Cardiac Asthma

CARDIAC ASTHMA (asthma cardiale). Any sudden attack of difficult breathing of varying intensity and duration is called asthma or suffocation. The old clinic distinguished a large number of asthmas, which would more correctly be called asthmatic states (dyspeptic, parasitic, sexual, neurotic, uremic A.). The most clearly defined symptom complex is bronchial asthma (see), which, for this reason, is relatively easily distinguished from the series of other asthmatic states, with which, however, it may be combined, making the picture difficult to evaluate. Most other asthmatic states are classified as cardiac asthma, which represents a symptom complex for which it is still difficult to find any precise formulation. The most characteristic features are considered to be sudden onset, following an unclear feeling of anxiety of the epileptic aura type, a feeling of constriction in the retrosternal area, fear turning into severe dyspnea, pallor, often followed by cyanosis, psychomotor agitation. All these phenomena, as a rule, occur at night. No regular dependence has been noted between the severity of anatomical or functional (objectively demonstrable) changes in the heart and the attacks of A. - For understanding the pathogenesis, it is important to note that the most widespread theory of respiratory regulation at present is Winterstein's "reactive" or "neutralization" theory. According to the latter, the stimulus for the normal activity of the respiratory center is mainly CO2 or any other acidic products of metabolism. The respiratory center is set at a certain concentration of H-ions close to neutral and is extremely sensitive to minimal deviations from this point toward an acidic reaction. The pathogenesis of the attack itself is reduced to the concept of acute stagnation in the pulmonary circulation due to dissociation between the right and left heart (the classic Traube theory). This leads to insufficient ventilation, accumulation of CO2 in the blood, and serves as a cause for hyperventilation (resp. dyspnea). The nocturnal nature of the attacks is explained by the greater retention of CO2 at night due to decreased respiratory metabolism. However, the question remained unexplained why the left ventricle weakens during rest and sleep if, as is generally believed, the basis of the condition lies in its anatomical change. Therefore, Fraenkel put forward the hypothesis of a disturbance in the balance "between the anatomically changed ventricle and its functional capacity," and F. A. Hoffmann, by analogy with angina pectoris, pointed to the possibility of a reflex from the anatomically changed periphery; in particular, he indicated on sclerotic changes in small vessels and lesions of nerve ganglia in the area of the cardiac apex, which, in his opinion, could explain the peculiar picture of the condition. Huchard considers it possible to adhere to the classic explanation of Traube only in some cases, proposing for other cases his concept of toxic alimentary dyspnea, reducing the attack to a combination of "toxic and nervous factors." According to modern concepts, this indefinite and vague interpretation by Huchard ("toxic alimentary dyspnea") fits into two types of dyspnea. First, the so-called "renal" dyspnea, caused by disturbance of acid-base balance (acidosis due to the kidney's loss of ability to excrete acidic metabolic products). This form can be partially eliminated or alleviated by appropriate diet (Beckmann), and in this respect the name toxic alimentary is still suitable for it. The second group is the so-called cerebral, centrogenic dyspnea (Straub, Meyer, Winterstein). In these cases, there is no acidosis, the blood reaction may even shift to the alkaline side. Therefore, in such cases, dyspnea must be explained by changes in the actual reaction directly in the fluid bathing the respiratory center; this change can be considered as a result of poor circulation (locally) in the cerebral vessels. Such dyspnea is often observed in organic hypertensives-arteriosclerotics, along with intermittent breathing (Cheyne-Stokes), for example, in the late stages of nephrosclerosis. Eppinger, Papp and Schwarz in 1924 demonstrated a sharp acceleration of blood flow during an attack of A., and along with expansion of the capillary network, in their opinion, a short circuit occurs (between arteries and veins through previously non-functioning smallest vessels). All this leads to overload of the pulmonary circulation, which the heart, especially an anatomically changed one, cannot cope with. In this acceleration they see the primary moment for the occurrence of the "asthmatic attack." Nevertheless, pathogenetically Eppinger, Papp and Schwarz reduce everything to the classic explanation of the attack (Traube): to stagnation in the pulmonary circulation on the basis of left ventricular insufficiency. Wassermann puts forward the concept of asthma as an