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Guiding resuscitation in shock: base excess or lactate?
Critical Care ( IF 8.8 ) Pub Date : 2024-07-18 , DOI: 10.1186/s13054-024-05039-2
Micah Liam Arthur Heldeweg _{1,

2} , Thomas Langer _{3,

4} , František Duška ₂

Affiliation

Base excess (BE) is a widely used parameter derived from blood gas analysis. A recent international study showed that 40% of surveyed anesthesia and critical care clinicians use BE to guide (intraoperative) fluid management, and that 25% of respondents prefer BE over lactate [1]. This is surprising as lactate production is directly increased by hypovolemia-associated tissue hypoxia, whilst BE is a simple calculation of the metabolic component of acid-base derangement.

In the 1960s, measuring lactate was laborious and time-consuming: a typical colorimetric measurement of lactate took up to eight hours, clearly limiting its clinical point-of-care use [2]. At the same time, Astrup and Siggaard-Andersen introduced BE, a marker to quantify metabolic acid-base derangements independent of concomitant carbon dioxide variations, i.e. respiratory acid-base disorders. Modern BE is a simple mathematical expression that corrects changes in bicarbonate for carbon dioxide variation by using the slope of an experimentally determined carbon dioxide titration curve [3].

In contrast to lactate, BE was able to provide an instant and inexpensive quantification of a metabolic acidosis, occurring, for example, during circulatory shock. Unsurprisingly, in this context, many researchers considered BE a surrogate indicator of oxygen debt and hypovolemia. BE was ideal in the predominantly healthy traumatology population: a single surrogate marker for hemorrhagic shock severity that could be used as a therapeutic trigger for transfusion management. Investigations demonstrated that BE was more accurate at quantifying the magnitude of blood loss during hemorrhagic shock than clinicians’ visual estimates of blood loss, volume replacement counts, blood pressure, or heart rate [4].

Development of refined electrode-based lactate measurement methods enabled direct and rapid assessment, starting the era of routine lactate measurement in the 1980s [2]. Nonetheless, some authors deemed lactate as clinically less useful than BE because of potential confounding factors: inflammation, sympathetic stimulation, drugs such as metformin, hepatic failure, and exogenous lactate may all lead to a hyperlactatemia in the absence of oxygen debt [4]. Moreover, lactate normalization depends on its clearance and may be delayed despite effective resuscitative measures. Indeed, hyperlactatemia may reflect other pathophysiological mechanisms unrelated to hemorrhagic shock [5]. However, any increase in endogenous lactate, by definition, leads to a decrease in BE. Moreover, BE is a composite marker and may be influenced by more factors than only hyperlactatemia: changes in strong electrolytes, such as sodium and chloride, weak acids, such as albumin or phosphate, and other unmeasured acids, such as ketones and toxins. Notably, resuscitation with a 0.9% saline solution leads to a hyperchloraemic metabolic acidosis with a decreased BE [3].

Nonetheless, research in traumatology continued to employ BE. A landmark Critical Care cohort study heralded ‘the renaissance of BE’: investigators found that BE may be superior to traditional vital parameters (heart rate, systolic blood pressure, and Glasgow coma scale) for identification of transfusion requirements in traumatology patients [3]. BE was subsequently included in the guidelines and the ATLS classification of hypovolemic shock, an internationally-used teaching and management instrument for resuscitation. This established a paradigm in traumatology and resuscitation management that permeated into emergency medicine, anesthesia, and critical care [1]. Unfortunately, the original study did not perform a direct comparison of the performance of lactate versus BE to predict transfusion requirements [3].

Meanwhile, routine point-of-care testing spread across emergency and critical care settings worldwide, and mounting evidence supported the value of serial lactate measurements in the evaluation of critically ill patients and their response to (fluid) therapy. Clinicians widely embraced lactate as the best-available single high-sensitivity indicator of shock severity and a central therapeutic trigger in resuscitation protocols. In critical care, appraising lactate jointly with central mixed venous oxygen saturation may (partially) offset its limited specificity [5].

Currently lactate, an underlying metabolic substrate of tissue hypoxia, can be directly, reliably, and serially measured [2]. Considering BE its surrogate is, in our opinion, anachronistic. However, as these parameters provide different information, their joint evaluation remains informative. Indeed, if BE cannot be fully explained by hyperlactatemia, there may be a concurrent acid-base derangement, which should be identified and addressed. The presence of an ‘alactic’ BE may therefore be etiologically and prognostically valuable in traumatology, and perhaps, critically ill patients [1, 4]. There is a burning need for studies directly comparing the utility of metabolic parameters such as BE, lactate and alactic BE as tailored resuscitation trigger and prognostic markers in acute hypovolemia.

