Jentzer Jacob C, Coons James C, Link Christopher B, Schmidhofer Mark
Department of Cardiology, UPMC-Presbyterian Hospital, Pittsburgh, PA, USA Department of Critical Care Medicine, UPMC-Presbyterian Hospital, Pittsburgh, PA.
Department of Cardiology, UPMC-Presbyterian Hospital, Pittsburgh, PA, USA University of Pittsburgh School of Pharmacy UPMC-Presbyterian Hospital, Pittsburgh, PA
J Cardiovasc Pharmacol Ther. 2015 May;20(3):249-60. doi: 10.1177/1074248414559838. Epub 2014 Nov 28.
This paper summarizes the pharmacologic properties of vasoactive medications used in the treatment of shock, including the inotropes and vasopressors. The clinical application of these therapies is discussed and recent studies describing their use and associated outcomes are also reported. Comprehension of hemodynamic principles and adrenergic and non-adrenergic receptor mechanisms are salient to the appropriate therapeutic utility of vasoactive medications for shock. Vasoactive medications can be classified based on their direct effects on vascular tone (vasoconstriction or vasodilation) and on the heart (presence or absence of positive inotropic effects). This classification highlights key similarities and differences with respect to pharmacology and hemodynamic effects. Vasopressors include pure vasoconstrictors (phenylephrine and vasopressin) and inoconstrictors (dopamine, norepinephrine, and epinephrine). Each of these medications acts as vasopressors to increase mean arterial pressure by augmenting vascular tone. Inotropes include inodilators (dobutamine and milrinone) and the aforementioned inoconstrictors. These medications act as inotropes by enhancing cardiac output through enhanced contractility. The inodilators also reduce afterload from systemic vasodilation. The relative hemodynamic effect of each agent varies depending on the dose administered, but is particularly apparent with dopamine. Recent large-scale clinical trials have evaluated vasopressors and determined that norepinephrine may be preferred as a first-line therapy for a broad range of shock states, most notably septic shock. Consequently, careful selection of vasoactive medications based on desired pharmacologic effects that are matched to the patient's underlying pathophysiology of shock may optimize hemodynamics while reducing the potential for adverse effects.
本文总结了用于治疗休克的血管活性药物的药理特性,包括强心药和血管升压药。讨论了这些疗法的临床应用,并报告了描述其使用情况及相关结果的近期研究。理解血流动力学原理以及肾上腺素能和非肾上腺素能受体机制对于血管活性药物在休克治疗中的适当应用至关重要。血管活性药物可根据其对血管张力(血管收缩或舒张)和心脏(有无正性肌力作用)的直接影响进行分类。这种分类突出了在药理学和血流动力学效应方面的关键异同。血管升压药包括纯血管收缩剂(去氧肾上腺素和血管加压素)和血管收缩性正性肌力药(多巴胺、去甲肾上腺素和肾上腺素)。这些药物中的每一种都作为血管升压药,通过增强血管张力来提高平均动脉压。强心药包括血管扩张性正性肌力药(多巴酚丁胺和米力农)以及上述血管收缩性正性肌力药。这些药物通过增强心肌收缩力来增加心输出量,从而起到强心作用。血管扩张性正性肌力药还可通过全身血管舒张降低后负荷。每种药物的相对血流动力学效应因给药剂量而异,但在多巴胺上表现得尤为明显。近期的大规模临床试验对血管升压药进行了评估,并确定去甲肾上腺素可能是治疗多种休克状态(最显著的是脓毒性休克)的一线首选疗法。因此,根据与患者潜在休克病理生理学相匹配的预期药理作用仔细选择血管活性药物,可能会优化血流动力学,同时降低不良反应的可能性。