Diminished placental vasculature, particularly on the fetal side of the placental vasculature, associates with fetal growth restriction. Aberrant feto-placental vascular structure impacts fetal growth but less clear are the implications for fetal cardiovascular development. Loading of the fetal heart is determined by incoming placental flow, and furthermore the fetal heart beats directly against resistance of the placental vascular bed. Thus placental haemodynamics likely have important influences on cardiac development. Moreover, in FGR, regional blood flow can change, with a higher proportion of blood coming from the placenta bypassing the fetal liver with increased perfusion of the fetal head and neck. These haemodynamic shifts impact fetal cardiovascular development, with both short and long-term health implications. To explore this placental-cardiovascular axis, we have utilised a range of models of glucocorticoid exposure in pregnancy. Glucocorticoids are critical for fetal maturation, including the heart, and in excess are known to reduce feto-placental vasculature and fetal growth. We have established that glucocorticoid receptor signalling is essential for gestational maturation in diastolic flow within the umbilical artery and that acute exposure to glucocorticoids in mouse pregnancy has gestation-dependent effects on fetal and placental haemodynamics. Utilising a rat model of chronic glucocorticoid exposure we have made significant advances in imaging and modelling the longitudinal haemodynamics of the feto-placental cardiovascular axis. These approaches will drive the development of more accurate diagnostic criteria for at-risk pregnancies, as well as the prediction of offspring health complications and consideration of preventative strategies.