Lactic acid levels are a useful adjunct in assessing perfusion in the intensive care unit (ICU). Lactate levels >2 mEq/L may reflect tissue ischemia. However, lactate levels may be confounded by various circumstances and are also prone to misinterpretation. When using lactate levels in clinical management, it is important to understand the physiology behind lactate production and the commonly held misconceptions about lactic acidosis.

When cells face insufficient oxygen to carry out their metabolic functions, they convert from aerobic to anaerobic metabolism. Without an available oxygen molecule, pyruvate is instead converted to lactate, contributing to an anion-gap acidosis. In other words, rather than yielding the complete 36 adenosine triphosphate (ATP) molecules for each mole of glucose, metabolism is halted at lactate, rendering only 2 ATP. The clearance of lactate (in the setting of adequate tissue perfusion) occurs in the liver, through one of two mechanisms. It may combine with oxygen with the end result being carbon dioxide, water, and bicarbonate:

CH₃CHOHCOO^– + 3O₂ → 2CO₂ + 2H₂O + HCO^–₃