This particular valvular defect occurs more frequently in women than in men, and between the ages of 10 and 30, and is generally the result of rheumatic endocarditis or ch.o.r.ea, perhaps 60 percent of mitral stenosis having this origin. Other causes are various infections or chronic disease, such as nephritis. Of course, like any valvular lesion, it may be a.s.sociated with other lesions, and sooner or later in many instances, when the left ventricle becomes dilated or weakened, mitral insufficiency also occurs.
It has sometimes seemed that high blood pressure has caused the left ventricle to act with such force as to irritate this mitral valve, and later develop from such irritation a sclerosis or narrowing, and stenosis occurs. It has been suggested that, though lime may be of advantage in heart weakness, as will be stated later, if the blood is overfull of calcium ions the valvular irritations may more readily have deposits of calcium, in other words, become calcareous, and therefore cause more obstruction. It is quite likely, however, that this sort of deposit is only a piece of the general calcification of tissue in arteriosclerosis and old age, and could not be caused by the administration of calcium to a younger patient, and might then occur in older patients even if substances containing much calcium were kept out of the dict. Calcium metabolisim in arteriosclerosis and in softening of the bones is not well understood.
Patients with this lesion are seriously handicapped when any congestion of the lungs occurs, such as pneumonia, pleurisy, or even bronchitis. Asthma is especially serious in these cases, and these patients rarely live to old age.
The pulse is generally slow, unless broken compensation occurs; dyspnea on exertion is a prominent symptom; the increased secretion of mucus in the bronchial tubes and throat is often troublesome, and there is liable to be considerable cough. If these patients have an acute heart attack, a feeling of suffocation is their worst symptom and the dyspnea may be great, although there may be no tachycardia, these hearts often acting slowly even when there is serious discomfort. When compensation fails, there is an occurrence of all the usual symptoms, as previously described.
The distinctive diagnostic physical sign of this lesion is the diastolic and perhaps presystolic murmur heard over the left ventricle, accentuated at the apex and transmitted some distance to the left of the heart. There is also an accentuated pulmonary closure. To palpation this lesion often gives a characteristic presystolic thrill at and around the apex.
The first symptoms of weakening of the compensation are irregularity in the beat and venous congestion of the head and face, causing bluing of the lips, often nosebleed, and sometimes hemoptysis and insomnia. Later the usual series of disturbances from dilatation of the right ventricle occurs. As previously stated, with the absence of good coronary circulation and the consequent impaired nutrition, the left ventricle may also dilate and the mitral valve may become insufficient. Sudden death from heart failure may occur with this lesion more frequently than with mitral insufficiency but less frequently than with aortic insufficiency.
A particularly dangerous period for women with this lesion is when the blood pressure rises after the menopause and the patients become full-blooded and begin to put on weight. Also, these patients always suffer more or less from cold extremities. In most cases they sleep best and with least disturbance with the head higher than one pillow.
Besides the usual treatment for broken compensation in patients with this lesion, digitalis is of the greatest value, and the slowing of the heart by it, allowing the left ventricle to be more completely filled with the blood coming through the narrowed mitral opening during the diastole, is the object desired. This drug acts similarly on both the right and left ventricles, and though there is no real occasion for stimulation of the left ventricle, and it is the right ventricle that is in trouble, dilated and failing, still a greater force of left ventricle contraction helps the peripheral circulation. The action on the right ventricle contributes greatly to the relief of the patient by sending the blood through the lungs and into the left auricle more forcibly. and the left ventricle receives an increased amount of blood, the congestion in the lungs is relieved, and the dyspnea improves. Perhaps there is no cla.s.s of cardiac diseases in which more frequent striking relief can be obtained than in these cases of mitral stenosis.
If the congestion of the lungs is very great, and death seems imminent from cardiac paralysis, if cyanosis is serious, and b.l.o.o.d.y.
frothy mucus is being expectorated, venesection and an intramuscular injection of aseptic ergot may be indicated. Digitalis should also be given, hypodermically perhaps, but its action would be too late if it was not aided by other more quickly acting drugs. The physician may often save life by such radical measures.
MITRAL INSUFFICIENCY: MITRAL REGURGITATION
This is the most frequent form of valvular disease of the heart, and is due to a shortening or thickening of the valves, or to some adhesion which does not permit the valve, to close properly, and the blood consequently regurgitates from the left ventricle into the left auricle during the contraction of the ventricle. Such regurgitation may occur without valvular disease if for any reason the left ventricle becomes dilated sufficiently to cause the valve to be insufficient. Such a dilatation can generally be cured by rest and treatment. As with mitral stenosis, the most frequent causes are rheumatism and ch.o.r.ea, with the occasional other causes as previously enumerated.
