COLLEGE OF OSTEOPATHIC PHYSICIANS AND SURGEONS LOS ANGELES, CALIFORNIA Radiograph of a Healthy Child's Chest. ^PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST BY RICHARD C. CBOT, M.D. x PHYSICIAN TO OUT-PATIENTS, MASSACHUSETTS GENERAL HOSPITAL ; ASSISTANT IN CLINICAL MEDICINE, HABVABD MEDICAL SCHOOL WITH ONE HUNDRED AND FORTY-TWO ILLUSTRATIONS NEW YORK WILLIAM WOOD 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 IN* EVIDENCE OF MY APPRECIATION OF THE EXAMPLE OF SINCERITY, COMMON SENSE, AND ENTHUSIASM ESTABLISHED BY HIM IN THE TEACHING AND THE PRACTICE OF MEDICINE 7 / 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 The correct books are too large ; the small books are out of date and repeat such well-worn myths as that the aortic second sound is normally louder than the pulmonic second, that aortic regurgitant murmurs are usually best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 adherent 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 permission 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 Rontyen Ray for permission to use two radiographs from that journal. ERRATA. 1. Page 35, line 7, for "expiration" read "inspiration". 2. Page 81, last line, first word, for "of" read "or". 3. Page 120, in the legend underneath Fig. 78, for "pulmonic" read "aortic". 4. Page 125, last line but one, for "found" read "sound". 5. Page 261, line 11, for "aphonic" read "aphonia". 6. Page 299, third paragraph, for "three" read "two". TABLE OF CONTENTS. PAGE INTRODUCTION, ............ 1 I. Methods of Examining the Thoracic Organs, ..... 1 II. Regional Anatomy of the Chest, 2 PAKT I. TECHNIQUE AND GENEEAL DIAGNOSIS. CHAPTER I. INSPECTION. I. SIZE, 5 II. SHAPE, 6 (a) The Rachitic Chest, 7 (b) The Paralytic Chest, 8 (c) The Barrel Chest, 9 III. DEFORMITIES, ........... 12 (a) Curvature of the Spine, . .12 (b) Flattening of One Side of the Chest, 14 (c) Prominence of One Side of the Chest, ..... 14 (d) Local Prominences, 15 IV. RESPIRATORY MOVEMENTS, ........ 16 (a) Normal Respiration, 16 (b) Anomalies of Expansion, 16 1. Diminished Expansion, 17 2. Increased Expansion, 18 (c) Dyspnoea, 18 V. THE RESPIRATORY RHYTHM, .21 (a) Asthmatic Breathing, . . . . ^ . . . .21 (b) Cheyne-Stokes Breathing, ....... 21 (c) Restrained Breathing, 22 (d) Shallow and Irregular Breathing, 22 (e) Stridulous Breathing, ........ 23 Viii TABLE OF CONTENTS. PAGE VI. DIAPHRAGMATIC MOVEMENTS (LitterTs Phenomenon), . . .23 VII. THE CARDIAC 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. ANEUIUSM AND OTHEK 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. (Edema 40 3. Pallor, . . 40 4. Jaundice, 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 Impulse 42 2. Thrills, 43 3. Tactile Fremitus, 44 4. Friction. Pleural or Pericardial, 4fc' 5. Palpable Rales .47 6. Tender Points, 48 7. Abnormal Pulsations ......... 48 8. Tumors 48 9. Temperature and Quality of the Skin. ..... 49 II. THE PULSE, 49 1. The Rate 51 2. Rhythm, 51 3. Compressibility, .......... 52 4. Size and Shape of Pulse Wave, 52 6. Tension, ........... 53 6. Size and Position of Artery. 55 7. Condition of Artery Walls, 55 TABLE OF CONTENTS. IX CHAPTER III. PERCUSSION. PAGE I. TECHNIQUE, ....... . . . .58 ^ Mediate Percussion, ......... 58 '' ( Immediate Percussion, ........ 58 (6) Auscultatory Percussion, ...... . 65 (c) Palpatory Percussion, ......... 67 II. PERCUSSION-RESONANCE OF THE NORMAL CHEST, . . . .67 (a) Vesicular Resonance, . . . . . . . .68 (b) Dulness and Flatness, ......... 68 (c) Tympanitic Resonance, ........ 70 (d) Cracked-pot Resonance, ........ 74 (e) Amphoric Resonance. ......... 75 (/) The Lung Reflex, ......... 76 III. SENSE OF RESISTANCE, ......... 76 CHAPTER IV. AUSCULTATION. 1. MEDIATE AND IMMEDIATE AUSCULTATION, . . 77 2. SELECTION OF A STETHOSCOPE, ........ 78 3. THE USE OF THE STETHOSCOPE, ........ 83 A. Selective Attention and What to Disregard, ... .84 B. Muscle Sounds, .......... 86 C. Other Sources of Error, ......... 88 4. AUSCULTATION OF THE LUNGS, ........ 91 I. Respiratory Types, ......... 92 (a) Vesicular Breathing, ........ 93 (b) Tubular Breathing, ...... . 95 (c) Broncho-vesicular Breathing, ...... 96 (d) Emphysematous Breathing, ....... 97 (e) Asthmatic Breathing ......... 97 (/) Cog-wheel Breathing, ........ 98 (g) Amphoric Breathing, ........ 98 (h) Metamorphosing Breathing, ....... 98 II. Differences between the Right and the Left Chest, . . .99 III. Pathological Modifications of Vesicular Breathing, . . .99 (a) Exaggerated Vesicular Breathing, . . . . . 99 (6) Diminished Vesicular Breathing. ..... 100 IV. Bronchial Breathing in Disease, ....... 102 PAGE V. Amphoric Breathing, 103 VI. Rales, .... 103 (a) Moist, 103 (b) Dry, 104 (c) Musical, 106 VII. Cough. Effects ou 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, . . . .111 (a) Succussion, . . . . . . . . . .111 (b) 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 (b) 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 (b) Weakening of Pulmonic Second Sound, . . . 121 (c) Accentuation of the Aortic Second Sound, . . .121 C/) Weakening of the Aortic Second Sound, . . . 121 (e) Accentuation of Both Second Sounds, . . . .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 (ei "Muffled "Heart Sounds, 124 4. SOUNDS AUDIBLE OVER THE PERIPHERAL VESSELS, .... 124 (a) Arterial Sounds, 124 (b) Venous Sounds, 125 TABLE OF CONTENTS. Xl CHAPTEK VI. (AUSCULTATION OF THE HEART CONTINUED.) CARDIAC MURMURS. PAGE I. TERMINOLOGY, 126 1. Mode of Production 126 2. Place of Murmurs in the Cardiac Cycle, 128 3. Point of Maximum Intensity, 129 4. Area of Transmission, ......... 130 5. Effects of Respiration, Exertion, and Position, .... 135 6. Intensity, Quality, and Length, 132-135 7. Relation to Heart Sounds,. 135 8. Metamorphosis of Murmurs, . 136 II. FUNCTIONAL MURMURS, ......... 136 III. CARDIO-RESPIRATORY MURMURS, ....... 138 IV. VENOUS MURMURS, 139 V. ARTERIAL MURMURS, . 140 PART II. DISEASES OF THE HEAKT. CHAPTER VII. VALVULAR LESIONS. 1. VALVULAR AND PARIETAL DISEASE, 141 2. THE ESTABLISHMENT AND FAILURE OF COMPENSATION, . . . 144 3. HYPERTROPHY AND DILATATION, 146 4. VALVULAR DISEASE, .......... 151 I. Mitral Regurgitation, 151 (a) Pre-compensatory Stage, 153 (b) Stage of Compensation 154 (c) Stage of Failing Compensation 158 (d) Differential Diagnosis 159 II. Mitral Stenosis, 161 1. First Stage, 163 2. Second Stage, 165 3. Third Stage, 166 4. Differential Diagnosis 167 III. Aortic Regurgitation, . 170 1. Inspection, .171 xii TABLE OF CONTENTS. PAGE (a) Arterial Jerking, . ....... 172 (6) Capillary Pulsation . . 17o 2. Palpation, 174 3. Percussion, 175 4. Auscultation, .......... 175 5. Summary and Differential Diagnosis, .... 178 6. Prognosis ... 179 7. Complications, ......... 179 IV. Aortic Stenosis 180 1. (a) The Murmur, 181 (6) The Pulse 183 (c) The Thrill 184 (d) Feeble Aortic Second Sound, 184 2. Differential Diagnosis, ........ 184 V. Tricuspid Regurgitation, ........ 187 1. (a) The Murmur, 188 (6) Venous Pulsation, 188 (c) Cardiac Dilatation, 189 (d) Feeble Pulmonic Second Sound 189 2. Differential Diagnosis, 190 VI. Tricuspid Stenosis, 191 VII. Pulmonary Regurgitation. . . . . . . . . 192 VIII. Pulmonary Stenosis, 193 IX. Combined Valvular Lesions 194 (a) Double Mitral Disease. ........ 195 (6) Aortic and Mitral Regurgitation 196 (c) Aortic Stenosis and Regurgitaiion. 197 CHAPTER VIII. PARIETAL DISEASE AND CARDIAC NEUROSES. I. ACUTE MYOCARDITIS, .......... 198 1 Acute Moycarditis 198 2. Chronic Myocarditis 199 3. Fatty Overgrowth 201 4. Fatty Degeneration. ......... 201 II. CARDIAC NECROSES, .......... 202 1. Tachycardia 202 2. Bradycardia 203 3. Arrhythmia, .......... 204 4. Palpitation 205 5. Congenital Heart Disease, 206 TABLE OF CONTENTS. xin 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 3. 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. HYDROPKRICARDIUM AND PNEUMOPERICAUI>IUM, ..... 219 CHAPTER X. THORACIC ANEURISM. 1. Abnormal Pulsation, 220 2. Tumor, 221 3. Thrill 222 4. Diastolic Shock, 222 5. Tracheal Tug, 223 6. Pressure Signs 224 7. Percussion Dulness, 224 8. Auscultation, 225 (a) Murmurs, 225 (6) Diastolic Shock Sound, 226 9. Radioscopy, 227 10. Summary 227 11. Diagnosis 229 PART III. DISEASES OF THE LUNGS AND PLEURA. CHAPTER XI. BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 1. TRACHEITIS, 233 2. BRONCHITIS, 233 xiv TABLE OF CONTENTS. PAGE (a) Physical Signs, 234 (6) Differential Diagnosis. ......... 235 3. CROUPOUS PNEUMONIA, .......... 237 (a) Inspection, 237 (6) Palpation 238 (c) Percussion, 238 (d) Auscultation, 239 (e) Summary, 242 (/) Differential Diagnosis, 242 4. BRONCHO-PNEUMONIA, .......... 244 5. POI.MONARY TUBERCULOSIS, ......... 245 (a) Incipient Tuberculosis, ........ 245 (6) Moderately Advanced Cases, 249 (c) Advanced Phthisis 252 (d) Anomalous Forms of Pulmonary Tuberculosis 256 CHAPTER XII. (DISEASES OF THE LUNGS, CONTINUED.) 1. EMPHYSEMA, 258 (a) Small-Lunged Emphysema, 258 (6) Large-Lunged Emphysema ........ 258 (c) Emphysema 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, 260 III. Pneumohydrothorax and Pneumopyothorax, 268 Differential Diagnosis of Pneumothorax and Pneumohydrothorax. . 270 IV. Pleurisy 271 1. Dry Pleurisy 271 TABLE OF CONTENTS. xv PACK 2. Pleuritic Effusion, 273 (a) Percussion, 273 (b) Auscultation 279 (c) Inspection and Palpation, ........ 