Department of Critical Care and Anesthesiology, CHU Montpellier, Hôpital Saint Eloi, 80 avenue Augustin Fliche, 34295 Montpellier Cedex 5, France.
Crit Care. 2011 Mar 11;15(2):206. doi: 10.1186/cc10023.
Diaphragmatic function is a major determinant of the ability to successfully wean patients from mechanical ventilation. However, the use of controlled mechanical ventilation in animal models results in a major reduction of diaphragmatic force-generating capacity together with structural injury and atrophy of diaphragm muscle fibers, a condition termed ventilator-induced diaphragmatic dysfunction (VIDD). Increased oxidative stress and exaggerated proteolysis in the diaphragm have been linked to the development of VIDD in animal models, but much less is known about the extent to which these phenomena occur in humans undergoing mechanical ventilation in the ICU. In the present review, we first briefly summarize the large body of evidence demonstrating the existence of VIDD in animal models, and outline the major cellular mechanisms that have been implicated in this process. We then relate these findings to very recently published data in critically ill patients, which have thus far been found to exhibit a remarkable degree of similarity with the animal model data. Hence, the human studies to date have indicated that mechanical ventilation is associated with increased oxidative stress, atrophy, and injury of diaphragmatic muscle fibers along with a rapid loss of diaphragmatic force production. These changes are, to a large extent, directly proportional to the duration of mechanical ventilation. In the context of these human data, we also review the methods that can be used in the clinical setting to diagnose and/or monitor the development of VIDD in critically ill patients. Finally, we discuss the potential for using different mechanical ventilation strategies and pharmacological approaches to prevent and/or to treat VIDD and suggest promising avenues for future research in this area.
膈肌功能是成功脱离机械通气的主要决定因素。然而，在动物模型中使用控制机械通气会导致膈肌产生能力的显著降低，同时伴随着膈肌纤维的结构损伤和萎缩，这种情况被称为呼吸机诱导的膈肌功能障碍（VIDD）。在动物模型中，膈肌中氧化应激的增加和蛋白水解的过度活跃与 VIDD 的发展有关，但在接受 ICU 机械通气的人类中，这些现象发生的程度知之甚少。在本综述中，我们首先简要总结了大量证据证明 VIDD 在动物模型中的存在，并概述了与该过程相关的主要细胞机制。然后，我们将这些发现与最近发表的危重病患者的数据联系起来，迄今为止，这些数据与动物模型数据表现出了非常显著的相似性。因此，迄今为止的人体研究表明，机械通气与氧化应激增加、膈肌纤维萎缩和损伤以及膈肌力量产生的迅速丧失有关。这些变化在很大程度上与机械通气的持续时间直接相关。在这些人体数据的背景下，我们还回顾了可以在临床环境中用于诊断和/或监测危重病患者 VIDD 发展的方法。最后，我们讨论了使用不同的机械通气策略和药理学方法来预防和/或治疗 VIDD 的潜力，并提出了该领域未来研究的有前途的途径。
