BACKGROUND Vasopressors are administered to critically ill patients with vasodilatory shock not responsive to volume resuscitation, and less often in cardiogenic shock, and hypovolemic shock. OBJECTIVES The objectives are to review safety and efficacy of vasopressors, pathophysiology, agents that decrease vasopressor dose, predictive biomarkers, β1-blockers, and directions for research. METHODS The quality of evidence was evaluated using Grading of Recommendations Assessment, Development, and Evaluation (GRADE). RESULTS Vasopressors bind adrenergic: α1, α2, β1, β2; vasopressin: AVPR1a, AVPR1B, AVPR2; angiotensin II: AG1, AG2; and dopamine: DA1, DA2 receptors inducing vasoconstriction. Vasopressor choice and dose vary because of patients and physician practice. Adverse effects include excessive vasoconstriction, organ ischemia, hyperglycemia, hyperlactatemia, tachycardia, and tachyarrhythmias. No randomized controlled trials of vasopressors showed a significant difference in 28-day mortality rate. Norepinephrine is the first-choice vasopressor in vasodilatory shock after adequate volume resuscitation. Some strategies that decrease norepinephrine dose (vasopressin, angiotensin II) have not decreased 28-day mortality while corticosteroids have decreased 28-day mortality significantly in some (two large trials) but not all trials. In norepinephrine-refractory patients, vasopressin or epinephrine may be added. A new vasopressor, angiotensin II, may be useful in profoundly hypotensive patients. Dobutamine may be added because vasopressors may decrease ventricular contractility. Dopamine is recommended only in bradycardic patients. There are potent vasopressors with limited evidence (e.g. methylene blue, metaraminol) and novel vasopressors in development (selepressin). CONCLUSIONS Norepinephrine is first choice followed by vasopressin or epinephrine. Angiotensin II and dopamine have limited indications. In future, predictive biomarkers may guide vasopressor selection and novel vasopressors may emerge.

中文翻译：

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重症休克患者的升压治疗。

背景技术血管加压药被施用于对容量复苏无反应的血管扩张性休克的重症患者，并且在心源性休克和低血容量性休克中较少使用。目的目的是审查血管加压药的安全性和有效性，病理生理学，降低血管加压药剂量的药物，预测性生物标志物，β1受体阻滞剂以及研究方向。方法采用推荐评估，发展和评估等级（GRADE）评估证据质量。结果血管升压药与肾上腺素结合：α1，α2，β1，β2；α1，α2，β1，β2。加压素：AVPR1a，AVPR1B，AVPR2; 血管紧张素II：AG1，AG2；和多巴胺：诱导血管收缩的DA1，DA2受体。血管加压药的选择和剂量因患者和医师的实践而异。不良反应包括过度血管收缩，器官缺血，高血糖，高乳酸血症，心动过速和快速性心律失常。没有任何血管加压药的随机对照试验显示28天死亡率有显着差异。去甲肾上腺素是适当的容量复苏后血管扩张性休克的首选血管加压药。在一些（两项大型试验）中，但并非所有试验中，降低去甲肾上腺素剂量的某些策略（血管加压素，血管紧张素II）并未降低28天死亡率，而皮质类固醇却显着降低了28天死亡率。在去甲肾上腺素难治性患者中，可加血管加压素或肾上腺素。一种新的升压药血管紧张素II可能对严重低血压的患者有用。可以添加多巴酚丁胺，因为血管加压药可能会降低心室收缩力。仅在心动过缓的患者中才建议使用多巴胺。有有效的升压药证据有限（例如 亚甲蓝，间氨基）和正在开发的新型升压药（Selepressin）。结论去甲肾上腺素是首选，其次是加压素或肾上腺素。血管紧张素II和多巴胺的适应症有限。将来，预测性生物标志物可能会指导血管加压药的选择，并且可能会出现新型血管加压药。