281 3. Pleural Thickening, 283 4. Encapsulated Pleural Effusions, 283 5. Pulsating Pleurisy and EnipyemaNecessitatis, ..... 284 6. Differential Diagnosis of Pleural Effusions, 284 CHAPTER XIV. ABSCESS, GANGRENE AND CANCER OF THE LUNG, PULMONARY ATELECTASIS, (EDEMA 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 THE 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 thorough 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 within 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. REGIONAL ANATOMY OF THE CHEST. It seems to me a mistake to divide the chest into arbitrary por- tions and to describe physical signs Avith 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 ribs in the axilla," and so on. When we want to state more exactly what part of the axilla anteroposteriorly is affected, we may refer to the " mid-axillary line " (see Fig. 1) ; or better, we may place the lesion by measuring the number of centimetres cl- inches from the median line of the sternum. In a similar way the place of the apex 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 the nipple 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 we desire to study, it becomes unnecessary to memorize any technical terms or to learn the position of any arbi- trary lines and divisions such as are frequently forced upon the FIG. l.-The Mid-Axillary Line. INTRODUCTION. 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 physical diagnosis. I mean (a) 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. Liver. - - . I _ I Left ventricle. Lower lobe of left lung. ~ Stomach. 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 (6) the percussion outlines of the heart, liver, and spleen. These outlines do not correspond in size with the actual dimensions of the organs within, 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 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 behind the ribs and covered by the ^ f * Upper lobe. , Lower lobe. Spleen. Lower lobe. Upper lobe. Middle lobe. _ Liver FIG. 3. Position of the Left Lung from tbe Sides and of the Spleen. FIG. 4. Position of the Right Lung from the Side, and of the Liver. liver. The normal pancreas 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 chest, 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 moving 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 combina- 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 in 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 child's and the adult's chest in health. A child's trunk, as compared with FIG. 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 backward, although indi- vidual variations in this respect are considerable, as Woods Hutch- inson has shown. In childhood the commonest pathological modifications are due INSPECTION. I to rickets ; in middle and later life to emphysema, phthisis, or old pleuritic disease. (a) The Hachitic Chest. The sternum generally projects ("pigeon breast"}, but in some cases, especially when rickets is combined with adenoid hyper- 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 eiisi- 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 " Harrison's groove " (Figs. 11 and 12). The lower margin of the ribs 1 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 chondro-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- maker 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 rosary " has been given (see Fig. 13). (ft) The "Paralytic Thorax." Fig. 14 conveys a better idea of this form of chest than any description. The normal anteroposterior flattening 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 ensif orm 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 (Woods Hutchinson). (See Fig. 128, page 251.) (c) The "Barrel Chest." 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. Nutrition of the Chest 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 FIG. 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 produce a marked falling 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. (j is often seen in states of pro- found unconsciousness from any cause, such 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 accompanied by a peculiar nodding movement of the INSPECTION. 23 head, the chin being 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 aighing type as Avell as very shallow. (e) Stridulous Breathing. 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. DIAPHRAGMATIC MOVEMENTS. Litten's Phenomenon. 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 1 (see Fig. 24). The observer stands at the patient's side and asks him to take a full breath. As the ribs rise with 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. 1 If it is inconvenient to move the patient's bed into the proper position with 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 observer. The shadow is best seen near L. hysteria and in some very stupid persons who cannot be made to understand what 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 about two and a half inches; with very forced breathing three and a half inches. The mechanism of this phenomenon is best understood by imagin- ing a coronal section of the thorax as seen from the front or buck (see Fig. 25). At the end of expiration, the diaphragm lies flat against the thorax from its attachment up to about the sixth rib. During inspiration it "peels off" as it descends and allows the edge of the lung to come down into the chink between the dia- phragm and thorax. This "peeling off" of the diaphragm and the descent of the lung during inspiration give rise to the moving shadow above described. By thus observing the excursion of the diaphragm we can obtain a good deal of information of clinical value. INSPECTION. 25 In pneumonia of the lower lobe, pleuritic effusion, 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 adhesions 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 abolish 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. 25. Excursion of the Diaphragm during Forced Respiration. R, Ribs ; E, position of the diaphragm at end of expiration ; J, position of diaphragm at end of inspiration. sion of the shadow. In persons who 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 arrays, inasmuch as 26 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. it furnishes us with the means of observing the diaphragmatic movements, on the importance of which so much stress has been laid by F. H. Williams and others, much more easily and cheaply than with the ic-rays, and upon the left side, more plainly as well. It also frees us 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, we obtain a very fair idea of the respiratory capacity of the individual. VII. OBSERVATION OF THE CARDIAC MOVEMENTS. (1) The Normal Cardiac, 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. 1 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 maximum impulse in adults is usually in the fifth intercostal space just inside the nipple line. In chil- dren under 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 interspace. In adults it is occasionally absent even in perfect health and under certain pathological condi- tions to be later mentioned. (a) The position of the impulse varies to a certain extent ac- cording to the position of the body. If the patient lies upon 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. 26). A slight shift to the right can also be brought about by lying upon the right side, and, as a rule, the im- 1 For a more detailed description of the normal position of the cardiac impulse, see next page. INSPECTION. 27 pulse is. less visible in the recumbent 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. 2. Showing Amount of Shifting of the Apex Impulse with Change of Position. The in- ner dot represents the position of the impulse when the patient lies on his back ; the outer dot corresponds to the position of the apex with patient on left side. (i) Relation of the maximum cardiac impulse to the 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 heart in order to determine how far the organ extends to the left and downward, it will not do to be guided by the posi- tion of the maximum 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 thus determined cor- responds usually not with the moy'innim impulse, but with the point farthest out and farthest down at which any rise and full syn- chronous with the heart beat can be felt (for further discussion of this point see below, p. 213). (c) Besides the definite and localized impulse which has just INSPECTION. 29 been described, it is often possible to see that a considerable section of the chest wall in the precordial region is lifted " en masse. " The phenomenon is the " Herzenstoss " of the Germans, with which the ' : Spitzenstoss " or apex impulse is contrasted. A variable amount of " Herzenstoss " can be seen and felt over any normal heart when it is acting rapidly and forcibly, and in thin, nervous subjects or in children even when the heart is beating quietly. It is more marked in cardiac neuroses or in cases in which 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 impossible to localize any one point to which we 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. ((/) Character of the cardiac impulse. 