Abstract

After completing this article, readers should be able to: 1. Explain the pathophysiology of fetal hypoxemia during uteroplacental circulatory insufficiency (UPI). 2. Describe the effect of UPI on nutritional substrates. 3. Delineate the potential and limitations of using Doppler flow velocity waveforms to guide delivery decisions in the presence of intrauterine growth restriction. Uteroplacental circulatory insufficiency (UPI) accounts for more than 70% of intrauterine growth restriction (IUGR) (1) and is associated with an increased risk of hypoxemic stress and nutritional deficiency. Both of these threats are concomitant and, to some extent, interrelated, but more importantly, both could lead to the feared complication of UPI—cerebral damage and secondary neurodevelopmental disabilities. To better appreciate the challenge involved in establishing the best time to deliver fetuses that have placental insufficiency, this article is divided in two parts. In the first section, present knowledge of the pathophysiology of fetal hypoxemia and nutritional deficiency in the context of UPI is reviewed briefly. The second section is devoted to a critical appraisal of the criteria currently applied to reach the decision that a fetus that has IUGR should be delivered. Fetal arterial oxygen (O2) concentrations are the result of relative proportions of blood that has different O2 saturations from various venous channels (the two venae cavae, the pulmonary veins, the coronary sinus, and the umbilical vein) draining into the cardiac cavities. Final arterial O2 saturation, therefore, predominantly is dictated by the volume of better-oxygenated blood arriving from the umbilical circulation. Normally, because of its low vascular resistance, the placenta accommodates 50% of the fetal combined cardiac output. Any change in this determinant part of venous return necessarily has a significant impact on intrauterine O2 delivery, even if Po2 in the umbilical vein is within normal range. Experimental (2)(3) and clinical (4 …

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