a) The Racldtlc Chest. The stennun generally projects {^^ pirjeon b)-east"), but in some cases, especially when rickets is combined with adenoid hyjier- trophy, there may be a depression at the root of the sternum re- sulting in the condition known as "funnel breast " ' (Figs. 5 and 6). Fig. 6.— Funnel Breast. The sides of the chest are compressed laterally and slope in to meet the sternum as the sides of a ship slope down to meet the keel (pectus carinatum) (Figs. 8, 9 and 10). From the origin of the eusi- form cartilage a depression or groove is to be seen running down- ward and outward to the axilla and corresponding nearly to the attachment of the diaphragm. This is sometimes spoken of as " Harriso7i's groove " (Figs. 11 and 12). The lower margin of the ribs ' In some cases this condition appears to be congenital. 8 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. in front often flares out, owing to the enlargement of the liver and spleen below and the pull of the diaphragm above. Along the line of the chondi'o-costal articulation there is to be felt, and sometimes Fig. 7. — Acquired Depression at the Root of the Ensifonn Cartilage. The patient Is a shoe- malver of seventy, who has all his life pressed against his breast bone the shoe on which he worked. seen, a line of eminences or swellings, to which the name of '' ra- chitic rosarij " has been given (see Fig. 18). (/;) The ''Paralytic Thorax.'' Fig. 14 conveys a better idea of this form of chest than any description. The normal anteroposterior flattenmg is exaggerated so that such persons are often spoken of as ^\flat-chested.'' The clavicles are very prominent, owing to falling in of the tissues INSPECTION. 9 above and below them; the shoulders are stooping, the scapulae prominent, and the neck is generally long. The angle where the ribs meet at the ensiform cartilage, the so-called " costal angle, " is in such cases very sharp. This type of chest has often been supposed to be characteristic of phthisis, but may be found in persons with perfectly healthy lungs. On the other hand, phthisis frequently Fig. 8.— Pigeon Breast. exists in persons with normally shaped chests or with abnormally deep chests (T\^oods Hutchinson). (See Eig. 128, page 251.) (e) The "Barrel Cliest." Nothing is less like a barrel than the '^ barrel chest." Its most striking characteristic is its greatly increased anteroposterior diam- eter, so that it approaches the form of the infant's chest. The costal angle is very obtuse, the shoulders are high, and the neck is short. The respiratory movements of the barrel chest will be spoken of later (see Figs. 15 and 16). 10 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. Xuti''itlo)i nf the Chi'st Walls. Emaciation is readily appreciated by inspection. The ribs are unusually prominent, the scapulae stand out, and the clavicles pro- ject. All this may be seen independently of any change in the Fk;. 9.— Pigeon Breast. shape of the chest such as was described above under the title of Paralytic Thorax. Tuberculosis of the apices of the lungs may ])roduce a marked fallhig in of the tissues above and below the clavicle independent of any emaciation of the chest itself. INSPECTION. 11 Fig. 10.— Pigeon Breast. 12 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. III. Deformities. The abnormalities just enumerated are symmetrical and affect the whole thorax. Under the head of Deformities, I shall consider chiefly such abnormalities as affect particular portions of the chest and not the thorax as a whole. (if) Sjitmil Curvatures and Twists. A good view of the patient's hack brings out best the lesser de- grees of lateral curvature, which are not at all infrequent in persons Fk;. 11.— HaiTi^oti's (.roovp. who are not aware of them. Slight degrees of deformity are best seen by marking with a skin-pencil the position of the spinous proc- esses (see Fig. 18). The more marked cases of lateral curvature, which are usually accompanied by a certain amount of tivisting, give rise to considerable displacement of the thoracic organs and render unreliable the usual bony lancbnarks, with reference to which we judge of the position of the intrathoracic organs. By such deformities the apex of the heart may l)e pushed up into the INSPECTION. 13 Fig. 13. — Harrison's Groove. fourth space or out into the axilla, or portions of the lungs may be compressed and made atelectatic. I. The bulging on the convex side of the curve may simulate an aneurismal tumor. II. Pott's disease of the spine should be looked for as a part Fig. 13.— Remains of Rachitic Rosary in a Boy of Seventeen. 14 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. of the routine inspection of the chest. It is sometimes better felt than seen. III. Abnormal rigidity of the spine, due to spondylitis defor- mans, is to be recognized by watching the movements of the spinal column as the patient bends forward and back. Where the verte- brae are locked together, as occurs in moderately advanced cases of this disease, the spine is maintained rigidly stiff, in- dependent of muscular sup- port. A similar stiffness of the spine may also be seen in early Pott's disease. It is here due mostly to mus- cular spasm. (h) FJatfenhuf of One Side of the Chest. In chronic phthisis, cir- rhosis of the lung, or long- standing pleuritic effusion, marked falling in of one side of the chest is often to be seen. This may be ap- parent in the upper and front portion, beneath the clavicle, or in the axilla, or in both situations (see Figs. The slirinkage of the affected side is made more ob- vious l)y contrast with the compensatory hypertrophy of the sound lung, which makes the sound side unusually full and prominent. Fi(i. U.- Till- raralylii- Thorax. 14 and 20). {(■) I'roiii'incnre noea may affect especially ins^firation, as, for example, when a foreign body lodges in the larynx, or in ordinary "'crou})." In such cases we speak of '"'' insplratonj (Ji/spiuea," distinguisliing it from " explrdtovy dyspna'a " such as occurs in asthma and emphy- sema. In the latter condition the breath seems to enter the chest readily, hut the difficulty is to get it out again. Expiration is greatly prolonged and often noisy. Combined t;y75es also occur in which both respiratory acts are difficult. Ahnovmalhj deep and fall respiration, without any appearance of difficulty in the process, is sometimes seen near the fatal termina- tion of cases of diabetes, the so - called diabetic dyspnoea. Slinp/le rapidity of hreatliing should be dis- tinguished from dyspncea of any type. In adults the normal rate of respi- ration is about 22 per minute. In children, it is considerably quicker and more irregular. It is not desirable to attempt here to enumerate all the causes which may lead to a quickening of the respi- ration. Among the com- moner are muscular exer- tion, emotional disturb- ance, diseases of the heart and lungs, and iluid or solid accumula- tions below the diaphragm, Avhich push up that muscle and cause it to encroach abnormally upon the thoracic cavity. ]\Iost of the in- fectious fevers are also apt to be accompanied by quickened breath- contraction of Left Chest. Empyema. 20 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. ing, especially but not exclusively when the fever is associated Avith a disease of the heart, lung, pleura, or pericardium. Sucking-in of the interspaces in the lower axillary regions or below the clavicles may be seen in connection with dyspnoea when- ever the lungs are jire- vented l)y some cause from properly expand- ing during inspiration. Negative pressure i s thus produced within the chest, aiul the at- mospheric p r e s s u r e Avithout pushes in the more elastic parts of the thorax. This phe- nomenon is seen in col- lapse or atelectasis of a portion or the Avhole of a lung, such as may occur in obstruction at the glottis (in Avhich case both sides are equally retracted) o r from occlusion of a bronchus. In the lat- ter CA^ent, the sucking-in of the interspaces during inspiration oc- curs only on the affected side.' ' Slight retraction of the lower interspaces in the axilla during inspiration is often seen in health. In disease this phenomenon is greatly exaggerated. Fig. 21.— Prominence of Right Side. Pleural Effusion. INSPECTION. 21 Y. C"hangp:.s ix the REspiKATftKY Rhythm. (c/) AstJi iiKitic Uri'dthuKj. In asthma the normal rhythm is reversed and the expiration becomes longer, instead of shorter, than inspiration. Inspiration may be represented only by a short gasp, while expiration becomes a prolonged wheeze lasting several times as long as inspiration. Dyspnoea is usually very marked. In emphysema we get very much the same type of breathing so far as rhythm is concerned, but the dyspnfjea is not usually so extreme and the auxiliary mus- cles of respiration are not so apt to be called into use. In many cases of emphysema one sees the thorax move all as one piece, " hii ctiirasse," owing to a senile fixation of the bones of the thorax from ossification of the cartilaginous portions. In hereditary syphilis this fixation may occur in youth or early middle age. (b) CJieijne-Stolces Breatlting. An anomaly of respiratory rhythm in which short, recurrent paroxysms of dyspnoea are preceded and followed by x^eriods in which no respiration occurs (apnoea). If we represent the normal resisiratory movement by an up-and-down line, as seen in Fig. 22, Fig. 2~.— Diagram to Represent Nonnal Breathiug-Rliytlim. the Cheyne-Stokes type of breathing would appear as in Fig 23. The period of apnoea may last from one to ten seconds ; then short, shallow respirations begin and increase rapidly, both in volume and in rate, until a maximum of marked dyspnoea is reached, Avhen a diminution in the rate and depth of the act begins, and the patient gradually returns to the apnosic state The length of the whole paroxysm may l)e from 30 to 70 seconds During the apnceic period the patient is apt to drop asleep for a few seconds and the pupils may become contracted When the paroxysm of dyspnaa 22 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. is at its lieiglit, lie is apt to cough aud shift his ijosition restlessly, or in case the whole phenomenon occurs during sleep he moves un- easily in his sleep at this period. Modified types of the phenome- non also occur, in which there is a rhythmic increase and decrease in the depth and rapidity of respiration but without any interven- ing period of apnoea. This type of breathing is most often seen in severe cases of cardiac, renal, or cerebral disease. It is generally more marked at night and may occur only at that time. In chil- dren it appears sometimes to be physiological during sleep. As a Fi(_;. :.';5.— Cheviie-Stokes Ivespiriitioii. rule, it is a sign of grave prognostic significance, but patients have been known to recover completely after Aveeks or even months of Cheyne-Stokes breathing. (f) Bestndni'd or '' C((tcJii/^^ livcdthlng. When the patient has a "stitch in the side," due to dry pleu- risy, intercostal neuralgia, or to other causes, the inspiration may be suddenly interrupted in the middle, owing to a seizure of jiain which makes the patient stop breathing as quickly as he can. The same conditions may produce very shallow breathing as the patient tries to avoid the pain Avhich a fall inspiration will cause. This type of restrained breathing is c^ten seen in pleurisy and pneumo- nia, and in the latter disease expiratio;! is often accompanied by a little moan or gnnit of discomfort. (fZ) Shdlloir (ind ivi-('(jHha' hveatliiiu/ is often seen in states of pro- found unconsciousness from any caiise, su(!h as apoplexy or poison- ing. A few deep respirations may be followed by a number of shallow and irregular ones. When death is imminent in any dis- ease, the respiration may become very irregular and gasping, and it is apt to be accomi)aiiit'd l)y a ])(M'uliar nodding inovement of the INSPECTION. 23 head, the chin bemg thrown quickly upward during inspiration, and falling slowly during expiration. I have known but one patient to recover after this type of breathing had set in. After severe hemorrhage the breathing may be of a sujlilny tijpe as well as very shallow. (e) Strhlulous Brcatlibuj. A high-pitched, crowing or barking sound is heard during inspi- ration when there is obstruction of the entrance of air at or near the glottis. This type of breathing occurs in spasm or oedema of the glottis, " croup," laryngismus stridulus, and forms the "whoop " in the paroxysms of whooping-cough. Laryngeal or tracheal ob- structions due to foreign bodies, or tumors within or pressure from without the air-tubes, may cause a similar type of respiration. It is in these cases especially that we see the sucking-in of the inter- spaces mentioned above (see p. 20). VI. DiAPHEAGilATIC MoVEMEXTS. Lltteii'' s PJienomenon. The normal movements of the diaphragm may be rendered vis- ible by the following procedure, suggested by Litten in 1892 : The patient lies upon his back with the chest bared and the feet pointed directly toward a window. Cross lights must be altogether ex- cluded by darkening any other windows which the room may con- tain' (see Fig. 24). The observer stands at the patient's side and asks him to take a full breath. As the ribs rise Avith the movement of inspiration, a short, narrow shadow moves doAvn along the axilla from about the seventh to about the ninth or tenth rib. During the expiration the shadow rises again to the point from which it started, but is less easily seen. This phenomenon is to be seen on both sides of the chest and sometimes in the epigastrium. ^ If it is inconvenient to move the patient's bed into the proper position vpith relation to the window, or if the foot-board interferes, or if the observa^ tion has to be made after dark, a dark lantern or other strong light held at the foot of the bed answers very well. All other light must, of course, be ex- cluded. 24 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. It is best seen in spare, muscular young persons of either sex, and is never absent in health except in those who are very fat, or who cannot or will not breathe deeply. The latter condition occurs in Fig. 24.— Litten's Diaphragm Shadow. Proper position of patient and of obsener. The shadow is best seen near L. hysteria and in some very stu])id persons who cannot be made to understand Avhat is meant by a full breath. In the observation of several thousand cases, I have never known it absent in health except under these conditions. In normal chests, the excursion of the shadow is al)out two and a half inches; with very forced breathing three and a half inclies. The mechanism of this phenomenon is best understood by imagin- ing a coronal section of the thorax as seen from the front or l)ack (see Fig. 25). At the end of expiration, the diaidiragm lies flat against the thorax from its attachment up to about the sixth rib. During inspiration it "jirr/s off" as it descends and allows the edge of the lung to come down into the cliink Ix^ween tlie dia- phragm and thorax. This "peeling off" of the diaphragm and the descent of the lung during ins])iration give rise to the moving shadow above described. By thus ol)serving the excursion of the diaphragm we can obtain a good deal of information of clinical value. INSPECTION. 2;j 111 pneumonia of the lower lobe, pleuritic eif'usion, extensive pleu- ritic adhesions, or in advanced cases of emphysema, the shadow is absent. This is explained by the fact that in pneumonia, pleuritic effusion, and emphysema the diaphragm is held off from the chest wall so that its movements communicate no shadow. In pleuritic adliesions the movements of the diaphragm are prevented. In early phthisis I have generally found the excursion of the dia- phragm diminished upon the affected side, owing to a loss of elasticity in the affected lung and in part probably to pleuritic adhesions. On the other hand, fluid or solid tumors below the dia- phragm, unless very large, do not prevent the descent of that muscle, and so do not aljolish the diaphragm shadow. In cases in which the diagnosis is in doubt between fluid in the right pleural cavity and an enlargement of the liver upward or a subdiaphragmatic ab- seess, the preservation of the Litten's phenomenon in the latter two affections may be of great value in diagnosis. Very large accumu- lations of ascitic fluid may so far restrain the diaphragmatic move- ments that no shadow can be seen. Great muscular weakness or debility may greatly diminish, but rarely if ever prevent, the excur- FiG. 23.— Excursion of the Diaphragm duiing Forced Respiration. R, Ribs ; E, position of tbe diaphragm at end of expiration ; J, position of diaphragm at end of inspiration. sion of the shadow. In persons Avho cannot be made to breathe deeply enough to bring it out, a hard cough will frequently render it visible. The use of this method of examination tends, to a certain ex- tent, to free us from the necessity of using the a-rays, inasmuch as 26 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. it furuislies i;s -with the means of observing tlie diapliragmatic movements, on the importance of which so much stress has been Liid l:»y F. H. Williams and others, much more easily and chea})ly than with the a-rays, and upon the left side, more plainly as well. It also frees ns to a considerable extent from the need of using the spirometer to determine the capacity of the lungs. By measuring the excursion of the phrenic shadow and taking account of the thoracic movement, Ave obtain a very fair idea of the respiratory capacity of the individual. YII. Observatiox of the Cardiac IMovemexts. (1) Tlie Xonnal Ccn/t"'' Impulse. With each systole of the heart there may be seen in the great majority of normal chests an outward movement of a small portion of the chest wall just inside and below the left nipple. This phe- nomenon is known as the cardiac impulse.' It is now generally admitted that the *' apex impulse " is caused by the impact of a portion of the right ventricle against the chest wall and not by the apex of the heart itself. [The bearings of this fact, which have not, I think, been generally appreciated, will be discussed pres- ently.] The position of the rndxliinmi impulse in adults is usually in the fifth intercostal space just inside the nipple line. In chil- dren imder the age of six it is often in the fourth interspace or behind the fifth rib; while in persons of advanced age it often de- scends as low as the sixth inters])ace. In adults it is occasionally absent even in perfect health ami under certain pathological condi- tions to be later mentioned. (/■/) The ]»osition of the impiilse varies to a certain extent ac- cording to the position of the body. If the patient lies u])on the left side, the heart's apex swings out toward the axilla, so that the visible impulse shifts from one to two and one-half inches to the left (see Fig. 2i\). A slight shift to the right can also be brought about by lying upon the right side, and, as a rule, the i])i- ' For a more detailed description of the iionnal position of the cardiac iuipiilsi', see next liagu. INSPECTION. 27 pulse is less visible in the reciijubent than in the upright position. Since the heart is lifted with each expiration by the rise of the dia- phragm and falls during inspiration, a corresponding change can be observed in the apex beat, which, in forced breathing, may shift as much as one interspace. Of the changes in the position of the im- pulse brought about by disease, I shall speak in a later paragraph. Fig. 2C.— Showing Amount of Sliifting of the Apex Impulse with Change of Position, The in- ner dot represents tlie position of the impulse wlien the patient lies on his back ; the outer dot corresponds to the position of the apex with patient on left side. (//) It(datio)i of the maximum canliao inqjidse to tJie apex of the heart. — I mentioned above that the maximum cardiac impulse is not due to the striking of the apex of the heart against the chest wall, but to the impact of a portion of the right ventricle. The practical importance of this fact is this: When we are trying to localize the 28 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. apex of the lieart in order to deterniine how far the organ extends to the left and downward, it will not do to be guided by the posi- tion of the VKixiinioii impulse, for the apex of the heart is almost always to be found three-fourths of an inch or more farther to the left (see Fig. 27) . This may be proved by percussion (vide infra, Fig. 27,— The Inner Dot is the Maximum Cardiac Impulse. That to the right is the true apex of the heart, as obtained by percussion. The ribs are numbered. p. 58). The true position of the cardiac apex tlius determined cor- responds usually not with the maxim imi iin})ulse, Init with the point farthest out and farthest down at which (niu rise and faU syn- chronous Avitli the heart beat can he felt (for further discussion of this point see below, j). 213). (c) Besides the deHiiitc and localized impulse Avhich has just INSPECTION. 29 been described, it is often possible to see that a considerable section of the chest wall in the jjrecordial region is lifted "e/i viasae." The phenomenon is the " Herzenstoss " of the Germans, with which the '■ Sjntzenstoss " or ajjex inipulse is contrasted. A variable amount of " Ilerzeni^triss" can he seen and felt over any normal heart when it is acting rapidly and forcibly, and in thin, nervous subjects or in children even Avhen the heart is beating quietly. It is more marked in cardiac neuroses or in cases in Avhich the heart is hypertrophied and in which there is more or less stiffening of the ribs with loss of their natural elasticity. At times it may be impossi])le to localize any one point to which Ave can give the name of apex impulse, and what we see is the rhythmical rise and fall of a section of the chest as large as the palm of the hand or larger. (d) Character of the cardiac imindse. — Palpation is considerably more effective than inspection in giving us information as to the na- ture of the cardiac movements which give rise to the "apex beat," but even inspection sometimes suffices to shoAv that the impulse has a heaving character or is of the nature of a short tap, a peristaltic Avave, or a diffuse slap against the chest Avail. In some cases a dis- tinct undulation can be seen passing from the apex region upAvard toAvard the base of the heart, or less often in the opposite direction. (2.) Displacement of the Cardiac Impulse. To one familiar Avith the jDosition, extent, and character of the normal cardiac impulse, any displacement of this impulse from its normal site or any superadded pulsation in another part of the chest is apparent at a glance. I Avill consider first the commonest forms of dislocation of the apex impulse. (a) Displaceinent of the cardiac im^ynlse due to /n/jjertrophi/ and dilatation of the heart. — By far the most common directions of dis- placement are toAvard the left axilla, or doAviiAvard. As a rule, it is displaced in both these directions at once. I shall return to this subject more in detail under the heading Cardiac Hypertroj^h}', but here I may say that enlargements of the left A'entricle tend espe- cially to displace the apex impulse doAvnward, while enlargements of 30 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. the right ventricle are more connuonly associated witli displacement of the impulse toward the axilla. (fi) Next to hypertrophy and dilatation of the heart jierhaps the commonest cause of dislocation of the cardiac impulse is jiressure from below the diaphragm. When the diaphragm is raised by a large accumulation of gas or fluid or by solid tumors of large size, we may see the apex beat in the fourth interspace and often an inch or more inside the ni}n>le line. (c) Of nearly equal frequency is displacement of the heart due to 2)leuritic effusion or to pneumothorax. "VMien a considerable amount of air or fluid accumulates in the left pleural cavity, the apex of the heart is displaced to the right so that it may be concealed behind the sternum or be visible beyond it to the right ; in extreme cases it may be dislocated as far as the right nipple. Right pleuritic effusions have far less effect upon the position of the cardiac impulse, but when a very large amount of fluid accumulates we may see the impulse displaced considerably toward the left axilla. {(1) I have mentioned causes tending to push the heart to the r'K/lif, to thti left, or vpward. Occasionally the heart is pushed (loirmrard by an aneurismal tumor or a neoplasm of the mediasti- num. In these cases there is usually more or less displacement to tlie left as well. In old age the aorta sags or stretches a little, and hence the apex l)eat niay descend to the sixth interspace. A similar stretching of the aorta may be produced by the weight of a liypertrophied heart (e) Displacement of the cardiac impulse resulting from adliesions of the pericardium, or of the i)leura, with sulisequent contraction, occurs \n jihvold 2)ht}iisls and in some cases of long-standing disease of the pleura. Through the effect of negative pressure the heart may be sucked into the space formerly occupied by a portion of the lung, when the latter has become contracted by disease. It seems likely, however, that in the majoritj^ of cases adliesions between the i)leura and pericardium play a part in such displacement. By these means the heart nuiy be displaced to the right of the sternum, as it is l)y left-sided pleuritic effusion. It is often drawn upward INSPECTION. 31 as well as to the right in such eases by the contraction which takes place in the upper part of the lung. More rarely we may see the heart drawn toward the left clavicle in fibroid phthisis of the left apex. (/) Distortion of the thorax due to spinal curvature or other causes may bring aljout a consideralile displacement of the heart from its normal position. ((j) Dextrocardia and Situs Inversus. — In. rare cases a displace- ment of the apex impulse to the right of the sternum may be due either to a transjiosition of all viscera [the liver being found upon the left, the spleen upon the right, etc.], or to dextrocardia, in which the heart alone is transposed while the other viscera retain their normal places (see Fig. 138, p. 302). Sam mar?/. The apex impulse is displaced by (a) Hypertrophy and dilatation of the heart. (b) Pressure from below the diaphragm. (c) Air or fluid in one pleural cavity, especially the left. (d) Aneurism, mediastmal growths, and sagging of the aorta. (e) Fibroid phthisis. (/) Spinal curvature. (^) Transposition of the heart or of all the viscera. (3) Aj)ex Itetraction. Before leaving the subject of the cardiac impulse it seems best to speak of those cases m which during systole we see a retraction of one or more interspaces at or near the point where the cardiac impulse normally appears. {«) lu by far the greater number of instances such retraction is due to negative pressure produced within the chest by the vigorous contraction of a more or less hypertrophied and dilated heart In these cases the retraction is usually to be seen in several inter- spaces. Such retraction is not at all uncommon and usually at- tracts no attention. (Jj) In rarer cases several interspaces, both in the precordial 32 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. region and in the left lower axilla and Lack, may l)e drawn in as a result of adhesions between the pericardium and the chest wall, such as form in cases of adherent j^ericardium and fibrous medias- tinitis (see below, pages 216 and 295). In a considerable i)ortion of healthy adults a pulsation at the epigastrium synchronous with the systole of the heart is to be seen from time to time. Such pulsation has often been treated as evi- dence of hypertrophy of the right ventricle of the heart, but this I believe to be an error. It is not at all uncommon to find, post mor- tem, considerable hypertrophy of the right ventricle in cases in which during life no epigastric pulsation has been visible, Avhile,.on the other liand, the heart is frequently found normal at autopsy in cases in v hich during life there has been marked epigastric pulsa- tion. In some cases such pulsation is to be explained as the trans- mission of the heart's impulse through the liver, or as a lifting of that organ by the movements of the abdominal aorta. In other cases it is more difficult to explain. (5) Visible Pidsatioiis due to {"/icorerljif/ of Portians of the Heart Nonii((Uij Covered hi/ the LwKja. One of the commonest causes of visible pulsations in ]>arts of the chest Avhere normally none is to be seen is retraetion of the luiuj. () Arfn'utl Phcnoinima. \. In thin or nervous persons pulsations are not infrequently to be seen in the carotids independent of any abnormal condition of the heart. 2. Very violent thrf)bl)iug of the carotids, more noticeable than INSPECTION. 37 that seen in liealtli, occnrs in many cases of aortic regnrgitation and occasionally in simple hypertrophy of the heart withont any valvnlar disease. From the same causes, visible pulsation may occur in the subclavian, axillary, brachial, and radial arteries, as well as in the large arterial trunks of the lower extremity. I lately examined a blacksmith Avhose heart was considerably enlarged by hard work, but without any valvular disease. Pulsa- FiG. 30.— Enlarged Tortuous Brachial Arteries (Arterio-sclerosis). tion was violent in all the peripheral arteries which I have just named. 3. In arterio-sclerosis occurring in spare, elderly men, with or without aortic regurgitation, one often notices a lateral excursion of the tortuous brachial arteries synchronous with every heart beat. An up-and-down pulsation may occur at the same time. Not infre- quently the arteries which are stiffened by deposition of lime salts (see below, page ho) stand out visibly as enlarged, tortuous cords upon the temple and along the inner side of the biceps muscle, (see Figs. 30 and 31) and occasionally the course of the radial artery 38 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. may be traced over a considerable distance in tlie forearm. In rare cases inequalities produced in the arterial wall by deposition of lime salts may be visible as well as palpable. (c) C(i2>Ularij Pulsation. If a microscopic slide is placed against the mucous membrane of the lower lip so as partially to blanch its surface, one may see, with X. n.,- \ Fig. 31.— Enlarged and Tortuous iiiuchial Artery (Arterio-sclerosis) . each beat of the lieart (in cases of aortic regurgitation and sometimes in other conditions), a delicate flushing of the blanched surface be- neath the glass slide. The same pulsation is sometimes to be ob- served under the finger nails, or may be still better brought out by drawing a pencil or other hard substance across the forehead so as to cause a line of hypersemia, at the edge of which the systolic flush- ing occurs. This phenomenon will be referred to again when we come to speak of aortic regurgitation. Here it suffices to say that it is not in any way ])eculiar to that disease, and occurs occasion- INSPECTION. 39 ally in health or iii conditions associated with low tension in the peripheral arteries, as well as in any area of inflammatory hyper- aemia (jumping toothache, throbbing felon, etc.). X. IXSPECTION" OF THE SkIX AXD MuCOUS MeMBRANES. Light may be thrown upon the diagnosis of diseases of the chest by observing the color and condition of the cutaneous surfaces as Avell as of the mucous membranes. We should look for the follow- ing conditions : (1) Cyanosis. (2) (Edema. (3) Pallor. (4) Jaundice. (5) Scars and eruptions. (1) Cyanosis. By cyanosis we mean a purplish or grayish-blue tint notice- able especially in the face, in the lips, and under the nails. There are many degrees of cyanosis, from the slight purplish tinge of the lips, Avhich a little overexertion or slight exposure to cold may bring out, up to the gray-blue color seen in advanced cases of pulmonary or cardiac disease, or the dark reddish-blue seen in congenital malfor- mations of the heart. Cyanosis makes a very different impression upon us when it is combined with pallor on the one hand or with jaundice on the other. When combined with pallor, one gets vari- ous ashy-gray tints, while the admixture of cyanosis and jaundice results in a color very difficult to describe, sometimes approaching a greenish hue. The commonest causes of cyanosis are : («) Valvular or parietal disease of the heart. (Ji) Emphysema. (c) Asthma. (il) Pneumonia. \e) Phthisis. (/) In some persons a certain degree of cyanosis of the lips exists despite perfect health. This is especially true of weather- beaten faces and those of the so-called "full-blooded" type. 40 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. A rare but very striking type of cyanosis is that seen in cases of congenital heart disease, in which the lips may be indigo blue in color or almost black while yet no dyspnoea is present. (2) (Ednini. CEdema^ or the accumulation of serous fluid in the subcutaneous spaces, is usually appreciated by palpation rather than by inspec- tion, but soxuetimes makes the face look very putfy, especially under the eyes This is not a common occurrence in diseases of the chest, in connection with which such oedema as takes place is tisually to be found in the lower extremities and is aj^preciable rather by palpation than by inspection. If we are not familiar Avith a patient's face, we often do not perceive in it the changes of out- line due to oedema which a friend would notice at once. Clothing is apt to leave grooves and marks wherever it presses tightly upon the oedematous tissues, as around the waist or over the shoulders. In the legs, the presence of oedema may be suggested by an unnatu- rally smooth, glossy apjiearance of the skin Such impressions, however, may ])e false unless controlled by paljjation, for simple obesity may produce very similar appearances. (;-J) Fall,,!'. Pallor suggests, though it does not in any way prove, anaemia, and ansemia is a characteristic of the commonest of all diseases of the chest — phthisis. It is also seen in certain varieties of cardiac disease. Pallor of the mucous membranes, as seen in the lips and conjunctivje, is much more a])t to be a sign of real anaemia than is pallor of the skin. At best, pallor is only a sign which suggests to us to look further into the case in one or another direction, and of itself proves nothing of importance. (4) Jdinidiee. The yellowish tint wldch appears in the skin, and especially in the conjunctivae, when the escape of liile from the liver is hindered, is sometimes to l)e seen in connection witli uncom])ensated heart INSPECTION. 41 disease when the liver is greatly distended by passive congestion Pneumonia is occasionally complicated by jaundice; but beyond this I know of no special connection between this symptom and diseases of the chest. (5) >Sc(/rs (iiid Eruptiuns. In cases of suspected syphilis of the lung or bronchi the pres- ence of scars and eruptions suggestive of syphilis may be useful in diagnosis. XI. EXLARGED GlAXDS. Eoutine inspection of the chest may reveal the presence of en- larged glands in the neck or axillae, and may thereby give us a clew to the nature of some mtrathoracic disease ; for example, the pres- ence of enlarged glands in the neck, especially if there are any scars, sinuses, or other evidence that suppuration is going on or has formerly taken place in them, suggests the possibility of j^ul- monary tuberculosis or of an enlargement of the bronchial and me- diastinal glands. Again, malignant disease of the chest is some- times associated with the metastatic nodules over the clavicle, and a microscoj)ic examination of them may thus reveal the nature of the intrathoracic disease to which they are secondary. Very large and matted masses of glands above the clavicle, Avhich have never suj^purated and have been painless and slow in their growth, sug- gest the presence of similar deposits in the mediastinum as a part of the symptom complex known as "Hodgkin's disease." The presence of a goitre or enlargement of the thyroid gland may ac- count for a well-marked dyspnoea. Syphilis produces general glandular enlargement ; the posterior cervical and the epitrochlear glands are often involved, but this is also the case in many diseases other than sjqDhilis. CHAPTER 11. PALPATION AND THE STUDY OF THE PULSE. I Palpatiox. The most important points to be determined by palpation — that is, by laying the hand upon the siirface of the chest — are : (1) The position and character of the apex heat of the heart. (2) The presence of a ^^ thrill" (see below). (3) The vibrations of the spoken voice (^^'' tactile fremitus"). (4) The presence of pleuritic or pericardial /r/rfio;;. Other less important data furnished by palpation will be men- tioned later. (1) The Ajjej' Beat. (a) In feeling for the apex impulse of the heart, one should first lay the palm of the hand lightly upon the chest just below the left nipple. In this way we can appreciate a good deal about the movements of the heart, and confirm or modify what Ave have learned by inspection. One learns, in the first place, whether the heart beat is rer/ular or not, and in case it is irregular, whether the beats are unequal in force or whether some are skipped ; further, one gets a more accurate idea than can be obtained through inspec- tion regarding the eharaeter of the cardiac moreinents. The power- ful heaving im])ulse suggesting a hypertrophied heart, the diffuse slap often felt in dilatation of the right ventricle, the sudden tap characteristic of mitral stenosis, the deliberate thrust occasionally met with in aortic stenosis, may be thus appreciated. {h) After this, it is best to lay the tips of two or three fingers over the point where the maximum impulse is to be seen, and fol- low it outward and downward until one arrives at the point farthest to the left and farthest down at which it is still possible to feel PALPATION AND THE STUDY OF THE PULSE. 43 any iij)-aud-(lown movement. This point usually corresponds with the apex of the heart, as determined by percussion. It does not correspond with the maxivmni cardiac impulse, but is often to be found at least an inch farther to the left and downward (see above, Fig. 27). Sometimes one can localize by palpation a cardiac impulse which is not visible ; on the other hand, in some cases we can see pulsations that we cannot feel. Both methods must be used in every case. The results obtained by palpation and inspection of the apex region give us the most r'^liable data that we have regarding the size of the heart. Percussion may be interfered with by the pres- ence of gas m the stomach, of fluid or adhesions in the pleural cav- ity, or by the ineptness of the observer, but it is almost always pos- sible with a little care to make out by a combination of palpation and inspection the position of the apex of the heart. Wlien we can neither feel it nor see it, we may have to fall back upon auscul- tation, considsring the apex of the heart to be at or near the point at which the heart sounds are heard loudest. "When endeavoring to find the apex of the heart, we must not forget that the position of the patient influences considerably the relation of the heart to the chest walls If the patient is leaning toward the left or lying on the left side, the apex will swing out several centimetres toward the left axilla. (2) ''Thrills." When feeling for the cardiac impulse with the palm of the hand, we are in a good position to notice the presence or absence of a very important physical sign to which we give the name of ''thrill." The feelmg imparted to the fingers by the throat of a purring cat is very much like the palpable " tli rill " over the pre- cordia in certain diseases of the heart to be mentioned later. It is a vibration of the chest wall, usually confined to a small area m the region of the apex impulse, but sometimes felt in the second right intercostal space or elsewhere in the precordial region. This vibra- tion or thrill almost ahvays occurs intermittently, i.e., only during 44 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. a portion of the cardiac cycle, "When felt iu the apex region, it usually occurs just before the cardiac impulse ; this fact we express by calling it a "presi/stoNc t/iriW; but occasionally we may feel a systolic thrill at the apex — one, that is, which accompanies the car- diac im])ulse. The word tit rill should be used to denote only a purring, vibrating sensation communicated to the fingers by the chest wall. It is incorrect to speak of a thrill as if it were some- thing audible. We must also distinguish a purring thrill from the slight shud- der or jarring which often accompanies the cardiac impulse in func- tional neuroses of the heart or in conditions of mental excitement. As a rule we can appreciate a thrill more easily if we lay the fingers very lightly upon the chest, using as little pressure as pos- sible. Firm pressure may prevent the occiirrence of the vibrations which we desire to investigate. Of the thrills felt over the base of the heart, more will be said in Chapter YII. (3) Vibrations Commuiiicatcd to the Chest Wall hy the Voice. " Tactile fremitus " is the name given to the sense of vibration communicated to the hand if the latter is laid upon the chest while the patient repeats some short phrase of words. The classical method of testing tactile fremitus is to ask the ^mtient to count "one, two, three," or to repeat the words ''ninety-nine " Avhile the palm of the hand is laid iiat upon the chest. The amount of fre- mitus to be obtained over a given part of the thorax varies, of course, according to the loudness of the words spoken, and is influenced also by the vowels contained in them. A certain uniformity is ob- tained by getting the patient to repeat always the same formula. Thus, he is likely to use the same amount of force each time he re- peats them and to use approximately the same pitch of voice. Other things being equal, the fremitus is greater in men than in Avomen, in adults than in children, and is more marked in those whose voices are low pitched than in those whose voices are rela- tively shrill The amount of fremitus also varies widely in differ- ent parts of the healthy chest A glance at Fig .'-52 will help us to realize this The parts sliaded darkest communicate to the fingers PALPATION AND THE STUDY OF THE PULSE. 45 the most marked fremitus, while iii the parts not shaded at all, lit- tle or no fremitus is felt. Intermediate degrees of vibration are represented by intermediate tints of shading. From this diagram we see at once (a) that the maximum of fremitus is to be obtained over the apex of the right lung in front, {b) that it is greater in the upper part of the chest than in the lower, and somewhat greater throughout the right chest than in corresponding parts of the left. Fig. 32.— Distribution of Tactile Fremitus. This natural inequality of the two sides of the chest cannot be too strongly emphasized. Comparatively little fremitus is to be felt over the scapulae be- hind, and still less in the precordial region in front. The outlines of the lungs can be quite accurately mapped out by means of the tactile fremitus in adults of low-pitched voice. In children, as has been already mentioned, fremitus is usually very slight and may be entirely absent, and in many women it is too slight to be of any considerable diagnostic value. Again, some very fat persons and those with thick chest walls transmit but little vibration to their chest Avails when they speak. On the other hand, in emaciated patients or in those with thin-walled, flexible chests, the amount of fremitus is relatively great. 