Chapter VI: Preface: To the First Edition (6)

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 associated with left-side endocarditis.

A special treatment of the heart, if any is needed, would probably not be indicated unless there was associated 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 space 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 associated with other lesions of the heart. It has been found to be associated 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 space 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.

ACUTE CARDIAC SYMPTOMS: ACUTE HEART ATTACK

It is not proposed here to describe the condition of sudden cardiac failure, or acute dilatation during disease, or after a severe heart strain, but to describe the terrible cardiac agony which occurs, sometimes repeatedly, with many patients who have valvular lesions. These patients may not have the symptoms of loss of compensation. Probably some one or more chambers of the heart become overdistended and act irregularly, or the blood is suddenly dammed up in the lungs, with the oppression and dyspnea caused by such passive congestion, or perhaps it is the right ventricle that is suddenly in serious trouble.

A physician receives an emergency call, and knows, if it is not a patient who has hysteria, that it is his duty to see the patient immediately. The friends of the patient all anxiously await the physician's arrival; front doors are often wide open, and the servants and the whole household are in a great state of excitement and anxiety. The position in which the patient will be found is that which he has learned gives him the greatest comfort. If the physician knows his patient, he will know how he will find him. He may lie sitting up in bed; he may be standing, leaning over a chair; he may be sitting in a chair leaning over a table or leaning over the back of another chair; but he is using every auxiliary muscle he possesses to respire. He is generally bathed in cold perspiration; the extremities are often icy cold; he calls for air, and to stop fanning all in one breath; he wishes the perspiration wiped off his brow, and nearly goes frantic while it is being done; there is agony depicted on his face; his eyes stare; his expirations are often groaning. Sometimes there is even incontinence of urine and feces, often hiccup or short coughs, perhaps vomiting, and possibly sharp pangs of pain in the cardiac region. A patient with these symptoms may die at any moment, and the wonder is that so many times one lives through these paroxysms.

The patient can hardly be questioned, can certainly not be carefully examined; and herein lies the advantage of the family physician who knows the patient and his heart, and in whom the patient has confidence.

In fact, this confidence which such a patient has in the physician who has more or less frequently aided him in weathering these terrible attacks is alone the greatest boon the patient can have.

MANAGEMENT

The immediate conditions to meet are the rapid fluttering heart, the nervous excitation and cardiac anxiety, and perhaps the most important of all, the vasomotor spasm that is often so pronounced. Physically we have, then, a heart with leaking or constricted valves; in either case more blood is entering the chambers of the heart than can be expelled in one contraction, while the peripheral resistance due to the spasm of the blood vessels, because of fear, becomes greater every minute and tends still more to interfere with the peripheral circulation and the complete emptying of the heart of its surplus blood. Owing to the well known stimulus to distention of hollow muscular organs, the heart contracts faster and faster.

Soon, by some disarrangement of the inhibitory apparatus, the pneumogastric nerves, the heart loses its governor, and the beats increase to even 150 a minute, with irregular contractions, the blood being sent through the arteries with irregular force, as evidenced by the varying volume of the pulse. At this time, with or without cardiac pain, which upsets the rhythm of the heart, the patient becomes frightened at the feeling of impending demise, and the cerebral reflexes begin to add to the cardiac difficulty. The breathing becomes nervously rapid, besides that which is due to the rapid heart. The chill of fear is added to the already contracted peripheral vessels, and the surface of the body becomes cold, the extremities sometimes intensely so. Next it seems as if the strongly contracted arterioles begin actually to prevent some of the peripheral circulation, the blood is piled up in the large arteries, and the venous circulation becomes more and more sluggish, while the lips, finger nails and forehead become cyanotic. Respiration becomes more rapid and deep; the inspiration being as strong as possible with every auxiliary muscle taking part, thus making the negative pressure in the chest aid in bringing the blood back through the veins. Part of the extra respiratory stimulus comes from the imperfectly aerated blood reaching the respiratory center.

Two factors may normally, without treatment, stop these paroxysms, and the "bad heart turn" may be cured spontaneously. The first of these is self-control. If the patient does not lose his head, by an effort of the will he saves himself from becoming nervous or frightened and therefore escapes the result of mental excitement; the increased peripheral blood pressure from fear does not occur, and in a shorter or longer time the heart quiets down. The physician recognizes this power, and gives his patient immediate assurance that he will soon be all right; the patient who knows his physician immediately feels this assurance and is quickly improved.

