THERAPEUTIC HYPOTHERMIA POST CARDIAC ARREST

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Recent studies have shown patients suffering from cardiac arrest are treated with mild therapeutic hypothermia is now recognized as standard therapy in patients resuscitated from out-of-hospital cardiac arrest (OHCA) leading to unexpected death 1 in 1500 adults each year in this hi tech world (Zheng et al 2001). Therapeutic hypothermia (TH) may increase survival and reduce the amount of neurologic damage after cardiac arrest. According to the recent guidelines, comatose survivors of out-of-hospital ventricular fibrillation cardiac arrest should be cooled with internal or external cooling techniques to a target temperature of 32 °C to 34 °C (patients with in-hospital cardiac arrest or other primary rhythms may also be cooled. This target temperature should be maintained for 12 to 24 hours, and after this cooling period the patients should be rewarmed at a rate of 0.25 °C to 0.5 °C hour to normothermia. Significant survival and functional benefit impelling increased acceptance of use of TH.
Healthcare professionals in the hospital settings has been recommended in cardiac arrest (CA) patients since the publication of two randomized clinical trials in 2002, the results of which demonstrated a significant improvement in neurologically intact survival for comatose CA patients presenting with ventricular fibrillation (VF) or ventricular tachycardia (VT) Current guidelines suggest that mild therapeutic hypothermia should also be considered in patients presenting with other rhythms although this has been less well studied.
The aim of this research study is to review current literature reviews on therapeutic hypothermia post cardiac arrest ,its benefit for a neurological outcome, in shockable and non shockable rhythms, in and out of hospi...

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...perfusion and oxygen supply to the brain for few minutes post cardiac arrest resume of reperfusion releases some enzymes which changes intracellular ions and causes cell death.This leads to free radical production, cytotoxic cascade, nitric oxide that ceases further injury to neurons (Nolan et al 2008).Neurological deficit can be a evident post cardiac arrest reperfusion injury however this damage could be alleviated by therapeutic hypothermia recommended by holzer et al (2005). The mechanism of action of therapeutic hypothermia is tought to be mediated by prevention of cerebral reperfusion injury stated by mark luscombe, john c andrezowski (2006) consequently holzer et al ,(2005,2009) suggest if the reperfusion injury occurs following cardiac arrest then it is necessary to use TH to bring to an endto the development of injury and also to overcome the condition.

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