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Increased effort during partial ventilatory support is not associated with lung damage in experimental acute lung injury
Intensive Care Medicine Experimental Pub Date : 2019-11-05 , DOI: 10.1186/s40635-019-0272-z
Dietrich Henzler 1, 2, 3, 4 , Alf Schmidt 1 , Zhaolin Xu 5 , Nada Ismaiel 2, 6 , Haibo Zhang 7, 8 , Arthur S Slutsky 7, 8 , Paolo Pelosi 9
Affiliation  

BackgroundAn on-going debate exists as to whether partial ventilatory support is lung protective in an acute phase of ARDS. So far, the effects of different respiratory efforts on the development of ventilator-associated lung injury (VALI) have been poorly understood.To test the hypothesis whether respiratory effort itself promotes VALI, acute lung injury (ALI) was induced in 48 Sprague Dawley rats by hydrochloric acid aspiration model. Hemodynamics, gas-exchange, and respiratory mechanics were measured after 4 h of ventilation in pressure control (PC), assist-control (AC), or pressure support with 100% (PS100), 60% (PS60), or 20% (PS20) of the driving pressure during PC. VALI was assessed by histological analysis and biological markers.ResultsALI was characterized by a decrease in PaO2/FiO2 from 447 ± 75 to 235 ± 90 mmHg (p < 0.001) and dynamic respiratory compliance from 0.53 ± 0.2 to 0.28 ± 0.1 ml/cmH2O (p < 0.001). There were no differences in hemodynamics or respiratory function among groups at baseline or after 4 h of ventilation. The reduction of mechanical pressure support was associated with a compensatory increase in an inspiratory effort such that peak inspiratory transpulmonary pressures were equal in all groups. The diffuse alveolar damage score showed significant lung injury but was similar among groups. Pro- and anti-inflammatory proteins in the bronchial fluid were comparable among groups.ConclusionsIn experimental ALI in rodents, the respiratory effort was increased by reducing the pressure support during partial ventilatory support. In the presence of a constant peak inspiratory transpulmonary pressure, an increased respiratory effort was not associated with worsening ventilator-associated lung injury measured by histologic score and biologic markers.

中文翻译:

部分通气支持期间增加的努力与实验性急性肺损伤的肺损伤无关

背景 关于部分通气支持在 ARDS 急性期是否具有肺保护作用,存在持续的争论。到目前为止,对不同呼吸努力对呼吸机相关肺损伤 (VALI) 发展的影响知之甚少。为了验证呼吸努力本身是否促进 VALI 的假设,在 48 只 Sprague Dawley 大鼠中诱导了急性肺损伤 (ALI)通过盐酸吸入模型。在压力控制 (PC)、辅助控制 (AC) 或 100% (PS100)、60% (PS60) 或 20% 压力支持通气 4 小时后测量血流动力学、气体交换和呼吸力学。 PS20) 的 PC 期间的驱动压力。VALI 通过组织学分析和生物标志物进行评估。 结果 ALI 的特征是 PaO2/FiO2 从 447 ± 75 降至 235 ± 90 mmHg(p < 0. 001) 和动态呼吸顺应性从 0.53 ± 0.2 到 0.28 ± 0.1 ml/cmH2O (p < 0.001)。在基线或通气 4 小时后,各组之间的血流动力学或呼吸功能没有差异。机械压力支持的减少与吸气努力的补偿性增加相关,因此所有组的吸气峰跨肺压相等。弥漫性肺泡损伤评分显示出明显的肺损伤,但组间相似。支气管液中的促炎蛋白和抗炎蛋白在各组之间具有可比性。结论在啮齿类动物的实验性 ALI 中,通过在部分通气支持期间降低压力支持来增加呼吸努力。在存在恒定的吸气跨肺压峰值时,
更新日期:2019-11-05
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