Lactic acid is generated as the end product of anaerobic metabolism of glucose and is disposed by gluconeogenesis or oxidation. Changes in the lactate pyruvate ratio are not necessarily indicative of tissue hypoxia. The plasma lactate concentration is the result of lactate production and lactate removal (hepatic and renal gluconeogenesis; oxidation by muscle, liver and kidney). Lactic acidosis is defined as a state of metabolic acidosis (arterial pH less than 7.3) due to an increase in the blood concentration of lactate (greater than 2 mEq/l). Lactic acidosis may occur with evidence of tissue hypoxemia (type A) or in its absence (type B). Lactic acidosis has been described in association with phenformin therapy, hereditary enzymatic defects, hematological malignancy, prolonged fasting, shock with or without septicemia and occasionally without any underlying disease ("idiopathic" lactic acidosis). The therapy of lactic acidosis consists of administration of sodium bicarbonate and restoration of adequate tissue perfusion; hemodialysis may be helpful to control sodium excess and possibly to remove phenformin. The effectiveness of methylene blue, glucose and insulin are not yet established.
乳酸是葡萄糖无氧代谢的终产物，可通过糖异生或氧化作用进行清除。乳酸/丙酮酸比值的变化不一定表明组织缺氧。血浆乳酸浓度是乳酸生成与清除（肝脏和肾脏的糖异生；肌肉、肝脏和肾脏的氧化作用）的结果。乳酸酸中毒定义为由于血液中乳酸浓度升高（大于2 mEq/L）导致的代谢性酸中毒状态（动脉pH值小于7.3）。乳酸酸中毒可能伴有组织低氧血症证据（A型），也可能无此证据（B型）。乳酸酸中毒已被描述与苯乙双胍治疗、遗传性酶缺陷、血液系统恶性肿瘤、长期禁食、伴有或不伴有败血症的休克有关，偶尔也可无任何基础疾病（“特发性”乳酸酸中毒）。乳酸酸中毒的治疗包括给予碳酸氢钠和恢复充足的组织灌注；血液透析可能有助于控制钠过量，并可能清除苯乙双胍。亚甲蓝、葡萄糖和胰岛素的有效性尚未确定。
