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
a bunch of shit can cause seizures. we know that
examples:
- genetic predisposition
- brain tumor/trauma
- infection/febrile illness
- hypoxia
- drug OD/withdrawal
- fatigue, stress
- methohexital
- ketamine
- demerol
- metabolic defects
metabolic defects that precipitate seizures
- hyper/hyponatremia
- hypomagnesemia
- hypocalcemia
- hypoglycemia
- alkalosis
anesthesia drugs that can precipitate seizures
- methohexital
- ketamine
- demerol
manifestations of partial seizures
motor, sensory, autonomic, or psych symptoms
where do generalized seizures originate
(plz reword)
bilaterally symmetric electrical activity
what is a petit mal seizure?
aka absence seizure
transient lapse in consciousness
manifestations of a grand mal seizure
aka tonic-clonic seizures
loss of consiousness → clonic activity → tonic motor activity
status epilepticus is a medical emergency
next
focus of preop eval for pts with seizures
- cause/triggers
- type of seizure
- medications
- last seizure
T/F - if a pt just has partial seizures it’s not as important that they continue AEDs throughout periop period
false - even a partial sz can progress to generalized sz
meds to avoid in pts with seizure disorders
- ketamine
- methohexital
- demerol
- atracurium/cisatracurium in large doses (metabolites)
NMB dosing considerations for pts with seizure disorders
probably will need to increase dose d/t hepatic enzyme induction (from sz meds)
meds and doses to terminate a seizure
- 50-100 mg Propofol
- 500-1000 mg Dilantin (slowly)
- 1-5 mg midazolam
most common causes of adult seizures
- mostly structural lesions (head trauma, tumors, stroke)
- metabolic abnormalities (liver failure, uremia, hypoglycemia, hyopcalcemia, drug tox, drug/ETOH withdrawal)
pt population assoc. with idiopathic seizures
kiddos (can carry into adulthood)
what is Parkinson’s disease
most common disorder involving motor tracts of EPS (controlled by basal ganglia and cerebellum)
what is primary parkinson’s?
degenerative disorder of substantia nigra
interferes with dopamine pathways to basal ganglia
onset > 50 yrs old
what causes secondary parkinson’s?
trauma, drugs, infection, toxins
(usually reversible)
principle feature of Parkinson’s
degeneration of dopaminergic pathways (inhibitory) and relative excess of cholinergic activity (excitatory)
classic signs of Parkinson’s
~trigger warning~
- skeletal muscle tremors
- rigidity
- akinesia of facial muscles
- often oily skin, seborrhea
- diaphragmatic spasms
- eventually includes muscles of chewing/swallowing
- upper airway involvement may restrict airflow
where does rigidity first occur in Parkinson’s
neck muscles
describe skeletal muscle tremors with Parkinson’s
rhythmic, usually at rest
usually disappear with voluntary movement
pill-rolling tremor
goal of parkinson’s treatment
increase concentration of dopamine in basal ganglia or decrease effects of ACh
side effects of L-dopa (Sinemet, Parcopa)
- dyskinesias
- confusion
- headache
- hallucinations
- orthostatic hypotension
- increased contractility
MOA of decarboxylase inhibitors for Parkinson’s
prevents conversion of levodopa to dopamine in periphery to optimize conversion in CNS
3 general med classes used to treat Parkinson’s
- Levodopa-dopamine precursors
- decarboxylase inhibitor
- anticholinergics
surgical treatment of Parkinson’s
deep brain stimulation - stimulates various nuclei in basal ganglia to relieve/help with tremor
intraop anesthesia concerns for deep brain stimulation treatment of Parkinson’s
- they’re awake :(
- sitting position - VAE risk
- avoid propofol/benzos
- avoid oversedation (little access to airway)
why should propofol and benzos be avoided with deep brain stimulation (Parkinson’s treatment)
alter recordings of nuclei and thus stimulation of appropriate place (brain area?)
