Department of Clinical Physiology, Lund University, Lund, Sweden.
Br J Anaesth. 2012 Oct;109(4):584-94. doi: 10.1093/bja/aes230. Epub 2012 Jul 29.
Low tidal volume (V(T)), PEEP, and low plateau pressure (P(PLAT)) are lung protective during acute respiratory distress syndrome (ARDS). This study tested the hypothesis that the aspiration of dead space (ASPIDS) together with computer simulation can help maintain gas exchange at these settings, thus promoting protection of the lungs.
ARDS was induced in pigs using surfactant perturbation plus an injurious ventilation strategy. One group then underwent 24 h protective ventilation, while control groups were ventilated using a conventional ventilation strategy at either high or low pressure. Pressure-volume curves (P(el)/V), blood gases, and haemodynamics were studied at 0, 4, 8, 16, and 24 h after the induction of ARDS and lung histology was evaluated.
The P(el)/V curves showed improvements in the protective strategy group and deterioration in both control groups. In the protective group, when respiratory rate (RR) was ≈ 60 bpm, better oxygenation and reduced shunt were found. Histological damage was significantly more severe in the high-pressure group. There were no differences in venous oxygen saturation and pulmonary vascular resistance between the groups.
The protective ventilation strategy of adequate pH or PaCO2 with minimal V(T), and high/safe P(PLAT) resulting in high PEEP was based on the avoidance of known lung-damaging phenomena. The approach is based upon the optimization of V(T), RR, PEEP, I/E, and dead space. This study does not lend itself to conclusions about the independent role of each of these features. However, dead space reduction is fundamental for achieving minimal V(T) at high RR. Classical physiology is applicable at high RR. Computer simulation optimizes ventilation and limiting of dead space using ASPIDS. Inspiratory P(el)/V curves recorded from PEEP or, even better, expiratory P(el)/V curves allow monitoring in ARDS.
小潮气量（V（T））、呼气末正压（PEEP）和低平台压（P（PLAT））在急性呼吸窘迫综合征（ARDS）期间具有肺保护作用。本研究检验了这样一个假设，即死腔（ASPIDS）的吸引加上计算机模拟可以帮助在这些设置下维持气体交换，从而促进肺的保护。
使用表面活性剂扰动加损伤性通气策略在猪中诱导 ARDS。一组随后接受 24 小时保护通气，而对照组则在高或低压力下使用常规通气策略进行通气。在 ARDS 诱导后 0、4、8、16 和 24 小时时研究压力-容积曲线（P（el）/V）、血气和血液动力学，并评估肺组织学。
P（el）/V 曲线显示保护策略组有所改善，而两组对照组均恶化。在保护组中，当呼吸频率（RR）约为 60 次/分时，发现氧合更好，分流减少。高压力组的组织学损伤明显更严重。各组之间静脉血氧饱和度和肺血管阻力无差异。
适当的 pH 或 PaCO2 与最小的 V（T）以及导致高 PEEP 的高/安全 P（PLAT）的保护通气策略是基于避免已知的肺损伤现象。该方法基于 V（T）、RR、PEEP、I/E 和死腔的优化。本研究无法得出关于这些特征各自独立作用的结论。然而，减少死腔对于在高 RR 下实现最小 V（T）至关重要。经典生理学在高 RR 时适用。计算机模拟使用 ASPIDS 优化通气和限制死腔。从 PEEP 记录的吸气 P（el）/V 曲线，甚至更好的是呼气 P（el）/V 曲线，允许在 ARDS 中进行监测。
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