Broche Ludovic, Perchiazzi Gaetano, Porra Liisa, Tannoia Angela, Pellegrini Mariangela, Derosa Savino, Sindaco Alessandra, Batista Borges João, Degrugilliers Loïc, Larsson Anders, Hedenstierna Göran, Wexler Anthony S, Bravin Alberto, Verbanck Sylvia, Smith Bradford J, Bates Jason H T, Bayat Sam
1European Synchrotron Radiation Facility, ID17 Biomedical Beamline, Grenoble, France.2Department of Pediatric Pulmonology, Université de Picardie Jules Verne, Inserm U1105 & Amiens University Hospital, Amiens, France.3Hedenstierna Laboratory, Department of Surgical Sciences, Section of Anaesthesiology & Critical Care, Uppsala University, Uppsala, Sweden.4Department of Emergency and Organ Transplant, University of Bari, Bari, Italy.5Department of Physics, University of Helsinki, Helsinki, Finland.6Helsinki University Central Hospital, Helsinki, Finland.7Pulmonary Division, Cardio-Pulmonary Department, Heart Institute (Incor), University of São Paulo, São Paulo, Brazil.8Hedenstierna Laboratory, Department of Medical Sciences, Clinical Physiology, Uppsala University, Uppsala, Sweden.9Department of Mechanical Engineering and Environmental Quality Laboratory, University of California Davis, Davis, CA.10Respiratory Division, University Hospital UZ Brussel, Brussels, Belgium.11Department of Medicine, University of Vermont, Burlington, VT.
Crit Care Med. 2017 Apr;45(4):687-694. doi: 10.1097/CCM.0000000000002234.
Positive pressure ventilation exposes the lung to mechanical stresses that can exacerbate injury. The exact mechanism of this pathologic process remains elusive. The goal of this study was to describe recruitment/derecruitment at acinar length scales over short-time frames and test the hypothesis that mechanical interdependence between neighboring lung units determines the spatial and temporal distributions of recruitment/derecruitment, using a computational model.
Experimental animal study.
International synchrotron radiation laboratory.
Four anesthetized rabbits, ventilated in pressure controlled mode.
The lung was consecutively imaged at ~ 1.5-minute intervals using phase-contrast synchrotron imaging, at positive end-expiratory pressures of 12, 9, 6, 3, and 0 cm H2O before and after lavage and mechanical ventilation induced injury. The extent and spatial distribution of recruitment/derecruitment was analyzed by subtracting subsequent images. In a realistic lung structure, we implemented a mechanistic model in which each unit has individual pressures and speeds of opening and closing. Derecruited and recruited lung fractions (Fderecruited, Frecruited) were computed based on the comparison of the aerated volumes at successive time points.
Alternative recruitment/derecruitment occurred in neighboring alveoli over short-time scales in all tested positive end-expiratory pressure levels and despite stable pressure controlled mode. The computational model reproduced this behavior only when parenchymal interdependence between neighboring acini was accounted for. Simulations closely mimicked the experimental magnitude of Fderecruited and Frecruited when mechanical interdependence was included, while its exclusion gave Frecruited values of zero at positive end-expiratory pressure greater than or equal to 3 cm H2O.
These findings give further insight into the microscopic behavior of the injured lung and provide a means of testing protective-ventilation strategies to prevent recruitment/derecruitment and subsequent lung damage.
正压通气会使肺暴露于可能加剧损伤的机械应力之下。这一病理过程的确切机制仍不清楚。本研究的目的是使用计算模型描述短时间内腺泡长度尺度上的再充盈/去充盈情况,并检验相邻肺单位之间的机械相互依存关系决定再充盈/去充盈的空间和时间分布这一假设。
实验动物研究。
国际同步加速器辐射实验室。
四只麻醉兔,采用压力控制模式通气。
在灌洗和机械通气诱导损伤前后,使用相衬同步加速器成像以约1.5分钟的间隔对肺进行连续成像,呼气末正压分别为12、9、6、3和0 cmH₂O。通过减去后续图像来分析再充盈/去充盈的范围和空间分布。在真实的肺结构中,我们实施了一个机制模型,其中每个单位都有各自的压力以及开放和关闭速度。根据连续时间点的充气量比较计算去充盈和再充盈的肺部分(F去充盈,F再充盈)。
在所有测试的呼气末正压水平下,尽管压力控制模式稳定,但在短时间尺度上相邻肺泡出现了交替的再充盈/去充盈。仅当考虑相邻腺泡之间的实质相互依存关系时,计算模型才重现了这种行为。当包括机械相互依存关系时,模拟结果紧密模仿了F去充盈和F再充盈的实验幅度,而排除该因素时,在呼气末正压大于或等于3 cmH₂O时,F再充盈值为零。
这些发现进一步深入了解了受损肺的微观行为,并提供了一种测试保护性通气策略以防止再充盈/去充盈及后续肺损伤的方法。