  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.
