degree of emphysema; crepitant râles at both bases, more marked on right side; vital capacity, 2600 cc. Heart: slight enlargement both to right and left with definite enlargement of right auricle (transverse diameter, M.L. 8.5 cm., M.R. 4.5 cm.); sounds of good quality, unaccompanied by murmurs; rhythm, irregular; rate, 60; blood pressure, 105-62. Moderate thickening of peripheral vessels. Abdomen: tenderness in epigastrium; enlargement of liver. Renal function: urine normal; phthalein, 32 per cent for two hours. Blood, cytology and Wassermann reaction negative. The patient had received digitalis from both the dispensary and her home physician, but the amount taken could not be accurately estimated.

The first electrocardiogram showed auricular flutter, auricular rate of 261; ventricular rate, 58. Vagus pressure in the neck was without influence. Exercise tolerance was very poor; she was unable to walk up one flight of stairs because of extreme dyspnea. No change in either auricular or ventricular rate resulted from the effort.

Quinidine sulphate to the point of toxicity, lowered the auricular rate but the flutter could not be broken. After leaving the hospital she took 20 grains of powdered digitalis. Examination on July 5 showed the cardiac mechanism to be unchanged. The day following that observation she experienced severe epigastric pain, weakness, orthopnea and swelling of the legs. When seen two weeks later, she had taken 30 grains of powdered digitalis and a small quantity of tinctur. At this time, color of the skin was bette, there was less cyanosis. The moisture in the chest had diminished, but was still present; vital capacity, 1500 cc., she said that the effort of blowing made her dizzy. A soft low-pitched diastolic murmur was heard at the apex of the heart. The pulse rate was 68. Blood pressure, 120-66. The electrocardiogram showed normal mechanism. This patient is still under observation. Her symptoms have persisted and at almost every examination there has been some sign of myocardial insufficiency (congestion of lungs or liver). The cardiac mechanism has continued normal.

Case 13. Male. Storekeeper. Age fiftyfive. On August 15, 1922, this patient came to Dr. L. L. Schwartz because of an acute exacerbation of a chronic dermatitis on the right leg. He had worked in a coal mine for twenty-six years but for the past eighteen years kept a small store. There had never been any cardiac symptoms until three days before his admission to the hospital, when he suddenly became very short of breath and said that deep breathing caused pain in the lower right chest. The first night he was obliged to sit up in a chair, but the dyspnea rapidly subsided and two nights later he rested with a single pillow. There was no palpitation. The past history was negative.

Examination. A large well developed man; muscular tone poor; body weight 148 pounds. Deep cyanosis of lips, oral mucosae, nose and fingers. No edema. Over the lower third of the right leg was a red brawny indurated area and the entire leg and thigh showed remnants of vesicle formation. The lungs showed a moderate grade of emphysema; the vital capacity was 2700 cc.; a few crepitant râles were present at the base of the right lung. Heart: not enlarged; sounds of good quality, without murmurs or accentuations. During the first examination there was noted a regular tachycardia, rate 152, which was not influenced by posture, breathing, exercise or vagal pressure; later in the day the heart rate was 96 and irregular; rates between 75 and 100 had been recorded by nurses and irregularity of pulse noted. Blood pressure, 130-90. The X-ray examination of the heart showed slight enlargement; the transverse diameter was 14.2 cm.; the right auricle was enlarged and the curve of the left distinctly exaggerated; the presence of flutter was recognized during the fluoroscopic examination. The electrocardiogram showed flutter, auricular rate 304, ventricular, 152. The pupils reacted rather poorly to light, but otherwise the neurological findings were normal. The blood was normal and the Wassermann reaction negative. Renal function good.

Quinidine was used both before and after digitalis; greater lowering of auricular rate was obtained by quinidine following

digitalis, but flutter continued. After 64 cc. of tincture of digitalis fibrillation occurred, to be followed after two days by normal rhythm.

Just before the conversion to fibrillation the blood pressure was 116-66 and the vital capacity had risen to 3500 cc. On the first day of normal rhythm the blood pressure was 144-76 and the vital capacity was 3850. No cardiac murmurs appeared. The cyanosis decreased. This patient has not been examined for one year but writes that he is working and has had no return of the symptoms for which he came to the hospital.

