Key result
Venovenous ECMO initiation significantly decreased the mean norepinephrine equivalent dose from 0.23 to 0.14 μm/kg/min at 24 hours (P<.001).
Why the study?
Some clinicians view concurrent vasopressors as a contraindication for venovenous ECMO, prompting an evaluation of how cannulation affects vasopressor requirements.
Does venovenous ECMO reduce vasopressor requirements in patients with severe respiratory failure?
Observational (n=108)
No
Does venovenous ECMO reduce vasopressor requirements in patients with severe respiratory failure?
Absolute Event Rate: 0.14% vs 0.23%
p-value: p=<.001
Venovenous ECMO initiation in patients with severe respiratory failure significantly reduces vasopressor requirements within 24 hours, suggesting that concurrent high-dose vasopressor use should not be an absolute contraindication to ECMO.
VV-ECMO initiation was associated with reduced vasopressor requirements at 24 hours; hypothesis-generating and should not yet change practice.
Background Venovenous extracorporeal membrane oxygenation (ECMO) is used increasingly for severe respiratory failure. Some ECMO clinicians may view concurrent vasopressors as a contraindication for venovenous ECMO. However, we noted improved vasopressor requirements after venovenous ECMO cannulation. Research Question How does venovenous ECMO affect vasopressor requirements in patients with respiratory failure? Methods This was a retrospective review of all venovenous ECMO initiations from December 2016 through December 31, 2023, at a large-volume ECMO center. The changes in norepinephrine equivalent dose and number of continuous IV vasopressors were determined immediately before and 24 hours after venovenous ECMO cannulation. This change was assessed by Wilcoxon signed-rank tests, and their associations with potential predictor variables (pH, Paco 2 , Pao 2 , and positive end-expiratory pressure) were examined by linear regressions. Results Two hundred five patients received venovenous ECMO during this time, with 108 patients taking vasopressors at ECMO cannulation and included in this analysis. The mean (SD) norepinephrine equivalent dose at ECMO initiation, 0.23 (0.29) μm/kg/min, to 24 hours after ECMO, 0.14 (0.23) μm/kg/min, decreased significantly ( P < .001). The mean (SD) number of pressors at ECMO initiation, 1.69 (0.92), to 24 hours later, 1.29 (1.04), decreased significantly ( P < .001). A significant decrease in positive end-expiratory pressure, mean airway pressure, and Paco 2 with a significant increase in pH and Pao 2 was found ( P ≤ .001 for all). The changes in pH ( P < .001) were associated with changes in norepinephrine equivalent dose and number of vasopressors after adjusting for baseline outcomes. Twenty-seven patients (25%) had received a norepinephrine equivalent dose of ≥ 0.3 μm/kg/min at ECMO initiation; of these, 16 patients (59.3%) survived to hospital discharge (compared with 51.9% survival among those with a lower norepinephrine equivalent dose at ECMO initiation; P = .66). Interpretation Our results show that patients' vasopressor requirements significantly decreased 24 hours after venovenous ECMO initiation, with a change in pH weakly associated with vasopressor improvement. The requirement of vasopressors, even norepinephrine equivalent dose of ≥ 0.3 μm/kg/min at the time of ECMO consideration, is not a clear contraindication to ECMO candidacy.
No takes yet. Share an insight, caveat, or question.
Odish et al. (2024) conducted an observational in severe respiratory failure (n=108). Venovenous extracorporeal membrane oxygenation (ECMO) vs. Baseline (immediately before cannulation) was evaluated on Norepinephrine equivalent dose (μm/kg/min) (p=<.001). Venovenous ECMO initiation significantly decreased the mean norepinephrine equivalent dose from 0.23 to 0.14 μm/kg/min at 24 hours (P<.001).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: