Cerebral resuscitation after cardiocirculatory arrest.
Cardiopulmonary resuscitation can restore spontaneous circulation in up to 50% of patients suffering from cardiac arrest. However, most of these patients still die during the postresuscitation period. Mortality is largely due to neuronal injury after global cerebral ischemia. There is, therefore, a clear need for therapies, which restore and protect brain function after cardiac arrest. Several years ago, mild therapeutic hypothermia was introduced into clinical practice. It represents the first treatment to improve both survival and neurological outcome of patients after out-of-hospital cardiac arrest, according to randomized clinical trials. In addition to therapeutic hypothermia, various other therapeutic options are currently being investigated experimentally and/or clinically. These include thrombolytic therapy, specific infusion regimens, or antiapoptotic drugs. In this article, we review both the pathophysiological background and the efficacy of different measures that might be useful for cerebral resuscitation.
Schneider
Andreas
A
Department of Anesthesiology and Postoperative Intensive Care Medicine, University of Cologne, Kerpener Strasse 62, 50937 Köln, Germany. andreas.schneider_@uk-koeln.de
Böttiger
Bernd W
BW
Popp
Erik
E
D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D016887:Cardiopulmonary Resuscitation; D002560:Cerebrovascular Circulation / Q000502:physiology*; D002561:Cerebrovascular Disorders / Q000628:therapy; D006323:Heart Arrest / Q000503:physiopathology* / Q000628:therapy*; D006801:Humans; D007036:Hypothermia, Induced; D008833:Microcirculation / Q000502:physiology