Department of Pharmacy, Mayo Clinic, Rochester, MN; Multidisciplinary Epidemiology and Translational Research in Intensive Care, Mayo Clinic, Rochester, MN.
Multidisciplinary Epidemiology and Translational Research in Intensive Care, Mayo Clinic, Rochester, MN; Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, MN.
Chest. 2021 Feb;159(2):596-605. doi: 10.1016/j.chest.2020.08.2074. Epub 2020 Aug 31.
Vasodilatory shock refractory to catecholamine vasopressors and arginine vasopressin is highly morbid and responsible for significant mortality. Synthetic angiotensin II is a potent vasoconstrictor that may be suitable for use in these patients.
What is the safety and effectiveness of angiotensin II and what variables are associated with a favorable hemodynamic response?
We performed a multicenter, retrospective study at five tertiary medical centers in the United States. The primary end point of hemodynamic responsiveness to angiotensin II was defined as attainment of mean arterial pressure (MAP) of ≥ 65 mm Hg with a stable or reduced total vasopressor dosage 3 h after drug initiation.
Of 270 included patients, 181 (67%) demonstrated hemodynamic responsiveness to angiotensin II. Responders showed a greater increase in MAP (+10.3 mm Hg vs +1.6 mm Hg, P < .001) and reduction in vasopressor dosage (-0.20 μg/kg/min vs +0.04 μg/kg/min; P < .001) compared with nonresponders at 3 h. Variables associated with favorable hemodynamic response included lower lactate concentration (OR 1.11; 95% CI, 1.05-1.17, P < .001) and receipt of vasopressin (OR, 6.05; 95% CI, 1.98-18.6; P = .002). In severity-adjusted multivariate analysis, hemodynamic responsiveness to angiotensin II was associated with reduced likelihood of 30-day mortality (hazard ratio, 0.50; 95% CI, 0.35-0.71; P < .001). Arrhythmias occurred in 28 patients (10%) and VTE was identified in 4 patients.
In postmarketing use for vasopressor-refractory shock, 67% of angiotensin II recipients demonstrated a favorable hemodynamic response. Patients with lower lactate concentrations and those receiving vasopressin were more likely to respond to angiotensin II. Patients who responded to angiotensin II experienced reduced mortality.
对儿茶酚胺血管加压药和精氨酸血管加压素无反应的血管扩张性休克病情严重,死亡率高。合成血管紧张素 II 是一种有效的血管收缩剂,可能适用于这些患者。
血管紧张素 II 的安全性和有效性如何,哪些变量与有利的血流动力学反应相关?
我们在美国五家三级医疗中心进行了一项多中心回顾性研究。血管紧张素 II 血流动力学反应的主要终点定义为药物起始后 3 小时平均动脉压(MAP)达到≥65mmHg,且总血管加压药剂量稳定或减少。
在 270 例纳入的患者中,181 例(67%)对血管紧张素 II 有血流动力学反应。与无反应者相比,反应者在 3 小时时 MAP 增加更多(+10.3mmHg 比+1.6mmHg,P<0.001),血管加压药剂量减少更多(-0.20μg/kg/min 比+0.04μg/kg/min,P<0.001)。与有利的血流动力学反应相关的变量包括较低的乳酸浓度(OR 1.11;95%CI,1.05-1.17,P<0.001)和接受血管加压素(OR,6.05;95%CI,1.98-18.6;P=0.002)。在严重程度调整的多变量分析中,对血管紧张素 II 的血流动力学反应与 30 天死亡率降低相关(风险比,0.50;95%CI,0.35-0.71;P<0.001)。28 例(10%)患者发生心律失常,4 例患者发生静脉血栓栓塞。
在血管加压药难治性休克的上市后使用中,67%的血管紧张素 II 接受者表现出有利的血流动力学反应。乳酸浓度较低和接受血管加压素的患者更有可能对血管紧张素 II 有反应。对血管紧张素 II 有反应的患者死亡率降低。