Instances occasionally occur in which a patient had an anginal attack, as denoted by facial anxiety, paleness, holding of the breath, and a slow, weak pulse, without real pain. This has been called angina sine dolore. The patient has an appearanece of anxious expectation, as though he feared something terrible was about to happen.
The position of the patient with true angina pectoris is characteristic. He stops still wherever he is, stands perfectly erect or bends his body backward, raises his chin, supports himself with one hand, leans against anything that is near him, and places his other hand over his heart, although he exercises very little pressure with this hand. The position assumed is that which will give the left chest the greatest unhampered expansion, as though he would relieve all pressure on the heart.
Besides the feeling of constriction, even to some spasm, perhaps, of the intercostal muscles, respiration is slowed or very shallow, because of the reflex desire of the patient not to add to the pain by breathing. The face is pale, the eyes show fear, and the whole expression is almost typical of cardiac anxiety. The patient feels that he is about to die. The pulse is generally slowed, may be irregular, and may not be felt at the wrist. The blood pressure has been found at times to be increased. It could of course be taken only in those cases in which there were more or less continued anginal pains; the true typical acute angina pectoris attack is over, or the patient is dead, before any blood pressure determination could be made. When there is more or less constant ache or frequent slight attacks of pain, the blood pressure may be raised by the causative disease, arteriosclerosis. During the acute attack with inefficient cardiac action and a diminished force and frequency of the beat, the peripheral blood pressure can only be lowered.
The duration of an acute attack, that is, the acute pain, is generally but a few seconds, sometimes a few minutes, and rarely has lasted for several hours. In the latter cases some obstruction to an artery has been found at necropsy, but not sufficient to stop the circulation at a vital point. Repeated slight attacks, more or less severe, may occur frequently throughout one or more days, or even perhaps a series of days, caused by the least exertion, even that of turning in bed.
While most cases of sudden death with cardiac pain are due to a local disease in or around the heart, it is quite probable that some disturbance in the medulla oblongata may cause acute inhibitory stoppage of the heart through the pneumogastric (vagi) nerves. The power of the pneumogastric reflex to inhibit the action of the heart is, of course, easily demonstrated pharmacologically. Clinically reflexes down these nerves interfering with the heart's action cause faintness and serious prostration, if not actual shock, and perhaps, at times, death. The most frequent cause of such a reflex is abdominal pain, perhaps due to some serious condition in the stomach, to gastralgia, to an intestinal twist, to intussusception or other obstruction, or to hepatic or renal colic. A severe nerve injury anywhere may cause such a heart reflex. Hence serious nerve pain must always be stopped almost immediately, else cardiac and vasomotor shock will occur. In serious pain morphin becomes a life saver.
MANAGEMENT
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. It is possible that a true angina may be due to a coronary artery disease or obstruction, and that a collateral circulation may become established and repair the deficiency. While this probably can take place, it must be rare.
Occasionally when the intense pain has ceased, the patient may be nauseated and actually vomit, or he may soon pass a large amount of urine of low specific gravity, or have a copious movement of the bowels.
The first attack, and subsequent ones more and more readily, are precipitated by any exertion which increases the work of the heart, as walking up hill, walking against the wind, going upstairs, physical strains, as suddenly getting out of bed, leaning over to put on the shoes, straining at stool, or even mental excitement. Exertion directly after eating a large meal is especially liable to precipitate an attack. Food which does not readily digest, or food which causes gastric flatulence may precipitate attacks. Any indiscretion in the use of coffee, tea, alcohol or tobacco may be the cause of the attack.
For treatment of the immediate pain, if the physician arrives soon enough, anything may be given which quickly relieves local or general arterial spasm and spasm of the muscles. The moment that the heart and its arterioles relax, the attack is often over. The most quickly acting drug for this purpose is amyl nitrite, inhaled. If amyl nitrite is not at hand, or has been found previously to cause considerable disturbance of the head or a feeling of prolonged faintness, nitroglycerin is the next most rapidly acting drug. It may be given hypodermically, or a tablet may be dissolved on the tongue. The amyl nitrite should be in the emergency case of the physician in the form of ampules, or may be carried by the patient after he has had one or more attacks. The ampules now come made of very thin glass with an absorbent and silk covering ready for crushing with the fingers, and are thus immediately ready for inhalation. One of these is generally all that it is necessary to use at any one time. Nitroglycerin, if given hypodermically, should be in dose of 1/100 grain. If given by mouth the dose should be the same, repeated in ten minutes if the pain has not stopped.