Thoracic Disease Research Unit, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Expert Rev Respir Med. 2010 Jun;4(3):373-85. doi: 10.1586/ers.10.28.
Although mechanical ventilation (MV) is a life-saving intervention for patients with acute respiratory distress syndrome (ARDS), it can aggravate or cause lung injury, known as ventilator-induced lung injury (VILI). The biophysical characteristics of heterogeneously injured ARDS lungs increase the parenchymal stress associated with breathing, which is further aggravated by MV. Cells, in particular those lining the capillaries, airways and alveoli, transform this strain into chemical signals (mechanotransduction). The interaction of reparative and injurious mechanotransductive pathways leads to VILI. Several attempts have been made to identify clinical surrogate measures of lung stress/strain (e.g., density changes in chest computed tomography, lower and upper inflection points of the pressure-volume curve, plateau pressure and inflammatory cytokine levels) that could be used to titrate MV. However, uncertainty about the topographical distribution of stress relative to that of the susceptibility of the cells and tissues to injury makes the existence of a single 'global' stress/strain injury threshold doubtful.
尽管机械通气（MV）是急性呼吸窘迫综合征（ARDS）患者的救命干预措施，但它会加重或导致肺损伤，称为呼吸机引起的肺损伤（VILI）。不均匀损伤的 ARDS 肺的生物物理特性会增加与呼吸相关的实质压力，MV 会进一步加重这种压力。细胞，特别是那些衬在毛细血管、气道和肺泡上的细胞，会将这种应变转化为化学信号（力学转导）。修复性和损伤性力学转导途径的相互作用导致了 VILI。已经有一些尝试来识别肺应激/应变的临床替代指标（例如，胸部计算机断层扫描密度变化、压力-容积曲线的下拐点和上拐点、平台压和炎症细胞因子水平），这些指标可用于调整 MV。然而，由于相对于细胞和组织对损伤的易感性，应激的空间分布不确定，使得存在单一的“整体”应激/应变损伤阈值这一说法值得怀疑。