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 show that the impulse has a heaving character or is of the nature of a short tap, a peristaltic wave, or a diffuse slap against the chest wall. In some cases a dis- tinct undulation can be seen passing from the apex region upward toward the base of the heart, or less often in the opposite direction. (2.) Displacement of the Cardiac Impulse. To one familiar with the position, 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 will consider first the commonest forms of dislocation of the apex impulse. (a) Displacement of the cardiac impulse due to hypertrophy and dilatation of the heart. By far the most common directions of dis- placement are toward the left axilla, or downward. 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 Hypertrophy, but here I may say that enlargements of the left ventricle tend espe- cially to displace the apex impulse downward, while enlargements of 30 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. the right ventricle are more commonly associated with displacement of the impulse toward the axilla. (ft) Next to hypertrophy and dilatation of the heart perhaps the commonest cause of dislocation of the cardiac impulse is pressure 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 nipple line. (c) Of nearly equal frequency is displacement of the heart due to pleuritic effusion or to pneumothorax. AYhen 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. Eight 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. (cT) I have mentioned causes tending to push the heart to the ri'/ltt, to the left, or upward. Occasionally the heart is pushed ) Pressure from below the diaphragm. (c) Air or fluid in one pleural cavity, especially the left. (d) Aneurism, mediastinal growths, and sagging of the aorta. (e) Fibroid phthisis. (/) Spinal curvatiire. (<7) Transposition of the heart or of all the viscera. (3) Apex Retraction. Before leaving the subject of the cardiac impulse it seems best to speak of those cases in which during systole we see a retraction of one or more interspaces at or near the point where the cardiac impulse normally appears. (a] In 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. (b) 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 back, may be drawn in as a result of adhesions between the pericardium and the chest wall, such as form in cases of adherent pericardium and fibrous medias- tinitis (see below, pages 216 and 295). (4) Epigastric Pulsation. In a considerable portion of healthy adults a piilsation 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, while, on the other hand, the heart is frequently found normal at autopsy in cases in vhich 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 Pulsations due to Uncovering of J'ortlons of the Jfi >/i'f Normally Covered \j the Linn/s. One of the commonest causes of visible pulsations in parts of the chest where normally none is to be seen is retract I on <>f the Ininj. (a) It is in chlorosis, perhaps, that we most frequently see such pulsations. In that disease, as in other' debilitated states, the lungs are often not adequately expanded owing to the superficiality of the respiration, and accordingly their margins do not cover as much of the surface of the heart as they do in healthy adults. This results in rendering visible, in the second, third, or fourth left interspace near the sternum, pulsations transmitted from the conus arteriosus or from the right ventricle. Less commonly, similar pul- sations may be seen on the right side of the sternum. (l>) A rarer cause of retraction of the lungs is fibroid phthisis or chronic interstitial pneumonia. In these diseases a very large INSPECTION. 33 area of pulsation may be seen in the precordial region owing to the entire uncovering of the heart by the retracted lung, even when the heart is not drawn out of its normal position. VIII. ANEURISM AND OTHER CAUSES OF ABNORMAL THORACIC PULSATION. So far I have spoken altogether of pulsations transmitted di- rectly to the thorax by the heart itself, but we have also to bear in FIG. ~'S. Position When Looking forSlight Aneurisinal Pulsation. mind that a dilated aorta may transmit to the chest wall pulsations which it is exceedingly important for us to recognize and properly to interpret. No disease is easier to recognize than aneurism when the groAvth has perforated the chest wall and appears as a tumor exter- nally, but it is much more important as well as much more difficult to recognize the disease w r hile it is confined within the thorax. In such cases, the movements transmitted from the aorta to the chest wall may be so slight that only the keenest and most thorough in- spection controlled by palpation will detect them. When slight pulsations are searched for, the patient should be put in a position 3 34 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. shown in Fig. 28, and the observer should place himself so that his eye is as nearly as possible on a level with the chest and looks across it so that he sees it in profile. In this position he can make out pulsations which are totally invisible if the patient sits facing the light. Pulsations due to aneurism are most apt to be seen in the first or second right interspace near the sternum, and not infrequently the clavicle and the adjacent parts may be seen to rise slightly with every beat of the heart, but in any part of the chest wall pulsa- tions due to an aneurism are occasionally to be seen, and should be looked for scrupulously Avhenever the symptoms of the case suggest the possibility of this disease (see below, p. 221). Pulsating Pleurisy. In cases of purulent pleurisy in which the pus has worked its way out betwen the ribs so that it is covered only by the skin and subcutaneous tissues, a pulsation transmitted from the heart may become visible, and the resemblance to the pulsation seen in aneu- rism may be confusing. Such pulsation is apt to be seen in the upper and front portions of the chest. Very rarely a pleuritic effu- sion which has not burrowed into the chest wall may transmit to the latter a wavy movement corresponding to the motions set up in the fluid by the cardiac contractions. IX. INSPECTION OF THE PERIPHERAL VESSELS. In a work dealing with diseases of the heart and lungs it is im- possible to avoid reference to vascular phenomena apparent in the neck or in the extremities, since such phenomena have a very direct bearing upon the interpretation of the conditions obtaining within the chest. Inspection plays a very large part in the study of these vascular phenomena. We should look for : () Venous phenomena. () Arterial phenomena. (c) Capillary phenomena. INSPECTION. 35 (a) Inspection of the Veins. 1. The condition of the veins of the neck is of considerable im- portance in the diagnosis of diseases of the heart and lungs. Where the tissues of the neck are more or less wasted the veins may be quite prominent even when no disease exists within the chest, and in such cases they may be more or less distended during each expi- ration, especially if dyspnoea or cough is present. If the veins are completely emptied during each expiration and on both sides of the neck, we can usually infer that there is an overdistention of the right side of the heart. When a similar phenomenon occurs on one side only, it may mean pressure upon one innominate vein. So far I have spoken of venous changes synchronous with respiration, but we may have also 2. A presystolic pulsation or undulation seen either in the ex- ternal jugular vein or in the bulbus jugularis between the two attachments of the stern oniastoid muscles. Such pulsation or undulation, which is to be seen just before each systole of the heart, is not necessarily anything abnormal and must be carefully distinguished from 3. Systolic venous pulsation, such as occurs in one of the most serious valvular diseases of the heart tricuspid re gurgitation. ' Systolic venous pulsation is more often seen upon the right side than upon the left side of the neck. There may be a wave during the systole of the auricle and another during the systole of the ven- tricle, the latter closely following the former. In any case in which a doubt arises whether a pulsation in the veins of the neck is due to tricuspid regurgitation, it is well to try the experiment of emptying the vein by stroking it from below upward. If it imme- diately fills from below, we may be practically certain that tricus- pid regurgitation is present. In the vast majority of cases of ve- nous pulsation due to other causes or occurring in healthy persons 1 A pulsating carotid may transmit an up-and-down motion to the veins overlying it. In such cases, if the veins be emptied by "milking" them up- ward, they will not refill from below. 36 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. a vein will not refill from below if emptied in the manner above described. 4. Rarely, superficial veins may be seen to pulsate in other parts of the body, especially in aortic regurgitation, and occasionally large and tortuous veins may be seen pulsating upon the chest wall, FIG. 29. Tortuous Veins on Chest and Abdomen. representing an attempt at collateral circulation when one or the other vena cava is compressed (Fig. 29). (&) Arterial Phenomena. 1. 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 throbbing of the carotids, more noticeable than INSPECTION. 