Key result
Angiotensin-II in ECMO patients is linked to ~4-point lower circuit exchange rates vs benchmark.
Why the study?
Angiotensin-II increases mean arterial pressure and reduces catecholamine requirements in shock, but concerns exist regarding thrombotic complications that could be particularly dangerous for patients requiring mechanical circulatory support devices.
Does angiotensin-II reduce vasopressor requirements without increasing thrombotic complications in adult patients requiring ECMO support?
Cohort (n=64)
Does angiotensin-II reduce vasopressor requirements without increasing thrombotic complications in adult patients requiring ECMO support?
In adult patients on ECMO, angiotensin-II was associated with statistically significant reductions in vasopressor requirements without an apparent increase in oxygenator/cannula exchange rates compared to benchmark data.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for angiotensin-II in ECMO shock; prospective RCTs needed before adoption.
Background Angiotensin-II has demonstrated the ability to increase mean arterial pressure and reduce catecholamine vasopressor requirements in critically ill patients in shock. However, concerns have been raised regarding thrombotic complications, which can be particularly dangerous for patients requiring mechanical circulatory support devices. Methods We conducted a retrospective, descriptive, cohort study evaluating the safety and hemodynamic effects of angiotensin-II in adults requiring extracorporeal membrane oxygenation support between December 31, 2019, and November 1, 2024. Safety outcomes included need for oxygenator or cannula exchange and thrombotic events. Efficacy was assessed by reduction in vasopressor requirements following the initiation of angiotensin-II. Results A total of 64 adult patients receiving angiotensin-II while on ECMO were included. The cohort was comprised of 28 venovenous, 31 venoarterial, and 5 hybrid configurations. Septic shock was the most common indication for angiotensin-II (40.6%), with a median therapy duration of 25.8 hours (IQR 13.99 to 42.73). Five patients (7.8%) required oxygenator or cannula exchange compared to the ELSO benchmark of 12.1%. Other thrombotic events included 1 pulmonary embolism and 5 ischemic strokes. The median baseline norepinephrine equivalent was 0.42 mcg/kg/min which was reduced by 0.02, 0.08, and 0.13 mcg/kg/min at 1-hour, 3-hours, and 6-hours, respectively, which were statistically significant with p-values <0.05. Conclusions In this retrospective cohort study angiotensin-II was associated with reductions in vasopressor requirements and improved hemodynamic stability, without an apparent signal of increased thrombotic complications. These findings support the potential role of angiotensin-II as an adjunct vasopressor in ECMO patients, though prospective studies are warranted.
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Montealegre et al. (2026) conducted a cohort in Shock requiring extracorporeal membrane oxygenation (ECMO) support (n=64). Angiotensin-II vs. ELSO benchmark (for oxygenator/cannula exchange) and baseline pre-treatment vasopressor requirements was evaluated on Need for oxygenator or cannula exchange, thrombotic events, and reduction in vasopressor requirements (p=<0.05). Angiotensin-II in ECMO patients reduced norepinephrine equivalents by /kg/min at 6 hours with a 7.8% oxygenator/cannula exchange rate vs the 12.1% ELSO benchmark.
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