Preventing Reperfusion Injury During Cardiac Arrest

Reperfusion injury is linked with several pathophysiological pathways leading to cell apoptosis. The metabolic processes associated with reperfusion injury are well described in the setting of a myocardial infarction and CVA and more recently in the setting of cardiac arrest. These processes include pro-apoptotic signaling and inflammatory response. The mitochondria plays a critical role and mitochondrial transition pore (MTP) opening and calcium release are important determinant in the apoptosis signaling.1,2 Increased no-flow and low-flow duration as well as poor quality of CPR are associated with more severe reperfusion injury.3 Return of spontaneous circulation is achieved in 20–40% of out-of-hospital cardiac arrests (OHCA) with resuscitation attempted.3 For these patients, reperfusion injury is responsible for increased in-hospital mortality, and consequently 40–50% of them will survive to be discharged from hosptial.3,4 Moreover, survivors frequently have persistent subtle cognitive impairment and some have severe neurological deficit.5,6 In addition, some have persistent heart failure. Therapeutic strategies developed to improve cardiac arrest survival (e.g., epinephrine use, extracorporeal CPR, etc.) may be successful in terms of increased survival but are often limited by the increase rate of reperfusion injury associated with prolonged CPR.7 Several strategies targeting different pathways have been developed in an effort to limit these lesions. First, optimiz...
Source: JEMS Patient Care - Category: Emergency Medicine Authors: Tags: Cardiac & Resuscitation Top Story Exclusive Articles Heart of America Source Type: news