meds to avoid in pts with Parkinson’s
- ketamine
- metoclopramide
- phenothiazines (Compazine, Thorazine)
- butyrophenones (Haldol, Droperidol)
- opioids (use carefully? predisposed to rigidity)
- succs (rare reports of hyperkalemia)
dosing considerations for nondepolarizing NMBs in Parkinson’s
generally normal
most common neurodegenerative disease
Alzheimer’s
how is Alzheimer’s characterized
slow decline in intellectual function (5 + years)
affects memory, judgment, decision making, emotional lability
late signs of Alzheimer’s
extrapyramidal symptoms
apraxias
aphasia
why do pts with Alzheimer’s have altered responses to many anesthetic drugs?
loss of gray matter
how does Alzheimer’s affect brain?
marked cortical atrophy with ventricular enlargement
patho of Alzheimer’s
proteins in neurons become twisted and distorted “neurofibrillary triangle”
“senile plaques” deposit that disrupt impulse transmission, esp. in cerebral cortex & hippocampus
consent considerations for Alzheimer’s pts
must get from someone legally able to provide - pt may not have cognitive ability to consent
pts with Alzheimer’s can have new-onset, temporary impairment after anesthesia that lasts how long?
1-3 days
considerations for giving anticholinergics to Alzheimer’s pts
avoid centrally acting (atropine, scopolamine) - add to confusion
use glycopyrrolate if needed
use of regional anesthesia in Alzheimer’s pt
no contraindications but consider how you will give anxiolysis and potential side effects
what is multiple sclerosis?
reversible demyelination at random and multiple sites in brain and spinal cord
inflammation eventually causes scarring
causes and etiology of MS
may be autoimmune initiated by a virus
primarily affects females 20-40 yrs old (2:1 vs. males)
central symptoms of MS
- fatigue
- cognitive impairment
- depression
- unstable mood
GI/GU symptoms of MS
- incontinence
- diarrhea or constipation
- urinary frequency or retention
airway symptoms of MS
- dysarthria
- dysphagia
visual symptoms of MS
- nystagmus
- optic neuritis
- diplopia
musculoskeletal symptoms of MS
- weakness
- spasms
- ataxia
sensation symptoms of MS
- pain
- hypoesthesias
- parasthesias
how is MS diagnosis confirmed?
CSF or MRI
if a pt with MS comes in for elective surgery and they just got over an exacerbation yesterday, is it ok to proceed?
nah - give them a biscuit
considerations for NMBs in pts with MS
if paresis or paralysis - no succs
can peripheral nerve blocks be used on pts with MS?
yup
can conduction still occur across demyelinated axons in MS pts?
yes - but affected by many things, including temperature
what is ALS?
neurodegenerative, rapidly progressive weakness of both upper and lower motor neurons
when does ALS typically present?
symptoms?
usually present in 50s or 60s
muscular weakness, atrophy, fasciculations, spasticity
anesthesia concerns for ALS pts
- aspiration risk
- no Succs (hyperkalemia risk)
- after 2-3 years, progresses to all skeletal muscles and pt has ventilation failure
what is Guillain Barre syndrome
what can cause it?
immunologic reaction against myelin sheath of peripheral nerves → sudden onset of paralysis, areflexia, and paresthesias
assoc. with URI/GI infections, Hodgkin’s disease, HIV
s/s Guillain Barre
weakness or paralysis that starts in the legs and spreads cephalad over several days
types of Guillian Barre
- acute inflammatory demyelinating polyneuropathy (75%)
- acute motor axonal neuropathy
- acute motor and sensory axonal neuropathy
peak disability of GBS
10-14 days
treatment of GBS
some respond to plasmapheresis
anesthesia concerns for GBS pts
~trigger warning, feel free to break this up~
- labile ANS - prepare for dysrhythmias and ANS instability
- respiratory insufficiency/paralysis, pharyngeal muscle weakness
- no succs
- regional is controversial
- hypotension with position change or small blood loss
- exaggerated HTN with laryngoscopy
common autonomic dysfunctions in GBS pts
- wide change in BP
- profuse diaphoresis
- gastroparesis
- tachycardia
- dysrhytmias
cycle of events leading to CVA
cell hypoxia → edema → activation of excitatory amino acids → creation of free radicals → calcium influx → (cell hypoxia)
what causes a CVA?
