This review discusses the mechanisms of neurologic damage during and after global cerebral ischemia caused by cardiac arrest. The different pathways of membrane destruction by radicals, free fatty acids, excitatory amino acids (neurotransmitters), calcium, glucose metabolism, and oxygen availability and demand in relation to metabolic rate are briefly discussed. The main focus of this review paper, however, lies in therapeutic (resuscitative) hypothermia after cardiac arrest. Two pioneering studies of the 1950s and four recent publications (in part preliminary results of ongoing studies) in humans are discussed in detail. The conclusions are as follows: (1) hypothermia holds promise as the only specific brain therapy after cardiac arrest so far; (2) hyperthermia is not tolerable after successful resuscitation; and (3) if the ongoing European multicenter trial of hypothermia after cardiac arrest finds a significant benefit to mild hypothermia, withholding hypothermia may be ethically hard to defend.
University Clinic of Emergency Medicine, Vienna, Austria.
Correspondence to Fritz Sterz, MD, University Clinic of Emergency Medicine, General Hospital Vienna, Waehringer Guertel 18-20/6/D, A-1090 Vienna, Austria; e-mail: email@example.com
Heidrun Losert is supported by the Laerdal Foundation for Acute Medicine. Michael Holzer was supported by BIOMED2 European Commission, DG XII for Science Research and Development, Directorate Life Science and Technologies, Biomedical and Health Research Division.