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自发性张力性气胸:它是什么,它存在吗?

Spontaneous tension pneumothorax: what is it and does it exist?

机构信息

Department of Thoracic Medicine, Cairns Base Hospital, Cairns, Queensland, Australia.

出版信息

Intern Med J. 2012 Oct;42(10):1157-60. doi: 10.1111/j.1445-5994.2012.02910.x.

Abstract

Tension pneumothorax is variously defined but is generally thought of as a pneumothorax in which the pressure of intrapleural gas exceeds atmospheric pressure, producing adverse effects, including mediastinal shift associated with cardiovascular collapse, often attributed to reduced venous return and kinking of the great vessels. The mechanism of tension pneumothorax is said to be a valvular defect in the visceral pleura such that air enters the pleural space in inspiration but cannot exit in expiration, leading to a progressive increase in pressure. However, as the driving pressure forcing air into the pleura in inspiration is atmospheric pressure, the pleural pressure can never exceed 1 atm during inspiration in a spontaneously breathing subject. Furthermore, all pneumothoraces must have pressures greater than atmospheric during expiration, or conventional treatment with intercostal tube drainage would not work. Pilot experiments have failed to show any re-entry of pleural gas into the lung in patients with persistent air leaks but no evidence of tension, suggesting these behave as valvular pneumothoraces. Case reports of tension pneumothorax in spontaneously breathing patients are rare, and most patients have other explanations for clinical deterioration. Although a large and rapidly expanding pneumothorax may require urgent intervention, it is unlikely that the effects are mediated by high intrapleural pressures. The term tension pneumothorax in spontaneously breathing patients should be reconsidered.

摘要

张力性气胸的定义多种多样,但通常被认为是一种胸膜腔内压力超过大气压的气胸,会产生不良影响,包括与心血管衰竭相关的纵隔移位,通常归因于静脉回流减少和大血管扭曲。张力性气胸的机制被认为是脏层胸膜的瓣膜缺陷,使得空气在吸气时进入胸膜腔,但在呼气时无法排出,导致压力逐渐增加。然而,由于在自主呼吸的受试者吸气时迫使空气进入胸膜腔的驱动力压力为大气压,因此胸膜压力在吸气期间永远不会超过 1 大气压。此外,所有气胸在呼气期间的压力必须大于大气压,否则常规的肋间管引流治疗就不会起作用。初步实验未能显示出在持续漏气但没有张力迹象的患者中胸膜气体重新进入肺部,这表明这些患者的气胸表现为瓣膜性气胸。在自主呼吸的患者中,张力性气胸的病例报告很少见,大多数患者的临床恶化有其他解释。尽管大且迅速扩张的气胸可能需要紧急干预,但高胸膜内压力不太可能是其作用机制。在自主呼吸的患者中,张力性气胸的术语应重新考虑。

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