46 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. Bearing in mind all these disparities — disparities both between persons of different age and different sex, and between the two sides of the chest ui any one person — we are in a position to appreciate the modifications to which disease gives rise and which may be of great impor- tance in diagnosis. These vari- ations are : {(t) Dimiuntion or absence of fremitus. (h) Increase or absence of fremitus. (fl) If the lung is j^ushed away from the chest wall by the presence of air or fluid in the pleural cavity, we get a diminu- tion or absence of tactile fremi- tus — diminution where the layer of fluid or air is very thin, al)- sence where it is of considerable thickness. (A) Solidification of the lung due to phthisis or jDneumonia is the commonest cause of an in- crease in tactile fremitus. Fur- ther details as to the variations in amount of fremitus in different diseases may be found in later chapters of this lK)()k. (4) Friftloii, J'Icdrol or I'crica rd'ud . In many cases of inflammatory roughening of tlie pleural sur- faces (" dry pleurisy ") a grating or rubl)ing of the two surfaces upon each other may be felt as well as heard during the movements of res})iration, and especially at the end of insjjiration. Such fric- tion is most often felt at the l)()ttom of tlie axdla, on one side or Fig. :33.-Sli(i\viiifr I'liint iFi :it Whirh I'louial Frictiou is Most Ofteu Hearcl. PALPATION AND THE STUDY OF THE PULSE. 47 the other, where the diaphragmatic pleura is in close apposition with the costal layer (see Fig. 3o, p. 46). Similarly, in roughening of the pericardial surfaces ("dry" or " plastic " pericarditis) it is occasionally possible to feel a grating or rubljing in the precordial region more or less synchronous with the heart's movements. Such friction is most often to be felt in the region of the fourth left costal cartilage (see Fig. 34). Palpable friction is of great value in diagnosis because it is a sign about which we can feel no doubt ; as such it frequently con- FiG. 34.— Sbowing Point (P) at Which Pericardial Friction Is Most Often Heard. firms our judgment in cases in which the auscultatory signs are less clear. Friction sounds heard with the stethoscope may be closely simulated by the rubbing of the stethoscope upon the skin, but pal- pable friction is simulated by nothing else, unless occasionally by (5) Fidp(ih](> Bides. Occasionally coarse, dry rales communicate a sensation to the hand placed upon the chest in the region beneath which the rales are produced; to the practised hand this sensation is quite diifer- ent from that produced by pleural friction, although the difference is hard to describe. 48 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. (6) Tender points upon the thorax. In intercostal neuralgia, dry pleurisy, necrosis of a rib, and sometimes in phthisis, one finds areas of marked tenderness in different parts of tlie chest. The position of the tender points in intercostal neuralgia generally corresponds with the point of exit of the intercostal nerves. These points are shown in Fig. 35. The tenderness in phthisis is most apt to be in the upper and front portions of the chest. In neurotic individuals we sometimes find a very superficial tenderness over parts of the thorax ; in such Fig. :i).— Showing Points of Exit of the Intercostal Nerves. cases pain is produced by very light pressure, but not by firm press- ure at the same })oint. (7) The presence of pulsations in parts of the chest where nor- mally there should be none is suggested by inspection and con- firmed by palpation. It is not necessary to repeat what Avas said above as to the commonest causes of such abnormal pulsations. When searching for slight, deei)-seated pulsation (e.f/., from an aortic aneurism), it is well to use l)imanual palpation, keeping one hand on the front of the chest and the other over a corresponding area in the back. (8) Fluctuation or elasticity in any tumor or projection from PALPATION AND THE STUDY OF THE PULSE. 49 the chest is a very iiuportant piece of informatiou which palpation may give us. (9) The temperature antl quality of the skin are often brought to our attention during palpation. After a little practice one can usually judge the temperature within a degree or two simply from the feeling of the skin. Any roughness or dryness of the skin (myxoedema, diabetes) is easily appreciated as we pass the hand over the surface of the thorax or down the arms. The same manipula- tion often brings to our attention in cases of alcoholism an unusu- ally smooth and satiny quality of the cutaneous surface. II. Thk Pulse. Fifty years ago the study of the pulse furnished the physician, with most of the available evidence regarding the condition of the heart. At present this is not the case. With the increase of our knowledge of the direct physical examination of the heart, the amount of information furnished exclusively by the pulse has pro- portionately decreased, until to-day, I think, it is a fact that there is but little to be learned by studying the pulse which could not be as well or better ascertained by examining the heart itself. Nevertheless, the radial pulse is still an important factor in diagnosis, prognosis, and treatment, and will remain so, because it gives us quickly, succinctly, and in almost every case a great deal of valuable information which it would take more time and trouble to obtain by examining the heart itself. As we feel the pulse, we get at once a fact of central importance in the case ; by the pulse the steps of our subsequent examination are guided. In emergen- cies or accidents- the pulse gives us our bearings and tells us whether or not the patient's condition is one demanding immediate succor — e.g., hypodermic stimulation — and whether the outlook is bright or dark. To gather this same information by examining the heart itself would mvolve losing valuable time. Again, when one has to s.?e a large number of patients in a short time, as in visiting a hospital ward or on the crowded days of private practice, the pulse is an invaluable short cut to some of the most important data. 4 50 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. Moreover, there are some important inferences which the pulse and onli/ the j^nl^f^ enables us to make. They are not numerous, but their value may be great. Delay iu one radial pulse when taken in connection with other signs may furnish decisive evidence of aneu- rism of the aortic arch ; aortic stenosis is a lesion Avhich cannot be diagnosed unless the pulse shows certain characteristic features; arterial degeneration may betray its presence .chiefly in the periph- eral arteries. Since, then, the condition of the pulse furnishes information of crucial importance in a few diseases, and is a quick, reliable, and convenient indication of the general condition of the circulation iu all cases, it is essential that we should study it most carefully both in health and in disease. How to Feel tJie Pulse. (a) We usually feel for the pulse in the radial artery because this is the most superflcial vessel which is readily available. Oc- casionall}', as when the wrists are swathed in surgical dressings or tied up in a straight-jacket, Ave make use of the temporal, facial, or carotid arteries. (i^) l^oth radials should always be felt at the same time. By making this a routine practice many mistakes are avoided and any difference in the two pulses is appreciated. (c) The tips of three fingers (never the thumb) should be laid upon the artery, and the following points noted : 1. The rate of the pulse. 2. The rJti/tlnu of the pulse (regular or irregular). 3. The amoiuit of force necessary to obliterate it [coynjiressi- hilitif) . 4. The size and shape of the pulse wave. 5. The extent to which the artery collapses between beats (tension) . 6. The sise and posit io?i of the arter;/. 7. The condition of the arteri/ walls. Each of these points will now be considered in detail. PALPATION AND THE STUDY OF THE PULSE. 51 1. The Rate of the Pulse. In the adult male the pulse averages 72 to the minute, in the female 80. In children it is considerably more frequent. At birth it averages about 130, and until the third year it is usually aljove 100. In some families as low pulse, 60 or less, is hereditary ; on the other hand, it is not very rare to observe a permanent pulse rate of 110 or more in a normal adult (see below, p. 202). Exercise or emo- tion quickens the pulse very markedly, and after food it is someAvhat accelerated. Some account of the causes of pathological quicken- ing or sloAving of the pulse will be found on pages 202 and 203. 2. Bhi/thm. The pulse may be irregular in force, in rhythm, or (as most commonly happens) in both respects. As a rule, irregularities in force are the more serious. Intermittence or irregularity in rhythm alone, means that the heart skips one or more beats at regular or irregular intervals. This may be a mere idiosyncrasy not associ- ated with an}^ evidence of disease. I have known several instances in which a perfectly sound person has been aware of such an irregu- larity throughovit life — the heart dropping regularly every third or fourth beat. Such rhythmical intermittence in health is not un- common. When beats are dropped, not at fixed intervals, but irregularly, the pulse waves usually vary in force as well. This combination of irregular cardiac rhythm with variations in the strength of the individual beats is very rarely seen in health and usually points to functional or structural disease of the heart. Special types of irregularity will be discussed later. In general it may be said [a) that irregularity in the force of the pulse beats is a serious sign, if overexertion and temporary toxic influences (tobacco, tea, etc. ) can be ruled out ; {h) that it is far more serious when occurring in connection with diseases of the aortic valve than in mitral disease ; and (c) that it often occurs in connection with sclerosis of the coronary arteries and myocarditis. 52 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. S. Compressibility. There is no single datum concerning tlie pulse more important than the amount of force needed to obliterate its beat. We have no more accurate method of measuring the compressibility of the pulse than the following : Let the tips of three fingers rest as usual on the radial artery Then gradually increase the pressure made upon the vessel with the finger nearest the patient's heart until the pulse wave is arrested and cannot be felt by the other fingers which rest loosely on the artery. The degree of force necessary to arrest the wave varies a great deal in different cases and at different times of day, but by trying the above manceuvre day after day in as many cases as possible one comes to possess a fairly accurate mental standard or picture of the compressibility of the average pulse, and is then able to estimate in any given case whether it is more or less compressible than usual. The compressibility of the pulse is a rough measure of the mus- cular power of the heart's beat, and therefore gives us direct infor- mation abou.t this important element in the patient's condition. 4- The Size and Shape of the Pulse TVave. Of the use of the sphygmograph for representing pulse waves I shall sjjeak later. The points discussed in this section are appre- ciable to the fingers. I. The size of the pulse wave — the height to Avhich it lifts the finger — depends on two factors : (a) The force of the cardiac contractions. (J)) The tightness or looseness of the artery {tension). If the arteries are contracted and small, the pulse wave corre- sponds, while if they are large and relaxed, it needs only a moder- ate degree of power m the heart to produce a high pulse wave. If the tension remains constant the size of the pulse wave depends on the force of the heart's contraction. If the heart power remains constant, the size of the pulse wave depends on the degree of vas- cular tension. Vascular tension is estimated in Avays to be de- scribed ])resently, and after allowing for it, we are enabled to esti- PALPATION AND THE STUDY OF THE PULSE. 53 mate the power of the heart's contractions from the height of the pulse wave, II. The shfqye of the 2^ulse vave is also of importance. («) It may have a very sharp summit, rising and falling back again suddenly; this is known as an ill-sustained pulse, and may be due to a lack of sustained propulsive power in the contracting heart muscle, to low vascular tension, or to a combination of the two causes. A weak heart when stimulated by alcohol often pro- duces such a pulse wave — deceptively high and giving at first an impression of power in the heart wall, but ill sustained and easily compressible. An exaggeration of this type of pulse is to be felt in aortic regurgitation (see Fig. 102). (1>) In sharp contrast with the above is the pulse wave which lifts the finger gradually and slowly, sustains it for a relatively long period, and then sinks gradually down again. Such a pulse with a " long plateau " instead of a shar^) peak is to be felt most distinctly in aortic stenosis, less often in mitral stenosis and other conditions (see Fig. 107). (c) The dicr'otic pulse wave is one in which the secondary wave, which the sphygmograi)h shows to be present in the normal pulse, is much exaggerated, so that a distinct " echo " of the primary wave is felt after each beat. If the heart is acting rapidly, this dicrotic wave does not have tiaie to fall before it is interrupted by the i^rimary wave of the next beat, and so appears in the sphygmo- graphic tracing as a part of the ujD-stroke of the primary wave. This is known as the ^^ anacrotic pulse." (d) The shape of the high-tension ])%dse rvave will be described in the next paragraph. 5. Tension . The degree of contraction of tlie vascular muscles determines the size of the artery and (to a great extent) the tension of the blood within it. But if the heart is acting feebly, there may be so little blood in the arteries that even when tightly contracted they do not subject the blood within them to any considerable degree of tension. To produce high tension, then, we need two factors : a 54 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. certain degree of power in the heart muscle, and contracted arteries. To produce low tension we need only relaxation of the arteries, and the heart may be either strong or weak. The 23i(he of low tension collapses between beats, so that the ar- tery is less palpable than usual or cannot be felt at all. Normally, Fig. 36.— Sphygmographie Tracing of Low Tension Pulse. the artery can just be made out between beats, and any consider- able lowering of arterial tension makes it altogether impalpable except during the period of the primary wave and of the dicrotic wave, which is often very well marked in pulses of low tension. The shape of the wave under these conditions has already been described (see Fig. 36). The pulse of high tension is percejitible between beats as a dis- tinct cord irliich am he rolled between the fingers, like one of the ten- Fin. 37.— Sphygmographic Tracing of High Tension Pulse. dons of the wrist. It is also difficult to compress in most cases, but this may depend rather on the heart's i)ower than on the degree of vascular tension. The i)ulse wave is usually of moderate height or low, and falls away slowly with little or no dicrotic wave (see Fig. 37). PALPATION AND THE STUDY OF THE PULSE. 55 6. The Size and Position of the Artery. I have often known errors to occur because a small artery is mistaken for a small ^>/f/./mji) On groimds of cleanHness (although the chest may be cov- ered with a towel so as to protect the auscultator to a certain extent). (c) Because we cannot conveniently reach the supracla^•icular or the upper axillary regions in this way. (•fZ) Because it is difficult to localize the different vahnilar areas and the sites of cardiac murmurs if immediate auscultation is em- ployed. On account of the latter objection the great majority of observ- ers now use the stethoscope to examine the heart. For the lungs, both methods are employed by most experienced auscultators. 78 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. (Personally, I have never yet learned to hear anything with my unaided ear which I could not hear better with a stethoscope, and the Bowles stethoscope seems to me to reach as large an area and as deep as the unaided ear. Nevertheless the weight of competent ophiion is against me and greater experience will doubtless show me my mistake.) "While learning the use of immediate auscultation it is best to close with the fingers the ear which is not in contact with the chest. With practice one comes to disregard outer noises and does not need to stop the ear. Mediate Auscultatiox. 1. Select toil of a Sti'tltosro^^e. (1) It is as rash for any one to select a stethoscope without first trying the fit of the ear pieces in his ears as it would be to buy a new hat without trying it on. AVhat suits A. very well is quite im- possible for B. It is true that one can get used to almost any stethoscope as one can to almost any hat, but it is not necessary to do so. The ear pieces of the ordinary stethoscope are often too small and rarely too large. In case of doubt, therefore, it is better to err upon the side of getting a stethoscope with too large rather than too small ends. (2) The binaural stethoscope, which is now almost exclusively used in tins country, maintains its position m the ears of the aus- cultator either through the pressure of a rubber strap stretched around the metal tubes leading to the ears, or by means of a steel spring connecting the tubes. Either variety is usually satisfactory, but I prefer a stethoscope made with a steel spring (see Fig. 48) because such a spring is far less likely to break or lose its elasticitj^ than a rubber strap. A rubber strap can always be added if this is desirable. It is important to pick out an instrument possessing a si)ring not strong enough to cause i)ain in the external meatus of the ear and yet strong enough to hold the ear })ieces firmly in i)lace. Persons with narrow heads need a much more powerful spring or strap tlmn would l)e convenient for i)ersons witli wide heads. AUSCULTATION. 79 (3) The rubber tul)ing used to join the metallic tubes to the chest piece of the instrument should be as flexible as possible (see Fig. 48). Stiff tubing (see Fig. 49) makes it necessary for the auscultator to move his head and body from place to place as the exam- ination of the chest pro- gresses, Avhile if flexible tubing is used the head need seldom be moved and a great deal of time and fatigue is thus saved. Stiff stetho- scopes are especially incon- venient when examining the axilla. (4) Jointed stethoscopes which fold up or take apart should be scrupulously avoided. They are a delu- sion and a snare, apt to come apart at critical mo- ments, and to snap and creak at the joints when in use, sometimes producing in this way sounds which may be easily mistaken for rales. Such an in- strument is no more portable nor compact than the ordinary form with flexible tubes. It has, therefore, no advantages over stethoscopes made in one piece and possesses disadvantages which are peculiarly annoying. (5) The Chest Piece.— The majority of the stethoscopes now in use have a chest j)iece of hard-rubber or wood with a diameter of about seven-eighths of an inch. Chest pieces of larger diameter than this are to be avoided as they are very difticult to maintain in close apposition Avith thin Fig. 49. — C a m m a n Stethoscope With Stiff Tubing and Rubber Strap. Fig. 4.S. — stethoscope Fitted With Long Flexible Tubes, Espe- cially Useful When Examining Children. 80 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. chests. To avoid this difficulty the chest piece is sometimes made of soft-rubber or its diameter still further reduced. (6) The Bowles Stetlioscope. — (See Figs. 50 and 51.) Within the last year there has been introduced an instrument which, for most purposes, seems to me far superior to any other form of stetho- scope with which I am acquainted. Its pe- culiarity is the chest piece, which consists of a very shal- low steel cup (see Fig. 52) over the mouth of Avhich a thin metal plate or a bit of pigskin is fastened. The metal or pigskin diaphragm serves simply to prevent the tissues of the chest from pro- jecting into the shallow cup of the chest piece when the latter is pressed against the chest, and does not in any other way contribute to the sounds which we hear with the instrument. This is proved by the fact that we can hear as well even when the diaphragm is cracked across in several directions. With this instrument al- most all sounds i)roduced Avithin the chest can be heard much more distinctly than in any other variety of stethoscope. Cardiac murmurs which are in- audible with any other stethoscope may be distinctly heard with this. Especially is this true of low-pitched murmurs due to aortic regur- gitation. Yet it is useful for examination not merely of the heart, but of the lungs as well. For any one who has difficulty in hearing the ordinary cardiac or respiratory sounds, or for one Avho is par- no. 50.— Bowles' Stetho scope. Front view. Fig. 51. — Bowles' Stethoscope. Back View. AUSCULTATION. 81 tially deaf, the instrument is invalualjle. Its flat chest piece makes it very useful m listenmg to the posterior portions of the lungs in cases of pneumonia in which the patient is too sick to be turned over or to sit up. "Without moving the patient at all we can work the chest piece m under the back of the patient by pressing down the bed-clothes, and m this way can listen to any part of the chest without moving the patient. A further advantage of the instru- ment is that it enables us to gain an api^roximately accurate idea of the heart sounds witliout undressing the patient. Respiratory /^ Fig. 52.— Chest Piece of Bowles' Stethoscope. On the right the shallow cup communicating with the ear tubes. On the left the diaphragm which covers the cup, and the ring which holds it in place. sounds cannot well be listened to through the clothes, as the rub- bing of the latter may simulate rales. There are two purposes for which I have found the Bowles stethoscope inferior to the ordinary stethoscope : (1) For listening over the apex of the lung for fine rales, e.y., in incipient phthisis. (2) For listening for snperfickd sounds, such as a friction rub of a presystolic murmur.' "When I desire to listen for fine rales at ^ It has frequently been observed, when listening with the ordinary stetho- scope, that a presystolic murmur can be better heard if only the very lightest pressure is made with the stethoscope. The fact that a thrill is communicated to the chest wall, and that that thrill is connected with the audible murmur explains my calling this murmur a superficial one. 6 82 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. an apex, for a friction rub, or for a presystolic murmur, I separate the chest piece of the Bowles stethoscope from the rubber tube which connects it with the rest of the instrument and slip on in its place the hard-rubber bell of an ordinary stethoscope, thereby converting the instrument mto one of the ordinary form. With an extra hard- rubber bell attached or kept in the pocket, the instrument is no more bulky than an ordinary stethoscope, and far more efficient. N^^ien used for listening to the res- piration, the Bowles instru- ment gives us information similar in some respects to that obtained by the use of the free ear — that is, we are through it enabled to ascer- tain by listening at one spot the condition of a much larger area of the chest than can in any other way be in- vestigated. Owing to the fact that both cardiac and respiratory sounds are magnified by the Bowles stethoscope, this instrument is especially well adapted for use Avith some sort of an attachment whereby several sets of ear pieces are so joined by tubing to one chest piece that several persons may listen at once. Bowles' multiple stethoscope, fitted for six and for twelve observers, is seen in Figs. 53 and 54, and the method of its use in Fig. 55. In the teaching of auscultation this instrument is of great value, saving as it does the time of the instructor and of the stu- dents and the strength of the patient. The sounds conducted through any one of the twelve tubes used in this instrument are Fig. 53.— Bowles' Multiple stethoscope for Six Stu- dents. AUSCULTATION. 83 as loud as those to be heard with a single instrument of the ordi- nary form, although far fainter than those to be heard with a single Bowles stethoscope. II. The Use of the Stetlioscope. Having secured an instrument which fits the ears satisfactorily, the beginner may get a good deal of practice by using it upon him- FiG. 54.— Bowles' Multiple Stethoscope for Twelve Students. self, especially upon his own heart. The chief point to be learned is to disregard various irrelevant sounds and to concentrate atten- tion upon those which are relevant. Almost any one hears enough with a stethoscope, and most beginners hear too much. No great keenness of hearing is required, for the sounds which we listen for are not, as a rule, difficult to hear if attention is concentrated upon them. 84 PHYSICAL DIAGyOSIS OF DISEASES OF THE CHEST. A. Si'h'ctlre Afff'uttoii and IVJiat to Disregard. Accordingly, the art of using a stethoscoi:)e successfully depends upon the acquisition of two powers — {a) A knoAvledge of what to disregard. (//) A selective atten- Fn;. .j").— Biiwlts' Mullipli; .stelboscope iu U.sf. Twelve stiuleiits listeiiiiifi at uiice tion or concentration \\])o\\ those sounds which we know to be of ini})ortance. Among the sounds Avhich we must learn to disregard are the following: (1) Noises ])rodu('('(l iu the room or its immediate neiglihorhood, but not connected with the i»atient himself. It is, of course, easier AUSCULTATIOX. 85 to listen iii a perfectly quiet room where there are no external noises which need to be excluded from attention, hut as the greater part of the student's work must be done in more or less noisy places, it is for the beginner a practical necessity to learn to with- draw his attention from the various sounds which reach his ear from the street, from other parts of the building, or from the room in which he is working. This is at first no easy matter, but can be accomplished witli practice. (2) AMien the power to disregard external noises has been ac- quired, a still further selection must be made among the sounds which come to the ear through the tubes of the stethoscope. Noises produced by friction of the chest piece of the stethoscope upon the skin are especially deceptive and may closely simulate a pleural or pericardial friction sound. It is well for the student to experiment upon the nature and extent of such " skin rubs " by deliberately moving the chest piece of the stethoscope upon the skin and listen- ing to the sounds so produced. ]\Iistakes can be avoided in the majority of cases by holding the chest piece of the stethoscope very firmly against the chest. This can be easily done when the patient is in the recumbent position, but Avhen the patient is sitting up it may be necessary to press so hard with the chest j)iece of the stethoscope as to throw the patient off his balance unless he is in some way supported ; accordingly, it is my practice in many cases to put the left arm around and behind the patient so as to form a support, against which he can lean when the chest piece of the stethoscope is pressed strongly against his chest. AMien listening to the back of the chest, the manoeu^TC is reversed. If the skin is A^ery dry, the ribs are very prominent, or the chest is thickly covered with hair, it may be impossible to prevent the occur- rence of adventitious sounds due to friction of the chest piece upon the chest, no matter how firmly the instrument is held. In case of doulit, and in any case in which a diagnosis of pleural or pericardial friction is in question, the surface of the chest, at the point where we desire to listen, should be moistened and any hair that may be present thoroughly Avetted Avith a sponge, so that it will lie fiat upon the chest. OtlierAvise the friction of the hair 86 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. under the chest piece of the stethoscope may simulate crepitant rales as closely as " skin rubs " simulate pleural friction. (3) The friction of the fingers of the auscultator upon the chest piece or on some other part of the stethoscope frequently gives rise to sounds closely resembling rales of one or another description. The nature of these soimds can be easily learned by intentionally moving the fingers upon the stethoscope. They are to be avoided by grasping the instrument as firmly as possible, and by touching it with as few fingers as will suffice to hold it close against the chest. (4) Noises produced by a shifting of the parts of the stetho- scope upon each other are especially frequent in stethoscopes made in several pieces and jointed together, A variety of snapping and cracking sounds, not at all unlike certain varieties of rales, may thus be produced, and if we are not iipon our guard, may lead to errors in diagnosis. Stethoscopes which have no hinges and which do not come apart are far less likely to trouble us in this way. (5) When a rubber band is used to press the ear pieces more firmly into the ears, a very peculiar sound may be produced by the breathing of the auscultator as it strikes upon the rubber strap. It is a loud musical note, and may be confused with coarse, dry rales. Wlien one has learned to recognize and to disregard the noises produced in the ways above indicated, there is still one set of sounds which are very frequently heard, yet which have no signifi- cance for physical diagnosis, and must therefore be disregarded; I refer to B. Muscle Sounds. Patients who liold themselves very erect while being exam- ined, or who for any reason contract the muscles of that portion of the chest over which we are listening, prodiice in these muscles a very peculiar and characteristic set of sounds. The contraction of any muscle in the body prodiujes sounds similar in quality to those heard over the chest, but of less intensity. Those who have the faculty of contracting the tensor tympani muscle at Avill can at any time listen to a typical muscle soiuul. A use ULTA TION. 87 Or close both ears with the lingers and strongly contract the uias- seter nmscle, with the teeth clenched. A high-pitched muscle sound will be heard. It is well also to have a patient contract one of the pectorals and then listen to the sound thus produced. In some cases a con- tinuous, low-pitched roar or drumming is all that we hear ; in other cases we hear nothing but the breath sounds during expiration, while during inspiration the breath sound is obscured by a series of short, dull, rumbling sounds, following each other at the rate of from hve to ten in a second. Occasionally the sound is like the puffing of the engine attached to a pile-driver, or like a stream of water fallmg upon a sheet of metal just slowly enough to be sepa- rated into drops and heard at a considerable distance. As already mentioned, we are especially apt to hear these muscle sounds dur- ing forced inspiration, owing to the contraction of voluntary mus- cles during that portion of the respiratory act. They are most often heard over the upper portion of the chest (over the pectorals in front and over the trapezius behind), but m some persons no part of the chest is free from them. It is a curious fact that we are not always able to detect by sight or touch the muscular con- tractions which give rise to these sounds, and the patient himself may be v/holly unaware of them. Under such circumstances they are not mfrequently mistaken for rales, and I am inclined to think that many of the sounds recorded as "crumplmg," "obscure," "muffled," "distant," or "indeterminate" rales are in reality due to muscular contractions. The adjectives " muffled " and " distant " give us an inkling as to the qualities which distinguish muscular sounds from rales. Eales are more clean cut, have a more distinct beginning and end, seem nearer to the ear, and possess more of a crackling or bubblmg quality than muscle sounds. I have made no attempt exhaustively to describe all the sounds due to muscular contractions and conducted to the ear by the steth- oscope, but have intended simply to call attention to the importance of studying them carefully. PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. C. Other Sources of Error. Another source of confusion, whicli for beginners is A^ery trouble- some, especially if they are using the ordinary form of stethoscope with a bell-shaped chest piece, arises in case the chest piece is not Fig. 5fi.— Sliowiii iinected.) held perfectly in apposition with the skin. If, for example, the stethoscope is slightly tilted to one side so that the bell is lifted from the skin at some point, or if one endeavors to listen over a very uneven part of the chest on which the bell of the stethoscope cannot be made to rest closely, a roar of external noises reaches the ear through the chink left between the chest piece and the chest. AUSCULTATION. 89 After a little practice one learns instantly to detect this condition of things and so to shift the position of the chest piece that exter- nal noises are totally excluded ; but by the Ijeginner, the peculiar babel of external noises which is heard whenever the stethoscope fails to fit closely against the chest is not easily recognized, and Fig. 5".— Accident to be Avoided. CStethoscope kinked.) hence he tends to attribute some of these external sounds to diseased conditions within the chest. Again, it is not until we have had considerable practice that our sense of hearing conies instantly to tell us when something is wrong about the stethoscope itself; when, for example, one of the tubes is blocked, kinked, or disconnected (see Figs. 56 and 57), or when we are holding the stethoscope upside down, so that the ear pieces point downward instead of upward (see Figs. 58 and 59). It is only when we have learned through long practice about how much we 90 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. ought to hear at a given point in the normal chest that we recognize at once the fact that we are not hearing as much as ive should^ in Fig. 58— Stethoscope Held Ripht Side Up. case some one of the above accidents has happened. Many begin- ners do not listen long enough in any one place, but move the chest piece of the stethoscope about rapidly from point to point, as they have seen experienced auscultators do; but it is remarkable how much more one can hear at a given point by simply persevering and listening to beat after beat, or In-eath after breath. It is sometimes Fig. 59.— stethoscope Held Wrong Side Up. difficult to avoid the impression that the sounds themselves have grown louder as we continue to listen, especially if Ave are in any A use UL TA TION. 91 doubt as to what we hear. Therefore, if we hear indistinctly, it is important to keep on listening, and to fix the attention successively upon each of the different elements in the sounds under consideration. In difficult cases we should use every possible aid toward concen- tration of the attention, and where it is possible, all sources of dis- traction should be eliminated. Thus, in any case of doubt, I think it is important for the auscultator to get himself into as comfort- able a position as he can, so that his attention is not distracted by his own jDhysical discomforts. Many auscultators shut their eyes when listenuig in a difficult case so as to avoid the distraction of impressions coming through the sense of sight. It goes without saying that if quiet can be secured in the room where we are work- ing, and outside it as well, we shall be enabled to listen much more profitably. AUSCULTATION OF THE LUNGS. In the majority of cases ordinary quiet breathing is not forcible enough to bring out the sounds on which we depend for the diag- nosis of the condition of the lungs. Deep or forced breathing is what Ave need. As a rule, the patient must be taught how to breathe deeply, which is best accomplished by personally demonstrating the act of deep breathing and then asking him to do the same. Two difficul- ties are encountered : {a) The patient may blow out his breath forcibly and with a noise, since that is what he is used to doing whenever he takes a long breath under ordinary circuuistances ; or (h) It may be that he cannot be made to take a deep breath at all. The first of these mistakes alters the sounds to be heard with the stethoscope in any part of the chest by disturbing both the rhythm and the pitch of the respiratory sounds. In this way the breathing may be made to sound tubular or asthmatic throughout a sound chest. This difficulty can sometimes be overcome by demon- strating to the patient that what you desire is to have him take a full breath and then simply let it go, but not blow it forcibly out. In some cases the patient cannot be taught this, and we have to get 92 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. on the best we can despite his mistakes. When he cannot be made to take a full breath at all, we can often accomplish the desired re- sult by getting him to cough. The breath just before and after a cougli is often of the type we desire. The use of voluntary cough in order to brmg out rales will be discussed later on. Another use- ful manoeuvre is to make the patient count aloud as long as he can with a single breath. The deep mspiration which he is forced to take after this task is of the type wliich we desire. I. Eespiratoky Types. In the normal chest two types of breathing are to be heard : (1) Tracheal, bronchial, or tubular breathing. (2) Vesicular breathing. Tracheal, hroncJiial, or tuhid'W hri'atlilng is to be heard in normal cases if the stethoscope is pressed agamst the trachea, and as a rule Fig. Oft.— Situation of the Trachea and Primary Bronchi. it can also be heard over the situation of the ])rimary bronchi, in front or behind (see Figs. 60 and 01). Vetih-ylar hreath'mr/ is to be heard over the remaining portions of the lung — that is, in the front of the thorax except where the heart AUSCULTATION. 93 and the liver come against the chest wall, in the back except where the presence of the scapulse obscures it, and throughout both axillae. (1) Characteristics of Vesictdm' Breathing. Vesicular breathing — that heard over the air vesicles or paren- chyma of the lung — has certam characteristics which I shall try to describe in terms of intensity, duration, and pitch. Fig. 61.— Situation of the Trachea and Primary Bronchi. Of the qualitij of the sounds heard over this portion of the lung there is little can be said ; it sounds somethmg like the swish of the wind in a grove of trees some distance off, and hence is sometimes spoken of as "breezy." The intensity, duration, and pitch of the inspiration as compared with that of the expiration may be represented as in Fig. 62. In this figure, as in all those to be used in description of respiratory sounds — (1) I represent the inspiration by an up-stroke and the expira- tion by a down-stroke (see the direction of the arrows in Fig. 62). (2) The length of the up-stroke as compared Avith that of the down-stroke corresponds to the length of inspiration compared with expiration. 94 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. (3) The fhlchiess of the iip-stroke as compared with the down- stroke rejjresents the intensltij of the iuspiratioii as compared with the expiration. (4) The pitcli of inspiration as compared with that of expi- ation is represented by the sharpness of the angle which the up- FiG. 62.-VesifuIar Breatb- FiG. 63.— Distant Vesicular FiG. 64. -Exaggerated Ve- ing. Breathing. sicular Breathing. stroke makes with the perpendicular as compared with that which the down-stroke makes with the perpendicular. The p'dcli of a roff may be thought of in this connection to remmd us of the mean- uig of these symbols. If now we look agam at Fig. 62 we see that when compared with expiration (the down-stroke), the inspiration is — [a) More intense. {b) Longer. (<•) Higher pitched. Our comparison is invariably made between inspiration and ex- piration, and not with any other sound as a standard. Now, this type of breathing (which, as I have said, is to be heard over every portion of the lung except those portions imme- diately adjacent to the primary bronchi), is not heard everywhere with equal intensity. It is best heard below the clavicles in front, in the axillae, and below the scapulae behind, but over the thin, lower edges of the lung, whether behind or at the sides, it is fee1)ler, though still retaining its characteristic type as revealed in the inspiration and expiration in respect to intensity, duration, and pitch. To represent distant vesicular l:)reathing graphically we have only to draw its symbol on a smaller scale (see Fig. 03). On AUSCULTATION. 95 the other hand, when one listens to the lungs of a person who has been exerting himself strongly, one hears the same type of respira- tion, but on a larger scale, which may then be represented as in Fig. 64. This last symbol may also be used to represent the respi- ration which we hear over normal but thin-walled chests ; for ex- ample, in children or in emaciated persons. It is sometimes known as "exaggerated" or ''puerile" respiration. When one lung is thrown out of use by disease so that increased work is brought upon the other, the breath sounds heard over the latter are increased and seem to be produced on a larger scale. Such breathing is some- times spoken of as " rough " breathing. It is very important to distinguish at the outset between the different ti/i^es of breathmg, one of which I have just described, and the different degrees of loudness with which any one tyjje of breath- ing may be heard. (2) Bronclikd or Tracheal Breatliing in Health. Bronchial breathing may be symbolically rej^resented as in Fig. 65, in which the increased length of the down stroke corresponds to the increased duration of exiDiration, and the greater thickness Fig. 65.— Bronohial Breath- ing of Moderate Intensity. Fig. 66.— Distant Bronchial Breathing. Fig. 67.— Very Loud Bron- chial Breathing. of both Imes corresponds to the greater intensity of both sounds, expiratory and inspiratory, while the sharp pitch of the " gahle " on both sides of the perpendicular corresponds to the high pitch of both sounds. Expiration, it will be noticed, slightly exceeds inspi- ration both in intensity and pitch, and considerably exceeds it in duration, while as compared with vesicular breathing almost all the 96 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. relations are reversed. Broncliial breathing has also a peculiar quality which can be better appreciated than described. In the healthy chest this type of breathing is to be heard if one listens over the trachea or primary bronchi (see above, Fig. 60), but practically one hardly ever listens over the trachea and bronchi except by mistake, and the importance of familiarizmg one's self with the type of respiration heard over these portions of the chest is due to the fact that in certain diseases, especially in i)neumonia and phthisis, we may hear bronchial breathing over the parcncJiijnia of the lung where normally vesicular breathing should be heard. The student should familiarize himself with each of these types of breathing, the vesicular and the bronchial, concentrating his at- tention as he listens first \ipon the inspiration and then upon the expiration, and comparing them with each other, first in duration, next in intensity, and lastly in pitch. To those who have not a musical ear, high-pitched sounds convey the general impression of being shrill, while low-pitched sounds sound hollow and empty, but the distinction between intensity and pitch is one comparatively difficult to master. Distant ])ronchial breathing may be repre- sented in Fig. QQ, and is to be heard over the back of the neck opposite the position of the trachea and bronchi. Fig. 67 repre- sents very loud bronchial breathing such as is sometimes heard in pneumonia. (3) BvoncJin-VcsiciiJo)' Bredthbig in Health. As indicated by its name, tliis type of breathing is intermediate between the two just described, hence the terms '4nixed breath- ing," or "atypical breathing " ("unbestimmt "). Its characteristics may be symbolized as in Fig. 68. In the normal chest one can be- come familiar with broncho-vesicular breathing, l)y examining the apex of the right lung, or by listening over the trachea or one of the primary bronchi, and then moving the stethoscope half an inch at a time toward one of the nipples. In the course of this journey one passes over points at which the breathing has, in varying de- grees, the characteristics intermediate between the bronchial type from which we started and the vesicular type toward which we are AUSCULTATION. 