In 50% of EMS-treated sudden cardiac arrest cases, the heart is restarted and the patient is transferred to a hospital. Some are unstable and die in the emergency department. Of those who can be stabilized and admitted to hospital, more than half will die in hospital, most of brain death. To close this gap, our researchers are investigating:
The clinical pathophysiology of globally ischemic brains: Hypoxic ischemic brain injury (HIBI) after cardiac arrest (CA) is a leading cause of mortality and long-term neurologic disability in survivors. The pathophysiology of HIBI encompasses a heterogeneous cascade that culminates in secondary brain injury and neuronal cell death. This begins with primary injury to the brain caused by the immediate cessation of cerebral blood flow following CA. Thereafter, the secondary injury of HIBI takes place in the hours and days following the initial CA and reperfusion. Among factors that may be implicated in this secondary injury include reperfusion injury, microcirculatory dysfunction, impaired cerebral autoregulation, hypoxemia, hyperoxia, hyperthermia, fluctuations in arterial carbon dioxide, and concomitant anemia. Clarifying the underlying pathophysiology of HIBI is imperative and has been the focus of considerable research to identify therapeutic targets.
Neuroprotection of the brain during ischemia and reperfusion: the value of NA-1, a neuroprotective drug currently undergoing clinical evaluation in stroke in the FRONTIER trial for post-cardiac arrest global ischemia in whole animal models.
