Abstract
The production of hyperlactatemia in the critically ill patient has previously been thought to be primarily related to anaerobic conditions. Newer data suggests that lactate accumulates under aerobic conditions in clinical settings that were previously thought to solely represent anaerobic processes. This review summarizes the present understanding of lactate metabolism and reviews the data supporting use of lactate determinations in the critical care setting. The use of lactate as a marker of inadequate tissue perfusion as well as its role as a prognostic indicator are discussed. The utility of managing lactic acidosis with various buffers is also reviewed.
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