Baseline fetal heart rates from 15 to 38 weeks gestation in normotensive and hypertensive pregnancies

Summary. To determine whether the fetal heart behaves differently in normotensive and hypertensive pregnancies, the changes in baseline fetal heart rate were investigated prospectively from 15 to 38 weeks gestation in 16 women who were normotensive at the time of booking in the antenatal clinic. Fetal heart rate recordings were made ultrasonically, and were computer-processed by the programs TELEPLOT and BASELINE. Those women who remained normotensive exhibited a decrease of fetal heart rate with advancing gestational age, but this did not occur in the six women who eventually developed hypertension.     

Baseline fetal heart rates from 15 to 38 weeks gestation in normotensive and hypertensive pregnancies

To determine whether the fetal heart behaves differently in normotensive and hypertensive pregnancies, the changes in baseline fetal heart rate were investigated prospectively from 15 to 38 weeks gestation in 16 women who were normotensive at the time of booking in the antenatal clinic. Fetal heart rate recordings were made ultrasonically, and were computer-processed by the programs TELEPLOT and BASELINE. Those women who remained normotensive exhibited a decrease of fetal heart rate with advancing gestational age, but this did not occur in the six women who eventually developed hypertension.     

Angiotensin II levels in hypertensive and normotensive pregnancies

Summary. We measured circulating angiotension II by radioimmunoassay in women with pregnancy-induced hypertension (  n = 54  ), and compared these values with those obtained in women with normal pregnancy (  n = 18  ) and in non pregnant women (  n = 20  ). Pregnant women had statistically significantly higher plasma angiotensin II [mean (SD): 41.3 (12.6) pg/ml] than non-pregnant women [  29.2 (11.3) pg/ml; P < 0.004  ]. Angiotensin II concentrations in women with pregnancy- induced hypertension [mean (SD): 31.7 (16.2) pg/ml] were, on average, 25% lower than in normal pregnancy (   P < 0.003  ) and resembled those obtained in non-pregnant women. The lowest angiotensin II levels were found in women with more severe forms of pregnancy-induced hypertension, such as proteinuric or superimposed pregnancy-induced hypertension. Review of the published studies on angiotensin II and our data suggest that the conflict among studies on angiotensin II levels in pregnancy-induced hypertension is largely due to the heterogeneity of the study populations in the various reports.     

Angiotensin II levels in hypertensive and normotensive pregnancies

We measured circulating angiotension II by radioimmunoassay in women with pregnancy-induced hypertension (n = 54), and compared these values with those obtained in women with normal pregnancy (n = 18) and in non pregnant women (n = 20). Pregnant women had statistically significantly higher plasma angiotensin II [mean (SD): 41.3 (12.6) pg/ml] than non-pregnant women [29.2 (11.3) pg/ml; P less than 0.004]. Angiotensin II concentrations in women with pregnancy-induced hypertension [mean (SD): 31.7 (16.2) pg/ml] were, on average, 25% lower than in normal pregnancy (P less than 0.003) and resembled those obtained in non-pregnant women. The lowest angiotensin II levels were found in women with more severe forms of pregnancy-induced hypertension, such as proteinuric or superimposed pregnancy-induced hypertension. Review of the published studies on angiotensin II and our data suggest that the conflict among studies on angiotensin II levels in pregnancy-induced hypertension is largely due to the heterogeneity of the study populations in the various reports.     

Antepartum fetal assessment in hypertensive pregnancies.

Antepartum fetal assessment in hypertensive pregnancies helps to prevent perinatal morbidity and mortality. The pathophysiology of chronic maternal hypertension often leads to placental insufficiency and fetal growth retardation. Current testing schemes include serial ultrasonographic assessment of fetal growth, placental morphology, and amniotic fluid volume; fetal heart rate testing using either non-stress or contraction stress methods; multiple parameter biophysical profile; and Doppler flow velocimetry of fetal umbilical and maternal uterine arteries. The values of individual and combined testing approaches are evaluated and an integrated scheme for fetal management, illustrated by case examples, is presented.     

