From the *Pneumologia, Ospedale San Paolo, Dipartimento di Scienze della Salute, Università degli Studi di Milano, Milan, Italy; †Department of Experimental Medicine, University of Milano-Bicocca, Italy; ‡Centro Cardiologico Monzino IRCCS, Milano, Italy; §Centro Cardiologico Monzino IRCCS, Dipartimento di Scienze Cliniche e di Comunità, Sezione cardiovascolare, Università di Milano, Milan, Italy; ∥Division of Pulmonary and Critical Care and Medicine, Department of Medicine, University of Washington, Seattle, Washington; and ¶Anesthesia and Intensive Care, Ospedale Niguarda Ca' Granda, Milano, Italy.
Anesth Analg. 2015 Feb;120(2):373-80. doi: 10.1213/ANE.0000000000000496.
An increased alveolar-arterial oxygen tension difference is frequent in anesthetized patients. In this study, we evaluated the effect on the lung of anesthesia, muscle paralysis, and a brief course of mechanical ventilation.
Lung diffusion for carbon monoxide (DLCO), including pulmonary capillary blood volume (Vc) and conductance of the alveolar-capillary membrane (DM), and pulmonary surfactant protein type B (a marker of alveolar damage) were measured in 45 patients without pulmonary disease undergoing extrathoracic surgery.
Anesthesia, muscle paralysis, and mechanical ventilation led to impairment of gas exchange, with a reduction of DLCO values immediately after anesthetic induction due to a concomitant reduction of both DM and Vc. While changes in DM were due to the reduction of lung volume, changes in Vc were not limited to volume loss, since the Vc/alveolar volume ratio decreased significantly. Although DLCO and its components decreased immediately after induction, none of the values decreased further at 1 and 3 hours. Surfactant protein type B, however, was unchanged immediately after anesthesia but increased at 1 hour after induction and further increased after 3 hours of anesthesia. The level of alveolar damage correlated with the reduction of lung perfusion and lung dynamic strain (i.e., ratio between tidal volume and end-expiratory lung volume).
A brief course of anesthesia and controlled ventilation leads to: (1) alveolar damage, which is correlated with lung strain and perfusion, and (2) impaired gas exchange mainly due to volume loss but also to reduced aerated lung perfusion.
麻醉患者常有肺泡-动脉氧分压差增大。本研究旨在评估麻醉、肌肉麻痹和短暂机械通气对肺的影响。
对 45 例无肺部疾病的行胸外手术患者，检测其一氧化碳肺弥散功能（DLCO），包括肺毛细血管血容量（Vc）和肺泡毛细血管膜通透性（DM）以及肺表面活性蛋白 B（肺泡损伤标志物）。
麻醉、肌肉麻痹和机械通气导致气体交换受损，麻醉诱导后即刻 DLCO 值下降，主要是由于 DM 和 Vc 同时降低。DM 的变化是由于肺容积减少所致，而 Vc 的变化不仅限于容积丢失，因为 Vc/肺泡容积比值显著降低。虽然 DLCO 及其各成分在诱导后即刻下降，但在 1 和 3 小时时均无进一步下降。然而，表面活性蛋白 B 立即麻醉后不变，但在诱导后 1 小时增加，并在麻醉后 3 小时进一步增加。肺泡损伤程度与肺灌注和肺动态应变（即潮气量与呼气末肺容积之比）的减少相关。
短暂的麻醉和控制性通气可导致：（1）肺泡损伤，与肺应变和灌注相关；（2）气体交换受损主要是由于容量丢失，也与充气肺灌注减少有关。
