-
Ultrasound in Obstetrics and Gynecology 10/2010; 36(S1):16. · 3.01 Impact Factor
-
Ultrasound in Obstetrics and Gynecology 10/2009; 34(S1):10. · 3.01 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To examine whether maternal indomethacin therapy affects human fetal pulmonary arterial vascular impedance without constriction of the ductus arteriosus and to determine the changes in the pulmonary arterial vascular impedance in the presence of ductal constriction.
In this cross-sectional study, 52 normal fetuses without maternal medication (control group), 33 fetuses without ductal constriction (Study group I) and 11 fetuses with ductal constriction (Study group II) during maternal indomethacin therapy between 24 and 34 weeks of gestation were examined by Doppler echo-cardiography. Blood velocity waveforms across the proximal right or left pulmonary artery were obtained and the pulsatility index (PI) of the proximal pulmonary arteries was calculated.
In the control group, the proximal pulmonary artery PI was higher (p < 0.0001) at 24-25 weeks (n = 7) (3.73 +/- 0.33; mean +/- SD) than at 33-34 week of gestation (n = 11) (2.98 +/- 0.27). The PI was constantly greater (p < 0.005) in Study group I than in the control group. However, in this group the mean average weekly decrease in the PI of the proximal pulmonary arteries was similar to that in the control group. After 26 weeks of gestation, the PI values in Study group II were significantly higher than in the control group (27 weeks: 4.12 vs. 3.34 (p < 0.005); 30 weeks: 4.48 vs. 3.14 (p < 0.0001); 34 weeks: 4.96 vs. 3.00 (p < 0.0001), respectively).
Human fetal pulmonary arterial vascular impedance is increased by maternal indomethacin therapy even without ductal constriction. In the presence of ductal constriction, the magnitude of the increase in the vascular impedance is related to the gestational age.
Ultrasound in Obstetrics and Gynecology 03/1999; 13(2):112-6. · 3.01 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The authors hypothesized that in utero tracheal occlusion would reverse the high impedance to pulmonary blood flow associated with congenital diaphragmatic hernia (CDH) and normalize the fetal physiological response to oxygen at term.
Three experimental groups were studied. Six fetal lambs (CDH group) underwent creation of a left CDH at 80 days' gestation, an additional six fetal lambs underwent left CDH creation at 80 days' gestation followed by fetal tracheal occlusion performed at 108 days' gestation (CDH + TO group), and four control fetal lambs (control group) underwent a sham procedure at 80 days gestation. All lambs were followed up at 2-week intervals by pulse wave Doppler echocardiography. At each time-point the pulsatility index (PI) was calculated for the left branch pulmonary artery from the Doppler blood velocity waveform. Near term (term, 145 days gestation) at 136 days gestation, measurements were repeated under maternal normoxia and hyperoxia. The fetal lungs were harvested and processed for morphometric analysis by radial alveolar counts (RAC) and lung-to-body-weight ratios (LBWR) as measures of lung growth.
At 136 days' gestation the PI of the CDH + TO group (2.88 +/- 0.29) and control group (3.97 +/- 0.37) were significantly lower compared with the PI of the CDH group (9.02 +/- 0.50). There was a significant decrease in the PI of both the CDH + TO group and the control group with maternal hyperoxia at term, whereas the CDH group showed no change. The lungs of the CDH group fetuses were significantly smaller by LBWR and RAC than both CDH + TO and control fetuses.
An elevated PI is associated with pulmonary hypoplasia, fetal tracheal occlusion reverses this finding, and results in a normal fetal physiological response to changes in oxygen tension at term.
Journal of Pediatric Surgery 08/1998; 33(7):1071-4; discussion 1074-5. · 1.45 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The aims of the present study were to determine whether maternal hyperoxygenation affects human fetal pulmonary circulation and whether there is a gestational age-related response in the fetal pulmonary circulation to maternal hyperoxygenation during the second half of gestation.
Twenty women between 20 and 26 weeks of gestation and 20 women between 31 and 36 weeks of gestation with normal singleton pregnancies were randomized to receive either 60% humidified oxygen or medical compressed air (room air) by a face mask. Fetal aortic and pulmonary valve; ductus arteriosus (DA); and right (RPA), left (LPA), and distal (DPA) pulmonary artery blood velocity waveforms were obtained by Doppler ultrasound before, during, and after maternal administration of either 60% oxygen or room air. Left and right ventricular cardiac outputs, DA volume blood flow, and RPA and LPA volume blood flows (Qp) were calculated. Foramen ovale volume blood flow (left ventricular cardiac output-Qp) was estimated. Pulsatility index (PI) values of DA, RPA, LPA, and DPA were calculated. Maternal hyperoxygenation did not change any of the measured fetal parameters between 20 and 26 weeks, whereas between 31 and 36 weeks, the PI values of RPA, LPA, and DPA decreased (P<.0001) and the PI of DA increased (P<.0001). In addition, Qp increased (P<.001), and DA volume blood flow (P<.01) and foramen ovale volume blood flow (P<.03) decreased. Left and right ventricular cardiac outputs were unchanged. All changes returned to baseline after maternal hyperoxygenation was discontinued.
