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

TL;DR

This paper reviews how fetal oxygen delivery, blood gases, and related physiological mechanisms change with gestational age, affecting fetal growth, motility, and survival, especially under hypoxemic conditions.

Contribution

It provides a comprehensive analysis of fetal oxygen dynamics, blood gas changes, and the physiological responses during gestation, highlighting mechanisms that maintain oxygen balance and their implications for fetal health.

Findings

Fetal oxygen diffusion is high but Po2 is lower than postnatal levels.

Fetal hypoxemia is poorly tolerated, but hemorrhage is tolerated.

Decreased oxygen delivery with gestation leads to reduced fetal oxygen consumption.

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.