Minton Jonathon, Sidebotham David A
Department of Anesthesia and Perioperative Medicine, The Alfred Hospital, Melbourne, Australia.
Department of Cardiothoracic Anesthesia and the Cardiovascular Intensive Care Unit, Auckland City Hospital, Auckland, New Zealand.
J Extra Corpor Technol. 2017 Mar;49(1):7-15.
The normal blood lactate level is 0-2 mmol/L, and a value above 3-5 mmol/L is variably used to define hyperlactatemia. In cardiac surgical patients, hyperlactatemia can arise from both hypoxic and non-hypoxic mechanisms. The major non-hypoxic mechanism is likely stress-induced accelerated aerobic metabolism, in which elevated lactate results from a mass effect on the lactate/pyruvate equilibrium. The lactate/pyruvate ratio is normal (<20) in this circumstance. Hyperlactatemia can also result from impaired global or regional oxygen delivery, in which case the lactate/pyruvate ratio is typically elevated (>20). Lactate is a strong anion that is virtually fully dissociated at physiological pH. As such, increased lactate concentration reduces the strong ion difference and exerts an acidifying effect on the blood. Hyperlactatemia in cardiac surgery patients has been categorized as either early or late onset. Early-onset hyperlactatemia is that which develops in the operating room or very early following intensive care unit (ICU) admission. Early-onset hyperlactatemia is strongly associated with adverse outcome and probably arises as a consequence of both hypoxic (e.g., microcirculatory shock) and non-hypoxic (accelerated aerobic metabolism) mechanisms. By contrast, late-onset hyperlactatemia is a benign, self-limiting condition that typically arises within 6-12 hours of ICU admission and spontaneously resolves within 24 hours. Late onset hyperlactatemia occurs in the absence of any evidence of global or regional tissue hypoxia. The mechanism of late onset hyperlactatemia is not understood. Hyperlactatemia is a common accompaniment to treatment with β-agonists such as epinephrine. Epinephrine-induced hyperlactatemia is thought to be due to accelerated aerobic metabolism and requires no specific intervention. Irrespective of the cause, the presence of hyperlactatemia should trigger a search for remedial causes of impaired tissue oxygenation, bearing in mind that normal-or even supranormal-indices of global oxygen delivery may exist despite regional tissue hypoperfusion.
正常血乳酸水平为0 - 2 mmol/L，3 - 5 mmol/L以上的值可用于不同程度地定义高乳酸血症。在心脏外科手术患者中，高乳酸血症可由缺氧和非缺氧机制引起。主要的非缺氧机制可能是应激诱导的有氧代谢加速，其中乳酸升高是由于对乳酸/丙酮酸平衡的质量效应。在这种情况下，乳酸/丙酮酸比值正常（<20）。高乳酸血症也可能由全身或局部氧输送受损引起，在这种情况下，乳酸/丙酮酸比值通常升高（>20）。乳酸是一种强阴离子，在生理pH值下几乎完全解离。因此，乳酸浓度升高会降低强离子差，并对血液产生酸化作用。心脏外科手术患者的高乳酸血症可分为早发或迟发。早发性高乳酸血症是指在手术室或重症监护病房（ICU）入院后很早发生的情况。早发性高乳酸血症与不良预后密切相关，可能是缺氧（如微循环休克）和非缺氧（有氧代谢加速）机制共同作用的结果。相比之下，迟发性高乳酸血症是一种良性的、自限性疾病，通常在ICU入院后6 - 12小时内出现，并在24小时内自发缓解。迟发性高乳酸血症发生时没有任何全身或局部组织缺氧的证据。迟发性高乳酸血症的机制尚不清楚。高乳酸血症是使用肾上腺素等β受体激动剂治疗时常见的伴随情况。肾上腺素诱导的高乳酸血症被认为是由于有氧代谢加速，不需要特殊干预。无论原因如何，高乳酸血症的存在都应促使寻找组织氧合受损的补救原因，同时要记住，尽管存在局部组织灌注不足，但可能存在正常甚至超常的全身氧输送指标。