Reactivity of the human fetal pulmonary circulation to maternal hyperoxygenation increases with advancing gestation; this suggests that fetal pulmonary circulation is under acquired vasoconstriction at least after 31 to 36 weeks of gestation.
Circulation 01/1998; 97(3):257-62. · 14.74 Impact Factor
-
Clinical Obstetrics and Gynecology 01/1998; 40(4):796-803. · 1.93 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Our objective was to determine whether abnormal loading conditions can modify human fetal right ventricular ejection force during the second half of pregnancy. By Doppler echocardiography, we studied 73 normal fetuses between 19 and 41 weeks of gestation, 27 fetuses with hypoplastic left heart syndrome (chronic volume overload) between 18 and 38 weeks of gestation, 14 fetuses with mild to moderate constriction of the ductus arteriosus (pulsatility index (PI) between 1.0 and 1.9) and seven fetuses with severe constriction (PI < 1.0) or occlusion of the ductus arteriosus (relatively acute pressure overload) between 28 and 34 weeks of gestation. In the normal and ductal constriction/occlusion groups, blood velocity waveforms were recorded at the level of the aortic and pulmonary valves, and in the group with hypoplastic left heart syndrome at the level of the pulmonary valve. The ventricular ejection forces were calculated. In the normal group, right (RVEF; r = 0.91, p < 0.0001) and left (LVEF; r = 0.86, p < 0.0001) ventricular ejection forces increased and were equal during the second half of gestation. In the group with hypoplastic left heart syndrome the RVEF increased (r = 0.76, p < 0.0001) with advancing gestation. The RVEF (p < 0.0005) and its average weekly increase (p < 0.0001) were greater in the hypoplastic left heart syndrome group than in the normal group. In the group with mild to moderate ductal constriction, both ventricular ejection forces were similar to those of the normal group. The RVEF (p < 0.003) and its average weekly increase (p < 0.03) were lower in the group with severe ductal constriction or occlusion than in the normal group. The LVEF did not differ from that of the normal group We conclude that chronic volume overload increases and relatively acute pressure overload decreases human fetal RVEF. The right ventricular performance is modified by abnormal loading conditions.
Ultrasound in Obstetrics and Gynecology 11/1997; 10(5):325-32. · 3.01 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: About 4% of pregnant women have concomitant cardiac disease and a few of these do not respond to medical therapy and require surgical correction during pregnancy. We report a unique case describing fetal hemodynamics and uterine blood flow before, during, and after maternal cardiopulmonary bypass, and compare them to normal reference values in the second trimester.
A woman with severe aortic regurgitation underwent aortic valve replacement at 19 weeks' gestation. A nonpulsatile cardiac pump was used for cardiopulmonary bypass, maintaining the mean arterial pressure at 77-90 mmHg, with a peak flow rate of 3.5-4.0 L/minute/m2 and core temperature of 34-35C throughout surgery. Blood velocity waveforms were recorded by Doppler ultrasound at the level of maternal main uterine artery and fetal vessels. Pulsatility index (PI) values were calculated. Preoperatively, fetal hemodynamic characteristics were within normal limits. Preoperatively, uterine artery PI was 3.9 (normal 0.5-1.5 at 20 weeks). Intraoperatively, fetal bradycardia ensued after aortic clamping (120 to 75 beats per minute), with a rise in umbilical artery PI (1.7 to 7.1) and disappearance of diastolic flow. The middle cerebral artery PI decreased (2.0 to 0.92) and the PI increased in the descending aorta (2.22 to 3.55), inferior vena cava (2.7 to 9.3), and ductus venosus (0.6 to 1.7). During bypass, after aortic clamping, nonpulsatile uterine artery flow was noted. Postoperatively, the uterine artery PI improved, to 1.0. Two days later, hydrocephalus and hydrops were observed.
Despite high peak flow rates, normal mean arterial pressure, and normothermia, fetal outcome was dismal. Nonpulsatile cardiopulmonary bypass under normothermia may not be able to meet the demands of the fetoplacental circulation.
Obstetrics and Gynecology 11/1996; 88(4 Pt 2):667-71. · 4.73 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: By using Doppler echocardiography, we determined the normal distribution of human fetal combined cardiac output (CCO) from the left and right ventricles. We also established weight-indexed pulmonary and systemic vascular resistances (Rpi and Rsi, respectively) and changes during the second half of pregnancy.
