The fetal circulation works in parallel with the dominant right ventricle, ejecting approximately 60% of the combined ventricular output. Three important communications exist between the two circulations (oval foramen and the arterial and venous ducts) that influence loading conditions. In particular, the determinants of fetal left ventricular filling differ considerably from those seen in the adult heart. Pulmonary venous return contributes only a small proportion to left ventricular preload because of the relatively low pulmonary blood flow in fetal life (rising from an estimated 11% to 25% of right ventricular output by the third trimester).¹ Left ventricular filling depends predominantly on patency of the oval foramen to allow the relatively oxygen-rich blood returning from the placental circulation, via the umbilical vein and venous duct, to stream through the right atrium and enter the left side of the heart.² The right ventricle fills from mostly upper body systemic venous return and the majority of its output is diverted away from the pulmonary circulation, via the arterial duct, to the descending aorta and thence to the placenta via the umbilical arteries. Hence the fetal right ventricle pumps against the systemic pressures of the lower fetal body and placental impedance, while the left ventricle ejects against the relatively high impedance of the fetal brain and upper body. Not surprisingly, ventricular loading is affected by the maturation of structures such as the placenta and changes in the impedance of the cerebral and placental vascular beds in response to hypoxaemia, as well as circulatory adaptations made by the fetus in response to intracardiac malformations.

MATURATIONAL CHANGES IN LOADING

Loading patterns alter throughout gestation; the ventricular pressure–volume loops of the chick embryo show an active response to increasing preload as the early myocardium organises.³ Mid trimester studies in the human fetus demonstrate the importance of trophoblastic invasion …