Authors have expressed reservations regarding the use of base deficit measured in umbilical artery blood samples to assess fetal well-being during the course of labor and to predict neonatal neurologic morbidity. Despite its integration into clinical practice for more than 50 years, obstetricians and maternal-fetal medicine specialists may not realize that this marker has significant limitations in accurately identifying neonatal metabolic acidosis as a proxy for fetal well-being. In brief, there are 2 large families of base deficit, namely whole blood and extracellular fluid. Both rely on equations that use normal adult acid-base characteristics (pH 7.40 and partial CO pressure of 40 mm Hg) that overlook the specificity of the normal in utero acid-base status of pH 7.27 and partial CO pressure of 54 mm Hg. In addition, it ignores the unique characteristic of the in utero fetal response to acute hypoxia. The dependence on placental circulation for CO elimination may lead to extremely high values (up to 130 to 150 mm Hg) during hypoxic events, a phenomenon that is absent in adults with acute metabolic acidosis who can hyperventilate. The dispute over if to include a correction for high partial CO pressure in the bicarbonate estimation, as presented in the Great Trans-Atlantic Debates, remains unresolved. The key constants computed for adult acid-base physiology in the current base deficit algorithms, without accounting for the impact of high partial CO pressure or other fetal characteristics of buffering capacity (eg, differences in body water content composition, plasma protein, and hemoglobin attributes), may lead to an overestimation of metabolic acidosis, especially in newborns who are experiencing hypercarbia during the early stages of the hypoxic response. These unrecognized limitations impact the base deficit results and may mislead clinicians on fetal well-being assessments when discussing the management of fetal heart rate monitoring and neonatal outcomes. Based on our arguments, we believe that it is prudent to consider an alternative to base deficit for drawing conclusions regarding fetal well-being during the course of birth management. We propose a marker specifically related to the newborn acid-base physiology––the neonatal eucapnic pH correction. This marker can be added to arterial cord blood gas analysis, and we have described how to interpret it as a marker of neonatal metabolic acidosis.

中文翻译：

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是时候停止使用碱缺乏来评估胎儿健康了吗？

作者对使用脐动脉血样测量的碱基缺乏来评估分娩过程中胎儿的健康状况和预测新生儿神经系统发病率表示保留。尽管它融入临床实践已有 50 多年，但产科医生和母胎医学专家可能没有意识到，该标记物在准确识别新生儿代谢性酸中毒作为胎儿健康指标方面存在重大局限性。简而言之，碱缺乏有两大类，即全血和细胞外液。两者都依赖于使用正常成人酸碱特征（pH 7.40 和 CO 分压 40 mm Hg）的方程，忽略了正常子宫酸碱状态（pH 7.27 和 CO 分压 54 mm Hg）的特异性。此外，它忽略了宫内胎儿对急性缺氧反应的独特特征。在缺氧事件中，依赖胎盘循环消除 CO 可能会导致极高的值（高达 130 至 150 mm Hg），这种现象在患有急性代谢性酸中毒且通气过度的成人中不存在。正如跨大西洋大辩论中提出的那样，关于是否在碳酸氢盐估算中包括对高二氧化碳分压的修正的争议仍未解决。在当前碱亏缺算法中计算成人酸碱生理学的关键常数，未考虑高二氧化碳分压或缓冲能力的其他胎儿特征的影响（例如，体内水含量成分、血浆蛋白和血红蛋白属性的差异） ），可能会导致代谢性酸中毒的高估，尤其是在缺氧反应早期阶段出现高碳酸血症的新生儿。这些未被认识到的局限性会影响基础赤字结果，并可能在讨论胎心率监测和新生儿结局的管理时误导临床医生对胎儿健康评估。根据我们的论点，我们认为，在分娩管理过程中，考虑采用碱基赤字的替代方案来得出有关胎儿健康的结论是明智的。我们提出了一个与新生儿酸碱生理学特别相关的标记——新生儿纯碳酸 pH 值校正。该标记物可以添加到动脉脐带血气分析中，我们已经描述了如何将其解释为新生儿代谢性酸中毒的标记物。