Early Exposure to Arterial Hyperoxia During Extracorporeal Membrane Oxygenator Support and Acute Brain Injury and Mortality in Patients With Cardiogenic Shock

Authors: Yang Y et al.

Anesthesia & Analgesia 142(2):326–334, February 2026

Summary

This retrospective cohort study from Beijing Anzhen Hospital examined whether early arterial hyperoxia during venoarterial extracorporeal membrane oxygenation (VA-ECMO) is associated with acute brain injury (ABI) and in-hospital mortality in patients with cardiogenic shock.

The investigators reviewed 481 adult patients receiving VA-ECMO between January 2017 and January 2024. Patients were stratified by PaO2 levels measured at 4 and 24 hours after ECMO initiation:

• Normoxia: 60–149 mm Hg

• Mild hyperoxia: 150–199 mm Hg

• Moderate hyperoxia: 200–299 mm Hg

• Severe hyperoxia: ≥300 mm Hg

The primary outcome was composite acute brain injury (ABI), which included:

• Ischemic stroke and intracranial hemorrhage

• Hypoxic-ischemic brain injury

• Neurological examination abnormalities

Acute brain injury occurred in 34.1% of patients (164 of 481), a strikingly high rate. Among ABI cases, ischemic stroke/intracranial hemorrhage made up nearly half.

There was a clear dose-dependent relationship between hyperoxia and ABI risk:

At 4 hours:

• Mild hyperoxia: OR 2.33

• Moderate hyperoxia: OR 4.16

• Severe hyperoxia: OR 6.10

At 24 hours:

• Mild hyperoxia: OR 3.44

• Moderate hyperoxia: OR 3.28

• Severe hyperoxia: OR 4.78

The association remained significant after multivariable adjustment, demonstrating a graded increase in ABI risk as PaO2 rose above 150 mm Hg.

Severe hyperoxia (PaO2 ≥300 mm Hg) at 24 hours was also independently associated with in-hospital mortality (OR 2.46).

What You Should Know

1. Hyperoxia is not benign during VA-ECMO. This study reinforces that PaO2 levels ≥150 mm Hg are associated with increased acute brain injury risk in cardiogenic shock patients.

2. The relationship appears dose-dependent. The higher the PaO2, the higher the risk—especially with severe hyperoxia ≥300 mm Hg.

3. Severe hyperoxia also predicts mortality. Maintaining very high arterial oxygen levels during VA-ECMO may worsen overall survival.

4. Early oxygen targets matter. Both 4-hour and 24-hour PaO2 levels were predictive, suggesting that early ECMO oxygen management is critical.

5. Clinical implication: Titrate ECMO sweep gas and ventilator FiO2 to avoid unnecessary hyperoxia, rather than defaulting to maximal oxygen delivery.

Key Points

• PaO2 ≥150 mm Hg at 4 and 24 hours post-VA-ECMO initiation predicts acute brain injury.

• PaO2 ≥300 mm Hg at 24 hours independently predicts in-hospital mortality.

• A clear dose-response relationship exists between hyperoxia severity and neurologic risk.

• Conservative oxygenation strategies may improve neurologic and survival outcomes in VA-ECMO patients with cardiogenic shock.

Thank you to Anesthesia & Analgesia for allowing us to summarize and share this important work advancing neurologic protection in high-risk ECMO patients.