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The effects of changes in PaCO2 on the circulation are complex, involving local vasodilation, vasodilation mediated by the pulmonary inflation reflex, and vasoconstriction due to effects on central vasomotor centers and peripheral chemoreceptors. One might anticipate that some or all of these might differ between the fetus in utero and the newborn. Distribution of cardiac output was measured in unanesthetized fetal (n = 6) and newborn (n = 7) sheep, using the radioactive microsphere technique. PaCO2 rose from 44 to 70 (fetus) and 38 to 60 torr (newborn) with the addition of CO2 to room air. In the fetus, there were significant increases in central nervous system (CNS), diaphragm, and lung blood flows. No organ showed a significant decrease in flow. Local vasodilation by CO2 was the likely cause of the increased flow to CNS. The large increase in pulmonary blood flow was most likely due to the associated rise in fetal PaO2 (23 to 28 torr) that accompanied respiratory acidosis and the presence of fetal breathing movements. The rise in diaphragmatic blood flow was likely the result of fetal breathing. In the newborn, CNS and diaphragm flows rose, but unlike the fetus, spleen and stomach flows decreased. These decreased flows in the hypercapnic newborn may have been due to stimulation of either central vasomotor centers or peripheral chemoreceptors.

Distribution of Cardiac Output in Fetal and Neonatal Lambs with Acute Respiratory Acidosis