Post Cardiac Arrest Syndrome in Adults and Pediatrics

Abstract

The high mortality rate of patients who initially achieve return of spontaneous circulation(ROSC) after cardiac arrest can be attributed to a unique pathophysiological process that involves multiple organs. The unique features of post cardiac arrest pathophysiology are often superimposed on the disease or injury that caused the cardiac arrest, as well as underlying comorbidities. The 4 key components of post–cardiac arrest syndrome are: Post–cardiac arrest brain injury, post–cardiac arrest myocardial dysfunction, systemic ischemia/reperfusion response and Persistent precipitating pathology. Post–cardiac arrest brain injury is considered a common cause of morbidity and mortality. The mechanisms of brain injury caused by cardiac arrest and resuscitation include excitotoxicity, disrupted calcium homeostasis, free radical formation, pathological protease cascades, and activation of cell-death signaling pathways. Several factors can potentially compromise cerebral oxygen delivery and cause secondary brain injury in the hours to days after cardiac arrest. These factors include hypotension, hypoxemia, impaired cerebrovascular autoregulation, brain edema, pyrexia, hyperglycemia, and seizures. Seizures may increase the cerebral metabolic r