The effect of maternal hypoxia on the fetus is a lowered PO2 in the umbilical vessels, a lowered hemoglobin oxygen saturation, a lowered pH (increased acidity), and an elevated PCO2 (Table 3.03).
The usual fetal response, in the short-term, is increased umbilical blood flow, bradycardia, increased arterial blood pressure, and the increased use of the glycolysis with increased lactate output. In addition, blood flow is redistributed mainly to the brain, heart, and placenta, the plasma titers of epinephrine and norepinephrine increase sharply, and oxygen consumption is decreased.
The bradycardic response contributes to this oxygen "sparing" mechanism. In the long-term, fetal hypoxia results in polycythemia and body growth retardation.
In the mother, hypoxia results in increased uterine blood flow and increased hyperventilation. The latter decreases maternal and fetal PCO2 and increases the CO2 gradient at the placenta.
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