the hand in exophthalmic goiter or in paralysis agitans.

According to Mackenzie, fibrillation of the auricles is found in from 60 to 70 per cent. of all cases of heart failure. I do not believe it is so common in this country. In 100 cases of heart failure of which I have graphic records, I found only thirty-five of fibrillation. That fibrillation of the auricles is a distinct clinical entity, there is no doubt. The recognition of this form of arhythmia is of more importance than the pathological lesion associated with it, not only from the fact that the heart failure

The symptomatology is quite characteristic. The diagnosis can be made in the vast majority of cases from the arterial pulse alone, which is usually fast, 80 to 170, and completely irregular. There are seldom any two pulse beats the same distance apart. Such a marked disorder of rhythm is not closely simulated by any other form of arhythmia. The explanation for the irregular pulse as given by Lewis is that there are multiple foci of impulse formation in the auricle and these impulses are showered in a haphazard manner on the bundle of His and carried to the ventricle. An example of this

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may be, and usually is, the result of disturbed. rhythm, but particularly because the rhythm can be influenced by drugs while the pathological lesion usually cannot.

Just why an auricle that is contracting rhythmically should suddenly cease to contract, and all fibers assume the state of fibrillary contraction, is not known. The assumption is that "the auricle is the seat of an electric disturbance of a peculiar yet distinct nature" (Lewis). It is certainly closely allied to auricular extrasystoles, paroxysmal tachycardia and auricular flutter. Its frequency in cases of mitral stenosis

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form of arhythmia is shown in Figure 11. As a result of this rapid and irregular contraction of the ventricle, there may be loss of tonicity and dilatation. The most important symptom is shortness of breath on exertion, which is usually present if the pulse rate is above 80 or 90. The usual picture of heart disease with dropsy and a swollen liver is absent, unless the heart becomes dilated. With the onset of fibrillation in mitral stenosis, the presystolic murmur, due to auricular systole, disappears, as the auricle does not contract, and is replaced by a diastolic decrescendo murmur.

would suggest irritability of the wall of the auricle on account of the increased intraauricular pressure as a possible factor. This form of arhythmia is extremely rare under 12 years of age. It sometimes occurs from overdosage of digitalis, which is especially true in cases of auricular flutter, but as a rule, when the drug is stopped, the rhythm becomes normal.

The valvular lesion most often associated with fibrillation is mitral stenosis, but cardiosclerosis in the aged has been equally as common a condition in the cases that I have seen. There is, however, no distinctive pathology. Sometimes a careful microscopical examination of the heart fails to reveal anything abnormal.

The onset of fibrillation is usually sudden, and, as a rule, persists throughout an individual's life. A few cases of paroxysmal fibrillation have been reported, but I have never seen any. The disturbance of rhythm lessens the efficiency of the heart in probably all cases. The duration of life in patients affected by it is from a few months to a few years.

It is in this form of heart failure that the best results can be obtained from the drugs of the digitalis group. In many of these cases there is no loss of tonicity or dilatation, the lessened cardiac efficiency being due solely to the rapid and irregular contraction of the ventricle. It is in this type of heart disease that digitalis causes a marked reduction of the pulse rate, while in

other forms of heart failure, with a regular pulse, the rate is influenced very little or not at all. In fibrillation cases it is usually safe to push the digitalis until it slows the pulse, unless the patient has fever.

There is much controversy over the best preparation of digitalis to use. Mackenzie, who isolated this group of heart cases as being the ones in which digitalis acts as a specific, always uses the tincture and says where it fails he has never seen results from any other preparation. Whichever preparation is used, it should be given until symptoms of its action appear, which are usually slow pulse, headache and vomiting, in the order named. Some patients require four times as much of the same preparation as others. One patient may respond in four days to one-half teaspoonful of the tincture three times a day, while another may take the same amount out of the same bottle for two or three weeks before any symptom of its action can be noticed. As a rule, digitalis or one of its allies has to be taken more or less continuously in order to keep the pulse rate at 80 or less. If quick results are desired, strophanthin may be given intravenously. I have used it in eighteen cases of fibrillation with excellent results in all, except one patient who had fever. When the pulse is rapid, 100 of a grain of strophanthin intravenously will usually reduce the rate one-third within one hour. One such dose every four to seven days is usually sufficient. In some patients it has to be repeated every day or two. The action of strophanthin is the same as digitalis. It is easily administered, practically painless and in over 300 injections that I have given there have been no bad results.

