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(Stroke. 2006;37:1638.)
© 2006 American Heart Association, Inc.
Editorials |
From the Stroke and Neurological Intensive Care, The Cleveland Clinic Foundation, Cleveland, OH.
Correspondence to Derk W. Krieger, Stroke and Neurological Intensive Care, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195. E-mail krieged@ccf.org
Key Words: cardiac arrest critical care hypothermia
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The great majority of patients who experience cardiac arrests expire after the event. Moreover, full neurological recovery occurs in only a small proportion of the survivors. Until recently no specific postarrest therapy was available to improve that outcome. Therapeutic cooling (32°C to 34°C for 12 to 24 hours) applied after cardiac arrest has been shown to improve this dismal situation. In 2002, two randomized clinical trials of mild therapeutic hypothermia applied to unconscious patients after successful resuscitation from cardiac arrest revealed that therapeutic cooling is capable of improving neurological outcome while reducing mortality.1,2 Both studies focused on an out-of-hospital population with ventricular-fibrillatory cardiac arrest and brief intervals to return of spontaneous circulation but remained comatose. These patients are considered the "sweetspot" population for a neuroprotective trial for this condition.
Current International Liaison Committee on Resuscitation (ILCOR) guidelines reflect those inclusion criteria recommending that unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32°C to 34°C for 12 to 24 hours when their initial rhythm was ventricular fibrillation. These recommendations also suggest that such cooling may also be beneficial for other rhythms or in-hospital cardiac arrest.3
There are several possible mechanisms by which mild hypothermia could improve neurological outcome when used after reperfusion. In normal brain, hypothermia has shown to reduce the cerebral metabolic rate for oxygen (CMRO2) by 6% for every 1°C reduction in brain temperature above 28°C. Although slowing metabolism may defend against brain injury in circulatory arrest, it is unlikely to explain
Related Article:
Stroke 2006 37: 1792-1797.
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