Induced Therapeutic Hypothermia After Cardiac Arrest Research Paper

Induced Therapeutic Hypothermia After Cardiac Arrest - Research Paper patternTDuring an open heart surgery, there is significant risk of neurological injury on account of the lack of oxygen supply to brain as the circulation comes to a halt. In the absence of oxygen, the brain undergoes anaerobic metabolism as reported by Michelle E. (2011). This leads to misuse to ATP dependent cellular functions with a resulting increase in calcium and glutamate excretion. The brain cells thus become more active, consuming more oxygen. With the increasing hypoxemia, further damage occurs direct to cell death. The resultant cerebral dropsy further enhances the damage. Also, as a result of all these processes, the blood-brain barrier also becomes ineffective further contributing to cerebral edema. As soon as the circulation returns by and by the heart starts pumping again, reperfusion injury occurs which adds up to the ongoing damage. Meanwhile, there is already an onset of the inflammatory re action as a result of cell death leading to a release of neutrophils and macrophages in an attempt to remove the cellular debris. The resultant production of free radicals also catalyses the damaging process thus worsening the cerebral edema. This vicious cycle continues leading to brain death. ROLE OF THERAPEUTIC HYPOTHERMIA IN PREVENTING NEUROLOGICAL DAMAGE Using the technique of therapeutic hypothermia can be useable to avoid all the above described damage. The therapeutically induced hypothermia after cardiac arrest takes following steps to decrease the extent of neurological damage 1. It stabilizes the release of calcium and glutamate thus decreasing the degree of cellular death, 2. It stabilizes the blood brain barrier, 3. It causes a suppression of the inflammatory response, 4. It reduces cerebral edema by the help oneself of above actions. INDUCED THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST 4 According to the report produced by Michelle E. (2011), there is a reduction in cerebral metabolism from 6% to 10% for every one degree Celcius drop in body temperature. This results in decreased oxygen requirements by the brain cells. Michelle E. (2011) simulates the cause of therapeutic hy