Serum lactate: Role in the assessment of microhemodynamics in critically ill patients

Many critically ill patients with stabilized hemodynamics die with signs of multiorgan failure. One of the reasons is the derangement of microcirculation and tissue perfusion. It has been shown that microcirculatory distress left uncorrected for 24 hours is single independent predictor of mortality in sepsis. Serum lactate is the only indicator of microcirculatory changes that is monitored routinely in all critically ill patients. It has been widely believed that hyperlactatemia in sepsis is marker of tissue hypoxia and indicates the existence of oxygen debt resulting from tissue hypoperfusion and anaerobic glycolysis. Attempts to correct hyperlactatemia by delivering supranormal oxygen amounts have failed in septic patients. The term ?shock? lactate refers to hyperlactatemia originating from oxygen debt. Human studies failed to demonstrate the relationship between hyperlactatemia and tissue hypo-perfusion in the late phase of sepsis. Adrenergic stimulation in sepsis and accelerated aerobic glycolysis have been proposed as a likely mechanism of hyperlactatemia. Both exogenous and endogenous catecholamines are correlated with septic hyperlactatemia. Aerobically generated lactate mediated by cytokines is called ?stress? lactate and may serve as a marker of hypermetabolism rather than tissue hyperperfusion. Many studies and guidelines recommend targeting resuscitation to normalize lactate in septic patients. These recommendations need to be taken with reserve. Since lactate serves, under stress, as a source of energy and can be used as a fuel for oxidation as well as for glucose production, attempts to normalize lactate might be even harmful. Although high lactate clearance, due to a correction of oxygen debt contributes to a better prognosis in sepsis, the unusual complexity of lactate makes it almost impossible to make an unambiguous therapeutic decision, when comes to a lactate-guided treatment in sepsis.