Response of the fetal heart to changes in load: from hyperplasia to heart failure

Abstract

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 in the remodelling of the placental spiral arteries to create a low impedance placental circulation against which the right ventricle ejects.⁴ This low resistance circuit is pivotal to permit appropriate fetal growth as the right ventricle (unlike the left) responds to increasing afterload with a fall in ventricular output. Left ventricular preload becomes more dependent on pulmonary venous return in the third trimester as the pulmonary circulation increases and the oval foramen becomes relatively restrictive, thus reducing the right to left shunt. This leads to volume loading of right sided structures that is usually well tolerated in later pregnancy and regresses after delivery with no apparent long term effects. Preparation for postnatal closure of the arterial duct is effected by “cushions” of tissue seen at the pulmonary end of the duct towards term. These contribute to the increasing afterload faced by the fetal right ventricle as a consequence of placental changes near term and may lead to increased systemic venous pressure in the fetus.