10. Neuro Flashcards
cerebral O2 consumption
20%
CMRO2
3-8 mL/100g/min
or 50 mL/min
where is CMRO2 the highest?
grey matter
what % of brain is gray?
40%
what % ofthe brain is white?
60%
total cerebral blood flow
15-20% of total CO
what ensures cerebral perfusion
redundancy via collateral flow in the circle of willis
CPP =
CPP = MAP - ICP
or
CPP = MAP - CVP
normal CPP
80-100 mmHg
cerebral autoregulation
60-160 mmHg
what do CPP < 50 mmHg indicate?
slowing EEG
cerebral PaCO2
20-80 mmHg
what crosses BBB
CO2
what does not cross BBB
ions
does met acidosis affect CBF
no
what is hypothermia impact on CBF and CMRO2
decr CBF
decr CMRO2
decr 10c causes
50% decr in CMRO2
incr 10c causes
2x CMRO2
what is the main determinent of viscosity?
HCt
what impacts tight junctions
size
charge
lipid solubility
protein binding
where is CSF produced
choroid plexus
ependymal cells of ventricles
CBF leak
CSF production per day
500 mL/day
CSF total volume
150 mL
CSF is _____ to plasma
isotonic to plasma
incr ICP compensatory mechanisms
CSF displace to spinal cord
incr CSF absorb
decr CSF production
decr cerebral blood vol
incr ICP can be indicated by what on radiology scans
> 0.5cm midline shift
midline shift is measures off of the
corpus collosum
normal CSF pressure
10 mmHg
what ICP triggers decr in cerebral blood vol?
ICP > 60 mmHg
iso CMR
decr
iso CBF
incr
iso CSF production
no change
iso CSF absorb
incr
iso CBV
incr
iso ICP
incr
des CMR
decr
des CBF
incr
des CSF
incr
des CSF absorb
decr
des CBV
incr
des ICP
incr
sevo CMR
decr
sevo CBF
incr
sevo CBV
incr
sevo ICP
incr
nitrous CMR
decr
nitrous CBF
incr
nitrous CSF
no change
nitrous CSF
no change
nitrous CBV
no change
nitrous ICP
incr
barbituates CMR
decr
barbituates CBF
decr
barbituates CSF
no change
barbituates CSF absorb
incr
barbituates CBV
decr
barbituates ICP
decr
etomidate CMR
decr
etomidate CBF
decr
etomindate CSF
no chagne
etomidate CSF absorb
incr
etomidate CBV
decr
etomidate ICP
decr
propofol CMR
decr
propofol CBF
decr
propofol CBV
decr
propofol ICP
decr
benzos CMR
decr
denzos CBF
decr
benzos CSF
no change
benzos CSF absorb
incr
benzos CBV
decr
benzos ICP
decr
ketamine CMR
no change
ketamine CBF
incrketa
ketamine CSF
no change
ketamine CSF absorb
decr
ketamine CBV
incr
ketamine ICP
incr
opioids CMR
no change
what do opioids change?
incr CSF absorption
lidocaine CMR
decr
lidocaine CBR
decr
lidocaine CBV
decr
lidociane ICP
decr
which inhaled agent has greatest effect on autoregulation
halothane
which inhaled agent has best CSF production/absorption dynamic
iso
most cerebral protective drug
barbituates
which drug can have possible seizure activity
etomidate
isoelectric
minimal brain activity
luxury perfusion
decr cerebral met demand
incr CBF
circ steal
ischemic areas max vasodilation
agents incr CBF
blood shunted away from ischemic areas
main goal for cerebral protection
incr O2 delivery
decr further decline
hypothermia effects
decr metabolic and basal rates
anesthetic effects
decr metabolic rates
nimodipine effects
prevents vasospasm
cerebral protection: carbia
normocarbia
cerebral protection avoid
avoid:
hTN
elevated CVPs
hyperglycemia
eeg
summation of excitatory and inhibitory postsynaptic potentials of cerebral cortex
EEG uses
ID inadequate BF to cortex
guide to reduction of cerebral metabolism
predict neuro outcome after brain injury
guage depth of anesthetic
fastes human brain waves
gamma
32-100Hz
slowest brain waves
delta
0.5-4 hz
brain wave
fast
gamma
beta
alpha
theta
delta
slow
eeg should be correlated with what
EKG
EEG changes with age
amplitude decr with ageq
ischemia on EEG
slow freq
preserved amplitude
CBF ischemic threshold
18
CBF infarction threshold
12
CBF normal
35-50
what is the difference between BIS 2 or 4 channel
BIS 4 can differentiate between hemispheric differences
BIS isoelectric
0
BIS GA
40-60
BIS MAC
60-80
BIS awake
100
BIS liitations
agents
age
hypothermia
neuro impairment
interference
ketamine ____ electric activity
incr
evoked potentials test
neural pathways
subcortical function
evoked potentials look at
amplitude
latency
ampliotude
voltage of signal
latency
time to illicit signal
Sensory evoked potentials
SSEPs
BAEPs - click
VEPs - goggles
which sensory evoked potentials are monitored with MEPs
SSEPs
which monitoring can you paralyze
sensory evoked potentials can be paralyzed
MEPs
TMEPs
SMEPs
stimulus needed for transcrania motors
> 400V via screw needle
who initiates spinal motor evoked potentials
surgeon directly stimualtes spinal cord
generally, all sedative and inhalational agents _____ amplitude and ________ latency
decr amplitude
incr latency
burst suppression dosing inhalational
> 1.5 MAC
which drugs cannot achieve burst suppression even at high doses?
