Neuro Diseases Flashcards
normal CBF
50 mL/100 g brain tissue when CPP 50-150 mmHg
approx 750 mL/min (15-20% of CO)
factors that govern CBF (5)
- CMRO2
- CPP
- PaCO2/O2 tension
- various meds (esp. volatiles)
- intracranial abnormalities
rate of CMRO2
what % of total body O2?
3-3.8 mL O2/100 g brain tissue/minute
20% of total body O2
what is most cerebral O2 consumption used for?
to generate ATP for neuronal electrical activity
result of high O2 consumption + low O2 reserve
what happens if not restored ASAP?
unconsciousness in 10 seconds if perfusion stopped
if not restored in 3-8 min - ATP stores depleted, cellular injury and death can occur
2 things that decrease CMRO2
hypothermia
anesthetic agents
2 things that increase CMRO2
hyperthermia
seizures
CPP =
what is a normal value?
MAP - ICP
normally 60-110 mmHg
T/F - if a pt has an ICP > 30 but normal MAP, CPP won’t change
false - CPP and thus CBF can change (whatever that means)
effect of CPP on EEG:
- CPP < 50 mmHg
- CPP 25-40 mmHg
- CPP < 25 mmHg
- < 50 = slowing on EEG
- 25-40 = flat EEG
- < 25 = possible irreversible brain damage
what determines CPP beyond 50-150 mmHg
pressure-dependent
how do increases and decreases in BP impact arteries?
increased BP = arterial constriction
decreased BP = arterial dilation
Effects of CBF in normotensive pt:
- CBF 35 mmHg
- CBF 150 mmHg
(shouldn’t this be in mL or something? sos)
- CBF 35 mmHg = ischemia (nausea, dizziness)
- CBF 150 mmHg = vessels maximally constricted, fluid forced out of vessel = cerebral edema
how does HTN affect autoregulation curve
shifts to right
chronic HTN - lower limit shifts upward
autoregulation lost or impaired with (3):
- intracranial tumors
- head trauma
- volatile anesthetics
most important extrinsic influence of CBF
PaCO2
(directly proportional)
how does CBF change with PaCO2 changes
CBF changes approx 1-2 mL/100 g/min per mmHg change in PaCO2
what PaCO2 is associated with shifting the PaCO2/CBF curve to the left
< 20
may have EEG changes
how does decreased PaCO2 affect:
- CSF pH
- vessels
- ischemia
- ICP
- increased CSF pH
- vasoconstriction
- increased cerebral ischemia
- decreased ICP
how does increased PaCO2 affect:
- CSF pH
- vessels
- ischemia
- ICP
- decreased CSF pH
- vasodilation
- decreased cerebral ischemia
- increased ICP
CBF is not significantly affected by decreased PaCO2 until threshold of ____
50
3 major effects of hypocapnia that lead to tissue hypoxia
(picture on slide 10)
- vasoconstriction
- increased neuronal excitability
- CSF alkalosis
how does CSF alkalosis r/t hyperventilation lead to tissue hypoxia
alkalosis → oxyhgb dissociation curve L shift → decreased O2 delivery → tissue hypoxia
how does neuronal excitability r/t hyperventilation lead to tissue hypoxia?
increased excitatory amino acids → increased O2 consumption → tissue hypoxia
how does vasoconstriction r/t hyperventilation lead to tissue hypoxia?
vasoconstriction → decreased CBF → decreased O2 supply → tissue hypoxia
how does vasoconstriction r/t hyperventilation affect ICP
vasoconstriction → decreased CBF → decreased CBV → brain relaxation/decreased ICP
how does hypocapnia impact TBI or brain bleed
~unclear~
how does hypothermia affect CMRO2 and CBF
both decrease
how does hyperthermia affect CMRO2 and CBF
both increase
how does hct affect viscosity
decreased Hct = decreased viscosity (also decreases O2 carrying capacity)
increased Hct = increased viscosity, decreased CBF
suggested optimal Hct for cerebral O2 delievry
30%
how do brain blood vessels create a blood-brain barrier?
