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.
Perioperative Pulmonary Atelectasis: Part I. Biology and Mechanisms
This article is featured in “This Month in Anesthesiology,” page A1.
Martin J. London, M.D., served as Handling Editor for this article.
C.Z. and D.L. contributed equally to this article.
Submitted for publication December 4, 2020. Accepted for publication July 13, 2021. Published online first on September 8, 2021.
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Congli Zeng, David Lagier, Jae-Woo Lee, Marcos F. Vidal Melo; Perioperative Pulmonary Atelectasis: Part I. Biology and Mechanisms. Anesthesiology 2022; 136:181–205 doi: https://doi.org/10.1097/ALN.0000000000003943
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