Cerebral Physiology after Cardiac Arrest

Despite the restoration of an adequate systemic blood pressure, local cerebral blood flow and hence cerebral perfusion after a cardiac arrest are severely impaired due to local increases in vasoconstrictors. This explains the observed lack of electrical activity on EEG despite adequate blood pressure following cardiac arrest. Immediately after resuscitation there is a period of multifocal no-reflow, followed by a period of transient global hyperaemia lasting 15-30 minutes, thereafter, cerebral blood flow becomes severely reduced while cerebral metabolic rate of oxygen gradually recovers. This is termed the delayed hypoperfusion phase. After 24 hours, cerebral blood flow and metabolism may be restored, remain low or there may be secondary hyperaemia. Multifocal no-reflow, is a phenomenon observed in animals following recovery from cardiac arrest, in which, despite the restoration of adequate blood pressure multiple areas of the brain have been shown to develop perfusion defects that range from a pin hole, up to 95% of the brain. The main factor determining cerebral blood flow following a cardiac arrest is the initial period of ischaemia prior to adequate resuscitation [14]. Clinically, these observations are supported by the loss of brainstem reflexes such as the gag reflex that indicate a loss of brainstem function.