Induced Hypothermia in Post Cardiac Arrest - Assignment Example

Induced Hypothermia in Post Cardiac Arrest Introduction Survival happens very rarely in a post cardiac arrest and of those who do survive there is however a high incidence of anoxic brain injury. Such injury or what is termed as the widespread cerebral ischemia normally results in severe neurologic damage. A number of authors (Felberg et al 2001; Bernard et al 2003) agree that this neurologic damage is the result of not only the cerebral anoxia occurring during the cardiac arrest, but also the reperfusion injury occurring with the return of spontaneous circulation. Correspondingly, their studies provide sufficient evidence in the literature that supports the use of induced hypothermia to prevent and limit this anoxic brain injury (Hypothermia After Cardiac Arrest Study Group 2003; Bernard et al. 1997). For therapeutic reasons, induced hypothermia is defined as the controlled lowering of a patient's temperature. Lowering the patient's core temperature to 32-34 C is typical and appropriate for post cardiac arrest according to Bernard & Buist (2003). Literature Review The use of hypothermia as a means of cerebral protection became established in the early days of cardiac surgery, the time when it was shown that hypothermia could prolong the safe period of circulatory arrest. From then on, hypothermic-perfusion-actively cooling body temperature down to 28 to 32 degrees Celsius during post cardiac arrest has been favored by the majority of surgeons for both valve surgery and CABG (Coronary Artery Bypass Graft). However, many surgeons argue that hypothermia is an unnecessary convention if systemic circulation is uninterrupted with the use of CPB (Cardiopulmonary Bypass and cerebral perfusion is assumed to be adequate. On one hand, the use of normothermicperfusion (maintaining body temperature at around 37 degrees or allowing to drift down without active cooling) has not produced any solid evidence from neither clinical practice nor prospective randomized trials. Hypothermia may also be induced for several medical purposes. As such, cardiac arrests necessitate a reduction in body temperature in order to slow down the metabolism but the case in point also resulted into patient becoming bradycardic and electrolytes going down after attaining 32 degrees of active cooling. A few trials have indicated that hypothermic perfusion may be beneficial and that normothermic perfusion is potentially harmful. Martin et al. (1994) were the first to report an increased rate of postoperative stroke, both early and late, in CABG patients randomized to normothermic perfusion (actively warmed to 35 degrees Celsius or higher). These findings have been questioned, because the use of retrograde cardioplegia in these patients could have increased the risk of cerebral embolism. More patients with neurologic deficits were also found in the group randomized to normothermia by Mora et al. (1996), although NP testing did not support a difference in outcome between the two groups. Only one study so far has suggested an effect of temperature on NP performance. Regragui et al. (1996) studied 70 patients randomized to three temperature groups: 28 C, 32 C, and 37 C. Normothermia was found to result in worse NP performance than the other two groups. However, both the small numbers of patients and the method of analysis of NP deterioration in the study caution against accepting this finding. The application of hypothermia in a post cardiac arrest may also protect the brain and spinal cord (Schepens et al. 1994). However, Colon R. et al. (1987) had found that it can also cause its own complications especially when the hypothermia is profound (Svensson et al. 1993). As an alternative, some surgeons like Gott (1972) have provided adjunctive intraoperative perfusion with temporary arterial shunts and partial extracorporeal bypass (Bloodwell et al. 1968) or retrograde cerebral perfusion during hypothermic circulatory arrest. Furthermore, there are other techniques that have been tried like the preoperative radiographic assessment of critical intercostal arteries (Ueda et al. 1990), intraoperative monitoring of somatosensory and motor evoked potentials (Kieffer et al. 1989), use of oxygen free radical scavengers to prevent reperfusion injury (Laschinger et al. 1987), administration of inrathecal agents to improve collateral flow to the spinal cord (Gerhardt et al. 1987), and the use of neuroplegic solutions such as calcium channel blockers (Svensson et al. 1986). Conclusion In view of the problem, doctors that insist on starting the active cooling are in line with protocol guidelines. As a support for the previous discussion, increased brain temperature contributes to ischemic brain damage in patients post cardiac arrest. Much of the studies have shown that induced hypothermia or lowering brain temperature for even a few degrees will decrease ischemic damage and have contributed in the improvement of neurological outcomes. This factual and proven statement is enough to support induced hypothermia in post cardiac arrest considering the proper protocols in doing so. References Bernard, S. A. et al. (1997). Clinical trial of induced hypothermia in comatosed survivors of out of hospital cardiac arrest. Annals of Emergency Medicine. 30(2), pp. 146-153. ---, (2002). Treatment of comatosed survivors of out of hospital cardiac arrest with induced hypothermia. New England Journal of Medicine. 346(8), pp. 557-563. --- & Buist, M. (2003). Induced hypothermia in critical care medicine: A review. Critical Care Medicine. 31(7), pp. 2041-2050. Bloodwell, R. D. et al. (1968). Partial cardiopulmonary bypass for pericardiectomy and resection of descending thoracic aortic aneurysms. Ann Thorac Surg. 6, p. 46. Colon, R. et al. (1987). Hypothermic regional perfusion for protection of the spinal cord during periods of ischemia. Ann Thorac Surg. 43, p. 639. Gerhardt, E. B. (1987). Spinal cord protection during ischemia: Comparison of mannitol, thiopental, and free-radical scavengers. Surg Forum. 4, p. 197. Gott, V. L. (1972). Heparinized shunts for thoracic vascular operations [editorial]. Ann Thorac Surg. 14, p. 219. Hypothermia After Cardiac Arrest Group (2002). Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. The New England Journal of Medicine. 346(8), pp. 549-556. Kieffer, E. et al. (1989). Preoperative spinal cord arteriography in aneurysmal disease of the descending thoracic and thoracoabdominal aorta: Preliminary results in 45 patients. Ann Vasc Surg. 3, p. 34. Laschinger, J. C. et al. (1987). Monitoring of somatosensory evoked potentials during surgical procedures on the thoracoabdominal aorta. I: Relationship of aortic cross-clamping duration, SEPs, and incidence of neurologic dysfunction. J Thorac Cardiovasc Surg. 94, p. 260. Martin, T. et al. (1994). Prospective, randomized trial of retrograde warm blood cardioplegia: Myocardial benefit and neurologic threat. Annals of Thoracic Surgery. 57, pp. 298-302. Mora, C. T. et al. (1996). The effect of temperature management during cardiopulmonary bypass on neurologic and neuropsychologic outcomes in patients undergoing coronary revascularization. Journal of Thoracic and Cardiovascular Surgery. 112, pp. 514-522. Regragui, I. et al. (1996). The effects of cardiopulmonary bypass temperature on neuropsychologic outcome after coronary artery operations: A prospective randomized trial. Journal of Thoracic and Cardiovascular Surgery. 112, pp. 1036-1045. Schepens MAAM et al. (1994). Surgical treatment of thoracoabdominal aortic aneurysms by simple crossclamping. Risk factors and late results. J Thorac Cardiovasc Surg. 107, p. 134. Svensson, L. G. et al. (1993). Deep hypothermia with circulatory arrest. Determinants of stroke and early mortality in 656 patients. J Thorac Cardiovasc Surg. 106, p. 19. Svensson, L. G. et al. (1990). Appraisal of cerebrospinal fluid alterations during aortic surgery with intrathecal papaverine administration and cerebrospinal fluid drainage. J Vase Surg. 11, p. 423. Ueda, Y. et al. (1990). Surgical treatment of aneurysm or dissection involving the ascending aorta and aortic arch, utilizing circulatory arrest and retrograde cerebral perfusion. J Cardiovasc Surg. 31, p. 553. Read More