Pathophysiology of lactic acidosis, and its clinical importance after cardiac surgery

In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation.The normal blood lactate concentration in unstressed patients is 0.5-1 mmol/L. Patients with critical illness can be considered to have normal lactate concentrations of less than 2 mmol/L. Hyperlactatemia is defined as a mild-to-moderate persistent increase in blood lactate concentration (2-5 mmol/L) without metabolic acidosis, whereas lactic acidosis is characterized by persistently increased blood lactate levels (usually >5 mmol/L) in association with metabolic acidosis (pH < 7.35).1,2 Lactic acidosis is associated with major metabolic dysregulation, tissue hypoperfusion, effects of certain drugs or toxins, or congenital abnormalities in carbohydrate metabolism. Cohen and Woods divided lactic acidosis into 2 categories: “type A”, associated with impaired delivery of oxygen to tissues (DO2) eg, hypotension, cyanosis, cool and clammy extremities, and “type B”, where lactic acidosis occurs in the presence of normal DO2