37 that seen in health, occurs in many cases of aortic regurgitation and occasionally in simple hypertrophy of the heart without any valvular 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 whose 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 55) 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 the forearm. In rare cases inequalities produced in the arterial wall by deposition of lime salts may be visible as well as palpable. (c) Capillary 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 FIG. 31. Enlarged and Tortuous Brachial Artery (Arteriosclerosis) . each beat of the heart (in cases of aortic re gurgitation 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 peculiar to that disease, and occurs occasion- INSPECTION. 39 ally in health or in conditions associated with low tension in the peripheral arteries, as well as in any area of inflammatory hyper- semia (jumping toothache, throbbing felon, etc.). X. INSPECTION OF THE SKIX AND 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 well as of the mucous membranes. We should look for the follow- ing conditions : (1) Cyanosis. (2) (Edema. (3) Pallor. t (4) Jaundice. (o) 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, which 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 : (a) Valvular or parietal disease of the heart. (l>~) 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) (Edema. CEdema, or the accumulation of serous fluid in the subcutaneous spaces, is usually appreciated by palpation rather than by inspec- tion, but sometimes makes the face look very puffy, 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 usually to be found in the lower extremities and is appreciable rather by palpation than by inspection. If we are not familiar with 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 appearance of the skin Such impressions, however, may be false unless controlled by palpation, for simple obesity may produce very similar appearances. (3) Pallor. Pallor suggests, though it does not in any way prove, anaemia, and anaemia 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 conjunctive, is much more apt 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) Jaundice. The yellowish tint which appears in the skin, and especially in the conjunctivae. when the escape of bile from the liver is hindered, is sometimes to be seen in connection with unconipensated 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) Scars and Eruptions. 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. ENLARGED G LANDS. Routine 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 intrathoracic 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 pul- monary tuberculosis or of an enlargement of the bronchial and nie- diastinal glands. Again, malignant disease of the chest is some- times associated with the metastatic nodules over the clavicle, and a microscopic 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, which have never suppurated 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 syphilis. CHAPTER II. PALPATION AND THE STUDY OF THE PULSE. I PALPATION. THE most important points to be determined by palpation that is, by laying the hand upon the surface of the chest are : (1) The position and character of the apex beat of the heart. (2) The presence of a " thrill " (see below) . (3) The vibrations of the spoken voice ( u tactile Jreinitus"). (4) The presence of pleuritic or pericardial friction. Other less important data furnished by palpation will be men- tioned later. (1) The Afjex Seat. (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 we have learned by inspection. One learns, in the first place, whether the heart beat is regular 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 character of the cardiac movements. The power- ful heaving impulse 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. (b) 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 up-and-down movement. This point usually corresponds with the apex of the heart, as determined by percussion. It does not correspond with the maximum 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 Ave 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 reliable data that we have regarding the size of the heart. Percussion may be interfered with by the pres- ence of gas in 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. When 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 feeling imparted to the fingers by the throat of a purring cat is very much like the palpable " thrill " 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 in 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 always occurs intermittently, i.e., only during 44 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. a portion of the cardiac cycle, When felt in the apex region, it usually occurs just before the cardiac impulse ; this fact we express by calling it a "presystolic tin-ill"; but occasionally we may feel a systolic thrill at the apex one, that is, which accompanies the car- diac impulse. The word thrill 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, iising as little pressure as pos- sible. Firm pressure may prevent the occurrence of the vibrations which we desire to investigate. Of the thrills felt over the base of the heart, more will be said in Chapter VII. (3) Vibrations Communicated to the Chest Wall by 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 patient to count "one, two, three," or to repeat the words "ninety-nine " w r hile the palm of the hand is laid flat 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 women, 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 32 will help us to realize this The parts shaded darkest communicate to the fingers PALPATION AND THE STUDY OF THE PULSE. 45 the most marked fremitus, while in 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 walls when they speak. On the other hand, in emaciated patients or in those ivith 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 in 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 : () Diminution or absence of fremitus. (i) Increase or absence of fremitus. (a) If the lung is pushed 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, ab- sence where it is of considerable thickness. (//) Solidification of the lung due to phthisis or pneumonia is the commonest cause of an ///- FIG. 33. Showing Point (F) at Whk-b Pleunil . ,., ., --, Friction is Most often Heard. crease in tactile f remitus. ther details as to the variations in amount of fremitus in different diseases may be found in later chapters of this book. (4) friction, PImral or 7V/vV<7/v//W. In many cases of inflammatory roughening of the pleural sur- faces (" dry pleurisy ") a grating or rubbing of the two surfaces upon each other may be felt as Avell as heard during the movements of respiration, and especially at the end of inspiration. Such fric- tion is most often felt at the bottom of the axilla, on one side or PALPATION AND THE STUDY OF THE PULSE. 47 the other, where the diaphragmatic pleura is in close apposition with the costal layer (see Fig. 33, p. 46). Similarly, in roughening of the pericardia! surfaces ("dry" or " plastic " pericarditis) it is occasionally possible to feel a grating or rubbing 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. Showing Point (P) at Which Perieardial 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 sinmlated by the rubbing of the stethoscope upon the skin, but pal- pable friction is simulated by nothing else, unless occasionally by (5) Palpable Rales. 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 differ- 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 the 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. 35. 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 point. (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 was said above as to the commonest causes of such abnormal pulsations. When searching for slight, deep-seated pulsation (>.ulsus rants, parvus, tardus" is, therefore, a most constant and important point in diagnosis, but unfortunately it is to be felt in perfection only in the very 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 1 "Occasionally, as noted by W. H. Dickinson, there is a musical murmur of great intensity in the region of the apex, probably due to a slight regurgita- tion at high pressure through the mitral valve." OSLEK. 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 in 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 Thrill. 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- tinued 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 indistinct, " 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 Diagnosis. 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 : () Roughening, stiffness, fenestration, or slight congenital mal- formation of the aortic valves. (&) Roughening or diffuse dilatation of the arch of the aorta. (c) Aneurism of the aorta or innominate artery. (c?) Functional murmurs. (e) Pulmonary stenosis. (/) Open ductus arteriosus. (g} Mitral re gurgitation. VALVULAR LESIONS. 