Therapeutic Hypothermia

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Practice development issues around Induced Therapeutic Hypothermia (ITH) on Cardiac Arrest Patients Contents
1. Introduction
2. Pathophysiological changes during cardiac arrest and return of spontaneous circulation 3. Physiological benefits of therapeutic hypothermia
4. Guideline for induced therapeutic hypothermia after cardiac arrest 5. The UHL guideline’s goal of therapeutic hypothermia
6. Preparation, Monitoring and Supportive therapy
7. Cooling Methods
8. The relative experience
9. The role of advanced clinical practitioner and multidisciplinary approach 10. Synthesis
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11. Conclusion
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1. Introduction
In UK, there are approximately 50,000 treated cardiac arrests, of which 5-30% of patients survive to leave the hospital every year (Intensive Care Society, 2008). The Majority of these patients have suffered ischemic brain injury, which results in severe disability or ultimately leads to death. Until recently, there has been no intervention proving a significant reduction in the incidence of brain injury in arrest survivors; however in recent years induced therapeutic hypothermia (ITH) has been used to improve the neurological outcome of comatose patients who had return of spontaneous circulation (ROSC) after resuscitation following sudden cardiac arrest (Holden & Makic 2006). Although it is an evidence-based method, it has its own limitations and complications. The purpose of this assignment is to look at the current practice in own area, supporting national and international recommendations, review current literature and evidence-based nursing implications in caring for those patients. The physiological benefits of hypothermia, multidisciplinary approach of clinically cooled patients, practice development issues around these patients and scope of advanced nursing practice will also be discussed. 2. Pathophysiological changes during cardiac arrest and return of spontaneous circulation Under normal circumstances, the brain takes 15% of the cardiac output and consumes 20% of total body oxygen supply (Girolami, Anthony & Froch, 1999).During cardiac arrest the blood supply to the brain decreases or stops, which leads to less or no oxygen supply to the brain causing loss of consciousness. This hypoxic state in the brain can cause depletion of glucose and adenosine triphosphate store (the brain’s source of energy) (Safar, Behringer, Bottiger, et al. 2002). In hypotensive state or no blood supply state to the brain, membrane depolarize, calcium influxes, glutamate is released leading to acidosis and lipases, proteases, and nucleases are activated contributing to cerebral oedema (Warner 1997, Safar & Behringer 2003). During the spontaneous return of circulation (SROC), further damage to the brain can occur. This is called reperfusion injury which causes series of process involving release of iron, free radicals, nitric oxide, catecholamine, renewed excitatory amino acid and calcium shifts (Warner 1997, Safar & Behringer 2003). These series of process will result in mitochondrial damage, DNA fragmentation, and cell death (Warner 1997, Safar & Behringer 2003). This process will continue for 3days (Safar & Behringer 2003). This process of injury and subsequent recovery varies depends upon the severity of injury (Girolami et al. 1999).The severity of injury can vary from reversible injury with full recovery to global irreversible injury leading to brain death (Girolami et al. 1999). The severity of injury is dependent on the length of ischemic state and the duration of reduced blood flow (Girlami et al. 1999). 3. Physiological benefits of therapeutic hypothermia

There are several research have been conducted on methods to improve neurological outcome after cardiac arrest including pharmacological approaches, methods to improve cerebral circulation and oxygenation and induced therapeutic...
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