We read with interest the article of Knutzen et al and the accompanying editorials of Drs Cahill and Olofsson in discussing the significance of base deficit (BD) in umbilical cord blood. Together the authors discuss the use of pH, BD _blood , BD _ECF , and lactate as to which represents the best predictor of neonatal morbidity. As noted by the authors, each of these parameters is interdependent and thus highly correlated.

The findings are similar to our prior study of newborn acidosis in which the relationship of cord blood values to adverse neonatal outcomes was similar, whether using pH or BE values. Although Knutzen et al indicated that BD did not add significantly to pH in a hierarchical logistic regression, it would be of interest to know whether pH added significantly to BD in a similar regression analysis. Knutzen states that “it is largely the hydrogen ion concentration that is responsible for cellular damage.” However, respiratory acidosis, which also results in an increase in hydrogen ion concentration, does not appear to produce cell damage.

Rather neural cell damage is likely more dependent on deprivation of glucose and oxygen, inflammatory cytokines, and a second-phase generation of oxygen-derived free radicals and excitatory amino acids. Consequently, each of these measures simply serve as a marker of tissue hypoxia rather than the putative injury-inducing factor. In fact, intracellular lactate production retards, not causes, acidosis.

Although a more predictive umbilical artery acidosis indicator can aid in directing neonatal care, it is critical that we recognize that the major goal of fetal monitoring during labor and delivery is the prevention of this acidosis, whether quantified by pH, BD _blood , BD _ECF , or lactate. Because of the inverse logarithmic function of pH, it cannot be utilized to time linear changes in fetal acid production in response to hypoxic stress. Knutzen et al suggests that BD may reflect the duration and severity of the hypoxic insult, findings that are confirmed in our studies in ovine fetuses. Human fetal heart rate patterns may be assessed in real time for quantification of BD changes in response to varying heart rate patterns. The awareness of patterns and rates of BD accumulation as well as BD thresholds for injury can aid in the prospective management of fetal heart rate tracings and potentially prevent adverse outcomes.