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血管加压药和正性肌力药的应用

Author
Scott Manaker, MD, PhD
Section Editor
Polly E Parsons, MD
Deputy Editor
Geraldine Finlay, MD
Translators
车京津, 主任医师

引言

血管加压药是一类引起血管收缩、从而升高平均动脉压(mean arterial pressure, MAP)的作用较强药物。血管加压药有别于正性肌力药，后者是增加心肌收缩力；但是，许多药物兼有血管加压作用和正性肌力作用。虽然许多血管加压药从20世纪40年代就已使用，但很少有临床对照试验直接比较这些药物或证实使用这类药物能够改善结局[1]。因此，通常使用这些药物的方式，很大程度上反映了专家的意见、动物实验的数据，以及使用组织氧合等替代终点来替代减轻病况和死亡风险。

基础的肾上腺素能受体生理学，以及围绕使用血管加压药和正性肌力药治疗休克的原则、并发症和争议，都将在此介绍。关于休克的鉴别诊断和对脓毒性休克患者使用血管加压药的问题，将单独讨论。 (参见“成人休克的定义、分类、病因及病理生理学”和“成人严重脓毒症及脓毒性休克的评估和治疗”)

受体的生理学

与血管加压活性有关的肾上腺素能受体的主要类别有α1、β1和β2肾上腺素受体及多巴胺受体[2,3]。

α肾上腺素受体 — 激活位于血管壁的α1肾上腺素受体，能够诱发显著的血管收缩。α1-肾上腺素受体也存在于心脏，可增加心脏收缩的持续时间而不增强心脏变时性。然而，尚不清楚这种现象的临床意义[4]。

β肾上腺素受体 — β1肾上腺素受体最常见于心脏，可介导正性肌力和正性频率作用，而只有轻微的血管收缩作用。刺激血管上的β2肾上腺素受体，能够诱发血管扩张。

                                   

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Literature review current through: 2017-06 . | This topic last updated: 2017-04-04.
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