[The surgical physiopathology of essential pulmonary emphysema and volume-reduction intervention]

The breaking of the interalveolar septa represents, in the pathogenetic mechanism of emphysema, a final event, common to the different etiologic agents. This elementary injury causes a series of consequences, essentially of mechanic-structural type (intrapulmonary aerial spaces-confining parenchyma collapse, bronchial obstruction, dead space augmentation) on the thin and articulate bronchoalveolar architecture, whose final rearrangement determines, at least in part, the clinical picture. In short, the break of alveolar septa involves the formation of intraparenchymal aerial spaces with collapse of the confining lung; the compensatory mechanism to this situation, involves the hyperexpansion of the thoracic cage and flattening of the diaphragm, with the aim of allowing ventilation of the healthy residual parenchyma. Because of the finite capability of expansion of the thoracic cage and of the diaphragm in respect to the theoretical capability of the lung of large intraparenchymal aerial spaces formation, it is easy to imagine that emphysema can cause a serious functional respiratory deficit even before a significant quantity of pulmonary parenchyma is destroyed by the pathogenic process. It may then be hypothesized that a simple reduction of the volume of the lung, even sacrificing a part of "working" parenchyma, might allow the residual lung to come back to a normal ventilation, wholly ameliorating the respiratory exchanges. The clinically more remarkable consequence of lung volume reduction is the amelioration of ventilation mechanics with a decreased respiratory work due to the shift of the tidal volume toward values less proximal to the maximal expandability of the thoracic wall and of the diaphragm. On the other end, it is possible to anticipate an equally significant effect on bronchial obstruction, due to the more favorable matching of the compliance of the thoracic wall and that of the lung. LVRS has significant effect on the TV sharing ratio between emphysematous spaces and residual healthy parenchyma; the hyperexpansion of the residual lung in fact causes the distension of the emphysematous spaces, continuing in the natural compensatory mechanism of the emphysema. The decreased ventilation and thus re-breathing of the residual emphysematous spaces, together with the improved ventilation may ameliorate hypercapnia. Obviously no direct effects can be expected from LVRS on the conditions of the alveolar membrane and thus on gas diffusion capacity through it. The time duration of the amelioration achieved with the lung volume reduction is still to be demonstrated.