Measurement of cardiac output in the second trimester identified women at risk for preeclampsia. Treatment with atenolol decreased the incidence of preeclampsia. Nulliparous and diabetic women at risk for preeclampsia were similar with regard to maternal hemodynamics, maternal weight, and renal function. Treatment with atenolol was associated with reduced infant birth weight.

No abstract

Early intervention with antihypertensive therapy was associated with a low rate of severe maternal hypertension and preterm delivery. The failure to adjust therapy in response to an excessive fall in cardiac output or increase in vascular resistance was associated with reduced fetal growth.

Early diagnosis of pulmonary hypertension is critical. Volume overload postpartum might significantly contribute to decompensation. We recommend a year of successful therapy after a response to vasodilator therapy and near-normal right ventricular function before pregnancy is considered. In complicated pregnancies, women must balance the best estimate of risk with the value they put on pregnancy.

Invasive and noninvasive investigations suggest that the hemodynamics of pregnant hypertensive patients are heterogeneous. Nineteen pregnant patients were evaluated before changes in antihypertensive therapy. Cardiac output was measured by Doppler technique. Blood pressure was measured by automated cuff. Systemic vascular resistance was calculated. Two distinct groups were identified on the basis of differences in cardiac output (p less than 0.0001) and systemic vascular resistance (p less than 0.0001). Those with high resistances were treated with hydralazine. A modest antihypertensive effect was achieved (-6.9 mmHg, p = 0.01), but systemic vascular resistance was dramatically reduced, (-534 dyne.sec.cm-5, p less than 0.0001) and was associated with a compensatory increase in cardiac output (2.0 liters/min, p less than 0.0001). Those with a high cardiac output were treated with atenolol. An antihypertensive effect was achieved, (-17.0 mm Hg, p = 0.008), which was associated with a reduction in cardiac output (-2.8 liters/min, p less than 0.0001).