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As this study has noted the pre-resuscitation period as well as the post-resuscitation period are both related to lipid peroxidation of membrane, DNA fragmentation prior to accelerated programmed cell death "apoptosis. Factors including arrest time, time for resuscitation, severity of reperfusion and core body temperature all are critical in the determination of neuronal functional recovery. Detrimental factors such as arrest time, resuscitation time, reperfusion severity, and core body temperature play vital role in determining neuronal functional recovery. Cooling of the patient's body can mitigation these negative effects in this chain of events and the prevention or minimization of the effects of the size of infarct as well as improvement of myocardial savage, reduction of left ventricular remodeling and more optimized long-term left ventricular function and a decrease in mortality of patients with cardiac arrest as cited by Kelly and Nolan (2010). Hypothermia benefits include neuroprotective protection. The series of steps related to ischemia and reperfusion are temperature dependent. Therefore, if the body is at cooled condition, the deleterious effect of these interlinked events has the potential to be controlled in nature. The goal of treatment of cardiac arrest patients is to prevent or to minimize the effects of infarct size, improve myocardial salvage, reduced left ventricular remodeling and better long-term left ventricular function with overall decreased mortality rates.

The neuroprotective effect of hypothermia includes a decrease in cerebral metabolism, barring the release of excitatory amino acid, reduction of oxygen free radical production and lipid peroxidation, a decrease in CSF platelet activating factor (PAF, and inhibition of cytoskeleton breakdown. Other benefits include enhancement of membrane stabilization, electrolyte redistribution, and normalization of intracellular water concentration and intracellular pH (stabilization of the blood-brain barrier). Further aided is restoring normal intracellular signaling, protein synthesis and gene expression by lower body temperature during cardiac arrest Furthermore, with therapeutic hypothermia can reduce the cardio toxic effect through induction of epicardial reflow, reduction of myocardial metabolic need and maintenance of intracellular high-energy phosphate reserves. (Bessman, 2010)

Induced therapeutic hypothermia are cardioprotective and neuroprotective effect as related to reduction of infarct size, anoxic brain injury and mortality; and reduction in risk of arrhythmias, a decrease in complications. There are risks associated with hypothermia including effects on multiple organ systems however; these risks can be greatly reduced in proper treatment and high-quality intensive care therapy. The use of pharmacological agents is indicated in therapeutic hypothermia and include such as sedatives, analgesics, and neuromuscular blocking agents. (NMBAs) It is evident that therapeutic hypothermia has provided advances in the treatment of cardiac arrest and specifically in terms of the cardioprotective and neuroprotective effect of the use of this method for treatment individuals with cardiac arrest incidents. It is important that hospital nursing staff be educated, trained and prepared to administer therapeutic hypothermia in the care of individuals with cardiac arrest and who are determined to be eligible for such treatment of cardiac arrest.