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The closure of the aortic valve is less typically sharp, showing that the blood vessels are not so thoroughly filled. The peripheral circulation is not so active, the blood pressure falls, and the heart becomes more rapid, especially on the least exertion. All of these signs indicate myocardial weakness. The treatment of this condition is largely preventive.
This condition of auricular fibrillation occurs occasionally in valvular disease, and perhaps most frequently in mitral stenosis; but it can occur without valvular lesions, and with any valvular lesion. If it occurs in younger patients, valvular disease is apt to be a cause; if in older patients, sclerosis or myocardial degeneration is generally present.
In serious pain morphin becomes a life saver. While a number of causes of true cardiac pain may be eliminated by improvement in any loss of compensation, by improvement of the heart tone, by more or less recovery from myocardial or endocardial inflammation, and by the withdrawal of nicotin, which may cause cardiac pains, still, true angina pectoris once occurring is likely to be caused by a progressive, incurable condition, and the attacks will become more frequent until the final one.
In probably nearly every case of diphtheria, unless of the mildest type, there is some myocardial involvement, even if not more than 25 percent of such cases show clinical symptoms of such heart injury. Tuberculosis of different parts of the body also, sooner or later, injures the heart; and the effect of syphilis on the heart is now well recognized.
As soon as the patient indicates that he can hold his breath no longer, the number of seconds is noted. A normal person should hold his breath from thirty to forty seconds without much subsequent dyspnea, while a patient with myocardial weakness can hold his breath only from ten to twenty seconds, and then much temporary dyspnea will follow.
An early occurrence of myocardial weakness shows a 50 percent probability that death will be caused by cardiac insufficiency. Heart pains comprise another important indicator of future cardiac death, perhaps not an angina.
Whether digitalis should be used when there is considered to be much myocardial degeneration is a question for individualization.
Unfortunately, during fever processes, digitalis in ordinary doses rarely slows the heart; and while it might slow the heart if given in large doses, it would also cause too powerful contractions of the ventricles. Digitalis is inadvisable if there is much endocardial inflammation, and especially if there is supposed or presumed to be acute myocardial inflammation.
These myocardial changes are sometimes associated with chronic pericarditis and chronic endocarditis, and may accompany or follow valvular disease of the heart. Failure of compensation in valvular disease and dilatation of the heart are sequences which occur sooner or later. The heart frequently becomes more rapid, not only with exertion and change of position to the erect, but even after eating.
It should be remembered that just before death venous pressure is likely to rise, and this may raise the diastolic pressure. With the progressive toxemia of typhoid fever the blood pressure will become lowered from the myocardial degeneration. As in other infections, the blood pressure will fall in scarlet fever; but if it suddenly rises, a kidney complication is to be looked for.
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