97 moving. Expiration is a little longer, intenser, or higher pitched than in vesicular breathing, and inspiration a little shorter, feebler, A Fig. 68.— Two Common Types of Broncho- Vesicular Breathing. Fig. 69.— Distant Broncho-Vesicular Breath- ing. or lower pitched ; but since these characteristics are variously com- bined, there are many subvarieties of broncho-vesicular breathing. Fig. 69 represents two types of distant broncho-vesicular breath- ing. (4) Empliijsematous BreutJiing. A glance at Fig. 70 will call up the most important features of this type of respiration. The inspiration is short and somewhat feeble, but not otherwise remarkable. The expiration is long, feeble, and low pitched. This type of breathing is the rule in elderly persons, particularly those of the male sex. (5) Asthmatic Breathinrj. Fig. 71 differs from emphysematous only in the greater intensity of the expiration. In this type of breathing, however, both sounds Fig. 70.— Emphysematous Breathing. Fig. 71. — Asthmatic Breathing, s, s, s. squeaking (musical) rales. are usually obscured to a great extent by the presence of pipuig and squeakuig rales (see below). 7 98 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. (6) Interrupted or " Cogwheel " Breathing. As a rule, only the inspiration is interrupted, being transformed into a series of short, jerky puffs as shown in Fig. 72. Very rarely the expiration is also divided into segments. When heard over the entire chest, cogwheel breathing is usually the result of nervous- ness, fatigue, or chilliness on the patient's part. "With the removal of these causes this type of respiration then disappears. If, on the other hand, cogwheel respiration is confined to a relatively small portion of the chest, and remains present despite the exclusion of Fig. 73.— Cogwheel Breathing. Fig. 73.— Metamorphosing Breathing. fatigue, nervousness, or cold, it points to a local catarrh in the finer bronchi such as to render difficult the entrance of air into the alve- oli. As such, it has a certain significance in the diagnosis of early phthisis, a significance similar to that of rales or other signs of localized bronchitis (see below) . (7) Am2)horic or Cavernous Breathing (see below, p. 103). (8) Metamorphosing Breathing. Occasionally, while we are listening to an inspiration of normal pitch, intensity, and quality, a sudden metamorphosis occurs and the tyi^e of breathing changes from vesicular to bronchial or amphoric (see Fig. 73), or the intensity of the l)reatli sounds may suddenly be increased without other change. These metamorphoses are usu- ally owing to the fact that a j^lugged bronchus is suddenly opened by the force of the insj)ired air, so that the sounds conducted througli it Ijecome audible. AUSCULTATION. 99 II. Differences betweex the Two Sides of the Chest. Over the apex of the right lung — that is, above the right clavi- cle in front, and above the spine of the scapula behind — one hears in the great majority of normal chests a distinctly broncho-vesicu- lar type of breathing. In a smaller number of cases this same type of breathing may be heard just below the right clavicle. These facts cannot be too strongly insisted upon, since it is only by bearing them in mind that we can avoid the mistake of diagnos- ing a beginning consolidation of the right apex where none exists. Breath sounds wJilch are j^sr/ectlf/ normal over the right a^^ex would mean serious disease if heard over similar 2)ortions of the left lung. It will be remembered that the apex of the right lung is also duller on percussion than the corresponding portion of the left, and that the voice sounds and tactile fremitus are normally more intense on the right (see Fig. 32). Occasionally one finds at the base of the right lung posteriorly a slightly feebler or more broncho-vesicular type of breathing than in the corresponding portion of the left lung. III. Pathological Modifications of Vesicular Breathing. Having now distinguished the different ty^^es of breathing and described their distribution in the normal chest, we must return to the normal or vesicular breathing in order to enumerate certain of its modifications which are important in diagnosis. (1) Exaggerated Vesicular Breathing (" Compensatorii'''' Breathing). [a) It has already been mentioned that in children or in adults with very thin and flexible chests the normal breath sounds are heard with relatively great distinctness ; also that after any exer- tion which leads to abnormally deep and forcible breathing a simi- lar increase in the intensity of the respiratory sounds naturally occurs. (l)) The term ^^ compen.mtonj hreathing,^^ or 'S'iearious " breath- ing, refers to vesicular breathing of an exaggerated type, such as is heard, for example, over the whole of one lung when the other lung 100 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. is thrown out of use by the pressure of an accumulation of air or fluid in the pleural cavity. A similar exaggeration of the breathing upon the sound side takes place when the other lung is solidified, as by tuberculosis, pneumonia, or malignant disease, or when it is compressed by the atUiesions following pleuritic effusion, or by a contraction of the bones of that side of the chest such as occurs in spinal curvature. (2) Dlmhilslied Vesicular Breath uif/. The causes of a diminution in the intensity of the breath sounds without any change in their type are very numerous. I shall men- tion them in an order corresponding as nearly as possible to the relative frequency of their occurrence. («) Fluid, Air, or Solid in the Fleural Caciti/. — Probably the commonest cause for a diminution or total abolition of normal breath sounds is an accumulation of fluid in the pleural cavity such as occurs in inflammation of the pleura or by transudation (hydro- thorax). In such cases the layer of fluid intervening between the lung and the stethoscope of the auscultator causes retraction of the lung so that little or no vesicular murmur is produced in it, and hence none is transmitted to the ear of the auscultator. An ac- cumulation of air in the pleural cavity (pneumothorax) may dimin- ish or abolish the breath sounds precisely as a layer of fluid does ; in a somewhat different way a thickening of the costal or pulmo- nary pleura or a malignant growth of the chest wall may render the breath sounds feeble or ])revent their being heard because the vibrations of the thoracic sounding-ljoard are thus deadened. Which- ever of these causes, fluid or air or solid, intervenes between the lung and the ear of the auscultator, the breath sounds are deadened or diminished without, as a rule, any modification of their type. The amount of such diminution depends roughly on the thickness of the layer of extraneous substance, whether fluid, air, or solid. Total absence of breath sounds may therefore be due to any one of these causes, provided the layer intervening between the lung and chest wall is of sufficient thickness to produce complete atelectasis of the lung or to deaden the vibrations of the chest Avail. AUSCULTATION. 101 [h) Em^jhysema of the Inwj, by destroying its elasticity and re- ducing the extent of its movements, makes the breath sounds rela- tively feeble, but seldom, if ever, abolishes them altogether. {c) In hroncliitls the breath sounds are usually considerably di- minished owing to the filling up of the bronchi with secretion. This diminution, however, usually attracts but little attention, owing to the fact that the buljbling and squeaking sounds, which result from the passage of air through the bronchial secretions, dis- tract our notice to such an extent that we find it difficult to con- centrate attention upon the breath sounds, even if we do not forget altogether to listen to them. NATien, hoAvever, we succeed in listen- ing throiKjh the rules to the breath sounds themselves, we usually notice that they are very feeble, especially over the lower two- thirds of the chest. Oedema of the Inur/ ma.y diminish the breath sounds in a similar way. (d) Pain in the thorax, such as is produced l)y dry pleurisy or intercostal neuralgia, diminishes the breath sounds because it leads the patient to restrain, so far as possible, the movements of his chest, and so of his lungs. If, for any other reason, the full ex- pansion of the lung does not take place, whether on account of the feebleness of the respiratory movements or because the lung is me- chanically hindered by the presence of pleuritic adhesions, the breath sounds are proportionately feeble. ((?) Occlusion of the npper air itassarjes, as by spasm or oedema of the glottis, renders the breathing very feeble on both sides of the chest. If one of the primary bronchi is occluded, as by a for- eign body or by pressure of a tumor or enlarged gland from without, we get a unilateral enfeeblement of the breathing over the corre- sponding lung. (/) Occasionally a jDaralysis of the muscles of respiration on one or both sides is found to result in a unilateral or bilateral enfeeble- ment of the breathing. It should be remembered, when estimating the intensity of the breathing, that the sounds heard over the right lung are, as a rule, slightly more feeble than those heard over the left lung in the normal chest. 102 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. IV. Broxchial or Tubular Breathing in Disease. (a) I have already described the occurrence of bronchial breath- ing in parts of the normal chest, namely, over the trachea and pri- mary bronchi. In disease, bronchial breathing may be heard else- where in the chest, and usually points to solidification of that i)ortion of lung from which it is conducted. It is heard most commonly in phthisis (see below, p. 2-49). (b) Croupous pneumonia is probably the next most frequent cause of bronchial breathing, although by no means every case of croupous pneumonia shows this sign. For a more detailed account of the conditions under which it does or does not occur in croupous pneumonia, see below, p 239. Lobular pneumonia is rarely mani- fested by tubular breathing. ((?) In about one-third of the cases of pleuritic effusion distant bronchial breathing is to be heard over the fluid. On account of the feebleness of the breath sounds in such cases they are often put down as absent, as we are so accustomed to associate intensity with the bronchial type of breathing. One should be always on the Avatch for any degree of intensity of ]n-onchial breathing from the feeblest to the most distinct. (fZ) Rarer causes of bronchial breathing are hemorrhagic infarc- tion of the lung, syphilis, or malignant disease, any one of which may cause a scdidification of a portion of the lung. V. BkoXCHO-Yk.-IKjULAR BllEATHlXCi IX DiSE \SE. Respiration of this type should be carefully distinguished from puerile or exaggerated breathing, in which we hear the normal vesic- ular respiration upon a large scale. I have already mentioned that broncho-vesicular breathing is normally to be heard over the apex of the right lung. In disease, broncho-vesicular breathing is heard in other ])ortions of the lung, and usually denotes a moderate degree of solidification of the lung, such as occurs in early phthisis or in the earliest and latest stages of croupous pneumonia. In cases of pleuritic effusion, one can usually hear broncho -vesicular breath- A use ULTA Tio.y. 103 ing over the iijiper })ortiun of the affected side, owing to the retrac- tion of the huig at that point. VI. Amphoric Bkeathing [Amphora = A Jfi.r). Respirations having a hollow, empty sound like that produced by bloAving across the top of a bottle, are occasionally heard in dis- ease over pulmonary cavities {e.[/., in phthisis) or in pneumothorax, i.e., under conditions in which the air passes in and out of a large empty cavity v.ithin the chest. Amphoric breathing never occurs in health. The pitch of both sounds is low, Lut that of expiration lover than that of inspiration. The intensity and duration of the sounds vary, and the distinguishing mark is their quality which resembles that of a whispered ''t6'Ao." VII. Eales. The term " rales " is applied to sounds produced by the passage of air through bronchi which contain mucus or pus, or Avhich are narrowed by swelling of their walls.' Rales are best classified as follows : (1) Moist or bubbling rales, including («) coarse, (Jj) medium, and ((") fine rales. (2) Dry or crackling rales (large, medium, or fine). The smallest varieties of this type are known as " crepitant " or " subcrepitant " rales. (3) Musical rales (high or low pitched). Each of these varieties will now be described more in detail. (1) Moist or Bubhling Rules. The nature of these is sufficiently indicated by their name. The coarsest or largest bubbles are those produced in the trachea, and ordinarily known as the ^^ death rattle." Tracheal rales occur ^ Kales are of all auscultatory phenomena the easiest to appreciate, pro- vided we exclude various accidental sounds which may be transmitted to the ear as a result of friction of the stethoscope against the skin or against the fingers of the observer. (See above, page 8(3.) 104 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. in any condition involving either profound unconsciousness or very great weakness, so that the secretions which accumulate in the trachea are not coughed out. Tracheal rales are by no means a sure precursor of death, although they are very common in the moribund state. They can usually be heard at some distance from the patient and without a stethoscope. In catarrh of the larger bronchi large bubbling rales are occasionally to be heard. In phthisical cavities one sometimes hears coarse, bubbling rales of a very metallic and gurgling quality (see below, p. 252). The finer grades of moist i rales correspond to the finer bronchi. i In the majority of cases moist rales are most numer- FiG 74— Expio- °^^^ during inspiration and especially during the latter sion of Fine part of this act. Their relation to respiration may be oAnsp^ration. represented graphically as in Fig. 74, using large dots for coarse rales and small dots for fine rSles. Musical rales can be symbolized by the letter S (squeaks). (2) Cracldinrj Rales. These differ from the preceding variety merely by the absence of any distinct Imbbling quality. They are usually to l)e heard in cases of bronchitis in which the secretions are miusually tenacioxis and viscid. They are especially apt to come at the end of inspira- tion, a large number being evolved in a very short space of time, so that one often speaks of an " explosion of fine crackling rales " at the end of inspiration. Crackling rales are to be heard in any one of the conditions in which bul)bling rales occur, but are more fre- quent in tuberciilosis than in simple bronchitis. Crepitcmt rales, which represent the finest sounds of this type, are very much like the noise which is heard when one takes a lock of hair between the thumb and first finger and rubs the hairs upon each other while holding them close to the ear. A very large num- ber of minute crackling sounds is heard following each other in rapid succession. To the inex]iorienced ear they may seem to blend into a continuous sound, but with practice the component parts may AUSCULTATION. 105 be clistingiiislied. This type of rales is especially apt to occur dur- ing inspiration alone, but not very infrequently they are heard during expiration as Avell. From subcrepitant rales they are dis- tinguished merely by their being still finer than the latter. ' Sub- crepitant rales are often mixed with sounds of a somewhat coarser type, while crepitant rales are usually all of a size. If the chest is covered with hair, sounds precisely like these two varieties of rales may be heard when the stethoscope is placed upon the hairy portions. To avoid mistaking these sounds for rales one must thoroughly' wet or grease the hair. Crejntant Rales in Atelectasis. Crepitant and subcrepitant rales are very often to be heard along the thin margins of the lungs at the base of the axillae and in the back, especially when a patient who is breathing superficially first begins to take deep breaths. In such cases, they usually disappear after the few first respirations, and are then to be explained by the tearing apart of the slightly agglutinated surfaces of the finer bron- chioles. It is by no means invariably the case, however, that such sub- crepitant rales are merely transitory in their occurrence. In a large number of cases they persist despite deep breathing. The fre- quency of subcrepitant rales, persistent or transitory, heard over the inferior margm of the normal lung at the bottom of the axilla, is shown by the following figiires : Out of 356 normal chests to which I have listened especially for these rSles, I found 228, or 61 per cent, which showed them on one or both sides. They are very rarely to be heard in persons under twenty years of age. After forty-five, on the other hand, it is unusual to find them absent. In my experience they are considerably more frequent in the situa- tion shown in Fig. 124 than in any other part of the lung, but they may be occasionally heard in the back or elsewhere. In ^-iew of lA distinction was formerlj' drawn between crepitant and snbcrepitant rales, on the ground that the latter were heard during both respiratory sounds and the former only during inspiration, but this distinction cannot be main- tained and is gradually being given up. 106 PHYSICAL DIAG^^OSIS OF DISEASES OF THE CHEST. these facts, it seems to Bie that we must recognize that it is almost if not quite physiological to find the finer varieties of crackling rales at the base of the axillae in persons over forty years old. I have supposed these rales to be due to a partial atelectasis result- ing from disease in the thin loAver margin of the lungs. Such por- tions of the lung are ordinarily not expanded unless the respirations are forced and deep. This explanation would agree with the obser- vations of Abranis, to Avhich I shall refer later (see below, p. 290). (b) Crepitant or subcrepitant rales are also to be heard in a certain portion of cases of pneumonia, in the very earliest stages and Avhen resolution is taking place ("creintans redux"). More rarely this type of rale may be heard in connection with tubercu- losis, infarction, or oedema of the lung. In certain cases of dry pleurisy there occur fine crackling sounds which can scarcely be differentiated from subcrepitant rales. I shall return to the description of them in speaking of pleural friction (see below, p. 271). (3) Musical Redes. The passage of air through bronchial tubes narrowed by in- flammatory swelluig of their lining membrane (bronchitis), gives rise not infrequently to a multitude of musical sounds. Such a stenosis occurring in relatively large bronchial tubes produces a deep-toned groaning sound, while narrowing of the finer tubes re- sults in 2*ipi^^(/) squeaking, tcJiistling noises of various qualities. Such sounds are often known as " (Ivg rules " in contradistinction to the '•'■huhhling rules''^ above described, but as many non-musical crackling rales have also a very dry sound, it seems to me best to apply the more distmctive term ^^ musical rales'' to all adventitious sounds of distinctly musical quality which are produced m the bronchi. Musical rales are of all adventitious sounds the easiest to recognize but also the most fugitive and changeable. They ap- pear now here, now there, shifting from minute to minute, and may totally disappear from the chest and reappear again within a very short time. This is to some extent true of all varieties of rales, but especially of the squeaking and groaning varieties. AUSCULTATION. 107 Musical rales are heard, as a rule, more distinctly during expira- tion, especially when they occur in connection with asthma or em- physema. In these diseases one may hear quite complicated chords from the combinations of rales which vary in pitch. VII. The Effects of Cough. The influence of coughing upon rales is usually very marked. Its effect may be either to intensify them and bring them out where they have not previously been heard, or to clear them away alto- gether. Other effects of coughing upon physical signs will be mentioned later on in the chapters on Pneumonia and Phthisis. VIII. Pleural Pkictiox. The surfaces of the healthy pleural cavity are lubricated with sufficient serum to make them pass noiselessly over each other dur- ing the movements of respiration. But when the tissues become abnormally dry, as in Asiatic cholera, or when the serous surfaces are roughened by the presence of a fibrinous exudation, as in ordi- nary pleurisy, the rubbing of the two pleural surfaces against one another produces peculiar and very characteristic sounds known as ^''pleural friction sounds." The favorite seat of pleural friction sounds is at the bottom of the axilla, i.e., where the lung makes the widest excursion and where the costal and diaphragmatic pleura are in close apposition (see Pig. 33) . In some cases pleural fric- tion sounds are to be heard altogether below the level of the hmg. In others they may extend up several inches above its lower mar- gin, and occasionally it happens that friction may be appreciated over the whole lung from the top to the bottom. Very rarely friction sounds are heard only at the apex of the lung in early tuberculosis. The sound of pleural friction may be closely imitated by hold- ing the thumb and forefinger close to the ear, and rubbing them past each other with strong pressure, or by pressing the palm of one hand over the ear and rubbing upon the back of this hand ^vith 108 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. the fingers of the other. Pleural friction is usually a catchy, jerky, interrupted, irregular sound, and is apt to occur during in- spiration only, and particularly at the end of this act. It may, however, be heard with both respiratory acts, but rarely if ever occurs during expiration alone. The intensity and quality of the sounds vary a great deal, so that they may be compared to (jrazinr/, nihhinrj, rasjnng, and creak'mtj sovinds. They are sometimes spoken of as " ledtlienj." As a rule, they seem very near to the ear, and are sometimes startlingly loud. In many cases they camiot be heard after the patient has taken a few full breaths, probably because the rough pleural surfaces are smoothed down temporarily by the fric- tion which deep breathing produces. After a short rest, however, and a period of superficial breathing, pleural friction sounds often return and can be heard for a short time with all their former in- tensity. They are increased by pressure exerted upon the outside of the chest wall. Such pressure had best be made with the hand or with the Bowles stethoscope, since the sharp edges of the chest- piece of the ordinary stethoscope may give rise to considerable pain ; but if such pressure is made with the hand, one must be careful not to let the hand shift its position upon the skin, else rubbing sounds may thus be produced Avhich perfectly simulate pleural friction. In well-marked cases jileuritic friction can be felt if the palm of the hand is laid over the suspected area; occa- sionally the sound is so loud that it can be heard by the patient himself or by those aromid him. In doubtful cases, or Avhen a friction sound appears to have disappeared, and when one wishes to bring it out again, there are several manoeuvres suggested by Abrams for obtaming this end. (a) Tlie Arm Mananivre. The patient suspends respiration altogether, and the arm upon the affected side is raised over the head by the patient himself or by the physician, as in performing Sylvester's method of artificial respiration. During this movement we listen over the suspected area. " By this manoeuvre the movement of the i:)arietal against the vis- ceral pleura is opi)osite in direction to that occurring during the A use ULTA TlOy. 109 resjjiratoiy act, aud for this reason tlie x*l*^i-^i"itic sound may often be elicited after it lias been exhausted in the ordinary act of breath- ing." (/>) The Decubital 2Ianoeuvre. " Let the patient lie upon the affected side for a minute or two, then let him rise quickly and suspend respiration. Noav listen over the affected area, at the same time directing the patient to take a deep breath." Pleuritic friction sounds are distinguished from rales by their greater superficiality, by their jerky, interrupted character, by the fact that they are but little influenced by cough, and that they are increased by pressure. It has already been mentioned, however, that there is one variety of sounds which we have every reason to thmk originate in the pleura, which cannot be distinguished from certain varieties of crackling bronchial rales. Such sounds occur chiefly in connection with phthisical processes, in which both pleu- risy and bronchitis are almost invariably j)resent, and it is seldom, of importance to distingaiish the two. IX. Auscultation" of the Spoke^t or Whispered Voice Souxds. The more important of these is : {a) The Whlsj)ered Voice. The patient is directed to whisper ''one, two, three," or "ninety -nine," while the auscultator listens over different portions of the chest to see to what degree the whispered syllables are trans- mitted. In the great majority of normal chests the whispered voice is to be heard only over the trachea and primary bronchi in front and behind, while over the remaining portions of the lung little or no sound is to be heard. When, on the other hand, solidi- fication of the lung is present, the whispered voice may be dis- tinctly heard over jDortions of the lung relatively distant from the trachea and bronchi ; for example, over the lower lobes of the lung behind. The usefulness of the whispered voice in the search for small areas of solidification or for the exact boundaries of a solidi- 110 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. fied area is very great, especially when we desire to save the patient the pain and fatigue of taking deep breaths. Whispered voice sounds are i)raetieally equivalent to a forced expiration and can be obtained with very little exertion on the patient's part. The in- creased transmission of the whispered voice is, in my opinion, a more delicate test for solidification than tubular breathing. The latter sign is present only when a considerable area of lung tissue is solidified, while the increase of the whispered voice may be ob- tained over much smaller areas. Eetraction of the lung above the level of a pleural effusion causes a moderate increase in the trans- mission of the whispered voice, and at times this increased or bron- chial whisper is to be heard over the fluid itself, probably by trans- mission from the compressed lung above. Where the lung is completely solidified the whispered words may be clearly distinguished over the affected area. In lesser de- grees of solidification the syllables are more or less blurred. (h) The. Spohni Voice. The evidence given us by listening for the spoken voice in vari- ous parts of the chest is considerably less in value than that obtained through the whispered voice. As a rule, it corresponds with the tactile fremitus, being increased in intensity by the same causes which increase tactile fremitus, viz., solidification or condensation of the lung, and decreased by the same causes which decrease tac- tile fremitus — namely, l)y the presence of air or water in the pleu- ral cavity, by the thickening of the pleura itself, or by an ob- struction of the bronchus leading to the part over which we are listening. In some cases the presence of solidification of the lung gives rise not merely to an increase in transmission of the spoken voice, l)ut to a change in its quality, so that it sounds abnormally concentrated, nasal, and near to the listener's ear. The latter change may be heard over areas where tactile fremitus is not in- creased, and even Avhere it is diminished. Wliere this change in the quality of the voice occurs, the actual words spoken can often be distinguished in a way not usually ])ossible over either normal or solidified lung. "Bronchoi)liony," or the distinct transmission AUSCULTATION. IH of audible words, and not merely of diffuse, unrecognizable voice sounds, is considerably commoner in the solidilications due to pneu- monia than in those due to phthisis; it occurs in some cases of pneumothorax and pulmonary cavity. (c) Egophony. Among the least important of the classical jDhysieal signs is a nasal or squeaky quality of the sounds which reach the observer's ear when the jiatient speaks in a natural voice. To this jjeculiar quality of voice the name of "egophony" has been given. It is most frequently heard in cases of moderate-sized pleuritic effusion just about the level of the lower angle of the scapula and in the vicinity of that point. Less often it is heard at the same level in front. It is very rarely heard in the upper portion of the chest and is by no means constant either in pleuritic effusion or in any other condition. A point at which it is heard corresponds not, as a rule, with the upper level of the accumulated fluid, as has been frequently supposed, but often with a point about an inch farther down. The presence of egophony is in no way distinctive of j^leu- ritic effusions and may be heard occasionally over solidified lung. X. Phenomena Peculiar to Pneumohydrothorax axd Pneu- MOPYOTHORAX. (1) Si(ccussion. Now and then a patient consults a physician, complaining that he hears noises inside him as if water were being shaken about. One such patient expressed himself to me to the effect that he felt "like a half -empty bottle." In the chest of such a patient, if one presses the ear against any portion of the thorax and then shakes the whole patient stronglj^, one may hear loud splashing sounds known technically as " sitccussioji." Such sounds are absolutely diagnostic of the presence of both air and fluid in the cavity over which they are heard. Very frequently they may be detected by the physician when the patient is not aAvare of their presence. Oe- 112 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. casionally tlie splashing of the fluid within may be felt as Avell as heard. It is essential, of course, to distinguish succussion due to the presence of air and fluid in the pleural cavity from similar sounds protluced in the stomach, but this is not at all difficult in the majority of cases. It is a bare possibility that succussion sounds may be due to the presence of air and fluid in the jiericar- dial cavity. It is important to remember that succussion is never to be heard in simple pleuritic effusion or hydrothorax. The presence of air, as well as liquid, in the pleural cavity is absolutely essential to the production of succussion sounds.' (2) Mi'faU'ic Tlnlde or Falllnfj-Di'op Sound. When listening over a pleural cavity which contains both air and fluid, one occasionally hears a liquid, tinkling sound, due pos- sibly to the impact of a drop of liquid falling from the relaxed lung above into the, accumulated fluid at the bottom of the pleural cavity, and possibly to rales produced in the tissues around the cavity. It is stated that this physical sign may in rare cases be observed in large-sized phthisical cavities as well as in pneumohy- drothorax and pneumopyothorax. (3) Tlte Lunrj-Flstula Sound. "When a perforation of the lung occurs below the level of the fluid accumulated in the pleural cavity, bubbles of air may be forced out from the lung and up through the fluid with a sound reminding one of that made by children when blowing soap-bubbles. ' It is well for the student to try for himself the following experiment, which I have found useful in impressing these facts upon the attention of classes in physical diagnosis: Fill an ordinary rubber hot-water bag to the brim with water. Invert it and squeeze out forcibly a certain amount (per- haps half) of the contents, by grasping the upper end of the bag and compress- ing it. While the water is thus being forced out, screw in the nozzle of the bag. Now shake the whole bag, and it will be found impossible to produce any splashing sounds owing to the fact that there is no air in the bag. Un- screw the nozzle, admit air, and then screw it in again. Now shake the bag again and hnul splashing will be easily lieard. CHAPTER V. AUSCULTATION OF THE HEAKT. I. "Valve Areas." Ix the routine examination of the heart, most observers listen in four places : (1) At the apex of the heart in the fifth intercostal space neai the nipple, the ^^ mitral area.'" Aortic area. Tricuspid area. — Pulmonic area. ..... Mitral area. Fig. 7.5.— The Valve Areas. (2) In the second left intercostal space near the sternum, the "pulmonic area." (3) In the second right intercostal space near the sternum, the "aortic area." (4) At the bottom of the sternum near the ensiform cartilage, the " tricuspid area. " These points are represented in Eig. 75 and are known as 8 114 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. ^^ valve areas." They do not correspond to the anatomical position of any one of the four valves, but experience has shown that sounds heard best at the apex can be proved (by post-mortem examination or otherwise) to be produced at the mitral orifice. Similarly sounds heard best in the second left intercostal space are proved to be produced at the pulmonary orifice ; those which are loudest at the second right intercostal space to be produced at the aortic orifice ; ' while those which are most distinct near the origin of the ensiform cartilage are produced at the tricuspid orifice. II. The Normal Heart Sounds. A glance at Fig. 75, Avhicli represents the anatomical positions of the four valves above referred to, illustrates what I said above ; namely, that the traditional valve areas do not correspond at all with the anatomical position of the valves. If now we listen in the ^'mitral area," that is, in the region of the apex impulse of the heart, keeping at the same time one finger on some point at which the cardiac impulse is palpable, one hears Avith each outward thrust of the heart a low, dull sound, and in the period between the heart beats a second sound, shorter and sharper in quality.'^ That which occurs with the cardiac impulse is known as the fir.^t noinid ; that which occurs between each two beats of the heart is known as the second sound. The second sound is geneially ad- mitted to be due to the closure of the semilunar valves The cause of the first sound has been a most fruitful source of discussion, and no one explanation of it can be said to be generally received. Per- haps the most commonly accepted view attributes the first or systolic sound of the heart to a coml)ination of two elements — («) The contraction of the heart muscle itself. (Jj) The sudden tautening of the mitral curtains. Following the second sound there is a pause corresponding to ' For exceptions to this rule, see below, page 176. '' The tirst sound of the heart, as heard at the apex, may be imitated by holding a linen handkerchief by the corners and suddenly tautening one of the borders. To imitate the second sound, use one-half the length of the border instead of the whole. AUSCULTATION OF THE HEART. 115 the diastole of the heart. Normally this pause occupies a little more time than the first and second sounds of the heart taken to- gether. In disease it may be much shortened. The first sound of the heart is not only longer and duller than the second (it is often spoken of as " booming " in contrast with the "snapi)hig" quality of the second sound) but is also considerably more intense, so that it gives us the impression of being accented like the first syllable of a trochaic rhythm. After a little practice one grows so accustomed to this rhythm that one is apt to rely uj^on -• Aortic valve. Pulmonic valve. Tricuspid valve. -——'-"/I '^^ ^^ ^^^ ^^* "T- Mitral valve. i Fig. 76.— Anatomical Position of tbe Cardiac Valves. his appreciation of the rhythm alone for the identification of the systolic sound. This is, however, an unsafe practice and leads to many errors. Our impression as to which of the two sounds of each cardiac cycle corresponds to systole should always be verified either by sight or touch. We must either see or feel the cardiac impulse and assure ourselves that it is synchronous with the heart sound which we take to be systolic' This point is of especial importance in the recognition and identification of cardiac murmurs, as will be seen presently. ' When the cardiac impulse can be neither seen nor felt, the pulsation of the carotid will generally guide us. The radial pulse is not a safe guide. 116 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. So far, I have been describing the normal heart sounds heard in the "mitral area," that is, at the apex of the heart. If now we listen over the pulmonary area (in the second left intercostal space), we find that the rhythm of the heart sounds has changed and that here the stress seems to fall upon the "second sound," ie., that corresponding to the beginning of diastole; in other words, the first sound of the heart is here heard more feebly and the second sound more distinctly. The sharp, snapping quality of the latter is here even more marked than at the aj^ex, and despite the feebleness of the first sound in this area we can usually recog- nize its relatively dull and prolonged quality Over the (lortic area {i.e., in the second right interspace) the rhythm is the same as in the pulmonary area, although the second sound may be either stronger or weaker than the corresponding sound on the other side of the sternum (see below, p. 118). Over the tricuspid area one hears sounds practically indistin- guishable in quality and in rhythm from those heard at the apex. When the chest walls are thick and the cardiac sounds feeble, it may be difficult to hear them at all. In such cases the heart sounds may be heard much more distinctly if the patient leans for- ward and toward his own left so as to bring the heart closer to the front of the chest. Such a position of the body also renders it easier to map out the outlines of the cardiac duhiess by percussion. In cardiac neuroses and during conditions of excitement or emo- tional strain, the first sound at the apex is not only very loud but has often a curious metaUlc reverberation {" cliqnetis mefaJlique'^) corresponding to the trembling, jarring cardiac impulse (often mis- taken for a thrill) which palpation reveals. III. Modifications ix the Intensity of the Heart Sounds. It has already been mentioned that in young persons with thin, elastic chests, the heart sounds are heard with greater intensity than in older persons whose chest walls are thicker and stiffer. In obese, indolent adults it is sometimes difficult to hear any heart sounds at all, while in young persons of excitable temperament the sounds may have a very intense and ringing quality. Under dis- AUSCULTATION OF THE HEART. 117 eased conditions either of the heart sounds may he increased or diminished in intensity. I shall consider (1) The First Sound at the Apex [sometimes Called the Mitral First Soundy (a) Increase in the length or intensity of the first sound at the apex of the heart occurs in any condition which causes the heart to act with unusual degree of force, such as bodily or mental exer- tion, or excitement. In the earlier stages of infectious fevers a similar increase in the intensity of this sound may sometimes be noted. Hypertrophy of the left ventricle sometimes has a similar effect upon the sound, but less often than one would suppose, while dilatation of the left ventricle, contrary to what one would suppose, is not infrequently associated with a loud, forcible first sound at the apex. In mitral stenosis the first sound is usually very intense and is often spoken of as a " thumpmg first sound " or as a " sharp slap." (h) Shortening and weakening of the first sound at the apex. In the course of contmued fevers and especially in t3rphoid fever the granular degeneration which takes place in the heart muscle is manifested by a shortening and weakening of the first sound at the apex, so that the two heart sounds come to seem much more alike than usual. In the later stages of typhoid, the first soimd may become almost inaudible. The sharp "vahailar " quality, which one notices in the first apex sound under these conditions, has been attributed to the fact that weakening of the myocardium has caused a suppression of one of the two elements which go to make up the first sound, namely, the muscular element, so that we hear only the short, sharp sound due to the tautening of the mitral curtains. Chronic myocarditis, or any other change in the heart wall which tends to enfeeble it, produces a weakening and shortening of the first sound similar to that just described. Simple weakness in the mitral first sound without any change in its duration or laitch may be due to fatty overgrowth of the heart, to emphysema or pericar- dial effusion in case the heart is covered by the distended lung or by the accumulated fluid. Among vahiilar diseases of the heart 118 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. the one most likely to be associated with a diminution in intensity of the first apex sound is mitral regurgitation. (c) Doubling of the first sound at the apex. It is not uncommon in healthy hearts to hear in the region of the apex impulse a doubling of the first sound so that it may be suggested by pronouncing the syllables "turrupp " or "trupp." In health this is especially apt to occur at the end of expiration. In disease it is associated Avith many different conditions involving an increase in the work of one or the other side of the heart. It seems, however, to be unusually frequent in myocarditis. (2) Jlodljications in the Second tSoir/ith as Heard at the Base of the Heart. Phi/siolor/ical Variations. — The relative intensity of the j^ul- monic second sound, when compared with the second sound heard in the conventional aortic area, varies a great deal at different pe- riods of life. Attention was first called to this by A^ierordt,' and it has of late years been recognized by the best authorities on dis- eases of the heart, though the majority of current text-books still repeat the mistaken statement that the aortic second sound is always louder than the pulmonic second in health. The work of Dr. Sarah R. Creighton, done in my clinic durmg the summer of 1899, showed that in 90 per cent of healthy chil- dren under ten years of age, the pulmonic second sound is loiuler than the aortic. In the next decade (from the tenth to the twen- tieth year) the pulmonic second sound is louder in two-thirds of the cases. About half of 207 cases, between the ages of twenty and twenty-nine, showed an accentuation of the pulmonic second, while after the thirtieth year the number of cases showing such accentua- tion became smaller with each decade, until after the sixtieth year we fonnd an accentuation of the aortic sernnd in sixtji-slr out ofslxtij- ehjht cases examined. These facts are exhibited in tabular form in ' Vierordt: "Die Jlessung der Intensitiit der Herztone" (Tubingen, 1885). See also Ilochsinger, "Die Auscultation des kindlichen Ilerzens"; Gibson, "Diseases of the Heart" (1898) ; Kosenbach, "Diseases of the Heart" (1900) ; Allbutt, "System of Medicine." AUSCULTATION OF THE HEART. 119 Figs. 77 and 78, and appear to show that the relative intensity of the two sounds in the aortic and pnlmonic arteries depends pri- marily upon tlie age of the individual, the pulmonic sound predomi- nating in youth and the aortic in old age, while in the period of middle life there is relatively little discrepancy between the two. Fig. 100%- 90%- 80%- 70%- 0-9 10-19 20-29 30-39 40-49 50-59 60-69 70-79 \ \ \ v m o tn z \ > D m CO \ 30%- or)(y \ \ 10%- \ ^ V —100% 90% —-80% -—70% —00% -—50% —40% —30% 20% 10% r.