Abstract

After fluid administration for vasodilatory shock, vasopressors are commonly infused. Causes of vasodilatory shock include septic shock, post-cardiovascular surgery, post-acute myocardial infarction, postsurgery, other causes of an intense systemic inflammatory response, and drug -associated anaphylaxis. Therapeutic vasopressors are hormones that activate receptors—adrenergic: α1, α2, β1, β2; angiotensin II: AG1, AG2; vasopressin: AVPR1a, AVPR1B, AVPR2; dopamine: DA1, DA2. Vasopressor choice and dose vary widely because of patient and physician practice heterogeneity. Vasopressor adverse effects are excessive vasoconstriction causing organ ischemia/infarction, hyperglycemia, hyperlactatemia, tachycardia, and tachyarrhythmias. To date, no randomized controlled trial (RCT) of vasopressors has shown a decreased 28-day mortality rate. There is a need for evidence regarding alternative vasopressors as first-line vasopressors. We emphasize that vasopressors should be administered simultaneously with fluid replacement to prevent and decrease duration of hypotension in shock with vasodilation. Norepinephrine is the first-choice vasopressor in septic and vasodilatory shock. Interventions that decrease norepinephrine dose (vasopressin, angiotensin II) have not decreased 28-day mortality significantly. In patients not responsive to norepinephrine, vasopressin or epinephrine may be added. Angiotensin II may be useful for rapid resuscitation of profoundly hypotensive patients. Inotropic agent(s) (e.g., dobutamine) may be needed if vasopressors decrease ventricular contractility. Dopamine has fallen to almost no-use recommendation because of adverse effects; angiotensin II is available clinically; there are potent vasopressors with scant literature (e.g., methylene blue); and the novel V1a agonist selepressin missed on its pivotal RCT primary outcome. In pediatric septic shock, vasopressors, epinephrine, and norepinephrine are recommended equally because there is no clear evidence that supports the use of one vasoactive agent. Dopamine is recommended when epinephrine or norepinephrine is not available. New strategies include perhaps patients will be started on several vasopressors with complementary mechanisms of action, patients may be selected for particular vasopressors according to predictive biomarkers, and novel vasopressors may emerge with fewer adverse effects.

Publication History

Publication Date:
20 August 2020 (online)

© 2020. Thieme. All rights reserved.

Thieme Medical Publishers
333 Seventh Avenue, New York, NY 10001, USA.

中文翻译：

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重症监护室的血管加压治疗。

摘要

血管扩张性休克输液后，通常会输注血管加压药。血管舒张性休克的原因包括感染性休克、心血管手术后、急性心肌梗塞后、手术后、强烈全身炎症反应的其他原因和药物相关的过敏反应。治疗性血管加压药是激活受体的激素 - 肾上腺素：α1、α2、β1、β2；血管紧张素 II：AG1、AG2；加压素：AVPR1a、AVPR1B、AVPR2；多巴胺：DA1、DA2。由于患者和医生实践的异质性，血管加压药的选择和剂量差异很大。血管加压药的副作用是过度的血管收缩导致器官缺血/梗塞、高血糖、高乳酸血症、心动过速和快速性心律失常。迄今为止，没有血管加压药的随机对照试验 (RCT) 显示 28 天死亡率降低。需要将替代血管升压药作为一线血管升压药的证据。我们强调血管升压药应与补液同时使用，以预防和减少休克伴血管舒张时低血压的持续时间。去甲肾上腺素是感染性和血管扩张性休克的首选血管加压药。降低去甲肾上腺素剂量（加压素、血管紧张素 II）的干预措施并未显着降低 28 天死亡率。对去甲肾上腺素无反应的患者，可加用加压素或肾上腺素。血管紧张素 II 可能对极低血压患者的快速复苏有用。如果血管加压药降低心室收缩力，可能需要正性肌力药物（例如多巴酚丁胺）。由于不良反应，多巴胺已降至几乎不使用的推荐；血管紧张素 II 在临床上可用；有有效的血管加压药，但文献很少（例如，亚甲蓝）；新的 V1a 激动剂 selepressin 错过了其关键的 RCT 主要结果。在小儿感染性休克中，同样推荐使用血管加压药、肾上腺素和去甲肾上腺素，因为没有明确的证据支持使用一种血管活性药物。当肾上腺素或去甲肾上腺素不可用时，建议使用多巴胺。新策略可能包括患者将 当肾上腺素或去甲肾上腺素不可用时，建议使用多巴胺。新策略可能包括患者将 当肾上腺素或去甲肾上腺素不可用时，建议使用多巴胺。新策略可能包括患者将开始使用几种具有互补作用机制的血管加压药，可以根据预测性生物标志物为患者选择特定的血管加压药，并且可能出现副作用较少的新型血管加压药。

出版历史

发布日期：
2020 年 8 月 20 日（在线）

© 2020。蒂姆。版权所有。

Thieme Medical Publishers
333 Seventh Avenue, New York, NY 10001, USA。