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 accentuation of the aortic second sound enables us, except in 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 re gurgitation, 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 dubiess on percussion and by its association with aortic regurgitation of long standing (see Fig. 100) . Roughening of the intima of the aorta (endaortitis) is always to be suspected in elderly patients with calcified and tortuous periph- 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 pulse 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 shows none of the characteristics of aortic stenosis. (d) Functional murmurs, sometimes known as "haemic," 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. largenient, by any palpable thrill, any diminution 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 usually on the left side of the sternum. In the rare cases in which this murmur is best heard in the aortic area it may be distinguished 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 pulse. (/) 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. (y) The systolic murmur of aortic stenosis may be heard loudly at the apex, and hence the lesion may be mistaken for mitral re gur- 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 uncomplicated, 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) when we have, in addition to the signs of aortic regurgitation, a systolic murmur and palpable thrill in the aortic area transmitted into the great vessels, a modification of the Corrigan pulse in the direction of the "pnh-us tardus, rn*. jun- 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 must be careful, however, to exclude a relative mitral insuffi- VALVULAR LESIONS. 187 ciency which, as has 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 much as aortic stenosis does. TRICUSPID REGURGITATIOX. Endocarditis affecting the tricuspid. valve is rare in post-fcetal 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 tricuspid dis- ease occur as a result of disease of the mitral valve and in the follow- ing manner : Hypertrophy of the right ventricle 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 regurgitatiou, 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 during life, and in all of them the valve was itself healthy but insufficient to close the dilated orifice. Gibson and some other writers believe that temporary tricuspid regurgitation is the commonest of all valve lesions, and results from weakening 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 pulmonary 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 regurgitatiou is recognized not as a relief but as a serious and probably fatal disaster. Physical S'ujns. (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) The Jfin'/nin: 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 up, but it is generally agreed that the tricuspid area is a large one, so that the murmur may be heard anywhere 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 pulsation in the external jugular veins and of the liver, which unfortunately is not always present, but which when present is pathognornonic. I have already explained (see p. 35) the distinc- tion between true systolic jugular pulsation, which is practically pathognonionic of tricuspid regurgitation, and simple presystolic undulation or distention of the same veins, which 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 l>elow, 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 eliminate these transmitted impulses one must be able to grasp the liver biinanually, 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 best 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 outline such as that shown in Fig. 108. The pulnionic 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. Differential Diagnosis. The statistics of the cases autopsied at the Massachusetts Gen- eral Hospital show that tricuspid regurgitation is less often recog- nized during life than any other val vular 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) Mitral Regvrgitation. 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 (a) 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). (&) Occasionally the two systolic murmurs are of different pitch or of different quality, and may be thus distinguished. (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 tricuspid 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 complicated by tricuspid regurgitation. (cT) In cases of doubt the phenomena 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 the pulmonic 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 Fro. 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 the cardiac cycle. TRICUSPID STENOSIS. 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 154 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. 1 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. Xarrow- 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 certain 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. PULMONARY REGURGITATIOX. Organic disease of the pulmonary valve is excessively rare in post-fostal life, but may occur as part of an acute ulcerative or septic endocarditis. A temporary functional regurgitation through the pulmonary valve may be brought about by any cause producing very lil'jJi ///v.w/r in the J>/>//H//>II-// artery. I have known two medical students with perfectly healthy hearts who 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 spaces and ceasing as soon as the breath was let out. Of the occur- rence of a murmur similarly produced under pathological condi- tions, especially in mitral stenosis, much has been written by Graham Steell. 1 Out of 87 cases collected from the post-mortem records of Guy's Hos- pital, 85, or 97 per cent, were associated with still more extensive mitral stenosis. VALVULAR LESIONS. 193 From the diastolic murmur of aortic regurgitation we 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 great vessels, and is never associated with a Corrigan pulse nor with capillary pulsa- tion. 1 The right ventricle is hypertrophied, the pulmonic second sound is sharply accented and followed immediately by the murmur. Evidences of septic embolism of the lungs are frequently. present and assist us in diagnosis. The regurgitation which may take place through the rigid cone of congenital pulmonary stenosis is not recognizable during life. PULMONAKY STENOSIS. 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 dyspnosa 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 (ft) Functional murmurs due to anaemia and debility or to severe muscular exertion, and possibly associated with a dilatation of the conus arteriosus. (!>} Uncovering of the couus arteriosus through lack of expan- sion of the lung. (c) Aortic stenosis. ((I) Mitral regurgitation. (e) Aneurism. (/) Roughening of the intima of the aortic arch. 1 By registering the variations of pressure in the tracheal column of air Gerhardt has shown graphically that a systolic pulsation of the pulmonary cap- illaries may occur in pulmonary regurgitation. With the stethoscope a sys- tolic whiff may be heard all over the lungs. 13 194 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. (a and &) 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 murmur of aortic stenosis is usually upon the right side of the sternum and is transmitted to the neck, whereas the murmur of pulmonary stenosis is never so transmitted and is not associated with characteristic changes in the pulse (see above, p. 183). (cT) The murmur of mitral reguryitation 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 pulmonary 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. (/) Koughening 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 LESIOXS. It is essential that the student should understand from the first that the number of murmurs audible in the precordia is no gauge for the number of valve lesions. We may have four distinct mur- 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 diastolic murmur 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 might be mitral stenosis and aortic stenosis as well, but since 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. () 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- 1st III I "'"' I I Illlllllllllh I Mil J FIG. 110. 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 present as well, whether it is possible to hear any regurgitant murmur or not (see Fig. 110). (>) 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 evidences of mitral stenosis and at another evidences of mitral re gurgitation alone. Either murmur may disappear altogether for a time and reappear subsequently. 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 Reyuryitation with jMitral Disease. The signs of mitral disease occurring in combination Avith aortic regurgitation do not differ essentially from those of pure Systolic murmur over dilated--' aortic arch. Maximum intensity and diastolic mur- ' m 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). The 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 Corrigan pulse is distinctly less sharp at the summit and rises and falls less abruptly. Capillary 1st 1st 2nd I 2nd FIG. 112. Showing 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 peripheral arteries is less often visible. (3) Aortic Reyurgitation ivith 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 re gurgitation 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- semia associated with it. " Cloudy swelling, " or granular degener- ation of the muscle fibres, is produced by relatively mild infections, while a general septicaemia due to pyogenic organisms may produce extensive fatty degeneration of the heart within a feAV days. The physical signs are those of cardiac weakness. 