Schmucker Bc

Pulmonary hypertension in pregnancy: treatment with pulmonary vasodilators.

OBJECTIVE To describe the clinical course of pregnancies complicated by pulmonary hypertension and treated with the pulmonary vasodilators nifedipine and prostacyclin. METHODS Four pregnant women with pulmonary hypertension were treated with pulmonary vasodilators. Therapy with oral nifedipine and intravenous prostacyclin was guided by right pulmonary artery catheterization and Doppler measurements of cardiac output. RESULTS Three of four women responded to vasodilator therapy and successfully completed their pregnancies. Two who conceived at least 1 year after successful treatment and normalized right ventricle function carried three uncomplicated pregnancies. The woman who did not respond died. Delay in diagnosis contributed to her outcome. Noninvasive measurement of cardiac output helped diagnosis of right ventricular failure and offered reassurance in women who remained compensated. Postpartum decompensation in one woman was characterized by a negative Starling response as central venous pressure increased from 4 to 11 mmHg. She responded positively to diuresis. CONCLUSION 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.

Treatment of hypertension in pregnancy: effect of atenolol on maternal disease, preterm delivery, and fetal growth.

OBJECTIVE To assess the impact of antihypertensive therapy initiated early in pregnancy on maternal and fetal outcomes. METHODS A retrospective review of patients treated in early pregnancy with atenolol was conducted. Therapy was directed by measurements of cardiac output. Fetal growth was analyzed with reference to prior pregnancy outcome, treatment inconsistent with standards present at the end of the study period, and year of treatment. Data were analyzed by paired and unpaired t‐test, analysis of variance for multiple comparisons, and linear regression. RESULTS Two hundred thirty‐five pregnancies at risk for preeclampsia were studied. Ten percent (n = 22) received additional therapy with furosemide; 20% (n = 48) with hydralazine. Six and one half percent had treatment inconsistencies. Fifty‐five percent had greater than 100 mg of proteinuria at baseline. One patient developed severe preeclampsia. Only 2.1% delivered before 32 weeks; 4.7% delivered before 34 weeks. Low percentile birth weight was strongly associated with a prior pregnancy with intrauterine growth restriction (P = 0.001), treatment inconsistency (P < .001), and a pregnancy earlier in our treatment experience (P < .001). Percentile birth weight increased from the 20th at the beginning of the study period to the 40th by the end (P = 0.002). CONCLUSION 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.

Low-dose, short-acting, angiotensin-converting enzyme inhibitors as rescue therapy in pregnancy

Objective To assess the risks and potential benefits of low-dose angiotensin-converting enzyme (ACE) inhibitor treatment in pregnancies complicated by severe hypertension. Methods A retrospective review of pregnant women treated with ACE inhibitors was conducted. Hemodynamics before and after treatment were assessed by using Doppler technique to measure cardiac output. Data were analyzed by using the Wilcoxon signed-rank test. Maternal and neonatal outcomes were assessed by chart review and phone interview. Results Ten pregnancies were identified in which ACE inhibitor therapy was initiated in pregnancy for severe, unresponsive vasoconstricted hypertension; three were complicated by severe chronic hypertension, 4 by renal insufficiency, and 3 by severe preeclampsia. Treatment was limited to a low-dose, short-acting ACE inhibitor (captopril, 12.5 to 25 mg/day). Treatment was associated with an increase in cardiac output from 5.7 ± 1.5 L/minute to 7.4 ± 1.4 L/minute (P < .01) and a reduction in total peripheral resistance from 1770 ± 670 to 1222 ± 271 dyne • sec • cm−5 (P = .005). No fetal or neonatal complications were observed. The probability of observing one or more adverse neonatal outcome in this sample, based on an assumed true risk of 5% and 10%, was calculated to be 12% and 50%, respectively. Conclusion Low-dose captopril therapy was associated with improvement in maternal hemodynamics and, in cases complicated by severe hypertension and renal insufficiency, successful continuation of pregnancy. Fetal and neonatal complications were not experienced, but complication rates of 5–10% could have been missed because of the small number of exposed pregnancies.

The hemodynamic effects of isometric exercise during late normal pregnancy

OBJECTIVE Our study was designed to evaluate the hemodynamic effects of isometric exercise in late normal pregnancy. STUDY DESIGN Study subjects were 10 healthy pregnant volunteers with uncomplicated singleton gestations between 25 and 36 weeks. Doppler methods were used to derive cardiac output, total peripheral resistance, and stroke volume before, during, and after a defined protocol of lower extremity isometric exercise. Hemodynamics and blood pressure were evaluated and compared. RESULTS Mean arterial blood pressure and total peripheral resistance increased during the performance of isometric effort (mean blood pressure +/- SD was 78.9 +/- 7.3 to 97.5 +/- 8.6 mm Hg; total peripheral resistance +/- SD was 924 +/- 148 to 1153 +/- 18.3 dyne.sec.cm-5; p < 0.002 and p < 0.001, respectively). Cardiac output remained unchanged throughout the study period. CONCLUSION In advanced normal pregnancy isometric exercise increases the mean arterial blood pressure by raising the total peripheral resistance.

Maternal Weight, Hemodynamics, and Preeclampsia

Objectives: To evaluate the relationship between the obesity, elevated cardiac output, and the development of preeclampsia.Methods: Maternal weight, mean arterial pressure, and cardiac output were analyzed from 9 preeclamptic, 81 gestationally hypertensive, and 89 normotensive pregnant women at 23 weeks gestation, 34 weeks gestation, and 6–8 weeks postpartum. Data were gathered prospectively and longitudinally as part of a previously described investigation. Cardiac output was measured by Doppler technique. Data were analyzed by multiple logistic regression. The data for cardiac output, weight, and mean arterial pressure were first modeled controlling for the effect of the parameter most strongly associated with preeclampsia. The data were modeled a second and third time controlling for the other two parameters.Results: Elevated cardiac output, mean arterial pressure, and maternal weight at 23 weeks and postpartum were each associated with the development of preeclampsia. After controlling for the effects...

Measurement of Cardiac Output During Pregnancy: Validation of Doppler Technique and Clinical Observations in Preeclampsia

In 12 patients requiring pulmonary artery catheterization, cardiac output was measured using Doppler and thermodilution techniques. The Doppler technique accurately predicted measurements made by thermodilution (r = 0.91; P < .001). Eighteen normal patients in the third trimester and 36 preeclamptics who had not been treated with medications other than magnesium sulfate were evaluated with Doppler alone. Of note was the heterogeneity among preeclamptics. Although their mean systemic vascular resistance was elevated, it ranged from 2256–648 dyne·sec·cm-5. Cardiac output ranged from 13.2–3.9 L/minute.