ketamine
benzos
opiates
nitrous
IV vs inhalational effect on evoked potentials
IV have less effect than inhalational
combination of drugs effect on evoked potentials
combination of drugs is additive
which evoked potentials are resistant to the effects of anesthetic gases
subcortical SEPs
(bc they have less synapses)
which VA is more inhibitory at higher doses
Des is more inhibitory than sevo at higher doses
hypoxia EEG
slows frequency
absence of electrical activity
hypotension EEG
bilateral
non specific
hypothermia EEG
dose depended suppression
what temperature has complete suppression
15-18C
hypotension effect on SSEPs
decr in amplitude
no change latency
hypotension effect on BAEPs
no change (high resistance)
hypothermia effect on evoked potentials
decr amplitude
incr latency
radiculopathy
nerve root compression
spondylosis
wear on bone or cartilage
which spine surgery requires vascular surgeon
ALIF
which spine surgery can cause tracheal compression and damage to RLN
ACDF
POVL
perioperative vision loss
POVL risk factors
time
large EBL
hTN
DM
obesity
smoking
neurogenic shock
trauma with transection cephalad to T6
disrupts descending sympa tracts
neurogenic shock has unopposed _____
unopposed parasympathetic activity
== HD instability
treat neurogenic shock
volume
+ norepi / vasopressin
AH T6
85%
AH T10
rare
AH management
decr afferent activity
how do you decr afferent activity in AH
regional anesthesia
high degree of anesthesia
AH adjuncts
clevidipine
hydralazine
propofol
AH and AD present with
unihibited sympathetic response below transection
reflex brady
cutaneous vasodilation
high afterload state
high afterload symptoms
pulm edema
LV overload
seizure
arrythmias
supratentorial
higher brain function
supratentorial mass SE
incr seizures
hemiplegia
aphasia
infratentorial
balance
proprioception
infratentorial mass SE
cerebellar dysfunction
brainstem compression
cerebellar dysfuncrtion SE
ataxia
nystagmus
dysarthria
brainstem compression SE
cranial nerve palsy
altered consciousness
resp abnormalities
oldes structure in brain
brainstem
cranial mass pre-op exams
mentation
sensory
motor
what should you avoid in cranial mass excision
pre-op versed
- obscures neural exam
- incr hypercarbia == incr ICP
cranial mass pts will have what abnormal labs
hyperglycemia
hypernatremia
ventriculostomy
drainage tube that surgeon places into ventricle of brain
ventriculostomy functions
drain CSF
monitory CSF pressure (measure ICP)
venticulostomy height
level of external acoustic meatus
what pressure is needed for ventriculostomy to drain
10 cmH2O
which paralytic can incr ICP
sux
(transient)
fluids for cranial mass pt
limited to prevent cerebral edema
HTN in cerebral pts
incr brain mass
incr EBL
hTN in cerebral pts
incr intra-op ischemia
hypocarbia ____ CBF
decr CBF
hypercarbia _____ CBF
incr CBF
hyperventilation will _____ CBF and ICP
transiently decr CBF and ICP for 6-8 hrs
biot
deep breath with periods of apnea
cheyne-stokes
varying periods of breaths
biot causes
spinal meningitis
head injury
cheyne stokes causes
brain tumors
injuries
brain stem functions
breathing
consciousness
BP/HR
sleep
functional/stereotactic procedures are used to treat
parkinsons
epilepsy
lesions (broca area)
where do aneurysms present
arterial bifucations
mortality for cerebral aneurysm rupture
33%
cerebral aneurysm treatment
coiling
clipping
AV malvormation
fistula in brain
AV malformation SE
extensive blood loss
anuerysm clipping requires a
type and cross
2 units of PRBCs in room
art line
MAP goal for unruptured aneurysm
60-80 mmHg
EtCO2 goal for unruptured aneyrusym
35 mmHg
(normocarbia)
temporary aneurysm clipping requires
cool pts to 35-45 deg
what is a temporary clip trial
to test how well the pt tolerates the clipping
what does anesthesia need to ensure prior to temp clipping
achieve burst suppression
circ arrest (longer duration)
temp clip MAP
90-100 mmHg
temp clip removed MAP
60-80 mmHg
what can be used to ensure burst suppression
150-250 mcg/kg/min propofol
what is ICG used for
to confirm flows after clipping
ICG dose
25 mg into 10 mL NS
2.5 mg/mL
final clipping MAP
70-90 mmHg
aneurysm rupture MAP
40-50 mmHg
what should you give if surgeon cannot contain ruptures
adenosine
PRBCs
rescue adenosine dose
0.3-0.4 mg/kg
what can you give for brain relaxation
decadron
mannitol
lasix
hyperventilation
hypertonic saline
when is keppra needed
anti-convulsant coverage during ruptured aneurysma
AVM higher flow rate =
higher flow rate = higher bleeding risk
