Table 2 Pathophysiologic summary of cerebral reperfusion injury after cardiac arrest
From: Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model
Pathophysiology | Mechanisms | Consequences |
|---|---|---|
Endothelial dysfunction | Impaired vasomotor control of blood flow, microthrombi formation, blood-brain barrier disruption | Impaired blood flow in microcirculation and limited oxygen delivery, cerebral edema |
Free radical formation | Activation of lytic cellular enzymes | Neuronal apoptosis and cell death |
Intracellular Ca2+ accumulation, | Mitochondrial toxicity, activation of cellular lytic enzymes | Reduced adenosine triphosphate production, cell death, apoptosis |
Impaired nitric oxide, | Vasoconstriction, “no reflow” | Reduced cerebral blood flow, cerebral ischemia |
Excitatory neurotransmitter release | Glutamate release | Excitotoxicity, seizures, apoptosis, cell death |