— Showing the Per Cent of Accentuated Pulmonic Second Sound in Each Decade Based on 1,000 cases. It is, therefore, far from true to suppose that we can obtain e\d- dence of a pathological increase in the intensity of either of the second sounds at the base of the heart simply by comparing it Avith the other. Pathological accentuation of the pulmonic second sound must mean a greater louchiess of this sound than should he expected at the age of the patient in question, and not simply a greater intensity than that of the aortic second sound. The same 120 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. observation obviously applies to accentuation of the aortic second sound. Both the aortic and the pulmonic second sounds are sometimes DECADES. I I I • I r I I .oy \ 0-9 10-191 20-29 30-39 ] 40-49 | 50-59 [ 60-69 | 70-79 i Fig. 78.— Showing the Per Cent of Accentuated Puhuonic Second Sound hi Each Decade. Based on 1,(M) cases. very intense during great emotional excitement or after muscular exertion, and sometimes without any obvious cause. Patliohx/icdl J'(tr!t't!(>)is. A. Accentuation of the Fuhiionic Serovd Soi/7ifL Pathological accentuation of the second sound occurs especially in conditions involving a backing up of blood in the lungs, such as occurs in stenosis or insufficiency of the mitral valve, or in obstruc AUSCULTATION OF THE HEART. 121 tive disease of the lungs (emijhyseiua, broncliitis, phthisis, chronic interstitial pneumonia). Indirectly accentuation of the pulmonic second sound points to hyi^ertrophy of the right ventricle, since without such hypertrophy the work of driving the blood through, the obstructed lung could not long be performed. If the right ven- tricle becomes weakened, the accentuation of the inilmonic second sound is no longer heard. B. Weakeninff of the P^dmonic Second Sound. AYeakenmg of the j)ulmonic second sound is a very serious symp- tom, sometimes to be observed in cases of pneumonia or cardiac disease near the fatal termination. It is thus a very important indication for prognosis, and is to be watched for with the greatest attention in such cases. C. Accentuation of the AoHie Second Soiind. I have already shown that the aortic second sound is louder than the corresponding sound in the pulmonary area in almost every individual over sixty years of age and in most of those over forty. A still greater intensity of the aortic second sound occurs — (ff) In interstitial nephritis or any other condition which in- creases arterial tension and so throws an increased amount of work upon the left ventricle. Indirectly, therefore, a pathologically loud aortic sound points directly to increased tension in the peripheral arteries and indirectly to hypertrophy of the left ventricle. (Ji) A similar increase in the intensity of the aortic second sound occurs in aneurism or diffuse dilatation of the aortic arch. I>. Diminution in the Intensitij of the Aortic Second Sound. AMienever the amount of blood thrown into the aorta by the contraction of the left ventricle is diminished, as is the case espe- cially in mitral stenosis and to a lesser degree in mitral regurgita- tion, the aortic second sound is weakened so that at the apex it may be inaudible. A similar effect is produced by any disease which weakens the walls of the left ventricle, such as fibrous niyo- 122 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. carditis, fatty degeneration, and cloudy swelling. Relaxation of the peripheral arteries has the same effect. In conditions of col- lapse the aortic second sound may be almost or quite inaudible. In persons past middle life the second sounds are often louder in the third or fourth interspace than in the second, so that if we listen only in the second space we may gain the false impression that the second sounds are feeble. Accentuation of both the second sounds at the base of the heart may occur in health from nervous causes or when the lungs are retracted by disease so as to uncover the conns arteriosus and the aortic arch. Under these conditions the second sound may be seen and felt as well as heard. In a similar way, an apparent in- crease in the intensity of either one of the second sounds at the base of the heart may be produced by a retraction of one or the other lung. Summai'ij. — (1) The mitral first sound is increased by hyi^er- trophy or dilatation of the left ventricle, and among valvular dis- eases especially by mitral stenosis. It is weakened or reduplicated by parietal disease of the heart. Any of these changes may occur temporarily from physiological causes. (2) The 2Julmonic second sound is usually more intense than the aortic in children and up to early adult life. Later the aortic second sound predominates. Pathological accentuation of the sec- ond pulmonic sound usually points to obstruction in the pulmonary circulation (mitral disease, emphysema, etc.). Weakening of the pulmonic second means failure of the right ventricle and is serious. (8) The aortic second sound is increased pathologically by any cause which increases the Avork of the left ventricle (arteriosclero- sis, chronic nephritis). It is diminished when the blood stream, thrown into the aorta by the left ventricle, is abnormally small (mitral disease, cardiac failure). (4) Changes in the tricuspid sounds are rarely recognizable, while changes in the first aortic and ])ulmonic sounds have little practical significance. AUSCULTATION OF THE HEART. 123 Modifications in the RJiijthin of the Cardiac Sounds. (1) Whenever the walls of the heart are greatly weakened by disease, for example, in the later weeks of a case of tyjihoid fever, the diastolic pause of the heart is shortened so that the car- diac sounds follow each other almost as regularly as the ticking of a clock; hence the term ''tick-tack heart." As this rhythm is not unlike that heard in the foetal heart, the name of ^^ emhnjocavdia '' is sometimes applied to it. The " tick-tack " rhythm may be heard in any form of cardiac disease after compensation has failed, or in any condition leading to collapse. (2) A less common change of rhythm is that produced by a shortening of the interval between the two heart sounds owing to an incompleteness of the contraction of the ventricle. This change may occur in any disease of the heart Avhen coni2)ensation fails. (3) TJie " Gallop Hhi/tlDn." — Shortening of the diastolic pause together with doubling of one or another of the cardiac sounds re- sults in our hearing at the apex of the heart three sounds instead of two, which follow each other in a rhythm suggesting the hoof beats of a galloping horse. Such a rhythm may occur temporarily in any heart which is excited or overworked from any cause, but when permanent is usually a sign of grave cardiac weakness. The rhythms so produced are usually anapaestic, -~^ --^ — ', ^-^ -~^ — ', ^>^ — ', or of Doubling of the Second Sounds at the Base of the Heart. — At the end of a long inspiration this change may be observed in al- most any healthy person if one listens at the base of the heart. It is still better brought out after muscular exertion or by holding the breath. In such cases it probably expresses the non-synchronous closure of the aortic and pulmonic valves, owing to increased press- ure in the pulmonary circulation. Similarly in diseased condi- tions, anything which increases the pressure either in the periph- eral arteries or in the pulmonary circulation, and thus throws increased work upon one or the other ventricle, will cause a doub- ling of the second sound as heard at the base of the heart. In mitral stenosis a double diastolic sound is usually to be 124 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. heard at the apex, and in the diagnosis of this disease this " double shock sound " during diastole may be an important piece of evi- dence, and may sometimes be -felt as well as heard. The " double shock sound " of mitral stenosis is not generally believed to repre- sent a doubling of the ordinary second sound, although it corre- sponds with diastole. Just what its mechanism is, is disputed. I have said nothing about modifications in the second sound at the apex, since this sound is now generally agreed to represent the aortic second sound transmitted by the left ventricle to the apex. The first sounds at the base of the heart have also not been dwelt upon, since they have no special importance in diagnosis. 3IetaUic Hairt Sounds. The presence of air in the immediate vicinity of the heart, as, for example, in pneumothorax or in gaseous distention of the stomach or intestine, may impart to the heart sounds a curious metallic quality such as is not heard under any other conditions. " J/?y^/«^," '' Prolan (jat ion, '^ or " Unclecniess" of the Heart tSounds. These terms are not infrequently met with in literature, but their use sliould, I think, be discontinued. The facts to which they refer should be explained either as faintness of the heart sounds, due to the causes above assigned, or as faint, short mur- murs. In their present usage such terms as " muffled " or " unclear " heart sounds represent chiefly an un clearness in the mind of the observer as to just what it is that he hears, and not any one recog- nized pathological condition in the heart. IV. Sounds Audiulk Ovkii thk Pkuii'hkral Vessels. (1) The normal heart sounds are in adults audil)le over the carotids and over the subclavian artei'ies. In childliood and youth only the second heart sound is thus audible. (2) In about 7 per cent of normal persons a systolic sound can be heard over the femoral artery. This sound is obviously not AUSCULTATION OF THE HEART. 125 transmitted from the heart, and is usually explained as a result of the sudden systolic tautening of the arterial wall. In aortic regurgitation this arterial sound is almost always audible not only in the femoral but in the brachial and even in the radial, and its intensity over the femoral becomes so great that the term " pistol-shot " sound has been applied to it. In fevers, exophthalmic goitre, lead poisoning, and other diseases, a similar arterial sound is to be heard much more frequently than in health. Venous Sounds. The violent closure of the venous valves in the jugular is some- times audible in cases of insufficiency of the tricuspid valve. The found has no clinical importance, and is difficult to distinguish owing to the presence of the carotid first sound mentioned above. CHAPTER VL AUSCULTATION OF THE HEART: CONTINUED. Cardiac Murmurs. (a) Termlnologi/. The word "murmur''^ is one of the most unfortunate of ail the terms used in the description of physical signs, No one of the various blowing, whistling, rolling, rumbling, or piping noises to which the term refers, sounds anything like a " murmur " in the ordinary sense of the word. Nevertheless, it does not seem best to try to replace it by any other term. The French word ^'souffle " is much more accurate and has become to some extent Anglicized. Under the head of cardiac murmurs are included all abnormal sounds produced within the heart itself. Pericardial friction sounds and those produced in that jiortion of the lung or jileura which overlies the heart are not considered "murmurs." (l>) Mode of F rod net ton. With rare exceptions all cardiac murmurs are produced at or near one of the valve orifices, either by disease of the valves them- selves resulting in shrivelling, thickening, stiffening, and narrowuig of the valve curtains, or by a stretcliing of the orifice into which the valves are inserted. Diseases of the valves tliemselves may lead to the production of murmurs : (rt) AMien tlie valves fail tt) close at the proper time (incompe- tence, insufficiency, or regurgitation). {h) When the valves fail to open at the proper time (stenosis or obstruction) . AUSCULTATION OF THE HEART. 127 (c) When the surfaces of the valves or of the parts immedi- ately adjacent are roughened so as to prevent the smooth flow of the blood over them. (d) When the orifice which the valves are meant to close is di- lated as a result of dilatation of the heart chamber of which it forms Fig. 79.— Diaerram to Illustrate the Production of a Cardiac Murmur Through Regurgitation from the Aorta or in an Aneurismal Sac. The arrow shows the direction of the blood cur- rent and the curled lines the audible blood eddies. the entrance or exit. The valves themselves cannot enlarge to keep pace with the enlargement of the orifice, and hence no longer suffice to reach across it. The presence of any one of these lesions gives rise to eddies in the blood current and thereby to the abnormal sounds to which we give the name murmurs.' (See Figs. 79, 80, and 81). When Fig. 80.— Diagram to Illustrate the Production of a Cardiac Murmur Through Stenosis of a Valve-Oriflce. valves fail to close and so allow the blood to pass back through them, Ave speak of the lesion as rer/urgitation, insvfficiencu, or in- competence : if, for example, the aortic valves fail to close after the left ventricle has thrown a column of blood into the aorta, some of this blood regurgitates through these valves into the ven- ' The method by which functional murmurs are produced will be discussed later. (See page 136.) 128 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. tricle from which it has just been expelled, and we speak of the lesion as "aortic rerj^irgitation,^^ and of the murmur so produced as an aortic reyurgitant murmur or a murmur of aortic regurgitation. A similar regurgitation from the left ventricle into the left auricle takes place in case the mitral valve fails to close at the beginning of systole. If, on the other hand, the mitral valve fails to open properly to admit the blood which should flow during diastole from the left auricle into the left ventricle, we speak of the condition as mitral sfetiosis or mitral ohstrnction. A similar narrowing of the aortic valves such as to hinder the egress of blood durmg the systole of the left ventricle is known as aortic stenosis or obstruction. Val- Fir,. 81.— Diagram to Illustrate the Production of Cardiac Murmurs Through Roughening of a Valve. vLilar lesions of the right side of the heart (tricuspid and pulmonic valves) are comparatively rare, but ai-e produced and named in a way similar to those just described. The facts most important to know about a murmur are : (1) Its place in the cardiac cycle. (2) Its point of maxunum intensity. (3) The area over which it can be heard. (4) The effects of exertion, respiration, or position upon it. Less important than the above are : (5) Its intensity. (6) Its quality. (7) Its length. (8) Its relation to the normal sounds of the heart. Each of these points will now be taken up in detail : (1) Time of Murmurs. — The first and most important thing to ascertain regarding a murmur is its relation to the normal cardiac cycle ; that is, whether it occurs during systole or during diastole, or in case it does not fill the whole of one of those periods, in what AUSCULTATION OF THE HEART. 129 part of systole or diastole it occurs. It must be borne in mind that the period of systole is considered as lasting from the beginning of the first soimd of the heart up to the occurrence of the second sound, Avhile diastole lasts from the beginning of the second sound mitil the beginning of the first sound in the next cycle. Any mur- mur occurring with the first sound of the heart, or at the time when the first sound should take place, or in any part of the period inter- vening between the first sound and the second, is held to be systolic. Murmurs which distinctly follow the first sound or do not begin until the first sound is ended are known as late systolic murmurs. On the other hand, it seems best, for reasons to be discussed more in detail later on, not to give the name of diastolic to all murmurs which occur within the diastolic period as above defined. Murmurs which occur during the last j)art of diastole and which run up to the first sound of the next cycle are usually known as ^^presystolic " murmurs. All other murmurs occurring during dias- tole are known as diastolic. The commonest of all the errors in the diagnosis of disease of the heart is to mistake systole for diastole, and thereby to misin- terpret the significance of a murmur heard during those periods. This mistake would never happen if we were always careful to make sure, by means of sight or touch, just when the systole of the heart occurs. This may be done by keeping one finger upon the apex impulse of the heart or upon the carotid artery while listening for murmurs, or, in case the apex impulse or the pulsa- tions of the carotid are better seen than felt, we can control by the eye the impressions gained by listening. It is never safe to trust our appreciation of the cardiac rhythm to tell us which is the first heart sound and which the second. The proof of this statement is given by the numberless mistakes made through disregarding it. Equally untrustAvorthy as a guide to the time of systole and dias- tole is the radial pulse, which follows the cardiac systole at an interval just long enough to mar our calculations. (2) Localizations of Mui-murs. — To localize a murmur is to find its point of maximum intensity, and this is of the greatest impor- tance ui diagnosis. Long experience has shown that murmurs 9 130 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. heard loudest iu the region of the apex beat (whether this is in the normal situation or displaced), are in the vast majority of cases pro- duced at the mitral valve. In about live per cent of the cases mitral murmurs may be best heard at a point midway betAveen the position of the normal cardiac impulse and the ensiform cartilage, or (very rarely) an inch or two above this situation. Murmurs heard most loudly in the second left intercostal space are almost invariably produced at the pulmonic orifice or just above it in the conus arteriosus. Murmurs whose maximum intensity is at the root of the ensi- form cartilage or within a radius of an inch and a half from this point are usually produced at the tricuspid orifice. Murmurs pro- duced at the aortic orifice may l)e heard best in the aortic area, but in a large proportion of cases are loudest on the other side of the sternum at or about the situation of the fourth left costal cartilage. Occasionally they are best heard at the apex of the heart or over the lower part of the sternum (see above. Fig. 103). (3) Transmission of Murmurs. — If a murmur is audible over sev- eral valve areas, the questions naturally arise: "How are Ave to knoAv whether Ave are dealing Avith a single A'alve lesion or Avith several? Is this one murmur or tAvo or three murmurs? " ObAd- ously the question can be asked only in case the murmur Avhich Ave find audible in various places occupies eA-erywhere the same time in the cardiac cycle. It must, for example, be CA^erywhere systolic or eA'eryAA'here diastolic. A systolic murmur at the apex cannot be supposed to ])oint to the same lesion as a diastolic murmur, no matter AAdiere the latter is heard. But if Ave hear a systolic mur- mur in various parts of the chest, say over the aortic, mitral, and triciispid regions, hoAV are Ave to knoAV whether the sound is simple or compound, Avhether produced at one valve orifice or at scA'cral? This question is sometimes difficult to answer, and in a giA'en case skilled obserA'ers may differ in their A'erdict, but, as a rule, the difficulty may be OA^ercome as folloAvs : (1) Experience and post-mortem examination haA'e shown that the murmur produced by each of tlie A-ahndar lesions has its oavu characteristic area of propagation, over Avhich it is heard Avith an in- AUSCULTATION OF THE HEART. 131 tensity which regularly diminishes as we recede from a maxltuam whose seat corresponds with some one of the valve areas just de- scriljed. These areas of jn-opagation are shoAvu in Figs. 91, 92, 95, and 100. Any murmur whose distribution does not extend beyond one of these areas, and which steadily and progressively diminishes in intensity as we move away from the valve area over which it is loudest; ma.y be a.ssumed to be d.ue to a. single valve lesion and no Fig. 82.— Mitral and Tricuspid Regurgitation. The intensity of the systolic murmur is least at the " waist " of the shaded area and increases as one approaches either end of it. more. Provided but one valve is diseased, this course of procedure gives satisfactory results. (2) When several valves are diseased and several murmiu-s may be expected, it is best to start at some one valve area, say hi the mitral or apex region, and move the stethoscope one-half an inch at a time toward one of the other valve areas, noting the intensity of any murmur we may hear at each of the different points passed over. As we move toward the tricuspid area, we may get an im- pression best expressed by Fig. 82. That is, a systolic murmur heard loudly at the apex may fade away as we move toAvard the ensiform, until at the point x (Fig. 82) it is almost inaudible. But as we go on in the same direction the murmur may begin to grow 132 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. louder (and perhaps to change in pitch and quality as well) until a maximum is reached at the tricuspid area, beyond which the mur- mur again fades out. These facts justify us in susj'ectin^/ that we are dealing with two murmurs, one produced at the tricuspid and one at the mitral ori- fice. The suspicion is more likely to be correct if there has been a change in the pitch and quality of the murmur as we neared the tricuspid orifice, and may be confirmed by the discovery of other evidences of a double lesion, yo diagnosis is satisfactory ichich rests on the evidence of muniiin-s alone. Changes in the size of the heart's chambers or in the pulmonary or peripheral circulations are the most important facts in the case. Nevertheless the effort to ascertam and graphically to represent the mtensity of cardiac ' murmurs as one listens along the line connecting the valve areas has its value. An "hour-glass" murmur, such as that represented in Fig. 82, generally means tifo-valve lesions. A similar "hour- glass " may be found to represent the auditory facts as we move from the mitral to the pulmonic or to the aortic areas (see Fig. 83), and, as in the previous case, arouses our suspicion that more than one valve is diseased. It must not be forgotten, however, that " a murmxir may travel some distance underground and emerge with a change of quality " ( AUbutt) . This is especially true of aortic murmurs, which are often heard well at the apex and at the aortic area, and faintly in the in- tervening space, probably owing to the interposition of the right ventricle. In such cases we must fall back upon the condition of the heart itself, as shown by inspection, })alpation, and i)ercussion, and upon the condition of the pulmonary and peripheral circulation, as shown in the other symptoms and signs of the cases (dropsy, cough, etc.). (4) Intensity of Mavmiu's. — Sometimes murmurs are so loud that they are audible to tlie i)atient himself or even at some dis- tance from the chest. In one case I was able to hear a murmur eight feet from the patient. Such cases are rare and usually not serious, for the gravity of the lesion is not at all proportional to AUSCULTATION OF THE HEART. 133 the loudness of the murmur; indeed, other things bemg equal, loud murmurs are less serious than faint ones, provided we are sure we are dealing with organic lesions. (On the distinction between the organic and functional murmurs, see below, p. 138.) A loud murmur means a powerful heart driving the blood strongly over the diseased valve. AVhen the heart begins to fail, tlie intensity of the murmur proportionately decreases because the blood does not floAv^ swiftly enough over the diseased valve to |)ro- fict. -Mitral Regurgitation and Aortic Stenosis. The systolic murmur is loudest at the ex- tremities of the shaded area and faintest at its " waist." duce as loud a sound as formerly. The gradual disappearance of a murmur laiown to be due to a vahnilar lesion is, therefore, a very grave sign, and its reappearance revives hope. Patients are not infrequently admitted to a hospital with valvular heart trouble which has gone on so long that the muscle of the heart is no longer strong enough to produce a murmur as it pumps the blood over the diseased valve. In such a case, under the iniluence of rest and cardiac tonics, one may observe the development of a murmur as the heart wall regains its power, and the louder the murmur be- comes the better the condition of the patient. On the other hand, when the existence of a valvular lesion has been delinitelv deter- 134 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. mmed, and yet the compensation remains perfectly good (for exam- l)le, in the endocarditis occurring in children in connection with chorea) , an increase in the loudness of the murmur may run paral- lel Avith the advance in the valvular lesion. In general the most important pomt about the intensity of a murmur is its Increase or decrease ivhile under observation, and not its louchiess at any one time. (5) Qualiti/ of Heart Murmurs.— It has been already mentioned that the quality of a heart murmur is never anything like the sound which we ordinarily designate by the word "murmur." The commonest type of heart murmur has a blowing quality, whence the old name oi ^'■hel/oa-s sound.'' The sound of the letter "f" pro- longed is not unlike the quality of certain murmurs. Blowing murmurs may be low-pitched like the sound of air passing through a large tube, or high-pitched approaching the sound of a whistle. This last type merges into that knoAvn as the viuslcal murmur, m Avhich there is a definite musical sound whose pitch can be identi- fied, liasjjlnff or tearing sounds often characterize the louder varieties of murmurs. Finally, there is one type of sound which, though included .under the general name murmur, differs entirely from any of the other sounds just described. This is the ^^presystolic roll,'' which has a rumbling or blubbering quality or may remind one of a short drum-roll. This murmur is always presystolic in time and usually associated with obstruction at the mitral or tricuspid valves. Not infrequently some part of a cardiac murmur Avill have a musical quality while the rest is simply blowing or rasping in character. Musical murmurs do not give us evidence either of an especially serious or especially mild type of disease. Their chief importance consists in the fact that they rarely exist without some valve lesion,' and are, therefore, of use in excluding the type of mur- mur known as ^'functional," presently to be discussed, and not due to valve disease. Very often ras])ing murmurs are associated either with the calcareous deposit upon a valve or very marked narrowing of the valve orifice. ' Rosenbach holds that they may be produced by adhesive pericarditis. AUSCULTATION OF THE HEART, 135 Murmurs may be accented at the beginning or the end ; that is, they may be of the crescendo type, growing louder toward the end, or of the decrescendo tyjDC with their maximum intensity at the beginnuig. Almost all murmurs are of the latter type except those associated with mitral or tricuspid obstruction. (6) Length of Murmurs. — Murmurs may occupy the Avdiole of systole, the whole of diastole, or only a portion of one of these i^eriods, but no conclusions can be drawn as to the severity of the valve lesion from the length of the murmur. A short mur- mur, especially if diastolic, may be of very serious prognostic im- port. (7) Relations to the Normal Sounds of the Heart. — Cardiac mur- murs may or may not replace the normal heart sounds. They may occur simultaneously with one or both sounds or between the sounds. These facts have a certain amount of significance in prog- nosis. Murmurs which entirely replace cardiac sounds usually mean a severer disease of the affected valve than murmurs which accom- pany, but do not replace, the normal heart sounds. Post-systolic or late systolic murmurs, which occur between the first and the second sound, are usually associated with a relatively slight degree of A^alvular disease. Late diastolic murmurs, on the other hand, have no such favorable significance. (8) Ejfects of Position, Exercise, and Respiration upon Cardiac Jlurraurs. — Almost all cardiac murmurs are affected to a greater or less extent by the position which the patient assumes while he is examined. Systolic murmurs which are inaudible while the patient is in a sitting or standing position may be quite easily heard when the patient lies down. On the other hand, a pre- systolic roll which is easily heard when the patient is sitting up may entirely disappear when he lies down. Diastolic murmurs are relatively little affected by the position of the patient, but in the majority of cases are somewhat louder in the upright posi- tion. The effects of exercise may perhaps be fitly mentioned here. Feeble murmurs may altogether disappear Avhen the patient is at rest, and under such circumstances may be made easily audible by 136 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. getting the patient to walk briskly up and doAvn the room a few times. Such lesions are usually comparatively slight.' On the other hand, murmurs which become more marked as a result of rest are generally of the severest type (see above, p. 132). Organic murmurs are usually better heard at the end of expira- tion and become fainter during inspiration as the expanding lung covers the heart. This is especially true of those produced at tlie mitral valve, and is in marked contrast with the variations of func- tional murmurs which are heard chiefly or exclusively at the end of inspiration. (9) ^Sudden MetamorijJwsis of Murmurs. — In acute endocarditis, when vegetations are rapidly forming and changing their shajje upon the valves, murmurs may appear and disappear very sud- denly. This metamorphosing character of cardiac murmurs, when taken in connection with other physical signs, may be a very im- portant factor in the diagnosis of acute endocarditis. In a similar way relaxation or rupture of one of the tendinous cords, occurring in the course of acute endocarditis, may effect a very sudden change in the auscultatory phenomena. " Functioned Ifurmurs." Not every nuirmur which is to be heard over the heart points to disease either in the valves or in the orifices of the heart. Perhaps the majority of all murmurs are thus unassociated with vahiilar disease, and to such the name of "accidental," "functional," or " hsemic " murmurs has been given. The origin of these " functional " murmurs has given rise to an immense amount of controversy, and it cannot be said that any one explanation is now generally agreed upon. To me the most plausible view is that which regards most of them as due either to a temporary or permanent dilatation of the conns arteriosus, or to pressure or suction exerted upon the overlapping lung margins by the cardiac contractions. This ex- plains only the systolic functional nnirmurs, which make up ninety- nine per cent, of all functional nuirmuvs. The diastolic functional murmurs, which undoubtedly occur, although with exceeding rarity, ' Foi' excei)tion to this sec below, page 101. AUSCULTATION OF THE HEART. 137 are probably clue to sounds produced in the veins of the neck and transmitted to the innominate or vena cava. Characteristics of Functional Murmurs. — (1) Almost all func- tional murmurs are systolic, as has before been mentioned. (2) The vast majority of them are heard best over the imlmonic valve in the second left intercostal space. From this point they are transmitted in all directions, and are frequently to be heard, al- though with less intensity, in the aortic and mitral areas. Occa- sionally they may have their maximum intensity in one of the latter positions. (3) As a rule, they are very soft and blowing in quality, though exceptionally they may be loud and rough. (4) They are not associated with any evidence of enlargement of the heart nor with accentuation of the pulmonic second sound.' (5) They are usually louder at the end of inspiration. (6) They are usually heard over a very limited area and not transmitted to the left axilla or to the back. (7) They are especially evanescent in character ; for example, they may appear at the end of a hard run or boat race or durmg an attack of fever, and disappear withm a few days or hours. Ees- piration, position, and exercise produce greater variations in them than in "organic" murmurs. (8) They are especially apt to be associated with anaemia, although the connection betAveen anseniia and functional heart mur- murs is by no means as close as has often been supposed. The severest types of anoemia, for example pernicious anaemia, may not be accompanied by any murmur, while, on the other hand, typical functional murmurs are often heard in patients whose blood is nor- mal, and even in full health. It should not be forgotten that a real, though temporary, leakage through the mitral or tricuspid valve may be associated with ana?mia or debilitated conditions owing to weakening of the papillary muscles or of the mitral sphincter. In such cases we find not the signs of a functional ' In chlorosis the second pulmonic sound is often very loud (owing to the retraction of the lungs and uncovering of the conus arteriosus) and associated with a systolic murmur. 138 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. nmruiur, as above described, but the evidence of au organic valve lesion hereafter to be described. The distinctions between organic and functional heart murmurs may be summed up as follows : Oi'fjanic murinurs may occupy any part of the cardiac cycle ; if systolic, they are usually transmitted either into the axilla and back or into the great vessels of the neck ; they are usually asso- ciated with evidences of cardiac enlargement and changes in the sec- ond sounds at the base of the heart, as well as with signs and symp- toms of stasis in other organs. Organic murmurs not infrequently have a musical or rasping quality, although this is by no means al- ways the case. They are rarely loudest in the pulmonic area and are relatively uninfluenced by respiration, position, or exercise. Functional innvmurs are almost ahvays systolic in time and usually heard with maximum intensity in the pulmonic area. They are rarely transmitted beyond the precordial region and are usually loudest at the end of mspiration. They are not accompanied by evidences of cardiac enlargement or pathological accentuation of the second sounds at the base of the heart, nor by signs of venous stasis or dropsy. They are very apt to be associated Avith aniemia or with some special attack upon the resources of the lx)dy {e.g., physical overstrain or fever), and to disappear when such forces are removed. They are usually soft in quality ; never musical. The very rare diastolic functional murmur occurs exclusively, so far as I am aware, in conditions of profound anasmia ; i.e. , when the haemo- globin is twenty-live per cent or less. It can be abolished by press- ure upon the bullnis jugularis, and can be observed, if folloAved up into the neck, to pass over gradually into a continuous venous hiim with a diastolic accent. Cai'dio-licspli'dfoi')/ Jfi/rin urs. When a portion of the free margin of the lung is fixed by ad- hesions in a position overla])ping the heart, the cardiac movements may rhythmically dis})laee the air in such piece of lung so as to give rise to sounds which at times closely simulate cardiac mur- murs. These conditions are most often to be found in the tongue- AUSCULTATION OF THE HEART. 139 like projection of the left lung, which normally overlaps the heart, but it is probably the case that cardio-respiratory murmurs may be produced without any adhesion of the lung to the pericardium under conditions not at present understood. Such murmurs may be heard under the left clavicle or below the angle of the left scap- ula, as well as near the apex of the heart, — less often in other parts of the chest. Cardio-respiratory murmurs may be either systolic or diastolic, but the vast majority of cases are systolic. The area over which they are audible is usually a very limited one. They are greatly affected by position and by respiration, and are heard most distinctly if not exclusively during inspiration, especially at the end of that act. (This fact is an important aid in distinguishing them from true cardiac murmurs, which are almost always fainter at the end of iirspiration.) They are also greatly affected by cough or forced respiration or by holding the breath, whereas cardiac murmurs are relatively little changed thereby. Pressure on the outside of the thorax and in their vicinity may greatly modify their in- tensity or quality, while organic cardiac murmurs are but little influenced by pressure. As a rule, they have the quality of nor- mal respiratory murmur, and sound like an inspiration interrupted by each diastole of the heart. In case the effect of the cardiac movements is exerted upon a piece of lung in which a catarrhal process is going on, we may have systolic or diastolic explosions of rales, or any type of respiratory murmur except the bronchial type, since this is produced in solid lung which could not be emptied or filled under the influence of the car- diac movements. Cardio-respiratory murmurs have no special diag- nostic significance, and are mentioned here only on account of the im- portance of not confusing them with true cardiac murmurs. They were formerly thought to indicate phthisis, but such is not the case. Murmurs of Venous Origin. I have already mentioned that the venous hum so often heard in the neck in cases of anaemia may be transmitted to the region of the base of the heart and heard there as a diastolic murmur owing 140 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. to the acceleration of the venous current by the aspiration of the right ventricle during diastole. Such murmurs are very rare and may usually be obliterated by pressure upon the bulbus jugularis, or even by the compression brought to bear upon the veins of the neck when the head is sharply turned to one side. They are heard better in the upright position and duruig inspiraticn. Arterial Murmurs. (1) Roughening of the arch of the aorta, due to chronic endo- carditis, is a frequent cause in elderly men of a systolic murmur, heard best at the ])ase of the heart and transmitted into the vessels of the neck. Such a murmur is sometimes accompanied by a pal- pable thrill. From cardiac murmurs it is distinguished by the lack of any other evidence of cardiac disease and the presence of marked arterio-sclerosis in the peripheral vessels (see further discussion under Aortic Stenosis, p. 180, and under Aneurism, p. 220) . (2) A narrowing of the lumen of the left subclavian artery, due to some abnormality in its course, may give rise to a systolic mur- mur heard close below the left claA-icle at its outer end. The mur- mur is greatly mfluenced by movements of the arm and especially by respiratory movements. During inspiration it is much louder, and at the end of a forced expiration it may disappear altogether. Occasionally such murmurs are transmitted through the clavicle so as to be audible above it. (3) Pressure exerted upon any of the superficial arteries (carot- id, femoral, etc.) produces a systolic murmur (see below, p. 178). Diastolic arterial murmurs are peculiar to aortic regurgitation. (4) Over the anterior fontanelle in infants and over the gravid uterus systolic murmurs are to be heard which are probably arterial in origin. PART II. DISEASES OF THE HEART. CHAPTER VII VALVULAR LESIONS. Clinically it is convenient to divide the ills which befall the heart into three classes : (1) Those which deform the cardiac valves (valvular lesions). (2) Those which weaken the heart wall (parietal disease). (3) Congenital malformations. Lesions which affect the cardiac valves without deforming them are not often recognizable durmg life. The vegetations of acute endocarditis' do not usually produce any peculiar physical signs until they have so far deformed or obstructed the valves as to pre- vent their opening or closing properly. The murmurs which are often heard over the heart in cases of acute articular rheumatism cannot be considered as evidence of vegetative endocarditis unless valvular deformities, and their re- sults in valvular obstruction or incompetency, ensue. The chordae tendinese may be ruptured or shortened, thickened, and welded to- gether into shapeless masses, but if these deformities do not affect the action of the valves we have no means of recognizing them dur- ing life. Congenital malformations are practically unrecognizable as such. If they do not affect the valves, we cannot with any cer- tainty make out what is wrong. For physical diagnosis, then, heart disease means either de- formed valves or weakened walls. Whatever else may exist, we are none the wiser for it unless the autopsy enlightens us. ' See Appendix. 142 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. In this cliapter I shall confine myself to the discussion of vahii- lar lesions and their results. Valvular lesions are of two types : (a) Those which jiroduce partial obstruction of a valve orifice or prcA'ent its opening fully {" ste^iosis'^). Wco»pi.l;t'.:=' il,-,I Rlr.su »lnif..r iiG. ^4.— Tlic Base of tlie Coiit rafted Heart Showing Spliincteric Action of the Muscular l''il)res Surrounding the Mitral and Tricuspid Valves. The outer dotted line is the outline of the relaxed heart. The inner dotted circles show the size of the mitral and tricuspid valves during diastole, a. Outline of the heart when relaxed ; b, outline of the relaxed tricuspid valve ; i\ outline of the mitral orifice during diastole. (b) Those which produce leakage through a valve orifice or prevent its closing effectively {^^ regurgitation,^^ ^' insufficienc}/," " incompf'tcneij ") . Stenosis results always from the stiffening, thickenhig, and con- traction of a valve. Kegurgitation, on the other hand, may be the result either of — VALVULAR LESIONS. 143 Mitral curtains. Cliordea tendinete. Papillary muscle. Circular or ««il — sphlncteric Qbres. Endocardium. (a) Deformity of a valve, or (li) "Weakening of the heart muscle. The mitral and tricuspid orifices are closed not simply by the shutting of their valves, but also in part by the sphincter-like ac- tion of the circular fibres of tlie heart wall (see Fig. 84) and the contraction of the papillary muscles (Fig. 85). In birds the tricuspid orifice has no valve and is closed wholly by the muscular sphincter of the heart wall. In conditions of acute car- diac failure, such as may oc- cur after a hard run, the papillary muscles are in all probability relaxed, so that the valve-flaps swing back into the auricle and permit re- gurgitation of blood from the ventricle. Vahuilar incom- petence, then, differs from valvular ohstruction in that the latter always involves deformity and stiffening of valves, while incompetence or leakage is often the result of deficient muscular action on the jiart of the heart wall. An obstructed valve is almost always leaky as well, since the same deformities which prevent a valve from opening usually prevent its closure; hid this rule does not trork haelxU'CD'd. A leaky valve is often not obstructed. It is leaky but not obstructed if the valve curtain has been practically de- stroyed by endocarditis; or, again, it is leaky but not obstructed if the leak represents muscular weakening of the mitral sphincter or of the papillary muscles. Pure stenosis is very rare. Pure regur- gitation is very common. Myocardium. Pericardium. Fig. bo. -The Mitral Valve Closed, Showing the Action of the Papillary Muscles. 144 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. When valves are so defonued that their orifice is hofh leaky and obstructed, we have what is known as a " combined " or " double " valve lesion. Since valvular lesions are recognized largely by their results^ first upon the walls of the heart itself and then upon the other organs of the body, it seems best to give some account of these results before passing on to the description of the individual le- sions in the heart itself. The results of valvular lesions are first conservative and later destructive. The conservative results are known as : The estaJAisliment of compensation throufjli hypertrophy. The destructive or degenerative results are known as : The failure of compensation through (or without) dilatation. I shall consider, then, {a) The establishment and the failure of compensation. (b) Cardiac hypertrojihy. (c) Cardiac dilatation. ESTABLISHMENT AND FAILURE OF COMPENSATION IN VALVULAR DISEASE OF THE HEART. "We may discriminate three periods in the progress of a case of valviilar heart disease : (1) The period before the establishment of compensation. (2) The period of compensation. (3) The period of failing or ruptured compensation. (1) Compensation JXat Yet Established. In most cases of acute valvular endocarditis, Avhether of the relatively benign or of the malignant type, there is a time Avhen the lesion is perfectly recognizable despite the fact that compensa- tory hypertrophy has not yet occurred. In some cases this period may last for months ; the heart is not enlarged, there is no accentu- ation of either second sound at the base, there is no venous stasis, and our diagnosis must rest solely u])on the presence and character- istics of the murmur. For exam])le, in early cases of mitral regur- VALVULAR LESIONS. 