Global ischaemia of the brain following cardiac arrest results in exhaustion of the available oxygen within 15 s and of brain glucose and adenosine within 5 min [I]. Cell membranes start to leak almost immediately, with the development of intracellular and interstitial oedema. In addition, the membrane calcium channels, which are voltage-dependent, open because of the alteration in the resting membrane potential, resulting in influx of Ca2+ into the cell. It is believed that Ca’+ triggers a cascade of events which result in neuronal damage. There is also an accumulation of acid, metabolites, free radicals, fatty acids and prostaglandins. If cardiopulmonary resuscitation is successful, there follows a period of reperfusion, which itself appears to damage cerebral cells. Electron microscopy reveals fairly evenly distributed changes in neurones within 5-7 min of circulatory arrest. If the circulation is not restored (e.g. in a decapitation model), it is claimed that the changes do not become irreversible for up to 60 min [2]. However, if reperfusion occurs, secondary changes occur which evolve into miliary microscopic cerebral infarcts [3]. A number of mechanisms have been proposed for the reperfusion phenomenon, including red cell sludging, capillary pinching, oedema, vasospasm, hypermetabolism, catecholamine release and acidosis, all of which impair delivery or utilisation of oxygen and result in a period of incomplete ischaemia. Incomplete ischaemia is known to be more harmful than complete ischaemia [4] because the continued, although reduced, supply of glucose is metabolised in the presence of an inadequate supply of oxygen, resulting in a rapid accumulation of lactate and a severe intracellular acidosis. Total cerebral blood flow (CBF) increases for a period of 15-30 min after an episode of global ischaemia [S]. CBF then declines below pre-arrest values [6], for reasons which are not totally understood, before increasing to supranormal levels again. However, for the reasons outlined above, the capillary circulation appears to be perfused inadequately even during the period of increased total CBF [7]. The period of increased CBF is accompanied by a transient increase in intracranial pressure (ICP), but ICP is seldom elevated greatly or for a prolonged period in adults unless the ischaemic period is very prolonged.