Lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L, which is often accompanied by a blood pH of less than 7.35 and a plasma bicarbonate concentration below 20 mmol/L. These values are commonly used in clinical practice; however, the absolute thresholds may vary depending on coexisting respiratory or metabolic acid–base disorders, which can partially mask or offset the expected acid-base changes. In contrast, hyperlactatemia refers to lactate levels above 2 mmol/L without associated acidosis.
Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although it is typically associated with an elevated anion gap, moderately increased lactate levels can occur with a normal anion gap, particularly in the presence of hypoalbuminemia, unless the gap is appropriately corrected.
Lactic acid is produced under normal physiological conditions and is commonly elevated in various disease states. Lactic acidosis occurs when lactate production exceeds clearance, most often due to impaired tissue oxygenation resulting from decreased oxygen delivery or mitochondrial dysfunction. When increased production is combined with impaired clearance, the severity of illness often worsens. Significantly elevated lactate levels can have profound hemodynamic consequences and may lead to multiple organ failure or death.
Serum lactate serves as both a marker of risk and a therapeutic target; the higher the level and the longer it remains elevated, the greater the risk of mortality. Clinicians should also recognize that hyperlactatemia can occur even in the presence of adequate tissue perfusion and oxygenation, whereas true lactic acidosis typically reflects hypoperfusion, altered carbohydrate metabolism, or medication-induced effects. Please see StatPearls' companion resource, "
Copyright © 2026, StatPearls Publishing LLC.