Skip to Main Content

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android


Virtually any pathologic process which affects the mother has the potential to affect the fetus. The type and severity of fetal impact will depend on many variables among which are whether the insult is acute or chronic, how the insult affects fetal oxygenation via oxygen delivery and uterine perfusion, and the ability to intervene based on gestational age and the hemodynamic and respiratory status of the mother. Critical to decision making in these situations is a basic understanding of fetal physiology as it relates to these functions.


The fetal impact of most critical maternal diseases depends on how well the mother is able to deliver oxygen to the fetus while simultaneously dealing with her own compromised state. Fetal oxygen delivery depends on adequacy of placental blood flow, sufficient differences between fetal and maternal partial pressures of oxygen, sufficient oxygen content (a function of oxygen carrying capacity of the maternal blood), and adequacy of placental surface area. Fetal oxygen delivery is inversely proportional to the thickness of the placental diffusing membrane. Except for maternal diseases that may lead to abruptio placentae, placental issues are generally static in critical care situations. Thus, critical factors which influence fetal well-being in critical care situations are essentially uteroplacental blood flow and maternal oxygen pressure/content.

Fetal red blood cells possess hemoglobin F, a form of hemoglobin which binds more avidly to oxygen than does (maternal) hemoglobin A. Therefore, the fetus thrives at much lower oxygen tensions than can its mother. Its ability to do so is based on a hemoglobin/oxygen dissociation curve that is shifted to the left of its mother’s as a result of its hemoglobin F (Fig. 22-1), thereby producing considerably higher oxygen saturations at lower partial pressures of oxygen. This is essential in the human placental, which has a parallel flow arrangement, usually described as “concurrent.” In this model (Fig. 22-2), the maximum fetal PO2 will be a few torr (mm Hg) less than that of the mother’s venous PO2. This is because at the end of the exchange loop, for oxygen to be continually exchanged in the direction of mother to fetus, fetal PO2 can never equal or exceed that of maternal venous blood. Thus, in healthy, normally perfused placentas, fetal venous blood (the oxygenated side of the fetal circuit) will have maximum PO2 values of about 35 torr, versus maternal venous PO2 ­values of 35 to 40 torr. At this PO2, the fetal blood will be roughly 70% saturated with oxygen. The fetus will maintain aerobic metabolism at saturations above 30% to 35% corresponding to a PO2 of 15 to 20 torr. This is important information when trying to understand the impact of maternal hypoxia with concomitant alterations in uterine blood flow, such as the mother with acute respiratory ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.