Table 1 Summary of mechanisms of secondary brain injury after hypoxic ischemic brain injury
From: Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model
Pathophysiology | Mechanisms | Consequences |
|---|---|---|
Microvascular dysfunction | Microthrombi, cerebral vasoconstriction, blood-brain barrier disruption | Increased cerebrovascular resistance, decreased CBF, decreased cerebral O2 delivery, vasogenic cerebral edema |
Cerebral edema | Vasogenic cerebral edema, cytotoxic cerebral edema | Increased ICP and decreased CPP, decreased CBF, herniation, brain death |
Anemia | Decreased arterial oxygen content | Cerebral ischemia |
Impaired autoregulation | Narrowed and right-shifted autoregulation | Pressure passive cerebral hemodynamics, cerebral ischemia and hyperemia |
Carbon dioxide | Hypocapnia-induced vasoconstriction, hypercapnia-induced vasodilation | Decreased CBF, cerebral ischemia, increased ICP, decreased CPP, decreased CBF |
Hyperoxia | Increased O2 free radicals | Neuronal cell dysfunction and cell death |
Hyperthermia | Increased CMRO2, decreased seizure threshold, induction of apoptosis | Neuronal cell metabolic crisis, cell death, nonconvulsive seizures, increased CMRO2, neuronal cell death |