Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Department of Physiotherapy, Faculty of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Crit Care. 2020 Jun 3;24(1):284. doi: 10.1186/s13054-020-03011-4.
We dissected total power into its primary components to resolve its relative contributions to tissue damage (VILI). We hypothesized that driving power or elastic (dynamic) power offers more precise VILI risk indicators than raw total power. The relative correlations of these three measures of power with VILI-induced histologic changes and injury biomarkers were determined using a rodent model of acute respiratory distress syndrome (ARDS). Herein, we have significantly extended the scope of our previous research.
Data analyses were performed in male Wistar rats that received endotoxin intratracheally to induce ARDS. After 24 h, they were randomized to 1 h of volume-controlled ventilation with low V = 6 ml/kg and different PEEP levels (3, 5.5, 7.5, 9.5, and 11 cmHO). Applied levels of driving power, dynamic power inclusive of PEEP, and total power were correlated with VILI indicators [lung histology and biological markers associated with inflammation (interleukin-6), alveolar stretch (amphiregulin), and epithelial (club cell protein (CC)-16) and endothelial (intercellular adhesion molecule-1) cell damage in lung tissue].
Driving power was higher at PEEP-11 than other PEEP levels. Dynamic power and total power increased progressively from PEEP-5.5 and PEEP-7.5, respectively, to PEEP-11. Driving power, dynamic power, and total power each correlated with the majority of VILI indicators. However, when correlations were performed from PEEP-3 to PEEP-9.5, no relationships were observed between driving power and VILI indicators, whereas dynamic power and total power remained well correlated with CC-16 expression, alveolar collapse, and lung hyperinflation.
In this mild-moderate ARDS model, dynamic power, not driving power alone, emerged as the key promoter of VILI. Moreover, hazards from driving power were conditioned by the requirement to pass a tidal stress threshold. When estimating VILI hazard from repeated mechanical strains, PEEP must not be disregarded as a major target for modification.
我们将总功率分解为其主要组成部分，以解决其对组织损伤（呼吸机相关性肺损伤，VILI）的相对贡献。我们假设驱动功率或弹性（动态）功率比原始总功率提供更精确的 VILI 风险指标。使用急性呼吸窘迫综合征（ARDS）的啮齿动物模型，确定了这三种功率测量与 VILI 诱导的组织学变化和损伤生物标志物的相对相关性。在这里，我们已经大大扩展了我们之前研究的范围。
对接受气管内内毒素的雄性 Wistar 大鼠进行数据分析，以诱导 ARDS。24 小时后，它们被随机分配到低 V（6ml/kg）和不同 PEEP 水平（3、5.5、7.5、9.5 和 11cmHO）的容量控制通气 1 小时。驱动功率、包含 PEEP 的动态功率和总功率的应用水平与 VILI 指标相关[肺组织中的炎症（白细胞介素-6）、肺泡拉伸（ Amphiregulin）、上皮（Club 细胞蛋白（CC）-16）和内皮（细胞间黏附分子-1）细胞损伤相关的生物标志物]。
PEEP-11 时的驱动功率高于其他 PEEP 水平。从 PEEP-5.5 开始，动态功率和总功率分别逐渐增加到 PEEP-11。驱动功率、动态功率和总功率均与大多数 VILI 指标相关。然而，当从 PEEP-3 到 PEEP-9.5 进行相关性分析时，驱动功率与 VILI 指标之间没有关系，而动态功率和总功率仍与 CC-16 表达、肺泡塌陷和肺过度充气密切相关。
在这种轻度中度 ARDS 模型中，动态功率而不是单独的驱动功率成为 VILI 的主要促进因素。此外，驱动功率的危险受到需要通过潮汐压力阈值的限制。在估计来自重复机械应变的 VILI 危险时，不能忽视 PEEP 作为主要修改目标。
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