Determinants of Fetal Oxygenation
The fetus develops in an environment of low oxygen tension relative to the mother. This is due to the design of the placenta. The maternal uterine blood vessels and the fetal umbilical blood vessels run in parallel and oxygen is exchanged passively. Consequently, fetal oxygen pressure can never exceed maternal venous oxygen pressure.
In light of the low oxygen tension of blood delivered to the fetus, other mechanisms must be used to enhance fetal oxygenation. In this respect, fetal hemoglobin plays an important role. Fetal hemoglobin has a higher affinity for oxygen relative to adult hemoglobin. Further, fetal hemoglobin is more highly concentrated as compared to adult hemoglobin, which increases the oxygen-carrying capacity of the fetal blood. An additional method enhancing fetal oxygenation is the increased perfusion rate of some fetal organs compared with adult organs. Animal models suggest relative blood flow to select fetal organs can be greater than twice that of the adult organs.[11,12]
Nevertheless, there are multiple areas where fetal oxygen delivery can be restricted. Fetal oxygen delivery can be impaired by respiratory, cardiovascular, or hematologic problems in the fetus. For example, umbilical blood flow can be disrupted due to compression. Placental blood flow can be disrupted due to placental infection, infarction, or abruption. Finally, maternal oxygen delivery to the fetus can be impaired due to major maternal respiratory, cardiovascular, or hematologic abnormalities. One such maternal respiratory condition is asthma, which may affect the fetus adversely, if its not controlled effectively.
Cite this: Asthma and Pregnancy: A Review - Medscape - Dec 29, 1998.
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