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Aims: To clarify the mechanism of hypoxic Fetal Heart Rate (FHR) by the actocardio-gram. Methods: Hypoxic rabbit heart rate and PaO 2 were studied. Long Term FHR Variability (LTV) was studied in physiologic sinusoidal FHR and anencephalic fetus, the acceleration in hypoxia, and by its electronic simulation and adult heart rate. Results: Anencephalic neonatal bradycardia was caused by the excitation of remained medulla oblongata. Rabbit's bradycardia was parallel to PaO 2 bunder 50 mm Hg, which disappeared after urethane anesthesia. Human fetal bradycardia was caused by the hypoxia, because fetal PaO2 is less than 50 mm Hg. FHR acceleration was evoked in the midbrain by the large fetal movement bursts, and minor movements evoked LTV. Physiological sinusoidal FHR was a particular form of LTV. Triangular acceleration was simulated by the electronic integral circuit, and by the triangular heart rate in adult exercises. Fetal outcome was correlated to the acceleration duration. Hypoxia damaged fetal brain in nonreactive FHR, loosing acceleration, and advanced hypoxia further damaged brain a few days after the loss of acceleration, showing the loss of LTV and bradycardia. The loss of LTV which was confirmed by the frequency power spectrum was rare, but its brain damage was as severe as the apnea of anencephalic neonate, which lost cerebral respiratory center. Conclusion: Hypoxic bradycardia was evoked by the excited medulla oblongata in the decreased PaO 2 , which was lower than 50 mm Hg. The hypoxia damaged fetus in fetal bradycardia, the losses of acceleration and LTV, in relation to fetal movements.

Actocardiographic Analysis of Fetal Hypoxia Detected by the Bradycardia, Loss of Fetal Heart Rate Acceleration, and Long Term Variability