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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.

A pregnant woman with an undiagnosed pheochromocytoma is described. Her presentation at 29 weeks' gestation was consistent with preeclampsia. Noninvasive measurement of cardiac output and ambulatory monitoring of blood pressure provided data that facilitated making the appropriate diagnosis and managing the patient until delivery at term.

The vasodilation of pregnancy is thought by many to be due to increased endothelial production of prostacyclin, a vasodilatory prostanoid. Indomethacin, a potent inhibitor of prostaglandin synthesis, is known to increase the maternal blood pressure response to angiotensin II infusion. We sought to measure directly the hemodynamic effects of a short course of indomethacin. Twenty-three healthy pregnant women with uncomplicated pregnancies between 26-32 weeks' gestation completed the study. Using Doppler technology, we determined cardiac output, stroke volume, and total peripheral resistance before and after three 25-mg doses of indomethacin. Although blood pressure did not change, peripheral resistance rose and stroke volume fell following indomethacin administration. Our findings support the hypothesis that indomethacin interferes with tonic prostaglandin-induced vasodilation in pregnancy. However, the increase in vascular resistance was very slight, suggesting that other vasodilators are also at work in pregnancy. We recommend that indomethacin be used judiciously in hypertensive pregnant patients until more information concerning possible adverse hemodynamic effects becomes available.

The aortic diameters of 89 normotensive pregnant women were compared with those of nine rigorously defined preeclamptic women and 59 women who required antihypertensive therapy. Over the course of normal pregnancy, the diameter increased significantly; it was larger in preeclamptic than in normotensive women throughout pregnancy. The aortic diameter in women with high-resistance hypertension was smaller than that in normotensive women and in those with high-output, low-resistance hypertension, but it was larger in women with low-resistance hypertension than in normotensive women. The aortic diameter increased after treatment of high-resistance hypertension with hydralazine, but decreased after treatment of high-output, low-resistance hypertension.

The hemodynamics of six pregnant women with hyperthyroidism were studied before and after therapy. Cardiac output was measured by Doppler technique, and blood pressure by automated cuff. When compared with values in euthyroid pregnant women, blood pressure (83.6 mmHg, P less than .001), heart rate (89.2 beats per minute, P less than .001), cardiac output (11.2 L/minute, P less than .001), and stroke volume (123 mL, P less than .001) were significantly elevated. Total peripheral resistance was significantly reduced (609 dyne.second.cm-5, P less than .001). Despite normalization of thyroid indices after therapy, cardiac output remained markedly elevated (9.7 L/minute, P less than .001) and vascular resistance remained reduced (708 dyne.second.cm-5, P = .01). Although the hemodynamics of pregnant thyrotoxic women normalize with therapy, they remain significantly hyperdynamic.

Central hemodynamic response to position change was assessed in 10 normotensive primiparous patients between 36 and 38 weeks' gestation. Studies were repeated between 11 and 13 weeks post partum. Compared with the left lateral position, we observed a mean 9% fall in cardiac output in the supine position and an 18% fall when patients were standing. When standing, these patients had a 30% increase in pulse and a 21% fall in left ventricular stroke work index. The orthostatic response after pregnancy was much more labile than that during the third trimester. These findings have important descriptive implications for the understanding of the human response to orthostasis during pregnancy, as well as clinical implications for patients at risk of uteroplacental insufficiency and for working women during pregnancy.

Preeclampsia is a disease unique to pregnancy that contributes substantially to maternal and fetal morbidity and mortality. The condition has been thought to be one of hypoperfusion in which increased vascular resistance characterizes the associated hypertension. This study was designed to test an alternative hypothesis, that preeclampsia is characterized by high cardiac output. In a blinded longitudinal study of nulliparas with uncomplicated pregnancies, cardiac output was measured serially by Doppler technique. Cardiac output was elevated throughout pregnancy in patients who became preeclamptic (P = .006). Six weeks postpartum, the hypertension of the preeclamptic subjects had resolved but cardiac output remained elevated (P = .001) and peripheral resistance remained lower than in the normotensive subjects (P = .001). This study demonstrates that preeclampsia is not a disease of systemic hypoperfusion and challenges most current models of the disease based on that assumption.

Preeclampsia is a common disease and as such is a significant contributor to maternal and neonatal morbidity and mortality. Despite the ubiquity of the disease and its public health impact, no comprehensive mechanism has been established. Therapy has been limited to bed rest and premature delivery. The purpose of this article is to examine preeclampsia from a hemodynamic point of view and to advance a hypothesis of disease mechanism.

The high incidence of pulmonary complications following evacuation of molar gestation at 16 weeks' size of greater (27%) prompted us to institute hemodynamic monitoring in seven of these patients in an effort to determine etiologies and possible modes of therapy for this potentially life-threatening complication. Our data indicate that following suction curettage with general anesthesia there appears to be impairment of ventricular performance of a transient nature as manifested by increases in central venous pressure, mean pulmonary artery pressure, and pulmonary capillary wedge pressure, despite a slight elevation in cardiac index and a decrease in systemic vascular resistance. The possible role of general anesthesia in the development of these changes, as well as the role of the colloid osmotic pressure to wedge gradient in the development of pulmonary complications, is discussed.

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).

A patient with pheochromocytoma diagnosed at 17 weeks' gestation was studied at rest, during an episode of paroxysmal hypertension, and during phenoxybenzamine treatment. Cardiac output was estimated noninvasively by Doppler technique. During paroxysmal hypertension, the mean blood pressure was 102 mmHg, cardiac output fell by 40%, and systemic vascular resistance rose by 250%. Phenoxybenzamine treatment did not change the resting cardiac output or systemic vascular resistance. These observations suggest that serious fetal compromise might occur even with mild episodes of hypertension associated with pheochromocytoma.

Ten patients with severe preeclampsia complicated by pulmonary edema were studied with invasive hemodynamic monitoring. Eight of 10 patients developed pulmonary edema during the postpartum period. Five patients had alterations in the colloid osmotic pressure--pulmonary artery wedge pressure gradient related to elevations in the pulmonary artery wedge pressure and a reduction in the colloid osmotic pressure. Three patients had hemodynamic findings consistent with pulmonary capillary leak. Two patients had evidence of left ventricular failure. In three of the patients, the central venous pressure was significantly lower than the simultaneously determined pulmonary artery wedge pressure during the acute phase of the pulmonary edema.

The effects of orthostatic stress on cardiac output and systemic vascular resistance have not been previously studied in pregnancy. A Doppler technique of measuring cardiac output was used to study 15 nonpregnant women, 14 pregnant women in the first trimester, and 16 pregnant women in the third trimester. Subjects were studied in recumbent, sitting, and standing positions. In each group, the change from recumbent to standing positions resulted in a fall in cardiac output of 1.7-1.8 L/minute (P = .001). Systemic vascular resistance rose in each group (P = .001). The magnitude of the rise was greatest in nonpregnant women and smallest in the third trimester (P = .005). The observed fall in cardiac output and rise in systemic vascular resistance may be clinically significant in pregnancies complicated by uteroplacental insufficiency.