independent condition, having nothing in common with ordinary cardiac (classic congestive) dyspnea. Asthma cardiale is most often found in arteriosclerotics, hypertensives suffering from aortic lesions;-in a word, in the so-called aortic heart. It is the result of functional insufficiency of the systemic circulation, which results in poor circulation in the cerebral centers;-in other words, A. s. is the result of oxygen starvation of the brain-anoxia. Retrograde congestive phenomena in the pulmonary circulation, as well as dyspnea itself, are of secondary nature. As additional factors contributing to understanding the genesis, Wassermann points to increased excitability of the respiratory and other centers (even beyond necessity). This is how Goldscheider explains the continuation of dyspnea after saturation of the blood with oxygen (resp. hyperventilation). The functional insufficiency of the systemic circulation manifests itself during sleep not because it is caused by the severity of anatomical changes, but because sleep promotes a decrease in the threshold of irritation of the centers. If we take into account that night is the parasympathetic time, when the vagus nerve is in a state of increased irritation (Bauer), then we can find the point of application for the action of oxygen starvation both in the respiratory center and in the heart and vessels (through the innervation apparatus). Thus, the described group of phenomena, in the opinion of the authors, can only conditionally be considered a cardiovascular symptom complex. This is especially true of asthmatic attacks in renal patients and diabetics, in whom the chemical factor predominates. Nevertheless, here too signs of weakening of cardiac activity are often present, which is not without significance in developing practical measures aimed at stopping and preventing attacks of suffocation. - Dyspeptic A. is also classified as A. s., since attacks of dyspnea, having their starting point in the gastrointestinal tract with its appendages, can occur only in individuals with weakened myocardium. It must be considered established that along with primary weakness of the heart, disorders of the innervation apparatus must be taken into account as an important factor determining the onset of the attack, and not only in the sense of a simple reflex affecting cardiac rhythm and filling of the vascular bed, but also of direct inotropic influence (on contractility of the muscle) of cardiac fibers of the vagus nerve. The high position of the diaphragm, causing difficulty in cardiac activity both by direct compression of the heart itself and by mechanical disturbance of coronary circulation, also has unquestionable significance. - So-called parasitic A. belongs to the same group of phenomena. The basis of sexual or "uterine" A. also lies in reflex connections-this time with the sexual apparatus. The dyspneic phenomena in the sexual neurosis described by M. Herz under the name of frenocardia also belong here: sudden cessation of breathing at the height of a deep inspiration together with severe pain outward from the nipple (tonic spasm of the diaphragm). More often than the developed picture of frenocardia, attacks of unsatisfied, "blocked" breathing (Atemsperre) are observed. "Asthmatic" attacks in hysteria (hysterical tachypnea) can only be mentioned here for the sake of differential diagnosis (see Bronchial Asthma). - Etiology and precipitating factors. Among changes in the cardiovascular system, arteriosclerosis is most often noted, then syphilitic lesions of the aorta, heart defects (mainly of the aortic valves), and finally degeneration of the heart muscle. Often, an attack of suffocation is preceded by physical exertion, emotional excitement, abundant food intake (the latter especially in individuals with "dyspeptic asthma"). Treatment. If Bohr considers dyspnea a useful reflex, and Koranyi sees in it the last attempt of the body to save itself, then it is more correct, in agreement with Fraenkel, Kiilbs and others, to consider it a threatening symptom, which ultimately testifies to the exhaustion of cardiac functions (primary and consecutive), and therefore requiring therapeutic measures.

Morphine is given first place to reduce the excitability of the respiratory center, since, even according to authors who recognize in A. only the significance of a protective reflex, 'dyspnea overshoots the mark' (Goldschider). In the presence of disorders in the cardiovascular system, treatment is conducted according to the plan for treatment in arteriosclerosis and diseases of the heart. Camphor, in combination with preparations of the digitalis group and theobromine, is used both during the attack and after it. In syphilitic etiology, specific therapy is indicated. The prognosis is always doubtful; if the attacks of cardiac asthma return through ever shorter intervals, the prognosis must be considered extremely unfavorable.