145 gitation due to chorea or rlieimiatisiu, the disease may be recog- iiized by the presence of a loud musical murmur heard in the back as well as at the apex and in the axilla. In the earlier stages of aortic regurgitation occurring in young people as a complication of rlieuniatic fever, there may be a])solutely no evidence of the valve lesion except the characteristic diastolic murmur. In most text- books of physical diagnosis I thmk too little attention is given to this stage of the disease. (2) The Period of Conqjensatlou. Valvular disease would, however, soon prove fatal were it not for the occurrence of compensatory hypertrophy of the heart walls. To a certain extent the heart contracts as a single muscle, and in- creases the size of all its walls in response to the demand for in- creased work; but as a rule the hypertrophy affects especially one ventricle — that ventricle, namely, upon which especially demand is made for mcreased power in order to overcome an increased resist- ance in the vascular circuit which it supplies with blood. What- ever mcreases the resistance in the lungs brings increased work upon the right ventricle ; whatever mcreases the resistance in the aorta or peripheral arteries increases the amount of work which the left ventricle must do. jSTow, any disease of the mitral valve, whether obstruction or leakage, results in engorgement of the lungs with blood, and hence demands an increased amount of work on the j)art of the right ventricle in order to force the blood through the overcrowded pul- monary vessels ; hence it is in mitral disease that we find the great- est compensatory hypertrophy of the right ventricle. On the other hand, it is obvious that obstruction at the aortic valves or in the peripheral arteries (arterio-sclerosis) demands an increase in power in the left ventricle, in order that the requisite amount of blood may be forced through arteries of reduced calibre, while if the aortic valve is so diseased that a part of the blood throAvn into the aorta by the left ventricle returns into that ven- tricle, its work is thereby greatly increased, since it has to contract upon a larger volume of blood. lb 146 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. In resjionse to these demands for increased work, the muscular wall of the left ventricle increases ui thickness, and compensation is thus established at the cost of an increased amount of work on the part of the heart.' (3) Failure of Comjjensatlon. Sooner or later in the vast majority of cases the heart, handi- capised as it is by a leakage or obstruction of one or more valves, becomes unable to meet the demands made upon it by the needs of the circulation. Failure of compensation is sometimes associated with dilatation of the heart and weakening of its Avails, but in many cases no such change can be found to account for its failure, and Ave haA^e to fall back upon changes in the nutrition of the heart Avail or upon some hypothetical derangement of the ner- vous mechanism of the organ as an explanation. AAliatever the cause may be, the result of ruptured compensation is ve7ions stasis ; that is, oedema or dropsy of various organs appears. If the left A'entricle is especially Aveakened, dropsy appears first in the legs, on account of the influence of gravity, soon after in the geni- tals, lungs, liver, and the serous caA'ities. Engorgement of the lungs is especially marked in cases of mitral disease Avith Aveakening of the right A'entricle, and is manifested by dyspnoea, cyanosis, cough, and htemoptysis. In many cases, hoAvcA^er, dropsy is very irregularly and unaccountably distri])uted, and does not follow the rules just given. In pure aortic disease, inicomplicated by leakage of the mitral vah-e, dropsy is a relatively late symptom, and dysp- noea and precordial pain (angina pectoris) are more prominent. HYPERTROPHY AND DILATATIOX. Since cardiac hypertrophy or dilatation are not in themseh-es diseases, but may occur in any disease of the heart (A'ah^iilar or parietal), it seems best to giA'e some account of them and of the methods by which they may be recognized, before taking up sepa- rately the different lesions Avith Avhich they are associated. ' Rosenbach brings forward evidence to show that the arteries, tlie lungs, and other organs actively assist in maintaining compensation. VALVULAR LESIONS. 147 1. Cardiac HypertroijJnj. Hypertrophy of the heart is usually due to the following causes : First (and most frequent) : Yahailar disease of the heart itself. Second: Obstruction of the flow of blood through the arteries owing to increase of arterial resistance, such as occurs in chronic nephritis and arterio-sclerosis. Third : Obstruction to the circula- tion of the blood through the lungs (emphysema, cirrhosis of the lung, fibroid phthisis). Fourth: Severe and prolonged muscular exertion (athlete's heart). In vahiilar disease the greatest degree of hypertrophy is to be seen usually in relatively young persons, and especially when the advance of the lesion is not very rapid. Hypertroi^hy of the heart in valvular disease is also influenced by the amount of muscular w^ork done by the patient, by the de- gree of vascular tension, and by the treatment. In the great major- ity of cases of hypertrophy, from whatever cause, both sides of the heart are affected, but we may distinguish cases in which one or the other ventricle in predominantly affected. (1) Cardiac hypertrophy affecting especially the left ventricle. {(i) The apex impulse is usually lower than normal, often in the sixth space, occasionally in the seventh or eighth.' It is also farther to the left than normal, but far less so than in cases in which the hypertrophy affects esi^ecially the right ventricle. The area of visible pulsation is usually increased, and a considerable por- tion of the chest wall may be seen to move with each systole of the heart, while frequently there is a systolic retraction of the inter- spaces in place of a systolic impulse. (h) Palpation confirms the results of inspection and shows us also that the apex impulse is unusually powerful. Percussion shows in many cases that the cardiac dulness is more intense and its area increased downward and to a lesser extent toward the left.'^ ' This is due partly to a stretching of the aorta, produced by the increased weight of the heart. -Post mortem hypertrophy of the left ventricle is often found despite the absence of the above signs iu life. 148 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. {c) If we listen in the region of tlie maximum cardiac impulse, we generally hear an unusually long and low-pitched first souiul, which may or may not be of a greater intensity than normal. A very loud first sound is much more characteristic of a cardiac neu- rosis than of pure hypertrophy of the left ventricle. The second sound at the apex (the aortic second sound trans- mitted) is usually much louder and sharper than usual. Ausculta- tion in the aortic area shows that the second sound at that point is loud and ringing in character. Not infrequently the peri2:)heral ar- teries (the subclavians, brachials, carotids, radials, and femorals) may be seen to pulsate with each systole of the heart. This sign is most frequently observed in cases of hypertrophy of the left ven- tricle, which are due to aortic regurgitation, l)ut is by no means' peculiar to this disease and may be repeatedly observed when the cardiac hypertrophy is due to neyjliritis or muscular work. I have frequently observed it in athletes, blacksmiths, and others whose muscular work is severe. The radial pulse wave has no constant characteristics, but de- pends rather upon the cause which has produced the hypertrophy than upon the hypertrophy itself. (2) Cardiac Hyptivtroplitj Affecting Espexialhj the Rujlit Ventricle. It is much more difficult to be certain of the existence of en- largement of the right ventricle than of the left. Practically we have but two relial>le physical signs: (a) Increase in the transverse diameter of the heart, as shown by the position of the a]>ex impidse and by percussion of the right and left borders of the heart; and {h) Accentuation of the pulmonic second sound, which is often palpable as well as audible. The apex beat is displaced both to the left and downward, hut espechillij to the left. In cases of long-standing mitral disease, the cardiac impulse may be felt in mid-axilla, several inches outside the nipple, and yet not lower down than tlie sixth intercostal space. In a small percentage of cases {i.e., when tlie right auricle is en- gorged), an increased area of dulness to the right of the sternum VALVULAR LESIONS. 149 may be demonstrated. Accentuation of the pulmonic second sound is almost invariably present in liyjjertrophy of the right ventricle, though it is not peculiar to that condition. It may be heard, for example, in cases of pneumonia when no such hypertrophy is pres- ent, Imt in the vast majority of cases of cardiac disease we may infer the presence and to some extent the amount of hypertrophy of the right ventricle from the presence of a greater or lesser ac- centuation of the pulmonic second sound. The radial pulse shows nothing characteristic of this type of hy|)ertrophy. Epigastric pulsation gives us no e\ddence of the existence of hypertrophy of the right ventricle, despite contrary statements in many text-books. Such pulsation is frequently to be seen in per- sons with normal hearts, and is frequently absent when the right ventricle is obviously hypertrophied. It is perhaps most often due to an unusually low position of the whole heart. Dilatation of the Heart. (1) Acute Dilatation. — Immediately after severe muscular exer- tion, as, for example, at the finish of a boat race, or of a two-mile run (especially in persons not properly trained), an acute dilatation of the heart may occur, and in debilitated or poorly nourished sub- jects such an acute dilatation may be serious or even fatal in its results. (2) Chronic dilatation comes on gradually as a result of vahii- lar disease or other cause, and gives rise to practically the same physical signs as those of acute dilatation, from which it differs chiefly as regards the accompanying physical phenomena and the prognosis. Briefly stated, the signs of dilatation of the heart, whether acute or chronic, are : (fi) Feebleness and irregxilarlty of the apex impulse and of the radial impulse, (V) enlargement of the heart, as indicated by inspec- tion, palpation, and percussion, and (sometimes) (c) mnrmurs indi- cative of stretching of one or another of the A-ahiilar orifices. 150 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. Dilatation of the Left Ventricle. Inspection shows little that is not better brought out by palpa- tion. Palpation reveals a feeble "flapping" cardiac impulse, or a vague shock displaced both downward and to the left and diffused over an abnormally large area of the chest wall. Percussion veri- fies the position of the cardiac impulse and sometimes shows an unusually blunt or rounded outline at the apex of the heart. On auscultation, the first sound is usually very short and sharp, but not feeble unless it is accompanied by a murmur. In case the mitral orifice is so stretched as to render the valve incompetent, or in case the muscles of the heart are so fatigued and weakened that they do not assist in closing the mitral orifice, a systolic murmur is to be heard at the apex of the heart. This murmur is transmitted to the axilla and back, but does not usually replace the first somid of the heart. The aortic second sound, as heard in the aortic area and at the apex, is feeble. Dilatation of the right ventricle of the heart is manifested by an increase in the area of cardiac duhiess to the right of the sternum (corresponding to the position of the right auricle), by feebleness of the pulmonic second sound together with signs of congestion and engorgement of the lungs, and often by a systolic murmur at the tricuspid valve; i.e., at or near the root of the ensiform cartilage. When this latter event occurs, one may have also systolic i)ulsation in the jugular veins and in the liver (see below, \). 188). In cases of acute dilatation, such as occur in infectious fevers or at the end of well-contested races, there is often to be heard a systolic murmur loudest in the pulmonary area and due very pos- sibly to a dilatation of the conns arteriosus. The diagnosis of dilatation of the heart seldom rests entirely upon })hysical signs referable to the heart itself. In acute cases our diagnosis is materially aided by a knowledge of the cause, which is often tolerably ol)vious. In chronic; cases the best evi- dence of dilatation is often that furnished by the venous stasis which results from it. VALVULAR LESIONS. 151 (4) CHRONIC VALVULAll DISEASE. I. MiTKAL ReGURGITATIOX. The commonest and on the whole the least serious of valvular lesions is incompetency of the mitral. It results in most cases from the shortening, stiffening, and thickening of the valve pro- duced by rheumatic endocarditis in early life. It is the lesion l)resent m most cases of chorea (see Figs. 86 and 87). Temporary and curable mitral regurgitation may result from weakening of the heart muscle, which normally assists in closing the mitral orifice through the sphincter-like contraction of its cir- cular fibres. Great muscular fatigue, such as is produced by a hard boat race, may result in a temporary relaxation of the mitral sphincter or of the papillary muscles sufficient to allow of genuine but tem- porary and curable regurgitation through the mitral orifice. In conditions of profound nervous debility and exhaustion, similar Aveakening of the cardiac muscles may allow of a leakage through the mitral, which ceases with the removal of its cause. Stress has recently been laid upon these points by Arnold and by ]\Iorton Prince. jMitral insufficiency due to stretching of the ring into which the valve is inserted occurs not unfrequently as a result of dilatation of the left ventricle, and is commonly known as relative insufficiency of the mitral valve. The valve orifice can enlarge, the valve can- not, and hence its curtains are insufficient to fill up the dilated ori- fice. This type of mitral insufficiency frequently results from aortic regurgitation with the dilatation of the left ventricle which that lesion produces, or from myocarditis, which weakens the heart wall until it dilates and widens the mitral orifice. The results of any form of mitral leakage are : 1. Dilatation or hypertroph]i of the left auricle, which has to receive blood both from the lungs and through the leaky mitral from the left ventricle. 2. The overfilled left auricle cannot receive the blood from the 152 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. lungs as readily as it should; hence the blood ''backs up " in the lungs and thereby increases the work which the right ventricle must do in order to force the blood through them. Thus result oedema of the lungs, and — '-Z)/j£ar./ira(J/?/?a/ Fig. 66.— Noniial Heart fiuring Systole. Mitral valve closed ; blood flowing through the open aortic valves into the aorta. Fig. 87.— Mitral Regurgitation. The heart is in systole and the arrows show the current flowing back in the left auricle as well as forward into the aorta. VALVULAR LESIONS. 153 (3) Hijpertropliij and dihifjttlon of the right ventricle, which in turn becomes sooner or later overcrowded so tliat the tricuspid valve gives way and tricuspid leakage occurs. (4) The capacity for hypertrophy possessed by the riglit auricle is soon exhausted, and we get then — (5) General venous stasis, which shows itself first as venous pulsation in the jugulars and in the liver and later in the tissues drained by the portal and peripheral veins. This venous stasis in- creases the work of the left ventricle, and so we get — (6) Hyi:)ertroxjhy and dilatation of the left ventricle. Hyper- trophy of the left ventricle is also produced by the increased work necessary to maintain some vestige of sphincter action at the leaky mitral orifice, as well as by the labor of contracting upon the extra quantity of blood delivered to it by the enlarged left auricle. At last the circle is complete. Every chamber in the heart is enlarged, overworked, and failure is imminent. Eeturning now to the signs of mitral regurgitation, we shall find it most convenient to consider first the type of regurgitation pro- duced by rheumatism and resulting in thickening, stiffening, and retraction of the valve. Physicai. Signs. (a) First Star/e — Prior to the Estahlishinent of Compensatio7i. We have but one characteristic physical sign : A systolic murmur heard loudest at the apex of the heart, trans- mitted to the back (below or inside the left scapula) and to the left axilla. The murmur is not infrequently musical in character, and when this is the case diagnosis is much easier. Systolic musical murmurs so transmitted do not occur without vahailar leakage. Kosenbach believes that adherent pericardium is capable of produc- ing such a murmur, but only, if I understand him rightly, in case there is a genuine mitral leakage due to the embarrassing embrace of the pericardium which prevents the mitral orifice from closing. "Functional" or "haemic" murmurs are rarely heard in the back, and very rarely, if ever, have a musical quality. 154 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. Cases of mitral regurgitation are not very often seen at this stage, Lilt in acute endocarditis after the fever and anaemia have subsided, or in chorea, such a murmur may exist for days or weeks before any accentuation of the puhnonic second sound or any en- largement of the heart appears. I have had the opportunity of verifying the diagnosis at autopsy in two such cases. (b) Second Stage — Conqjensatlou EstuhlisJied. As long as compensation remains perfect, the only evidence of regurgitation may be that obtained by auscultation, and I shall accordingly begin with this rather than hi the traditional Avay Avith inspection, palpation, and percussion. The distinguishmg auscultatory phenomeua in cases of Avell-' compensated mitral insufficiency are: (a) A systolic murmur Avhose maximum intensity is at or near the apex impulse of the heart, but which is also to be heard in the left axilla and in the back below or inside the angle of the left scapula (so far the signs are those of the first stage, above de- scribed). (h) A pathological accentuation of the puhnonic second sound. This is the minimum of evidence upon Avhich it is justifiable to make the diagnosis of compensated mitral regurgitation. In the vast majority of cases, however, our diagnosis is confirmed by the following additional data : (c) Enlargement of the heart as shown by inspection, palpation, and percussion, [d) Evidence of congestion of the lungs (dyspnoea, orthopnoea, cough, cyanosis, hemoptysis), as well as of the general venous sys- tem (engorgement of the liver, oedema of the legs, ascites, etc.). The pulse in well-compensated cases shows no considerable abnormality. When compensation begins to fail, or sometimes be- fore that time, the most characteristic thing about the pulse is its marked irregularity both in force and rhythm. Such irregularity is at once more common and less serioxis in mitral disease than in that of any other valve ; it may continue for years and be compat- ible with very tolerable health. VALVULAR LESIONS. 155 Keturning now to the details of the sketch just given, we will take up Urst — (a) The Murmur. — In children, the murmur of mitral regurgita- tion may be among the loudest of all murmurs to be heard in val- Ist I 1st 2nd 2nd. Fig. 88.— Diagram to Represent Systolic Mitral Murmur. The heavy lines represent the normal cardiac sounds and the light lines the uuu-mur, which in this case does not replace the first sound and " tapers " off characteristically at the end. ^n.ilar disease, but this does not necessarily imply that the lesion is a very severe one. A murmur which groics louder under observa- tion in a well-compensated valvular lesion may mean an advance of the disease, but if the case is first seen after compensation has failed a faint, variable whiff in the mitral area may mean the se- verest tjqje of lesion. As the patient improves under the influence of rest and cardiac tonics, such a murmur may grow very much louder, or a murmur previously inaudible may appear. The length of the murmur varies a great deal in different cases and is not of any great practical importance. It rarely ends abruptly, but usually "tails off" at the end of systole (see Fig. 88). Musical murmurs are heard more often in mitral regurgitation than in any other valve lesion, but the musical quality rarely lasts throughout the whole duration of tlie murmur, contrasting in this respect with musical murmurs produced at the aortic valve. The 2iid I 2nd I I I Fig. 89.— Systolic Mitral Murmur Replacing the First Sound of the Heart. first sound of the heart may or may not be replaced by the murmur (see Fig. 89). When the sound persists and is heard either with or before the murmur, one can infer that the lesion is relatively slight in comparison Avith cases in which the first sound is wholly 156 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. obliterated. Fust-systoric or late sz/sfoUc murmurs, whieli are occa- sionally heard in mitral regurgitation, are said to point to a rela- tively slight amount of disease in the valve (see Fig. 90). Kosen- Ist I 2nd 1st 1 2nd Fig. 90.— Late Systolic Murmur. Tbe flrst sound is clear and an interval intervenes between it and the murmur. bach claims that the late systolic murmur is always due to organic disease of the valves and never occurs as a functional murmur. When compensation fails, the murmur may altogether disappear for a time, and if the patient is then seen for the first time and dies without rallying under treatment, it may be impossible to Pulmonic second accented. Systolic murmur loudest lie re. Fig. 91.— Mitral Regurgitation. The murmur is heard over the shaded area as well as in the back. make the diagnosis. The very worst cases, then, are those in which there is no murmur at all. The murmur of mitral regurgitation is conducted in all directions, but especially toward the axilla and to the back (not around the chest, but directly). In the latter situation it is usually louder VALVULAR LESIONS. 157 than it is in mid-axilla, and occasionally it is heard as loudly in the back as anywhere else. This is no doubt owing to the position of the left auricle (see Figs. 91 and 92). (b) After compensation is established and as long as it lasts an accentuation of the 2)idinonw second sound is almost invariably to be made out, and may be so marked that we can feel and see it, as well as hear it. Not infrequently one can also see and feel the pulsation of the conns arteriosus — not the left auricle — in the second and third left intercostal space. (It may be well to mention again Systolic murmur. Fig. 93.— Mitral Regurgitation. Murmur heard over the shaded area. here that by accentuation of the pulmonic second sound one does not mean merely that it is louder or sharj^er in quality than the aortic second sound, since this is true in the vast majority of cases in healthy individuals under thirty years of age. Pathological ac- centuation of the pulmonic second sound means a greater intensity of the sound than we have a rigid to expect at the age of the individ- nal in question.) Occasionally the pulmonic second sound is redu- plicated, but as a rule this points to an accompanying stenosis of the mitral valve. At the apex the second sound (i.e., the trans- mitted aortic second) is not infrequently wanting altogether, owing 158 PHYSrCAL DIAGNOSIS OF DISEASES OF THE CHEST. to the relatively small amount of Llood which recoils upon the aortic '^alves. (f) Enlarge))ii')it of the Ueavt, and more especially of the right ventricle, is generally to Ije made out, and in the majority of cases tnis enlargement is manifested by, displacement of the apex impulse both downward and toward the left, but more especially to the left. Percussion confirms the results of inspection and palpation regarding the position of the cardiac impulse. The normal sub- sternal dulness is increased in intensity, and we can sometimes demonstrate an enlargement of the heart toward the right (see Fig. 91). In children (in whom adhesive pericarditis often complicates the disease) a systolic thrill may not infrequently be felt at the apex, and the precordia may l)e Ijulged, and even in adults such a systolic thrill is not so rare as some writers Avould have us sup- pose. (f/) TIte pulse, as said above, shows nothing characteristic at any stage of the disease. While compensation lasts, there is usually nothing abnormal about the pulse, although it may be somewhat irregular in force and rhythm, and may be weak when compared to the powerful beat at the apex in case the regurgitant stream is a very large one. Irregularity at this period is less common in pure mitral regurgitation tlian in cases complicated by stenosis. (r) Third Staije — FdUliKj Compensation. "When compensation l^egins to fail, the pulse becomes weak and irregular, and many heart beats fail to reach the wrist, but there is still lujtliing (;liaracteristic about the pulse, which differs in no respect from that of any case of cardiac weakness of whatever nature. (e) Evidence of venous stasis, first in the lungs and later in the liver, lower extremities, and serous cavities, does not show itself so long as compensation is sufficient, but when the heart begins to fail the patient begins to complain not only of palpitation and car- diac distress, but of dyspnea, orthoi)n(]ea, and cough, and examina- tion reveals a greater or lesser degree of cyanosis with j^^dmo- VALVULAR LESIONS. 159 nary oedema manifested by crackling rales at the base of the lungs posteriorly, and possibly also by haemoptysis or by evidences of hydrothorax (see below, p. 266). If compensation is not re-estab- lished, the right ventricle dilates, the tricuspid becomes mcompe- tent, the liver becomes enlarged and tender, dropsy becomes gen- eral, the heart and pulse become more and more rapid and irregular, the heart murmur disappears and is replaced by a confusion of short vaho-ilar sounds, '■' (jallop rhythm'''' or ^' delirium cordis," often considerably obscured by the noisy, labored breathing with numer- ous moist rales. In a patient seen for the first time in such a con- dition diagnosis may be impossible, yet mitral disease of some tjrpe may usually be suspected, since murmurs produced at the aortic valve are not so apt to disappear when compensation fails. The relative tricuspid insufficiency which often occurs is likely to mani- fest itself by an enlargement of the right auricle, sometimes demon- strable by percussion and later by venous pulsation in the neck and in the liver. {d) Differential Diagnosis. • The murmur of mitral regurgitation may be confused with (1) Tricuspid regtirgitation. (2) Functional murmurs. (3) Stenosis or roughening of the aortic valves. (1) The post-mortem records of the Massachusetts General Hospital show that in the presence of a murmur due to mitral re- gurgitation it is very easy to fail altogether to recognize a tricuspid regurgitant murmur. Only 5 out of 29 cases of tricuspid regurgi- tation found at autopsy were recognized during life. AUbutt's figures from Guy's Hospital are similar. In the majority of these cases, mitral regurgitation was the lesion on Avhieh attention was concentrated during the patient's life. This is all the more excus- able because the tricuspid area is so wide and uncertain. jNIurmurs produced at the tricuspid orifice are sometimes lieard Avith maxi- mum intensity just inside the apex impulse, and if we have also a mitral regurgitant murmur, it may be impossible under such cir- cumstances to distinguish it from the tricuspid murmur. Some- 160 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. times the two are of different pitch, but more often tricuspid regur- gitation must be recognized indirect/ 1/ if at all, i.e., through the evidence given by venous pulsation in the jugular veins and in the liver. Tricuspid murmurs are not transmitted to the left axilla and do not cause accentuation of the pulmonic second sound, al- though they are compatible with such accentuation. They are to be distinguished from the murmurs of mitral regurgitation by their different seat of maximum intensity, possibly by a difference in pitch, but most clearly by the concomitant phenomena of venous pulsation above mentioned. (2) " Functional " murmurs are usually systolic and may have their maximum intensity at the apex of the heart, but in the great majority of cases they are heard best over the pulmonic valve or- just inside or outside the apex beat (Potain). They are famt or inaudible at the end of expiration, and are more influenced by position than organic murmurs are. In the upright position they are often very faint. They are rarely transmitted beyond the preeordia and are unaccompanied by any evidences of enlargement of the heart, by any pathological accentuation of the pulmonic second soimd,' or any evidences of engorgement of the lungs or general venoiis system. (3) Roughening or narroAving of the aortic valves may produce a systolic murmur with maximum intensity in the second right in- tercostal space, but this murmur is not infrequently heard all over the preeordia and quite plainly at the apex, so that it may simulate the murmur of mitral regurgitation. The aortic murmur may in- deed be heard more plainly at the apex than at any other point ex- cejjt the second right intercostal space, OAving to the fact that the right ventricle, which occupies most of the precordial region be- tween the aortic and mitral areas, does not lend itself Avell to the propagation of certain types of cardiac murmurs. Under these circumstances "a loud, rough aortic murmur may be heard at the ' It must be remembered that hi chlorosis, a disease in which functional murmurs are especially prone to occur, the pulmonic second sound is often surprisingly loud, owing to a retraction of the left lung, which uncovers the root of the pulmonic artery. VALVULAR LESIONS. 161 apex as a smooth murmur of a different tone " (Broadbent) . Such a murmur is not, however, likely to be conducted to the axilla or heard beneath the left scapula, nor to be accompanied by accentua- tion of the puhnonic second sound nor evidences of engorgement of the lungs and general venous system. II. Mitral Stenosis. harrowing or obstruction of the mitral orifice is almost invari- ably the result of a chronic endocarditis which gradually glues to- gether the two flaps of the valve until only a funnel-shaped open- ing or a slit like a buttonhole is left (see Figs. 93 and 94). As we examine post mortem the tiny slit which may be all that is left of the mitral orifice in a case of long standing, it is difficult to con- ceive how sufficient blood to carry on the needs of the circulation could be forced through such an insignificant opening. Usually a slow and gradually developed lesion, mitral stenosis often represents the later stages of a process which in its earlier phases produced pure mitral regurgitation. By some observers the advent of stenosis is regarded as representing an attempt at com- pensation for a reduction of the previous mitral leakage. Others consider that the stenosis simply increases the damage which the valve has suffered. A remarkable fact never satisfactorily explained is the predilec- tion of mitral stenosis for the female sex. A large proportion of the cases — seventy-six per cent in my series — occur in women. It is also curious that so many cases are associated with pul- monary tuberculosis. Plii/sical Si(/ns. Mitral stenosis may exist for many years without giving rise to any physical signs by which it may be recognized, and even after signs have begun to show themselves they are more fleetmg and mconstant than in any other valvular lesion of the heart. In the early stages of the disease the heart may appear to be entirely nor- mal if the patient is at rest, and especially if examined in the re- cumbent position, characteristic signs being elicited only by exer- 11 162 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. tion ; or again a murmur which is easily audihle with the patient in the upright position may disappear iji the recumbent position ; or a murmur may be heard at one visit, at the next it may be im- possible to elicit it by any manoeuvre, Avhile at the third visit it may y^) Trieusi^id obstruction. Luckily for us as diagnosticians, stenosis of the tricuspid valve is a very rare lesion. Like mitral stenosis it is manifested by a joresystolic rollmg murmur whose pomt of maximum intensity is sometimes over the traditional tricuspid area, but may be at a point so near the mitral area as to be easily confused with stenosis of the latter valve. The difficulty of distinguishing tricuspid stenosis from mitral stenosis is further mcreased by the fact that the two lesions almost invariably occur in conjunction. Hence we have two presystolic murmurs, perhaps with slightly different jjoints of maximum inten- sity and possibly with a difference in quality, but often quite un- distingiiishable from each other. Li the vast majority of cases, therefore, tricuspid stenosis is first recognized at the autopsy, and the diagnosis is at best a very difficult one. (c) Broadbent, Eosenbach, and others have noticed m children who have just passed through an attack of pericarditis a rumljliiig murmur near the apex of the heart, which suggests the murmur of mitral stenosis. It is distinguished from the latter, however, by the absence of any accentuation of the first sound at the apex, as well as by the conditions of its occurrence and by its transiency. Such cases are important, smce their prognosis is much more favorable than that of mitral stenosis. Phear (Lancet, September 21, 1895) investigated 46 cases in which a presystolic murmur was observed during life and no mitral lesion found at autopsy. In 17 of these there was aortic regurgi- tation at autopsy ; in 20 of these there was adlierent pericardium at autopsy ; in 9 nothing more than dilatation of the left ventricle was found. In none of these cases was the snapping first sound, so common in mitral stenosis, recorded durmg life. It should be remembered that patients suffering from mitral stenosis are very frequently unaware of any cardiac trouble, and seek ad^dce for antemia, wasting, debility, gastric or pulmonary complaints. This is less often true in other forms of valvular dis- 170 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. ease. We should be especially on our guard in cases of supposed "nervous arrhythmia" or "tobacco heart," if there has been an at- tack of rheumatism or chorea previously. Such cases may present no signs of disease except the irregularity — yet may turn out to be mitral stenosis. IV. AoKTKJ KE(iUK(iITATIOX. Ivheumatic endocarditis usually occurs in early life and most often attacks the mitral valve. The commonest cause of aortic dis- ease on the other hand — arterio-selerosis — is a disease of late mid- L/^fi^a/ {fi^^. Fir,. 99.— Diastole in Aortic Regurgitation. The blood is flowing back through the stumpy and incompetent aortic valves. die life, and attacks men much more often than women. "Wlien we think of aortic regurgitation, the picture that rises before lis is usually that of a man past middle life and most often from the classes who live by manual labor. Nevertheless cases occur at all ages and in both sexes, and rheumatic endocarditis does not spare the aortic cusps altogether by any means. Whether produced by arterio-selerosis extending down from the aorta, or by rheumatic or sei:)tic endocarditis, the lesion which re- sults in aortic regurgitation is usually a thklten'mfj and sliortenlng of the cusps (see Fig. 99). In rare cases an aortic cusp may be ruptured as a result of violent muscular effort, and the signs and VALVULAR LESIONS. 171 symptoms of regurgitation then ai)}>ear suddenly. But as a rule the lesion comes on slowly and insidiously, and unless discovered accidentally or in the course of routine physical examination it may exist unnoticed for years. Dropsy and cyanosis are relatively late and rare, and the symptoms which first appear are usually those of dyspufjea and precordial distress. It is a disputed point whether relative and temporary aortic insufficiency due to stretching of the aortic orifice ever occurs. If it does occur, it is certainly exceedingly rare, as the aortic rmg is very tough and inelastic. Dilatation of the aortic arch — practically diffuse aneurism — oc- curs in almost everij case of aortic regurgitation, and produces sev- eral important physical signs. This complication is a very well- known one, but has not, I think, been sufficiently insisted on in text-books of physical diagnosis. It forms part of that general enlargement of the arterial tree which is so characteristic of the disease. PJLijsical Signs. Inspection reveals more that is important in this disease than in any other valvular lesion. In extreme cases the patient's face or hand may blush visibly with every systole. Not infrequently one can make the diagnosis across the room or in the street by not- ing the violent throbbing of the carotids, which may be such as to shake the jDerson's whole head and trunk, and even the bed on which he lies. No other lesion is so apt to cause a heaving of the whole chest and a bobbing of the head, and no other lesion so often causes a bulging of the precordia, for in no other lesion is the en- largement of the heart so great (cor bovimtm or ox-heart) . The throbbing of the dilated aorta can often be felt and sometimes seen in the suprasternal notch or in the second right interspace. Not only the carotids but the subclavians, the brachials and radials, the femoral and anterior tibial, and even the digital and dorsalis pedis arteries may visibly pulsate, and the characteristic jerking quality of the pulse may be seen as well as felt. This visible pul- sation in the peripheral arteries, while very characteristic of aortic 172 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. regurgitation, is occasionally seen in cases of simple hypertrophy of the heart from hard muscular work (e.[/., in athletes). If the ar- teries are extensively calcified, their pulsation become much less marked. The peculiar conditions of the circulation whereby it is " changed into a series of discontinuous discharges as if from a catapult" (All- butt) throws a great tensile strain upon all the arteries, and results, in almost every long-standing case, in increasing both their length Pulsation at the jiigulum. Dulness and pnl- satinn corre- ,- sponiling to the dilated aortic arch. Pulsating car- otids. Diastolic murmur. Displaced cardiac impulse. Fig. 100.— Aortic Regurgitation, Showing Position of the Diafjtolic Murmur and Areas of Visible Pulsation. and their diameter. The visible arterial trunks become tortuous and distended, while thes arch of the aorta is diffusely dilated and becomes practically an aneurism (see Fig. 100). "With each heart beat the snaky arteries are often jerked to one side as well as made to throb. Inspection of the region of the cardiac impulse almost always shows a very marked displacement of the apex beat both downward and outward (but especially the former), corresponding to the hy- pertrophy of the left ventricle, which is usually very great, and to VALVULAR LESIOXS. 173 the downward, sagging of the enlarged aorta. In a small propor- tion of the cases no enlargement of the heart is to be demonstrated. This was true of 5 out of the last 67 cases which I have notes of, and generally denotes an early and slight lesion. Xot at all infre- quently one finds a systolic retraction of the intersj^aces near the apex beat instead of a systolic impulse. This is probably due to the negative pressure produced within the chest by the powerful contraction of an hypertrophied heart. In the suprasternal notch one often feels as well as sees a marked systolic pulsation trans- mitted from the arch of the dilated aorta, and sometimes mistaken for saccular aneurism. Arterial pulsation of the liver and spleen are rarely demon- strable by a combination of sight and touch. Cajjillari/ Pulsation. If one passes the end of a pencil or other hard substance once or twice across the patient's forehead, and then watches the red mark so produced, one can often see a systolic flushing of the hyper- semic area with each beat of the heart. This is by far the best method of eliciting this phenomenon. It may also be seen if a glass slide is pressed against the mucous membrane of the lip so as pai- tially to blanch it, or if one presses upon the finger-nail so as par- tially to drive the blood from under it ; but in both these manoeuvres error may result from inequality in the pressure made by the ob- server upon the glass slide or upon the nail. Very slight movements of the observer's fingers, even such as are caused by his own pulse, may give rise to changes simulating capillary pulsation. Capillary pulsation of normal tissues is not often seen in any condition other than aortic' regurgitation, yet occasionally one meets with it in diseases which produce very low tension of the pulse, such as phthisis or typhoid, anaemic and neurasthenic conditions, and I have twice seen it in perfectly healthy persons. In such cases the pulsation is usually less marked than in aortic regurgitation. Rarely pulsation may be detected in the peripheral veins. ' Jumping toothache and throbbing felon are common examples of capil- lary pulsation in inflamed areas. 174 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. Paljjafion. Palpation verifies the position of the cardiac impulse and the heaving of the whole chest wall suggested by inspection. The shock of the heart is very powerful and deliberate unless dilatation Fig. 101.— Spliygmographic Tracing from Normal Pulse. is extreme, when it becomes wavy and diffuse. In the supracla\'ic- ular notch a systolic thrill is often to be felt. A diastolic thrill in the precordia is very rare. T/tL' jjulse is important, usually characteristic. The wave rises Fig. 102.— SphyprmooTaphio Tracing of the "Pk/.shs rr?er" in Aortic Regurgitation. Its col- lapsing character is well shown. very suddenly and to an unusual height, then collapses completel" and with great rapidity (pulsus celer) (see Figs. 101, 102). This type of pulse, which is known as the " Corrigan pulse " or "water-hammer pulse," is exaggerated if one raises the patient's arm above the head so as to make the force of gravity aid in emp- tying the artery. The quality of the pulse in aortic regurgitation VALVULAR LESIONS. 