Abstract
Cardiovascular disease remains the leading cause of death in the Western world, with as many as 400,000 Americans and 700,000 Europeans sustaining cardiac arrest each year [1]. Though the initial success of cardiopulmonary resuscitation (CPR) is approximately 39%, the majority of victims die within 72 h of hospital admission [2–4]. Patients successfully resuscitated following cardiac arrest in fact often present with what is now termed “postresuscitation disease” [5]. Most prominent among these diseases are postresuscitation myocardial failure and ischaemic brain damage. Severe postresuscitation heart contractile failure has been implicated as one of the most important mechanism causing these fatal outcomes [6–9]. However, morbidity and mortality after successful CPR also largely depends on recovery of neurologic function. Up to 30% of survivors of cardiac arrest manifest permanent brain damage [10–12], and in some instances, only 2–12% of resuscitated patients are discharged from hospital without neurological dysfunction [13].
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Fumagalli, F., Ristagno, G. (2011). Nasopharyngeal Cooling During Cardiopulmonary Resuscitation. In: Gullo, A. (eds) Anaesthesia, Pharmacology, Intensive Care and Emergency Medicine A.P.I.C.E.. Springer, Milano. https://doi.org/10.1007/978-88-470-2014-6_12
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DOI: https://doi.org/10.1007/978-88-470-2014-6_12
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