Angiotensin II for Vasodilatory Hypotension in Patients Requiring Mechanical Circulatory Support

Background: Patients supported on mechanical circulatory support devices experience vasodilatory hypotension due to high surface area exposure to nonbiological and non-endothelialized surfaces. Angiotensin II has been studied in general settings of vasodilatory shock, however concerns exist regarding the use of this vasopressor in patients with pre-existing cardiac failure. The objective of this study was to assess the systemic and central hemodynamic effects of angiotensin II in patients with primary cardiac or respiratory failure requiring treatment with mechanical circulatory support devices. Methods: Multicenter retrospective observational study of adults supported on a mechanical circulatory support device who received angiotensin II for vasodilatory shock. The primary outcome was the intraindividual change from baseline in mean arterial pressure (MAP) and vasopressor dosage after angiotensin II. Results: Fifty patients were included with mechanical circulatory devices that were primarily used for cardiac failure (n = 41) or respiratory failure (n = 9). At angiotensin II initiation, the norepinephrine equivalent vasopressor dosage was 0.44 (0.34, 0.64) and 0.47 (0.33, 0.73) mcg/kg/min in the cardiac and respiratory groups, respectively. In the cardiac group, MAP increased from 60 to 70 mmHg (intraindividual P < .001) in the 1 h after angiotensin II initiation and the vasopressor dosage declined by 0.04 mcg/kg/min (intraindividual P < .001). By 12 h, the vasopressor dosage declined by 0.16 mcg/kg/min (P = .001). There were no significant changes in cardiac index or mean pulmonary artery pressure throughout the 12 h following angiotensin II. In the respiratory group, similar but nonsignificant effects at 1 h on MAP (61-81 mmHg, P = .26) and vasopressor dosage (decline by 0.13 mcg/kg/min, P = .06) were observed. Conclusions: In patients requiring mechanical circulatory support for cardiac failure, angiotensin II produced beneficial systemic hemodynamic effects without negatively impacting cardiac function or pulmonary pressures. The systemic hemodynamic effects in those with respiratory failure were nonsignificant due to limited sample size.

Medienart:

E-Artikel

Erscheinungsjahr:

2023

Erschienen:

2023

Enthalten in:

Zur Gesamtaufnahme - volume:38

Enthalten in:

Journal of intensive care medicine - 38(2023), 5 vom: 12. Mai, Seite 464-471

Sprache:

Englisch

Beteiligte Personen:

Wieruszewski, Patrick M [VerfasserIn]
Seelhammer, Troy G [VerfasserIn]
Barreto, Erin F [VerfasserIn]
Busse, Laurence W [VerfasserIn]
Chow, Jonathan H [VerfasserIn]
Davison, Danielle L [VerfasserIn]
Gaglani, Bhavita [VerfasserIn]
Khanna, Ashish K [VerfasserIn]
Ten Lohuis, Caitlin C [VerfasserIn]
Mara, Kristin C [VerfasserIn]
Wittwer, Erica D [VerfasserIn]

Links:

Volltext

Themen:

11128-99-7
Angiotensin II
Distributive shock
Hypotension
Journal Article
Mechanical support
Multicenter Study
Observational Study
Vasoconstrictor Agents
Vasodilatory shock
Vasopressors

Anmerkungen:

Date Completed 04.04.2023

Date Revised 04.04.2023

published: Print-Electronic

Citation Status MEDLINE

doi:

10.1177/08850666221145864

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM350361932