Lactate metabolism and regional lactate exchange after cardiac surgery

Abstract

Tissue perfusion is at risk during cardiac surgery and in the immediate postoperative period. The association of low blood flow with metabolic acidosis and accumulation of lactate perioperatively has been well established. With the improvements in cardiopulmonary bypass and overall hemodynamic management, severe peri- and postoperative hypoperfusion has become rare. Despite the rarity of severe postoperative complications, several lines of evidence suggest that episodes of less severe hypoperfusion and borderline tissue oxygenation are relatively common, although generally well tolerated. Measurement of blood lactate levels is widely used to assess the adequacy of tissue perfusion. The interpretation of elevated blood lactate levels is limited by several confounding variables. Acute changes in acid-base balance, interorgan substrate flux, peripheral and visceral tissue perfusion, and hepatic lactate uptake will all influence blood lactate levels and may occur during and after cardiac surgery. Peri- and postoperative hyperlactatemia are rare occurrences and their presence may indicate inadequate tissue perfusion. Based on regional blood flow and lactate exchange measurements, we suggest that hyperlactatemia after cardiac surgery is a sign of inadequate or marginal tissue perfusion of the hepatosplanchnic region, as well as other tissues. In this article we briefly review: a) the normal physiology of lactate metabolism and the various causes of hyperlactatemia; b) studies on lactate levels during and after cardiac surgery; c) the evidence of insufficient or marginal tissue perfusion peri- and postoperatively; and d) the pathophysiology of postoperative increases in blood lactate based on regional lactate kinetics.