HIBI - Pathophysiology
Subclassification: pediatric, in-hospital (IHCA, higher ROSC), and out-of-hospital (OHCA, lower survival). "Two-Hit" Model: Primary[β¦] brain injury from ischemia during pulselessness β made worse by reperfusion[β¦] injury via ROS and inflammation.
Impaired aerobic metabolism β loss of ATP β anoxic depolarization β cytotoxic edema[β¦].
Increased anaerobic metabolism β lactate accumulation β intracellular acidosis β increased intracellular Ca+2 β mitochondrial toxicity[β¦].
Disproportionately hits metabolically active structures: cortex, hippocampus, basal ganglia, thalami, cerebellar vermis[β¦].
Secondary[β¦] brain injury: neuroinflammation from imbalance between O2 delivery and metabolic demand.
Triggers: fever, seizures[β¦], cerebral edema, and disrupted autoregulation.
The lower limit of cerebral autoregulation shifts right[β¦] or is absent β CPP insufficient even at normal MAP.

