ordinary inspiration the sound became elicited; at the acme of inspiration it was most marked; towards the close of expiration it was feeble, or lost altogether. To distinguish these differences, a slow and full respiration was necessary. When the respiration was quick and feeble, the new sound was always presented at the systole, so that it seemed then to be exclusively connected with the heart. The late Dr. Snow saw this case with me, and on two occasions confirmed all the facts I have named above.

A second example of pulsatile crepitation occurred to me in a case which I attended with Mr. Gaskell, of Chelsea. The patient, a young man, twenty-one years of age, the son of a well-known solicitor, after an acute attack of inflammatory fever, which assumed a remittent rather than a rheumatic type, but during which the endocardium became implicated, suffered severely from the effects of chronic endocardial mischief. When I saw him three months before his death, I diagnosed mitral and aortic disease, with hypertrophy of the heart, and tubercle of the left lung. I saw him weekly, Mr. Gaskell attending in the intervals. During one of these intervals, our patient had an acute attack of pleuritic pain in the left side, which lasted four days, and embarrassed the breathing very considerably. On examining the chest at my next visit, I was surprised to find an exocardial sound, identical in character with that I have described as present in the previous case. The sound was at the base of the heart and to the left side. As before, it was super

ficial, local, an accompaniment of the systole, painfully distinct, and subject to similar modifications, as in the last named case, during inspiration and expiration. Mr. Gaskell and I often listened to this sound for many minutes together. I put an iodine mark round the spot externally, where the sound was best heard; the ring, not larger than a crown-piece, localised the position of the sound until the death of the patient.

I met with a third case in which the same sound was presented, in a child who came before me at the Royal Infirmary for Diseases of the Chest. This child was the subject of the chronic effects of hoopingcough. There were distinct physical indications of enlarged bronchi, emphysema of the right lung, and hypertrophy of the heart. The ordinary systolic and diastolic sounds were, in this instance, unattended by murmur. The exocardial sound existed again at the base of the heart, and bearing to the left side. It was coincident with the systole, and was also modified by the respiration, being prevented by a long expiration and brought out by inspiration; but, as the child could not be taught to inspire and expire by rule, the facts were not always well defined. Unfortunately, I am unable to follow out the history of this case further. The child either died, or was taken for treatment to some other Institution. She was brought to the Infirmary but once.

The above three cases were published in my pre

vious essay; but since then I have met with an instance in which the pulsatile crepitation was detected at another portion of the thorax. A private patient, who called on me one morning from the north of England, complained of symptoms which indicated the presence of phthisis. He was a tall, thin, anæmic young man, who had been much confined in an office, at the desk. He had suffered slightly from hæmoptysis, had nightsweats, and was losing flesh and strength. The right lung, at the apex, rendered unmistakable evidence of tubercular deposition in an early stage. On the left side there were, here and there, bronchial cooings; and the posterior part of this lung had been the seat of sharp pleuritic pains. On placing the stethoscope to the left of the vertebral column, and very low downat the base, in fact, of the left lung at its posterior and inner margin-I caught a pulsatile crepitation, much finer than that which had been observed in the preceding cases, but unquestionably governed by the same influences. When a long expiration was made, the crepitation was lost; when a long inspiration was made, it reappeared. This might have indicated nothing more than crepitation from tubercle; but the sound happened only in conjunction with the action of the heart, being coincident with the systole, synchronous with the pulse, and as perfect in its occurrence as the pulse itself. It was obviously connected, therefore, with aortic pulsation.

Analysing the auscultatory symptom thus described, we are led to trace it to a point connecting it with the acts both of respiration and of circulation. It is pro

duced only in the precincts of a pulsating structure, such as the heart or a large artery; and it is obviously brought out by the action of the pulsating organ. In so far, then, it is a circulatory sound. But, again, it is not capable of being elicited except in the chest, nor there unless the lungs be distended with air; the air in the lungs may be held in the statical condition, but it must be present. Hence the sound is strictly compounded of two acts; one, inspiratory or predisposing; another, pulsatory and exciting.

The cases in which the sound is met with are all of a kind in which there are signs of thoracic disease. In two of the cases cited, there were extensive cardiac lesions; in one there was mitral murmur, and evidence of enlargement of the whole heart: in the other, the physical indications pointed out the existence of mitral and aortic disease, also with great enlargement. In the remaining cases, the circulatory apparatus was apparently healthy. In all the cases there was marked pulmonic disease, which offered one analogous fact throughout, viz., unmistakable signs of pre-existent pleurisy; two of the patients had also been sufferers from long standing bronchial disorder and emphysema; the other two gave evidence of tubercle.

CAUSE AND CAUSATION OF PULSATILE PULMONIC

CREPITATION.

The study of these facts of diagnosis, taken in connection with the character of the pulsatile crepitation itself, led me early to the cause of the sound. It occurred

to me in the case of Mrs. K., that a portion of the left lung, at the point where it partially envelopes the left side of the heart, had been drawn downwards by pleuritic adhesion, and bound to the thoracic wall immediately over the heart; that the piece of lung thus placed was subjected to the impulse of the heart during systole; and that, when the lung was inflated on inspiration, the sudden compression, produced by the impulse, elicited the crepitation by forcible expulsion of air from the air-vesicles. I explained this view to Dr. Snow, who concurred with me entirely. In the succeeding two cases the same explanation presented itself; in the last case a like exposition was suggested, except that in this example the aorta, instead of the heart, was the pulsating body. Let me now show how far this diagnosis was proved correct.

Post mortem Facts. The first two cases above recorded ended fatally, and both, curiously enough, exactly six weeks after the occurrence of the pulsatile crepitation. I look upon this circumstance, of course, only as coincidental. The first patient died slowly, from exhaustion. The second died while he was sitting up in bed, laughing at some passing

event.

The post mortem examination, in the first case, revealed no disease of the segments of the mitral valve itself; but in the left ventricle, immediately below the valve, and to the left side, there was firmly attached to the endocardial membrane a rounded concretion, the base of which was of the size of a shilling, and the projection of which into the ventricle