“…With additional centralization, or the development of late decelerations on the fetal heart rate tracing, significantly lower oxygen content and pH values are associated with a concomitant rise in carbon dioxide and lactate in cord artery blood [14,94,95]. With the loss or reversal of end-diastolic flow in the umbilical artery a significant worsening of hypoxemia and acidemia can be detected [ Animal studies using invasive techniques [15,17,74,87] and noninvasive studies using Doppler sonography in the human fetus indicate that intrauterine hypoxemia due to uteroplacental insufficiency is associated with a redistribution in cardiac output in favor of the left ventricle providing preferential perfusion of the brain as well as the myocardium [2,68,76,77]. This is achieved by a relative decrease of left ventricular afterload in the presence of high right ventricular afterload caused by high resistance in the fetoplacental circulation.…”