Mechanisms of Cerebral Injury
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show | Brain accounts for 20% of body oxygen consumption
Depletion of oxygen occurs within 10 sec of cessation of blood flow
Conversion to anaerobic metabolism occurs within 2-4 minutes
ATP supplies exhausted within 4-5 minutes
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Hypoxia | show 🗑
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show | Severe or total loss of blood supply
Can be to the entire brain (cardiac arrest) or to a focal area (stroke)
Small focal areas have advantage of collateral circulation
Global or Focal
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show | if 1 vessel is blocked due to a stroke, cells that are further away, but close to another blood vessel can get blood supply from other vessel feeding area nearby. It’s getting a lower pressure of blood, but it’s getting some.
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show | Blood flow inadequate to meet the metabolic needs of the entire brain
Cardiac arrests, shock, or severe dysrhythmias
Failure of Na/K ATPase pump causes neuronal edema
Calcium influx causes release of intracellular digestive enzymes
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Global Ischemia (cont) | show 🗑
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Excitotoxicity Amino Acids | show 🗑
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show | NMDA-subtype of glutamate receptors, opens and allows sodium and calcium to enter the cell-results in prolonged action potentials, swelling
iontropic receptor which allows na and ca to passively move into cell– edema & prolonged action potential
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Excitotoxicity Calcium | show 🗑
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Excitotoxicity excess Glutamate | show 🗑
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Excess Glutamate and O2 | show 🗑
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show | Return of oxygen to ischemic cells can lead to oxygen free fradical formation, and allows inflammatory cells to enter the ischemic area
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show | Leads to lipid peroxidation of the cell membrane, which activates the arachadonic acid cascade, leading to more free radical formation
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Reperfusion Injury | show 🗑
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show | Calcium channel blocker that is preferential for cerebral blood vessels. Approved for prophylaxis vs brain injury after intracranial aneurysm rupture
Being investigated for prevention of some of the deleterious effects of excess glutamate/excitotoxicity
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Intracranial Pressure | show 🗑
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Intracrania Pressure s/s | show 🗑
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show | Bradycardia, hypertension (with widening pulse pressure), and irregular respiratory pattern
Pulse pressure: difference between sys and diastole– so systolic will raise and diastolic won’t
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Monroe-Kellie's Hypothesis | show 🗑
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Modified Monroe-Kellie Hypothesis | show 🗑
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Cerebral Perfusion Pressure (CPP) | show 🗑
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Artificially raise Blood Pressure | show 🗑
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Brain Herniation General | show 🗑
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show | Falx Cerebri: between hemispheres
Tentorium Cerebelli: above cerebellum
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show | Cingulate Herniation (subfalcine herniation): Cingulate gyrus beneath the falx cerebri. Greatest danger from compression of blood vessels
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show | Uncal Herniation (transtentorial herniation): : Medial aspect of temporal lobe protrudes over the tentorial edge. Ipsilateral pupil dilatation. Can interfere with RAS
Ipsilateral: pupil dilated with ICP, they maybe have herniation of that side
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show | Central Herniation: Downward displacement of hemispheres, basal ganglia, diencephalon and midbrain through tentorial incisura. Slowly dilating pupils
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show | Tonsillar Herniation: Cereballar tonsils through foramen magnum, compression of medulla. Less common but high mortality in short period of time. See changes in HR, BP, constricted pupils, ataxic breathing.
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Cerebral Edema | show 🗑
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Institial Cerebral Edema | show 🗑
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Vasogenic Edema | show 🗑
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show | Increase in fluid matter in intracellular space, mostly gray matter. Caused by water intoxication, severe ischemia, hypoxia, acidosis, and brain trauma.
Cause: water intox, dilutional hyponatremia
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show | Corticosteroid therapy for localized edema (such as inflammation around a tumor).
Controversial in use of generalized edema
Unsure of mechanism of action, but appears to stabilize the cell membrane and scavenger free radicals
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Mannitol (Osmitrol) | show 🗑
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show | Apendymals: coriod plexus in 2 lateral vent & will travel down into 3rd vent, thru aqueduct into 4th vent & has openings that allow it to free float down spinal cord & around the brain
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Noncommunicating Hydrocephalus | show 🗑
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Communicating Hydrocephalus | show 🗑
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