ABSTRACT
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.
Subject(s)
Computer Simulation , Ultrasonography, Doppler/methods , Ultrasonography, Prenatal , Umbilical Arteries/diagnostic imaging , Animals , Blood Flow Velocity , Blood Pressure , Female , Fetal Monitoring , Humans , Models, Cardiovascular , Placenta/blood supply , Pregnancy , Pulsatile Flow , Rheology , Sheep , Umbilical Arteries/physiology , Vascular ResistanceABSTRACT
Electrical analog models of the umbilical circulation were developed based on hemodynamic measurements in fetal sheep. The umbilical artery was represented by a transmission line and the placenta by a resistive load. Model predictions of input impedance and pressure and flow waveforms agreed with in vivo measurements under baseline conditions, following placental embolization, and during angiotensin II infusion. A unique positive impedance phase observed at the heart rate frequency under baseline conditions was best explained by the unusual viscoelastic properties of the umbilical arterial wall and small load reflections. Furthermore, a short, less vasoactive segment of the umbilical artery in the retroperitoneal space had a large impact on the input impedance of the umbilical circulation, which was particularly apparent when the artery was constricted during angiotensin II infusion. The model indicated that reflections arising near the approximate location where the first arterial branches leave the main umbilical artery have a measurable impact on impedance spectra when load reflections are low.
