Epon palpation near the apex, usually somewhat inside of it, may be felt a re markable purring thrill, which will be found to be presystolie in time and to terminate with a distinct shock corre sponding to the beginning of cardiac systole. This shock may be felt over three or four intercostal spaces to the left of the sternum. Its origin is a mat ter of considerable speculation, but not as yet of demonstration.
On percussion the cardiac area will be found to be increased transversely to the right of the sternum. On the left it often reaches somewhat higher than normal, but laterally not much beyond the nor mal limits.
On auscultation at or inside the apex is heard a presystolic murmur of a char acteristic quality. It is more or less rub bing, rumbling, or churning, and ter minates with a sharp valvular sound cor responding to the shock felt by the hand. Immediately following this sound, if the ease is one of pure mitral obstruction, is a brief pause, and then a fainter valvular sound is heard corresponding to the sec ond sound of the heart.
If the case is one of stenosis and re gurgitation combined, the first sharp valvular sound is followed by a systolic The character of the typical presys tolic murmur of mitral stenosis is so dis tinctive that it would seem to the writer possible to establish a diagnosis of mitral stenosis upon this sound alone without other evidence.
At the base of the heart in the second left space is heard a sharply-accented and usually reduplicated sound, corre sponding to the closure of the pulmonary valves under tension.
In cases of failing compensation, the thrill may be difficult to feel. It may sometimes then be perceived by appos ing the palm of the hand lightly to the chest-wall, when a very faint and ex tremely circumscribed thrill may be de tected. With a dilated heart the aus cultatory sounds also are indistinct. It may be impossible to recognize the ex istence of mitral stenosis in a patient seen then for the first time. If, how ever, compensation be restored wholly or in part, the murmur may reappear. The time of the murmur may be post-diastolic or middiastolic rather than strictly sys tolic. The pulse is small, regular, and sometimes of rather high tension. When compensation fails, it becomes weak, frequent, irregular, and intermittent. ' Tricuspid stenosis may give rise to a presystolic murmur, situated to the right of the sternum; but this disease is ex tremely rare unless congenital, and when it does occur is apt to be secondary to chronic lesions of the left side of the heart. Persons born with tricuspid stenosis are apt to be simultaneously affected with other abnormalities which entail speedy death.
The late Austin Flint called attention to the presystolic murmur frequently heard in cases of aortic regurgitation at the apex of the heart, and ascribed it to the influence of the blood-current falling into the left ventricle through the incompetent aortic valves. This murmur is associated with the ordinary signs of aortic regurgitation and is not accompanied by the peculiar thrill felt in mitral stcnosis; nor is it followed by the systolic shock above described.
Etiology.—Earely the lesion may be congenital. In most instances it is the result of valvular endocarditis due to rheumatism or chorea or some other of the children's diseases. Amemia and chlorosis have also been thought to have some influence in promoting its occur rence.
Pathology.—Mitral stenosis is almost invariably associated with a greater or less degree of mitral regurgitation. By itself, mitral stenosis does not cause much enlargement of the heart. The left ven tricle may be of normal size or smaller. The left auricle and right ventricle are, however, much dilated and hypertro phied. The valves may be changed to a variable extent. In the most extreme cases the auriculo-ventricular orifice is scarcely big enough to admit the head of a pin. The left auricle often contains thrombi. Sometimes the great enlarge ment of the left auricle causes pressure paralysis of the left recurrent laryn eeal nerve—the same lesion which is t, caused, more often, by thoracic aneurism.
Analysis of the cases of mitral stenosis found at autopsy at Guy's Hospital dur ing the ten years, 1886 to 1895, inclusive. There were 4791 necropsies, in 196, or 4 per cent., of which the initial orifice measured three and a half inches or less. The stenosed orifice exceeded two and a quarter inches (one finger) in circumfer ence in 108 eases. and measured too and a quarter inches or less in 85. Of the 196 cases. 107 were females and S9 males. The average age of death for both males and females was the same—thirty-eight and a third years. In 32 instances tri cuspid and mitral stenosis occurred to gether. Of these 21 were females and 11 males. The tricuspid stenosis accom panied almost exclusively the severe form of mitral disease which was present in 24 of the total 32 cases. In "a large proportion" of all the cases the aortic valves were thickened, distorted. or otherwise defective, but were seldom re ferred to as stenosed. Excluding the eases for 1886, there were 77 cases of severe and 96 of the slighter form of mitral stenosis for the other nine years.