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Virtually any pathologic process which affects the mother has the potential to affect the fetus. The type and severity of the 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 the fetal physiology as it relates to these functions.




The fetal impact of most critical diseases in the mother will depend on how well the mother is able to continue to deliver oxygen to the fetus while at the same time dealing with her own compromised state. Fetal oxygen delivery depends on placental blood flow, differences in partial pressure of oxygen between mother and fetus, oxygen content (a function of oxygen carrying capacity of the maternal blood), the placental surface area, and is inversely proportional to the thickness of the placental diffusing membrane. In diseases that primarily affect the mother, except for those that may lead to abruptio placentae, placental issues remain constant and the critical issues become blood flow and oxygen pressure and content.


The fetus functions at a much lower oxygen tension than its air breathing counterpart. Its ability to do so is based on a hemoglobin/oxygen dissociation curve that is to the left of its mother (Fig. 22-1) allowing a considerably higher oxygen saturation at lower partial pressures of oxygen. This is absolutely essential in the human placental model which has a type of parallel flow that has been described as “concurrent." In this flow model (Fig. 22-2) the maximum fetal PO2 will be a few torr 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, the fetal PO2 can never exceed that of maternal venous blood. Thus, in the healthy, normally perfused placenta, fetal venous blood (the oxygenated side of the fetal circuit) will have a maximum PO2 of about 35 given that mother’s venous PO2 of 35 to 40. At this PO2, the fetal blood is about 70% saturated with oxygen. The fetus will maintain aerobic metabolism at saturations above 30% to 35% corresponding to a PO2 of 15 to 20. This is important information when trying to understand the impact of maternal hypoxia with alterations in uterine blood flow, such as with the mother with acute respiratory illnesses and especially with a mother on a ventilator. Maternal anemia will significantly alter the level at which anaerobic metabolism and acidosis may occur since reduced levels of hemoglobin will reduce the absolute amount of oxygen the blood will carry at a ...

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