The second factor in spontaneous cure of the heart attack is relaxation. The exhaustion from the respiratory muscular efforts, together with the drowsy condition caused by the cerebral hyperemia and from the imperfectly aerated blood, causes finally a dulling of the mental acuity, and the nervous excitement abates, which, with the exhaustion, gives a relaxation of peripheral arterioles: the resistance to the flow of the blood is removed, the surface of the body becomes warm, the heart quiets down by the equalization of the circulation, and the paroxysm is over.

DRUGS

The part the nervous system plays in this paroxysm is shown by the good result obtained from injections of morphin, even when there is no pain; hence the action of morphin is directly in line with the natural resolution of the symptoms: it quiets the nervous system, causes drowsiness, relaxes spasm, and thus causes increased peripheral circulation; many times this is the only treatment necessary.

During these heart attacks it is more than useless to administer any drug by the stomach, as in this condition there will be no absorption, even if there is no vomiting.

While morphin is generally indicated, as just suggested, a very large dose should not be given, lest the activity of the respiratory center be impaired (it is already in trouble), and undoubtedly death may easily be caused by an overaction of morphin during these heart attacks. The addition of atropin to the morphin will prevent depression from the morphin. Also, atropin sometimes quiets cardiac pain, but it will not steady the heart, may irritate it, and will increase vasomotor tension, although peripheral nerve irritation may be diminished. Hence a fair dose of morphin hypodermicaly with a small dose of atropin, if respiratory depression is feared, is a physiologic method of bettering the condition. In this kind of heart attack a drug which often acts well is nitroglycerin. It may be given hypodermically in a dose of from 1/200 to 1/100 grain, or a tablet may be dissolved on the tongue, and the dose be repeated once or twice at fifteen-minute intervals, until there is throbbing in the forehead, which shows that a sufficient amount of the drug has been administered. This headache will generally not last long. In the meantime the peripheral blood vessels are relaxed, the surface of the body becomes warm, the heart quiets, and the attack is over. To hasten the action of nitroglycerin (that is, to equalize the circulation) a hot foot-bath is often valuable. Amyl nitrite may be inhaled with the same object in view, but the action is very intense, the prostration often severe, and unless there is angina pectoris, nitroglycerin is much better.

The symptoms of a heart attack may not be quite those described above; they may be those of sudden dilatation or semiparalysis of the heart, in which the prostration is intense and the patient is unable to sit up, although he may be leaning against several pillows. There is dyspnea, but the patient cannot aid respiration with the auxiliary muscles by holding the arms and shoulders tense or obtaining support from the aruls; in fact, the arms are almost strengthless. The surface of the body may be warm, and the arms may be warm except the hands; the feet, ankles and legs may be cold. There is generally more or less cyanosis, although the face may be pale. The finger nails often show venous stasis. In these cases the blood pressure is subnormal, the pulse may be hardly perceptible, and there is none of the tension of the body from fear. The patient may be fearful, but lie is completely collapsed. Such an attack may occur suddenly in a heart that is perfectly compensating, or it may accompany general edemas and dropsies.

If the emergency is excessively urgent, the lungs filling up with blood, moist rales beginning to occur, and frothy and blood-tinged sputum being coughed up, venesection may be indicated; combined with proper hypodermic medication it may save life, and does at times. In fact, a patient who shows every sign of fatal cardiac collapse may be saved. (one of the best drugs to administer to such patient is an aseptic ergot, injected intramuscularly.) The drug of all drugs for future action (as it will not act immediately) is digitalis, given hypodermically.

Whether digitalis shall be given at all, or how large the dose shall be depends on whether or not the patient has been taking digitalis in large quantities.

He may already be overpowered with digitalis. In that case it would be contraindicated.

Stroplianthin, especially when given intravenously, has been found to be a quickly acting circulatory stimulant. The dose of strophanthin, Merck, ranges from 1/500 to l/200 grain. The intravenous dose of strophanthin, Thoms, is about 1/130 grain. It should not be repeated within a day or two, if at all. Ampules of strophanthin in solution for intravenous use are now available.

Atropin in a dose of 1/150 grain, and strychnin in a dose of 1/40 or 1/30 grain are valuable aids in stimulating the circulation under these conditions. The atropin should not be repeated. The strychnin may be repeated in three, four or five hours, depending on the size of the previous close.

