I read with concern the article by Leung et al in which the authors conclude that "cord arterial pH deteriorates with bradycardia-to-delivery interval when the underlying cause of fetal distress is irreversible, but not so otherwise." Fetal arterial base excess, which correlates closely with lactate levels, can be used to quantify rates of metabolic acidosis change in response to varying levels of fetal hypoxic stress (Ross MG. Base excess during cord occlusion. Am J Obstet Gynecol 2003; 189:1811-2 [letter]). In contrast, the lack of utility of pH to measure changes per time of fetal compromise is well recognized because cord arterial pH has two "fatal" limitations. Firstly, arterial pH is highly dependent on pCO2 values, which result in respiratory, not metabolic, acidosis. Because fetal levels of pCO2 may exceed 100 mm Hg, pH changes can obscure the degree of metabolic acidosis.
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