Definition.—Mitral stenosis is a constriction of the left auriculo-ventricular orifice, usually due to valvular endocarditis, though it may be congenital.
Etiology.—Any cause that will give rise to endocarditis should be considered a producing factor of mitral stenosis; sub-acute rheumatism being responsible for the largest per cent of cases, though chorea and chlorosis are responsible for many, and most likely explains the greater frequency of the disease in females—about four to one.
The infectious fevers, especially measles, scarlet fever, and diphtheria, are also causal factors, while whooping-cough, no doubt, gives rise to valvular lesions from the straining of the valves induced by severe paroxysms of coughing.
It is a disease of early and middle life, rarely occurring after the age of fifty. Stenosis may be due to infiltration of the valvular ring, the valves remaining normal, though this is very rare.
Congenital stenosis has been noted, but is of very rare occurrence.
Pathology.—The morbid changes that take place in the valves, give rise, in most cases, to narrowing of the orifice. These changes consist in thickening and rigidity of the segments, and chordae tendineae, and frequently a fusion of the segments at their edges; not infrequently there are calcareous deposits. These changes convert the valves into a funnel, the base extending into ihe ventricle.
The degree of stenosis and shape varies. In one it will be circular, and so small as to scarcely admit a goose-quill, while in another it will be flattened, giving rise to a small, narrow slit—the "buttonhole'" mitral. The funnel-shaped opening is usually found in young subjects, and rarely in old patients, while the buttonhole slit is rarely found in the young, and nearly always in elderly patients.
Sometimes there will be vegetations upon the valves, obstructing the flow of blood, and in this way the size of the opening is reduced. In nearly all of these cases there will be more or less insufficiency as well as stenosis.
The changes in the heart are as follows: Owing to the diminished opening, less blood is forced into the left ventricle, and, as a result, the ventricle atrophies, the atrophic changes at times extending into the aorta. As a result of the stenosis, the auricle is not completely emptied, hence dilatation, and, later, hypertrophy follows, thus enabling the auricle to expel the blood through the small orifice; later, there is thinning of the walls.
This dilatation and hypertrophy necessarily call for increased work from the pulmonary vessels, which, in turn, become more or less thickened. The lungs become congested, and this constant tension in the lesser circulation is followed by induration of lung-tissue, sclerosis of the vessels, and sometimes by hemorrhagic infarcts. Pepper speaks of a case where atheromatous deposits in the pulmonary vessels were found to their remotest branches, the left lung being almost solid and airless.
The hypertrophy of the left auricle, for a time, compensates for the great resistance at the mitral orifice, and the patient suffers but little. Sooner or later, however, the auricle can not maintain this equilibrium, congestion of the lungs becomes more marked, and the right heart comes to the relief by taking on dilatation and hypertrophy, which aids the parts already enlarged for compensatory efforts, and the patient's life is still further prolonged; finally, however, the dilatation increases, the tricuspid valves are unable to effect a perfect closure, and tricuspid insufficiency is the result, with congestion of the general circulation and that cyanotic condition prophetic of a fatal issue.
When the stenosis is only moderate and there is mitral incompetency as well, there will be slight hypertrophy of the left ventricle. The apex of the heart is made up almost entirely of the hypertrophied right ventricle.
Symptoms.—The subjective symptoms during the stage of compensation are few and unreliable and may be entirely absent; when present, they are due to emotional excitement or physical exertion, such as going upstairs or performing some unusual muscular effort. The symptoms developed are the result of pulmonary congestion, and consist of dyspnea and cough, attended, at first, by expectoration of frothy mucus, which becomes bloodstained later on.
In the early stage, before compensation gives way, there is evidence of a defective blood-supply to the brain, which is seen in the pallor of the face and mucous membranes. Owing to the small amount of blood thrown into the left ventricle, the pulse becomes small, frequent, and irregular. A sharp stitchlike pain is frequently present in the apex region, and undue exertion may be attended by hemoptysis.
After compensation gives way, the symptoms become quite pronounced, and are almost identical with those of mitral insufficiency, for in a large number of cases the lesion is a combined one. Owing to pulmonary obstruction, the dyspnea becomes constant, and is greatly exaggerated on exertion. The face now becomes dusky, and the veins of the neck are distended and pulsation is visible. The liver becomes swollen, with thickening of the bile-ducts, causing jaundice, more or less pronounced. The urine becomes scanty, high-colored, and contains albumen. Dropsical effusion begins in the feet, rapidly extending up the limbs to the body, general dropsy resulting.
If vegetative deposits become loosened, they may float off into the general current, and give rise to embolism of the brain, kidney, or spleen, in which case local symptoms would determine the seat of disturbance.
Physical Signs.—Inspection.—If there be exaggerated hypertrophy of the right ventricle, there will be undue prominence, especially in children, over the lower half of the sternum and the fifth and sixth costal cartilages, otherwise the chest remains normal. The apex beat may be seen in the normal position, though chiefly over the lower sternum and adjacent cartilage.
Increased tension of the pulmonary artery will frequently be shown by a visible pulsation in the second, and sometimes the third and fourth, intercostal spaces. Epigastric pulsation is seen when there is great congestion of the liver. When compensation fails, the impulse of the heart becomes weak, and sometimes can not be seen, though pulsation may be seen in the enlarged veins of the neck.
Palpation.—A presystolic thrill, harsh or grating in character, and terminating in a sudden shock, synchronous with the pulse, is pathognomonic of mitral stenosis. It is best heard during expiration, and over the third and fourth interspaces. When absent, it may be made to appear by rapidly clapping the hands over the head.
The apex beat is felt more forcibly over the lower sternum and over the third and fourth interspaces. Epigastric pulsation is often pronounced, especially when there is enlargement of the liver. The pulse, owing to the weak impulse of the left ventricle, is small though regular during the period of compensation. When compensation fails, the pulse becomes irregular.
Percussion.—Where there is excessive hypertrophy of the right ventricle dullness may extend to the right nipple line. If the left auricle be greatly dilated, there will be extension of dullness to the left of the sternum as high as the second rib. Where there is marked pulmonary engorgement, there may be dullness over the entire left lung, and, if care be not exercised, it may be mistaken for consolidation of phthisis. Increase in transverse dullness will suggest an associated hypertrophy of the left ventricle.
Auscultation.—In well-marked cases a presystolic murmur, prolonged and of a harsh, rumbling character, may be heard within and above the normal apex beat. The area is quite limited, and, when compensation fails, may disappear entirely. If palpation be practiced at the same time, the murmur and thrill will be found to be synchronous. The murmur terminates suddenly with a distinct shock.
The first sound, sharp and distinct, following immediately after the rumbling sound, is another characteristic symptom, and is probably due to the sudden closure of the tricuspid valve, induced by hypertrophy of the right ventricle. This sound may be present when the murmur has not been heard, or when it has disappeared. The second sound at the pulmonic cartilage is of a sharp, ringing character. These adventitious sounds are more distinct and readily heard before failure of compensation, and are of great value in determining- the valvular lesion.
Diagnosis.—The characteristic features that point to mitral stenosis are, first, a presystolic murmur, prolonged, harsh, and rumbling, heard above yet near the apex; second, a presystolic thrill at the apex, synchronous with the murmur; third, the sharp, ringing character of the pulmonic sound; fourth, the increased dullness extending to the right of the sternum; fifth, the small, regular pulse before compensation, followed by a small, irregular pulse after compensation; sixth, wavy pulsations of the veins of the neck.