Effect of flow change on brain injury during an experimental model of differential hypoxaemia in cardiogenic shock supported by extracorporeal membrane oxygenation

Abstract

Differential hypoxaemia (DH) is common in patients supported by femoral veno-arterial extracorporeal membrane oxygenation (V-A ECMO) and can cause cerebral hypoxaemia. To date, no models have studied the direct impact of flow on cerebral damage. We investigated the impact of V-A ECMO flow on brain injury in an ovine model of DH. After inducing severe cardiorespiratory failure and providing ECMO support, we randomised six sheep into two groups: low flow (LF) in which ECMO was set at 2.5 L min−1 ensuring that the brain was entirely perfused by the native heart and lungs, and high flow (HF) in which ECMO was set at 4.5 L min−1 ensuring that the brain was at least partially perfused by ECMO. We used invasive (oxygenation tension—PbTO2, and cerebral microdialysis) and non-invasive (near infrared spectroscopy—NIRS) neuromonitoring, and euthanised animals after five hours for histological analysis. Cerebral oxygenation was significantly improved in the HF group as shown by higher PbTO2 levels (+ 215% vs − 58%, p = 0.043) and NIRS (67 ± 5% vs 49 ± 4%, p = 0.003). The HF group showed significantly less severe brain injury than the LF group in terms of neuronal shrinkage, congestion and perivascular oedema (p < 0.0001). Cerebral microdialysis values in the LF group all reached the pathological thresholds, even though no statistical difference was found between the two groups. Differential hypoxaemia can lead to cerebral damage after only a few hours and mandates a thorough neuromonitoring of patients. An increase in ECMO flow was an effective strategy to reduce such damages.

Hypoxic-Ischemic Brain Injury in ECMO: Pathophysiology, Neuromonitoring, and Therapeutic Opportunities

“…An increase in cerebral metabolites suggestive of anaerobic metabolism, such as lactate, pyruvate, and the lactate-to-pyruvate ratio further corroborated the presence of HIBI in the low-flow group. Inadequate oxygenation, as observed through continuous brain tissue oxygen (PbtO 2 ) and near-infrared spectroscopy (NIRS), was consistent with the hypoxia and hypoperfusion seen in HIBI in the low-flow group [44]. In summary, preclinical studies investigating HIBI in ECMO appear to demonstrate mitigation of HIBI resulting from the institution of ECMO with adequate flow and blood pressure.…”