Jagan Nikhil, Morrow Lee E, Walters Ryan W, Plambeck Robert W, Patel Tej M, Moore Douglas R, Malesker Mark A
Division of Pulmonary & Critical Care, Creighton University School of Medicine, 7710 Mercy Road, Suite 410, Omaha, NE, 68124, USA.
VA Nebraska-Western Iowa, Section of Pulmonary and Critical Care, Omaha, USA.
Ann Intensive Care. 2021 Feb 5;11(1):24. doi: 10.1186/s13613-021-00805-9.
Diametrically opposed positions exist regarding the deleterious effects of elevated lactate. There are data suggesting that it is a detrimental proxy for tissue hypoperfusion and anaerobic metabolism in sepsis and an alternative viewpoint is that some of the hyperlactatemia produced maybe adaptive. This study was conducted to explore the relationship between serum lactate levels, mean arterial blood pressure (MAP), and sympathetic stimulation in patients with sepsis.
Retrospective analysis of prospectively collected clinical data from four community-based hospitals and one academic medical center. 8173 adults were included. Heart rate (HR) was used as a surrogate marker of sympathetic stimulation. HR, MAP, and lactate levels were measured upon presentation.
MAP and HR interacted to affect lactate levels with the highest levels observed in patients with low MAP and high HR (3.6 mmol/L) and the lowest in patients with high MAP and low HR (2.2 mmol/L). The overall mortality rate was 12.4%. Each 10 beats/min increase in HR increased the odds of death 6.0% (95% CI 2.6% to 9.4%), each 1 mmol/L increase in lactate increased the odds of death 20.8% (95% CI 17.4% to 24.2%), whereas each 10 mmHg increase in MAP reduced the odds of death 12.3% (95% CI 9.2% to 15.4%). However, HR did not moderate or mediate the association between lactate and death.
In septic patients, lactate production was associated with increased sympathetic activity (HR ≥ 90) and hypotension (MAP < 65 mmHg) and was a significant predictor of mortality. Because HR, lactate, and MAP were associated with mortality, our data support the present strategy of using these measurements to gauge severity of illness upon presentation. Since HR did not moderate or mediate the association between lactate and death, criticisms alleging that lactate caused by sympathetic stimulation is adaptive (i.e., less harmful) do not appear substantiated.
关于乳酸水平升高的有害影响存在截然不同的观点。有数据表明,在脓毒症中它是组织灌注不足和无氧代谢的有害替代指标,而另一种观点认为,产生的一些高乳酸血症可能具有适应性。本研究旨在探讨脓毒症患者血清乳酸水平、平均动脉血压(MAP)和交感神经刺激之间的关系。
对来自四家社区医院和一家学术医疗中心前瞻性收集的临床数据进行回顾性分析。纳入8173名成年人。心率(HR)用作交感神经刺激的替代指标。就诊时测量HR、MAP和乳酸水平。
MAP和HR相互作用影响乳酸水平,MAP低且HR高的患者乳酸水平最高(3.6 mmol/L),MAP高且HR低的患者乳酸水平最低(2.2 mmol/L)。总死亡率为12.4%。HR每增加10次/分钟,死亡几率增加6.0%(95%CI 2.6%至9.4%),乳酸每增加1 mmol/L,死亡几率增加20.8%(95%CI 17.4%至24.2%),而MAP每增加10 mmHg,死亡几率降低12.3%(95%CI 9.2%至15.4%)。然而,HR并未调节或介导乳酸与死亡之间的关联。
在脓毒症患者中,乳酸生成与交感神经活动增加(HR≥90)和低血压(MAP<65 mmHg)相关,并且是死亡率的重要预测指标。由于HR、乳酸和MAP与死亡率相关,我们的数据支持目前使用这些测量指标来评估就诊时疾病严重程度的策略。由于HR并未调节或介导乳酸与死亡之间的关联,声称由交感神经刺激引起的乳酸具有适应性(即危害较小)的批评似乎没有依据。