This lesion, though not so common as the mitral lesion, is of not infrequent occurrence in children and young adults as a sequence of acute rheumatic endocarditis. If it occurs later in life it generally is associated with aortic narrowing, and is a part of the general endarteritis and perhaps atheroma of the aorta. Sometimes it is caused by strenuous exertion apparently rupturing the valve.
This form of valvular disease frequently ends in sudden death. On the other hand, it is astonishing how active a person may be with this really terrible cardiac defect. This lesion, from the frequent overdistention of the left ventricle, is one which often causes pain. While the left ventricle enlarges enormously to overcome the extra distention due to the blood entering the ventricle from both directions, the muscle sooner or later becomes degenerated from poor coronary circulation. Unless the left ventricle can do its work well enough to maintain an adequate pressure of blood in the aorta, the coronary circulation is insufficient, and chronic myocarditis is the result. If the left ventricle has maintained this pressure for a long time, edemas are not common unless the cardiac weakness is serious and generally permanently serious: that is, slight weakness, in this lesion, does not give edemas as does slight loss of compensation in mitral disease, and unless the weakness of the ventricle is serious, the lungs are not much affected.
The physical sign of this lesion is the diastolic murmur, which is loudest of the base of the heart, is accentuated over the aortic orifice, and is transmitted up into the neck and the subclavians, and down over the heart and down the sternum with marked pulsation, of the arteries (Corrigan pulse) and often of some of the peripheral veins, notably of the arms and throat.
If the left ventricle becomes dilated the mitral valve may become insufficient, when the usual lung symptoms occur, with hypertrophy of the right ventricle; and if it fails, the usual venous symptoms of loss of compensation follow. This lesion not infrequently causes epistaxis, hemoptysis and hematemesis.
Digitalis is always of value in these cases, but it should not be pushed. If a heart is slowed too much, the regurgitation into the left ventricle is increased. Therefore such hearts should not be slowed to less than eighty beats per minute, or sudden anemia of the brain and sudden death may occur. These patients must not do hard work.
TRICUSPID INSUFFICIENCY
This rarely, if ever, occurs alone; it is generally a sequence of other valvular defects, and represents an overworked, dilated right ventricle. It may, however, occur from lesions of the lungs which impede the blood flow through them. Such are fibroid changes in the lungs, emphysema, prolonged chronic bronchitis, the last stages of pulmonary tuberculosis, old neglected pleurisies with cirrhosis or fibrosis of the lung, and repeated attacks of asthma—anything, whether valvular defect or pulmonary circulatory disturbance, which increases the pressure ahead and the work of this ventricle.
The symptoms are those of loss of compensation as described under other valvular lesions. There may be jugular pulsation, especially evident in the external jugular on the left side. The liver enlarges and may pulsate. There are edemas, dropsies, ascites and perhaps hemorrhages. The heart is enlarged and there is a soft systolic blow heard at the lower end of the sternum. The dyspnea is sometimes very great, and cyanosis may be present, especially during paroxysms of coughing.
This lesion of the heart is always benefited by digitalis, but the continuance of the improvement and its amount depend, of course, on the cause of the dilatation of the ventricle. Strychnin is often of advantage. These patients should rarely receive vasodilators, and hot baths, overheating, overloading the stomach and vigorous purging should never be allowed. Sometimes improvement will not take place until ascitic or pleuritic fluid, if present, has been removed.