Maternal renal artery Doppler velocimetry in normotensive pregnancies and pregnancies complicated by hypertensive disorders.

Hypertensive disorders in pregnancy contribute to substantial maternal and perinatal morbidity and mortality. Clinically, these disorders are characterized by hypertension and proteinuria. However, these signs appear some time after the physiologic derangements have been initiated. The primary objectives of this study were as follows: 1) to establish baseline values for the maternal renal artery systolic-diastolic ratio (S/D) as a function of gestational age in normal pregnancies, and 2) to determine whether renal artery blood flow indices can accurately identify those pregnancies complicated by, or destined to develop, hypertensive disorders. Using a pulsed Doppler scanner, maternal renal artery duplex evaluation was performed in four groups of women: normotensive nonpregnant, normotensive pregnant, chronic hypertensive pregnant, and preeclamptic. In 30 normotensive pregnant women followed longitudinally, no change was noted in the renal artery S/D as gestational age advanced, with mean (+/- SD) values of 2.5 +/- 0.20 and 2.6 +/- 0.21 for the left and right sides, respectively. No clinically meaningful discriminations were detected when the four groups were compared. We conclude that maternal renal artery Doppler waveforms are not significantly altered by either pregnancy or hypertensive complications in pregnancy.     

Umbilical flow waveforms versus fetal biophysical profile in hypertensive pregnancies

The pulsatility index (PI) of the umbilical arteries was measured in 40 hypertensive pregnancies. Doppler-velocimetric data were kept unknown to the clinical staff. An abnormal PI was found in 79% of cases in which an abnormal fetal growth in utero had been diagnosed by ultrasonographic measurements. Serial PI findings showed worsening figures in most of the cases with an abnormal fetal growth, irrespective of the last absolute value. Amniotic fluid estimation and PI data were significantly correlated. PI values were markedly abnormal in fetuses with non-reactive heart-rate tracings. A high sensitivity and an optimal specificity were found for umbilical PI versus the diagnosis of fetal growth retardation made by the coexistence of different biophysical criteria. However, false normal results may occur. 62% of the newborns weighed below the 5th percentile. The sensitivity of abnormal PI values to detect these light fetuses resulted to be only 67%. However the prevalence of neonatal morbidity in fetuses with abnormal PI values was 74%, while morbidity occurred only in 14% of cases with normal PI values. In hypertensive pregnancies, this simple velocimetric parameter proved to correlate with abnormal biophysical monitoring and complicated neonatal outcomes.     

Placental grading with ultrasound in hypertensive and normotensive pregnancies. A prospective, consecutive study

Placental grading was studied prospectively with real-time ultrasound in 654 consecutive pregnancies. The placental maturation was clearly demonstrated in both unselected and hypertensive pregnancies. No differences in placental grading were found between normotensive and hypertensive pregnancies. Fetal outcome was not associated with different placental grades and a grade III placenta was not predictive of an adverse outcome. The value of antenatal placental grading in unselective and hypertensive pregnancies could not be demonstrated.     

Blood velocity waveforms of the fetal aorta in normal and hypertensive pregnancies

Blood velocity waveforms were studied using a combination of real-time and Doppler ultrasonic equipment, a spectral analyzer, and on-line computer in the thoracic descending aorta of the human fetus. In 43 normal pregnancies (weeks 30 to 42) the median of mean velocity was 26.5 (24.1 to 27.9) cm/sec, that of the end-diastolic velocity 10.9 (7.9 to 13.4) cm/sec, the velocity acceleration 718.9 (620.3 to 844.1) cm/sec2, the resistance index 0.84 (0.80 to 0.89), and the pulsatility index was 2.49 (1.94 to 3.10). No differences in these values were observed in the fetuses of noncomplicated hypertensive pregnancies (N = 32), whereas the resistance index increased and the mean velocity and end-diastolic velocity decreased if fetal growth retardation was associated with maternal hypertension (N = 14). In the subgroup of fetal distress (N = 6), all of these parameters except velocity acceleration differed from the normal values, reflecting increased peripheral vascular resistance. This method may be of value in the follow-up of fetal well-being in risk pregnancies by giving an early sign of hemodynamic changes in developing hypoxia.     