Case 14. Physician. Age sixty-seven. This patient was first seen on April 9, 1923. He complained of abdominal pain and vomiting which had followed an accident in November, 1922, when he was struck by an automobile. There had been a head injury and he was mentally confused. The heart appeared to be slightly enlarged; no murmurs were heard; the rhythm was irregular; apex rate 86 (at rest in bed); blood pressure 120-70; the radial and temporal vessels were thickened. There was slight cyanosis of lips and oral mucosae; crepitant râles were heard at the bases of the lungs and there was slight edema of the ankles. An electrocardiogram showed auricular flutter; the ventricular rate was 148, irregular 2:1-3:1 response; respiratory movements were indicated in the curve; during quiet breathing the auricular rate was 324, during inspiration, 335. Three days later the mechanism was normal. Before coming to the hospital a small amount of digitalis had been taken. No medication was given and the signs of congestion had disappeared before the normal rhythm was recorded.

In September, 1923, the patient returned to the hospital because of the persistent abdominal symptoms. The heart was not enlarged (transverse diameter, 11 cm.) and the aorta was normal; no murmurs were heard; the mechanism was normal; blood pressure, 104-75. There were no signs of myocardial insufficiency. The vital capacity of the lungs was 5100 cc. A gastro-enterostomy to relieve duodenal obstruction was performed, from which he recovered promptly.

Case 15. Female. Cook. Age thirtynine. Admitted November 8, 1923, complaining of shortness of breath, spitting of blood and swelling of legs. Expectoration of bright red blood began five days before admission. The patient had inflammatory rheumatism when a small child but could not give the age. She had been unable to work for the past eighteen months because of rheumatism, shortness of breath and intermittent edema of legs.

The diagnosis made was mitral stenosis, subacute bacterial endocarditis (an hemolytic streptococcus in blood stream), nephritis. The heart was enlarged, left border at anterior axillary line, and there was advanced myocardial failure. Physical signs indicated infarction in lower lobe of right lung. Signs of phlebitis of the right subclavian or right axillary vein appeared on the second day. There was no improvement and death occurred nine days after admission.

The patient had taken digitalis before coming to the hospital but the amount could not be estimated. The pulse rate recorded by the house officer on admission was 100 and regular; the charted rates for that afternoon were 100 and 108. Between the hours of 3:30 p.m. on November 8 and 10:00 a.m. of the next morning 22.5 cc. of tincture of digitalis were given. At 4:00 p.m. the nurse's record for the pulse rate was 144. On November 10 while sitting up eating lunch the apex rate was 130 and regular; leaning on back-rest, long periods of coupled rhythm occurred (personal observation). On November 12, the apex beat was regular, rate 158; an electrocardiogram showed auricular flutter, auricular rate 320, ventricular, 159. It is not possible to say whether flutter was present on admission or was produced by digitalis given, but it is remarkable that after flutter was recognized a 2:1 response was maintained throughout the period of observation (compare case 4). The reactions to quinidine have been given in table 3.

Case 16. Male. Age fifty-three. This patient developed exophthalmic goiter twenty-two years ago. He has suffered from nervousness, palpitation and tachycardia but his general condition has been

fair and continued his work as a tile setter until six weeks before admission to the hospital (November 28, 1923) when he began to have cardiac pain on exertion.

Examination. A poorly developed and poorly nourished man. Body weight, 120; usual weight, 140. There was marked exophthalmos; the pupils were dilated; reaction to light and accommodation normal. The heart was slightly enlarged. Systolic murmurs were heard at base and apex and over the latter, a late diastolic murmur without presystolic accentuation; at the base, the second sound was split and the aortic second was tympanitic. Rhythm grossly irregular. Blood pressure, 116-54. Vessels moderately thickened. X-ray examination showed moderate enlargement, transverse diameter, M.R. 5. cm., M.L. 8.5 cm.; diameter of aortic shadow in transverse position, 6.1 cm. The signs of myocardial insufficiency were cyanosis, slight edema and moisture at base of right lung. The reflexes were sluggish and the right epitrochlear gland was palpable. The Wassermann reaction was negative. The vital capacity of the lungs was 2700 cc. The basal metabolic rate was 25 per cent above normal. The first electrocardiogram showed auricular flutter, auricular rate 291, ventricular 105; there were frequent aberrant ventricular beats. Immediately following exercise (walking rapidly), the rate was 290-100. Vagal pressure was without effect.

The next morning, fibrillation was present, rate 435-118. Quinidine sulphate 0.8 gram was given at 10:05 a.m. At 12:35 p.m., pure flutter, was recorded, rate, 246-82, 2:1-4:1 response; 1:05 p.m., 238-112. 1:35 p.m., normal mechanism, rate 93; P-R, 0.20 sec. Blood pressure 104-58. The following morning the rhythm was normal save for occasional periods of "coupling" due to premature auricular beats. The blood pressure was the same and there was no improvement in vital capacity. That afternoon the patient developed hysterical amaurosis (urine obtained that evening showed absence of quinidine when tested with Mayer's reagent). Two days later the pulse rate was 128 and grossly irregular. No further studies were made.

