Lactate in Sepsis and Trauma - Hindrance or Help?

Lactic Acid and Shock

Lactic acid, formed by the reduction of pyruvate in the Embden-Meyerhof pathway, is normally converted back to pyruvate prior to its entry into the oxygen-dependent citrate cycle. In the presence of hypoxemia or shock (which may be simply defined as inadequate tissue perfusion), aerobic glycolysis is impaired and lactate and hydrogen ions accumulate. This results in acidosis, impaired mitochondrial energy production, disturbed ionic homeostasis across cell membranes, and reduced functional capacity of tissue cells [1].

The impact of shock on individual organs depends on their functional activity, basal metabolic requirement, capacity for autoregulation and high energy phosphate reserves. Metabolic derangements occur early in the kidney and liver and late in the heart and brain. Skeletal muscle tolerates considerable ischemia but vast amounts of lactic acid are produced. Reperfusion increases systemic lactate levels and can disturb vital organ function.

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