Chapter 20 - Observations on the evolution of human fetal acidosis

Abstract

Publisher Summary This chapter provides some observations on the evolution of human fetal acidosis. When human fetal hypoxia occurs, acidosis develops as a result of carbon dioxide retention and lactate accumulation, although it has never been clearly established if hypercapnia and lacticacidemia occur simultaneously or separately. It has been postulated that the acidosis due to hypercapnia is more acute, transitory, and of earlier onset than that due to lacticacidemia that results from a more severe hypoxic insult, develops more slowly, lasts longer, and is, therefore, more harmful to the fetus. The lack of understanding of the evolution of fetal acidosis has been compounded by difficulty in measuring lactate in the small samples obtained from the fetal scalp. The indirect measures of the lactate concentration have been made using the base excess, the base excess calculated at a hemoglobin concentration of 5g/100 ml, or the pH after equilibration of the blood sample with carbon dioxide at a tension of 40 mmHg. The good correlation between rising PCO 2 values and falling pH values and between rising lactate values and falling pH values implies that hypercapnia and lacticacidemia are principally responsible for causing a fall in pH. The poor correlation between the base deficit and lactate values suggests that the base deficit is a poor measure of lacticacidemia.