922 Rialto Building.

RESPIRATORY DISTURBANCES IN HEART DISEASE *

GEORGE HOWARD HOXIE, A.M., M.D. KANSAS CITY, MO.

My attention was drawn to this subject by a case in my practice, of which the following is an outline of the history.

C. R., male, aged 49, accustomed to vigorous life although engaged in wholesale merchandizing, seen first March 25, 1913, because of an attack of asthma. He had been troubled for many weeks with a "rasping in his lungs." He stated that he had been subject to bronchitis and pleurisy. Aside from his statement that he had palpitation of the heart and that his right ear "roared," his history was unimportant. Examination showed a bounding pulse of 80; temperature 98; blood-pressure 170. systolic, and 40 or

*Read in the General Session of the Missouri State Medical Association, at the Fifty-Seventh Annual Meeting held at Joplin, May 12-14, 1914.

less diastolic. No normal valve-closure sounds were heard anywhere over the chest but were replaced by high-pitched musical notes. The apex beat was heaving and outside the nipple line. The right margin of the heart dulness was to the right of the right margin of the sternum. The lungs were filled with rhonchi and whistling râles. The Karrell treatment without drugs freed him of his distress. On the 27th his bloodpressure was 150 and 40, the pulse still 80. He was able to leave the house in a few days and on April 7 came to my office where his blood-pressure was 170 (systolic) and 10 (diastolic), his pulse 72. At that time the systolic sound over the sternum consisted of a dull rumble accompanied by a musical bruit while the diastolic sound was short and of better quality. He felt well. He left the city in a few days and spent the summer at a suburban lake living in a shack, doing much of his own work and free from much discomfort.

In the fall he went to Los Angeles and while there fell sick with heart trouble. He was put into a hospital and was told of his approaching end, the diagnosis being aneurysm. But he insisted on being brought home and reached Kansas City Nov. 6, 1913, in very fair condition. The nurse who brought him reported that the pulse had varied from 52 to 110, and that he expectorated blood every night-the amount of frothy blood sputum being about 2 ounces a night. His symptoms were best controlled by morphin, 1/16 grain, hypodermatically administered. His physician had been administering strophanthus, 4 drops of the tincture every four to six hours. He was greatly emaciated, very weak, and had a bedsore in his left hip. I found his pulse about 92, his blood-pressure 160 systolic, and 50 diastolic, and his temperature ranging from 97.5 to 98.4, respiration 18-24. urine (on the 7th) showed no albumin but some granular casts, acidity 50-60, sp. gr. 1023, phosphates heavy.

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The chest examination showed general emphysematous enlargement with the consequent lack of dull areas. The breath sounds were rough and prolonged, and along the base of the right lung were many pleuritic râles. The heart sounds were replaced at all orifices by dull murmurs and were of the same general character as six months before. Examination of the sputum showed a general mixed infection but no B. tuberculosis.

On the 9th the blood-pressure was 130. The diastolic third sound terminated at 50, and the muffled sound at 10. Temperature 96.5. Pulse 72. Urine 17 ounces and cloudy. Patient coughed up masses of mucus and blood when turned on his left side.

On the 13th he was decidedly improved. Temperature 98.4. Pulse 84. Skin of better color. Bedsore healed. Some indigestion. Was able to be put into chair. But on the 14th, during the night, he had "spells" when, as it seemed to him, his heart stopped beating and he could not get his breath (StokesAdams syndrome?). These attacks wakened him out of sleep and were apparently over by the time he called his nurse. His pulse, however, between attacks was the same as usual and his respiration regular.

On the 19th his feet began to swell and his temperature went to 99. The attacks of oppression at night continued. The patient would cough only when the bronchi were irritated or when he changed his position. The blood-pressure on the 23d was 150 and 70, the pulse 100.

On the 24th he exhibited during my visit the Biot type of respiration but apparently during the apneic period the pulse was fairly regular at a rate of 120. Temperature 96. The rate of respiration varied from time to time, even during the day, and the apneic periods were more frequent in the night, probably because of the decreased pressure during sleep. Atropin did not give as much relief as morphin and

under moderate doses of the latter the breathing was fairly regular and the sense of precordial oppression was absent. The blood-pressure remained at about 150 systolic, and 60 diastolic.

On the 26th the breath had something of a uremic odor and the urine was very scanty-only 5 to 10 ounces. Under the influence of milk diet and magnesium sulphate the amount was 15 ounces the next day. On the 28th it had reached 48 ounces. The respiration on this date varied from 18 to 32 per minute. There were no attacks of oppression.

