MECHANISMS OF VENTILATOR-INDUCED LUNG INJURY
MECHANISMS OF VENTILATOR-INDUCED LUNG INJURY
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DOI：
10.1097/00003246-199301000-00024
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发表时间：
1993-01-01
影响因子：
8.8
通讯作者：
PEEVY, KJ
中科院分区：
文献类型：
--
作者：
PARKER, JC;HERNANDEZ, LA;PEEVY, KJ
目标.描述呼吸机引起的肺损伤的生理机制，并确定导致此类损伤的主要呼吸机和宿主依赖性风险因素。与呼吸机所致气压伤和肺病理生理学相关的基础科学和临床研究。研究选择：强调与特定机制相关的对照、实验研究和临床研究。数据提取：优先考虑具有定量终点的研究，以评估损伤和因果关系。数据合成：整合相关研究，以尽可能获得损伤的基本机制。结论：高潮气量通气可增加血管滤过压，造成毛细血管内皮、上皮和基底膜的应力性断裂，并导致肺破裂。机械损伤导致液体、蛋白质和血液泄漏到组织和空气间隙中，或空气泄漏到组织间隙中。这个过程之后是炎症反应，可能是对感染的防御能力降低。肺损伤的诱发因素是高峰吸气量和压力、高平均气道压力、肺和胸壁结构不成熟、表面活性物质不足或失活以及既存肺病。在治疗性通气过程中，通过防止功能性肺单位过度膨胀，可以将损伤降至最低。
Objectives. To describe the physiologic mechanisms of ventilator-induced lung injury and to define the major ventilator and host-dependent risk factors that contribute to such injury.Data Sources. Basic science and clinical studies related to ventilator-induced barotrauma and lung pathophysiology.Study Selection: Emphasis on controlled, experimental studies and clinical studies related to specific mechanisms.Data Extraction: Preference given to studies with quantitative end-points to assess damage and causal relationships.Data Synthesis: Related studies are integrated to obtain basic mechanisms of damage where possible.Conclusions: Ventilation with high tidal volumes can increase vascular filtration pressures; produce stress fractures of capillary endothelium, epithelium, and basement membrane; and cause lung rupture. Mechanical damage leads to leakage of fluid, protein, and blood into tissue and air spaces or leakage of air into tissue spaces. This process is followed by an inflammatory response and possibly a reduced defense against infection. Predisposing factors for lung injury are high peak inspiratory volumes and pressures, a high mean airway pressure, structural immaturity of lung and chest wall, surfactant insufficiency or inactivation, and preexisting lung disease. Damage can be minimized by preventing overdistention of functional lung units during therapeutic ventilation.