Nazari S
Dipartimento di Chirurgia, IRCCS San Matteo, Pavia.
Minerva Chir. 1998 Nov;53(11):899-918.
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.
在肺气肿的发病机制中，肺泡间隔的破坏是一个最终事件，是不同病因所共有的。这种基本损伤会引发一系列后果，主要是机械结构类型的（肺内气腔 - 限制实质塌陷、支气管阻塞、无效腔增大），作用于纤细且相互连接的支气管肺泡结构，其最终的重新排列至少部分地决定了临床症状。简而言之，肺泡间隔的破坏涉及肺实质内气腔的形成以及限制肺的塌陷；针对这种情况的代偿机制包括胸廓过度扩张和膈肌扁平，目的是使健康的残余实质得以通气。由于胸廓和膈肌的扩张能力相对于肺形成大的肺实质内气腔的理论能力有限，很容易想象，即使在大量肺实质被致病过程破坏之前，肺气肿也可能导致严重的功能性呼吸缺陷。因此可以推测，即使牺牲一部分“工作”实质，单纯减少肺的体积，可能会使残余肺恢复正常通气，从而完全改善呼吸交换。肺体积缩小在临床上更显著的后果是通气力学的改善，由于潮气量向更远离胸壁和膈肌最大扩张能力的值转移，呼吸功降低。另一方面，由于胸壁和肺的顺应性更有利的匹配，有可能预期对支气管阻塞有同样显著的影响。肺减容术（LVRS）对肺气肿气腔和残余健康实质之间的潮气量分配比例有显著影响；残余肺的过度扩张实际上导致肺气肿气腔的扩张，这是肺气肿自然代偿机制的延续。残余肺气肿气腔通气减少进而出现再呼吸，加上通气改善，可能会改善高碳酸血症。显然，不能预期肺减容术对肺泡膜状况以及由此对通过肺泡膜的气体扩散能力有直接影响。肺体积缩小所实现的改善的持续时间仍有待证明。
