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呼吸机诱导性肺损伤的机制。

Mechanisms of ventilator-induced lung injury.

作者信息

Parker J C, Hernandez L A, Peevy K J

机构信息

Department of Physiology, University of South Alabama, College of Medicine, Mobile 36688.

出版信息

Crit Care Med. 1993 Jan;21(1):131-43. doi: 10.1097/00003246-199301000-00024.

Abstract

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 SOURCE

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.

摘要

目的

描述呼吸机所致肺损伤的生理机制,并确定导致此类损伤的主要呼吸机相关及宿主相关危险因素。

资料来源

与呼吸机所致气压伤和肺病理生理学相关的基础科学及临床研究。

研究选择

重点关注与特定机制相关的对照实验研究和临床研究。

资料提取

优先选择具有定量终点以评估损伤及因果关系的研究。

资料综合

尽可能整合相关研究以获取损伤的基本机制。

结论

高潮气量通气可增加血管滤过压;导致毛细血管内皮、上皮及基底膜的应力性骨折;并引起肺破裂。机械性损伤导致液体、蛋白质和血液漏入组织及气腔,或空气漏入组织间隙。此过程之后会引发炎症反应,并可能降低抗感染防御能力。肺损伤的易感因素包括吸气峰容积和压力过高、平均气道压过高、肺和胸壁结构不成熟、表面活性物质不足或失活以及既往存在的肺部疾病。通过在治疗性通气期间防止功能性肺单位过度扩张,可将损伤降至最低。

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