Metabolic Acidosis

Lactic Acidosis

• Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Impaired tissue oxygenation, leading to increased anaerobic metabolism, is usually responsible for the rise in lactate production.
• Types:
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  • Type A lactic acidosis (hypoxic type) is associated with impaired tissue oxygenation due to tissue hypoperfusion in shock (due to hypovolemia, cardiac failure, or sepsis) or during a cardiopulmonary arrest. In some of these patients, concurrent respiratory acidosis contributes to the acidemia.
  • Type B lactic acidosis (non-hypoxic type - also due to delayed clearance through renal dysfunction) includes those in which the findings of systemic hypoperfusion are not apparent. Type B lactic acidosis may be due to a toxin-induced impairment of cellular metabolism or regional areas of ischemia. Causes of type B lactic acidoses include metformin therapy in patients with type 2 diabetes, tumor-induced lactic acidosis, alcoholism and drug-induced mitochondrial dysfunction in HIV-infected patients.
  • D-lactic acidosis is a unique form of acidosis that occurs in patients with short bowel syndrome or other forms of malabsorption. Glucose and starch are metabolized in the colon into D-lactic acid, which is then absorbed into the systemic circulation.
• The primary aim of therapy for lactic acidosis is reversal of the underlying disease (eg, shock).
• The role of exogenous bicarbonate therapy in patients with lactic acidosis is controversial. Most experts believe that it is appropriate to use bicarbonate in acutely ill patients with profound lactic acidosis and acidemia (arterial pH less than 7.1 and serum bicarbonate 6 meq/L or less). Such severe acidemia may produce hemodynamic instability as a result of reduced left ventricular contractility, arterial vasodilation, and impaired responsiveness to catecholamines.