Conclusions

The medical management of brain injury in patients following cardiopulmonary arrest needs a comprehensive approach, starting with the control of the primary hypoxic-ischemic injury from the cessation of blood flow during the arrest and suboptimal perfusion during resuscitation prior to ROSC, to the prevention of secondary insults to the brain (cerebral

Figure 2 Percentage mortality in the placebo groups of clinical trials for brain injury after cardiac arrest (1986-2002). Abbreviations: BRCT, Brain Resuscitation Clinical Trials; HACA, Hypothermia After Cardiac Arrest.

edema, seizures) and reversal of extra-CNS related injuries from such systemic causes as persistent hypoperfusion, hyperthermia and hyperglycemia. Thus far, therapeutic hypothermia (32-34°C) for 12 to 24 hours is the only therapeutic modality that has demonstrated efficacy in improving both survival and functional outcomes following cardiopulmonary arrest. The successful institution of therapeutic hypothermia requires the proper utilization of the methods and devices and timing of cooling and rewarming and prevention of accompanying complications. The extensive preclinical and translational research leading to the favorable results with therapeutic hypothermia proved that brain injury after CA can be ameliorated to yield clinical improvement. Efforts are now on the way to further improve outcomes by enhancing the methods of inducing hypothermia and understanding the optimal period of therapy. Although clinical trials with pharmacological agents have not proven to be beneficial in this paradigm, further studies of agents with novel mechanisms or the use hypothermia in combination with pharmacological neuroprotection hold promise in the future.

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