Blood flows at the aortic and pulmonary valve annuli (LVCO and RVCO, respectively), right and left pulmonary arteries (QP), and ductus arteriosus (QDA) were calculated in 63 normal fetuses. Foramen ovale blood flow (QFO = LVCO-QP) was estimated. From 20 to 30 weeks of gestation, the proportion of QP of the CCO increased (from 13% to 25%, P < .001), while the proportion of QFO decreased (from 34% to 18%, P < .001). After 30 weeks, the proportions of QP and QFO were unchanged. At 38 weeks, the proportion of RVCO (60%) was higher (P < .05) than that of LVCO (40%). The proportion of QDA did not change significantly. The correlation between RVCO calculated from blood flow through the pulmonary valve and from QDA and QP was good (r = .97, P < .0001). RPi (P < .001) decreased from 20 to 30 weeks of gestation. From 30 to 38 weeks, RPi increased (P < .0001). Rsi increased (P < .001) from 20 to 38 weeks. The ratio of RPi to RSi decreased (P < .01) from 20 to 30 weeks and later remained unchanged.
The human fetal pulmonary circulation has an important role in the distribution of cardiac output.
Circulation 10/1996; 94(5):1068-73. · 14.74 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Our purpose was to establish normal physiologic parameters in the fetal proximal and distal branch pulmonary arterial vascular impedance during the second half of pregnancy and to analyze relationships between proximal and distal pulmonary arterial blood velocity waveforms.
In this cross-sectional study 100 uncomplicated singleton pregnancies were studied by pulsed color Doppler techniques between 18 and 41 weeks of gestation (median 30 weeks). Both right and left proximal (immediately after the bifurcation of the main pulmonary artery) and distal (beyond the first bifurcation of the branch pulmonary artery) pulmonary artery blood velocity waveforms were recorded and pulsatility index values were calculated. Peak systolic velocities and time-to-peak-velocity intervals were measured. Time-to-peak-velocity intervals were also analyzed at the level of aortic and pulmonary valves and at the ductus arteriosus. Right and left pulmonary artery diameters and right lung length were measured.
In both right and left proximal and distal pulmonary arteries pulsatility index values decreased (p < 0.0001) and the peak systolic velocities (p < 0.003) and time-to-peak-velocity intervals (p < 0.0001) increased during the second half of pregnancy. In the proximal pulmonary arteries the pulsatility index values decreased linearly until 34 to 35 weeks of gestation and in the distal pulmonary arteries until 31 weeks of gestation. Thereafter they remained unchanged. In pulmonary arteries time-to-peak-velocity intervals were shorter (p < 0.01) than at the pulmonary valve level. There were no significant differences between the right or left pulmonary arteries in the pulsatility index values, peak systolic velocities, time-to-peak-velocity intervals, or pulmonary artery diameters. In the proximal pulmonary arteries the pulsatility index values (p < 0.02) and peak systolic velocities (p < 0.0001) were higher and time-to-peak-velocity intervals (p < 0.0001) were longer than in the distal pulmonary arteries. There was a 2.5-fold increase in pulmonary artery diameters and right lung length.
Fetal branch pulmonary arterial vascular impedance decreases significantly during the second half of pregnancy. The linear decrease in vascular impedance during the second trimester and in the beginning of the third trimester may be related to the growth of the lung and the increase in the number of resistance vessels. During the latter part of the third trimester pulmonary vascular impedance does not decrease further.
American Journal of Obstetrics and Gynecology 06/1996; 174(5):1441-9. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Background. We hypothesized that ephedrine and phenylephrine are equal with respect to uterine and placental haemodynamics and fetal acid-base status after exposure to maternal hypoxaemia and hypotension in a chronic sheep model of increased placental vascular resistance (RUA). Methods. At 114-135 days gestation, chronically instrumented fetal sheep underwent placental embolization leading to increased RUA. Twenty-four hours after embolization, the ewes were anaesthetized and randomized to receive boluses of ephedrine (n=7) or phenylephrine (n=6) for epidural-induced hypotension after maternal hypoxaemia. Uterine (QUtA) and placental (QUA) volume blood flows and uterine vascular resistance (RUtA) and RUA were recorded. Uterine (PIUtA) and umbilical artery (PIUA) pulsatility indices were obtained by Doppler ultrasonography. Fetal arterial blood samples were analysed for acid-base values and lactate concentrations. Results. During hypotension, QUtA, fetal pH, BE, and Po2 decreased whereas RUtA ,P I UtA ,R UA, and fetal lactate concentration increased. With ephedrine, QUtA, RUtA ,P I UtA, RUA, and fetal Po2 returned to baseline. Fetal pH, BE, and lactate concentration did not change from hypotensive values. With phenylephrine, QUtA remained lower (P=0.007) and RUtA (P=0.007), PIUtA (P=0.013), and RUA (P=0.050) higher than at baseline. Fetal Po2 returned to baseline and fetal pH and BE did not change from hypotensive values. However, fetal lactate concentration increased further (mean difference 1.49, 95% confidence interval 0.72-2.26 mmol litre� 1; P=0.004). Conclusions. In a chronic sheep model of increased placental vascular resistance, compared with ephedrine administration, phenylephrine administration was associated with impaired uterine and placental haemodynamics and increased fetal lactate concentrations. Br J Anaesth 2006; 96: 231-7
