Abstract
BACKGROUND: Patients on venoarterial extracorporeal membrane oxygenation (VA-ECMO) are frequently managed with varying degrees of hyperoxia. Existing data suggest that higher levels of Pao 2 correlate with worsened outcome in patients receiving ECMO support. We hypothesized that higher levels of Pao 2 during VA-ECMO support would correlate with an increased risk of acute brain injury (ABI) in critically ill patients with cardiogenic shock (CS). To test our hypothesis, we performed a retrospective review of patients receiving VA-ECMO for CS at a tertiary medical center. METHODS: Data from patients who received ECMO support for CS between January 2017 and January 2024 were retrospectively collected from Beijing Anzhen Hospital, Capital Medical University. Patients were categorized into 4 groups based on their Pa o2 values after 24 hours of ECMO: normoxia (Pa o2 60-149 mm Hg), mild hyperoxia (Pa o2 150-199 mm Hg), moderate hyperoxia (Pa o2 200-299 mm Hg), and severe hyperoxia (Pa o2 ≥300 mm Hg). ABI was categorized as ischemic stroke (IS) + intracranial hemorrhage (ICH), hypoxic-ischemic brain injury (HIBI), and neurological examination abnormalities (NEA). The rate of ABI and in-hospital mortality was evaluated using univariate and multivariable logistic regression analyses. RESULTS: Among 481 CS patients supported by VA-ECMO, 164 (34.1%) experienced ABI, with subtypes including IS + ICH (n = 73, 44.5%), HIBI (n = 25, 5.20%), and NEA (n = 66, 13.7%). The multivariable logistic regression for composite ABI at 4 hours post-ECMO revealed a dose-dependent association with hyperoxia severity: mild (odds ratio [OR], 2.33; 95% confidence interval [CI], 1.10-4.96), moderate (OR, 4.16; 95% CI, 2.16-8.02), and severe hyperoxia (OR, 6.10; 95% CI, 3.33-11.2). This dose-response pattern persisted at 24 hours (mild: OR, 3.44 and 95% CI, 1.88-6.29; moderate: OR, 3.28 and 95% CI, 1.80-5.97; severe: OR, 4.78 and 95% CI, 2.14-11.2). Severe hyperoxia (OR, 2.46; 95% CI, 1.25-4.84) was identified as an independent predictor of in-hospital mortality. CONCLUSIONS: Hyperoxia (Pa o2 ≥150 mm Hg) at both 4 and 24 hours post-ECMO initiation was significantly associated with ABI, while severe hyperoxia (Pa o2 ≥300 mm Hg) at 24 hours correlated with in-hospital mortality.