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呼吸机相关性肺损伤及其对临床管理的启示。

Ventilator-induced lung injury and implications for clinical management.

作者信息

Edibam C

机构信息

Department of Critical Care Medicine, Flinders Medical Centre, Adelaide, South Australia.

出版信息

Crit Care Resusc. 2000 Dec;2(4):269-77.

Abstract

OBJECTIVE

To review recent studies in pathogenesis and management of ventilator-induced lung injury.

DATA SOURCES

Articles and published reviews on ventilator-induced lung injury, barotrauma and acute lung injury.

SUMMARY OF REVIEW

This review summarises the important differences between clinically apparent 'barotrauma' and the more subtle changes in lung structure and function associated with ventilation. Of great importance is the understanding that as the underlying lung injury worsens, the degree of injury from mechanical ventilation increases. An inflammatory process results from mechanical stimuli and this may contribute to distant organ dysfunction. A great deal of knowledge has been obtained from the use of animal models, however, one must be cautious about extrapolating these findings directly to the clinical setting without the use of adequately designed clinical trials. Tidal volume reduction and higher levels of PEEP and recruitment manoeuvres should be employed given the available evidence. The use of high frequency techniques, surfactant therapy despite their past track record, may prove to be exciting 're-discoveries'.

CONCLUSIONS

Ventilator-induced lung injury is an iatrogenic disturbance that increases morbidity and mortality associated with acute respiratory distress syndrome. Tidal volume reduction and increased levels of PEEP have reduced inflammatory mediators and the mortality associated with ARDS.

摘要

目的

综述呼吸机相关性肺损伤发病机制及治疗的近期研究。

资料来源

关于呼吸机相关性肺损伤、气压伤和急性肺损伤的文章及已发表的综述。

综述总结

本综述总结了临床上明显的“气压伤”与通气相关的肺结构和功能更细微变化之间的重要差异。重要的是要认识到,随着潜在肺损伤的加重,机械通气造成的损伤程度会增加。机械刺激会引发炎症反应,这可能导致远隔器官功能障碍。通过动物模型已获得了大量知识,然而,在没有充分设计的临床试验的情况下,直接将这些发现外推至临床时必须谨慎。鉴于现有证据,应采用减少潮气量、提高呼气末正压水平及实施肺复张手法。高频技术、表面活性剂治疗尽管过去效果不佳,但可能会成为令人兴奋的“重新发现”。

结论

呼吸机相关性肺损伤是一种医源性干扰,会增加急性呼吸窘迫综合征的发病率和死亡率。减少潮气量和提高呼气末正压水平可减少炎症介质并降低急性呼吸窘迫综合征的死亡率。

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