Pulmonary lactate release in patients with sepsis and the adult respiratory distress syndrome
Pulmonary lactate release in patients with sepsis and the adult respiratory distress syndrome
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DOI：
10.1016/s0883-9441(96)90014-3
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发表时间：
1996-03-01
影响因子：
3.7
通讯作者：
Gutierrez, G
中科院分区：
文献类型：
--
作者：
Brown, SD;Clark, C;Gutierrez, G
目的：脓毒症患者动脉血乳酸浓度升高被解释为外周非肺组织缺氧的证据。这些患者通常会出现肺功能衰竭，表现为急性呼吸窘迫综合征(ARDS)。由于组织缺氧或炎症，脓毒症和ARDS患者的肺可能成为乳酸释放到循环中的来源。材料和方法：测定19例脓毒症患者的肺乳酸释放，动脉乳酸大于或等于2.2 mm，胃粘膜pH<7.30。正常的胃粘膜pH可作为内脏充氧的标志。同时采集动脉血和混合静脉血，计算肺乳酸释放量，作为心脏指数和血浆L乳酸浓度差值的乘积。结果：轻度或无肺损伤(肺损伤评分<lt；1)患者的肺产生乳酸明显少于中、重度肺损伤(肺损伤评分≥1)(P<；.005)。肺损伤评分与肺乳酸释放量呈正相关(r(2)=0.73；P<；0.0001)。这种关系主要是由于混合静脉-动脉乳酸差值的增加(r(2)=.59)。肺损伤评分与心脏指数呈弱相关(r(2)=0.32)。动脉血乳酸浓度与肺乳酸释放、全身氧转运或全身氧耗均无相关性。结论：脓毒症和ARDS患者的肺可能会产生乳酸。肺乳酸释放与肺损伤的严重程度相关。在将动脉乳酸浓度解释为全身缺氧的指标时，应考虑肺乳酸释放的贡献。(C)W.B.桑德斯公司1996年
Purpose: Elevated arterial lactate concentrations in patients with sepsis have been interpreted as evidence of peripheral, nonpulmonary tissue hypoxia. These patients often develop pulmonary failure manifested by the acute respiratory distress syndrome (ARDS). As the result of tissue hypoxia or inflammation, the lungs of patients with sepsis and ARDS may become a source of lactate release into the circulation.Materials and methods: Pulmonary lactate release was measured in 19 patients with sepsis, arterial lactate greater than or equal to 2.2 mm, and gastric mucosal pH > 7.30. A normal gastric mucosal pH served as a marker of adequate splanchnic oxygenation. Pulmonary lactate release was computed as the product of the cardiac index and the difference in plasma L-lactate concentration in simultaneously obtained arterial and mixed venous blood samples. Lung injury was graded with the Lung Injury Score using radiographic and physiologic data.Results: The lungs of patients with minimal or no lung injury (lung injury score < 1) produced significantly less lactate than those with moderate or severe lung injury (lung injury score greater than or equal to 1) (P < .005). The Lung Injury Score correlated with pulmonary lactate release (r(2) = .73; P < .0001). This relationship resulted primarily from increases in mixed venous-arterial lactate differences (r(2) = .59). The Lung Injury Score correlated weakly with the cardiac index (r(2) = .32). Arterial lactate concentration did not correlate with pulmonary lactate release, systemic oxygen transport, or systemic oxygen consumption.Conclusions: The lungs of patients with sepsis and ARDS may produce lactate. Pulmonary lactate release correlates with the severity of lung injury. The contribution of pulmonary lactate release should be considered when interpreting arterial lactate concentration as an index of systemic hypoxia. (C) 1996 by W.B. Saunders Company