The.

On the 30th the pulse began to intermit. systolic pressure was still at times as high as 152. The diastolic varied from 20 to 44. The pulse rate varied from 160 to 88.

On December 5 the periodic breathing returned, with the scanty urine, and periods of irregular heart action. Since November 13 he had shown very little trouble on the part of the lungs no bloody sputum, no pain. The periodic respiration was again quieted by morphin and the irregular heart action brought to regularity by strophanthin (Thoms) 1 per cent. solution-10 drops every six hours.

He had another smothering attack on the 8th and by the 11th the attacks became frequent and he had become edematous to the knees.

On the 14th he had frequent attacks of periodic breathing in which the apnea would continue for a full minute. During these attacks the pulse was feeble and irregular, but did not stop.

On the 15th he became stuporous and from that time gradually sank into deeper coma until he died on the morning of the 20th.

duction of the following brief summary of my findings.

The interpretation of the irregularities of the respiratory rhythm has received rather scant attention in our literature. For years and still in many quarters-the only type of periodic respiration recognized was the Cheyne-Stokes. But in 1876 Biot called attention to a variation of this type that he had found in meningitis in which the cessation and resumption of respiration were not gradual, but abrupt and with fullsized breaths. And in these last years emphasis has been laid on the Stokes-Adams syndrome in which we find a cessation of respiration that may or may not be coupled with a loss of consciousness.

The Cause of the Rhythm.-Recently, however, the problem of respiratory rhythm in general, and of dyspnea and periodic respiration in particular has been vigorously attacked in several different clinics, and it would seem as if we had now sufficient data for understanding the respiratory changes. Of the recent contributions the following seem to be most important: Röver1 discusses the causes of alterations in the respiratory rhythm. He finds that the pur

The post-mortem examination (10 hours after death and after embalming) showed the right lung adherent on all sides. The lower lobe was of the consistency and appearance of spleen and tore in removal from the posterior wall. The upper lobes dripped foam. One scar at apex. The left lung was adherent to the pericardium and posteriorly along the median line. Along this line was an abscess sac from which pus had apparently been emptied by the embalmer. The whole left lung except this small area was filled with foam. In this area (perhaps 1 by 4 inches) the same splenic infiltration was observed.

The heart was large-some six inches in horizontal measure. Left ventricle hypertrophied. Right atrium greatly dilated. Coronary arteries sclerotic but still patent. Mitralis atheromatous and insufficient. Aortic valve stenotic and dilated. Aorta dilated and studded with patches of yellow as well as of white thickening. The patches were not stellate, but had their axes parallel to the course of the vessel.

Abdominal organs normal except for congestion. Kidneys showed small infarcts.

The heart muscle was degenerated and along the area of the bundle of His were patches of calcification; but the bundle itself seemed intact.

The findings were so different from those usually prophesied in cases where the Biot type of respiration occurs that I began a search of the literature for an explanation. And because I believe that others may have to face a similar problem, I ask your indulgence for the intro

pose of respiration is the arterializing of the blood, not the excretion of the CO2. The respiratory center is stimulated by the circulating acids. If oxygen is lacking, if the partial tension in the blood is too low for oxygen to flow into the tissues, a suffocation, an asphyxiation, of the tissues including the respiratory center follows.

In such case the presence of other acids, acids formed by the incomplete oxidation of the tissues, furnishes a stimulus to extraordinary efforts at ventilating the lungs. The purpose of this effort is not to reduce the acidity of the blood or to expel the CO2, but rather to bring. oxygen to the tissues. For example, in such diseases as diabetes, the acids in the blood are so much more powerful in their attraction to hemoglobin than the CO, that the latter cannot unite with the hemoglobin of the blood. It follows again that the blood does not drain the CO, out of the tissues. Therefore the oxygen cannot gain entrance to the tissues. It follows again that the tissue combustion is incomplete and the end-products of CO, and water are not reached. and the acidosis is increased. Therefore, in 1. Zeitschrift für klinische Medicin, Ixxvii, 228.

order to overcome this asphyxiation of the tissues the blood is hurried through the arteries and veins more rapidly and the respiration increased-all usually without result. In gout a similar condition prevails on account of the uric acid increase. So this theory checks at least for these two diseases and seems plausible enough to be considered as the real explanation. This forms the chemical basis for the respiratory rhythm.

