Umbilical artery half peak systolic velocity deceleration time throughout pregnancy and its role in fetuses with bradycardia

2007 ◽  
Vol 30 (7) ◽  
pp. 952-957 ◽  
Author(s):  
J. C. Bustos ◽  
M. Paublo ◽  
P. Ramirez ◽  
W. Sepulveda
Keyword(s):  
Umbilical Artery ◽  
Peak Systolic Velocity ◽  
Deceleration Time

Umbilical Artery Half-Peak Systolic Velocity Deceleration Time in Fetal Growth Restriction

2015 ◽  
Vol 40 (2) ◽  
pp. 128-134 ◽  
Author(s):  
Juan Carlos Bustos ◽  
Vivian Gonzalez ◽  
Waldo Sepulveda
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Perinatal Outcome ◽  
Umbilical Artery ◽  
Perinatal Death ◽  
Peak Systolic Velocity ◽  
Growth Restriction ◽  
Ultrasound Evaluation ◽  
Diastolic Velocity ◽  
Deceleration Time

Objective: To study the umbilical artery (UA) half-peak systolic velocity deceleration time (hPSV-DT) in pregnancies complicated by fetal growth restriction (FGR). Methods: The study included 266 singleton, high-risk pregnancies with an estimated fetal weight <10th percentile, which were examined between 24 and 40 weeks' gestation and delivered within a week from the last ultrasound evaluation. UA hPSV-DT was measured with Doppler ultrasound in the same wave used to measure the pulsatility index. UA hPSV-DT values were correlated with perinatal outcome. Results: UA hPSV-DT <5th percentile was found in 87 and 98% of fetuses with moderate and severe FGR, respectively. 94% of fetuses with a UA hPSV-DT <90 ms had poor perinatal outcome including perinatal death or prolonged admission to the neonatal intensive care unit. None of the fetuses had a UA hPSV-DT <70 ms. Perinatal death occurred in 39 fetuses; UA hPSV-DT was abnormal in all of them, with 95% of these fetuses having values of ≤120 ms. In the group of fetuses with absent/reverse end-diastolic velocity in the UA, the perinatal mortality rate was 51% for those with a UA hPSV-DT ≤90 ms and only 23% for those having a UA hPSV-DT >90 ms (p < 0.01). Conclusions: UA hPSV-DT seems to be a useful technique in the evaluation of pregnancies at risk for FGR and perinatal death. Additionally, hPSV-DT was shown to be a good predictor of perinatal death, with values of <90 ms corresponding to imminent risk of intrauterine demise and values of <70 ms being likely to be incompatible with intrauterine life.

Umbilical artery pulsatility index and half-peak systolic velocity in second- and third-trimester fetuses with trisomy 18 and 13

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Juan Carlos Bustos ◽  
Denise Vega ◽  
Waldo Sepulveda
Keyword(s):  
Gestational Age ◽  
Pulsatility Index ◽  
Umbilical Artery ◽  
Peak Systolic Velocity ◽  
Trisomy 18 ◽  
Trisomy 13 ◽  
Doppler Velocimetry ◽  
Third Trimester ◽  
High Prevalence ◽  
Deceleration Time

Abstract Objectives To analyze umbilical artery (UA) Doppler velocimetry and its possible role in placenta-mediated fetal growth restriction (FGR) in second- and third-trimester fetuses with trisomy 18 and 13. Methods UA pulsatility index (PI) and half-peak systolic velocity deceleration time (hPSV-DT) were measured in fetuses with trisomy 18 and 13. Correlation with gestational age, birthweight, and perinatal outcome was analyzed. Results A total of 80 measurements were taken from 33 fetuses with trisomy 18 and 19 with trisomy 13. Overall, there was a high prevalence of abnormal UA Doppler velocimetry. In fetuses with trisomy 18, 54% (27/50) of the UA PI values and 58% (29/50) of the UA hPSV-DT values were abnormal. In fetuses with trisomy 13, 80% (24/30) of the UA PI values and 87% (26/30) of the UA hPSV-DT values were abnormal. The prevalence of abnormal UA Doppler velocimetry increased with gestational age in both types of aneuploidy. However, this trend was only significant for trisomy 13 (p<0.05). All fetuses with trisomy 18 and 86% of fetuses with trisomy 13 were classified at birth as FGR. There were no perinatal survivors in this series. Conclusions A high prevalence of abnormal UA Doppler velocimetry was found in second- and third-trimester fetuses with trisomy 18 and 13, which further increased with gestational age. These results may well correlate with alterations described previously in the placenta, suggesting placental insufficiency has an important role in the development of FGR in these autosomal aneuploid fetuses.

