Time-domain representations of the fetal aorto-pulmonary circulation were carried out to study hemodynamic consequences of congenital diaphragmatic hernia (CDH) and the effects of endothelin-receptor antagonist(ERA) (tezosentan, 3mg.45min-1). In 10 controls and 7 CDH lamb fetuses (28 ewes) on day 135, the isthmic aortic (iAo) and LPA flows (Q) and iAo, PA and left-auricle (LA) pressures (P) , discrete-triggered P and Q waveforms were modelized as P(t) and Q(t) functions to obtain hemodynamic profiles, pulsatile waves (P,Q and entry impedance Ze), and P,Q hysteresis loops. In controls, blood propelling energy was accounted for by biventricular ejection flow waves (kinetic energy) and by flow-driven pressure waves (potential energy) with low Ze. Weak fetal pulmonary perfusion was ensured by reverse flows from PA branches to the DA and aortic isthmus. ERA-blockade using tezosentan slightly increased the forward flow but largely increased diastolic backward flow. In CHD-fetuses, the static component overrode phasic flows that were detrimental to reverse flows and the direction of diastolic isthmic flow changed to forward. Decreased cardiac output, flattened pressure waves, and increased forward Ze promoted backward flow to the detriment of forward flow (especially during diastole). Additionally intrapulmonary arteriovenous shunting was ineffective. Slowing of cardiac output, dampening of energetic pressure waves and pulsatility, and heightening of phasic impedances contributed to lowering of aorto-pulmonary blood flows. We speculate that reverse pulmonary flow is a physiological requirement to protect the fetal pulmonary circulation from the prominent RV stream and to enhance blood flow to the fetal heart and brain.