Hyperoxia and End-Organ Complications Among Cardiogenic Shock Patients Supported by Venoarterial Extracorporeal Membrane Oxygenation.

OBJECTIVES

To investigate whether severe hyperoxia predisposes to end-organ complications and whether these complications contribute to in-hospital mortality among cardiogenic shock (CS) patients supported in venoarterial extracorporeal membrane oxygenation (VA-ECMO).

DESIGN

Adult patients with CS from the Extracorporeal Life Support Organization Registry between 2010 and 2023 were categorized into normoxia (Pa o2 60-150 mm Hg), mild hyperoxia (Pa o2 151-300 mm Hg), and severe hyperoxia (Pa o2 > 300 mm Hg) based on their Pa o2 at 24 hours. The primary outcome was in-hospital mortality. End-organ complications were analyzed using multivariate logistic regression models, and causal mediation analysis was performed to estimate the direct and indirect effects of hyperoxia on mortality.

SETTING

Multicenter, multinational prospective cohort study.

PATIENTS: Adults with CS supported on VA-ECMO.

INTERVENTIONS: Partial pressure of oxygen at 24 hours after VA-ECMO cannulation.

MEASUREMENTS/MAIN

RESULTS

A total of 10,541 patients were included (normoxia: 48.4%, mild hyperoxia: 30.0%, severe hyperoxia: 21.5%). There was higher in-hospital mortality in patients with severe hyperoxia (71.7%, adjusted OR [aOR]: 2.17; 95% CI, 1.19-2.50) and mild hyperoxia (63.8%, aOR: 1.34; 95% CI, 1.19-1.50) compared normoxia (52.7%; referent group). Severe hyperoxia was associated with more end-organ complications, which incrementally predicted higher mortality (aOR: 1.42; 95% CI, 1.25-1.61). Mediation analysis demonstrated that hyperoxia primary exerted a direct effect on mortality (86%), with contributions from neurologic (3.1%), hepatic (3.9%), renal (3.5%), and bleeding (2.3%) complications.

CONCLUSIONS

Severe hyperoxia in patients with CS receiving VA-ECMO is associated with increased mortality and more end-organ complications. However, most of the effect of severe hyperoxia on mortality occurs via direct effects, independent of end-organ complications. These findings highlight the potential direct toxicity of hyperoxia and underscore the need for strategies to optimize oxygen delivery in this critically ill population.