cLactate(P) is the concentration of lactate in plasma. The systematic symbol for arterial blood is cLactate(aP). The analyzer symbol may be cLac.
What does cLactate tell you
Lactate is a metabolite of pyruvate, the product of the glycolytic pathways and the substrate for the citric acid cycle. Lactate is a normal intermediary metabolite and is present at low levels (< 1.5 mmol/L) in the blood of healthy individuals.
Main lactate sources in healthy individuals are the red blood cells, the skin, and the central nervous system. Circulating lactate is eliminated by extraction and further metabolism, mainly in the liver, kidneys, and myocardium.
The blood lactate level depends on the balance between production and elimination. Consequently, elevated blood lactate levels (hyperlactatemia, possibly lactic acidosis) may be due to excess production, decreased elimination, or both.
cLactate reference range (adult): 0.5-1.6 mmol/L (4.5-14.4 mg/dL)
A persistently elevated or rising blood lactate level in a critically ill patient is alarming and most often indicates excessive lactate production. Hyperlactatemia is common in shock states and is strongly associated with a worsening prognosis. Thus, a high blood lactate level in a patient in shock on admission is highly predictive of progression to Multiple Organ Failure (MOF); persistent hyperlactatemia more than 6 hours after admission is predictive of increased mortality (see Figere below).
Hyperlactatemia often precedes the development of clinical shock or vital organ dysfunction by several hours and consequently lactate STAT monitoring may facilitate early intervention.
Regular (e.g., every 2 hours) sampling for blood lactate is valuable for monitoring the effect of interventions or the spontaneous resolution of critical illness. More frequent sampling may be relevant in patients who are hemodynamically unstable and/or who show signs of vital organ dysfunction. When monitoring lactate serially for the evaluation of a patient’s status, the trend in lactate levels is more important than are the absolute values.
Excessive lactate production due to tissue hypoxia, whether systemic (e.g., possibly in sepsis) or regional (e.g., in splanchnic ischemia or intestinal infarction), is of primary clinical concern. Persistent hyperlactatemia always warrants further investigation, mainly to exclude tissue hypoxia. Whether tissue hypoxia is caused by poor circulation (ischemia), insufficient oxygen uptake in the lungs (hypoxemia), hemoglobin-related deficiencies in oxygen transport and/or release (anemia, dyshemoglobinemia, and/or ODC shifts), these are all factors that may possibly be corrected.
It must, however, be realized that the pathogenesis of hyperlactatemia is multifactorial (see Table). Recent research suggests that hyperlactatemia in critically ill patients only occasionally may be attributed to tissue hypoxia alone. Even so, any component of anaerobic glycolysis (i.e., due to hypoxia) must be sought as a primary target for interventions.
Causes of hyperlactatemia
Excessive production of lactate
- Increased pyruvate production:
Anaerobic: Tissue hypoxia (shock, cardiac failure, localized ischemia, severe anemia, hypoxemia, strenuous muscular exercise, generalized seizures)
Aerobic: Hypermetabolism, systemic inflammation (increased PMN activity, e.g., sepsis), respiratory alkalosis, beta2-adrenergic catecholamine treatment
- Decreased pyruvate metabolism:
Changes in intracellular redox potential (e.g., ethanol intoxication)
Inhibition of PDH complex function (severe thiamine deficiency, endotoxin)
Dysfunction of ”respiratory chain” (drug intoxication: salicylate, biguanide, isoniazide, cyanide)
- Decreased lactate clearance:
Hepatic hypoperfusion and/or failure
Lactate as an indicator of mortality:
Probability of hospital mortality as related to blood lactate concentration in critically ill patients. (Adapted from references  and ).