Neuro Flashcards
Cerebral metabolism
Brain consumes 20% of total body oxygen –> most used to generate ATP for neuronal activity
CMRO2
50 mL/min
- greatest in the grey matter of cortex
Main energy for brain?
glucose ~ 5 mg/100g/min
- glucose transport into the brain independent of insulin
ketones during starvation
Cerebral blood flow
varies w/ metabolic activity = parallels CMRO2
50 mL/100g
CBF governed by CMRO2, CPP, PaCO2, PaO2
CBF regulation
- Cerebral Perfusion Pressure = MAP-ICP
- Autoregulation
- Extrinsic Mechanisms
Cerebral Perfusion Pressure
~80-100 mmHg
MAP - ICP
Intracranial Pressure
~10 mmHg
Autoregulation of CBF
cerebral vasculature dilates/constricts as necessary
- autoregulation between 60-160 mmHg
- drop in CPP = vasodilation to increase blood flow
- rise in CPP = vasoconstriction to decrease blood flow
Relationship between pressure and volume of CBF
1 mmHg = 1 mL of blood
Extrinsic mechanisms of blood flow
CBF is directly proportional to PaCO2
- this is secondary to changes in CSF [H+]
*only marked changes in PaO2 result in blood flow changes
Temperature effect on CBF
hypothermia = reduced CMR + CBF (protective) hyperthermia = increased CMR + CBF
Responsiveness of brain areas to CO2
Cerebrum > cerebellum > spinal cord
Blood brain barrier
vascular junctional endothelial cells in cerebrum are nearly fused together
- lipid bilayer allows lipid soluble substances through
Plasma hypertonicity effect on BBB
water moves out of brain (shrink)
Plasma hypotonicity effect on BBB
water moves into brain (swell)
Sustained increases in ICP
lead to herniation –> skull and contents are a rigid structure
- compensation of reducing CBF by vasoconstriction is quickly maxed out
Transmural pressure on an aneurysm?
with a large acute drop in ICP (CSF leak/drain) the MAP can lead to an aneurysm rupture
Hyperventilation effect on ICP?
Dropping the PaCO2 will lead to a reduction in CBF and reduced ICP –> this will last approximately 6 hrs
Volatile effects on CNS
- All volatiles reduce CMR and CMRO2 (protective)
2. All cause dilation of cerebral vasculature –> increase CBF
IV Anesthetic effects on CNS
- Reduce CMR and CMRO2 (protective)
2. Cerebral vasoconstriction –> reduce CBF and therefore reduce ICP
Ketamine effects on CNS
- No change in CMR and CMRO2
- Dilates cerebral vasculature and increases CBF and ICP
*However, NMDA antagonism may be protective against neuronal injury (blocks glutamate)
Opioids effect on CNS
not much except respiratory depression can lead to increase PaCO2 and thus increase CBF and ICP
Vasopressors
with normal autoregulation –> no effect really
Vasodilators
cerebral vasodilation –> increased CBF and ICP
Cerebral Ischemia Pathophysiology
brain utilized O2 reserves very quickly –> ischemia starts quickly
- ion derangements release glutamate which activates NMDA –> Ca2+ entry into cells –> damage to neurons