Lactic acidosis occurs when lactate production exceeds lactate clearance, resulting in serum lactate levels above 4 mmol/L (or >2 mmol/L with concurrent metabolic acidosis). Lactate is the end product of anaerobic glycolysis -- when cells cannot perform oxidative phosphorylation (aerobic metabolism) due to insufficient oxygen delivery or mitochondrial dysfunction, pyruvate is converted to lactate by lactate dehydrogenase (LDH) to regenerate NAD+ and allow glycolysis to continue. Lactic acidosis is classified into two types. Type A (hypoxic) is caused by tissue hypoperfusion and hypoxia: septic shock (most common cause -- both distributive shock reducing oxygen delivery AND mitochondrial dysfunction from inflammatory mediators), cardiogenic shock (pump failure reducing cardiac output), hypovolemic shock (blood/fluid loss reducing circulating volume), severe anemia (reduced oxygen-carrying capacity), carbon monoxide poisoning (displaces oxygen from hemoglobin), and mesenteric ischemia. Type B (non-hypoxic) occurs without overt tissue hypoxia: metformin toxicity (inhibits mitochondrial complex I), liver failure (impaired lactate clearance -- the liver normally clears 60% of circulating lactate via the Cori cycle), thiamine deficiency (thiamine is a cofactor for pyruvate dehydrogenase, which converts pyruvate to acetyl-CoA for the Krebs cycle),...