Preeclampsia and Fetal Growth Restriction: Intervillous Space Pressure

This chapter examines how increased intervillous space pressure caused by obstruction of uterine venous return might (1) directly and immediately reduce fetoplacental perfusion by the compression of already-existing chorionic villi (causing “sluice flow”), (2) reduce the beneficial flow shear stress within chorionic vessels, which is necessary for future villus growth, and (3) open subplacental myometrial arteriovenous shunts, which may exist in part to function as a “pressure relief valve” in situations of increased intervillous space pressure. For all these reasons, it may be important that intervillous space pressure remains low during gestation. Flow shear stress is an important emerging concept in placental health. Brisk fetal chorionic perfusion causes the release of growth factors which promote downstream growth of more chorionic villi. The end result of adequate flow shear stress is that the placenta is able to grow and seek out oxygen in order to keep pace with the needs of the developing fetus. Placental insufficiency is characterized by a high pulsatility index of the umbilical artery Doppler velocity waveform, and this abnormality of the waveform is consistent with a high resistance and low compliance (or “high impedance”) chorionic vasculature. Increased intervillous space pressure may externally compress chorionic vessels and produce a stiff chorionic vasculature with these Doppler waveform changes. The author theorizes that one cause of placental insufficiency and fetal growth restriction may be the increased intervillous space pressure and the high impedance chorionic (fetal) vasculature produced by obstruction of uterine venous return. Positional increases in pulsatility indices have been sought in women who assume the supine position from a lateral position, and some studies show the expected increases but others do not. These studies have limitations due to (1) their incorrect assumption that the supine position invariably causes obstruction of uterine venous return and that the lateral position invariably relieves it, (2) the participation in the studies of only low-risk and non-obese patients, and (3) the possibly delayed time course of development of the anticipated umbilical artery Doppler changes. These studies need to be repeated in higher-risk and obese patients and over longer time periods. They also should be performed using maternal cardiac output changes to objectively determine the presence or absence of obstruction of uterine venous return, rather than making assumptions about the presence or absence of venous obstruction based on maternal position alone.