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机械通气时的肺应力和应变:有安全阈值吗?

Lung stress and strain during mechanical ventilation: any safe threshold?

机构信息

Dipartimento di Anestesiologia, Terapia Intensiva e Scienze Dermatologiche, Università degli Studi di Milano, Milan, Italy.

出版信息

Am J Respir Crit Care Med. 2011 May 15;183(10):1354-62. doi: 10.1164/rccm.201010-1757OC. Epub 2011 Feb 4.

Abstract

RATIONALE

Unphysiologic strain (the ratio between tidal volume and functional residual capacity) and stress (the transpulmonary pressure) can cause ventilator-induced lung damage.

OBJECTIVES

To identify a strain-stress threshold (if any) above which ventilator-induced lung damage can occur.

METHODS

Twenty-nine healthy pigs were mechanically ventilated for 54 hours with a tidal volume producing a strain between 0.45 and 3.30. Ventilator-induced lung damage was defined as net increase in lung weight.

MEASUREMENTS AND MAIN RESULTS

Initial lung weight and functional residual capacity were measured with computed tomography. Final lung weight was measured using a balance. After setting tidal volume, data collection included respiratory system mechanics, gas exchange and hemodynamics (every 6 h); cytokine levels in serum (every 12 h) and bronchoalveolar lavage fluid (end of the experiment); and blood laboratory examination (start and end of the experiment). Two clusters of animals could be clearly identified: animals that increased their lung weight (n = 14) and those that did not (n = 15). Tidal volume was 38 ± 9 ml/kg in the former and 22 ± 8 ml/kg in the latter group, corresponding to a strain of 2.16 ± 0.58 and 1.29 ± 0.57 and a stress of 13 ± 5 and 8 ± 3 cm H(2)O, respectively. Lung weight gain was associated with deterioration in respiratory system mechanics, gas exchange, and hemodynamics, pulmonary and systemic inflammation and multiple organ dysfunction.

CONCLUSIONS

In healthy pigs, ventilator-induced lung damage develops only when a strain greater than 1.5-2 is reached or overcome. Because of differences in intrinsic lung properties, caution is warranted in translating these findings to humans.

摘要

背景

生理应变(潮气量与功能残气量之比)和应切力(跨肺压)可导致呼吸机相关性肺损伤。

目的

确定能导致呼吸机相关性肺损伤的应变-应切力阈值(如果存在的话)。

方法

29 只健康猪用潮气量为 0.45 至 3.30 的呼吸机通气 54 小时,该潮气量可产生介于 0.45 至 3.30 的应变。以肺重量的净增加来定义呼吸机相关性肺损伤。

测量和主要结果

初始肺重量和功能残气量用计算机断层扫描测定。终末肺重量用天平测定。设定潮气量后,每 6 小时收集一次呼吸系统力学、气体交换和血液动力学数据;每 12 小时收集一次血清和支气管肺泡灌洗液中的细胞因子水平(实验结束时);每 6 小时收集一次血液实验室检查结果(实验开始和结束时)。可明确地将两组动物区分开来:肺重量增加的动物(n = 14)和肺重量未增加的动物(n = 15)。前者的潮气量为 38 ± 9 ml/kg,后者为 22 ± 8 ml/kg,相应的应变分别为 2.16 ± 0.58 和 1.29 ± 0.57,应切力分别为 13 ± 5 和 8 ± 3 cm H(2)O。肺重量增加与呼吸系统力学、气体交换和血液动力学恶化、肺和全身炎症以及多器官功能障碍有关。

结论

在健康猪中,只有当达到或超过 1.5-2 的应变时才会发生呼吸机相关性肺损伤。由于内在肺特性的差异,在将这些发现转化为人类时需要谨慎。

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