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. Irregularity and increasing rapidity are omi- nous signs which may be appreciated in the radial pulse, 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 obtained during life (although at autopsy it is not in- frequently found), 1 but in acute articular rheumatism an acute dila- tation of the heart appears to be a frequent complication, independ- 1 Henchen's recent monograph on this subject, "Ueber die acute Herzdila- tation bei acuten Infectionskrankheiten," Jena, 1899, does not seem to me convincing. PARIETAL DISEASE. 199 ent of the existence of any valvular disease. Attention has been especially called to this point by Lees and Boynton (British Med. Jour., July 2, 1898) and by S. West. IXFLUEXZA is also complicated not infrequently by acute cardiac dilatation. Chronic Myocarditis (" Weakened Heart "). Fatty or fibroid changes in the heart wall occurring in chronic disease are usually the result of sclerosis of the coronary arteries and imperfect nutrition of the myocardium, but chronic toxaemias, like pernicious anaemia, may also produce a very high grade of fatty degeneration of the heart and especially of the papillary muscles. Whether fatty or fibroid changes predominate, the physical signs are the same. Physical Signs of Chronic Myocarditis. For the recognition of these changes in the myocardium our present methods of physical examination are always unsatisfactory and often wholly inadequate. Extensive degenerations of the heart -wall are not infrequently found at autopsy when there has been no reason to suspect them during life. On the other hand, the autopsy often fails to substantiate a diagnosis of degeneration of the heart muscle, although all the physical signs traditionally associated with this condition were present during life. 1 To a con- siderable extent, therefore, our diagnosis of myocarditis must de- pend upon the history and symptoms of the case ; physical exami- nation can sometimes supplement these, sometimes not. Symptoms of cardiac weakness developing in a man past middle life, especially in a patient who shows evidences of arterio-sclerosis or high ar- terial tension, or who has suffered from the effects of alcohol and syphilis, suggest parietal disease of the heart, fatty or fibroid. The probability is increased if there have been attacks of angina pectoris, Cheyne-Stokes breathing, or of syncope. Inspection and palpation may reveal nothing abnormal, or there 1 A well-known Boston pathologist recently told me that he had neyer known a case of myocarditis correctly diagnosed during life. 200 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. may be an unusually diffuse, slapping cardiac impulse associated perhaps with a displacement of the apex beat to the left and down- ward. Marked irregularity of the heart beat, both in force and in rhythm, is sometimes demonstrable by these methods, and an in- crease in the area of cardiac dulness ma} 7 " be demonstrable in case dilatation has followed the weakening of the heart wall. Auscvlta- tion may reveal nothing abnormal except that the aortic second sound is unusually sharp; in some cases feeble ) Weakness and irregularity of the cardiac sounds, when due to nervous affection of the heart and unassociated with parietal or valvular 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 present, 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, hi 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 positively made. We sus- pect it under the conditions above described, but no greater cer- tainty can be attained. Fatty Degeneration. There are no physical signs by which fatty degeneration of the heart can be distinguished from other pathological changes which result in weakening 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 anaemia, 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 in the section on Myocar- ditis (see p. 198). CARDIAC XEUROSES. Tachycardia (Rapid 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. Temporarily 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 independent malady is Paroxysmal Tachycardia. As indicated in the name, the attacks of this disease are apt to begin and to cease suddenly. They may last a few 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 aphasia 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 (Slow 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. (ft) Toxaemia; 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 intracranial pressure, as in meningitis, cere- bral hemorrhage, depressed fracture of the skull. Possibly in this category belong the cases of bradycardia sometimes seen in epilep- tiforni or during syncopal attacks. Bradycardia from any one of these causes is apt to be of comparatively short duration. II Permanent Lradycardia is most often associated with coro- nary sclerosis and myocarditis. 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. Not infrequently many pulsations of the heart are not of sufficient force to transmit a wave to the radial artery, and the mistake should never be made of diagnosing bradycardia simply by counting the radial pulse. Arrhythmia. 1. Physiological Arrhyth mia. 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 during expiration. Any psychical disturb- ance or muscular exertion may produce irregularity as well as a quickening of the heart -beat. Rarely the pulse 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 "jiaradozica? pulse," 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 itself, patho- logical arrhythmia is most frequently seen in persons who have used tobacco or tea to excess, or in dyspepsia. In these conditions it is often combined with palpitation and becomes thereby very distress- ing to the patient. In connection with cardiac disease the follow- ing types of arrhythmia may be distinguished : () Paradoxical Pulse. Any cause which leads to weakening of the heart's action may occasionally be associated with paradoxical pulse. Fibrous pericarditis has been supposed to be frequently associated with this type of arrhythmia, but if so it is by no means its only cause. (6) The bigeminal pulse is seen most frequently in cases of un- conipensated 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 unusually 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 ("trireminal pi i he "). (c) Embryocardia, 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 fretal heart. Any case of uncompensated heart disease, whether valvular or parietal, may be associated with this disturbance of rhythm. (cT) The rjallop rhythm. Owing to a reduplication of one of the heart sounds (usually the second), AVC 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- tible to the indiridunl." The essential point is that the individual becomes conscious of each beat of his heart, whether or no the heart action is in any way abnormal. (rt) 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. (V) The effect of high altitudes, or of even a moderate eleva- tion (1,500 feet) is sufficient to produce in many healthy persons a quickening 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 heart shows nothing more than unusually loud and ringing heart sounds, but since palpitation is often associated with arrhythmia of one or another type we 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 symp- tom. CONGENITAL HEAET DISEASE. From, 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. Pulmonary 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. (1} 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, pulmo- 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 differential diagnosis of this lesion, see above, p. 193. 2. Defects in the Ventricular Septum. The loud systolic murmur produced by the rush of blood 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 palpable thrill. With almost every other form of congenital heart disease in which 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. (P"atency of the foramen ovale, if unassociated 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 kind.) 3. Persistence of the Ductus Arteriosus. The most characteristic sign is a loud, vibratory systolic mur- mur with its intensity at the base of the heart and unassociated u-ith hypertrophy of either ventricle. If complicated with stenosis at or close above the pubnonary valves, persistence of the ductus arte- riosus cannot be diagnosed, as the murmur produced by it cannot with certainty be distinguished from that of the pulmonary ste- nosis, and the presence 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 borne out by post-mortem evidence. The signs produced by 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, we may summarize the signs of the other lesions as follows : (ft) 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. (b) If there is no thrill and no hypertrophy, the lesion is prob- ably a defect in the ventricular septum. (c) If there is a thrill but no hypertrophy, the lesion is probably a patent ductus arteriosus. (d) If there is a thrill and hypertrophy of the right ventricle, the lesion is probably pulmonic stenosis, especially if the pulmonic second sound is feeble. CHAPTER IX. DISEASES OF THE PERICAKDIUM. I. PERICARDITIS. THREE forms are recognized clinically : (1) Plastic, dry, or fibrin ous 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 during 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 pneumonia 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 "pericardial friction " which is usually to be appreciated by auscultation alone, but may occasionally be felt as well. Characteristic pericardial friction is a rough, irregular, yrating or shuffling sound which oc- 14 210 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. curs irregularly and interruptedly during the larger part of each cardiac cycle. It is almost never accurately synchronous either with systole or diastole, but overlaps the cardiac sounds, and en- croaches upon the pauses in the heart cycle. It is seldom exactly the same in any two successive cardiac cycles and differs thereby from sounds produced within the heart itself. Pericardial friction seems very near to the ear and may often be increased by pressure J^J I Pericardial friction. FIG. 113. Showing Most Frequent Site of Audible Pericardial 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 ; bnt not infrequently it may be heard at the base of the heart or over the whole precordial region. The sounds are fainter if the patient 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 wall. 