Evolution of lactate/pyruvate and arterial ketone body ratios in the early course of catecholamine-treated septic shock
Evolution of lactate/pyruvate and arterial ketone body ratios in the early course of catecholamine-treated septic shock
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DOI：
10.1097/00003246-200001000-00019
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发表时间：
2000-01-01
影响因子：
8.8
通讯作者：
Larcan, A
中科院分区：
文献类型：
--
作者：
Levy, B;Sadoune, LO;Larcan, A
目的：测定儿茶酚胺治疗的脓毒性休克不同阶段的动脉乳酸/丙酮酸（UP）和动脉酮体比值，作为细胞质和线粒体氧化还原状态的反映，并将其与氧转运减少的休克患者的正常值和病理值进行比较（心源性休克），并评估乳酸的时间进程，VP比率和感染性休克死亡率之间的关系。设计：前瞻性，观察性人体研究。设置：一所大学的重症监护病房。患者：60名连续的成年患者，他们发生了脓毒性休克和乳酸酸中毒，需要给予血管加压药。20例重症监护室中无休克、败血症和缺氧且乳酸值正常的患者和10例心源性休克患者也进行了研究。测量：血流动力学测量，动脉和混合静脉血气，动脉乳酸和丙酮酸浓度，以及动脉酮体比率在引入儿茶酚胺后4小时内和24小时后进行了测量。主要结果15名患者（25%）在感染性休克的前24小时内死亡，这些早期死亡者的血乳酸浓度（12.2 +/- 3 vs 4.6 +/- 1.3 mmol/L; p <0.01）和VP比值（37 +/- 4 vs 20 +/- 1; p <0.01）高于后期死亡者。未发现动脉酮体比存在差异（0.41 +/- 0.1 vs 0.50 +/- 0.06）。45名患者存活>24小时，包括25名存活者和20名非存活者。虽然存活者和非存活者的初始乳酸浓度没有差异，（分别为4.1 +/- 0.4和4.6 +/- 0.3），VP比（分别为19 +/- 1和20 +/- 1）和动脉酮体比（分别为0.5 +/-0.06和0.52 +/-0.07），存活者的血乳酸和UP比率在前24小时内显著降低（分别为2.8 +/-0.4和14 +/-1; p <0.05）。而在非存活者中稳定（分别为4 +/-0.3和22 +/-1）。尽管存活者和非存活者在24小时后恢复到正常值，但存活者的动脉酮体比率较高（1.72 +/-0.17对1.09 +/-0.15; p <0.05）。乳酸和UP比率密切相关（r（2）= 0.8，p <0.0001）。心源性休克组，乳酸浓度为4 +/- 1 mmol/L，UP比率为40 +/- 6，动脉酮体比率为0.2 +/- 0.05。死亡率为60%。结论：本研究的主要结果是，血流动力学不稳定的脓毒症患者需要接受儿茶酚胺治疗时出现乳酸酸中毒，UP比值升高，动脉酮体比值降低，提示细胞质和线粒体氧化还原状态下降。乳酸酸中毒的持续时间与多器官衰竭和死亡的发生相关。
Objectives: To measure arterial lactate/pyruvate (UP) and arterial ketone body ratios as reflection of cytoplasmic and mitochondrial redox state at different stages of catecholamine-treated septic shock and compare them with normal and pathologic values obtained in patients in shock who have decreased oxygen transport (cardiogenic shock), and to assess the relationship between the time course of lactate, VP ratio, and mortality in septic shock.Design: Prospective, observational human study.Setting: A university intensive care unit.Patients: Sixty consecutive adult patients who developed septic shock and lactic acidosis requiring the administration of vasopressors. Twenty patients in the intensive care unit without shack, sepsis, and hypoxia and with normal lactate values and 10 patients with cardiogenic shock were also studied.Measurements: Hemodynamic measurements, arterial and mixed venous blood gases, arterial lactate and pyruvate concentrations, and arterial ketone body ratio were measured within 4 hrs after the introduction of catecholamine and 24 hrs later.Main Results.. Fifteen patients (25%) died within the first 24 hrs of septic shock, and these early fatalities had a higher blood lactate (12.2 +/- 3 versus 4.6 +/- 1.3 mmol/L; p < .01) concentration and a higher VP ratio (37 +/- 4 versus 20 +/- 1; p < .01) than those who died later. No difference was found for arterial ketone body ratio (0.41 +/- 0.1 verses 0.50 +/- 0.06). Forty-five patients survived >24 hrs including 25 survivors and 20 nonsurvivors. Although there was no difference between survivors and nonsurvivors in initial lactate concentration (4.1 +/- 0.4 and 4.6 +/- 0.3, respectively), VP ratio (19 +/- 1 and 20 +/- 1, respectively), and arterial ketone body ratio (0.5 +/- 0.06 and 0.52 +/- 0.07, respectively), blood lactate and UP ratio significantly decreased during the first 24 hrs in the survivors (2.8 +/- 0.4 and 14 +/- 1, respectively; p < .05). and were stable in the nonsurvivors (4 +/- 0.3 and 22 +/- 1, respectively) Although returning to normal values after 24 hrs in survivors and nonsurvivors, arterial ketone body ratio was higher in survivors (1.72 +/- 0.17 versus 1.09 +/- 0.15; p < .05). Lactate and UP ratio were closely correlated (r(2) = .8, p < .0001). In the cardiogenic shock group, lactate concentration was 4 +/- 1 mmol/L, UP ratio was 40 +/- 6, and arterial ketone body ratio was 0.2 +/- 0.05. The mortality rate was 60%.Conclusions: The main result of the present study is that hemodynamically unstable patients with sepsis needing catecholamine therapy had a lactic acidosis with an elevated UP ratio and a decreased arterial ketone body ratio, suggesting a decrease in cytoplasmic and mitochondrial redox state. The duration of lactic acidosis is associated with the development of multiple organ failure and death.