Pulmonary atelectasis is common in the perioperative period. Physiologically, it is produced when collapsing forces derived from positive pleural pressure and surface tension overcome expanding forces from alveolar pressure and parenchymal tethering. Atelectasis impairs blood oxygenation and reduces lung compliance. It is increasingly recognized that it can also induce local tissue biologic responses, such as inflammation, local immune dysfunction, and damage of the alveolar-capillary barrier, with potential loss of lung fluid clearance, increased lung protein permeability, and susceptibility to infection, factors that can initiate or exaggerate lung injury. Mechanical ventilation of a heterogeneously aerated lung (e.g., in the presence of atelectatic lung tissue) involves biomechanical processes that may precipitate further lung damage: concentration of mechanical forces, propagation of gas-liquid interfaces, and remote overdistension. Knowledge of such pathophysiologic mechanisms of atelectasis and their consequences in the healthy and diseased lung should guide optimal clinical management.

中文翻译：

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围手术期肺不张：第一部分。生物学和机制。


肺不张在围手术期很常见。从生理学上讲，当胸膜正压和表面张力产生的塌陷力克服肺泡压力和实质束缚的扩张力时，就会产生这种情况。肺不张会损害血液氧合并降低肺顺应性。人们越来越认识到，它还可以诱导局部组织生物反应，例如炎症、局部免疫功能障碍和肺泡毛细血管屏障损伤，并可能导致肺液体清除能力丧失、肺蛋白通透性增加和对感染的易感性。可能引发或加剧肺损伤。不均匀通气的肺（例如，存在肺不张的肺组织）的机械通气涉及可能导致进一步肺损伤的生物力学过程：机械力的集中、气液界面的传播以及远程过度扩张。了解肺不张的病理生理机制及其对健康和患病肺部的影响应指导最佳的临床治疗。