Use of Therapeutic Hypothermia in the Treatment of Cardiac Arrest

¶ … Therapeutic Hypothermia in the Treatment of Cardiac Arrest

This work has examined the use of hypothermia in treating cardiac arrest, which is an important scientific advance especially for the American Heart Association's goal of reducing mortality rates associated with heart disease by 25%. (Nichols, 2008) The health status of individuals has suffered due to modernization of life in general however, medical advances in the area of cardiac arrests and particularly in the area of neurological functional recovery due to the hypoxic -- ischemic insults developed during and after the cardiac arrest as noted by Bessman (2010)

In addition, only 11% to 48% of surviving patients are noted with positive neuro functional clinical impact upon discharge. Therapeutic hypothermia is stated to result in a gain of 0.66 life years adjusted for quality when compared with normothermia treatment as noted by Merchant (2009). Eligibility is based upon criteria set by The Hypothermia After Cardiac Arrest (HACA) in a cost-effective treatment also noted by Merchant (2009). It has been reported that the guidelines for cardiopulmonary resuscitation and emergency cardiovascular care in relation to the hypothermia use places an emphasis on the initial rhythm VF (ventricular fibrillation) in adult patients with return of spontaneous circulation after out-of-hospital cardiac arrest, and patients with non-VF arrest out-of-hospital or with in-hospital arrest should be cooled to 32-34°C for 12-24 hours as cited in Bessman (2010). Sedatives or anesthetics are used in inducing therapeutic hypothermia both with and without narcotic infusion for managing pain.

Landmark clinical trials including those of Bernard and colleagues in an Australian study and HACA Group in a European study that the use of therapeutic hypothermia is successful in treating cardiac arrest patients and that this treatment results in a higher rate of physiological recovery. This is because the blood circulation interruption results in global ischemia. Ischemia involves depletion of oxygen, glucose and adenosine triphosphate (ATP) reserves in the brain and in what is a cascade of events including Ca2+ shifts, brain tissue lactic acidosis, and free fatty acids, osmolality, and extracellular concentration of excitatory amino acids (EAA's) like glutamate the hippocampus, neocortex, and cerebellum affected with the possibility of a cerebral injury due to cardiac arrest leading to eventual potential cerebral edema and seizures and/or brain death as cited in Holzer (2002).

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)