[Pathophysiology of postcardiac arrest syndrome]

Postcardiac arrest syndrome is characterized by the following: 1) hypoxic-ischemic brain injury, 2) postresuscitation myocardial dysfunction, 3) systemic ischemia/reperfusion injury, and 4) the persistent precipitating pathology. Pathophysiologically, no flow during cardiac arrest leads to global ischemia of all tissues, which already initiates early inflammatory processes. Subsequently, reperfusion (during cardiopulmonary resuscitation and after return of spontaneous circulation) triggers a complex cascade of events, including systemic inflammation, endothelial activation and procoagulant processes and-in the presence of oxygen-the formation of tissue-damaging reactive oxygen species. Taken together this may cause microcirculatory disturbances and myocardial dysfunction leading to shock and hypoperfusion and ultimately to organ failure. Furthermore, disruption of the blood-brain barrier and cerebral autoregulation cause ongoing neuronal death. Ultimately, the exaggerated inflammation may lead to an immunoparalytic state, making survivors susceptible to severe (nosocomial) infections in the postresuscitation course.