In conclusion, the current literature does not advocate for a single, optimal metabolic resuscitation trigger. Clinicians should integrate multiple metabolic variables with clinical parameters to decide the resuscitation strategy and evaluate its effect. Until direct comparisons are available, there is good rationale to suggest that, mechanistically, lactate is a more appropriate resuscitation trigger, whilst BE remains useful in identifying acid-base derangements superimposed on lactic acidosis.

No datasets were generated or analysed during the current study.

Heldeweg MLA, Stohlmann JAH, Loer SA. Base excess and lactate for guidance of peri-operative fluid management: a survey of anaesthetists, residents and intensive care physicians attending 2022 ESAIC in Milan. Eur J Anaesthesiol. 2023;40(8):610–2.
Article PubMed Google Scholar
Weil MH, Tang W. Forty-five-year evolution of stat blood and plasma lactate measurement to guide critical care. Clin Chem. 2009;55(11):2053–4. https://doi.org/10.1373/clinchem.2009.133553.
Article CAS PubMed Google Scholar
Berend K. Diagnostic use of base excess in acid-base disorders. N Engl J Med. 2018;378(15):1419–28. https://doi.org/10.1056/NEJMra1711860.
Article CAS PubMed Google Scholar
Rixen D, Siegel JH. Bench-to-bedside review: oxygen debt and its metabolic correlates as quantifiers of the severity of hemorrhagic and post-traumatic shock. Crit Care. 2005;9(5):441–53. https://doi.org/10.1186/cc3526.
Article PubMed PubMed Central Google Scholar
Vincent JL, Quintairos E, Silva A, Couto L Jr, Taccone FS. The value of blood lactate kinetics in critically ill patients: a systematic review. Crit Care. 2016;20(1):257. https://doi.org/10.1186/s13054-016-1403-5.
Article PubMed PubMed Central Google Scholar

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Authors and Affiliations

Department of Intensive Care Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands
Micah Liam Arthur Heldeweg
Department of Anaesthesia and Intensive Care Medicine, The Third Faculty of Medicine, Charles University, FNKV University Hospital, Prague, Czech Republic
Micah Liam Arthur Heldeweg & František Duška
Department of Medicine and Surgery, University of Milan-Bicocca, Monza, Italy
Thomas Langer
Department of Anesthesia and Intensive Care Medicine, Niguarda Ca’ Granda, Milan, Italy
Thomas Langer

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MLAH, TL, and FD were responsible for the conception of the work. MLAH was responsible for the first draft of the manuscript. Subsequently all authors provided critical revisions for until the final manuscript was completed. All authors read and approved the final manuscript and ensured that questions related to the accuracy or integrity of any part of the work were investigated and resolved.

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Correspondence to Micah Liam Arthur Heldeweg.

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Heldeweg, M.L.A., Langer, T. & Duška, F. Guiding resuscitation in shock: base excess or lactate?. Crit Care 28, 249 (2024). https://doi.org/10.1186/s13054-024-05039-2

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Received: 29 June 2024
Accepted: 13 July 2024
Published: 18 July 2024
DOI: https://doi.org/10.1186/s13054-024-05039-2

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Keywords

Base excess
Base deficit
Lactate
Metabolic acidosis
Resuscitation
Fluid management

中文翻译：

休克时指导复苏：碱过量还是乳酸过量？

碱过量（BE）是血气分析中广泛使用的参数。最近的一项国际研究表明，40% 的受访麻醉和重症监护临床医生使用 BE 来指导（术中）液体管理，25% 的受访者更喜欢 BE 而不是乳酸 [1]。这令人惊讶，因为低血容量相关组织缺氧直接增加了乳酸的产生，而 BE 是酸碱紊乱代谢成分的简单计算。

在 1960 年代，测量乳酸既费力又耗时：乳酸的典型比色测量需要长达 8 小时，这明显限制了其临床护理使用 [2]。与此同时，Astrup 和 Siggaard-Andersen 引入了 BE，这是一种量化代谢酸碱紊乱的标志物，独立于伴随的二氧化碳变化，即呼吸性酸碱紊乱。现代 BE 是一种简单的数学表达式，它通过使用实验确定的二氧化碳滴定曲线的斜率来校正碳酸氢盐的变化 [3]。

与乳酸相比，BE 能够即时且廉价地量化代谢性酸中毒，例如，发生在循环休克期间。不出所料，在这种情况下，许多研究人员认为 BE 是氧债和低血容量的替代指标。BE 在以健康的创伤学人群为主的人群中是理想的：出血性休克严重程度的单一替代标志物，可用作输血管理的治疗触发因素。研究表明，与临床医生对失血量、容量替代计数、血压或心率的目视估计相比，BE 在量化失血性休克期间失血量方面更准确 [4]。

