During pregnancy, hormonally mediated changes in blood volume, red cell mass, and heart rate result in a 50% increase in intravascular volume and cardiac output, peaking during the second trimester and remaining constant through the remainder of the pregnancy (1). Gestational hormones, circulating prostaglandins, and the low-resistance vascular bed in the placenta result in concomitant decreases in peripheral vascular resistance and blood pressure. During labor and delivery, pain and uterine contractions result in additional increases in cardiac output and blood pressure. Immediately following delivery, relief of caval compression and autotransfusion from the emptied and contracted uterus produce a further increase in cardiac output. The hemodynamic changes of pregnancy persist for at least several days postpartum and may not fully resolve until the sixth postpartum month.