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围手术期肺不张的发生机制。

Mechanisms of atelectasis in the perioperative period.

机构信息

Uppsala University, Dept of Medical Sciences, Clinical Physiology, 751 85 Uppsala, Sweden.

出版信息

Best Pract Res Clin Anaesthesiol. 2010 Jun;24(2):157-69. doi: 10.1016/j.bpa.2009.12.002.

Abstract

Atelectasis appears in about 90% of all patients who are anaesthetised. Up to 15-20% of the lung is regularly collapsed at its base during uneventful anaesthesia prior to any surgery being carried out. Atelectasis can persist for several days in the postoperative period. It is likely to be a focus of infection and may contribute to pulmonary complications. A major cause of anaesthesia-induced lung collapse is the use of high oxygen concentration during induction and maintenance of anaesthesia together with the use of anaesthetics that cause loss of muscle tone and fall in functional residual capacity (a common action of almost all anaesthetics). This causes absorption atelectasis behind closed airways. Compression of lung tissue and loss of surfactant or surfactant function are additional potential causes of atelectasis. Ventilation of the lungs with pure oxygen after a vital capacity manoeuvre that had re-opened a previously collapsed lung tissue results in rapid reappearance of atelectasis. If 40% O2 in nitrogen is used for ventilation of the lungs, atelectasis reappears slowly. A post-oxygenation manoeuvre is regularly performed to reduce the risk of hypoxaemia during awakening. However, a combination of oxygenation and airway suctioning will most likely cause new atelectasis. Recruitment at the end of the anaesthesia followed by ventilation with 100% O2 causes new atelectasis before anaesthesia is terminated but not with ventilation with lower fraction of inspired oxygen (FIO2). Thus, recruitment must be followed by ventilation with moderate FIO2.

摘要

肺不张在所有接受麻醉的患者中约占 90%。在进行任何手术之前,在无并发症的麻醉期间,多达 15-20%的肺在其基底处通常会塌陷。肺不张在术后可能会持续数天。它很可能成为感染的焦点,并可能导致肺部并发症。麻醉引起的肺塌陷的一个主要原因是在诱导和维持麻醉期间使用高浓度氧气,以及使用导致肌肉张力丧失和功能残气量下降的麻醉剂(几乎所有麻醉剂的共同作用)。这会导致闭合气道后面的吸收性肺不张。肺组织的压缩和表面活性剂或表面活性剂功能的丧失是肺不张的其他潜在原因。在先前塌陷的肺组织重新开放后,通过肺活量操作对肺部进行纯氧通气会导致肺不张迅速再次出现。如果用 40%氧气和 60%氮气对肺部进行通气,肺不张会缓慢再次出现。经常进行氧合后操作以降低苏醒期间缺氧的风险。然而,氧合和气道抽吸的组合很可能会导致新的肺不张。麻醉结束时的复张,然后用 100%氧气通气,会在麻醉结束前导致新的肺不张,但用较低吸氧分数(FIO2)通气则不会。因此,复张后必须用中等 FIO2通气。

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