Keller John H, Kendric Kayla J, LeSaint Kathy T
Department of Emergency Medicine, University of California San Francisco, San Francisco, California, USA.
California Poison Control System, San Francisco Division, San Francisco, California, USA.
Case Rep Crit Care. 2024 Dec 11;2024:7543758. doi: 10.1155/crcc/7543758. eCollection 2024.
Coingestion of cardiovascular drugs with angiotensin-converting enzyme inhibitors (ACEIs) can be associated with refractory shock derangements complicated by vasopressor resistance, prompting the use of novel, unconventional, or uncommonly used agents. A young adult male presented to the emergency department (ED) 10 h after ingesting lisinopril and amlodipine. On arrival, he was hypotensive with a blood pressure of 72/39 mmHg. In addition to crystalloid fluids, he was incrementally started on four vasopressors including norepinephrine, phenylephrine, epinephrine, and vasopressin without improvement in mean arterial pressure (MAP). He was then administered methylene blue, calcium gluconate, and hyperinsulinemic euglycemia therapy after discussion with medical toxicology. Shortly afterwards, he was started on an angiotensin II infusion with an improvement in MAP to a goal of > 65 mmHg. Despite evidence of efficacy in refractory vasodilatory shock secondary to sepsis, there is a paucity of data on the use of angiotensin II as an adjunctive vasopressor in drug-induced shock. We report a case of successful use of angiotensin II in combined lisinopril and amlodipine overdose refractory to conventional vasopressor support. Combined overdose of ACEIs with calcium channel blockers (CCBs) has been shown to cause more significant hypotension and higher vasopressor requirements than overdose of CCBs alone. This may be due to the synergism between CCBs and ACEIs, where the normal homeostatic mechanism of the renin-angiotensin-aldosterone system (RAAS) activation in response to shock is now inhibited, leading to decreased compensatory vasoconstriction via angiotensin II and decreased endogenous catecholamine release. We hypothesize that angiotensin II may have been of particular benefit in this patient given the likelihood that reduced angiotensin II levels were contributing to his refractory shock.
心血管药物与血管紧张素转换酶抑制剂(ACEIs)同时摄入可能会导致难治性休克紊乱,并伴有血管升压药抵抗,从而促使使用新型、非常规或不常用的药物。一名年轻成年男性在服用赖诺普利和氨氯地平10小时后被送往急诊科。到达时,他血压过低,收缩压为72/39mmHg。除了晶体液外,他还逐渐开始使用四种血管升压药,包括去甲肾上腺素、去氧肾上腺素、肾上腺素和血管加压素,但平均动脉压(MAP)没有改善。在与药物毒理学专家讨论后,给他使用了亚甲蓝、葡萄糖酸钙和高胰岛素正常血糖疗法。不久之后,他开始输注血管紧张素II,MAP提高到>65mmHg的目标值。尽管有证据表明血管紧张素II在脓毒症继发的难治性血管舒张性休克中有效,但关于其在药物性休克中作为辅助血管升压药使用的数据却很少。我们报告了一例成功使用血管紧张素II治疗赖诺普利和氨氯地平联合过量中毒且对传统血管升压药支持无效的病例。已证明,ACEIs与钙通道阻滞剂(CCBs)联合过量中毒比单独过量服用CCBs可导致更显著的低血压和更高的血管升压药需求。这可能是由于CCBs与ACEIs之间的协同作用,即休克时肾素-血管紧张素-醛固酮系统(RAAS)激活的正常稳态机制现在受到抑制,导致通过血管紧张素II的代偿性血管收缩减少以及内源性儿茶酚胺释放减少。我们推测,鉴于血管紧张素II水平降低可能导致该患者难治性休克,血管紧张素II可能对该患者特别有益。