Telias Irene, Madorno Matías, Pham Tài, Coudroy Rémi, Mellado Artigas Ricard, Baedorf-Kassis Elias, Chen Chang-Wen, Spadaro Savino, Chiumello Davide, Beitler Jeremy, Kondili Eumorfia, Tiribelli Norberto, Fredes Sebastian, Becher Tobias, Dres Martin, Liu Kuan, Terzi Nicolas, Guérin Claude, Mauri Tommaso, Roca Oriol, Mancebo Jordi, Rodriguez Nuria, Arnal Jean-Michel, Goligher Ewan C, Diehl Jean-Luc, Jochmans Sébastien, Beloncle François, Rittayamai Nuttapol, Mojoli Francesco, Heunks Leo, de Vries Heder, Zhou Jian-Xin, Guervilly Christophe, Brochard Laurent
University of Toronto, Interdepartmental Division of Critical Care Medicine, Toronto, Ontario, Canada;
MBMed SA, Buenos Aires, Argentina.
Am J Respir Crit Care Med. 2025 Jul 23. doi: 10.1164/rccm.202411-2155OC.
Excessive stress (distending pressure), strain (volume deformation), and drop in inspiratory alveolar pressure are proposed mechanisms for patient self-inflicted lung injury.
To dissect the influence of inspiratory effort, respiratory mechanics, and ventilation mode on lung stress, strain, and drop in inspiratory alveolar pressure; and explore their impact on oxygenation and lung compliance.
International cohort study analyzing respiratory recordings (esophageal pressure) of patients with acute hypoxemic respiratory failure. Association between muscular pressure (Pmus), surrogates of stress (driving trans-alveolar pressure), strain (tidal volume), and inspiratory alveolar pressure relative to PEEP were explored with mixed-models, including interactions for ventilation mode, respiratory system elastance, and synchrony. Association between these and changes in oxygenation and lung compliance were explored.
60 patients from 15 centers represented 528 recordings (339,796 breaths). For each cmHO Pmus increase there was an increase in driving trans-alveolar pressure (median[CI 95%] 0.28[0.27-0.29]cmHO) and tidal volume (0.16[0.16-0.17]ml/kg of predicted body weight) and decrease in alveolar pressure (-0.25[0.24-0.6]cmHO, p<0.001). Volume-control ventilation showed less increase in stress and strain surrogates than pressure-targeted modes, but more drop in alveolar pressure (p<0.001, Pmus:mode interaction). Breath-stacking was infrequent and associated with higher stress. Lower inspiratory alveolar pressure relative to PEEP was associated with subsequent worsening oxygenation (p=0.04) and higher stress with worsening lung compliance (p=0.023).
Strong efforts are associated with high surrogates for lung stress, strain, and lower inspiratory alveolar pressure relative to PEEP, differently according to the mode of ventilation, being associated with subsequent worsening oxygenation and lung compliance.
过高的压力（扩张压力）、应变（容积变形）以及吸气时肺泡压力下降被认为是患者自身造成肺损伤的机制。
剖析吸气努力、呼吸力学和通气模式对肺压力、应变以及吸气时肺泡压力下降的影响；并探究它们对氧合和肺顺应性的影响。
一项国际队列研究，分析急性低氧性呼吸衰竭患者的呼吸记录（食管压力）。采用混合模型探讨肌肉压力（Pmus）、压力替代指标（驱动跨肺泡压）、应变（潮气量）以及相对于呼气末正压（PEEP）的吸气肺泡压力之间的关联，包括通气模式、呼吸系统弹性和同步性的相互作用。探究这些指标与氧合和肺顺应性变化之间的关联。
来自15个中心的60例患者共有528份记录（339,796次呼吸）。Pmus每增加1cmH₂O，驱动跨肺泡压增加（中位数[95%置信区间]0.28[0.27 - 0.29]cmH₂O），潮气量增加（0.16[0.16 - 0.17]ml/kg预测体重），肺泡压力降低（-0.25[0.24 - 0.6]cmH₂O，p<0.001）。容量控制通气模式下压力和应变替代指标的增加幅度小于压力目标模式，但肺泡压力下降幅度更大（p<0.001，Pmus:模式相互作用）。呼吸叠加不常见且与更高的压力相关。相对于PEEP，较低的吸气肺泡压力与随后氧合恶化相关（p = 0.04），较高的压力与肺顺应性恶化相关（p = 0.023）。
较大的努力与较高的肺压力、应变替代指标以及相对于PEEP较低的吸气肺泡压力相关，根据通气模式的不同，这与随后的氧合恶化和肺顺应性下降有关。