The characteristic murmur of this lesion is a systolic blow, accentuated at the apex, transmitted to the left of the thorax, generally heard in the back, near the lower end of the scapula, and transmitted upward over the precordia.
Of all cardiac lesions, this is the safest one to have. Sudden death is unusual, the compensation of the heart seems to be most readily maintained, and the patient is not so greatly dangered by overexertion or by inflammations in the lungs. As in mitral stenosis, any increase in blood pressure--whether the normal increase after the age of 40, any continued earlier high tension, or increase from occupation or exercise--is serious as causing the left ventricle to act more strenuously, so that more blood is forced back into the left auricle, the lungs become congested, and the right ventricle, sooner or later, becomes incompetent.
When compensation fails with these patients, the first sign is pendent edema of the feet, ankles and legs; subsequently, if there is progressive failure of compensation, the usual symptoms occur.
The treatment is princ.i.p.ally rest and digitalis, and the recovery of compensation is often almost phenomenal. Patients with this lesion are likely to be children and young adults, and the heart muscle readily responds as a rule to the treatment inaugurated. Later, in these patients, or if the lesion occurs in older patients, the return to compensation does not occur so readily. If the condition is developed from a myocarditis or from fatty degeneration of the heart, it may be impossible to cause the left ventricle to improve so much as to overcome this relative dilatation or relative insufficiency of the valve. If the dilatation of the left ventricle is due to some poisoning such as nicotin, with proper treatment-- stopping the use of tobacco, administration of digitalis, and rest-- the heart muscle will generally recover and the valve again properly close.
AORTIC STENOSIS: AORTIC OBSTRUCTION
Valvular disease at the aortic orifice is much less common than at the mitral orifice, and while stenosis or obstruction is less common from rheumatism or acute inflammatory endocarditis than is insufficiency of this valve, a narrowing or at least the clinical sign of narrowing, denoted by a systolic blow at the base of the heart over the aortic opening, is in arteriosclerosis and old age of frequent occurrence. If such narrowing occurs without aortic insufficiency at the age at which it usually occurs, it may not seriously affect the heart. It may follow acute endocarditis, but it most frequently follows chronic endocarditis or atheroma, in which the aortic valves become thickened and more or less rigid; this condition most frequently occurs in men.
Anything that tends to increase arterial tension, as tobacco, lead or hard work, or anything that tends to cause arterial disease, as alcohol or syphilis, is often the cause of this lesion.
At times the edges of the valves may grow together from ulcerative inflammation, and the lumen thus be diminished in size; or projecting vegetations may interfere with the opening of the valve and with the flow of blood. With such narrowing the left ventricle more or less rapidly hypertrophies to overcome its increased work.
The murmur caused by this lesion is a systolic one, either accentuated in the second intercostal s.p.a.ce at the right of the sternum, or perhaps heard loudest just to the left of the sternum in this region. The murmur is also transmitted up the arteries into the neck, and may at times be heard in the subclavian arteries. It may also be transmitted downward over the heart. The pulse is slow, the apex of the rise of the sphymographic arterial tracing is more or less sustained and rounded, and the rise is much less than normal.
If this lesion occurs in old age, there is general arterial disease present, and the tension and compressibility of the arteries vary, depending on how much they are hardened. The disturbed circulation is evidenced by imperfect peripheral circulation and capillary sluggishly, with at times pendent edema of the feet and ankles, but, perhaps, little congestion of the lungs. The left ventricle being sufficient, there is no damming back through the left auricle to the lungs. The left ventricle may, however, become weakened, either by some sudden strain or by a chronic myocarditis, and relative insufficiency of the mitral valve may occur. The subsequent symptoms are typically those of loss of compensation.
This lesion may allow a patient to live for years, provided no other serious disturbance of the heart occurs, such as myocarditis or coronary disease; but sooner or later, with the failing force of the blood flow and the lessened aortic pressure, slight attacks of anemia of the brain occur, causing syncope or fainting. Also, sooner or later these patients have little cardiac pains. They begin to "sense" their hearts. There may not be actual anginas, but a little feeling of discomfort, with perhaps pains shooting up into the neck, or a feeling of pressure under the sternum. Little excitements or overexertions are likely to make the heart attempt to contract more rapidly than it is able to drive the blood through the narrowed orifice, and this alone causes cardiac discomfort and the feeling of cardiac oppression.
