Lactate metabolism.

Lactate is the end product of the anaerobic metabolism of glucose, and its accumulation in the blood signals an increase in production or a decrease in utilization, or both. The most common etiology of lactic acidosis is hypoperfusion, which represents an imbalance between systemic oxygen demand and oxygen availability with resultant tissue hypoxia. A wide variety of other etiologies of hyperlactatemia have been identified or implicated. However, most of these are uncommon causes, and many actually represent an associated perfusion failure. Clinical recognition of hyperlactatemia is facilitated by an awareness of the clinical settings in which it is likely to occur. Serum electrolyte and arterial blood gas studies are helpful to recognize lactic acidosis, but direct assay of blood lactate is necessary to identify milder degrees of lactate elevation, to confirm and quantitate the severity of more severe degrees, and to monitor the progress of therapy. Therapy should be directed toward measures to ensure adequate systemic oxygen delivery and specific treatment of the underlying causes.