175 is clue to the fact that a large volume of l)loocl is suddenly and for- cibly thrown into the aorta by the hypertrophied and dilated left ventricle, thus causing the characteristically sharp and sudden rise in the peripheral arteries. The arteries then empty themselves in two directions at once, forward into the capillaries and backward into the heart through the incompetent aortic valves; hence the sudden collapse in the pulse which, together with its sharp and sudden rise, are its important characteristics. The arteries are large and often elongated so as to be thrown into curves. Xot infrequently one can demonstrate that the radial pulse is delayed or follows the apex impulse after a longer interval than in normal persons. "While compensation lasts, the pulse is usually regular in force and rhythm. Irregvlarity is therefore on esjyecially grave sign, much more so than in any other valvular lesion. Percussion. Percussion adds but little to the information obtained by inspec- tion and palpation, but verifies the results of these methods of in- vestigation respecting the increased size of the heart, and especially of the left ventricle, which may reach enormous dimensions, espe- cially in cases occurring in young persons. The heart may be increased to more than four times its normal v'eirjht. Auscultation. In rare cases there may be absolutely no murmur and the diag- nosis may be unpossible during life, though it may be suspected by reason of the above-mentioned signs in the peripheral arteries. But although the murmur is seldom entirely absent, it is often so faint as to be easily overlooked. This is especially true in cases occurring in elderly people, and when the patient has been for a considerable time at rest. The difficulty of recognizing certain cases of aortic regurgitation during life is shown by the fact that out of sixty-five cases of aortic regurgitation demonstrated at au- topsy in the INIassachusetts General Hospital, only forty-four were recogfuized durinsr life. 176 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. In the majority of cases, however, the characteristic diastolic muDiinr is easily heard if one listens in the right place, and when heard it is the most distinctire and trustu-orthij of all cardiaG mur- murs. It almost invariably points to aortic regnrgitation and to nothing else. The murmur of aortic regurgitation, as has been already men- tioned, is diastolic in time/ Its inaxiniaiit iuti:iisitij is usualli/ not Fig. 103.— Position of the Point of Maximum Intensity of tbe Murmur of Aortic Regurgitation. The dots are most thickly congregated where the murmur is oftenest heard. in the conventional aortic area {second ri/jJit interspace), hut on the left side of the sternum about the level of the fourth left costal carti- lage. In about one-tenth of the cases, and especially when the aortic arch is much dilated, the murmur is best heard in the con- ventional aortic area. Occasionally there are two points at Avhich it may be loudly heard — one in the second riglit interspace and the other at or near the apex of tlie heart, wliile Ijetween these points ' Another murmur, systolic in time, which almost always accompanies the diastolic murmur, is usually due to roughening of the edges of the aortic valves or to dilatation of the aortic arch. This murmur must not be assumed to mean aortic stenosis (see below, p. 184 J. VALVULAR LESIONS. 177 the niurnuu- is faint. This is probably due to the fact that the left ventricle, through which the niunuur is conducted, approaches the surface of the chest only at the apex, while the intermediate space is occupied by the right ventricle, which often fails readily to trans- mit umrniurs produced at the aortic orifice. Less frequently the murmur of aortic regurgitation is heard with maxmium intensity at the second or third left costal cartilage or in the region of the ensiform cartilage (see Fig. 103). From its seat of maximum intensity (I.e., usually from the fourth left costal cartilage) the murmur is transmitted in all direc- tions, but not often beyond the precordia. In about one-third of the cases it is transmitted to the left axilla or even to the back. It is sometimes to be heard in the subclavian artery and the great vessels of the neck; in other cases two heart sounds are 1st 1st I 2nd I 2nd Fig. 104.— Short Diastolic Murmur Not Replacing the Second Sound. audible in the carotid, but no murmur. The murmur is usually blowing and relatively high pitched, sometimes musical. Its inten- sity varies much, but is most marked at the beginning of the mur- mur, giving the impression of an accent there. It may occupy the whole of diastole or only a small portion of it — usually the earlier portion (see Fig. 104). Late diastolic murmurs are rare. The mur- mur may or may not replace the second sound of the heart. Broad- bent believes that when it does not obliterate the second sound, the lesion is usually less severe than when only the murmur is to be heard. AUbutt dissents from this opinion. In listening for the aortic second sound with a view to gauging the severity of the lesion, it is best to apply the stethoscope over the right carotid artery, as here we are less apt to be confused by the murmur or by the pulmonic second sound. The position of the patient's body has but little eifect upon the murmur — less than upon murmurs produced at the mitral orifice. 12 178 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. The first sound at the apex is generally loud and long. There is no accentuation of the pulmonic second. Over the larger peripheral arteries, especially over the femoral artery, one hears in most cases a sharp, short systolic sound ("jhs- tol-shot sound ") due to the sudden filling of the unusually empty artery ; this sound is merely an exaggeration of what may be heard in health. Pressure with the stethoscope will usually bring out a systolic murmur (as also in health), and occasionally a diastolic' murmur as well (Duroziez's sign). This diastolic murmur in the perii)heral arteries, obtained on pressure with the stethoscope, is practically never heard except in aortic regurgitation. It is thought by some to be due to the regurgitant current in the great vessels which in very marked cases may extend as far as the femoral ar- tery. Duroziez's sign is a conq^aratively rare one, not present in most cases of aortic regurgitation, and usually disappears when compensation fails. Sn/iijnari/ and Differential Diagnosis. A diastolic murmur heard with the maximum intensity about the fourth left costal eartilage (less often in the second right inter- space or at the apex) gives us almost complete assurance of the existence of aortic regurgitation. From pulmonary regurgitation, an exceedingly rare lesion, the disease is distinguished by the pres- ence of predominating hypertrophy of the left ventricle with a heaving apex impulse and by the foUoAving arterial phenomena: (fi') Visible pulsation in the peripheral arteries. (h) Capillary pulsation, (c) "Corrigan " jjulse. ((/) "Pistol-shot sound" in the femoral artery. (e) Duroziez's sign. The very rare functional diastolic murmur, transmitted from the veins of the neck and heard over the base of the heart in cases of grave anaemia, may be obliterated by ])ressure over the bullous jugularis. Such jn-essure has no effect upon the murmur of aortic regurgitation. It must be remembered that aortic regurgitant murmurs are VALVULAR LESIONS. 179 often exceedingly faint, and should Ije listened for Vv^ith. the greatest care and under the most favorable conditions. ]£stlin((fi()n of the Kxioit dad Gravity of the Lesion. The extent of the lesion is roughly ^jroportional to — • (0) The amount of hypertroj^hy of the left ventricle. [h) The degree to Avhich the i)ulse collapses during diastole (provided the radial is not so much calcified as to make collapse imj^ossible) . {(') The degree to which the murmur replaces the second sound as heard over the right carotid artery (Broadbent). Irregularity of the pulse is a far more serious sign in this dis- ease than in lesions of the mitral valve, and indicates the beginning of a serious failure of compensation. Another grave sign is a diminution in the intensity of the murmur. Complications. (1) Dilatation of the Aorta. — Diffuse dilatation of the aortic arch is usually associated with aortic regurgitation and may produce a characteristic area of dulness to the right of the sternum (see Fig. 100). ISTot^nfrequently this dilatation is the cause of a systolic murmur to be heard over the region of the aortic arch and in the great vessels of the neck. (2) Roughening of the Aortic Valves. — In the great majority of cases of aortic regurgitation the valves are sufficiently roughened to produce a systolic murmur as the blood flows over them. This murmur is heard at or near the conventional aortic area, and may be transmitted into the carotids. (The relation of these murmurs to the diagnosis of aortic stenosis will be considered with the latter lesion.) (3) The return of arterial blood through the aortic valves into .the left ventricle produces in. time l)oth hypertroph}^ and dilatation of this chamber, and results ultimately in a stretching of the mitral orifice which renders the mitral curtains imcompetent. The result is a " rehdive mitral insufficienci/,'^ i.e., one in which the mitral valve 180 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. is intact but too short to reach across the oriiice Avhich it is in- tended to close. Such an insufficiency of the mitral occurs in most well-marked cases ; it temporarily relieves the overdistention of the left venti'icle and often the accompanying angina, although at the cost of engorguig the lungs.' (4) The Austin Flint Murmur. — The majority of cases of aortic regurgitation are accompanied by a presystolic murmur at the apex, ■which may be due to a genuine mitral stenosis or may be produced in the manner suggested by Austin Flint. (For a fuller discussion of this murmur see above, p. 168.) (5) Aortic stenosis frequently supervenes in cases of aortic re- gurgitation, and results in a more or less temporary improvement in the patient's condition. It has the effect of increasing the intensity of the diastolic murmur, since the regurgitating stream has to pass through a smaller opening. The general visible arterial pulsation becomes much less marked if stenosis supervenes on regurgitation. AORTKJ STEXOSIS. Uncomplicated aortic stenosis is by far the rarest of the vahii- lar lesions of the left side of the heart, as well as the most difficult to recognize. Out of two hundred and fifty-two autopsies made at the Massachusetts General Hospital in cases of valvular disease there was not one of uncomplicated aortic stenosis. Twenty -nine cases occurred in combination with aortic regurgitation. During life the diagnosis of aortic stenosis is frequently made, but often on insufficient evidence — i.e., uptjn the evidence of a systolic murmur heard with maximum intensity in the second right intercostal space and transmitted into the vessels of the neck. Such a nnirmur does indeed occur in aortic stenosis, but is by no means peculiar to this condition. Of the other diseases which produce a similar murmur more will be said under Differential Diagnosis. ' This relative insufiflciency of the mitral valve has been tenued its "safety- vahe" action, but the safety is but temporary and dearly bought. VALVULAR LESIONS. 181 the followinsr evi- For the diagnosis of aortic stenosis we need dence : (1) A systolic niurniuv heard best in the second right intercostal space and transmitted to the neck. (2) The characteristic pulse (ride infra). (3) A palpable thrill (usually). (4) Absence or great enfeeblement of the aortic second sound. Of these signs the characteristic jjvhe is probably the most im- '/^/^J/is^ Fig. 105.— Aortic Stenosis. The heart is in systole and the blood column is obstructed by the narrowed aortic ring. The mitral is closed (as it should be). portant, and no diagnosis of aortic stenosis is possible without it. The heart may or may not be enlarged. Each of these points will now be described more in detail. (1) TJie Murmur. (a) The maxivunn infensifi/ of the murmur, as has already been said, is usually in the second right intercostal space near the ster- num or a little above that point near the sterno-clavicular articula- tion, but it is by no means uncommon to find it lower down, i.e., in the third, fourth, or fifth right interspace, and occasionally it is best heard to the left of the sternum in the second or third inter- costal space. (//) The time of the murmur is hife s>/sto/ir; that is, 182 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. it follows tlie apex impulse at an aj^preciable interval, contrasting in this respect with the systolic murmur usually to be heard in mitral regurgitation, (c) The mvirmur is usually ivideJy transmit- ted, often being audible over the whole chest and occasionally over the skull and the arterial trunks of the extremities (see Fig. 106). It is usually heard less well over that portion of the precordia oc- cupied by the right ventricle, while, on the other hand, it is rela- tively loud in the region of the apex impulse, whither it is trans- mitted through the left ventricle. The same line of transmission Maximum intensity (if systolic mur- mur and tlirill. Fig. 106.— Aortic Stenosis. The murmur is audible over the shaded area and sometimes over the whole chest. was mentioned al)ove as characteristic of the murmur of aortic re- giirgitation in many cases. The murmur is also to be heard over the carotids and subclavians, and can often be traced over the tho- racic aorta along the spine and down the arms. Until compensation fails the murmur is apt to be a very loud one, especially in the recumbent position ; it is occasionally au- dible at some distance from the chest, and is often rough and vibrating, sometimes musical or croaking. Its length is unusually great, extending throughout the whole of systole, but to this rule there are occasional excej^tions. The first sound in the aortic re- VALVULAR LESIOXS. 183 gion is altogether obliterated, as a rule, and the second sound is either absent or very feeble.' (2) The Pulse. Owing to the opposition encountered by the left ventricle in its attempt to force blood into the aorta, its contraction is apt to be prolonged ; hence the pulse wave rises gradually and late, and falls mcay slotclt/. This is shown very well in sphygniographic tracings (see Fig. 107) . But further, the blood thrown into the aorta by the left ventricle is prevented, by the narrowing of the aortic valves, from striking upon and expanding the arteries Avith its ordinary force ; hence the pulse wave is not only slow to rise but suiall in Fig. 107.— Sphygmographic Tracing of the Pulse in Uncomplicated Aortic Stenosis. Compare with the normal pulse wave and with that of aortic regurgitation (page 174). helgJit, contrastmg strongly with the powerful apex beat ("pulsus pa7'vus"). Again, the delay in the emptying of the left ventricle, brought about by the obstruction at the aortic valves, renders the contractions of the heart relatively infrequent, and hence the pulse is infrequent (pulsus rams) as well as small and slow to rise. The "pulsus rarus, parvus, tardus" is, therefore, a most constant and important point in diagnosis, but unfortunately it is to be felt in perfection only in the rer// rare cases in which aortic stenosis occurs uncomplicated. When stenosis is combined with regurgita- tion, as is almost always the case, the above-described qualities of the pulse are greatly modified as a result of the regurgitation. It is also to be remembered that the pulse of aortic stenosis is by no ' "Occasionally, as noted by W. H. Dickinson, there is a musical murmnr of great intensity in tlie region of tlie apex, probably due to a slight regiu'gita- tion at high pressure through the mitral valve."— Uslek. 184 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. means unalterable and does not exhibit its typical plateau at all times. A less characteristic, but decidedly frequent, variation in the pulse wave of aortic stenosis is the anacrotic curve. The slow, long pulse with a long plateau at the summit is seen also m some cases of mitral stenosis and renal disease, and is not peculiar to aortic stenosis, but taken in connection with the other signs of the disease it has great value in diagnosis. (3) The ThrUJ. In the majority of cases an intense purring vibration may be felt if the hand is laid over the upper portion of the sternum, espe- cially over the second right intercostal space. This thrill is con-- tinned into the carotids, can occasionally be felt at the apex, and rarely over a considerable area of the chest. It is a very important aid in the diagnosis of aortic stenosis, but is by no means pathog- nomonic, since aneurism may produce a precisely similar vibration of the chest wall. The heart is slightly enlarged to the left and downward as a rule, but the apex impulse is unusually indistmct, '* a well-defined and deliberate push of no great violence" (Broadbent). Corre- sponding to the protracted sustained systole the first sound at the apex is dull and long, but not very loud. Differential Diaf/nosis. A systolic murmur heard loudest in the second right intercostal space is by no means peculiar to aortic stenosis, but may be due to any of the following conditions : (a) Roughening, stilfness, fenestration, or slight congenital mal- formation of tlie aortic valves. {b) Eoughening or diffuse dilatation of the arch of the aorta. (c) Aneurism of the aorta or innominate artery. (d) Functional murmxirs. (e) Pulmonary stenosis. (/) ^M'^^i ductus arteriosus. ((/) ]\Iitral regurgitation. VALVULAR LESIOXS. 185 (a and b) The great majority of such systolic murmurs at the base of the heart, first appearing after middle life, are due to the causes mentioned above under a, b, and c. In such cases it is usu- ally combined with accentuation and ringing quality of the aortic second sound owing to the arterio -sclerosis and high arterial tension, associated with the changes which produce the murmur, This arrevfiiatlon of the aortic second sound enables us, except m extraor- dinarily rare cases, to exclude aortic stenosis, in which the intensity of the aortic second sound is almost always much reduced. Diffuse dilatation of the aorta, such as often accompanies aortic regurgitation, is a frequent cause of a systolic murmur loudest in the second right interspace. This may be recognized in certain, cases by the characteristic area of dulness on percussion and by its association with aortic regurgitation of long standing (see Fig. 100). Roughening of the intima of the aorta {endaovtitls') is always to be suspected in elderly patients with calcified and tortuous perij^h- eral arteries, and such a condition of the aorta doubtless favors the occurrence of a murmur, especially when accompanied by a slight degree of dilatation. The absence of a thrill and a long, slow l^ulse with a low maximum serves to distinguish such murmurs from those of aortic stenosis. (c) Aneurism of the ascending arch of the aorta or of the in- nominate artery may give rise to every sign of aortic stenosis except the characteristic pulse and the diminution of the aortic second sound. In aneurism we may have a well-marked tactile thrill and a loud systolic murmur transmitted into the neck, but there is usually some pulsation to be felt in the second right intercostal space and often some difference in the pulses or in the pupils, as well as a history of pain and symptoms of pressure upon the tra- chea and bronchi or recurrent laryngeal nerve. In aneurism the aortic second sound is usually loud and accompanied by a shock, and the pulse sIioavs none of the characteristics of aortic stenosis. (rf) Functional murmurs, sometimes known as ''haeniic," are occasionally best heard in the aortic area instead of in their usual situation (second left intercostal space). They occur especially in young, anaemic persons, are not accompanied by any cardiac en- 186 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. largement, by any palpable thrill, any diminntion in the aortic second sound, or any distinctive abnormalities in the pulse. (e) Pulmonary stenosis, an exceedingly rare lesion, is mani- fested by a systolic murmur and by a thrill whose maximum inten- sity is usiially on the left side of the sternum. In the rare cases in which tliis murmur is best heard in the aortic area it may be distinguislied from the murmur of aortic stenosis by the fact that it is not transmitted into the vessels of the neck, has no effect upon the aortic second sound, and is not accompanied by the character- istic changes in the jiulse. (/) The murmur due to persistence of the ductus arteriosus may last through systole and into diastole ; it may be accompanied by a thrill, but does not affect the aortic second sound nor the pulse. {(/) The systolic murmur of aortic stenosis may be heard loudly at the apex, and hence the lesion may be mistaken for mitral regur- gitation. But the maximum intensity of the murmur of aortic stenosis is almost invariably in the aortic area, and its association with a thrill and a long, slow pulse should enable us easily to dif- ferentiate the two lesions. By the foregoing differentiae aortic stenosis may be distinguished from the other conditions which resemble it, provided it occurs uncouiplicated, but unfortunately this is very rare. As a rule, it occurs in connection with aortic regurgitation, and its characteristic signs are therefore obscured or greatly modified by the signs of the latter disease. We may suspect it in such cases (provided the mi- tral valve is sufficient) Mdien Ave have, in addition to the signs of aortic regurgitation, a systolic murmur and palpable thrill in the aortic area transmitted into tlie great vessels, a modification of the Corrigan jmlse in the direction of the "pN/siis tardus, varus, par- vus," and less visible arterial pulsation than is to be expected in pure aortic regurgitation. Occasionally one can watch the development of an aortic steno- sis out of what was formerly a pure regurgitant lesion, the stenosis gradually modifying the characteristics of the previous condition. One juust be careful, however, to exclude a relative mitral insuffi- VALVULAR LESIOi^S. 187 cieney which, as lias been already mentioned above, is very apt to supervene in cases of aortic disease, owing to dilatation of the mi- tral orifice, and which may modify the characteristic signs of aortic regurgitation very luuch as aortic stenosis does. TEICUSPID REGURGITATIOX. Endocarditis affecting the tricuspid valve is rare in post-foetal life ; in the foetus it is not so uncommon. In cases of ulcerative or malignant endocarditis occuring in adult life, the tricuspid valve is occasionally involved, but the majority of cases of tricusijid dis- ease occur as a result of disease of the mitral valve and in the follow- ing manner : Hypertrophy of the right v^entricle occurs as a result of the mitral disease, is followed in time by dilatation, and with this dilatation comes a stretching of the ring of insertion of the tricuspid valve, and hence a regurgitation through that valve. Tri- cuspid regurgitation, then, occurs in the latest stages of almost every case of mitral disease and sometimes during the severer at- tacks of failing compensation. Out of 405 autopsies at Guy's Hospital in which evidence of tricuspid regurgitation was found, 271, or two-thirds, resulted from mitral disease, 68 from myocardial degeneration, 55 from pulmonary disease (bronchitis, emphysema, cirrhosis of the lung) . Very few of these cases had been diagnosed durmg life, and in all of them the valve was itself healthy but insufficient to close the dilated orifice. Gibson and some other Avriters believe that temporary tricuspid regurgitation is the commonest of all valve lesions, and results from Aveakening of the right ventricle in connection with states of anae- mia, gastric atony, fever, and many other conditions. It is very difficult to prove or disprove such an assertion. Tricuspid regurgitation is often referred to as serving like the opening of a " safety valve " to relieve a temporary jDulmonary en- gorgement. This " safety-valve " action, however, may be most disastrous in its consequences to the organism as a whole, despite the temporary relief which it affords to the overfilled lungs. The engorgement is simply transferred to the liver and thence to the 188 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. abdominal organs and the lower extremities, so that as a rule the advent of tricuspid regurgitation is recognized not as a relief but as a serious and probably fatal disaster. PJiyslcal Signs. (1) A systolic murmur is heard loudest at or near the fifth left costal cartilage. (2) Systolic venous pulsation in the jugulars and in the liver. (3) Engorgement of the right auricle producing an area of dul- ness beyond the right sternal margin. (4) Intense cyanosis. (1) TJie Murmur. — The maximum intensity of the systolic mur- mur of tricuspid regurgitation is usually near the junction of the fifth or sixth left costal cartilages with the sternum. Leube finds the murmur a rib higher u}), but it is generally agreed that the tricuspid area is a large one, so that the murmur may be heard any^vhere over the lower part of the sternum or even to the right of it. On the other hand, there are some tricuspid murmurs which are best heard at a point midway between the apex impulse and the ensiform carti- lage. The murmur is not widely transmitted and is usually inaudi- ble in the back ; at the end of expiration its intensity is increased. In some cases we have no evidence of tricuspid regurgitation other than the murmur just described, but — (2) Of more importance in diagnosis is the presence of a sys- tolic inilsation in the external jugular veins and of the liver, which unfortunately is not always present, but which when present is pathognomonic. I have already explained (see ]). oH) the distinc- tion between true s>/.^fo/ic jugular pulsation, which is practically pathognomonic of tricuspid regurgitation, and simple presystolic undulation or distention of the same veins, Avhich has no necessary relation to this disease. The decisive test is the effort permanently to empty the vein by stroking it upward from below. If it in- stantly refills from below and continues to pulsate, tricuspid regur- gitation is almost certainly present. If, on the other hand, it does not refill from below, the cause must be sought elsewhere. VALVULAR LESIONS. 189 Pulsation in the liver must be distinguished from the ''jogging " motion which may be transmitted to it from the abdominal aorta or from the right ventricle. To elimhiate these transmitted impulses one must be able to grasp the liver bimanually, one hand in front and one resting on the lower ribs behind, and to feel it distinctly ex- pand with every systole, or else to take . its edge in the hand and to feel it enlarge in one's grasp with every beat of the heart. Dilated right auricle. Systolic murmur. — — Enlarged and pul- sating liver. Fig. 108.— Tricuspid Regurgitation. The murmur is heard hest over the shaded area. Pressure upon the liver often causes increased distention and pulsa- tion of the external jugulars if tricuspid regurgitation is present. (3) Enlargement of the heart, both to the right and to the left, as well as downward, can usually be demonstrated. In rare cases a dilatation of the right auricle may be suggested by a percussion outlme such as that shown in Fig. 108. The pulmonic second sound is usually not accented. The im- portance of this in differential diagnosis will be mentioned pres- ently. If a progressive diminution in the intensity of the sound occurs under observation, the prognosis is very grave. (4) Cyanosis is usually very great, and dyspnoea and pulmonary oedema often make the patient's condition a desperate one. 190 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. Different id I Diarjn os is. The statistics of the cases autopsiecl at the INIassachusetts Gen- eral Hospital show that tricuspid regurgitation is less often recog- nized during life than any other vahoilar lesion. The diagnosis was made ante mortem on only five out of twenty-nine cases. This is due to the following facts: {a) Tricuspid regurgitation may be present and yet give rise to no physical signs which can be recognized during life. (b) Tricuspid regurgitation occurs most frequently in connec- tion with mitral regurgitation ; hence its signs are frequently masked by those of the latter lesion. It is, therefore, a matter of great importance as well as of great difficulty to distinguish tricus- pid regurgitation from (1) Ilitml Begurgitation. The difficulties are obvious. The murmur of mitral regurgita- tion has its maximum intensity not more than an inch or two from the point at which the tricuspid murmur is best heard. Both are systolic in time. They are, therefore, to be distinguished only — (rt) In case we can demonstrate that there are two areas in which a systolic murmur is heard with relatively great intensity, with an intervening space over which the murmur is less clearly to be heard (see Fig. 109). {It) Occasionally the two systolic murmurs are of different pitch or of different quality, and may be thus distinguislied. (c) Tricuspid murmurs are not transmitted into the left axilla and are rarely audible in the back, and this fact is of value in case we have to distinguish between uncomplicated tricusi)id regurgitation and uncomplicated mitral regurgitation. Unfortunately these le- sions are very apt to occur simultaneously, so that in practice our efforts are generally directed toward distinguishing between a pure mitral regurgitation and one com})licated l>y tricuspid regurgitation. (d) In cases of doubt the ])lienomena of venous pulsation in the jugulars and in the liver are decisive if present, but their absence proves nothing. VALVULAR LESIONS. 191 (e) Accentuation of tlie itulnionic second sound is almost inva- riably present in uncomplicated mitral disease and is apt to disap- pear in case the tricuspid begins to leak, since engorgement of the lungs is thereby for the time relieved, but in many cases the pul- monic second sound remains most unaccountably strong even when the tricuspid is obviously leaking. (2) From "functional" systolic murmurs tricuspid insufficiency may generally be distinguished by the fact that its murmur is best Fig. 109.— Two Systolic Murmurs (Mitral and Tricuspid) with a " Vanishing Point " between. heard in the neighborhood of the ensiform cartilage, and not in the second right intercostal space where most functional murmurs have their seat of maximum intensity. Functional murmurs are unac- companied by venous pulsation, cardiac dilatation, or cyanosis. (3) Occasionally a pericardial friction rub simulates the mur- mur of tricuspid insufficiency, but, as a rule, pericardial friction is much more irregular in the time of its occurrence and is not regu- larly synchronous with any definite portion of tlie cardiac cycle. Tricuspid Stexosis. One of the rarest of valve lesions is narrowing of the tricuspid valve. No case has come under my observation, and in 1898, Her- 192 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. rick was able to collect but 15-4 cases from the world's literature. Out of these 154 cases, 138, or 90 per cent, were combined with mitral stenosis, and only 12 times has tricuspid stenosis been known to occur alone.' These observations account for the fact that tri- cuspid stenosis has hardly ever been recognized during life, since the murmur to which it gives rise is identical in time and quality and nearly identical in position with that of mitral stenosis. Narrow- ing of the tricuspid valve is to be diagnosed, therefore, only by the recognition of a presystolic murmur best heard in the tricuspid area and distinguished either by its pitch, quality, or position from the other presystolic murmur due to the mitral stenosis which is almost certam to accompany it. The heart is usually enlarged, especially in its transverse direc- tion, but the enlargement is just such as mitral stenosis produces, and does not aid our diagnosis at all. The diagnosis is still further complicated in many cases by the presence of an aortic stenosis in addition to a similar lesion at the tricuspid and mitral valves, so that it seems likely that in the future as in the past the lesion will be discovered first at autopsy. PuLMOXARY Regurgitation. Organic disease of the pulmonary valve is excessively rare in post-foetal life, but may occur as part of an acute ulcerative or septic endocarditis. A temjwrari/ functional regurgitation through the pulmonary valve may be brought about by any cause producing very Jilffh jJ^'f^ssure in the pidnionanj artery. I have known two medical students with perfectly healthy hearts Avho were able, by prolonged holding of the breath, to produce a short, high-pitched diastolic murmur best heard in the second and third left intercostal si:)aces and ceasing as soon as the breath was let out. Of the occur- rence of a murmur similarly i)roduced under pathological condi- tions, especially in mitral stenosis, much has been written by Graham Steell. ' Out of 87 cases collected from the post-mortem records of Guy's Hos- pital, 8.5, or 07 per cent, were associated with still more extensive mitral stenosis. VALVULAR LESIOXS. 193 From the diastolic iniirmur of aortic regurgitation Ave may dis- tinguish the diastolic murmur of pulmonary incompetency by the fact that the latter is best heard over the pulmonary valve, is never transmitted to the apex of the heart nor to the gi-eat vessels, and is never associated with a Corrigan pulse nor with capillary pulsa- tion.' The right ventricle is hA^jertrophied, the pulmonic second sound is sharply accented and followed immediately by the murmur. E\-idences of se^jtic embolism of the lungs are frequently jjresent and assist us in diagnosis. The regurgitation which may take place through the rigid cone of congenital pulmonary stenosis is not recognizable during life. PULMOXARY StEXOSIS. Among the rare congenital lesions of the heart valves this is probably the commonest. The heart, and particularly the right ventricle, is much enlarged. There is a history of cyanosis and dyspnoea since birth. A systolic thrill is usually to be felt in the second left intercostal space, and a loud systolic murmur is heard in the same area. The pulmonic second sound is weak. The region in which this murmur is best heard has been happily termed the " region of romance " on account of the multiplicity of mysterious murmurs which have been heard there. The systolic murmur of pulmonary stenosis must be distinguished from («) Fimctional murmurs due to anaemia and debility' or to severe muscular exertion, and possibly associated with a dilatation of the conus arteriosus. (h) Uncovering of the conus arteriosus through lack of expan- sion of the lung. (c) Aortic stenosis. (d) !Mitral regurgitation. (e) Aneurism. (/) Koughening of the mtima of the aortic arch. ' By registering the variations of pressure in the tracheal column of air Gerhardt has shown giaphically that a .systolic pulsation of the pulmonary cap- illaries may occur in pulmouarj- regurgitation. With the stethoscope a sys- tolic whiff inav be heard all over the lungs. 13' 194 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. (a and b) Functional murmurs, and those produced in the conus arteriosus, are rarely if ever accompanied by a thrill, are rarely so loud as the murmur of pulmonary stenosis, and are not associated with dyspnoea, cyanosis, and enlargement of the right ventricle. (c) The murmui- of aortic stenosis is usually upon the right side of the sternum and is transmitted to the neck, whereas the murmur of i)ulmonary stenosis is never so transmitted and is not associated with characteristic changes in the pulse (see above, p. 183). (d) The murmur of viitral regurgitation is occasionally loudest in the region of the pulmonary valve, but differs from the murmur of pulmonary stenosis in being, as a rule, transmitted to the back and axilla and associated with an accentuation of the pulmonary second sound. (e) Aneurism may present a systolic murmur and thrill similar to those found in puhnonary stenosis, but may usually be distin- guished from the latter by the presence of the positive signs of aneur- ism, viz. — pulsation, and dulness in the region of the murmur, and signs of pressure on the trachea or on other structures in the medi- astinum. (/) Roughening of the aortic arch occurs after middle life, while pulmonary stenosis is usually congenital. The murmur due to roughening may be transmitted into the carotids ; that of pul- monary stenosis never. Enlargement of the right ventricle is char- acteristic of pulmonary stenosis, but not of aortic roughening. COMBINED VALVULAR LESIONS. It is essential that the student should understand from the first that the number of murmurs audible in the precordia is no gauge for tlie number of valve lesions. "We may have four distinct nnu- murs, yet every valve sound except one. This is often the case in aortic regurgitation — systolic and diastolic murmurs at the base of the heart, systolic and presystolic at the apex, yet no valve in- jured except the aortic. In such a case the systolic aortic murmur is due to roughening of the aortic valve. The systolic apex mur- mur results from relative mitral leakage (with a sound valve). The presystolic apex murmur is of the " Flint " type. Hence in this VALVULAR LESIONS. 195 case the diastolk niurniur alone of the four audible murmurs is due to a valvular lesion. It is a good rule not to multiply causes unnecessarily, and to explain as many signs as possible under a single hypothesis. In the above example the mitral leak might be due to an old endocar- ditis, and there mirjlit be mitral stenosis and aortic stenosis as well, but smce we can explain all the signs as results — direct and indirect — of one lesion (aortic regurgitation) it is better to do so, and post- mortem experience shows that our diagnosis is more likely to be right when it is made according to this principle. The most frequent combinations are : (1) Mitral regurgitation with mitral stenosis. (2) Aortic regurgitation with mitral regurgitation (with or with- out stenosis). (3) Aortic regurgitation with aortic stenosis, with or without mitral disease. (1) Double Mitral Disease. (a) It very frequently happens that the mitral valve is found to be both narrowed and incompetent at autopsy when only one of these lesions had been diagnosed during life. In fact mitral steno- Ist III. 2nd M I Fig. no.— Mitral Stenosis and Regurgitation, showing relation of murmur to first heart sound sis is almost never found at autopsy without an associated regurgi- tation, so that it is fairly safe to assume, whenever one makes the diagnosis of mitral stenosis, that mitral regurgitation is j^resent as well, whether it is possible to hear any regurgitant murmur or not (see Fig. 110). (l>) On the other hand, with a double mitral lesion one may have only the regurgitant murmur at the mitral valve and nothing to suggest stenosis unless it be a surprising sharpness of the first mitral sound. In chronic cases the changeableness of the murmurs both in type and position is extraordinary. One often finds at one 196 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. visit evideuces of mitral stenosis and at another evidences of mitral regurgitation alone. Either murmur may disappear altogether for a time and reappear subsequentl3^ This is peculiarly true of the pre- systolic murmur, which is notoriously one of the most fleeting and uncertain of all physical signs. As a rule the same inflammatory changes which produce mitral regurgitation in early life result as they extend in narrowing the mitral valve, so that the signs of stenosis come to predominate in later years. Coincidently with this narrowing of the diseased valve a certain amount of improvement in the patient's symptoms may take place, and Rosenbach regards the advent of stenosis in such a case as an attempt at a regenerative or compensatory change. In many cases, however, no such amelioration of the symptoms follows. (2) Aortic Iie(jur(jit(itlo)i icitlt Jlitral Disease. The signs of mitral disease occurring in combination with aortic regurgitation do not differ essentially from those of pure Systolic murmur over dilated*--/--' aortic arch. Maximum intensity and diastolic inur- ni u r, conducted up and down. --——Systolic murmur. Fig. 111.— Aortic and Mitral Regurgitation. The shaded areas are those in which the murmurs are loudest. mitral disease except that the enlargement of the heart is apt to be more general and correspond less exclusively to the right ven- tricle (see Figs. Ill and 112). Th(; manifestations of the aortic le- VALVULAR LESIONS. 197 sion, on the other hand, are considerably modified by their associa- tion with the mitral disease. The Corrigau pulse is distinctly less sharp at the summit and rises and falls less abruptly. Capillary 1st 1st III! '^^ lllll ~"'^ iillliiin'i lliiiiiiiiiiii lillliiiiinn llliiiiii Ill, Fig. 113.— Sliowing Relation of Murmurs to Heart Sound in Regurgitation at the Aortic and Mitral Valves. pulse is less likely to be present, and the throbbing of the perijjheral arteries is less often visible. (3) Aortic Regurfjitation with Aortic Stenosis. If the aortic valves are narrowed as well as incompetent, we find very much the same modification of the physical signs charac- teristic of aortic regurgitation as is produced by the advent of a mitral lesion ; that is to say, the throbbing in the peripheral ar- teries is less violent, the characteristics of the radial pulse are less marked, and the capillary pulsation is not always to be obtained at all. Indeed, this blunting of all the typical manifestations of aortic regurgitation may give us material aid in the diagnosis of aortic stenosis, provided always that the mitral valve is still per- forming its function. (4) The association of mitral disease with tricuspid insufficiency has been already described on p. 159. CHAPTER VIII. PARIETAL DISEASE.— CARDIAC NEUROSES.— CONGENI- TAL MALFORMATIONS OF THE HEART. Parietal Disease of the Heart. Acute Myocarditis. The myocardium is seriously, though not incurably, affected in all continued fevers, owing less to the fever itself than to the tox- aemia associated with it. "Cloudy swelling," or granular degener- ation of the muscle fibres, is produced by relatively mild infections, Avhile a general septicaemia due to pyogenic organisms may produce extensive /«/f// degeneration of the heart within a few days. The physical signs are those of cardiac tceakness. The most significant change is in the quality of the first sound at the apex of the heart, which becomes gradually shorter and feebler until its quality is like that of the second sounds, while its feebleness makes the second sounds seem accented by comparison. Soft blowing systolic murmurs may develop at the pulmonary orifice, less often at the apex or over the aortic valve. The apex impulse becomes progressively feebler and more like a tap than a push. Irregxdarity and increasing rapidity are omi- nous signs which may be appreciated in the radial i)ulse, but still better by auscultation of the heart itself. In most of the acute in- fections evidence of dilatation of the weakened cardiac chambers is rarely to be oljtained during life (although at autopsy it is not in- frequently found),' but in acute articular rheumatism an acute dila- tation of the heart appears to be a frequent complication, independ- ' Henchen's recent monogi-aph on this subject, "Ueber die acute Herzdila- tation bei acuten Infectioiiskiankheiten," Jena, 1899, does not seem to me convincing. PARIETAL DISEASE. 199 ent of the existence of any vahiilar disease. Attention has been especially called to this point by Lees and Boyntou (Bjutiah M) Accentuation of the aortic second sound. (c) A diffuse slapping cardiac impulse. (d) Reduplication of some of the cardiac sounds (gallop rhythm), (e) Evidences of cardiac dilatation. (/) ]\Iurniurs — especially the murmur of mitral insufficiency which often occurs as a result of dilatation of the valve orifices and weakening of the cardiac muscle. I) lift' rent la I Diar/nosis. "We have to distinguish myocarditis from — (a) Uncomplicated valvular lesions. (h) Cardiac neuroses. PARIETAL DISEASE. 201 (r/) It has been already pointed out that vahiilar lesions do not necessarily give rise to any ninrniurs when compensation has failed. Under such circumstances one hears only irregular and weak heart sounds, as in myocarditis. The history of a long-standing vahii- lar trouble, a knowledge of the previous existence of murmurs, the age, method of onset, and symptoms of the case may assist us in the diagnosis. Cases of myocarditis are less likely to be associated with extensive dropsy than are cases of valvular disease whose com- pensation has been ruptured. (h) "Weakness and irregularity of the cardiac sounds, when due to nervous affection of the heart and unassociated with parietal or vahiilar changes, is usually less marked after slight exertion. The heart "rises to the occasion" if the weakness is a functional one. On the other hand, if fatty or fibroid changes are jiresent, the signs and symptoms are much aggravated by any exertion. In some cases of myocarditis the pulse is excessively slow and shows no signs of weakness. This point will be referred to again in the chapter on Bradycardia. Fatty Overgrowth. An abnormally large accumulation of fat about the heart may be suspected if, in a very obese person, signs of cardiac embarrass- ment (dyspnoea, palpitation) are present, and if on examination we find that the heart sounds are feeble and distant but preserve the normal difference from each other. When the heart wall is seri- ously weakened (as in the later weeks of typhoid), the heart sounds become more alike owing to the shortening of the first sound. In fatty overgrowth this is not the case. The diagnosis, however, cannot be jiositively made. We sus- pect it under the conditions above described, but no greater cer- tainty can be attained. Fatty Degeiieration. There are no physical signs by which fatty degeneration of the heart can be distinguished from other pathological changes which result in weakenmg the heart walls. An extensive degree of fatty 202 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. degeneration is often seen post mortem in cases of pernicious ansemia, although the heart sounds have been clear, regular, and in all re- spects normal during life. The little we know of the physical signs common to fatty degeneration and to other forms of parietal disease of the heart has been included m the section on Myocar- ditis (see p. 198). Cardiac Neuroses. Tachucanlia (Kap'id Heart). Simple quickening of the pulse rate, or tachycardia, which may pass altogether unnoticed by the patient himself, is to be distin- guished from palpitation, in which the heart beats, whether rapid or not, force themselves upon the patient's attention. The pulse rate may vary a great deal in health, A classmate of mine at the Harvard Medical School had a pulse never slower than 120, yet his heart and other organs were entirely sound. Such cases are not very uncommon, especially in women. Temj)orarily the pulse rate may be greatly increased, not only by exercise and emotion, but by the influence of fever, of gastric disturbances, or of the menopause. Such a tachycardia is not always of brief duration. The effects of a great mental shock may produce an acceleration of the pulse which persists for days or even weeks after the shock. Among organic diseases associated with weakening of the pulse the commonest are those of the heart itself. Next to them, exoph- thalmic goitre, tumors or hemorrhage in the medulla, and obscure diseases of the female organs of generation, are the most frequent causes of tachycardia. The only form of tachycardia which is worthy to be considered as a more or less indei)eudent malady is Pa roxys mal Ta clt yea rdia. As indicated in the name, the attacks of tliis disease are apt to begin and to cease siiddcnhj. They may last a fcAv hours or several days. The pulse becomes frightfully rapid, often 200 per minute or more. Bristowe records a case with a pulse of 308 per minute. CARDIAC NEUROSES. 203 In the radial artery the pulse beat may be impalpable. The heart sounds are regular and clear, but the diastolic pause is shortened and the first sound becomes short and "valvular," resembling the sec- ond ("tic-tac heart"). The paroxysm may be associated with ajjhasia and abnormal sensations in the left arm. Occasionally the heart becomes dilated, and oedema of the lungs, albuminuria, and other manifestations of stasis appear. As a rule, however, paroxys- mal tachycardia can be distinguished from the rapid heart-beat associated with cardiac dilatation by the fact that the heart remains perfectly regular. This . same fact also assists us in excluding the cardiac neuroses due to tobacco, tea, and other poisons. From the tachycardia of Graves' disease the affection now in consideration differs by its paroxysmal and intermittent character. ■ Bradycardia ( Shiv Heart). In many healthy adults the heart seldom beats over 50 times a minute . I. Among the causes which may produce for a short time an abnormally slow heart-beat are : (a) Exhaustion; for example, after fevers, after parturition, or severe muscular exertion. (h) Toxoimia ; for example, jaundice, uraemia, auto-intoxications in dyspepsia. (c) In certain hysterical and melancholic states and in neurotic children, the pulse may be exceedingly slow. Pain has also a ten- dency to retard the pulse. (d) An increase of intrac7-a7iial pressure, as in menuigitis, cere- bral hemorrhage, depressed fracture of the skull. Possibly in this category belong the cases of bradycardia sometimes seen in epilep- tiform or during syncopal attacks. Bradycardia from any one of these causes is apt to be of comparatively short duration. II. Permanent hradjjcardia is most often associated with coro- nary sclerosis and myocarditi:^. In this disease the pulse may re- main below 40 for months or years, though strong and regular, yet the patient may be free from disagreeable symptoms of any kind. The rate of the heart-beat cannot always be estimated by counting 204 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. the radial pulse. !N"ot infrequentl}' many pulsations of the heart are not of sutticient force to transmit a wave to the radial artery, and the mistake should never be made of diagnosing bradycardia simply by counting the radial j^ulse. An'/ri/thmla. 1. Phys'wlorjkal Arrhyth in la . — Arrhythmia, or irregularity in the force or rhythm of the heart-beat, is to a certain extent physiologi- cal. The heart normally beats a little faster and a little more strongly during inspiration than duruig expiration. Any psychical distur])- ance or muscular exertion may produce irregularity as well as a quickening of the heart-beat. Earely the jiulse may be irregular throughout life in perfectly healthy persons. This irregularity is usually of rhythm alone; every second or third beat may be regu- larly omitted without the individual knowing anything about it or feeling any disagreeable symptoms connected with it. More rarely the heart's beats may be permanently irregular in force as well as rhythm despite the absence of any discoverable disease. In children the pulse is especially apt to be irregular, and dur- ing sleep some children show that modification of rhythm known as the ^^paradoxical indse,''^ which consists in a quickening of the pulse with diminution in volume during inspiration. (2) If we leave on one side diseases of the heart '\t^Q\i, ixitho- logical arrJir/tlunia is most frequently seen in persons who have used tobacco or tea to excess, or in dyspepsia. In these conditions it is often combined Avith palpitation and becomes thereby very distress- ing to the patient. In connection with cardiac disease the follow- ing tyi)es of arrhythmia may be distinguished : (a) Paradoxical Pulse. — Any cause which leads to weakening of the heart's action may occasionally be associated Avith paradoxical pulse. Fibrous pericarditis has been supposed to be frequently associated Avith this type of arrhythmia, but if so it is by no means its only cause. (b) The bigeminal puhe is seen most frequently in cases of un- compensated heart disease (particularly mitral stenosis) after the administration of digitalis. Every other beat is weak or abortive CARDIAC NEUROSES. 205 and is succeeded by an luiusiially long pause. Sometimes every third beat is of the abortive type, or an unusually long interval may divide the heart-beats into groups of three ("trireuiinal pulse"). (c) Einhri/ocardia, or the *'tic-tac heart," represents a shorten- ing of the diastolic pause and of the first sound of the heart so that it resembles the second sound, as in the foetal heart. Any case of uncompensated heart disease, whether valvular or parietal, may be associated with this disturbance of rhythm. ((/) The (jallop rliijthin. Owmg to a reduplication of one of the heart sounds (usually the second), we may have three sounds instead of two with each beat of the heart, the sounds possessing a rhythm which reminds us of the hoof -beats of a galloping horse (see p. 123). This rhythm is heard especially in the failing heart of interstitial nephritis or cor- onary sclerosis. (e) Delirium cordis is a term used to express any great irregu- larity and rapidity of the heart-beats which cannot be reduced to a single type or rhythm. It is seen in the gravest stages of uncom- pensated heart disease. Palpitation. Defined by Osier as "irregular or forcible heart action percep- tihle to the individual.^' The essential point is that the indi^ddual becomes conscious of each beat of his heart, whether or no the heart action is in any way abnormal. («) In irritable conditions of the nervous system, such as occur at puberty, at climacteric, or in neurasthenic persons, palpitation may be very distressing. Temporary disturbances, such as fright, may produce a similar and more or less lasting effect. (h) The effect of high altitudes, or of even a moderate eleva- tion (1,500 feet) is sufficient to produce in many healthy persons a cpiickening and strengthening of the heart's action, so that sleep may be prevented. After a few nights this condition usually passes off, provided the heart is sound. (c) Abuse of tobacco and tea have a similar effect. 206 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. Auscultation of a palpitating lieart sliows nothing more than unusually loud and ringing heart sounds, but since palpitation is often associated with arrhythmia of one or another type Ave must be careful to exclude the palpitation symptomatic of acute dilatation of the heart, such as may occur in debilitated persons after violent or unusual exertion. In this condition the area of cardiac dulness is increased and dyspnoea upon slight exertion becomes marked. It goes without saying that in almost any case of organic disease of the heart palpitation may be a very marked and distressing sym})- tom. CONGENITAL HEAET DISEASE. Erom the time of birth it is noticed that the child is markedly and permanently cyanosed, hence the term "blue baby." Dyspnoea is often, though not always, present, and may interfere with suck- ing. The cyanosis is practically sufficient in itself for the diag- nosis. Among congenital diseases of the heart the commonest and the most important (because it is less likely than any of the others to prove immediately fatal) is : 1. Puhnonanj Stenosis. This lesion is usually the result of foetal endocarditis, and is often associated with malformations and defects, such as patency of the foramen ovale and persistence of the ductus arteriosus. The physical signs of pulmonary stenosis are : (a) A palpable systolic thrill most distinct in the pulmonary area. (b) A loud murmur (often rough or musical) heard best in the same region, but usually transmitted to all parts of the chest. (c) A weak or absent pulmonic second sound. (d) An increased area of cardiac dulness corresponding to the right ventricle. Unlike most other varieties of congenital heart disease, jiulmo- nary stenosis is compatible with life for many years, and "blue babies " with this lesion may grow up and enjoy good health, al- CONGENITAL HEART DISEASE. 207 though usually subject to pulmonary disorders (pneumonia or tu- berculosis). For a discussion of the ditferential diagnosis of this lesion, see above, p. 193. 2. Defects in the Ventrleular Septum. The loud si/stolic murmur produced by the rush of l^lood through an opening between the ventricles is heard, as a rule, over the whole precordia. Its point of maximum intensity differs in different cases, but is hardly ever near the apex of the heart. The most im- portant diagnostic point is the absence of a i:)alpable thrill. "With almost every other form of congenital heart disease in Avhich a loud murmur is audible, there is a thrill as well Hypertrophy of both ventricles may be present, but is seldom marked in uncomplicated cases. (^Patencn of tlie foramen ocale, if luiassociated with other de- fects, does not usually produce any murmur or other signs by which it can be recognized during life, and causes no symptoms of any kuid.) 3. Persistence oftlie Ductus Arteriosus. The most characteristic sign is a loud, vibratory systolic mur- mur with its intensity at the base of the heart and unassociated v:ith hypertroijhy of extlier ventricle. If complicated with stenosis at or close above the puhnonary valves, persistence of the ductus arte- riosus cannot be diagnosed, as the murmur produced by it cannot with certainty be distmguished from that of the pulmonary ste- nosis, and the ]3resence of hypertrophy of the right ventricle de- prives us of the one relatively characteristic mark of a patent arte- rial duct. It has been claimed that a murmur persisting through systole and into diastole is diagnostic of an open arterial duct, but this supposition is not l)orne out by post-mortem evidence. The signs produced liy the other varieties of congenital heart disease, such as aortic stenosis and tricuspid or mitral lesions, do not differ materially from those characterizing those lesions in 208 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. adults. Excluding these, Ave may summarize the signs of the other lesions as follows : (a) Practically all cases of congenital heart disease, which pro- duce any physical signs beyond cyanosis and dyspnoea, manifest themselves by a loud systolic murmur heard all over the precordia and often throughout the chest. Its maximum intensity is usually at or near the base of the heart. "V (7^) If there is no tlirlll and no litipevtroplty, the lesion is prob- ably a defect in the ventricular se})tum. (e) If there is a tlrriU hut no hi/pevti-ophi/, the lesion is probably a patent ductus arteriosus. (d) If there is a thrill tmd In/pcrtroplnj of the right ventricle, the lesion is probably pulmonic stenosis, especially if the pulmonic second sound is feeble. CHAPTER IX. DISEASES OF THE PERICARDIUM. I. Pekicakditis. Three forms are recognized clinically : (1) Plastic, dry, or fibrinous pericarditis. (2) Pericarditis with effusion (serous or purulent). (3) Pericardial adhesions or adherent pericardium. Fibrinous pericarditis may be fully developed without giving rise to any physical signs that can be appreciated durmg life. In several cases of pneumonia in which I suspected that pericarditis might be present, I have listened most carefully for evidences of the disease and been unable to discover any ; yet at autopsy it was found fully developed — :the typical shaggy heart. We have every reason to believe, therefore, that pericarditis is frequently present but unrecognized, especially in j)neumonia and in the rheumatic at- tacks of children. On the other hand, it may give rise to very marked signs which are the result of — (a) The rubbing of the roughened pericardial surfaces against one another when set in motion by the cardiac contractions. (b) The presence of fluid in the pericardial sac. (c) The interference with cardiac contractions brought about by obliteration of the pericardial sac together with the results of ad- hesions between the pericardium and the surrounding structures. (1) Dry or Fibrinous Pericarditis. The diagnosis rests upon a single physical sign — '^jjericardial friction " — which is usually to be appreciated by auscultation alone, but may occasionally be felt as well. Characteristic jDcricardial friction is a rough, irregular, grating or shuffling sound which oc- 14 210 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. curs irregularly aud interruptedly during the larger part of each. cardiac cycle. It is almost never accurately synchronous either with systole or diastole, but ocerlaps the cardiac sounds, and en- croaches upon the pauses in the heart cycle. It is seldom exactly the same in any two successive cardiac cj^cles and differs thereby from sounds yjroduced within the heart itself. Pericardial friction seems very near to the ear and may often be increased by pressure Pericai'dial friction. Fig. 113.— Showing Most Frequent Site of Audible Pericarriial Friction. with the stethoscope ; it is not materially influenced by the respi- ratory movements. It is best heard in the majority of cases in the position shown in Fig. 113 ; that is, over that portion of the heart which lies near- est to the chest wall and is not covered by the margins of the lungs ; but not infrequently it may be heard at the base of the heart or over the whole precordial region. The sounds are fainter if 'the ])atient lies on the right side, and sometimes intensified if, while sitting or standing, he leans forward and toward the left, so as to bring the heart into closer apposition with the chest Avail. Pericardial friction sounds often change rapidly from hour to hour, and may disappear and reappear in the course of a day. DISEASES OF THE PERICARDIUM. 211 111 rare cases tlie friction may occur only during systole or only during diastole. In suck cases the diagnosis between pericardial and intracardial sounds may be very difficult. DlFFEKENTIAL DIAGNOSIS. (ji) Pleuro-Pericard'ud Friction. Fibrinous inflammation affecting that part of the pleura which overlaps the heart may give rise to sounds altogether indistinguisli- aljle from those of true pericardial friction when the inflamed pleu- ral surfaces are made to grate against one another by the move- ments of the heart. Such sounds are sometimes increased in intensity during forced respiration and disappear at the end of expiration, while true pericardial friction is usually best heard if the breath is held at the end of expiration. If a friction sound heard in the pericardial region ceases altogether when the breath is held, we may be sure that it is produced in the pleura and not ill the pericardium, but in many cases the diagnosis cannot be made correctly. {h) Intracardiac Murmurs. From murmurs due to valvular disease of the heart, pericardial friction can usually be distinguished by the fact that the sounds to which it gives rise do not accurately correspond either with systole or diastole, and do not occupy constantly any one portion of either of these periods. Cardiac murmurs are more regular, seem less superficial, and vary less with position and from hour to hour. Pressure with the stethoscope does not increase so considerably the intensity of intracardiac murmurs. ^Mien endocarditis and peri- carditis occur simultaneously, it may be very difficult to distinguish the two sets of sounds thus produced. The pericartlial friction is usually recognized with comparatively little difficulty, but it is hard to make sure whether in addition we hear endocardial mur- murs as well. 212 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. (2) Pericardial Effusiox. Following the libriiious exudation, which roughens the pericar- dial surface and produces the friction sounds just described, serum may accumulate in the pericardial sac. Its quantity may exceed but slightly the amount of fluid normally present in the pericar- dium, or may be so great as to embarrass the cardiac movements and finally to arrest them altogether. In chronic (usually tubercu- lous) cases, the pericardium may become stretched so as to hold a quart or more without seriously interfering with the heart's action, while a much smaller quantity, if effused so rapidly that the peri- cardium has no time to accommodate itself by stretching, will prove, rapidly fatal. Hydropericardium denotes a dropsy of the pericardium occur- ring by transudation as part of a general dropsy in cases of renal disease or cardial weakness. The physical sigjis to which it gives rise do not differ from those of an inflammatory effusion, and, ac- cordingly, all that is said of the latter in the following section may be taken as equally an account of the signs of hydropericardium. Hsemopericardium, or blood in the pericardial sac, due to stabs or to ruptures of the heart, is usually so rapidly fatal that no physical signs are recognizable. PliijslcaJ Sif/iis of Pcrii'itrdidl Effusion. In most cases a pericardial friction rub has been observed prior to the time of the fluid accumulation. The presence of fluid in the pericardial sac is shown chiefly in three ways : (1) By ^;erc».s.s/o«, which demonstrates an area of duhiess more or less characteristic (see below). ♦ (2) By au,sridtafion, which may reveal an unexpected feebleness in the heart sounds when compared with tlie power shown in the radial pulse. (3) By the signs and symptoms oi jji-essiox exerted by the i)eri- cardial effusion upon surroiuiding structures. Bulging of the precordia is occasionally to be seen in cliihb'en ; DISEASES OF THE PERICARDIUM. 213 ill adults we soiiietiiiies observe a flattening of the interspaces just to the right of the sternum between the third and sixth ribs. (1) The Area of Percussion Dulness. — (a) One of the most char- acteristic jioints is the unusual ' extension of the percussion duliiess a considerable distance to the left and beyond the cardiac impulse. (/*) ISText to this, it is important to notice a change in the angle made by the junction of the horizontal line corresj)onding to the upper limit of hepatic dulness and the nearly perpendicular line corresponding to the right border of the heart. In health this Tympany, _i — - Dulness, Cardiac impulse. Liver dulness. ''' Fig. lU.— Percussion Dulness in Pericardial Effusion, with Tympanitic Resonance Under the Left Clavicle. cardio-hepatic angle is approximately a right angle ; in pericardial effusion it is much more obtuse (see Fig. 114). Rotch has called attention to the importance of dulness in the fifth right intercostal space as a sign of pericardial effusion, but a similar dulness may be produced by enlargement of the liver. Except for the two points mentioned above (the unusual extension of the dulness to the left of the cardiac impulse and the blunting of the cardio-hepatic angle), there seems to me to be nothing charac- teristic about the area of dulness produced by pericardial friction. ' In health the cardiac duliiess extends about three-fourths of an inch be- yond the cardiac impulse, but in pericardial effusion the difference is gi-eater. 214 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. The "pear-shaped" or triangular area of percussion dnlness men- tioned by many Avriters has not been present in cases which have come under my observation. In large etfusions percussion reso- nance may be diminished in the left back, and under the left clav- icle the percussion note may be tympanitic from relaxation of the lung. Traube's semilunar space may be obliterated, but this occurs also in pleuritic effusions. In some cases the area of dnlness may be modified by change in the patient's position. After marking out the area of percussion dubiess with the patient in the upright jiosition, let him lie upon his right side. The right border of the area of dnlness will some- times move considerably farther to the right. A dilated heart can be made to shift in a similar way, l)ut to a lesser extent. Compar- atively little change takes place if the patient lies on his left side, and no important information is elicited by placing him flat on his back or by getting him to lean forAvard. Unfortunately, it is only with moderate-sized effusions occur- ring in a pericardial sac free from adliesions to the surrounding parts that this shifting can be made out. Large effusions may not shift apyjreciably, and less than 150 c.c. of fluid probably cannot be recognized by this or by any other method. But with large effu- sions the lateral extension of the area of dnlness may be so great as to be almost distinctive in itself, i.e., from the middle of the left axilla nearly to the right nipple. (2) The feebleness of the heart sounds, especially those at the apex, is of diagnostic importance only in the rare cases when it oc- curs in connection Avith a relatiA'ely normal condition of the radial pulse. In most diseases feeble heart sounds are associated Avith a Aveak pulse, but occasionally in pericardial effusion the pulse may be of good quality, although the heart sounds are heard A\ath diffi- culty. Broncho-A^esicular breathing Avith increased voice sounds may be heard over the tympanitic area beloAv the left clavicle and occa- sionally betAA'^een the scapula? behind. Tliis is a result of comiDres- sion of the lung. (3) Pressure exerted by tlu3 pericardial exu^'ation iipon sur- DISEASES OF THE PERICARDIUM. 215 rounding stvnctures may give rise to (ly,s})ncea, especially of a paroxysmal type, to dysphagia, to aphonia, and to an irritating cough. The "paradoxical pulse," small and feeble during inspira- tion, is occasionally to be seen, but is by no means peculiar to this condition and has no considerable diagnostic importance. (4) Inspection and xmlpation usually help us very little, but two jDoints are occasionally demonstrable by these methods : (rt) A smoothing out of the intercostal depression in the precor- dial region, especially near the right border of the sternum between the third and the sixth ribs. (/>) A progressive dimmution of the intensity of the apex im- pulse until it may be altogether lost. If this change occurs while the i^atient is under observation, and especially if the apex impulse reajypears or becomes more distinct when the patient lies on the right side, it is of considerable diagnostic value. In conditions other than jiericardial effusion, the apex impulse becomes less visible in the right-sided decubitus. Dtjferentlol Diagnosis. (1) Our chief difficulty is to distinguish the disease from hyper- trophy and dilatation of the heart. In the latter, which often com- plicates acute articular rheumatism with or Avithout plastic pericar- ditis, the apex impulse is often very indistinct to sight and touch as in pericardial effusion. But the area of dulness is less likely to extend beyond the apex impulse to the left or to modify the cardio- hepatic angle, or to shift when the patient lies on the right side. Pressure symptoms are absent, and there a,re no areas of broncho- vesicular breathing with tympanitic resonance under the left clavicle or in the axilla. Yet not infrequently these differentiae do not serve us, and the diagnosis can be made only b}^ puncture. (2) I have tAvice known cases of eiicapsulated empyema mistaken for pericardial effusion. In one case a needle introduced in the fifth intercostal space below the nipple drew pus from what turned out later to be a localized purulent pleurisy, but the diagnosis was not made until a rib had been removed and the region thoroughly explored. It is not rare for pleuritic effusions to gather first 216 PHYSICAL DIAGyOSIS OF DISEASES OF THE CHEST. ill this situation, viz., just outside the apex impulse in the left axilla. Such effusions may gravitate A-ery slowly to the bottom of the pleural cavity or may become encapsulated and remain in their original and very deceptive position. In such cases the signs of compression of the left lung are similar to those produced by a pericardial effusion, and the results of punctures may be equivocal as in the case just mentioned. If there is cuv/ dulness, even a very narrow zone, in the left axilla between the fifth and eighth ribs, though there be none in the back, the likelihood of pleurisy should be suggested. As between pleuritic and pericardial effusion the presence of a good pulse and the absence of marked dyspnoea favors the former. In the two cases above referred to in which encapsulated pleurisy was mistaken for pericarditis, the general condition of the patient struck me at the time as surprisingly good for pericarditis. If both pleurisy and pericarditis are present, the area of peri- cardial dulness is not characteristic until the pleuritic fluid has been drawn off. The persistence of dulness in the cardio-hepatic angle and beyond the apex beat after a left pleurisy has been emptied by tapping, and after the heart has had time to return to its normal position, should make us suspect a pericardial effusion. Despite the utmost care and thoroughness in physical examina- tion, many cases of pericardial effusion go unrecognized, especially in infants, in elderly ])ersons, or when the lung borders are adher- ent to the pericardium or to the chest Avail. In the rheumatic attacks of children, it should be remembered that pericarditis is even more common than endocarditis. Adherent Fericard'uiiti . In the majority of cases the diagnosis cannot be made during life, unless the pericardium is adherent, not only to the heart, but to the walls of the chest as well. When this combination of peri- carditis with chronic mediastinitis is present, the diagnosis may be suggested by {(i) A systolic retraction of the chest wall in the region of the DISEASES OF THE PERICARDIUM. 217 apex impulse at the base of the left axilla and in the region of the eleventh and twelfth ribs in the left back (Broadbent's sign). 8uch retraction is more marked during a deep inspiration. (It should be remembered that systolic retraction of the interspaces in the vicinity of the apex is very commonly seen m cases of cardiac hy- pertrophy from any cause, owing to the negative pressure produced within the chest by the contraction of a powerful heart.) A quick rebound of the cardiac apex at the time of diastole (the diastolic shock) is said to be characteristic of pericardial adhesions, but is often absent. (h) Collapse of the cervical veins during diastole has been no- ticed by Friedreich, and the paradoxical pulse, above described, is said to be more marked in adherent pericardium than in any other known condition. Most recent Avriters, however, place no reliance upon it. (r) When the lungs are adherent to the pericardium or to the chest wall, as is not uncommonly the case, the absence of the phrenic ]Dhenomenon (Litten's signs) and of any respiratory excursion of the pulmonary margins may be demonstrated. Since pericardial adhesions are most often due to tuberculosis, the discovery of tu- berculosis in the lung or elsewhere may be of aid in diagnosis. ((/) Broadbent considers that the absence of any shift in the position of the apex beat, with respiration or change of patient's position, is an imjiortant point in favor of mediastino-pericarditis. In health and in val\ailar or parietal disease of the heart, the apex beat will swing from one to two inches to the left when the patient lies on his left side, and the descent of the diaphragm during full inspiration lowers the position of the cardiac impulse considerably. (e) The presence of hypertrophy or dilatation affecting espe- cially the right side of the heart, and not accounted for by the existence of any disease of the cardiac valves, of the lung, or of the kidney, should make us suspect pericardial and mediastinal adhesions. Such adhesions embarrass especially the right A'en- tricle, because it is the right ventricle far more than the left which becomes attached to the chest Avail. The left ventricle is more nearly free. 218 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. (/) Since the sj^ace enclosed by the divergent costal cartilage just below the ensiforni is but loosely associated with the ceu~ tral tendon of the diaphragm, Broadbent looks especially at thi'i t FIG. 115. Fi(i. 110. Figs. 115, 116.— Adherent Pericardium, Ascites. point for evidence of mediastinal or pericardial adhesions, the effect of which is to arrest completely tlie slight respiratory inove- ments of tliis i)art of tlie abdominal Avail. (_'/) Adherent pericardiimi, o'-cuvring as a jiai't of a widespread DISEASES OF THE PERICARDIUM. 219 chain of librous processes involving tlie i)leni'a, the mediastinum, and tlie peritoneum, may give rise in young persons to a train of symptoms and signs suggesting cirrhosis of the liver. Ascites collects, the liver is enlarged, yet there are no signs in the heart, kidneys, or blood sufficient to explain the condition. In any such case adherent pericardium should be considered. Figs. 115 and IIG show the appearance in cases of this kind in which the diagnosis was verified by autopsy. Suminai'i/. The diagnosis of adherent pericardium with chronic mediastini- tis is suggested by [a) Systolic retraction of the loAver intercostal spaces in the left axilla and in the left back, followed by a diastolic rebound. {I)) The absence of any change in the position of the apex im- pulse with respiration or change of position. (<■) The presence of hypertrophy and dilatation of the right ventricle without obvious cause. ((/) The absence of any respiratory excursion of the lung bor- ders near the heart and of the abdommal wall at the costal angle. (e) The presence of signs like those of hepatic cirrhosis in a 3^oung person and without any obvious cause. CHAPTER X. THORACIC AXEURISM. Aneurism of the Thokacic Aorta. For clinical purposes thoracic aneurisms may be dirided into the diffuse and the saccular. Saccular aneurisms of the ascending or descending portion of the arch of the aorta are apt to penetrate the chest wall, while aneurism of the transverse aorta or diffuse dilatations of the whole aortic arch are more likely to extend within the chest without erodmg tlie thoracic bones. Practically any aneurism Avhich penetrates the thoracic bones may be inferred to be saccular, but if no such penetration takes place, it may be im- possible to make out whether the dilatation is diffuse or circum- scribed. I shall consider : I. The signs of the j^resence of aneurism. II. The evidences of its seat. Inspection and 2)a^p'(tion give us most of the important informa- tion in the diagnosis of aneurism. The patient should be placed in the position shown m Fig. 117, so that the light will strike obliquely across the siirface of the chest, and the observer should be so placed that his eyes are as nearly as possible at the level at that part of the chest at which he hopes to see pulsation. In the majority of cases of aneurism some abnormal 2'>ilsatlon may be made out either to the right of the sternum in front or in Abnormal ^^^ region of the left scapula behind. If the aneiir- Pulsation. ism is large, a considerable area of the chest wall may be lifted with each beat of the heart; with smaller growths the pulsating area may be small and sharply circumscribed. Not in- frequently an abnormal i)ulsation at the sternal notch or in the THORACIC ASEUEISM. 221 neck may be observed. Other causes of abnormal pulsations in the chest, such as dislocation or uncovering of the heart, must of course be excluded. Pulsations due to aneurism can sometimes be distinctly seen to occur later than the apex impulse of the heart. Palpation controls tiie results of inspection, but at times a pul- sation may be seen better than felt ; at others may be felt better than seen. Bimanual palpation — one hand over the suspected area in front and one in a corresponding position behind— is useful. If the aneurism involves the ascending portion of the aortic Fig. 117.— Position Wtien Looiiiug for Siifrlit Aneurismal Pulsation. arch, it is likely sooner or later to erode the right margin of the sternum and the adjacent j^arts of the second or third costal car- tilages and appear externally as a round SAvelling in which a systolic pulsation is to be seen and felt. This pulsation is almost always distinctly expansile in character, and differs in this respect from the up-and-down motion which may be communicated to a tumor of the chest wall b}' the beatmg of a normal aorta. The tumor is usually firm, rarely soft, and may be as hard as any variety of malignant new growth. Occasionally 222 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. the thickness of the lamenated clot within it is so great that no pulsations ai-e transmitted to the surface. "Whether the aneurism penetrates the chest or not, it is often possible to feel over it a vibratinq t/t r ill, wsnally s»/s- to/ic in time. If the layer of lamellated clot in the sac is very thick, the thrill is less ajjt to be felt. More important in diagnosis is a diastolic shock or tap which is appreciated by laying the palm of the hand lightly over the affected Fig. 118.— Aneiirismal Tumor (A). The arrow B points to a guumiatous swelling neartheen- sifortn cartilage. The radiograpbic appearances of this case are shown below (Fig. 131). area. This diastolic shock is due to the recoil of the blood in the di- lated aorta, and is one of the most important and characteristic signs Diastolic i'l aneurism. As the wall of the sac becomes weaker. Shock, tlie intensity of this shock diminishes. This diastolic shock may be appreciated over the trachea also, and is thought by some to have even more significance Avhen felt in this situation. Of special im])ortance in aneurism of the transverse arch is the sign known as the t radical tii'j. The arch of the aorta runs over THORACIC ANEURISM. 223 the left priinaiy bronclius in such a way that when the aorta is dilated, the bronchus is pressed upon with each expansile pulsation Tracheal of ^^^^ artery. This systolic pressure transmitted to Tug. the trachea produces a distinct downward tug upon it with each systole of the heart. The tug is best felt by making the patient throw l:)ack his head so as to put the trachea upon a stretch. The physician then stands Ijehind him and gently presses the tips of the fingers of both hands up under the lower border of the cri- FIG. 119.— Aneurism Tumor Perforatin.'i'oncko-j)neumo7iia. In many cases of lobular or broncho-pneumonia the l^hysical signs are exclusively those of the coexisting bronchitis. In such cases the diagnosis of bronchitis is not Avrong, but does not cover the Avhole ground. I shall discuss further under broncho-pneumonia the evidence which leads us to suspect that something more than bronchitis is present. (4) Muscle sounds. Under certain circumstances (cold, nervousness), the rumbling noises produced by muscular contractions in the chest wall may simu- late rales so closely that the diagnosis of bronchitis may be strongly suggested. The differentiation between rales and muscle soiinds has already been discussed (see above, }). 87). (5) Atelectatic cfepitation. Crackling rales heard over the thin margins of the lungs at the base of the axilla or along the edges of the manubrium are often due to atelectasis (see above). From bronchitis tliey are distinguished by their situation and by the lack of symptoms. They are best heard at the jioint shown in Fig. 124. Clironic Bvoncliitis. So far as the l)ronf'hitis itself is concerned, there may he no difference in the physical signs between the acute and chronic forms Fig. 124.— The Dots are Placed over the Area where Atelecta- tic Crepitation is Oftenest Heard. BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 237 of the disease; Imt in the latter one almost invariably finds asso- ciated Avitli the bronehitis itself a considerable degree of eni})hy- senia, of asthma, or of both conditions. Indeed, the foreground of the clmical 2)icture and the bulk of the physical sign are made up by the emphysema and asthma, rather than by the bronchitis itself. Accordingly, I shall not discuss chronic bronchitis any further at this point, but will return to the subject in the chapter on Emphy- sema. CEOUPOUS PXEUMOXIA. In its typical form croujDous or fibrinous pneumonia produces solidification of one or more lobes, usually the lower, the process being accurately bounded by the interlobular fissures. Although the physical signs of the earlier stages differ considerably from those of the later ones, there seems to be no sufficient ground for markmg off stages of engorgement and of red and gray hepatiza- tion, for dbi'icalbj these stages cannot be distmguished. The solidification may begm in the deeper parts of the lung (''^ coitral pneuuionia"), ^o that no physical signs are obtamable until later in the course of the disease, when the process extends to the surface of the lung. Massive pneumonia, in which the bronchi as well as the air cells are plugged with fibrin and leucocytes, is a relatively rare form of the disease, but possesses great clinical importance on account of the marked resemblance between its physical signs and those of pleural effusion. The frequency of endocarditis and pericarditis in connection with lobar pneumonia, especially with those of the left side, should be borne in mmd. Physical Signs. (a) Inspection. — The aspect of the patient frequently suggests the diagnosis ; the face is anxious, often flushed or slightly cya- nosed, the flush sometimes affecting most strikingly the side of the face corresponding to the lung affected.' Herpetic vesicles ("cold ^ Pevliaps because the patient is apt to lie upon the aiifected side. 238 PHYSIC AI DIAGNOSIS OF DISEASES OF THE CHEST. sores '') are often to be seen around the mouth or nose. The rapid, difficult breathing is at once noticable, and expiration is often ac- companied by a grunt. The use of the accessory muscles of respi- ration and the dilatation of the nostrils attract attention. The combination of marked dyspnoea with absence of dropsy is met with more frequently in pneumonia than in any other disease. Both sides of the chest usually move alike, but occasionally the affected side shows deficient ex2)ansion especially in the later stages of the disease, and the other side of the chest shows increased re- spiratory movements (compensatory). Rarely the pulsations of the heart may be transmitted to the chest Avail through the affected lung. "When pneumonia attacks a feeble old man, or follows injuries (surgical pneumonia), its onset may be insidious, and none of the phenomena just described may be seen. {h) Palfjatlon. — In the great major it u of cases tactile fremitus is viai'lcedhj increased over the affected area,^ but in case the bronchi are occluded by secretions or fibrinous exudate, fremitus may be di- minislied or altogether absent. A few hard coughs will sometimes clear out the tubes and thus materially assist the diagnosis. Occa- sionally an increase in superficial temperature of the affected side may be noticed by palpation, and rarely one feels a friction rub due to the fibrinous pleurisy which almost invariably accompanies the disease. {c) Pcrcussioib. — Overtlie area affected tlie percussion note is (jener- ally dull and may he almost flat, except in the earliest and latest stages of the disease, in which it may have a tympanitic quality Avith or Avithout an element of slight dulness. More marked tympany is usually x)resent OATr the unaffected lobes of the diseased lung (that is, over the upper lobes in the great majority of cases.) The conditions just described rejiresent the great majority of cases, but the folloAving exceptions occur : (1) In the pneumonias of children, and occasionally in adults, dulness may be absent. ' By u.sing the edge instead of the flat of the hand the boundaries of sol- idified lobe.s may often be very accurately marked out by means of the tactile fremitus. BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 239 (2) When the lower lobe of the left lung is affected, a distmctly tympanitic quality may be transmitted to the consolidated area from a distended stomach or colon. (3) In rare cases, the percussion over the consolidated area may be of a metallic quality, or produce the " cracked-pot " sound. (4) In central pneumonia there may be no change in the percus- sion note, or it may be unusually full and deep so that the sound side seems dull by comparison. A solidified lobe increases so much in size that the area of dul- ness corresponding to it often seems incredibly large. Thus, al- though the lower lobe reaches in health not more than half-Avay up the scapula, when solidified it produces duhiess throughout nearly the whole back. The right base is the most frequent seat of pneumonic solidifica- tions, but the dulness corresponding to it is often first noticeable in the posterior axillary line. A dulness appreciable only in the front of the chest is almost sure to correspond to the upper lobe, while signs in the lower part of the right axilla correspond to the middle lobe. Many cases of central pneumonia first appear at the surface in one or the other axilla. As regards the amount of solidification needed to produce per- cussion dulness, Wintrich says that the minimum is a patch 5 cm. in diameter, 2 cm. deep, and superficially situated. Percussion often makes us aware of an increased resistance or diminished elasticity of the affected side, although the resistance is seldom as marked as in large pleural effusions. (d) Auscultafiou. — In the great majority of cases typical tubular breathing is to be heard over the affected area. Since a whisper is practically a forced expiration, this tuhvlar qualiff/ is ver}'- well brought out if the patient is made to whisper "one, two, three," or any other succession of syllables, and by this method the fatigue and pain of deep breathing may be saved. By this use of the whispered voice one may accurately mark out the boundaries of the consolidated area, and demonstrate in many cases that it coincides with the boundaries of one lobe of the lung. In the earliest stages of the disease the breathing may be bron- 240 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. cho- vesicular ; more often it is feeble or suppressed over the con- solidated area, and "crepitant rales," that is, very line crackling sounds, may be heard at the end of inspiration, but these are much more common in the stage of resolution' ("crepitans redux '"). If some of the smaller bronchi are blocked, as is not infre- quently the case, resjDiration is absent or very feeble, and such cases are often mistaken for pleuritic effusion. In pneumonia of the upper lobe it is not rare for bronchial breathing to be absent even Avithout plugging of the bronchi. In cases of "central pneumonia," that is, when the area of solidification is in the interior of the organ, there may be no change in the breath sounds, or a bronchial element may be faintly audible on auscultation with the unaided ear, and only by this method. The mtensity of the spoken or whispered voice is greatly in- creased over the area of consolidation, and sometimes the words can be distmguished. The nasal twang known as ^'' eynplion;/" is occasionally to be heard. In the majority of cases, as Jias been already stated, the right lower lobe posteriorly is affected, so that the consolidated area is immediately in apposition with the spmal column. Under these circumstances, it is not at all imcommon to hear bronchial breathing transmitted from the consolidated lobe to a narrow zone close along the spinal column on the sound side. Such a zone is often mistaken for consolidation (see Fig. 125). The signs are usually less marked in the axilla and in the front of the lung, but in a minority of cases, and especially when the upper lobes are affected, the signs are wholly in the front. When searching for evidences of consolidation in persons susjDected to have pneumonia, one should never omit to examine the apices and venj summit of the armpit, pressing the stetlioscoj^e up behind the anterior fold of the axilla. In examining the posterior lobes, when the patient is too Aveak to sit up and is loath even to turn upon the side, the Bowles steth- ' Crepitant r2,les are rarely heard in the pneumonias of infancy and old age. They are not peculiar to pneumonia, but occur in pulmonary rcdema or hemorrhagic infarction— conditions easily distinguished from pneumonia. BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 241 oscope is a great couveiiience, owing to the ease Avith wliich its flat- tened extremity may be worked iii between the patient and the bed- clothes without causing any discomfort. When resolution begms, the signs may suddenly and completely disai)pear within a few hours. More frequently the bronchial breathing is modified to broncho- vesicular, dulness and broncho- phony become less marked, fine crackling rales (crej^itans redux) or coarser moist bubbles appear, and the lung gradually returns to its normal condition within a period of three or four days. In the __ _- Tympany. Bronchial breathing transmitted by _ spinal column to sound lung. Solidification. Fig. 135.