It is necessary to construct, insofar as possible on the basis of actual observations, a conceptual framework of the pathology and pathogenesis of pulmonary emphysema before considering the vascular changes. This task is made difficult by lack of knowledge of anatomic detail, especially in quantitative terms and as it is in the living; by the reversible nature of certain mechanisms, such as obstruction of bronchioles by mucus; and by the indubitable existence of important functional phenomena such as bronchospasm or vasospasm that may not be reflected anatomically. It is also possible that several mechanisms may be necessary in the evolution of pulmonary emphysema and that these may differ at various stages in the development of the lesions. Consequently, much remains hypothetical, and disagreements in interpretation among different observers have been wide and virulent (1-9).

For present purposes, emphysema will be defined as an overexpansion of distal air spaces, usually accompanied by loss of the septa among them." Distal air spaces" is used to imply that, not only alveolated substance, but also distal orders of bronchioles, may be involved in any of these processes. In particular, what is referred to as a" bulla" usually represents a much more proximal distribution than that of a single respiratory bronchiole. Transitions exist to" honey-comb lung" brought about, in part, by ingrowth of bronchial epithelium into altered air spaces by way of the canals of Lambert (10). In many instances there are superimposed, to a varying extent additional lesions such as focal fibrosis and