Abstract
From simultaneous tracings of the volume of tidal air and of intra-pleural pressure in emphysema, an almost complete loss of pulmonary elasticity can be demonstrated. This loss can be more simply, but not so accurately, demonstrated by changes in tracings of the vital capacity. These afford a crude clinical test for the loss of pulmonary elasticity in emphysema. Characteristic changes in the lung volume and its subdivisions are described and an explanation for these changes advanced, on the basis of loss of pulmonary elasticity. Evidence is presented, based on this loss, that the peripheral, distended and relatively ischemic alveoli are overventilated at the expense of the deeper and more normal ones. The subsequent diminution of the effective tidal air is held responsible for some, if not all, of the anoxemia and CO2 retention observed in emphysema. Expiration in emphysema is the result of a positive intrapleural pressure, generated by active muscular effort. The functional drawbacks of this type of expiration are emphasized, in particular diminution in the excursion of the diaphragm, with consequent impairment of inspira-tory efficiency. The emphysematous subject is incapable of effective hyperventilation, although this is called for by the diminution in the volume of effective tidal air.