The most common sequel of asthma is emphysema. The bronchial tubes being more or less completely closed, either by contraction of their muscular fibres or by plugs of thick, viscid mucus, the air pent up in the parts beyond the obstruction is subjected to the negative pressure produced by the exaggerated inspiratory act, becomes rarefied, and, in obedience to the diminished resistance induced by the partial vacuum in the thorax, causes distension of the air-cells. This condition continues until, the tubes having again become pervious, the natural elasticity of the lung-tissue, aided by the expiratory muscles, forces out the air and permits them to return to their natural size. This is the transitory emphysema to which we have already alluded. Germain Sée[8] regards it as analogous to the paralytic emphysema which occurs the moment the pneumogastric is divided. With repeated attacks the air-cells lose their elasticity and remain permanently dilated. Owing to the constant distension, the walls of the alveolæ become more and more attenuated, until, finally giving way, two or more of them coalesce, forming one large cell. The symptoms of this condition are the same as those of ordinary vesicular emphysema. [Footnote 8: _Op. cit._, p. 637.] 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 {190} 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.