In Canada, more than 50,000 cardiac arrest (i.e. “heart attack”) patients simultaneously suffer from brain injury due to reduced brain blood flow and oxygen delivery. Primary brain injury occurs following the initial reduction in brain blood flow following cardiac arrest, and in some cases, secondary brain injury occurs after brain blood flow is restored to normal levels. However, the physiological mechanism(s) responsible for secondary brain injury following cardiac arrest remain unclear, and the data available in humans are very limited. We hypothesize that a key contributor to secondary brain injury following cardiac arrest is due to consequential activation of the human body’s innate immune system, which signals for excess brain inflammation and results in cellular damage. The proposed investigation, which will be conducted at Vancouver General Hospital, aims to measure key biological markers to quantify brain inflammation in post cardiac arrest patients. The findings from this study will improve our overall understanding of the mechanism(s) that contribute to brain injury characterized by reductions in blood flow and will potentially identify potential therapeutic targets and improve quality of life in these patients.