cerebral perfusion is interrupted, depriving brain of O2 and glucose
most common surgeries r/t CVA
- open heart for valve disease
- surgery on thoracic aorta
mortality with intraop stroke
25%
risk for periop stroke with GA + history of CV disease
0.4-3%
***prior stroke or hx of TIA = increased risk of periop CVA***
:|
risk factors for CVA (10)
- HTN
- diabetes
- cigarettes
- drug abuse
- age > 75
- CAD
- hyperlipidemia
- Afib
- hereditary
- prior stroke/hx TIA
conditions assoc. with thrombotic CVA
- atherosclerosis
- diabetes
- hypercoagulability
- dehydration
- arteritis
- polycythemia vera
- HTN
what causes a thrombotic CVA?
arterial occlusion caused by thrombi in carotid or cerebral vessels
what causes an embolic CVA?
fragments break from thrombi formed outside brain
conditions assoc. with embolic CVA
- Afib
- endocarditis
- prosthetic valve
- carotid disease
- valvular and aortic surgeries
most common cause of hemorrhagic CVA
other causes?
HTN (60-80%)
also - ruptured aneurysm, AVM, bleeding tumor, coag defects
headaches often assoc. with what type of CVA?
hemorrhagic
treatment of a thrombotic or embolic stroke
IV fibrinolytic within 3 hours of symptom onset
T/F - a pt with a suspected thrombotic or embolic stroke should be given a fibrinolytic ASAP
(this seems like an issue for the ER but)
false - don’t give until CT scan has r/o hemorrhage
when should a suspected stroke pt not be given fibrinolytics
- hx or evidence of bleed
- known AVM, aneurysm, neoplasm
- plt < 100
- INR > 1.7
- stroke, NSGY, or head trauma within past 3 months
NMB considerations for CVA
resistance in paretic limb
monitor TOF in nonparetic limb
no succs
effects of CVA in the area of infarct
- loss of autoregulation
- loss of CO2 responsiveness
- loss of BBB integrity
BP goal for HTN pt with CVA
keep slightly higher than normal
pts with cerebrovascular disease at greatest risk for stroke
- open heart procedures with valvular diseases
- CAD with ascending aortic atherosclerosis
- diseases of thoracic aorta
risks for pts with cerebrovascular disease in noncardiac surgeries
risks assoc. with hyper or hypotension
effects of pulse pressures > 80 mmHg
endothelial injury → hypoperfusion or embolism
how does HTN affect BBB
sustained HTN = BBB breakdown
how long does it take for blood flow abnormalities, BBB, and CO2 responsiveness to heal/resolve after a stroke?
blood flow abnormalities - 2 wks
BBB/CO2 responsiveness - 4 wks
consults required before proceeding with elective surgery in pts with hx TIA
neuro and CV
cases we might see pts with cerebrovascular diseases
- emboli removal
- carotid endarterectomy
- endovascular procedures
- hematoma evacuation
- decompressive crani
things to have ready for a pt with cerebrovascular disease
art line
IV vasodilators
beta blockers
symptoms of spinal cord disorders
- loss of sensation
- weakness/paralysis of extremities
- reflex changes (hyper or hypo)
- bladder/bowel incontinence
- back pain
- muscle spasms
causes of spinal cord disorders (3)
- trauma
- infection/abscess
- autoimmune disorders
airway considerations for spinal cord disorders
- keep head neutral
- possible obstruction/edema
- RLN damage
CV issues in pts with spinal cord disorders
- reflex bradycardia
- arrythmias
- hyper and hypotension
which CN is responsible for each of these s/s of increased ICP?
- blurred vision
- inability to adduct eyes
- inability to abduct eyes
- blurred vision - CN II
- adduct - CN III
- abduct - CN VI
what are watershed infarcts?
hypoperfusion and necrosis in areas most distal to arterial blood supply
(??? sos her explanation didn’t really make sense to me so I googled it and its kinda different from what she said)