Effects of diazoxide on maternal and fetal circulations in normotensive and hypertensive pregnant sheep

Diazoxide is a potent antihypertensive agent due to its peripheral vasodilator action. For this reason it is used in the management of hypertensive crises in pregnancy. To assess the effects of an intravenous bolus injection of diazoxide on maternal and fetal hemodynamics an experimental study was performed in 11 chronically instrumented pregnant sheep. In six ewes hypertension was induced by surgical removal of one kidney and reduction of arterial blood flow to the remaining kidney (one-kidney renovascular hypertension). The other five ewes remained normotensive. In a second operation, one week after the first one, the animals were equipped with electromagnetic flow transducers and catheters for monitoring of blood flow in a renal, a uterine, and an umbilical artery and for measurement of maternal and fetal arterial blood pressures, and blood sampling. Maternal heart rate was derived from the arterial pressure curve, fetal heart rate from a fetal ECG. Experiments were begun on the third day after the second operation. In each experiment a bolus of 300 mg of diazoxide was administered intravenously, with or without rapid simultaneous infusion of 500 ml of a plasma expander. A total of 17 experiments were performed in the one-kidney hypertensive ewes (Group H), nine with and eight without plasma expander. In the five normotensive animals (Group NH) 10 experiments were done, four with and six without plasma expansion. During the control periods maternal arterial pressure was approximately 30 mm Hg higher in Group H than in Group NH. In Group H also maternal heart rate, and renal and uterine vascular resistances were significantly elevated. All fetal variables were equal in both groups. Administration of diazoxide without simultaneous plasma expansion resulted in both groups in a significant fall in maternal arterial pressure, a rise in maternal heart rate, and a fall in uterine and renal blood flows with a rise in vascular resistance. Fetal arterial pressure and umbilical blood flow showed no significant changes, but fetal heart rate showed a transient fall together with a drop in fetal pO2 and pH, although acidosis did not occur. When diazoxide was combined with a plasma expander maternal blood pressure did not change significantly in Group NH, but fell in Group H. Maternal heart rate rose significantly in both groups. The decrease in uterine and renal blood flows which occurred when diazoxide was given without plasma expansion was not observed.(ABSTRACT TRUNCATED AT 400 WORDS)     

Reduced fetal platelet counts in pregnancies with abnormal Doppler umbilical flow waveforms

Fetal and maternal platelet counts were correlated with antenatal assessment of the umbilical-placental waveform. Forty singleton pregnancies were studied using Doppler ultrasound, and placental resistance was categorized as normal or high according to the systolic/diastolic ratio. We performed platelet counts on maternal and cord blood taken at the time of cesarean section. The high-resistance group had a mean fetal platelet count (218 +/- 53 x 10(3)/microliters) significantly lower than that of the normal-resistance group (314 +/- 76 x 10(3)/microliters) (P less than .001). This difference was evident in both the hypertensive and nonhypertensive subgroups of the high-resistance group. There was no difference in mean maternal platelet counts between the high- and normal-resistance groups.     