Dyspnea in Heart Disease.-Siebeck of Heidelberg, and his pupil Reinhardt, have taken up the specific problem of the variations of respiration in heart disease. Their work has been experimental and may be outlined as follows: Siebeck finds that in cardiac dyspnea, the real capacity of the lungs is decreased. This is brought about by increased rigidity of the walls. Next he finds that the mixture of gases in the alveoli is not uniform, as in normal lungs. And third, more of the inspired air is immediately breathed out than in normal lungs. This causes the oxygen of the inspired air to be less fully utilized than in normal lungs. Furthermore, there is less CO, breathed out than normally, and for this reason also the blood (and there

capacity little CO2 retention exists; on the other hand in some cases enormous overflow occurs. It follows, therefore, that the purely mechanical interference with the respiration found in cardiac insufficiency is sufficient to explain the occurrence of cardiac dyspnea. On the other hand, the work of Porges, Leimdörfer and Markovici shows that the alveolar gas-tension is decreased. Cardiac dyspnea is therefore comparable to that due to lack of oxygen, or to that in acidosis (Haldane). Therefore, in cardiac dyspnea two factors are present: (1) the mechanical and (2) the chemical.

The matter of acidosis in cardiorenal patients is discussed by Lewis. He calls attention to the two types of dyspnea: (1) those with and (2) those without cyanosis. In the latter type he finds a decrease in the alkalinity of the blood. The cause of the increased acidity of the blood lies, of course, in the incomplete combustion and excretion of the proteid molecule. In such cases the morbid anatomy at the post-mortem examination is not commensurate with the amount of functional disturbance. It follows, therefore, that in such cases the dyspnea is capable of being ameliorated and need not

fore the tissues) of cardiopaths contains more CO2 than that of normal persons. All these factors bring about the increased activity of the lungs in order to equalize conditions.

Reinhardt brings Siebeck's investigations to more definite conclusions. Stated categorically, they are:

1. The vital capacity of the lungs in all cases of cardiac insufficiency is lowered, in some cases from 20 to 25 per cent. of the normal.

2. In the lighter cases, and in all cases where the congestion includes only the peripheral circulation, the change in respiration is small.

3. In all the more severe cases, the ventilation of the lungs is rendered more difficult, and this shows itself as cardiac dyspnea. This consists in an increase in the volume of air respired, which is brought about by an increase in the frequency with the maintenance of the normal depth of the individual breath.

4. The experiments in breathing in air containing increased percentages of CO2 show (a) that in severe cases less CO2 can be endured; (b) that a percentage of CO, much lower than normal is sufficient to cause an increase of the respiratory effort; (c) the absolute CO, values show that in the severer cases with reduced vital

2. Deutsches Archiv für klin. Med., cvii, 1912, p. 252. 3. Deutsches Archiv für klin. Med., Band III, p. 465.

therefore be of such grave prognostic importance as the dyspnea of the other type.

Causes of Periodic Respiration. - Eyster calls attention to another factor in rhythm disturbances, and that is the relation of bloodpressure to periodic respiration. His point was that periodic respiration occurs whenever the blood-pressure alternately rises and falls above and below the level of intracranial pressure. The respirations become active with the rise and die away with the fall of blood-pressure. This finding shows that even in intracranial types of periodic respiration the heart and vasomotor system are of distinct influence.

More recently Clark and Hamill have published' their observations of circulatory changes in cases of periodic respiration. Their first case shows a Biot type of respiration and the postmortem examination revealed myocardial degeneration as the essential lesion. This tallies closely with my case.

In the same journal (p. 393) Barbour shows that in all periodic respiration the cardiac element is essential. He distinguishes the two types of periodic respiration as (1) the cardiac, and (2) the vasomotor. The blood-pressure in

4. Zeitschrift für klin. Med., Band 77, 1913, p. 447.

5. British Med. Jour., Nov. 29, 1913, p. 1417.

6. Jour. Exper. Med., 1906, viii, 565.

7. Jour. Pharm. and Exper. Therapeutics, March, 1914, p. 357.

its relation to intracranial pressure is, however, in both types the determinant factor in the production of periodicity. In the cardiac type the blood-pressure falls near the end of apnea and rises when the respirations become weaker. In the vasomotor type the blood-pressure rises near the end of apnea, only to fall soon after the first respiration. Of course, a depression of the medulla (as by morphin), or of the heart muscle would initiate or influence markedly such a periodicity.