Case 17. Male. Age forty-seven. This patient complained of rapid beating of his heart on exertion, or with excitement; he said that at times there was a continuous tremor about the heart. If he continued his exertion he became faint and slightly dizzy; this disappeared after resting for a few minutes. These symptoms had been present for about six weeks; the onset could not be accurately dated. Seventeen years ago he had a similar attack which lasted for about one month. The past history has no bearing on the present symptoms. He is a traveling salesman whose work involves much walking and the carrying of a 40 pound case.

Examination. Heart not enlarged to percussion; no murmurs; aortic second sound accentuated and tympanitic; rate 144 with occasional dropped beats. X-ray examination showed enlargement of right auricle and a widened aorta of increased density. Flutter was easily recognized in the movements of the right auricle. There was slight congestion at bases of lungs.

The electrocardiogram showed flutter, A-288, V-144. Vagal stimulation caused an increase in auricular rate and a fall in ventricular; both phases were proportional to the degree of stimulation. Following exercise (hopping on one foot) there was slight rise in auricular rate and a marked increase in ventricular, to approximately 260, which continued for thirty-eight seconds, after which 2:1 response returned (fig. 3). The rhythm became normal about four and one-half hours after the administration of 0.8 gram of quinidine. Certain comparative figures are tabulated:

(1) RITCHIE, W. T.: Auricular flutter. Edinburgh and London, 1914.

(2) BLACKFORD AND WILLIUS: Auricular flutter. Arch. Int. Med., 1918, xxi, 147.

(3) KEATING, J. H., AND HAJEK, J.: Auricular flutter with report of cases. Amer. Jour. Med. Sci., 1922, clxiv, 656.

(4) WEDD, A. M.: Notes on the action of certain drugs in clinical flutter. Heart, 1924, xi, 87.

(5) HOLMES, G. W., AND WHITE, P. D.: Auricular flutter detected by the fluoroscope. Jour. Amer. Med. Assoc., 1917, lxviii, 844.

(6) WIGGERS, C. J.: The nature of muscular contraction in auricular fibrillation and flutter. Amer. Jour. Physiol., 1922, lxii, 310.

(7) DE BOER, S.: On fibrillation of the heart. Jour. Physiol., 1921, liv, 400. (8) LEWIS, T., AND OTHERS: Series of papers on fibrillation and flutter in Heart, vii and viii.

(9) ROTHBERGER, C. J.: Neue Theorien über Flimmern und Flattern. Klinische Wochenschrift, 1922, no. 2, 82. (10) MEAKINS, J.: Auricular flutter and its treatment. Can. Med. Assoc. Jour., 1919, ix, 7, 606.

(11) COWAN AND RITCHIE: Diseases of the heart. London, 1922, 156.

(12) KORNS, H. M.: An experimental and clinical study of quinidine sulphate. Arch. Int. Med., 1923, xxxi, 36. (13) HEARD, J. D., AND STRAUSS, A. E.: Auricular flutter. Arch. Int. Med.,

1917, xx, 409.

(14) LEWIS, T., DRURY, A. N., AND ILIESCU, C. C.: Some observations upon atropine and strophanthin. Heart, 1921, ix, 21.

(15) LEWIS, T.: The law of cardiac muscle. Quart. Jour. Med., 1921, xlvi, 339. (16) Rothberger and WintERBERG: Über Vorhofflimmern und Vorhofflattern. Pflüger's Archiv f. d. ges. Physiologie, 1915, clx, 42.

(17) LEWIS, T.: The action of digitalis in case of auricular fibrillation and flutter. Amer. Jour. Med. Sci., 1922, clxiv, 157.

(18) LEWIS, T., DRURY, A. N., WEDD, A. M.,

AND ILIESCU, C. C.: Observations upon the action of certain drugs upon fibrillation of the auricles. Heart, 1922, ix, 207.

(19) BRODY, J. G.: The effect of quinidine on striped muscle. Jour. Amer. Med. Assoc., 1922, lxxix, 354.

(20) GALLAVARDIN AND GRAVIER: La quinidine dans l'auricular flutter. Lyon Medical, March 10, 1923.

(21) WOLFERTH, C. C.: The present status of quinidine therapy. Ann. Clin. Med., 1923, ii, 123.

(22) ORR, J.: Brit. Med. Jour., 1921, ii, 576.