A model of in utero ventilation was used to elucidate the mechanisms by which left ventricular (LV) output increases with the transition from a fetal to a neonatal circulation. Using a conductance catheter, LV volumes were measured in seven anesthetized, near-term fetal sheep. Pressure-volume data was recorded before and with oxygen ventilation and again after occlusion of the umbilical cord. Ventilation caused increases in LV end-diastolic volume (2.3 2 0.9 to 2.9 2 0.6 mL/kg; p < 0.05), stroke volume (1.2 2 0.3 to 1.9 2 0.2 mL/kg; p < 0.001), and ejection fraction (52.8 + 11.1 to 66.4 + 8.8%; p < 0.001).Contractile state, as assessed by end-systolic elastance, did not change during the transition. Heart rate also remained ' constant. Afterload, as assessed by effective arterial elastance, decreased from 1.80 2 0.37 to 1.04 2 0.33 kPa/mL @ < 0.01). Occlusion of the umbilical cord did not result in any further change in hemodynamic parameters.Pressure-volume analysis revealed that a decrease in effective LV afterload and an increased LV end-diastolic volume are the major determinants of, and contribute comparably to, the profound increase in LV output with in lttero ventilation. Enhanced contractility is not required for the increase in LV output to occur. (Pediatr Res 36: 373-379, 1994) Abbreviations LV, left ventricle RV, right ventricle dP/dt,,,, the maximum of the first time derivative of the LV pressure wave form E,,, end-systolic elastance E,,,, effective arterial elastance (afterload opposing LV ejection) PV, pressure-volume Adaptation of the fetus to extrauterine life involves a number of rapidly occurring processes. Among these, the initiation of breathing and the transition from a fetal to a neonatal circulation are the paramount events. In the fetal heart, which is characterized by RV dominance (1-3), the ventricles operate in parallel. After birth, the ventricles function serially and LV output increases 2-to 3-fold (4-10). The mechanism by which the L V increases its output to such an extent remains a mystery.In utero ventilation is associated with a marked increase in LV output identical with the increase observed in the immediate postpartum state. Either an increase in end-diastolic volume, ejection fraction, or both may underlie the augmented LV stroke volume. Ejection fraction could increase due to an increase in contractility or a reduction in afterload. Augmented LV end-diastolic volume as a result of increased pulmonary venous return (1 1-15) and an increase in contractility (16, 17) have both been suggested to play a role in augmenting LV output at birth. Because systemic pressure is increased or unchanged at birth, it has been suggested that a decrease in afterload is unlikely to occur (18). On the other hand, afterload may decrease due to the exposure of the LV to the pulmonary circulation through the patent ductus arteriosus (19). The individual contribution of each component to the augmentation of LV performance at birth is unknown. We applied the conductance catheter technique to the in...