The "weight" of fetal growth restriction in 437 hypertensive pregnancies

Objective Our objective was to evaluate the outcomes of the hypertensive and preeclamptic pregnancies with or without fetal growth restriction (FGR).Methods We retrospectively studied 437 hypertensive pregnant women treated by calcium antagonists and divided in four groups: Gestational hypertension (GH) with or without FGR (GH-AGA: 244; GH-FGR: 78) and preeclampsia (PE) with or without FGR (PE-AGA: 76; PE-FGR: 39). Outcomes considered were: the need for a second-line treatment, prolongation of the pregnancy after diagnosis, duration of treatment in puerperium, gestational age at delivery, neonatal birth weight, perinatal mortality and neonatal malformations.Results A second line treatment was added in: GH-AGA: 15.4% vs. GH-FGR: 32.8%; PE-AGA: 28% vs. PE-FGR: 50%. We found a significant difference in delivery delay after diagnosis (31.3±5.4 vs. 20.7±3.4 days and 35.3±4.5 vs. 22.2±3.1; p<0.001). Gestational age at delivery was (p<0.001): 35.5±2.3 vs. 35.6±2.5 and 34.4±1.7 vs. 33.1±2.3. A significant difference in birth weight was (p<0.001): 2,271±759.1 vs. 1,817.59±396.9 and 2,196±685.17 vs. 1,465.80±441.7. Mortality was 2.56% (2 cases) for GH-FGR and 10.2% (4 cases) for PE-FGR. No neonates showed malformations.Conclusions Gestational hypertension and preeclampsia increase the risk of low birth weight, on the other hand the fetal growth restriction is a determinant factor for the outcome of hypertensive and preeclamptic pregnancy, perinatal morbidity and mortality of the fetus and for the management and treatment efficacy of the mother.     

Maternal and fetal haemodynamics in hypertensive pregnancies during maternal treatment with intravenous hydralazine or labetalol

Summary. Intravenous treatment with 10 mg of hydralazine or 100 mg of labetalol was randomly allocated to 30 hypertensive pregnant women. Umbilical artery flow velocity waveforms were recorded using a pulsed Doppler duplex scanner (ATL Mk V) and umbilical artery pulsatility index (PI) and fetal heart rate (FHR) were derived from these recordings. Maternal blood pressure decreased significantly after both drugs. Maternal pulse rate increased after hydralazine but did not change significantly after labetalol. FHR did not change significantly after hydralazine but decreased after labetalol. PI decreased after hydralazine and increased after labetalol-most fetuses showed little change but a few in each group showed large changes in PI, as did two of five additional patients studied. We attributed the decrease in PI in some fetuses after hydralazine to vasodilation, and the increase in PI in some fetuses after labetalol to vasoconstriction in the fetoplacental circulation, suggesting that fetal beta-blockade may occur after maternal treatment with labetalol.     

Maternal and fetal haemodynamics in hypertensive pregnancies during maternal treatment with intravenous hydralazine or labetalol

Intravenous treatment with 10 mg of hydralazine or 100 mg of labetalol was randomly allocated to 30 hypertensive pregnant women. Umbilical artery flow velocity waveforms were recorded using a pulsed Doppler duplex scanner (ATL Mk V) and umbilical artery pulsatility index (PI) and fetal heart rate (FHR) were derived from these recordings. Maternal blood pressure decreased significantly after both drugs. Maternal pulse rate increased after hydralazine but did not change significantly after labetalol. FHR did not change significantly after hydralazine but decreased after labetalol. PI decreased after hydralazine and increased after labetalol--most fetuses showed little change but a few in each group showed large changes in PI, as did two of five additional patients studied. We attributed the decrease in PI in some fetuses after hydralazine to vasodilation, and the increase in PI in some fetuses after labetalol to vasoconstriction in the fetoplacental circulation, suggesting that fetal beta-blockade may occur after maternal treatment with labetalol.     

Autonomic heart-rate control in response to standing in toxemic and normotensive primigravid pregnancies

Heart-rate changes after transition from a supine to a standing posture were measured in 12 hypertensive and 12 normotensive primigravid women, in their last trimester of gestation. The subjects beat-to-beat heart-rate (HR) changes were recorded on both an ordinary cardiotocograph and on magnetic tape. The hypertensive patient group (1) reached an HR-maximum after standing up in a significantly shorter period of time and (2) had a significantly lower HR during 1 min erect posture. A population threatened by pregnancy-induced hypertension might be detected by using the non-invasive method of recording the maternal beat-to-beat heart-rate changes after transition to the standing posture, even before the onset of hypertension.