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 In rare cases the friction may occur only during systole or only during diastole. In such cases the diagnosis between pericardial and iutracardial sounds may be very difficult. DIFFERENTIAL DIAGNOSIS. (a) Plewo- Pericardial Friction. Fibrinous inflammation affecting that part of the pleura which overlaps the heart may give rise to sounds altogether indistinguish- able 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 in the pericardium, but in many cases the diagnosis cannot be made correctly. (&) Intmcardiac 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. When endocarditis and peri- carditis occur simultaneously, it may be very difficult to distinguish the two sets of sounds thus produced. The pericardial 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 EFFUSION*. Following the fibrin ous 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 signs 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. Physical Signs of Pericardial 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 percussion, which demonstrates an area of dulness more or less characteristic (see below). (2) By auscultation, which may reveal an unexpected feebleness in the heart sounds when compared with the power shown in the radial pulse. (3) By the signs and symptoms of pressure exerted by the peri- cardial effusion upon surrounding structures. Bulging of the precordia is occasionally to be seen in children ; DISEASES OF THE PERICARDIUM. 213 in adults we sometimes 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 points is the unusual ' extension of the percussion dulness a considerable distance to the left and beyond the cardiac impulse. (/;) Next to this, it is important to notice a change in the angle made by the junction of the horizontal line corresponding to the upper limit of hepatic dulness and the nearly perpendicular line corresponding to the right border of the heart. In health this Tympany, _ J Dulness, Cardiac impulse. Liver dulness. FIG. 114. Percussion Dulness in Pericardial Effusion, with Tympanitic Kcsonance 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. 1 In health the cardiac dulness extends about three-fourths of an inch be- yond the cardiac impulse, but in pericardial effusion the difference is greater. 214 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. The " pear-shaped " or triangular area of percussion clulness men- tioned by many writers has not been present in cases which have come under my observation. In large effusions 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 dulness may be modified by change in the patient's position. After marking out the area of percussion dulness with the patient in the upright position, let him lie upon his right side. The right border of the area of dulness will some- times move considerably farther to the right. A dilated heart can be made to shift in a similar way, but 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 forward. Unfortunately, it is only with moderate-sized effusions occur- ring in a pericardial sac free from adhesions to the surrounding parts that this shifting can be made out. Large effusions may not shift appreciably, 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 dulness 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 with a relatively normal condition of the radial pulse. In most diseases feeble heart sounds are associated with a weak pulse, but occasionally in pericardial effusion the p\ilse may be of good quality, although the heart sounds are heard with diffi- culty. Broncho-vesicular breathing with increased voice sounds may be heard over the tympanitic area below the left clavicle and occa- sionally between the scapulae behind. This is a result of compres- sion of the lung. (3) Pressure exerted by the pericardial exudation upon sur- DISEASES OF THE PERICARDIUM. 215 rounding structures may give rise to dyspnoea, 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 110 means peculiar to this condition and has no considerable diagnostic importance. (4) Inspection and palpation usually help us very little, but two points are occasionally demonstrable by these methods : () 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. (V) A progressive diminution of the intensity of the apex im- pulse until it may be altogether lost. If this change occurs while the patient is under observation, and especially if the apex impulse ri'tippears or becomes more distinct when the patient lies on the right side, it is of considerable diagnostic value. In conditions other than pericardial effusion, the apex impulse becomes less visible in the right-sided decubitus. Differential 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 without 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 are 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 by puncture. (2) I have twice known cases of encapsulated 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 DIAGNOSIS OF DISEASES OF THE CHEST. in this situation, viz., just outside the apex impulse in the left axilla. Such effusions may gravitate very 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 any 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 persons, or when the lung borders are adher- ent to the pericardium or to the chest wall. In the rheumatic attacks of children, it should be remembered that pericarditis is even more common than endocarditis. Adherent Pcr'n-i/ rii'nnn. 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. \Vlien this combination of peri- carditis with chronic mediastinitis is present, the diagnosis may be suggested by (a) 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). Such 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 in 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. (&) 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 writers, however, place no reliance upon it. (c) When the lungs are adherent to the pericardium or to the chest wall, as is not uncommonly the case, the absence of the phrenic phenomenon (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. (rf) 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 important point in favor of mediastino-pericarditis. In health and in valvular or parietal disease of the heart, the apex beat will sAving from one to tAvo inches to the left when the patient lies on his left side, and the descent of the diaphragm during full inspiration loAvers 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 mecliastinal adhesions. Such adhesions embarrass especially the right ven- tricle, because it is the right ventricle far more than the left which becomes attached to the chest wall. The left ventricle is more nearly free. 218 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. (/) Since the space enclosed by the divergent costal cartilage just below the ensiform is but loosely associated with the cen- tral tendon of the diaphragm, Broadbent looks especially at thr* FIG. 115. FIG. 116. FIGS. 115, 116. Adherent Pericardium, Ascites. point for evidence of mediastinal or pericardial adhesions, the effect of which is to arrest completely the slight respiratory move- ments of this part of the abdominal wall. (y) Adherent pericardium, occurring as a part of a widespread DISEASES OF THE PERICARDIUM. 