Pathophysiology of fetal distress has not been elucidated completely so far. But there has been a rapid progress in the studies both in vitro and in vivo which investigated the causes of neuronal death by hypoxia. At the initiation of hypoxemia, elevation of fetal blood pressure will occur due to constriction of fetal peripheral vessels, and this results in fetal heart rate slowing and respiratory compromise. During moderate hypoxemia, circulating blood is redistributed to the brain, heart and adrenals at the expense of peripheral organs (lung, skin, etc). During prolonged hypoxemia, blood flow to the brain stem is maintained and even greater than that in other brain regions. Neuronal activity of brain stem, an autonomic center, is important for survival of a fetus. As hypoxia progresses, glucose in metabolized anaerobically, lactate concentration elevates, and concentrations of high-energy phosphates decrease in the cerebrum. When cerebral metabolism has collapsed finally, neuronal membranes depolarize, voltage-gated Ca+2 channels open and Ca+2 flux into the cytoplasm increases. These changes result in neuronal death. It is considered that glutamates, oxygen radicals and other substances are involved in the increase of Ca+2 influx. These studies suggest that hypoxic stimulation should be avoided in the chronically deteriorating fetus for prevention of unrecognized fetal brain damage.