Heart rate and flow velocity variability as determined from umbilical Doppler velocimetry at 10–20 weeks of gestation

1998 ◽  
Vol 95 (5) ◽  
pp. 539-545 ◽  
Author(s):  
Nicolette T. C. URSEM ◽  
Piet C. STRUIJK ◽  
Wim C. J. HOP ◽  
Edward B. CLARK ◽  
Bradley B. KELLER ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Flow Velocity ◽  
Fetal Heart Rate ◽  
Umbilical Artery ◽  
Parasympathetic Nervous System ◽  
Fetal Heart ◽  
Peak Systolic Velocity ◽  
Fetal Heart Rate Variability ◽  
Artery Flow

1.The aim of this study was to define from umbilical artery flow velocity waveforms absolute peak systolic and time-averaged velocity, fetal heart rate, fetal heart rate variability and flow velocity variability, and the relation between fetal heart rate and velocity variables in early pregnancy. 2.A total of 108 women presenting with a normal pregnancy from 10 to 20 weeks of gestation consented to participate in a cross-sectional study design. Doppler ultrasound recordings were made from the free-floating loop of the umbilical cord. 3.Umbilical artery peak systolic and time-averaged velocity increased at 10–20 weeks, whereas fetal heart rate decreased at 10–15 weeks of gestation and plateaued thereafter. Umbilical artery peak systolic velocity variability and fetal heart rate variability increased at 10–20 and 15–20 weeks respectively. 4.The inverse relationship between umbilical artery flow velocity and fetal heart rate at 10–15 weeks of gestation suggests that the Frank–Starling mechanism regulates cardiovascular control as early as the late first and early second trimesters of pregnancy. A different underlying mechanism is suggested for the observed variability profiles in heart rate and umbilical artery peak systolic velocity. It is speculated that heart rate variability is mediated by maturation of the parasympathetic nervous system, whereas peak systolic velocity variability reflects the activation of a haemodynamic feedback mechanism.

Developmental changes in hemodynamics of uterine artery, utero- and umbilicoplacental, and vitelline circulations in mouse throughout gestation

2006 ◽  
Vol 291 (3) ◽  
pp. H1421-H1428 ◽  
Author(s):  
Junwu Mu ◽  
S. Lee Adamson
Keyword(s):  
Uterine Artery ◽  
Umbilical Artery ◽  
Resistance Index ◽  
Peak Systolic Velocity ◽  
Normal Pregnancy ◽  
Ultrasound Biomicroscopy ◽  
Placental Development ◽  
Diastolic Velocity ◽  
Early Onset Preeclampsia ◽  
Arterial Canal

In human pregnancy, abnormal placental hemodynamics likely contribute to the etiology of early-onset preeclampsia and fetal intrauterine growth restriction. The mouse is increasingly being deployed to study normal and abnormal mammalian placental development, yet the placental hemodynamics in normal pregnancy in mice is currently unknown. We used ultrasound biomicroscopy to noninvasively image and record Doppler blood velocity waveforms from the maternal and embryonic placental circulations in mice throughout gestation. In the uterine artery, peak systolic velocity (PSV) increased significantly from 23 ± 2 (SE) to 59 ± 3 cm/s, and end-diastolic velocity (EDV) increased from 7 ± 1 to 28 ± 2 cm/s in nonpregnant versus full-term females so that the uterine arterial resistance index (RI) decreased from 0.70 ± 0.02 to 0.53 ± 0.02. Velocities in the maternal arterial canal in the placenta were low and nearly steady and increased from 0.9 ± 0.03 cm/s at embryonic day 10.5 (E10.5) to 2.4 ± 0.07 cm/s at E18.5. PSV in the umbilical artery increased steadily from 0.8 ± 0.1 cm/s at E8.5 to 15 ± 0.6 cm/s at E18.5, whereas PSV in the vitelline artery increased from 0.6 ± 0.1 cm/s at E8.5 to 4 ± 0.2 cm/s at E13.5 and then remained stable to term. In the umbilical artery, the EDV detection rate was 0% at ≤E14.5 and 94% at E18.5, and the RI decreased from 1 to 0.82 ± 0.01 during this interval. We conclude that ultrasound biomicroscopy can be used to monitor placental hemodynamics during pregnancy in mice. These results provide novel information concerning the development of the vitelline and placental circulations in mice and reveal strong similarities in placental hemodynamics between mice and humans.

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