基于精细电极的乳酸测量方法的发展实现了直接和快速的评估，开启了 1980 年代常规乳酸测量的时代 [2]。尽管如此，一些作者认为乳酸在临床上不如 BE 有用，因为存在潜在的混杂因素：炎症、交感神经刺激、二甲双胍等药物、肝功能衰竭和外源性乳酸都可能导致无氧债务的高乳酸血症 [4]。此外，乳酸正常化取决于其清除率，尽管采取了有效的复苏措施，但可能会延迟。事实上，高乳酸血症可能反映了与失血性休克无关的其他病理生理机制[5]。然而，根据定义，内源性乳酸的任何增加都会导致 BE 的降低。此外，BE 是一种复合标志物，可能受更多因素的影响，而不仅仅是高乳酸血症：强电解质的变化，如钠和氯化物，弱酸，如白蛋白或磷酸盐，以及其他未测量的酸，如酮和毒素。值得注意的是，使用 0.9% 生理盐水进行复苏会导致高氯血症性代谢性酸中毒，伴 BE 降低 [3]。

尽管如此，创伤学研究继续使用 BE。一项具有里程碑意义的重症监护队列研究预示着“BE 的复兴”：研究人员发现，在识别创伤患者输血需求方面，BE 可能优于传统的生命参数（心率、收缩压和格拉斯哥昏迷量表）[3]。BE 随后被纳入指南和 ATLS 低血容量性休克分类，这是一种国际通用的复苏教学和管理工具。这建立了创伤学和复苏管理的范式，并渗透到急诊医学、麻醉和重症监护中[1]。遗憾的是，最初的研究并未直接比较乳酸与 BE 的性能以预测输血需求 [3]。

与此同时，常规即时检测遍布全球急诊和重症监护机构，越来越多的证据支持连续乳酸测量在评估危重患者及其对（液体）治疗的反应方面的价值。临床医生广泛认为乳酸是休克严重程度的最佳单一高敏感性指标，也是复苏方案中的核心治疗触发因素。在危重症诊疗中，联合评估乳酸和中心静脉血氧饱和度可能（部分）抵消其有限的特异性[5]。

目前，乳酸是组织缺氧的潜在代谢底物，可以直接、可靠和连续地测量 [2]。在我们看来，将 BE 视为它的替代物是不合时宜的。然而，由于这些参数提供的信息不同，它们的联合评估仍然具有信息量。事实上，如果 BE 不能用高乳酸血症完全解释，则可能存在并发酸碱紊乱，应予以识别和解决。因此，“无酸性”BE 的存在可能在创伤学和危重患者中具有病因学和预后价值 [1， 4]。迫切需要研究直接比较代谢参数（如 BE、乳酸和乳酸 BE）作为急性低血容量中量身定制的复苏触发因素和预后标志物的效用。

总之，目前的文献并不提倡单一的、最佳的代谢复苏触发因素。临床医生应将多个代谢变量与临床参数相结合，以决定复苏策略并评估其效果。在获得直接比较之前，有充分的理由表明，从机制上讲，乳酸是更合适的复苏触发因素，而 BE 在识别乳酸性酸中毒叠加的酸碱紊乱方面仍然有用。

在当前研究期间没有生成或分析数据集。

Heldeweg MLA， Stohlmann JAH， Loer SA.碱过量和乳酸指导围手术期液体管理：对在米兰参加 2022 年 ESAIC 的麻醉师、住院医师和重症监护医生的调查。Eur J 麻醉剂。2023;40(8):610–2.

文章 PubMed 谷歌学术
Weil MH， Tang W. 统计血液和血浆乳酸测量指导重症监护的 45 年演变。临床化学 2009;55(11):2053–4.https://doi.org/10.1373/clinchem.2009.133553。

论文 CAS PubMed Google Scholar
Berend K. 碱过量在酸碱紊乱中的诊断使用。N Engl J Med. 2018 年;378（15）：1419-28 https://doi.org/10.1056/NEJMra1711860。

论文 CAS PubMed Google Scholar
Rixen D，Siegel JH。从实验室到床旁回顾：氧债务及其代谢相关性作为出血性和创伤后休克严重程度的量化指标。暴击护理。2005;9(5):441–53.https://doi.org/10.1186/cc3526。

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荷兰阿姆斯特丹大学医学中心重症监护医学系

米卡·利亚姆（Micah Liam）亚瑟·赫尔德维格（Arthur Heldeweg）
捷克共和国布拉格 FNKV 大学医院查理大学第三医学院麻醉和重症监护医学系
Micah Liam Arthur Heldeweg & František Duška
意大利蒙扎米兰比可卡大学内外科系
托马斯·兰格
麻醉和重症监护医学科， Niguarda Ca' Granda，米兰，意大利
托马斯·兰格

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