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Báo cáo y học: Mild induced hypothermia after out-of-hospital cardiac arrest: persisting doubts about patient safet
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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Mild induced hypothermia after out-of-hospital cardiac arrest: persisting doubts about patient safety...
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Báo cáo y học: " Mild induced hypothermia after out-of-hospital cardiac arrest: persisting doubts about patient safet" Available online http://ccforum.com/content/11/4/420LetterMild induced hypothermia after out-of-hospital cardiac arrest:persisting doubts about patient safetyBhavesh M Patel, Alyssa B Chapital, Mohamed Y Rady and Joel S LarsonDepartment of Critical Care Medicine, Mayo Clinic Hospital, Mayo Clinic Arizona, 5777 East Mayo Boulevard, Phoenix, AZ 85054, USACorresponding author: Mohamed Y Rady, rady.mohamed@mayo.eduPublished: 27 August 2007 Critical Care 2007, 11:420 (doi:10.1186/cc6084)This article is online at http://ccforum.com/content/11/4/420© 2007 BioMed Central LtdSee related research by Pichon et al., http://ccforum.com/content/11/3/R71In a study of the endovascular cooling system Alsius stability [4]. The survival benefit for out-of-hospital cardiacCoolGard™ combined with the Icy™ venous catheter, Pichon arrest from an early intervention for coronary reperfusion andand colleagues concluded the effectiveness and safety of restoration of optimal cardiac performance substantiallymild induced hypothermia (MIH) after out-of-hospital cardiac exceeds the survival benefit from MIH [5].arrest resuscitation [1]. We are troubled because the studyhas reproduced several safety concerns about MIH that have Fourth, MIH can prolong and augment the activation ofnot been confronted. inflammatory cytokines [6]; manifesting with rebound hyperthermia upon re-warming (74% of MIH cases) [1]. TheFirst, the sixfold increase of the nosocomial bloodstream cytokine response to MIH can diminish the favorable neuro-infection rate (13% versus control 2%) is most probably protective effect, and can perhaps exacerbate acute organrelated to insertion of endovascular catheters for MIH [1]. injury.Bloodstream infection in patients with endovascular catheterscan become a significant cause of preventable morbidity and Fifth, the concurrent use of muscle relaxants in MIH maymortality [2]. conceal clinical signs of epileptic activity after cardiopulmonary resuscitation and hypoxic insult to the brain. ContinuousSecond, it is unclear why hypokalemia (75% of MIH cases) monitoring of the electroencephalogram is necessary towas dismissed as a factor for the incidence of cardiac detect and treat provoked epileptic activity, otherwisedysrhythmia [1]. Temperature changes induce electrolyte secondary neuronal injury can progress during MIH [7].shifts and thus influence the depolarization and repolarization Immediate neurophysiologic studies after cardiopulmonarytimes and the conduction velocity of action potentials within resuscitation suggest that MIH has a limited therapeuticthe myocardium, promoting aberrant conduction pathways. benefit for neurologic salvage or protection [8].Electrolyte abnormalities associated with MIH can influenceelectrophysiological parameters of the myocardium, triggering It is imperative to recognize that MIH as a treatment modalitydysrhythmia [3]. after cardiopulmonary resuscitation has a narrow safety margin, and its misapplication can lead to unintendedThird, it can be argued that MIH may have contributed to deleterious consequences [9]. Pichon and colleaguesrefractory cardiogenic shock and early death. MIH blunts the highlight several safety concerns that must be addressedmyocardial response to inotropic medications and increases before recommending the broad application of endovascularthe requirement for vasopressors to maintain hemodynamic cooling devices in clinical practice.Authors’ responseNicolas Pichon and Bruno FrançoisWe assent to the potential relationship between the develop- future specific studies may provide clarity about thisment of nosocomial bloodstream infection and MIH, and relationship. Moreover, we agree that hypothermia probablyMIH = mild induced hypothermia. ...
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Báo cáo y học: " Mild induced hypothermia after out-of-hospital cardiac arrest: persisting doubts about patient safet" Available online http://ccforum.com/content/11/4/420LetterMild induced hypothermia after out-of-hospital cardiac arrest:persisting doubts about patient safetyBhavesh M Patel, Alyssa B Chapital, Mohamed Y Rady and Joel S LarsonDepartment of Critical Care Medicine, Mayo Clinic Hospital, Mayo Clinic Arizona, 5777 East Mayo Boulevard, Phoenix, AZ 85054, USACorresponding author: Mohamed Y Rady, rady.mohamed@mayo.eduPublished: 27 August 2007 Critical Care 2007, 11:420 (doi:10.1186/cc6084)This article is online at http://ccforum.com/content/11/4/420© 2007 BioMed Central LtdSee related research by Pichon et al., http://ccforum.com/content/11/3/R71In a study of the endovascular cooling system Alsius stability [4]. The survival benefit for out-of-hospital cardiacCoolGard™ combined with the Icy™ venous catheter, Pichon arrest from an early intervention for coronary reperfusion andand colleagues concluded the effectiveness and safety of restoration of optimal cardiac performance substantiallymild induced hypothermia (MIH) after out-of-hospital cardiac exceeds the survival benefit from MIH [5].arrest resuscitation [1]. We are troubled because the studyhas reproduced several safety concerns about MIH that have Fourth, MIH can prolong and augment the activation ofnot been confronted. inflammatory cytokines [6]; manifesting with rebound hyperthermia upon re-warming (74% of MIH cases) [1]. TheFirst, the sixfold increase of the nosocomial bloodstream cytokine response to MIH can diminish the favorable neuro-infection rate (13% versus control 2%) is most probably protective effect, and can perhaps exacerbate acute organrelated to insertion of endovascular catheters for MIH [1]. injury.Bloodstream infection in patients with endovascular catheterscan become a significant cause of preventable morbidity and Fifth, the concurrent use of muscle relaxants in MIH maymortality [2]. conceal clinical signs of epileptic activity after cardiopulmonary resuscitation and hypoxic insult to the brain. ContinuousSecond, it is unclear why hypokalemia (75% of MIH cases) monitoring of the electroencephalogram is necessary towas dismissed as a factor for the incidence of cardiac detect and treat provoked epileptic activity, otherwisedysrhythmia [1]. Temperature changes induce electrolyte secondary neuronal injury can progress during MIH [7].shifts and thus influence the depolarization and repolarization Immediate neurophysiologic studies after cardiopulmonarytimes and the conduction velocity of action potentials within resuscitation suggest that MIH has a limited therapeuticthe myocardium, promoting aberrant conduction pathways. benefit for neurologic salvage or protection [8].Electrolyte abnormalities associated with MIH can influenceelectrophysiological parameters of the myocardium, triggering It is imperative to recognize that MIH as a treatment modalitydysrhythmia [3]. after cardiopulmonary resuscitation has a narrow safety margin, and its misapplication can lead to unintendedThird, it can be argued that MIH may have contributed to deleterious consequences [9]. Pichon and colleaguesrefractory cardiogenic shock and early death. MIH blunts the highlight several safety concerns that must be addressedmyocardial response to inotropic medications and increases before recommending the broad application of endovascularthe requirement for vasopressors to maintain hemodynamic cooling devices in clinical practice.Authors’ responseNicolas Pichon and Bruno FrançoisWe assent to the potential relationship between the develop- future specific studies may provide clarity about thisment of nosocomial bloodstream infection and MIH, and relationship. Moreover, we agree that hypothermia probablyMIH = mild induced hypothermia. ...
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