| INTRODUC TI ONIn the last two decades, research on the ductus venosus (DV) has been the subject of large observational and interventional clinical trials, 1-3 as well as many clinical studies focused on human pregnancies affected by fetal growth restriction. 4-7 These studies were based on consistent observations made in animal experiments [8][9][10] and human pregnancies. 5,11,12 The DV is a critical crossroads for the umbilical vein flow to perform complex tasks during gestation to balance fetal brain and body growth. 13 It plays an important role in circulatory adaptation to hypoxia in early severe fetal growth restriction (FGR), but the mechanisms remain controversial. 5,11,12 Both hypoxemia-associated dilation of isthmic region of the DV as well as cardiac dysfunction associated with increased afterload have been implicated as the determinants of abnormal DV Doppler velocity waveforms. Here we consider the evidence underpinning assumptions on the DV waveform in relation to its clinical applicability.
| EMB RYOLOGY AND ANATOMYAt 6 weeks of gestation, the embryological development of hepatic circulation endows the human embryo, as well as most other mammals, with a peculiar venous channel, the ductus venosus, that originates at the hepatic venous crossroad (Figure 1). 14 The DV resembles
AbstractThe ductus venosus plays a critical role in circulatory adaptation to hypoxia in fetal growth restriction but the mechanisms still remain controversial. Increased shunting of blood through the ductus venosus under hypoxic conditions has been shown in animal and human studies. The hemodynamic laws governing the accelerated flow in