Silva Pedro Leme, Scharffenberg Martin, Rocco Patricia Rieken Macedo
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G-014, Ilha Do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.
Department of Anesthesiology and Intensive Care Medicine, Pulmonary Engineering Group, University Hospital Carl Gustav Carus at Technische Universität Dresden, Dresden, Germany.
Intensive Care Med Exp. 2023 Nov 27;11(1):82. doi: 10.1186/s40635-023-00569-5.
Mechanical ventilation is a life-saving therapy in several clinical situations, promoting gas exchange and providing rest to the respiratory muscles. However, mechanical ventilation may cause hemodynamic instability and pulmonary structural damage, which is known as ventilator-induced lung injury (VILI). The four main injury mechanisms associated with VILI are as follows: barotrauma/volutrauma caused by overstretching the lung tissues; atelectrauma, caused by repeated opening and closing of the alveoli resulting in shear stress; and biotrauma, the resulting biological response to tissue damage, which leads to lung and multi-organ failure. This narrative review elucidates the mechanisms underlying the pathogenesis, progression, and resolution of VILI and discusses the strategies that can mitigate VILI. Different static variables (peak, plateau, and driving pressures, positive end-expiratory pressure, and tidal volume) and dynamic variables (respiratory rate, airflow amplitude, and inspiratory time fraction) can contribute to VILI. Moreover, the potential for lung injury depends on tissue vulnerability, mechanical power (energy applied per unit of time), and the duration of that exposure. According to the current evidence based on models of acute respiratory distress syndrome and VILI, the following strategies are proposed to provide lung protection: keep the lungs partially collapsed (SaO > 88%), avoid opening and closing of collapsed alveoli, and gently ventilate aerated regions while keeping collapsed and consolidated areas at rest. Additional mechanisms, such as subject-ventilator asynchrony, cumulative power, and intensity, as well as the damaging threshold (stress-strain level at which tidal damage is initiated), are under experimental investigation and may enhance the understanding of VILI.
机械通气在多种临床情况下是一种挽救生命的治疗方法，可促进气体交换并使呼吸肌得到休息。然而，机械通气可能会导致血流动力学不稳定和肺结构损伤，这被称为呼吸机诱导的肺损伤（VILI）。与VILI相关的四种主要损伤机制如下：肺组织过度伸展导致的气压伤/容积伤；肺泡反复开闭导致剪切应力引起的肺不张伤；以及生物伤，即对组织损伤产生的生物学反应，可导致肺和多器官功能衰竭。这篇叙述性综述阐明了VILI发病机制、进展和缓解的潜在机制，并讨论了可减轻VILI的策略。不同的静态变量（峰值、平台压和驱动压、呼气末正压和潮气量）和动态变量（呼吸频率、气流幅度和吸气时间分数）都可能导致VILI。此外，肺损伤的可能性取决于组织易损性、机械功率（单位时间施加的能量）以及暴露持续时间。根据目前基于急性呼吸窘迫综合征和VILI模型的证据，提出以下肺保护策略：使肺部分塌陷（SaO > 88%），避免塌陷肺泡的开闭，并在保持塌陷和实变区域静止的同时轻柔地对通气区域进行通气。其他机制，如人机不同步、累积功率和强度，以及损伤阈值（引发潮气量损伤的应力应变水平），正在进行实验研究，可能会增进对VILI的理解。
