Pathophysiology of brain resuscitation after cardiac arrest

Cerebrocirculatory arrest induced by cardiac failure differs from other for ms of brain ischemia mainly by the fact, that the quality of the reperfusio n of the brain depends on the speed and quality of cardiac resuscitation. T he severity of brain injury after cardiac arrest is, therefore, a function of post-cardiac arrest hemodynamics. Under most practical conditions of car diopulmonary resuscitation, post-ischemic recirculation disturbances such a s the no-reflow phenomenon or the post-ischemic hypoperfusion syndrome as w ell as rite associated morphological lesions cannot be prevented after card iac arrest of more than 8-10 min. Optimizing extrathoracal cardiopulmonary resuscitation prolongs brain revival to 15 min, and direct intrathoracal ca rdiac massage or the use of extracorporeal circulation extends the recovery time to about 30 min. However, even this time is still markedly shouter th an that observed after isolated brain ischemia. Brain recovery after cardia c arrest is, therefore, mainly limited by the speed and quality of cardiac resuscitation. Molecular mechanisms of brain injury such as excitotoxicity, free radical-m ediated injury, nitric oxide toxicity mitochondrial and endoplasmic reticul um dysfunction or DNA fragmentations are of much lesser importance and prob ably contribute little to the final functional outcome. However with improv ements of cardiac resuscitation, molecular disturbances will become more do minant, and additional neuroprotective interventions may be required to fur ther improve functional recovery. Powerful therapeutical strategies for the prevention of molecular brain injury are already available and if necessar y: can be combined with cardioprotective interventions.