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The morbid anatomical factors in the production of right heart hypertrophy and failure in emphysema have been reviewed with reference to 44 cases studied by standard histological methods and by post-mortem pulmonary arteriography. The most important factors in raising the pulmonary vascular resistance in these cases are considered to be vascular deformity and pressure by the emphysematous spaces on the adjacent branches of the pulmonary artery. Precapillary bronchopulmonary arterial anastomoses may be of importance in those cases where areas of localized bronchiectasis are present. Intimal fibrosis of the pulmonary arterioles, destruction of the pulmonary vascular bed, and thromboembolic phenomena were thought to be of only minor importance in the production of cor pulmonale in emphysema.

The pathological features of 20 cases dying in status asthmaticus have been studied. In gross sections the lungs showed no emphysema, but mucus plugs in the air passages and focal areas of collapse were outstanding features. Five cases showed cystic bronchiectasis which was of a similar distribution to the focal areas of collapse, occurring in the upper lobes as commonly as in the lower lobes.Histologically, shedding of the ciliated bronchial mucosal cells was prominent and this is attributed to a transudation of oedema fluid from the submucosa. Areas of regeneration of the mucosa, with the presence of simple stratified epithelium, were seen frequently. The loss of the ciliated respiratory epithelium and the transudation of oedema fluid into the bronchial lumen, with interference with the action of the remaining ciliated cells, are considered to be the essential factors in the failure of clearance of the bronchial secretions in asthma. It is postulated that bronchospasm plays little or no part in the shedding of the bronchial mucosa or in the pathogenesis of the asthmatic attack.