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体外膜肺氧合治疗的急性呼吸窘迫综合征患者中,超保护性通气与窒息通气的生理研究

Ultraprotective versus apneic ventilation in acute respiratory distress syndrome patients with extracorporeal membrane oxygenation: a physiological study.

作者信息

Graf Peter T, Boesing Christoph, Brumm Isabel, Biehler Jonas, Müller Kei Wieland, Thiel Manfred, Pelosi Paolo, Rocco Patricia R M, Luecke Thomas, Krebs Joerg

机构信息

Department of Anesthesiology and Critical Care Medicine, University Medical Centre Mannheim, Medical Faculty Mannheim of the University of Heidelberg, Theodor-Kutzer Ufer 1-3, 68167, Mannheim, Germany.

Institute for Computational Mechanics, Technical University Munich, Boltzmannstraße 15, 85748, Garching, Germany.

出版信息

J Intensive Care. 2022 Mar 7;10(1):12. doi: 10.1186/s40560-022-00604-9.

DOI:10.1186/s40560-022-00604-9
PMID:35256012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8900404/
Abstract

BACKGROUND

Even an ultraprotective ventilation strategy in severe acute respiratory distress syndrome (ARDS) patients treated with extracorporeal membrane oxygenation (ECMO) might induce ventilator-induced lung injury and apneic ventilation with the sole application of positive end-expiratory pressure may, therefore, be an alternative ventilation strategy. We, therefore, compared the effects of ultraprotective ventilation with apneic ventilation on oxygenation, oxygen delivery, respiratory system mechanics, hemodynamics, strain, air distribution and recruitment of the lung parenchyma in ARDS patients with ECMO.

METHODS

In a prospective, monocentric physiological study, 24 patients with severe ARDS managed with ECMO were ventilated using ultraprotective ventilation (tidal volume 3 ml/kg of predicted body weight) with a fraction of inspired oxygen (FiO) of 21%, 50% and 90%. Patients were then treated with apneic ventilation with analogous FiO. The primary endpoint was the effect of the ventilation strategy on oxygenation and oxygen delivery. The secondary endpoints were mechanical power, stress, regional air distribution, lung recruitment and the resulting strain, evaluated by chest computed tomography, associated with the application of PEEP (apneic ventilation) and/or low V (ultraprotective ventilation).

RESULTS

Protective ventilation, compared to apneic ventilation, improved oxygenation (arterial partial pressure of oxygen, p < 0.001 with FiO of 50% and 90%) and reduced cardiac output. Both ventilation strategies preserved oxygen delivery independent of the FiO. Protective ventilation increased driving pressure, stress, strain, mechanical power, as well as induced additional recruitment in the non-dependent lung compared to apneic ventilation.

CONCLUSIONS

In patients with severe ARDS managed with ECMO, ultraprotective ventilation compared to apneic ventilation improved oxygenation, but increased stress, strain, and mechanical power. Apneic ventilation might be considered as one of the options in the initial phase of ECMO treatment in severe ARDS patients to facilitate lung rest and prevent ventilator-induced lung injury.

TRIAL REGISTRATION

German Clinical Trials Register (DRKS00013967). Registered 02/09/2018. https://www.drks.de/drks_web/navigate.do?navigationId=trial.HTML&TRIAL_ID=DRKS00013967 .

摘要

背景

即使在接受体外膜肺氧合(ECMO)治疗的重症急性呼吸窘迫综合征(ARDS)患者中采用超保护性通气策略,也可能导致呼吸机诱导的肺损伤,因此仅应用呼气末正压进行无呼吸通气可能是一种替代通气策略。因此,我们比较了超保护性通气与无呼吸通气对接受ECMO治疗的ARDS患者的氧合、氧输送、呼吸系统力学、血流动力学、应变、气体分布和肺实质复张的影响。

方法

在一项前瞻性、单中心生理学研究中,对24例接受ECMO治疗的重症ARDS患者采用超保护性通气(潮气量为预测体重的3 ml/kg),吸入氧分数(FiO)分别为21%、50%和90%。然后对患者采用类似FiO的无呼吸通气治疗。主要终点是通气策略对氧合和氧输送的影响。次要终点是机械功率、应力、区域气体分布、肺复张以及由此产生的应变,通过胸部计算机断层扫描评估,与呼气末正压(无呼吸通气)和/或低潮气量(超保护性通气)的应用相关。

结果

与无呼吸通气相比,保护性通气改善了氧合(在FiO为50%和90%时,动脉血氧分压,p < 0.001)并降低了心输出量。两种通气策略均能保持氧输送,与FiO无关。与无呼吸通气相比,保护性通气增加了驱动压力、应力、应变、机械功率,并在非下垂肺中诱导了额外的复张。

结论

在接受ECMO治疗的重症ARDS患者中,与无呼吸通气相比,超保护性通气改善了氧合,但增加了应力、应变和机械功率。无呼吸通气可被视为重症ARDS患者ECMO治疗初始阶段的选择之一,以促进肺休息并预防呼吸机诱导的肺损伤。

试验注册

德国临床试验注册中心(DRKS00013967)。于2018年9月2日注册。https://www.drks.de/drks_web/navigate.do?navigationId=trial.HTML&TRIAL_ID=DRKS00013967 。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73f/8900404/df4a5615a969/40560_2022_604_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73f/8900404/0469a83d03dc/40560_2022_604_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73f/8900404/df4a5615a969/40560_2022_604_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73f/8900404/0469a83d03dc/40560_2022_604_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73f/8900404/df4a5615a969/40560_2022_604_Fig2_HTML.jpg

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