Two separate barriers form the alveolar–capillary barrier, the microvascular endothelium, and the alveolar epithelium. ( A and B ) In normal lungs ( A ), the alveolar inflation and vascular perfusion are associated with low stress and are not injurious. Neutrophils can release oxidants, proteases, leukotrienes, and other proinflammatory molecules, such as platelet-activating factor (PAF). IL-1 can also stimulate the production of extracellular matrix by fibroblasts. In the airspace, alveolar macrophages secrete cytokines, interleukin (IL)-1, -6, -8, and -10, and tumor necrosis factor (TNF)-α, which act locally to stimulate chemotaxis and activate neutrophils. Neutrophils adhere to the injured capillary endothelium and migrate through the interstitium into the alveolar airspace. In addition to collapse, derecruited lungs also become fluid filled. Injury to type II cells disrupts normal epithelial fluid transport, impairing the removal of edema fluid from the alveolar space. As the derecruited lungs cause epithelial injury and loss of epithelial integrity, both type I and type II alveolar cells are damaged. However, with time, this leads to an inflammatory reaction. The initial injury is simple collapse of alveoli. This figure depicts the advanced stage of lung injury caused by atelectasis. Both epithelial and endothelial injury may initiate or propagate lung injury. Because the blood vessels are compressed, perfusion may be traumatic because of flow-induced disruption of the microvascular endothelium. In contrast, with atelectasis ( B ), alveolar inflation and deflation may be heterogeneous, and the resulting airway stress causes epithelial injury. Etiology and Pathogenesis of Atelectasisįig. In addition, we discuss the impact of atelectasis and of its prevention in ALI. 3This article reviews the causes, nature, and consequences of atelectasis, focusing on the role of atelectasis in development of perioperative morbidity, and illustrates how preventive measures could impact perioperative health. It is now known that atelectasis occurs in the most dependent parts of the lung of 90% of patients who are anesthetized and plays an important role in gas exchange abnormalities and reduced static compliance associated with acute lung injury (ALI). 2thus demonstrated their concept of a progressive alveolar collapse during general anesthesia with mechanical ventilation. 1Pulmonary atelectasis was suspected as the major cause, based on the observation of a successive decrease in lung compliance and the partial pressure of arterial oxygen (Pao 2), both of which returned toward normal after deep inflations of the lung. IT has been known for decades that in patients with previously normal lungs, general anesthesia is associated with impaired oxygenation.
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