The cardiac nerves in which the pain is seated are doubtless sensory fibres of the pneumogastrics. Their anatomical connections with the brachial plexus will explain the extension of pain to the left upper extremities. To account for the pain in parts which have no direct connection with the cardiac nerves, it may be assumed that in angina, as in other neuralgic affections, a centripetal influence conveyed to the nervous centres may occasion pain referable to different situations. This explains the shifting of pains which is one of the diagnostic traits of neuralgia. The explanation of the disturbed rhythm of the heart's action so often coexisting with the neuralgic pain is not more difficult than in cases of functional disorder disconnected from angina. For what is to be said of the rationale the reader is referred to that portion of this article which treats of Functional Disorders of the Heart.
Angina, as a purely functional affection—that is, not symptomatic of any organic lesion of the heart, and not due to any structural change in, nor mechanical pressure upon, nerves—is obscure as regards its pathology and etiology, but not more so than many other neuralgic affections. As already stated, cases in which it is thus purely functional are few in number—fewer even than has been supposed, because there is reason to believe that lesions have been overlooked. Moreover, cases which have been reported render it probable that in some instances in which the heart has been found free from appreciable lesions nerves entering into the cardiac plexuses may be the seat of structural changes or may be subject to pressure from a morbid growth. But there are cases in which no lesions are discernible during life, and in which the existence of lesions is disproved by complete recovery. The affection under these circumstances must be regarded as purely functional. There is no positive knowledge of the etiology in these cases. The affection has been attributed to gout, to hysteria, to the action of cold, to the use of tobacco, and to other causes. These causes may have a certain amount of agency, but there is an unknown intervening link in their etiological connection concerning which, in the present state of our knowledge, it is useless to speculate.
Age and sex have an undoubted influence in the etiology. The affection very rarely occurs under middle life, and it occurs in men much oftener than in women.
PROGNOSIS.—As a very rare exception to the rule, a single paroxysm only may occur, the patient living for many years without any recurrence. Recurring paroxysms sometimes are separated by long intervals—weeks, months, and years. In the majority of cases, however, paroxysms recur with more and more frequency and with increasing severity. Under these circumstances death may take place after a long period of suffering.
The liability to sudden death is an important point in the prognosis. This may occur in the first paroxysm. An instance has fallen under my observation within a few months, there having been no signs previously indicative of disease of the heart. Calcareous obstruction of the coronary arteries was the lesion found after death. A person subject to paroxysms of angina must be considered as in more or less danger of sudden death with the recurrence of each paroxysm. The physician should be sufficiently impressed with the importance of this fact. While it is doubtful whether it be the physician's duty to apprise the patient of the fact, the danger should always be communicated to some discreet relative or friend. To do this is a duty which the physician owes to himself as well as to the patient. If he omit it, he exposes himself to censure should sudden death unexpectedly take place. The mildness of the paroxysms which have already occurred does not afford a positive security against the liability to a severe and fatal paroxysm. But it is a hopeful consideration that paroxysms may recur more or less frequently for an indefinite period without proving fatal. At this time I am cognizant of three cases in which paroxysms have recurred frequently for several years, the patients, with that exception, having had fair health. Let not the physician, therefore, predict with positiveness that a patient with angina will die sooner or later in a paroxysm. The uncertainty is a ground of encouragement as well as for apprehension.
The coexistence of organic disease of the heart and the nature of the cardiac lesions have a very important bearing on the prognosis. The danger is in proportion to the importance of these. Recovery is never to be expected when the affection is associated with well-marked cardiac lesions, and there is always great danger in the recurrence of paroxysms when the associated lesions are in themselves dangerous. Lesions which give rise to free aortic regurgitation and to fatty degeneration of the heart involve more or less danger of sudden death, irrespective of angina. It is evidence of greatly increased danger if paroxysm of angina be superadded.
During a paroxysm of angina the immediate danger is to be estimated by the symptoms denoting disturbance of the heart's action. The danger is great in proportion as the action of the heart is feeble, irregular, or intermitting. Per contra, the danger is less in proportion as the deviation from the normal force and rhythm is small. It may be said that there is no danger so long as the heart's action remains unaffected, but the disturbance may be slight or wanting at the outset of a paroxysm and afterward become fatally great.
A favorable prognosis may be entertained when there are no signs of cardiac lesion, and when there is little or no disturbance of the heart's action during the paroxysms. Let it be borne in mind that such cases are exceptional and extremely rare. Let it also be borne in mind that lesions especially apt to be associated with fatal paroxysms may be latent—namely, obstruction of the coronary arteries and fatty degeneration. The latter fact renders it proper that a favorable prognosis should always be formed with a reservation, while the fact that recovery takes place in a few well-marked cases of angina renders it improper to withhold encouragement whenever lesions are not discoverable and the paroxysms are not accompanied by alarming symptoms referable to the heart's action. The long tolerance of the affection in some cases is not to be lost sight of with reference to the encouragement which may be fairly derived therefrom.
The immediate cause of sudden death in a paroxysm is probably an arrest of the heart's action in diastole, or such a degree of diminution of the force of its action that the accumulation of blood within its cavities induces paralysis from distension.
TREATMENT.—It is important that a paroxysm of angina be treated as soon as possible, not alone with a view to the relief of pain, but to remove immediate danger. If the physician be present, an opiate in a form to act promptly should be given either by the mouth or hypodermically; the latter mode is to be preferred. Laudanum or a solution of a salt of morphia is the most eligible form if given by the mouth. If the heart's action be weak and irregular, a diffusible stimulant is indicated. If at once available, chloric ether, Hoffman's anodyne, and the compound tincture of lavender act efficiently. If these be not at hand, an alcoholic stimulant should be given, diluted but little, and the doses repeated at short intervals until the paroxysm ends and the disturbed action of the heart has ceased. The duration of paroxysms is generally so short that a physician is rarely present unless they recur after brief intervals. A patient, therefore, subject to angina should be provided with remedies and instructions as to their use at the instant a paroxysm occurs. The amyl nitrite, first recommended in this affection by Brunton, is a remedy of signal benefit in some cases. From two to five minims may be inhaled at the commencement of the paroxysm. It is especially indicated when the characters of the pulse denote arterial tension. Caution is to be exercised in its use if there be notable weakness of the heart's action. Sinapisms, stimulating embrocations, and fomentations applied to the chest have a certain measure of utility, but they should not take the place nor delay the use of remedies which are more efficient.