Owing to partial occlusion of the afferent bronchi and the altered conditions of pressure mentioned, the blood accumulates in the capillaries during the paroxysm, the lung-cells do not receive their adequate supply of air, and oxygenation is imperfect. In the early stages of the disease this congestion is only temporary, and disappears with the removal of the obstruction, but in those cases in which the attacks are severe and frequent the vessels lose their contractility and remain permanently congested.
The state of chronic congestion just mentioned is occasionally attended with serous exudation into the interalveolar tissue, which by pressing upon the adjacent air-cells causes their obliteration. This oedema, with the remains of the compressed air-cells and the viscid mucus stagnating in the finer tubes, forms the little islets of carnified tissue known as lobular pneumonia.
The most frequent change observed in the bronchial tubes in old cases of asthma is hypertrophy of their muscular fibres, causing thickening of their walls and diminished calibre. In other cases they are dilated, but this condition is due more to the concomitant bronchial catarrh than to the asthma.
Obstructed in its course through the lungs, the venous blood accumulates in the pulmonary artery, and, pressing back upon the right ventricle, excites it to increased action, which in the course of time leads to hypertrophy of its muscular fibres and dilatation of its cavity.
In the early stages of asthma, the face is usually pale during the intervals between the paroxysms, but when the latter become more frequent the impeded circulation causes stasis in the peripheral vessels. The imperfectly-oxygenated blood gives the face a dusky hue, and in severe cases it may become bluish or even violet-colored. The eyes are prominent, owing to the enlargement of the orbital veins (Sée), and the conjunctivæ congested and watery.9
9 For a description of symptoms of the above-mentioned secondary affections the reader is referred to the articles on [EMPHYSEMA] and [HEART DISEASE].
ETIOLOGY.—Predisposing Causes.—Every one is not liable to asthma, and the fact that out of a large number exposed to its exciting causes only a few are attacked justifies the assumption that there is an inherent tendency to the disease. That this tendency is hereditary in its nature is conceded by every prominent writer on asthma except Lebert, who believes this to be only occasionally the case. Thus, of 35 cases collected by Salter, heredity could be traced in 14, of whom 7 inherited the disease from the father, and the remainder from grandparents and other relations. Ramadge gives an instance in which the disease appeared in four generations: an asthmatic father had four children, three of whom inherited the disease; one of the daughters married, and of her two children one became asthmatic; the other escaped, but the disease reappeared in one of her children.10
10 Germain Sée, op. cit., p. 668.
The hereditary tendency may skip one generation, as is the case with Steavenson,11 who inherited asthma from his grandfather, his father's generation having been entirely free from the disease. In other cases it may alternate with some other neurosis or with gout or rheumatism; for instance, the children of an asthmatic father may be epileptic or gouty and the grandchildren asthmatic, or the asthmatic tendency may develop in one child of an asthmatic family and the gouty diathesis in another. It is by no means necessary for the hereditary transmission of the disease that the father should be asthmatic when the child is conceived, as there are many cases recorded in which asthma developed in children whose fathers had completely recovered before they contracted marriage and never had any subsequent return of the disease.
11 W. E. Steavenson, Spasmodic Asthma, London, 1882, p. 8.