Lactic alkalosis in a patient on veno-venous extracorporeal membrane oxygenation: A case report

Lactic alkalosis, defined as an increase in circulating lactate in the setting of elevated extracellular pH, has been described in both in vivo and in vitro settings, often under conditions of acute respiratory alkalosis. However, its occurrence in the context of extracorporeal membrane oxygenation (ECMO) has not been previously reported.

A 59-year-old man underwent coronary artery bypass grafting (CABG). Postoperatively, he developed respiratory failure necessitating veno-venous ECMO. Fluctuations in lactate were observed across ECMO circuit sampling points-pre-oxygenator, post-oxygenator, and arterial line-coinciding with changes in serum pH and PCO₂. Notably, lactate rose in tandem with an increase in pH and decrease in PCO₂ during increased sweep gas flow, consistent with ex-vivo lactic alkalosis.

Lactic alkalosis is believed to result from proton-coupled lactate export via monocarboxylate transporters (MCT1), and enhanced glycolysis in erythrocytes due to pH-stimulated phosphofructokinase activity. Prior reports describe hyperlactatemia in patients with an acute respiratory alkalosis. This case adds novel ECMO-specific considerations: aggressive CO₂ clearance may rapidly shift pH and influence lactate kinetics ex vivo. To our knowledge, this is the first reported instance of lactic alkalosis temporally linked to ECMO sweep gas manipulation, highlighting a unique and benign biochemical artifact.