Ductus venosus velocimetry in acute fetal acidemia and impending fetal death in a sheep model of increased placental vascular resistance.
We investigated whether hypoxemia without acidemia affects ductus venosus (DV) blood velocity waveform pattern in sheep fetuses with intact placenta and whether worsening acidemia and impending fetal death are related to changes in DV velocimetry in fetuses with increased placental vascular resistance. A total of 34 fetuses were instrumented at 115-136/145 days of gestation. Placental embolization was performed in 22 fetuses on the fourth postoperative day, 24 h before the experiment. The control group was comprised of 12 fetuses with intact placenta. The experimental protocol consisted of fetal hypoxemia that was induced by replacing maternal inhaled oxygen with medical air. To further deteriorate fetal oxygenation and blood-gas status, uterine artery volume blood flow was reduced by maternal hypotension. Fetuses that underwent placental embolization were divided into two groups according to fetal outcome. Group 1 consisted of 12 fetuses that completed the experiment, and group 2 comprised 10 fetuses that died during the experiment. DV pulsatility index for veins (PIV) and fetal cardiac outputs (COs) were calculated. Placental volume blood flow, fetal blood pressures, and acid base and lactate values were monitored invasively. On the experimental day, the mean gestational age did not differ significantly between the groups. In groups 1 and 2, the baseline mean DV PIV and fetal COs were not statistically significantly different from the control group. In the control group, the DV PIV values increased significantly with hypoxemia. In groups 1 and 2, the DV PIV values did not change significantly, even with worsening acidemia and imminent fetal death in group 2. During the experiment, the fetal COs remained unchanged. We conclude that fetal hypoxemia increases the pulsatility of DV blood velocity waveform pattern. In fetuses with elevated placental vascular resistance, DV pulsatility does not increase further in the presence of severe and worsening fetal acidemia and impending fetal death.
Mäkikallio
Kaarin
K
Dept. of Obstetrics and Gynecology, University of Oulu, Finland.
Acharya
Ganesh
G
Erkinaro
Tiina
T
Kavasmaa
Tomi
T
Haapsamo
Mervi
M
Huhta
James C
JC
Räsänen
Juha
J
D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D005227:Fatty Acids / Q000097:blood*; D005260:Female; D005313:Fetal Death / Q000503:physiopathology*; D005333:Fetus / Q000098:blood supply*; D006339:Heart Rate / Q000502:physiology; D000860:Hypoxia / Q000503:physiopathology; D023421:Models, Animal; D010920:Placenta / Q000098:blood supply*; D011247:Pregnancy; D012039:Regional Blood Flow / Q000502:physiology; D012756:Sheep; D014471:Umbilical Veins / Q000196:embryology; D014655:Vascular Resistance / Q000502:physiology*; D014680:Veins / Q000502:physiology*; D014682:Vena Cava, Inferior / Q000196:embryology
D005227:Fatty Acids