Degenerative lung disease includes diffuse hypertrophic emphysema, bullous emphysema, and "vanishing" or "cotton-candy" lung. It is the author's concept that all of the above clinical entities are stages of one disease with a common etiological factor, namely obliterative vascular disease of both the bronchial and pulmonary systems. It is thought that this vascular disease starts in the bronchial arterial system, which, through its ramifications, influences the pulmonary arterial system through the vasa vasorum. The lack of nutrient blood supply first causes destruction of the elastic fibers with resultant fibrosis in the alveolar spaces. With the increasing loss of nutrient blood supply, this destructive process may progress until the main lobar bronchi and vessels have been destroyed. All stages of lung destruction may exist at the same time in the same lung. Our concept of the vascular pathogenesis of pulmonary emphysema arose from observations made prior to 1949 during surgery on emphysematous patients who were being operated for other disease, such as carcinoma, bronchiectasis, etc. In some instances, emphysema was unexpectedly encountered at operation. It was noted that in areas of degenerated or bullous disease there was a paucity or absence of bleeding. These areas represented actual destruction of lung parenchyma-not simply pleural or superficial parenchymal changes although such was suggested by their protrusion above the surface of the lung. There was a gradation from the gross changes of hypertrophic emphysema to complete degeneration of a segment or lobe suggesting that this was the same disease in various stages. Under intratracheal anesthesia these emphysematous lungs, especially the destroyed areas, filled readily with air but expiration was difficult because of the loss of lung elasticity. The clinical entity of degenerative lung disease does not include compensatory emphysema, the trapping of air behind a foreign body, bronchospasm as seen in asthma, pulmonary cysts, or subpleural blebs. In blebs, tension results from the mechanical trapping of airl8 with secondary compression of normal lung tissue between the chest wall and the hilum. This differs from bullae in which there is an absence of tension. Bullae involve lung parenchyma, and are associated with hypertrophic emphy~erna.~~ Blebs compress adjacent lung tissue because of the positive pressure within them, whereas bullae have bronchial pressures, negative or positive depending upon the phase of respiration, and they progressively enlarge because of their inelastic nature and may gradually stretch with respiration until they fill the chest cavity ("stretched cysts").lg Tension blebs may also become large enough to fill a hemithorax. In the latter