Fig. 1
From: Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model
A schematic demonstrating the various microvascular and cellular pathophysiologic consequences which occur during the primary and secondary injury in hypoxic ischemic brain injury (HIBI). Decreased cerebral oxygen delivery manifests as reduced neuronal aerobic metabolism, causing reduced cellular adenosine triphosphate (ATP) production. Intracellular calcium accumulation leads to mitochondrial toxicity and further reduced ATP production. Inability to sustain cellular respiration results in cell death and apoptosis. Additionally, in the microvasculature, endothelial dysfunction leads to a porous blood-brain barrier, formation of cerebral edema, formation of microthrombi and limitation of cerebral blood flow with exacerbation of cellular ischemia. AQP 4 Aquaporin-4, RBC Red blood cells, WBC White blood cells