De Backer D, Creteur J, Zhang H, Norrenberg M, Vincent J L
Department of Intensive Care, Erasme University Hospital, Free University of Brussels, Belgium.
Am J Respir Crit Care Med. 1997 Oct;156(4 Pt 1):1099-104. doi: 10.1164/ajrccm.156.4.9701048.
Arteriovenous differences in lactate (AVLAC) across the lungs are usually small and close to zero. However, it has recently been reported that the lungs can produce increased amounts of lactate in some patients with acute respiratory distress syndrome (ARDS). The aim of this study was to evaluate lactate production in various types of acute lung injury requiring mechanical ventilation and hemodynamic monitoring. Since the differences involved are usually small, minor errors in lactate measurement could greatly influence AVLAC. Based on an analysis of these errors (see text for details), we averaged five arterial and venous samples for each measurement. We investigated 122 patients: 43 with acute lung injury (ALI), nine with cardiogenic pulmonary edema (CPE), 37 with bronchopneumonia (BPN), seven with single lung transplantation (LTX), and 26 with other causes of respiratory failure (OTHER). There was no difference in arterial lactate between the various groups. AVLAC was higher in patients with ALI than in the other groups (0.20+/-0.23 versus 0.07+/-0.11 mEq/L). In patients with ALI, AVLAC was proportional to the Murray's lung injury score (-0.032+/-0.032x; r = 0.46, p < 0.01). Lung lactate production was calculated as the product of the cardiac index times AVLAC and was significantly higher in patients with ALI than in the other groups (0.69+/-0.88 versus 0.19+/-0.30 mEq/min; p < 0.05). In patients with ALI, lung lactate production was inversely related to the PaO2/FIO2 (1.42 - 0.005x; r = 0.35, p < 0.05) but directly related to the venous admixture (-0.36 + 0.003x; r = 0.49, p < 0.01) and the lung injury score (-0.19 + 0.36x; r = 0.45, p < 0.01). Lung lactate production was not significantly related to arterial lactate levels. These data indicate that AVLAC and lung lactate production can be increased in patients with ARDS but remain within the normal range in other types of respiratory failure.
经肺动静脉的乳酸差异（AVLAC）通常很小，接近于零。然而，最近有报道称，在一些急性呼吸窘迫综合征（ARDS）患者中，肺可产生更多的乳酸。本研究的目的是评估各类需要机械通气和血流动力学监测的急性肺损伤中的乳酸生成情况。由于所涉及的差异通常较小，乳酸测量中的微小误差可能会极大地影响AVLAC。基于对这些误差的分析（详见正文），我们对每次测量的五个动脉和静脉样本进行了平均。我们研究了122例患者：43例急性肺损伤（ALI）患者、9例心源性肺水肿（CPE）患者、37例支气管肺炎（BPN）患者、7例单肺移植（LTX）患者以及26例其他呼吸衰竭病因（OTHER）患者。各亚组之间的动脉血乳酸水平无差异。ALI患者的AVLAC高于其他组（0.20±0.23对0.07±0.11 mEq/L）。在ALI患者中，AVLAC与Murray肺损伤评分呈正相关（-0.032±0.032x；r = 0.46，p < 0.01）。肺乳酸生成量通过心指数乘以AVLAC计算得出，ALI患者的肺乳酸生成量显著高于其他组（0.69±0.88对0.19±0.30 mEq/min；p < 0.05）。在ALI患者中，肺乳酸生成量与PaO2/FIO2呈负相关（1.42 - 0.005x；r = 0.35，p < 0.
