Department of Medicine, University of Colorado, Aurora, Colorado.
Am J Respir Crit Care Med. 2022 Jan 15;205(2):152-160. doi: 10.1164/rccm.202107-1690CP.
Ventilator-induced lung injury (VILI) is currently ascribed to volutrauma and/or atelectrauma, but the effect of constant Vt ventilation (CVtV) has received little attention. This Perspective summarizes the literature documenting that CVtV causes VILI and reviews the mechanisms by which it occurs. Surfactant is continuously inactivated, depleted, displaced, or desorbed as a function of the duration of ventilation, the Vt, the level of positive end-expiratory pressure (PEEP), and possibly the respiratory rate. Accordingly, surfactant must be continuously replenished, and secretion primarily depends on intermittent delivery of large ventilatory excursions. The surfactant abnormalities resulting from CVtV result in atelectasis and VILI. Although surfactant secretion is reduced by the absence of intermittent deep breaths, continuous administration of large Vts depletes surfactant and impairs subsequent secretion. Low or normal lung volumes result in desorption of surfactant. PEEP can be protective by reducing surface film collapse and subsequent film rupture on reexpansion, and/or by reducing surfactant displacement into the airways, but PEEP can also downregulate surfactant release. The effect of CVtV on surfactant is complex. If attention is not paid to facilitating surfactant secretion and limiting its inactivation, depletion, desorption, or displacement, surface tension will increase and atelectasis and VILI will occur.
呼吸机相关性肺损伤（VILI）目前归因于容积伤和/或肺不张伤，但持续容量控制通气（CVtV）的影响尚未得到太多关注。本观点总结了记录 CVtV 导致 VILI 的文献，并回顾了其发生的机制。随着通气时间、潮气量、呼气末正压（PEEP）水平的延长和可能的呼吸频率的延长，表面活性物质不断被灭活、耗尽、移位或解吸。因此，表面活性物质必须不断补充，分泌主要取决于间歇性大通气的输送。由于 CVtV，表面活性物质异常导致肺不张和 VILI。虽然间歇性深呼气的缺失会减少表面活性物质的分泌，但持续给予大的潮气量会耗尽表面活性物质并损害随后的分泌。低或正常的肺容量会导致表面活性物质的解吸。PEEP 可以通过减少表面膜塌陷和再扩张后的膜破裂，以及/或通过减少表面活性物质向气道的移位来起到保护作用，但 PEEP 也可以下调表面活性物质的释放。CVtV 对表面活性物质的影响是复杂的。如果不注意促进表面活性物质的分泌并限制其失活、耗竭、解吸或移位，表面张力将增加，肺不张和 VILI 将发生。
