Delineating the pathophysiology of hypoxic ischemic brain injury after cardiac arrest to identify therapeutic targets

The main determinant of patient outcome following revival from cardiac arrest (heart stops pumping blood and oxygen to the body) is the brain injury that occurs in the days after hospital admission. This injury, termed hypoxic ischemic brain injury, partly arises from a lack of oxygen delivery to the brain after resuscitation. The cornerstone of post-cardiac arrest management has involved increasing the delivery of oxygen to the brain to facilitate recovery.  This logic assumes that the transport of oxygen from the blood system into the brain tissue is normal after cardiac arrest. I have recently demonstrated that this assumption is not true and in fact, in a large proportion of post-cardiac arrest patients demonstrate an inability to unload oxygen into the brain from the blood vessels. The mechanisms explaining this observation are unclear and not accounted by tests including CT and MRI scans. Therefore, another approach is required.

My project involves using a series of novel blood tests that arise from structures in the brain that are responsible for oxygen transfer. Identifying the precise structures that inhibit oxygen delivery into the brain will lead to further research aimed at identifying therapeutic targets.