Curley Gerard F, Laffey John G, Zhang Haibo, Slutsky Arthur S
Department of Anesthesia, St Michael's Hospital, and the Critical Illness and Injury Research Centre, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, Ontario, Canada; Department of Anesthesia, University of Toronto, Toronto, Ontario, Canada.
Department of Anesthesia, St Michael's Hospital, and the Critical Illness and Injury Research Centre, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, Ontario, Canada; Department of Anesthesia, University of Toronto, Toronto, Ontario, Canada; Department of Physiology, University of Toronto, Toronto, Ontario, Canada.
Chest. 2016 Nov;150(5):1109-1117. doi: 10.1016/j.chest.2016.07.019. Epub 2016 Jul 29.
The pathophysiological mechanisms by which mechanical ventilation can contribute to lung injury, termed "ventilator-induced lung injury" (VILI), is increasingly well understood. "Biotrauma" describes the release of mediators by injurious ventilatory strategies, which can lead to lung and distal organ injury. Insights from preclinical models demonstrating that traditional high tidal volumes drove the inflammatory response helped lead to clinical trials demonstrating lower mortality in patients who underwent ventilation with a lower-tidal-volume strategy. Other approaches that minimize VILI, such as higher positive end-expiratory pressure, prone positioning, and neuromuscular blockade have each been demonstrated to decrease indices of activation of the inflammatory response. This review examines the evolution of our understanding of the mechanisms underlying VILI, particularly regarding biotrauma. We will assess evidence that ventilatory and other "adjunctive" strategies that decrease biotrauma offer great potential to minimize the adverse consequences of VILI and to improve the outcomes of patients with respiratory failure.
机械通气导致肺损伤(称为“呼吸机诱导的肺损伤”,即VILI)的病理生理机制已越来越为人所熟知。“生物创伤”描述了有害通气策略导致的介质释放,这可能会导致肺和远端器官损伤。临床前模型的研究结果表明,传统的高潮气量会引发炎症反应,这有助于推动临床试验,结果显示采用低潮气量策略进行通气的患者死亡率更低。其他可将VILI降至最低的方法,如较高的呼气末正压、俯卧位和神经肌肉阻滞,均已被证明可降低炎症反应的激活指标。本综述探讨了我们对VILI潜在机制,特别是生物创伤的理解的演变。我们将评估相关证据,即减少生物创伤的通气及其他“辅助”策略,在将VILI的不良后果降至最低并改善呼吸衰竭患者的预后方面具有巨大潜力。