(pic on slide 13)
tight junctions (no pores) create the barrier
what things move easily across the BBB?
what things are restricted?
lipid-soluble things move easily - CO2, O2, H2O, most anesthetics
restricted: ionized or large molecular weight
conditions that disrupt BBB (8)
- severe HTN (chronic or acute, new onset)
- strokes
- trauma
- tumors
- infection
- hypercapniea
- hypoxia
- sustained seizures
if the BBB is disrupted, what is fluid movement dependent on?
hydrostatic pressure (not osmotic gradient)
major function of CSF
protect CNS against trauma
where is CSF formed?
choroid plexus of cerebral ventricles (mostly lateral)
2 ways CSF is produced
- ultrafiltration and secretion by cells of choroid plexus
- passage of water, electrolytes, and other things across BBB
she said she wouldn’t ask specifics about CSF flow through the brain but to be familiar with it? so peek at the pic on slide 16
:)
how much CSF do adults produce
21 mL/hr (500 mL/day)
total CSF volume
150 mL
what % of the cranial vault is made up by:
- brain
- blood
- CSF
- brain - 80%
- blood - 12%
- CSF - 8%
where is ICP measured?
lateral ventricles or over cerebral cortex
what is the Monroe-Kellie Doctrine?
any increase in one compartment (brain, blood, CSF) must be offset by equal reduction in another to avoid increased ICP
ICP values:
- normal
- mild increase
- moderate increase
- severe increase
- normal: 5-10 mmHg
- mild: 20-30 mmHg
- moderate: 30-40 mmHg
- severe: > 40 mmHg
blood pressure effects of cerebral blood volume are dependent on?
autoregulation of CBF
where is a subfalcine herniation?
what are the adverse effects?
cingulate gyrus under falx cerebri
compression of anterior cerebral artery → midline shift
where is a transtentorial herniation?
what are the adverse effects?
uncinate gyrus through tentorium cerebelli
brainstem compression → altered consciousness, gaze defects, ocular reflex defects, hemodynamic and resp failure → death
what is a transcalvarial herniation?
any area beneath a defect in the skull
what can herniate through foramen magnum
cerebellar tonsils
stupid question sry
where is an uncal herniation?
adverse effect?
medial portion of temporal lobe
causes oculomotor nerve dysfunction → pupil dilation, ptosis, lateral deviation of affected eye
s/s cerebral tonsils herniating through foramen magnum
cardiac and resp dysfunction indicating medullary dysfunction
leads to death
s/s increased ICP
HA, nausea, pupil dilation, blurred vision, decreased LOC, seizures, coma, blah blah
Cushing’s Triad
irregular respirations
increased BP
decreased HR
how do brain tumors directly and indirectly increase ICP?
directly d/t size
indirectly d/t edema in surrounding tissue
inner brain things that increase ICP (5)
- brain tumors
- brain bleeds
- brain hematoma
- infection (meningitis, encephalitis)
- aqueductal stenosis
inner brain things that increase ICP (5)
- brain tumors
- brain bleeds
- brain hematoma
- infection (meningitis, encephalitis)
- aqueductal stenosis
what is aqueductal stenosis?
what disorder is seen in ⅓ of these pts?
congenital narrowing of cerebral aqueduct connecting 3rd and 4th ventricles
⅓ have seizures
interventions to decrease ICP (9)
a bunch of ish but we already know this
- elevate HOB
- head neutral
- hyperventilation
- CSF drainage
- hypothermia
- hyperosmotic drugs
- corticosteroids
- cerebral vasoconstrictors
- HTN control
dose of mannitol to decrease ICP
20% mannitol
0.25-1 g/kg IV
cerebral vasoconstrictors that can decrease ICP
barbiturates
propofol
MAP goal when giving antihypertensives to decrease ICP
> 70
underlying mechanisms of seizure disorders
- loss of inhibitory activity
- enhanced release of excitatory amino acids
- enhanced neuronal firing d/t voltage-mediated Ca2+ current
