Pham Diem, Ward Harrison, Yong Brian, Mahendra Raj Jayanand, Awad Mariam, Harvey Martyn, Doherty Steven, Cave Grant
Department of Intensive Care Medicine, Tamworth Rural Referral Hospital, Tamworth, New South Wales, Australia.
Emergency Department, Waikato Hospital, Hamilton, New Zealand.
Emerg Med Australas. 2021 Feb;33(1):82-87. doi: 10.1111/1742-6723.13584. Epub 2020 Aug 18.
Elevated serum lactate has long been considered an important marker of sepsis severity. Increasing evidence supports catecholamine-stimulated aerobic glycolysis being a major contributor to the hyperlactataemia seen in sepsis. Beta-blockade may blunt such catecholamine mediated rise in lactate analogous to the way it can mask tachycardia. This could impact the way we evaluate sepsis severity and adequacy of initial treatment. The objective of this study is to investigate whether septic patients who were on beta-blocker treatment at presentation have lower serum lactate level.
Using a retrospective cohort design we gathered data on patients admitted to our base hospital intensive care unit with APACHE III diagnosis of sepsis and septic shock during the 2017 calendar year. Serum lactate, current medications, presenting vital signs, illness severity scores, laboratory data and mortality outcome were extracted from patients' medical record and the unit's clinical database.
Of 189 records analysed, 49 patients were concurrently prescribed beta-blockers. More beta-blocked patients were male, beta-blocked patients were older, and a greater proportion of beta blocked patients had their first lactate measured as an inpatient. After regression to correct for identified significant covariates mean serum lactate was 0.87 (95% confidence interval 0.05-1.69) mmol/L lower in those prescribed beta blockers.
In our cohort pre-existing beta blocker treatment was associated with lower serum lactate measurements in patients presenting with sepsis. Pre-existing beta blocker treatment may reduce serum lactate at presentation in patients with sepsis.
长期以来，血清乳酸水平升高一直被视为脓毒症严重程度的重要指标。越来越多的证据支持儿茶酚胺刺激的有氧糖酵解是脓毒症中高乳酸血症的主要原因。β受体阻滞剂可能会抑制儿茶酚胺介导的乳酸升高，类似于它可以掩盖心动过速的方式。这可能会影响我们评估脓毒症严重程度和初始治疗充分性的方式。本研究的目的是调查入院时接受β受体阻滞剂治疗的脓毒症患者血清乳酸水平是否较低。
采用回顾性队列设计，我们收集了2017年期间入住我院重症监护病房且APACHE III诊断为脓毒症和脓毒性休克患者的数据。从患者的病历和科室临床数据库中提取血清乳酸、当前用药、入院时生命体征、疾病严重程度评分、实验室数据和死亡率结果。
在分析的189份记录中，49例患者同时使用了β受体阻滞剂。使用β受体阻滞剂的男性患者更多，年龄更大，且更大比例的使用β受体阻滞剂的患者首次乳酸测量是在住院期间进行的。在对确定的显著协变量进行校正的回归分析后，使用β受体阻滞剂的患者平均血清乳酸水平低0.87（95%置信区间0.05 - 1.69）mmol/L。
在我们的队列中，既往使用β受体阻滞剂治疗与脓毒症患者较低的血清乳酸测量值相关。既往使用β受体阻滞剂治疗可能会降低脓毒症患者入院时的血清乳酸水平。
