Intrauterine asphyxia and the breakdown of physiologic circulatory compensation in fetal sheep.

In response to acute hypoxemia, the fetus invokes physiologic compensatory mechanisms that cause a preferential redistribution of the circulation to sustain the brain, heart, and adrenal gland and maintain blood flow to the placenta. These mechanisms are available for a limited time and eventually the fetus is no longer able to maintain preferential perfusion and decompensation occurs. To identify the relationship between hypoxemia with severe acidemia and the breakdown of circulatory compensation, we decreased uterine blood flow in 10 chronically instrumented pregnant sheep. We measured fetal blood gases and pH, arterial and central venous pressures, heart rate, combined ventricular output, and regional blood flow distribution during hypoxemia with severe acidemia and when a fixed-baseline sustained bradycardia (agonal) heart rate pattern developed. Hypoxemia with severe acidemia was characterized by markedly decreased blood flow to most organs; however, the preferential perfusion of the brain, heart, adrenal gland, and placenta was still present. An agonal heart rate pattern was characterized by complete cardiovascular collapse. This study demonstrates that circulatory compensation is present in fetal sheep affected by deficiency of oxygen delivery despite hypoxemia with severe acidemia.