Deep hypothermic circulatory arrest has become an essential technique to allow repair of complex congenital cardiac lesions in children. The arrested state has concerned the surgeon, cardiologist, and anesthesiologist alike, and yet deep hypothermic circulatory arrest has been highly successful with a low incidence of neurologic sequelae. Studies of cerebral blood flow and cerebral oxygenation demonstrate that the arrest hypothermic brain does not develop the immediate postarrest hyperemia or hyperoxia seen in normothermic ischemic brain models. However, both hypothermic and normothermic ischemic brains exhibit hypoperfusion beyond the immediate recirculation period, likely coupled with a reduced cerebral metabolic rate. That the hypothermic arrested brain likely becomes anoxic and recovery of the anoxic brain depends in large part on recirculatory hemodynamics suggests that the lack of hyperemia and hyperoxia may play more major roles than was previously believed. The mechanism of protection may be related to suppression of oxygen free radicals.