Lactic acidosis causes a decrease in serum bicarbonate concentration that is similar in magnitude to the increase in the lactate concentration. Lactate is a metabolizable organic anion that, when oxidized, will generate bicarbonate. Thus, if the stimulus to lactic acid production is eliminated by successful treatment of the underlying disease (eg, restoration of perfusion in a patient with shock), oxidative processes will metabolize the accumulated lactate and regenerate bicarbonate. This will correct the metabolic acidosis and reduce the anion gap.
The role of exogenous bicarbonate therapy in patients with lactic acidosis is controversial [1-5]. Most, but not all, experts believe that it is appropriate to use bicarbonate in acutely ill patients with profound lactic acidosis and acidemia (arterial pH less than 7.1). Such severe acidemia may produce hemodynamic instability as a result of reduced left ventricular contractility, arterial vasodilation, and impaired responsiveness to catecholamines [1,5-10].
The role of bicarbonate therapy and alternative buffering agents in patients with lactic acidosis will be discussed in this topic. The causes of lactic acidosis, the approach to the adult with metabolic acidosis, and the treatment of shock in adults are presented elsewhere. (See "Causes of lactic acidosis" and "Approach to the adult with metabolic acidosis" and "Treatment of severe hypovolemia or hypovolemic shock in adults".)
The use of bicarbonate dialysis to correct lactic acidosis caused by metformin is discussed separately. (See "Metformin poisoning".)
OVERVIEW OF THERAPY
The following general approach applies to the use of bicarbonate therapy in patients with lactic acidosis: