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Hypothermia

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Submitted By jbella027
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The incidence of out-of –hospital cardiac arrest is a common event, particularly in the Western world. There are 110,000 deaths from coronary disease in the United Kingdom each year, of which 75% are due to sudden cardiac death (Schilling et al., 1998; DoH 2005). Despite nearly 40 years of pre-hospital advance life support, the survival rate of hospital discharge following out-of-hospital cardiac arrest is very poor. Among the few survivors to hospital discharge, neurologic impairment often remains a lasting morbidity (Becker et al., 1993).
A large body of evidence from animal models indicate that hyperthermia (a temperature higher than the threshold value of 37C) due to brain injury or ischemia can exacerbate the degree of permanent neurological damage following cardiac arrest. Each degree Celsius higher than 37C can cause cerebral destruction through increased metabolic expenditure, excitatory neurotransmitters resulting in calcium cellular reflux and accumulation of oxygen free radicals (Busto et al., 1987).
To improve the outcome of patients who survive cardiac arrest requires not only reducing the ischemic process as quickly as possible, caused by cardiac arrest, but also preventing post resuscitation syndrome caused from reperfusion (Safar, 1993). Cerebral reperfusion after successful resuscitation can trigger harmful chemical cascades such as oxygen free radical production which can result in multifocal brain damage. Therapeutic hypothermia (TH) is considered as an effective method for reducing the deleterious neurological outcomes in patients who have out-of-hospital cardiac arrest. Clinical and animal studies have shown that TH following cardiac arrest reduces both the cerebral metabolic rate and oxygen demand and it is thought to attenuate reperfusion injury, global inflammation and endothelial dysfunction, all consequences of cerebral ischemia.
Over the last decade several research trials have demonstrated that the induction and...

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