Downstream determinants of pulsatility of the mean velocity waveform in the umbilical artery as predicted by a computer model.
An electrical analog model of the umbilicoplacental circulation that was based on hemodynamic measurements in fetal sheep was used to predict the mean blood velocity waveform in the umbilical artery. A 300% increase in placental resistance reduced the normally forward diastolic blood velocity in the umbilical artery nearly to zero. When resistance was normal, variations in umbilical arterial wall thickness (h) and elastic modulus (E) had little effect on the velocity waveform, whereas a 20% increase in radius (a) halved the ratio of the diastolic-to-systolic blood velocity (D/S). When placental resistance was high, abnormal umbilical arterial wall properties (a large, or h or E small) further reduced D/S. We conclude that high placental resistance, low umbilical arterial resistance, or a combination of high placental resistance with abnormal umbilical arterial wall properties are the primary downstream determinants of elevated pulsatility in umbilical arterial blood velocity.
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Program in Development and Fetal Health, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
Adamson
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D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure; D003198:Computer Simulation; D005260:Female; D005323:Fetal Monitoring; D006801:Humans; D008955:Models, Cardiovascular; D010920:Placenta / Q000098:blood supply; D011247:Pregnancy; D011673:Pulsatile Flow; D012212:Rheology; D012756:Sheep; D018608:Ultrasonography, Doppler / Q000379:methods*; D016216:Ultrasonography, Prenatal; D014469:Umbilical Arteries / Q000000981:diagnostic imaging* / Q000502:physiology; D014655:Vascular Resistance