Placental hypoxia is associated with maternal hypertension, placental insufficiency and fetal growth restriction. In the pregnant guinea pig, prenatal hypoxia during early gestation inhibits cytotrophoblast invasion of spiral arteries, increases maternal blood pressure and induces fetal growth restriction. This study evaluated the impact of chronic maternal hypoxia on fetal heart structure with 4D echocardiography with spatio-temporal image correlation and tomographic ultrasound (STIC-TUI) and uterine and umbilical artery resistance/pulsatility indices and fetal heart function using pulsed wave Doppler ultrasound. Pregnant guinea pigs were exposed to either normoxia (N=7) or hypoxia (10.5%O₂; N=9) at 28-30d gestation and studied at term. Fetal heart structure and outflow tracts were evaluated in the four chamber view. Fetal heart diastolic function was assessed by E/A ratios of both ventricles and systolic function by the myocardial performance index (or Tie) of left ventricles of normoxic (N=21) and hypoxic (N=17) fetuses. There were no structural abnormalities in fetal hearts. However, hypoxia induced asymmetric fetal growth restriction and increased the relative placental weight compared to normoxic controls. Hypoxia increased Doppler resistance/pulsatility of uterine but not umbilical arteries, had no effect on the Tie index, and increased the E/A ratio in left but not right ventricles. Thus, early and prolonged hypoxia increases uterine artery resistance, stimulates placental compensation, and generates fetal growth restriction at term. Further, the enhanced cardiac diastolic filling with no changes in systolic function or umbilical artery resistance suggests that the fetal guinea pig undergoes a compensated, adaptive response of the systemic circulation to prolonged hypoxia exposure.