Hoover's remarks constitute the only clinical discussion of apnea in cardiovascular disease that I have found. There are several reports, however, where a Stokes-Adams syndrome has been noted and yet no injury to the bundle of His found at the post-mortem examination. This fact emphasizes again the importance of studying more carefully the respiratory irregularities of our patients, for the very good reason that entirely different measures should be taken to combat a heart-block from those needed for apnea caused by medullary anemia. Hoover's remarks are so pertinent that I wish to quote them:

"In cardiovascular disease we see occasional lapses of respiratory activity which assume either Biot's or Cheyne-Stokes type of respiration. A man, 60

con

est sign of impariment in the gross hydraulics of his blood circulation so far as the right heart, pulmonary circulation, liver or the pendant parts were cerned. There were no signs of respiratory involvement during his waking hours, but the instant the added factor of sleep ensued there was induced a sufficient anemia of the respiratory center to cause apnea, and automatic respiration was resumed only after the partial pressure of carbonic acid in the blood reached a point sufficient to arouse his depressed respiratory center to action. This train of events explains those cases of arterial sclerosis which waken with suffocation during the early hours of the night when sleep is most profound, and when examined during their attacks reveal no signs of pulmonary stasis, no emphysema or bronchial râles and no change in character or rate of the arterial pulse. It is not a dyspnea; it is a prolonged hyperapnea, and has for its basis circulatory changes in the medulla which are not sufficient to produce symptoms during the waking hours, but with the diminution of blood supply to the encephalon which comes with profound slumber a sufficient anemia of the medulla occurs to produce hypesthesia of the respiratory center.

"All the cases of Cheyne-Stokes respiration which are produced in cardiovascular disease by the injection of small amounts of morphin occur in elderly people or patients with arterial disease. In all these patients we have the cumulative effect of morphin on a respiratory center already affected by an impaired blood supply. The patient above described recovered from his respiratory symptoms after taking nitroglycerin and caffein citrate, a further proof of the theory I have presented.

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years old, with chronic aortitis, general arterial sclerosis, chronic interstitial nephritis and moderate hypertrophy and dilatation of the left ventricle, had for three months been suffering from nocturnal dyspnea, followed by prolonged apnea. For a year the patient had wakened frequently at night suffering from intense air-hunger; after breathing deeply for several minutes he would be able to go to sleep and rest for the remainder of the night. These attacks all came during the first hours of sleep. For three months he had been greatly distressed by complete suspension of respiration directly he fell asleep, and then awakened with, intense air-hunger, which was relieved after a few minutes rapid deep breathing.

"It was discovered he could avoid this period of intense air-hunger if he were awakened directly apnea commenced. So his wife would watch him as he fell asleep and waken him the instant respiration ceased. This plan enabled the patient to escape the period of air-hunger which always followed spontaneous wakenings. Very commonly he would have to be awakened as often as a dozen times before respiration would continue after falling asleep.

"This patient presented a type of Biot's respiration, a modification of Cheyne-Stokes respiration in which apnea and hyperapnea alternate without the gradual increase and diminution in rate and depth of respiration which intervene between the periods of apnea in Cheyne-Stokes phenomenon. Owing to sclerosis of the basilar arteries with consequent impairment of blood supply to the medulla he suffered what may be termed intermittent claudication of the respiratory center. There was not the slight8. Jour. Am. Med. Assn., July 20, 1907, p. 237 et seq.

"A man, 71 years old, had Biot's type of respiration, i. e., sharply alternating periods of apnea and hyperapnea. The periods of apnea lasted as long as Sixty-seven seconds. There were clinical signs of arterial sclerosis, high blood-pressure, pulse of long duration, hypertrophy and dilatation of both right and left ventricles of the heart, and renal infarcts. During the periods of prolonged apnea the patient talked irrationally and incoherently; during the periods of apnea there was profound slumber. This clinical picture had continued for nearly three weeks when nitroglycerin, 1/100 gr. every hour, and 5 gr. of caffein citrate every three hours, were given. Though there was moderate edema of the legs, the improvement which followed the treatment could not be ascribed to increased renal elimination. Biot's respiration ceased and the mental symptoms all disappeared within a few hours. The patient died suddenly two days later with symptoms of embolus in the pulmonary artery."

CONCLUSIONS

We may conclude then that in cardiac cases two factors are at work in the production of irregular respiration. They are, first, the mechanical insufficiency of the lungs because of the damming back of the blood in the lungs and of the lowered blood-pressure; and, second, the oxygen lack at the medulla. The first is mechanical and the second is chemical. The first produces increased efforts at respiration