Fetal Cardiac Function and Venous Circulation - Experiences with Velocity Vector Imaging

Abstract: Placental dysfunction resulting in intrauterine growth restriction (IUGR) is a common complication of pregnany and severe IUGR, with ensuing fetal hypoxia is an important cause of perinatal mortality and morbidity. Doppler studies of fetal and maternal vessels are routinely used for fetal surveillance and alterations in fetal venous blood flow has been demonstrated as a late sign of fetal compromise. However, the role of venous blood flow investigations in decisions on delivery has not been clearly defined and abnormal ductus venosus blood flow has shown moderate accuracy in predicting adverse perinatal outcome. The mechanisms behind ductus venosus dilatation in fetal hypoxia, the transmissions of pulses in the fetal venous system and the association between venous blood flow and cardiac function have also not been completely clarified. We investigated ductus venosus and umbilical venous blood flow patterns and the association between alterations in the two vessels and adverse perinatal outcome. Changes in ductus venosus blood flow during systole occurred more rarely than diastolic changes and were more often associated with adverse periatal outcome. UV-pulsations seemed to be an independent indicator of fetal compromise, regardless of ductus venosus pulsatility index for veins (PIV), which was not a reliable indicator of fetal compromise as an isolated finding. The heart is a crucial organ for fetal adaptation to placental insufficiency. Studies have indicated cardiac damage and remodelling during chronic hypoxia and estimations of cardiac function may therefore be useful for fetal surveillance in IUGR. The best suited parameters, however, remain to be established. Methods that analyze cardiac deformation have recently been developed and have shown promise. Using the novel speckle tracking technique Velocity Vector Imaging, strain, strain rate and velocity of the ventricular and atrial walls were measured in a cohort of 250 healthy fetuses and compared to results in a group of 38 fetuses with signs of impaired placental function. Reference ranges were constructed for the control group. Cardiac strain did not differ between the control and study groups and there was no association between ductus venosus PIV, umbilical vein pulsations and ventricular or atrial strain, strain rate or velocity. This indicates that during fetal hypoxia, circulatory redistribution results in preservation of cardiac deformation thereby maintaining cardiac output intact