Abstract
Extract: Maternal respiratory alkalosis from hyperventilation before delivery has been associated with depression and acidosis of some newborn infants. In these in utero studies of 6 primate fetuses, acute maternal hyperventilation significantly increased both the maternal and the fetal pH and thus increased the oxygen affinities of maternal and fetal hemoglobins. In comparison with the control period, during hyperventilation 71 % more CO2 was removed from the uterus and its contents. The average O2 consumption by the uterus and placenta, 3.4 ml/min, and the fetus, 2.1 ml/min was unchanged during hyperventilation. Mean pO2 in the umbilical vein during hyperventilation fell to 24.8 mm Hg and saturation to 65%, and umbilical blood flow increased from 40 to 45 ml/min. Average uterine blood flow decreased slightly during hyperventilation. During these same comparison periods, neither maternal and fetal heart rate nor arterial venous pressures changed significantly. Thus, although pO2 and saturation in the umbilical and uterine venous blood decreased, the amount of oxygen delivered to each fetus remained relatively constant due in part to an increase in umbilical blood flow and to shifts in the oxygen dissociation curves of fetal and adult hemoglobins.
Speculation: A number of interrelated physiologic adjustments may take place on both sides of the placenta in response to maternal respiratory alkalosis in the primate without necessarily resulting in untoward effects on the fetus. However, any of a variety of additional clinical complications, particularly those that interfere with umbilical or uterine blood flow, might exceed the limits of intrauterine adjustment and compromise fetal oxygenation.
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Behrman, R., Parer, J. & Novy, M. Acute Maternal Respiratory Alkalosis (Hyperventilation) in the Pregnant Rhesus Monkey. Pediatr Res 1, 354–363 (1967). https://doi.org/10.1203/00006450-196709000-00003
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DOI: https://doi.org/10.1203/00006450-196709000-00003