219 chain of fibrous processes involving the pleura, the mediastinum, and the 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 11G show the appearance in cases of this kind in which the diagnosis was verified by autopsy. Summary. The diagnosis of adherent pericardium with chronic mediastini- tis is suggested by () Systolic retraction of the lower intercostal spaces in the left axilla and in the left back, followed by a diastolic rebound. (li) The absence of any change in the position of the apex im- pulse with respiration or change of position. (c) The presence of hypertrophy and dilatation of the right ventricle without obvious cause. ((Z) The absence of any respiratory excursion of the lung bor- ders near the heart and of the abdominal wall at the costal angle. (c) The presence of signs like those of hepatic cirrhosis in a young person and without any obvious cause. CHAPTER X. THORACIC ANEURISM. ANEURISM OF THE THORACIC AORTA. FOR clinical purposes thoracic aneurisms may be divided 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 eroding the thoracic bones. Practically any aneurism which 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 presence of aneurism. II. The evidences of its seat. Inspection and palpation give us most of the important informa- tion in the diagnosis of aneurism. The patient should be placed in the position shown in Fig. 117, so that the light will strike obliquely across the surface 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 pulsation may be made out either to the right of the sternum in front or in Abnormal the region of the left scapula behind. If the aneur- 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 pulsation at the sternal notch or in the THORACIC ANEURISM. 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 the 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 When Looking for Slight Aneurismal Pulsation. arch, it is likely sooner or later to erode the right margin of the sternum and the adjacent parts of the second or third costal car- tilages and appear externally as a round swelling in Tumor. wn j cn a S y S t o lic 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 by the beating 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 lamellated clot within it is so great that no pulsations are transmitted to the surface. "Whether the aneurism penetrates the chest or not, it is often possible to feel over it a ri/n-itfiitr/ t/t fill, usually sys- tolic in time. If the layer of lamellated clot in the sac is very thick, the thrill is less apt to be felt. More important in diagnosis is a ilitistnllr shock or tap which is appreciated by laying the palm of the hand lightly over the affected FIG. 118. Aneurismal Tumor (A). The arrow D points to a guumiatous swelling near the en- siform cartilage. The radiographic appearances of this case are shown below (Fig. 121). 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* 1 aneurism. As the wall of the sac becomes weaker, Shock, the 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 when felt in this situation. Of special importance in aneurism of the transverse arch is the sign known as the tmcheul tufj. The arch of the aorta runs over THORACIC ANEURISM. 223 the left primary bronchus in such a way that when the aorta is dilated, the bronchus is pressed upon with each expansile pulsation Tracheal f the 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 back his head so as to put the trachea upon a stretch. The physician then stands behind him and gently presses the tips of the fingers of both hands up under the lower border of the cri- FiG. IW.-Aneurism Tumor Perforating the Sternum at A. At B there is a gummatous mass. (See below. Fig. 121, a radiograph of this case). coid cartilage. In feeling thus for the tracheal tug as transmitted to the cricoid cartilage certain precautions must be observed : (a) One must distinguish the tracheal tug from a simple pulsa- tion transmitted to the superficial tissues by the vessels under- neath. Such pulsation makes the tissues move out and in rather than up and down. (1} A tracheal tug felt only during inspiration has no patho- logical significance and is frequently present in health. While preparing to try for the tracheal tug we may notice whether there is any dislocation of the trachea, as shown by the 224 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. displacement of Ad?.m's apple. Other and less important signs of aneurism, which are due to the pressure of the dilated aorta upon the nerves or vessels of the mediastinum, are : (1) Inequality of the pupils. (2) Inequality of the radial pulses. (3) (Edema and cyanosis of one arm or of one side of the neck and head. (4) Pain in one arm from the pressure of an aneurism involving the subclavian artery upon the brachial plexus. (5) Clubbing of the fingers of one hand (rare). (6) Prominence of one eye (rare). (7) Flushing or sweating of one side of the face (very rare). Contraction or dilatation of the pupil is due to an irritative or paralytic affection of the sympathetic nerves. This symptom is much commoner than the other effect cf pressure upon the sympa- thetic nerves ; namely, flushing or sweating of one side of the face. In comparing the pulses in the two radials we must bear in mind the possibility of a congenital difference between them, due to a difference either in the size of the arteries or in their position, and also that a tumor pressing on the subclavian may affect the pulse exactly as an aneurism. The pulse wave upon the affected side (most often the left) may be either less in volume or later in time than the wave in the other radial artery, according as the pulse wave is actually delayed in the aneurismal sac or merely diminished by it. In marked cases the pulse upon the affected side may be nearly or quite absent. On the other hand the inequality of the pulses may be so slight that the sphygmograph has to be employed to demonstrate differences in the shape of the wave not perceptible to the fingers. Examination of the heart itself may show some dislocation of the organ to the left and downward, owing to the direct pressure of the aneurismal sac. II. Percussion. If the aneurism is deep-seated, the results of percussion are negative. If, on the other hand, it be situated immediately be- 225 neath the sternum or close under the thoracic wall, an area of dul- ness, not present in the normal chest, may be mapped out. The outlines most commonly seen in such cases are shown in Fig. 120. \Yhen the aneurism involves the descending aorta, an area of dulness may be found in the region of the left scapula or below it, and pul- sation may be detected in the same area. III. Auscultation. The signs revealed by auscultation are not of much diagnostic value as a rule. In about one-half of the cases of sacculated aneu- Aneurismal dulness. _(\_ L - Heart dulness. FIG. 120. Diagram of Percussion Dulness in Aortic Aneurism. rism there are no sounds or murmurs to be heard over the tumor. In other cases a systolic murmur, the audible counterpart of the vibratile thrill, may be heard over the area of pulsation, tumor, or dulness corresponding to the aneurismal sac. This systolic mur- mur may be due to many causes other than aneurism, and has noth- ing characteristic about it. A similar systolic sound is sometimes heard over the trachea (Drummond's sign) or in the mouth, if the patient closes his lips around the pectoral extremity of the steth- oscope (Sansom's sign). A loud, low-pitched diastolic sound, corresponding to the pal- 15 226 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. pable diastolic shock, is generally to be heard in the aortic region. This diastolic sound, which is probably not produced by the aortic valves, is remarkably deep-toned and loud, and is, on the Avhole, the most important sign of aneurism revealed by auscultation. If a portion of either lung is directly pressed upon by the an- eurisnial sac, we may have the signs of condensation of the lung in the area pressed upon (slight dulness, broncho-vesicular breath- ing, and exaggerated voice sounds). If one of the primary bronchi From the front. From behind. FIG. 121. Radiograph of Case whose Photograph is Reproduced as Figs. 118 and 119. In the right-hand cut are shown the appearances seen from behind. The left-hand cut, A, A, aneurismal sac; B, heart displaced ; C. liver (not in focus). is pressed upon, as occasionally happens, atelectasis of the corre- sponding lung may be manifested by the usual signs (dulness, ab- sence of tactile fremitus and of respiratory and vocal sounds). Since aneurism is frequently associated with regurgitation at the aortic valve, a diastolic murmur is not infrequently to be heard. If the aneurismal sac is of very great size, the pulse wave in the femorals may be obliterated, as happened in a case described by Osier. THORACIC ANEURISM. 227 IV. Radioscopy. With the fluoroscope and through photography one can often make out a shadow corresponding to the position of the aneurism. Dilated aortic arch. Hypertrophied heart. FIG. 123. Aortic Regurgitation with Diffuse Dilatation of the Aortic Arch. Front view. The position of the shadow is best explained by reference to Figs 121, 122, and 123. Summary. The most important signs of aneurism are : 1. Abnormal pulsation visible or palpable 2. Tumor over which a 3. Thrill and a 228 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 4. Diastolic shock may be felt. 5. Tracheal tuy. 6. Pressure siyns (unequal pulses, pupils, hoarseness, pain, etc.)= 7. Dulness on percussion over the suspected area. 8. Loud, low-}; itched aort!<- si.-n,/id sound. 9. Systolic murmur (least important of all). Aneurismalsac. Heart displaced downward by the aneurism. FK;. 12}. Extensive Aortic Aneurism Displacing the Heart. 10. Radioscopy may demonstrate a shadow higher up than that corresponding to the heart and extending beyond that produced by the sternum, spinal column, and great vessels. Diagnosis of the S<-at of the Lesion. (a) Aneurism of the ascending arch generally approaches or penetrates the chest wall in the vicinity of the secoml r!!) "Cracked-pot resonance " on percussion. (c) Coarse, gurgling rales. (