Fetal oxygen delivery and consumption and blood gases in relation to gestational age

Abstract

Fetal oxygen delivery and consumption and blood gases in relation to gestational age. Oxygen crosses the placenta by diffusion and placental permeability to O_2 is high. Thus, the fetus receives adequate amounts, but vascular Po_2 is much lower than after birth. Studies of sustained fetal hypoxemia and acute 40-45% hemorrhage show that hypoxemia is not tolerated whereas hemorrhage is. This suggests that if fetal Po_2 falls markedly, O_2 diffusion from blood to tissue is impaired. Uterine blood and umbilical blood flows/fetal weight fall progressively with advancing gestation. This results in fetal hypoxemia, an increase in Pco_2, and decrease in pH. This decreases fetal O_2 delivery, and in fetal lambs and horses there is a decrease in fetal O_2 consumption. The decrease in O_2 demands is linked to a decrease in fetal breathing and body movements and growth rate. The decrease in fetal motility is due to an increase in fetal plasma PGE2 concentration, which begins at ~120 days GA in sheep and is due to the prepartum rise in fetal cortisol. Also, adenosine administration to fetal lambs decreases fetal breathing and REM sleep and the plasma adenosine concentration increases in late gestation. The fetal plasma levels of neurosteroids, which suppress fetal motility, increase with advancing gestation. The prepartum cortisol rise also inhibits fetal growth. In normal pregnancies, these mechanisms operate effectively to maintain an appropriate balance between fetal oxygen consumption and delivery. However, in pregnancies with either further reduce O_2 delivery or increase fetal O_2 demands, the mismatch between O_2 delivery and consumption may worsen leading to IUGR, hypoxic organ damage or stillbirth.

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