The pathologic physiology of bronchial asthma is manifested by an edema of the mucous membranes and a spasm of the smooth muscle of the bronchi and bronchioles. The air passages become closed, and owing to this closure, there is subsequent difficulty in breathing, particularly in expiration. As a result of prolonged and frequent attacks of this type of dyspnea, the lungs become distended and emphysema supervenes. In the latter condition, the alveoli are distended, causing a flattening of the alveolar wall with consequent narrowing, tearing and even destruction of the capillaries, which results in diminution of alveolar circulation and increased pressure within the pulmonary arteries. Theoretically, this should result in increased work for the right ventricle.
This assumption seems to be borne out by Kahn,1 who concluded from an electrocardiographic study of fifty cases of bronchial asthma that the majority of his patients demonstrated a state of hypertrophy of