Of all quickly acting stimulants, none is better than camphor in saturated solution in sterile oil as may be obtained in ampules. Alcohol is absolutely contraindicated in the latter condition. In the former kind of heart attack, vasodilation from a large close of whisky or brandy may be of value. The dose should be large to cause immediate increased peripheral circulation, dilation, and even a little stupefaction of the central nervous system, and it may be effectual in a way not dissimilar to the action of morphiti.

TREATMENT OF BROKEN COMPENSATION

The consideration of this subject will include the following topics:
A. Hygiene.
B. Diet.
C. Elimination.
D. Physical measures.
E. Medication.
1. Cardiac Tonics: Digiralis, strophanthus, caffein, strychnin.
2. Cardiac Stimulants: Camphor, alcohol, ammonia.
3. Vasodilators: Nitrites, iodids, thyroid extract.
4. Cardiac Nutritives: Iron, calcium.
5. Cardiac Emergency Drugs: Ergot, suprarenal active principle,
pituitary active principle, atropin, morphin, and also some
of the drugs already mentioned.

A. HYGIENE

Of all treatment for broken compensation or dilated heart, nothing equals rest in bed. Sometimes it is the only treatment that is needed. The rigidness of this rest, the length of time that it should endure, and the period at which relaxation of such rest should be allowed depend entirely on the individual patient; no rule can be established. Most of the symptoms must disappear before exercise is allowed. Perhaps a not infrequent exception to the rule is when cardiac weakness, generally a inyocarditis, develops in a patient after 50. It is not always wise to keep such a patient in bed; he may be rested and his exercise greatly restricted, but sometimes it is difficult to get him out of bed if he is kept there any length of time.

Fresh air, sunlight and anything else that makes the bedroom attractive and cheerful are essential and will aid in the recovery. The kind of nurse that is needed, trained, untrained, or a member of the family, and the amount of company or entertainment allowed must be decided for the individual patient. The patient must be distinctly individualized and the proper measures taken to give mental and physical rest, to prevent excitement, worry, melancholia and depression, and to improve the general nutrition of the body as well as the condition of the heart.

Each occurrence of broken compensation in valvular disease causes another attack of cardiac weakness to occur with less excuse than before, and several serious attacks of broken compensation mean before long the loss of the heart muscle's ability to recover, so that permanent dilatation occurs.

B. DIET

The food given should be just sufficient for the needs of the body; the patient should not be overfed or underfed. Any large bulk of food or liquid should not be given. Pressure on the heart causes discomfort and is therefore inadvisable. Food that causes flatulence should be avoided. Theoretically the patient should receive a little meat, an egg or two, cereal or bread, a small amount of simple vegetables, a little fruit, often milk, a sufficient amount of noneffervescent water, perhaps a cup of chocolate or cocoa, a simple dessert, sometimes ice cream; in other words, a varied, limited diet containing all the elements that are necessary to good nutrition. The diet should be varied from day to day to encourage the appetite.

It has for several years been recognized that a salt-free diet in dropsies due to disease of the kidneys is a valuable aid in causing absorption of such exudates and of preventing greater exudations. For this reason a salt-free diet is often ordered in dropsies occurring in valvular disease. Its value, however, is not so great as in kidney lesions, and if it causes hardship to the patient it should not be continued rigorously. On the other hand, large amounts of salt should of course be interdicted.

A most valuable aid in dropsies due to heart deficiencies is the so- called dry diet, which means that as little liquid as possible should be taken in order that the patient's blood may resorb the exudate in the tissues and not have the blood vessels filled or overfilled with liquid from the gastro-intestinal tract. When dropsy is present, or even when serious pendent edemas are present, the patient should drink as little liquid as possible with his meals, and between meals should sip water rather than drink a large quantity of it. This is one of tile reasons that a large milk diet, even with kidney disturbance due to cardiac lesions, is generally inadvisable. With cardiac or general circulatory weakness, a laige amount of liquid to flush out the kidneys and the whole system, so long ordered for all kidney defects or mistakes in metabolism, is a seribus mistake. The Karel diet is described in the section on cardiovascular-renal disease.

Whether it is better to give three or four small meals a day or to give a small amount of nourishment every three hours during the daytime must again depend on the individual and his ability to digest without fermentation and putrefaction or discomfort. As previously urged, not too much fluid, even milk, though it digest perfectly, should be given, as the greater the amount of fluid the greater the amount of work thrown on the heart.