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Crit Care. 2017 Dec 28;21(1):324. doi: 10.1186/s13054-017-1896-6.

The effect of angiotensin II on blood pressure in patients with circulatory shock: a structured review of the literature.

Author information

1
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. laurence.w.busse@emory.edu.
2
Division of Pulmonary & Critical Care, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
3
Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
4
Department of Critical Care, King's College London, Guy's & St Thomas' NHS Foundation Hospital, London, SE1 7EH, UK.
5
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.

Abstract

BACKGROUND:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

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.

KEYWORDS:

Angiotensin II; Cardiac arrest; Cardiogenic shock; Distributive shock; Vasoconstrictor; Vasopressor

PMID:
29282149
PMCID:
PMC5745607
DOI:
10.1186/s13054-017-1896-6
[Indexed for MEDLINE]
Free PMC Article

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