The controversial role of the ductus venosus in hypoxic human fetuses

Abstract

| 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

ISUOG Practice Guidelines: diagnosis and management of small‐for‐gestational‐age fetus and fetal growth restriction

“…Alterations in the ductus venosus flow velocity waveform, especially absent or reversed a-wave, are caused by progressive dilatation of the ductus venosus isthmus in order to increase the blood flow toward the heart, in an attempt to compensate for extreme oxygen deprivation 24 . Others consider that absent or reversed a-wave in the ductus venosus is a consequence of increased intra-atrial pressure due to high cardiac afterload (increased vascular placental resistance) and/or a direct effect of fetal acidemia on myocardial cell function 25 .…”

Fetal cardiovascular hemodynamics in type 1 diabetic pregnancies at near‐term gestation

“…It must be kept in mind that ductus venosus blood flow profile is also affected by the amount of umbilical venous blood return from the placenta and the caliber of ductus venosus that is mainly regulated by fetal po 2 . 23 The pulsatility of fetal aortic isthmus blood flow velocity waveform was greater in T1DM pregnancies than in the controls at near-term gestation. In fetal circulation, the aortic isthmus has an important physiological role allowing communication between the left and right ventricular outputs that are arranged in parallel.…”

“…Our findings suggest that the inferior vena cava blood flow profile could be more sensitive than the ductus venosus to changes in cardiac function, at least in maternal T1DM pregnancies. It must be kept in mind that ductus venosus blood flow profile is also affected by the amount of umbilical venous blood return from the placenta and the caliber of ductus venosus that is mainly regulated by fetal p o 2 23 …”

Diagnosis and management of fetal growth restriction: the ISUOG guideline and comparison with the SMFM guideline

“…Extremely low values of short-term variation (STV) in computerized analysis of CTG (cCTG) is a reliable predictor of metabolic acidemia at delivery or intrauterine death [48][49][50][51][52][53][54][55] . Increased pulsatility in the ductus venosus (DV) reflects myocardial decompensation resulting in increased end-diastolic ventricular pressure and decreased forward flow velocities during atrial contraction (a-wave) as early changes and absent or reversed flow as late changes of its waveform 56 . These changes might also reflect a progressive dilatation of the DV as an adaptive response to worsening hypoxemia 56 .…”