Department of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Emory University, Emory St. Joseph's Hospital, 5665 Peachtree Dunwoody Road, Atlanta, GA, 30342, USA.
Division of Pulmonary & Critical Care, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
Crit Care. 2017 Dec 28;21(1):324. doi: 10.1186/s13054-017-1896-6.
Circulatory shock is a common syndrome with a high mortality and limited therapeutic options. Despite its discovery and use in clinical and experimental settings more than a half-century ago, angiotensin II (Ang II) has only been recently evaluated as a vasopressor in distributive shock. We examined existing literature for associations between Ang II and the resolution of circulatory shock.
We searched PubMed, MEDLINE, Ovid, and Embase to identify all English literature accounts of intravenous Ang II in humans for the treatment of shock (systolic blood pressure [SBP] ≤ 90 mmHg or a mean arterial pressure [MAP] ≤ 65 mmHg), and hand-searched the references of extracted papers for further studies meeting inclusion criteria. Of 3743 articles identified, 24 studies including 353 patients met inclusion criteria. Complete data existed for 276 patients. Extracted data included study type, publication year, demographics, type of shock, dosing of Ang II or other vasoactive medications, and changes in BP, lactate, and urine output. BP effects were grouped according to type of shock, with additional analyses completed for patients with absent blood pressure. Shock was distributive (n = 225), cardiogenic (n = 38), or from other causes (n = 90). Blood pressure as absent in 18 patients.
For the 276 patients with complete data, MAP rose by 23.4% from 63.3 mmHg to 78.1 mmHg in response to Ang II (dose range: 15 ng/kg/min to 60 mcg/min). SBP rose by 125.2% from 56.9 mmHg to 128.2 mmHg (dose range: 0.2 mcg/min to a 1500 mcg bolus). A total of 271 patients with complete data were determined to exhibit a BP effect which was directly associated with Ang II. Subgroups (patients with cardiogenic, septic, and other types of shock) exhibited similar increases in BP. In patients with absent BP, deemed to be cardiac arrest, return of spontaneous circulation (ROSC) was achieved, and BP increased by an average of 107.3 mmHg in 11 of 18 patients. The remaining seven patients with cardiac arrest did not respond.
Intravenous Ang II is associated with increased BP in patients with cardiogenic, distributive, and unclassified shock. A role may exist for Ang II in restoring circulation in cardiac arrest.
循环休克是一种常见的综合征,死亡率高,治疗选择有限。尽管血管紧张素 II(Ang II)在半个多世纪前在临床和实验环境中被发现并使用,但它最近才被评估为分布性休克的血管加压药。我们研究了现有的文献,以了解 Ang II 与循环休克缓解之间的关系。
我们在 PubMed、MEDLINE、Ovid 和 Embase 上搜索了所有关于静脉注射 Ang II 治疗休克(收缩压[SBP]≤90mmHg 或平均动脉压[MAP]≤65mmHg)的人类英文文献,并对提取文献的参考文献进行了手工搜索,以寻找符合纳入标准的进一步研究。在确定的 3743 篇文章中,有 24 项研究包括 353 名患者符合纳入标准。有 276 名患者有完整的数据。提取的数据包括研究类型、出版年份、人口统计学、休克类型、Ang II 或其他血管活性药物的剂量以及血压、乳酸和尿量的变化。根据休克类型对血压效应进行分组,并对血压缺失的患者进行了额外分析。休克为分布性(n=225)、心源性(n=38)或其他原因(n=90)。18 名患者血压缺失。
对于有完整数据的 276 名患者,MAP 从 63.3mmHg 升高到 78.1mmHg,升高了 23.4%,这是对 Ang II 的反应(剂量范围:15ng/kg/min 至 60mcg/min)。SBP 从 56.9mmHg 升高到 128.2mmHg,升高了 125.2%(剂量范围:0.2mcg/min 至 1500mcg 推注)。共有 271 名有完整数据的患者被确定具有与 Ang II 直接相关的血压效应。亚组(心源性、感染性和其他类型休克患者)的血压也有类似的升高。在血压缺失的患者中,被认为是心搏骤停,自主循环恢复(ROSC)得以实现,18 名患者中的 11 名患者的血压平均升高了 107.3mmHg。其余 7 名心搏骤停的患者没有反应。
静脉注射 Ang II 与心源性、分布性和未分类休克患者的血压升高有关。Ang II 在恢复心脏骤停患者的循环中可能有作用。