Unmasking the Impact of Oxygenator-Induced Hypocapnia on Blood Lactate in Veno-Arterial Extracorporeal Membrane Oxygenation

Abstract

Extracorporeal membrane oxygenation (ECMO) is often associated with disturbances in acid/base status that can be triggered by the underlying pathology or the ECMO circuit itself. Extracorporeal membrane oxygenation is known to cause hypocapnia, but the impact of reduced partial pressure of carbon dioxide (pCO2) on biomarkers of tissue perfusion during veno-arterial (VA)-ECMO has not been evaluated. To study the impact of low pCO2 on perfusion indices in VA-ECMO, we placed Sprague–Dawley rats on an established VA-ECMO circuit using either an oxygen/carbon dioxide mixture (O2 95%, CO2 5%) or 100% O2 delivered through the oxygenator (n = 5 per cohort). Animals receiving 100% O2 developed a significant VA CO2 difference (pCO2 gap) and rising blood lactate levels that were inversely proportional to the decrease in pCO2 values. In contrast, pCO2 gap and lactate levels remained similar to pre-ECMO baseline levels in animals receiving the O2/CO2 mixture. More importantly, there was no significant difference in venous oxygen saturation (SvO2) between the two groups, suggesting that elevated blood lactate levels observed in the rats receiving 100% O2 were a response to oxygenator induced hypocapnia and alkaline pH rather than reduced perfusion or underlying tissue hypoxia. These findings have implications in clinical and experimental extracorporeal support contexts.