It is essential, then, that these patients should not hasten and should not become excited; and any drug or stimulant which would cause cardiac excitement is bad for them. On the other hand, these are the very patients in whom, sometimes, alcohol in small doses may be advisable, especially if the patient is old; and a dose of alcohol used medicinally when an attack of cardiac disturbance is present is good treatment. The quick dilatation is valuable.
Nitroglycerin will also do good work in these cases, and with high blood tension may be the only safe drug for the patient to have on hand. As soon as his attack occurs, with or without real angina pectoris, let him dissolve in his mouth a nitroglycerin tablet. If he feels faint, he will feel better the moment he lies down, and in this instance he may be improved by a cup of coffee, or a dose of caffein or camphor.
If the left ventricle becomes still weaker and shows signs of serious weakness, or if there is actual dilatation, the question of whether or not digitalis should be used is a subject for careful decision. The left ventricle should not be forced to act too st.u.r.dily against this aortic resistance. Consequently the dose of digitalis must be small. On the other hand, it frequently happens, especially in old age, that myocarditis or fatty degeneration has already occurred before this cardiac weakness develops in the presence of aortic narrowing, and digitalis may not be indicated at all. We cannot tell how far degeneration may have gone, however, and small doses of digitalis used tentatively and carefully, perhaps 5 drops of an active tincture two or three times a day, and then the drug carefully increased to a little larger dose to see whether improvement takes place, is the only way to ascertain whether or not digitalis can be used with advantage. If it increases the cardiac pain and distress, it should not be used. Strychnin is then the drug relied on, with such other general medication as is needed, combined with the coincident administration of nitroglycerin, which may also be given in conjunction with digitalis, if deemed advisable.
Generally, however, if a heart with aortic stenosis needs stimulation, the blood pressure is generally none too high, although there may be arteriosclerosis present. Therefore when nitroglycerin is indicated to lower blood pressure, digitalis is not usually indicated; when digitalis is indicated to aid the heart, nitroglycerin is generally not indicated. These patients must have high blood pressure to sustain perfect circulation at the base of the brain.
Patients who have this lesion should not use tobacco in large amounts, or sometimes even small amounts, as tobacco raises the blood pressure and thus puts more work on the left ventricle; in the second place, if the left ventricle is failing, much tobacco may hasten its debility. On the other hand, with a failing left ventricle and a long previous use of tobacco, it is no time to prohibit its use absolutely. A failing heart and the sudden stoppage of tobacco may prove a serious combination.
AORTIC INSUFFICIENCY: AORTIC REGURGITATION
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 a.s.sociated 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.
TRICUSPID STENOSIS: TRICUSPID OBSTRUCTION
This is rare and probably always congenital, and is supposed to be due to an inflammation of the endocardium during intra-uterine life.
In early childhood it is possible that it may be a.s.sociated with left-side endocarditis.
A special treatment of the heart, if any is needed, would probably not be indicated unless there was a.s.sociated tricuspid insufficiency, when digitalis might be used.
PULMONARY INSUFFICIENCY: PULMONARY REGURGITATION
If this rare condition occurs, it is probably congenital. A distinctive murmur of this insufficiency would be diastolic and accentuated in the second intercostal s.p.a.ce on the left of the sternum. It should be remembered that aortic murmurs are often more plainly heard at the left of the sternum. Sooner or later, if this lesion is actually present, the right ventricle dilates and cyanosis and dyspnea occur. Digitalis would therefore be indicated.
PULMONARY STENOSIS: PULMONARY OBSTRUCTION
If stenosis is actually present in this location, the lesion is probably congenital. It might occur after a serious acute infectious endocarditis, but then it would be a.s.sociated with other lesions of the heart. It has been found to be a.s.sociated with such congenital lesions of the heart as an open foramen ovale or foramen Botalli, or with an imperfect ventricular septum, and perhaps with tricuspid stenosis--in short, a cardiac congenital defect. The right ventricle becomes hypertrophied, if the child lives to overcome the obstruction.
The physical sign is a systolic blow at the second intercostal s.p.a.ce on the left; but as just stated, such a murmur must surely be dissociated from an aortic murmur if found to develop after babyhood, and it should also be diagnosed from the frequently occurring hemic, basic and systolic murmurs; that is, if signs of pulmonary lesions are not heard soon after birth or in early babyhood, the diagnosis of pulmonary defects can be made only by exclusion.
Unless the right ventricle is found later to be in trouble, there is no treatment for this condition. If the right ventricle dilates, digitalis may be of benefit.