— Diagram of Signs in Pneumonia. active stages of the disease the entire absence of rales is very char- acteristic. In about 19 per cent, of the cases the solidification of the lung persists after the fall of the temperature ; indeed, it may be weeks or even months before it clears up, and yet the lung may be perfectly sound in the end. On the other hand, abscess or gan- grene may develop in the solidified lobe, or the latter may be trans- formed uito a mass of tough fibrous tissue, and the adjacent portion of the chest may fall in (cirrhosis of the lung, chronic interstitial pneumonia). " Wandevlng ^j;iei) The breathing may be fichle but vesicular in character, or it may be absent, in case bronchi are plugged ; from the same cause (<') Tactile fremitus may be diminished. A hard cough may clear out the bronchi and produce a sudden metamorphosis of the physical signs Avith a return to the normal tyi>e. In these atypical cases, we have to fall back upon the symp- toms, the history, the blood, and sputa for help in the diagnosis. Dee])-seated pneumonic processes may appear at the surface in out-of-the-way places, e.g., at the summit of the axilla, and the area of demonstrable physical signs may be no larger than a silver dollar. A thorough examination of every inch of the chest is therefore essential in douljtful cases. In the later stages of the disease crepitant or other tine rales often a])pear, and the signs of solidification suddenly or gradually disappear. Dlffi'VI'lit'lIll I>i) A slight dijuinution in the excursion of the diaphragm on the affected side, as shoAvn by Litten's diaphragm shadow. (r) Slight diminution in the intensity of the respiratory mur- mur, with or Avithout interrupted inspiration i^''' cor/- ir heel breatlt- inA \ \ \ r Tympany ; (absent voice; ^p—^s \ /i\ \ Air^ - breathing ab- Displacedcardiac -'" J\ ({v^r'^^X /C^i~~r:::>1 A / sent or distant impulse. WSSy^/XfX'- k^Jai^ lamphoric. Dulness, shifting with change of po- sition^ (fluid;. Fig. 133.— Pneumohydrothorax with Displaced Heart. area corresponding to the position of the fluid, an area of dulness may be easily marked out by percussion, and this area sli ifts very laarkedhj with change of position. The shifting dulness of pneu- mohydrothorax is strongly in contrast with the difficulty of obtain- ing any such shift in ordinary pleuritic effusion (see Fig 132) (The distinction between "o^j/e/i pneumotliorax," in which the rent in the lung through which the air escaped in the pleura re- mains ojien, and ^^ closed pnenmotliorax," in which the rent has become obliterated — is one which cannot be established by physi- cal signs alone. It is often said that amphoric breathing, and espe- cially an amphoric ring to the voice and cough sounds, denote an 270 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. open pneumothorax, but post-mortem evidence does not bear this out. Practically an open pnevmiothorax is one in which the amount of effused air increases, and closed pneumothorax is one in which the physical signs remain stationary ) Differential Dia (ptosis The distinction between pneumothorax and emphysema has al- ready been discussed (see p. 260). (a) When the air in the pleural sac is under such tension tliat the percussion note is dull, the physical signs may simulate pleu- ritic effusion, but real flatness, such as characterizes effusion, has not, so far as I know, been recorded in pneumothorax, and the sense of resistance on percussing is much greater over fluid than over air. In case of doubt puncture is decisive . {b) Acute pneumothorax, coming on as it does with symptoms of collapse and great shock, may be mistaken for angina pectoris, cardiac failure, embolism of the pulmonary artery, or acute pulmo- nary tympanites (see above, p. 262). From all these it can be distinguished by the presence of am- phoric or metallic sounds, which are never to be obtained in the other affections named. (c) Hernia of the intestine through the diaphragm, or great weakening of the diaphragmatic muscular fibres, may allow the intestines to encroach upon the thoracic cavity and simulate pneumo- thorax very closely. The history and course of the case, the ab- dominal pain, vomiting, and indicanuria, generally suftice to distin- guish the condition. The i)eristalsis of the intestine may go on even in the thorax, and gurgling metallic sounds corresponding to it and unlike anything produced in the thorax itself may be audible The distinction between open and closed pneumothorax, to which I have already alluded, is far less important than the presence or absence of (a) Pulmonary tuberculosis (Ji) Encapsulating adliesions in wliich the air is confined to a circumscribed area (a) Tlie examination of the sputa and of the comjjressed lung DISEASES AFFECTING THE PLEURAL CAVITY. 271 may yield evidence regarding tuberculosis. On the sound side the compensatory hypertrophy covers up foci of dulness or rales so that it is dittlcult to make out much. (0) Encapsulated pneumothorax gives us practically all the signs of a phthisical cavity, from whicli it is distinguished by the fact that with a cavity the nutrition of the patient is almost always much worse. Encapsulated })neumothorax needs no treatment. Hence the importance of distinguishing it from the non-encapsulated form of the disease, in whicli treatment is essential. TLEURLSY. Clinically, we deal with three types : (a) Dry or plastic pleurisy. (6) Pleuritic effusion, serous or purulent. (c) Pleural thickening. (a) Dry or Plastic Pleurisy. Doubtless many cases run their course without being recognized. The frequency with which iDleuritic adhesions are found post mor- tem would seem to indicate this. It is usually the characteristic stitch in the side which suggests physical exammation. The pain and the physical signs resulting from the fibrinous exudation are usually situated at the bottom of the axilla where the diaphragmatic and costal layers of the pleura are in close apposition. Doubtless the pleuritic inflammation is not by any means limited to this spot, but it is here that the two layers of the pleura make the largest excursion while in apposition with each other. In the vast majority of cases, then, the physical signs are situated at the spot indicated in Fig. 133. Occasionally pleuritic friction is to be heard in the precordial region, and after the absorption of a pleuritic effusion evidences of fibrinous exudation in the upper parts of the chest are sometimes demonstrable. Most rarely of all, evidence of plastic pleurisy may be found at the apex of the lung in connection with early phthisis. In diaphragmatic pleurisy, wlien the fibrinous exudation is espe- 272 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. cially marked iipou the diapliraginatic pleura, friction sounds may be heard over the region of the attachment of the diaphragm in front and behind as well as in the axillae. Hiccup often occurs and gives exquisite pain. • Our diagnosis is based upon a single physical sign, pleuritic f fiction. The nature of this sound and the manoeuvres for elicitmg it have already been described (see above, p. 108), and I ■will here only recapitulate what was there said. During the first few deep breaths one hears, while listenmg over the painful area, a grating or rubbing sound usually somewhat jerky and interrupted, most marked at the latter part of inspiration, but often audible throughout the whole respiratory act. After a few breaths it often disappears, but Avill usually reap- pear if the patient lies for a short time upon the affected side, and then sits up and breathes deeply. In marked cases the rubbing of the inflamed pleural sur- faces may be felt as well as heard, and it is not very rare for the patient to be able to feel and hear it himself. Pleuritic fric- tion may be present and loud without giving rise to any pain. On the other hand, the pain may be intense, and yet the friction -rub barely audible. When heard at the summit of the chest, as in cases of incipient phthisis, pleural fric- tion produces only a famt grazing sound, mucli more delicate and elusive than the sounds produced at the base of the chest. Occasionally the distinctive rubbing or grating sounds are more or less commingled with or replaced by crackling sounds indistin- guishable from the drier varieties of rales. It is now, I think, generally believed that such sounds may originate in the ])leura as Fig. 133.— Showing the Point at which Pleural Friction is most Often Heard. DISEASES AFFECTING THE PLEURAL CAVITY. 273 well as within the lung. The greatest care should be taken to prevent any shifting or slipping of the stethoscope upon the surface of the chest, as by such means sounds exactly like those of pleural friction may be transmitted to the ear. In case of doubt one should always wet or grease the skin so that the stethoscope can- not slip. Musde sounds are sometimes taken for pleural friction, Ijut they are bilateral, usually low-pitched, sound less superficial than pleu- ral friction, and are not increased by pressure. When listening for friction at the base of the left axilla, I have once or twice been puzzled by some low-pitched rumbling sounds occurring at the end of inspiration, and due (as afterward appeared) to gas in the stom- ach which shifted its position with each descent of the diaphragm. In children friction sou.nds and pleuritic pain are much less common than in adults, and the signs first recognizable are those of effusion. In adults the presence of a very thick layer of fat may make it difficult or impossible to feel or hear pleural friction. The breath sounds over the affected area are usually absent or greatly diminished, owing to the restraint in the respiratory move- ments due to pain. ^Mot infrequently pleuritic friction may be heard altogether below the level of the lung, [b) Pleuritic Effusion. jNIany cases are latent, and the patients consult the physician on account of slight cough, weakness, or gastric trouble, so that the effusion is first discovered in the course of routme physical ex- amination. Since it is usually the results of percussion w^hich first put us on the right track, I shall take up first Percussion. 1. A small effusion first shows as an area of dulness (a) Just below the angle of the scapula. {h) In the left axilla between the fifth and the eighth rib. (c) Obliterating Traube's semilunar area of tympany; or * (d) In the right front near the angle made by the cardiac and hepatic lines of dulness (see Fig. 134). 18 274 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. Ill the routine percussion of the chest, therefore, one should never leave out these areas. A small effusion is most easily de- tected in children or in adults with thin chest walls, provided our percussion is not too llea^'y. An effusion amounting to a pint should always be recognizable, and smaller amounts have frequently been diagnosed and proved by puncture. The amount of a pleuritic effusion is roughly proportional to the area of dulness on percussion, Imt not accurately. It is very common to find on puncture an amount of fluid much greater than Area of dulness due to small -cf' 1~ pleural effusion. ^■•-^ ' Area of cardiac dulness. Fig. 134.— Small Pleural Effusion Accumulating: (in part) near the Right Border of the Heart. could have been suspected from the percussion outlines ; on the other hand, the dulness may be extensive and intense on account of great inflammatory thickening of the costal pleura, by the accumulation of layer after layer of fibrinous exudate and its organization into fibrous plates, while very little fluid remains within. The amount of dulness depends also upon the thickness and elasti- city of the chest wall and the degree of collapse of the lung within. 2. Large Effusions. — "When the amount of fluid is large, the dul- ness may extend througliout the whole of one side of the chest with the exception of a small area above the clavicle or over the primary bronchus in front. This area gives a high-pitched ft/mpanitic note, DISEASES AFFECTING THE PLEURAL CAVITY. 275 provided the bronchi reiuaiu open, as they almost always d(j. This tympany is high-pitched and sometimes astonishingly clear. I re- cently saw a case in which the note abo^'e the clavicle Av^as almost indistinguishable with the eyes shut from that obtamed in the epi- gastrium. Occasionally "cracked-pot" resonance may be obtained in the tympanitic area. The pitch changes if the patient opens and closes his mouth while we percuss ("Williams' tracheal tone"). The dulness over the lower portions of a large effusiou is usual- ly veri/ marked, and the percussing finger feels a greatly increased Normal resonance and vesicular breathing. Tympany, voice and — "f r e 111 i t u s i !i - creased. Flatness, no breath- ing, voice sounds, or fremitus. Zone of condensed lung above the fluid. . Exaggerated (com- pensatory) breath- ing and r e s o - nance. Fig. 135.— Diagram to Illustrate Physical Signs in Moderate-Sized Effusion in the Left Pleura. resistance to its blows when compared with the elastic rebound of the sound side. 3. Moderate Effusions. — Three zones of resonance can often be mapped out in the back : at the base dulness or flatness, above that a zone of mingled dulness and tympany, and at the top normal resonance. The lowest zone corresponds to the fluid, the middle zone to the condensed lung immediately above it, and the top zone to the relatively unaffected part of the lung (see Fig, 135). Kot infrequently there is no middle zone but simply dulness below and resonance above, as is usually the case in the axilla and front. 276 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. The position of the effusion depends only in part upon the in- fluence of gravity, and is greatly influenced by capillarity and the degree of retraction of the lungs. Consequently the surface of the fluid is hardly ever horizontal except in very large accumula- tions. AVith the patient in an upright position it usually reaches a higher level in the axilla than in the back. Xear the sjjine and near the sternum (in right-sided effusions) the line corrresponding to the level of the fluid may rise sharply. The 8-curve of Ellis, as worked out so elaborately by Garland, varies still further the uneven line which corresponds to the sur- Triangular space dull until patient has eoug-hecl and hreatlied deeply. Area of dulness bdunded above by the S-curve of Ellis. Fig. lo6.-Tlie S-Curve of Ellis. face of the fluid (see Fig, 13G). This curve can be obtained only after the patient has, by cough and forced breathmg, expanded the lung as fully as possible. All these curves are to be found with tlie patient in the uiDright position. None of them has any considerable diagnostic impor- tance, and the chief point to be remembered is that the upper sixr- face of the fluid, not being settled by gravity alone, is hardly ever horizontal. With change in the jiosition of the ]iatient the level of the fluid sometimes changes very slowly and irregularly, and sometimes does DISEASES AFFECTING THE PLEURAL CAVITY. 277 not ehiiuge at all. If, for purposes of thorough examination, we raise to a sitting posture a patient who has been for some days or weeks in bed, we should never begin the examination at once, since it may take some minutes for the lungs and the fluid to accommo- date themselves to the new position. It is well also to get the patient to cough and to take a number of full breaths before the examination is begun. To test the mobility of the fluid with change of the patient's position, mark out the upper limit of the duluess in the back with the patient in the upright position. Then let the patient lie face downward upon a couch, and, after waiting a few minutes, percuss the previously dull area. It may be found to have become resonant.* When the fluid is absorbed or removed by tapping, one would expect an immediate return of the percussion resonance. But in fact the resonance returns very slowly and is wholly unreliable as a test of the amount of absorption which has occurred. Thickened pleura and atelectatic lung may abolish resonance long after the fluid is all gone. We depend here far more upon the evidence ob- tained by auscultation and palpation and on the general condition of the patient. To determine the returning elasticity of the lung and the degree of movability of its lower border, percussion is very useful during the stage of absorption. After percussing out the lower border of pulmonary resonance in the back, the patient is directed to take a long breath and hold it. If the lung expands, the area of percus- sion resonance will increase downward. Percussion aids us in determining whether neighboring organs are displaced by the pressure of the accumulated fluid. The liver is often pushed down, the spleen verj/ rarely. Dislocation of fife- heart is one of the most important of all the signs of pleural effu- sion, and is often the crucial point in differential diagnosis. It is ' This test, however, is somewhat fallacious and of very litt'.e diagnostic value, since the lungs tend ta swing up toward the back when the patient lies prone, even vjfien no fluid is present, and increase of resonance in the back with this change of position might, therefore, occur when the dulness was due to thickened pleura and not to tluid. 278 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. a very striking and at first surprising fact that a left-sided effusion displaces the heart far more than a right-sided effusion of the same size. Small or moderate right-sided effusions often do not displace the heart at all. With left-sided effusions, unless very small, we find the area of cardiac dulness shifted toward the right and often projecting be- yond the right edge of the sternum (see Fig. 134). (Inspection and palpation often give us even more valuable information on this lioint. See below, p. 281.) We must be careful to distinguish such an area of dulness at the right sternal margin from that which niay be prodiiced in right-sided effusions by the fluid itself (see above). As mentioned above, a right pleural effusion may very early show itself as an area of dulness along the right sternal margin. Light ijercussion will usually demonstrate that this dulness is con- tinuous with a narrow strip of flatness at the base of the axilla (ninth and tenth ribs). Such an effusion is late in creeping up the axilla. It api^ears first and disappears first along the right margin of the sternum. On tlie sound side the percussion resonance is often increased, owing to com2:)ensatory hypertrophy of the sound lung; the dia- phragm is pushed down and the borders of the heart or of the liver may l)e encroached iipon. When the hyper-resonance of the sound side is i)resent, it should warn us to percuss lightly over the effu- sion, else Ave may bring out the resonance of the distended hmg. Sum ma)-// of Percussion ,S!r/))s. — (1) Flatness corresponding roughly to the position of the fluid. (2) Tympany al)ove the level of tlie fluid over the condensed lung. (o) The level of the fluid is seldom quite horizontal. « (4) Shifting of the fluid with change of position is rare, slow, and has little or no importance in diagnosis. Exce2Jtions and PossUile Errors. — («) Great muscular pain and S])asm may produce an area of dulness which simulates that of pleural effusions, especially as the auscultatory signs may be equally misleading. A hypodermic of mori)hine will dispel the dubiess along with the pain if it is due to muscular cramp. DISEASES AFFECTING THE PLEURAL CAVITY. 279 (b) If the lung on the affected side fails to retract (owing to emphysema or adhesions to the chest wall), the area of dubiess and its intensity will be much dmiinished. ((') It must be remembered that dulness in Traube's space may be due to solidification of the lung, to tumors, or to overfilling of the stomach and intestine with food, as well as to j^leural effu- sion ; also that the size of the tympanitic sj^ace varies greatly in health. (d) Earely percussion may be tympanitic over an effusion at the left base owing to distention of the stomach or colon. (e) The diagnosis between fluid and thickened pleura will be considered later. Auscultation. The auscultatory phenomena vary greatly in different cases, and in the same case at different times, because the essential condi- tions are subject to similar variations. Whatever sounds are jjro- duced in the lungs or in the bronchi riiai/ he heard over the fluid un- less interfered with by inflammatory thickening of the costal xjl^ura. Fluid transmits sounds xvell, but there may be no breath sounds pro- duced and hence none audible over the fluid. Or tubular sounds only may be produced because only the bronchi remain open, the rest of the lung being collapsed. Or again, if rales or friction sounds are produced in the lung, they, too, may be transmitted to the fluid and may (alas I) deter the timid " observer " from tappmg. In about two-thirds of all large effusions no breathmg at all is audible over the area of flatness on percussion. In the remaming third, and especially in children, tubular breathing, sometimes feeble, sometimes very intense, is to be heard.. In moderate effusions there are often three zones in the back At the bottom we hear nothing, in the middle zone distant bron- chial or broncho-vesicular breathing, while at the summit of the chest the breathing is normal. The voice sounds corres^Dond When breath soinuls are absent, the voice sounds are likewise absent When the breathing is tubu- 280 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. lar, the voice, and especially the whisper, is also tubular and inten- sified. That is, wlienever the bronchi are open, the lung retracted, and the cJiest walls thin, the breathing, voice, and whisper ivill corre- spond to the tracheal and bronchial sounds. Since children have es- jDecially thin fchest walls, these bronchial sounds are esi^ecially fre- quent and intense in children.' Near the angle of the scapula and in a corresponding position in front, the sound of the spoken voice may have a peculiar high- pitched, nasal twang, to which the term ego phony is applied. This sign has no importance in diagnosis, since it is not constant, and not peculiar to fluid accumulations Hales are rarely produced in the retracted lung, and so are rarely to be heard over the fluid. All these sounds may be diminished or abolished if the costal pleura is greatly thickened The influence of cough upon the lung, and so upon the sounds produced in it and transmitted through the fluid, may be very great and very puzzling Eales may appear or disappear, breathing change in quality or intensity, and in the differential diagnosis of difficult cases the patient should always be made to cough and then breathe deeply before the examination is completed. In very large effusions, when only the primary bronchi are open, there may be signs like those of pulmona-'-y cavity at the site of the bronchi in front or behind (amphoric breathing, large metallic rales, etc.). Over the sound lung the breathing is exaggerated and extends unusually far down in the back and axilla, owing to hyper- trophy of the lung. The heart sounds may be absent at the apex owing to disloca- tion of the heart. In left-sided effusions the apex sounds are ofttn loudest near the ensiform cartilage or beyond the right margin of the sternum. Right-sided effusions liav'e much less effect ui)on the heart, Init occasionally we find the heart sounds loudest at the left of the nipple or in the axilla. Since many cases of ])leural effusion are due to tuberculosis, we 'Bacelh's theory — that the whispered voice is conducted through serum but not through pus — is not boi-ne out by facts. DISEASES AFFECTING THE PLEURAL CAVITY. 281 should iievt-r oiuit to search for evidences of this disease at the apex of the lung uu the soioid side, since experience has shown that phthisis is more a})t to begin here than on the side of the effusion. tSii iiniiiti-i/ of Auscaltdturij Sujns. (1) In most eases voice and breath sounds are alxsent or very- feeble over the area occupied by the fluid. (2) In a minority of the cases the breathing and voice sounds may be tubular and intensified, especially in children. (3) Over the condensed lung at the summit of the chest the breathing is bronchial or broncho- vesicular, according to the degree of condensation. If the amount of fluid is small, the layer of con- densed lung occupies the middle zone of the chest and the breath- ing is normal at the top of the chest. (4) Rales and friction sounds are rarely heard over fluid. (5) On the sound side the breathing is exaggerated. (6) The heart sounds may be absent at the apex and present in the left axilla or to the right of the sternum owing to dislocation. of the heart. Inspection and Palpation. The most important information given us by inspection and palpation relates to the displacement of various organs by the pres- sure of the accumulated fluid. In left-sided pleuritic effusions the heart is usually displaced considerably toward the right, even when the level of the fluid reaches no higher than the sixth rib in the nipple line. The apex impulse is to be seen and felt to the right of the sternum, somewhere between the third and the seventh rib, when a large amount of fluid is present. With smaller effusions one may find the apex beat lifting the sternum or close to its left border. The position of the heart may be confirmed by percussion. The spleen is scarcely ever displaced. Right-sided effusions are far less likely to displace the heart, and it is only Avhen a large amount of fluid is present tliat the apex of the heart is pushed outward beyond the nipple. INIoderate right- sided effusions often j)roduce no dislocation of the heart whatever. The liver is often considerably pushed down by a right-sided pleu- 282 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. ritic elf usion, and its edge may be palpable several inches below the costal margin. Its upper margin cannot be determined by percus- sion, as it merges into the flatness produced by the fluid accumula- tion above it. Tactile fremitus is almost invariably absent or greatly dimin- ished over the areas corresponding to the fluid ; just above the level of the fluid it is often increased. Occasionally a slight fulness of the affected side may be recog- nized by inspection, and the interspaces may be less readily visible than upon the sound side. Bulging of the interspaces I have never observed. When the accumulation of fluid is large the respiratory movements upon the affected side are somewhat diminished,' the shoulder is raised, and the spine curved toward the affected side. The diaphragm is depressed, and Litten's sign therefore absent. There are no reliable means for distinguishing purulent from serous effusions. The whispered voice may be transmitted through either pus or serum. But we know that in children two-thirds of all effusions are purulent, while in adults three-fourths of them are serous. Phijsical Si(jns During Ahsor^jtion of Fh'ural Effusions. When the fluid begins to disappear, either si)ontaneously or as a result of treatment, the dulness very gradually disappears and the lireath sovmds, voice sounds, and fremitus reappear. In case the heart has been dislocated, its return to its normal position is often much slower than one would anticipate, and indeed all the l)hysical signs are disappointingly slow to clear up even after tap- ping. Pleural frictioii appears when the roughened pleural surfaces, which have been held apart l)y the fluid, are allowed by the disap- pearance of the latter to come into apposition again. Owing to pul- monary atelectasis and permanent thickening of the pleura, con- siderable dulness often remains for weeks after the fluid has been absorbed. ' I have purposely made but little of the chauees in the shape of the chest produced by pleuritic effusions, as it has seemed to me that by far too much stress has usually been laid upon such signs. DISEASES AFFECTING THE PLEURAL CAVITY. 283 (r-) Pleural Thk'kexixg. In persons who have previously suffered from pleurisy with effusion, and in many who have never to their knowladge had any such trouble, a considerable thickening of the pleural membrane with adhesion of the costal and visceral layers may l)e manifested by the following signs : (1) Dulness on percussion, sometimes slight, sometimes marked. (2) Diminished vesicular respiration. (3) Diminished voice sounds and tactile fremitus. (4) Absence of Litten's jDhenomenon and diminution in the normal respiratory excursion of the chest. These signs are most apt to be found at the base of the lung behind and in the axilla. Occasionally a similar thickening may be demonstrated throughout the whole extent of the pleura, and the limg failing to expand, the chest may fall in as a result of atmos- pheric pressure (see Fig. 20). The ribs approximate and may overlajj, the spine becomes curved, the shoulder lowered, the scapula prominent, and the whole side shrunken. The heart may be drawn over toward the affected side. In the diagnosis of pleural thickenmg Rosenbach's "palpatory puncture " is sometimes our only resource. Under antiseptic pre- cautions a hollow needle is pushed between the ribs and into the pleural ca\'ity. As ihe needle forces its way through the tough fibrous, or perhaps calcified, pleura, the degree and kind of resist- ance are very enlightening. Again, the amount of mobility of the point after the chest wall has been pierced tells us whether the needle is free in a cavity, entangled in a nest of adhesions, or fixed in a solid " carnified " lung. There is no danger if the needle is sterile. Encapsulated Pleural Effusiox. Small accumulations of serum or pus may be walled off by ad- hesions so that the fluid does not gravitate to the lovv'est part of the pleural cavity or spread itself laterally as it would if free. 284 PHYSICAL DIAGNOSIS OF DISEASES. OF THE CHEST. Such localized eiiusions are most apt to be found in the lower axil- lary regions or behind — sometimes between th5 base of the lung and the diaphragm, and more rarely between the lobes of one of the lungs or higher up. I have twice seen an enca])sulated purulent effusion so close to the left margin of the heart that the diagnosis of pericardial effusion was made. The diagnosis of encapsulated pleural effusion is a difficult one and oftentimes cannot be made except by puncture. The signs are those of fluid in the pleura, but anomalously placed. Even punc- ture may fail to clear up the difficulty, since the needle may pass entirely through the pouch of fluid and into some structure behind so that no fluid is obtained. PuLSATixG Pleurisy (Empyema Necessitatis). Under conditions not altogether understood the movements transmitted l)y the heart to a pleural effusion (usually purulent) may be visible externally as a circumscriljed pulsating swelling near the precordial region, or as a diffuse undulation of a considerable portion of the chest wall. Sometimes this pulsation is visible be- cause the fluid has worked its way out through the thoracic wall and is covered only by the skin and subcutaneous tissues, but occa- sionally pulsation in a pleural effusion becomes visible, although no such perforation of the chest wall has occurred. The condition is a rare one, and is of importance only because it may be mistaken for an aneurism, from which, however, it should be readily distinguished by the al)sence of a palpable thrill or dias- tolic shock and by the evidence of fluid in the pleura. Differential Diagnosis of I'letkitic Effusiox. The following conditions are not infrequently mistaken for pleuritic effusion : (1) Croupous pneumonia with occlusion of the bronchi. (2) Pleural thickening, with pulmonary atelectasis. (3) Subdiaphragmatic abscess or abscess of the liver. In croupous ])neumonia with plugging of the bronchi one may DISEASES AFFECTING THE PLEURAL CAVITY. 285 have present all the ])liysical signs of pleuritic effusion cxrcpt dis- place/// cut '// f/ie /i(;'iijhho/-l//(j ()/•(/(( /IS. The presence or absence of such displacement, together Avith the history, symptoms, and course of the case, is therefore our mainstay in distinguishing the two diseases. From ordi/Ki/'ij croupous pucunionia (without occlusion of the bronchi") pleuritic effusion differs in that it produces a greater de- gree of dulness and a diminution of the spoken voice sounds and tactile fremitus. Bronchial breathmg and bronchial whisper may be heard either over solid lung or over fluid accumulation, although the bronchial sounds are usually feeble and distant in the latter condition. The displacement of the neighboring organs is of im- portance here as in all diagnoses in which pleuritic effusion is a possibility. In pleuritic effusion we can sometimes determine that the line marking the upper limit of dulness shifts with cliange of the patient's position. This is, of course, impossible in pneumo- nia. A few hard coughs may open tip an occluded bronchus and so clear up the diagnosis at once. In doubtful cases the patient should always be made to cough and breathe deeply before the examination is finished. It should always be remembered that one may have both pneu- monia and pleuritic effusion at the same time, and that pneumonia is often followed by a purulent effusion. In children the bronchi are especially prone to become occluded even as a result of a simple bronchitis, and we must then differentiate between atelectasis and efifusion — in the main by the use of the criteria just described. (2) It is sometimes almost impossible to distinguish small fluid accximulations in the pleural cavity from pleural thickening with puhnonary atelectasis. In both conditions one finds dulness, dimi- nution of the voice sounds, respiration, and tactile fremitus, and absence of Litten's phenomenon, but the tactile fremitus is usually more diminished when fliiid is present than in simple pleural thick- ening and atelectasis. An area of dulness which shifts with change of position points to pleuritic effusion. The presence of friction sounds over the suspected area speaks strongly in favor of pleural thickening, but it is possible to hear friction sounds over fluid, 286 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. probably because they are conducted from a point higher up in the chest at which no iiuid is present. In doubtful cases the diagnosis can and sliould be cleared up by j^unctiire. (3) In two cases I have known enlargement of the liver due to multiple abscesses to be mistaken for empyema. In both condi- tions, one finds in the right back dulness on percussion as high as mid-scapula, with absence of voice sounds, breath sounds, and fremitus. These conditions are due in one case to the presence of fluid between the lung and the chest wall, and in the other case to Fig. 137.— Area of Dulness in Solitary (tropical) Abscess of the Liver. the liver which pushes up the lung together with the diaphragm. ]5y physical signs alone I do not see how this diagnosis is possible, though Litten's sign may be of use, since the shadow is absent in empyema and sometimes present in moderate-sized subdia- l)hragmatic accumulations. Some of the symptoms, such as chills, sweating, and irregular fever, are common to both conditions. A careful consideration of the history and the associated signs and symptoms may help us to decide. Large solitary abscess of the liver, occurring as it almost in- varialjly does in the posterior portion of the right lobe, produces an area of flatness on percussion, which rises to a much higher level in DISEASES AFFECTING THE PLEURAL CAVITY. 287 the axilla and l)ack than in front or near the sternum (see Fig. 137), and may be in this way distinguished from empyema; but when the liver contains many small abscesses, as in suppurative cholangitis, this peculiar line of dulness is not present. (d) Rare diseases, such as cancer or hydatid of the lung, may be mistaken for pleuritic effusion. The history of the case and the results of exploratory puncture usually clear up the difficulty. CHAPTER XIV. ABSCESS, GAXGRENE, AND CANCER OF THE LUNG, PULMONARY ATELECTASIS, CEDEMA, AND HYPO- STATIC CONGESTION. Abscess and Gaxgrexe of the Luxg. I consider these two affections together because the physical signs, exclusive of the sputa, do not diifer materially in the two affections. In some cases there may be no physical signs at all, and the diagnosis is made from the character of sputa and from a knowledge of the etiology and symptomatology of the case. Li other cases we find nothing more than a patch of coarse rales or a small area of solidification, over Avhich distant bronchial breatliing, with increased voice sound and fremitus, may be appreciated. Rarely there may be slight dulness on percussion, but as a rule the area is not sufficiently large or sufficiently superficial to produce this. One may find the signs of cavity (amphoric breatliing, cracked-pot resonance, and gurgling rales), but this is unusual. Gangrene of the lung is not a common disease. The diagnosis usually rests altogether upon the smell and appearance of the sputa. In fetid bronchitis one may have sputa of equal foulness, but the odor is different. The finding of elastic tissue in the sputa proves the existence of something more than bronchitis. Pulmonary abscess, Avhich, like gangrene, is a rare aifection, is often simulated by the breaking of an empyema into the huig and the emptying of the pus through a bronchus. Large quantities of pus are expectorated in such a condition, and abscess of the lung is suggested, but tlie other physical signs are those of empyema and should be easily recognized as such. The finding oi elastic Jibres is the crucial point in tlu^. diagnosis of intrapulmonary abscess, ABSCESS, GANGRENE, AND CANCER OF THE LUNG. 289 whetlier due to tlie tubercle l)acillus or to otlier organisms. Tuber- culous abscess (cavity) is usually near the summit of the lung, and other varieties of abscess are near the base, but often there are no [thysical signs by which we can distinctly localize the })rocess. Maligxaxt Disease of the Luxg. In its earlier stages this affection is often mistaken f Pericardium, diseases of, 209, 219 Pericarditis, 209 adliesive, 32, 210 plastic, 209 with effusion, 212 Phthisis, 252 Pleural thickening, 283 Pleurisy, 271-284 encapsulated, 283 plastic, 271 pulsating, 284 with effusion, 273 Pneumonia, croupous, 237 inhalation, 244 Pneumohydrothorax, 208 Pneumothorax, 111, 200 Pulmonary abscess, 290 atelectasis, 104, 292 emphysema, 258 gangrene, 290 oedema, 293 regurgitation, 192 stenosis, 193 tubercidosis, 245 tympanites, 202 Pulmonic second sound, 120 Pulsation, abnormal, 48 Pulse, 49 capillary, 173 compressibility of, 52 Corrigan's, 172 dicrotic, 52 rate, 51 rhythm, 51 tension, 53 wave, size and shape of, 52 Rachitis, effects on the thorax, 7 Radioscopy, 227, 298 Rales, 103 bilateral, 2'PA crepitant, 105 dry, 104 moist, 104 musical, 106 palpable, 47 subcrepitant, 105 unilateral, 245 Resistance, sense of, 76 Resonance (see Percussion), 67 Respiration, amphoric, 98 asthmatic, 21, 97, 203 bronchial or tubular, 95 broncho-vesicular, 90 Cheyne-Stokes, 22 cogwheel, 98 diminished, 100, 279 em]3hysematous, 97 exaggerated, 99, 200, 279 metamorphosing, 98 normal, 08 restrained, 22 shallow, 23 stridulous, 23 types of, 92 vesicular, 93 Rhythm, cardiac, 123, 165 modifications of, 123, 165 respiratory, 21 Sphyg.mograph, 235 Stethoscope, choice of, 78 use of, 83 Succussiou, 111 Syphilis of the lung, 264 Tachycardia, 202 Tactile fremitits (see Premitus). 44 310 INDEX. Tension of the pulse, 53 Thrills. 43 in aneurism, 222 in aortic stenosis, 184 in congenital heart disease, 20G, 208 in mitral stenosis, 1G4 Tracheal tug, 223 Tracheitis, 233 Tricuspid regurgitation, 187 stenosis, 101 Tuberculosis, advanced, 249 incipient, 245 pulmonary, 244 Tumors, 15, 48, 221, 291, 293 Valve areas, 113 lesions, 151-197 Valvular disease, 141, 151-197 heart sounds, 117, 199, 202 Venous murmur, 139 pulsations, 35, 188 sound, 125 Ventricle, left, hypertrophy of, 147 right, hypertrophy of, 148 Ventricular septum, defects in, 207 Voice sounds, spoken, 110 whispered, 109, 238 1 COLUMBIA UNIVERSITY LIBRARIES This book is due on the date indicated below, or at the expiration of a definite period after the date of borrowing, as provided by the rules of the Library or by special ar- rangement with the Librarian in charge. DATE BORROWED DATE DUE DATE BORROWED DATE DUE JUL 2 5 19/ 2 C2e(l t40)MIOO o VV