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N934 Advanced Principles II - Christine > Neurophysiology > Flashcards

Neurophysiology Flashcards

1
Q

the brain receives blood from two distinct arteries which are

A 
internal carotid artery (anterior circulation)
vertebral arteries (posterior circulation)
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2
Q

blood traveling through the vertebral arteries

A

branches of subclavian artery, enter base of skull through the foramen magnum and run along the medulla and join in the pons forming the basilar artery which then branches into 2 posterior cerebral arteries

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3
Q

the 2 posterior cerebral arteries primarily supply which lobes of the brain

A

occipital

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4
Q

blood traveling through the internal carotid branches

A

enter through base of skull pass through the cavernous sinus and divided into anterior and middle cerebral artery

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5
Q

a major site of aneurysm and atherosclerosis is

A

middle cerebral artery

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6
Q

cerebral blood flow varies with

A

metabolic activity 10-300 mL/100g/min

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7
Q

total cerebral blood flow in adults averages

A

750 mL/min

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8
Q

brain receives ___ of cardiac output

A

15-20%

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9
Q

average cerebral blood flow to the gray matter is

A

80 mL/100g/min

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10
Q

average cerebral blood flow to the white matter is

A

20 mL/100g/min

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11
Q

cerebral impairment occurs when cerebral blood flow is

A

20-25 mL/100g/min

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12
Q

flat EEG occurs when cerebral blood flow is

A

15-20 mL/100g/min

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13
Q

irreversible brain damage is associated with cerebral blood flow below

A

10 mL/100g/min

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14
Q

how can we assess CBF in the clinical setting?

A

transcranial doppler, brain tissue oximetry, intracerebral microdialysis, and near infrared spectroscopy

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15
Q

near infrared spectroscopy

A

receptors detect the reflected light from superficial and deep structures
largely reflects the absorption of venous hemoglobin
NOT pulsatile arterial flow

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16
Q

neuro events can occur when rSO2

A

rSO2 <40% or change in rSO2 of >25% from baseline

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17
Q

CPP =

A

MAP - ICP

CVP may be substituted for ICP

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18
Q

ICP normal value

A

< 10-15 mmHg

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19
Q

CPP normal value

A

80-100 mmHg

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20
Q

CPP < 50 =

A

slowing eeg

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21
Q

CPP 25 - 40 =

A

flat eeg

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22
Q

CPP maintained < 25 =

A

irreversible brain damage

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23
Q

increase in CPP =

A

cerebral vasoconstriction (limit CBF)

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24
Q

decrease in CPP =

A

cerebral vasodilation (increase CBF)

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25
Q

myogenic autoregulation

A

intrinsic response of smooth muscle in cerebral arterioles

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26
Q

metabolic autoregulation

A

metabolic demands determine arteriolar tone

tissue demand > blood flow

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27
Q

release of tissue metabolites causes

A

vasodilation = increase flow

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28
Q

CBF remains nearly constant between MAPs of

A

60-160 mmHg

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29
Q

MAP greater than ____ can disrupt the BBB and may result in ____

A

150-160 mmHg; cerebral edema and hemorrhage

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30
Q

factors effecting CBF

A

PaCO2, PaO2, temperature, viscosity, autonomic influences, age

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31
Q

the most important extrinsic influences on CBF are

A

respiratory gas tensions-particularly PaCO2

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32
Q

CBF directly proportionate to PaCO2 between

A

tensions 20-80 mmHg

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33
Q

blood flow changes ____ per 1 mmHg change in PaCO2

A

1-2 mL/100g/min

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34
Q

What happens if you give HCO3?

A

HCO3 ions do not passively cross BBB so HCO3 doesn’t acutely affect CBF

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35
Q

acute metabolic acidosis has ____ on CBF

A

little effect

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36
Q

CBF is directly proportional to PaCO2 until PaCO2 is

A

< 25 mmHg

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37
Q

sensitivity of CBF to changes in PaCO2 is

A

positively correlated with resting levels of CBF

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38
Q

inhaled anesthetics ___ CBF

A

increase which increases cerebrovascular reactivity to carbon dioxide

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39
Q

marker hyperventilation shifts the oxy-hemoglobin dissociation curve to the ___

A

left which may result in EEG changes suggestive of cerebral impairment

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40
Q

alkalosis causes ____ affinity of Hgb for O2 and therefore ____ release of O2

A

increased; decreased

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41
Q

acute restoration of a normal PaCO2 value will result in

A

a significant CSF acidosis (after sustained period of hyperventilation/hypocapnia)

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42
Q

CSF acidosis results in ___ CBF after surgery

A

increased which will increase ICP

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43
Q

PaO2 less than ___ rapidly increases CBF

A

50 mmHg

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44
Q

vasodilation mediated via

A

release of neuronal nitric oxide, open ATP dependent K+ channels, rostral ventrolateral medulla

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45
Q

CBF changes ___ per 1 degree C

A

5-7%

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46
Q

CMR decreases by ___ per 1 degree C

A

6-7%

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47
Q

CMRO2 decreases by ____ per 1 degree C

A

7%

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48
Q

____ determines viscosity

A

hematocrit

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49
Q

a decrease in Hct = ____ viscosity and ____ CBF

A

decrease; increase

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50
Q

optimal cerebral oxygen delivery may occur at Hct of

A

30%

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51
Q

sympathetic innervation = ____ CBF

A

decrease

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52
Q

parasympathetic innervation = ____ CBF

A

increase

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53
Q

how does age affect the brain

A

progressive loss of neurons = loss of myelinated fibers = loss of white matter = loss of synapses

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54
Q

at age 80 CBF and CMRO2 decrease by

A

15-20%

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55
Q

the brain normally consumes ___ of total body oxygen

A

20%

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56
Q

cerebral metabolic rate

A

3-3.8 mL/100g/min = 50 mL/min

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57
Q

O2 is mostly consumed in the

A

gray matter

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58
Q

interruption of cerebral perfusion =

A

unconsciousness in 10 seconds

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59
Q

if O2 is not restored in 3- 8 minutes

A

depletion of ATP and irreversible cellular injury

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60
Q

which areas are most sensitive to hypoxic injury

A

hippocampus and cerebellum

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61
Q

brain glucose consumption

A

5 mg/100g/min

90% is metabolized aerobically

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62
Q

hypoglycemia =

A

brain injury

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63
Q

hyperglycemia =

A

exacerbated hypoxic injury

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64
Q

blood brain barrier

A

lipid soluble substances freely pass, ionized molecules restricted, large molecules restricted

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65
Q

what freely crosses the blood brain barrier

A

o2, co2, lipid soluble molecules, water

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66
Q

what is restricted through the blood brain barrier

A

ions, plasma proteins, large molecules

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67
Q

things that could disrupt the blood brain barrier

A

HTN, tumor, trauma, stroke, infection, marked hypercapnia, hypoxia, and sustained seizure

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68
Q

where is csf formed

A

in the choroid plexus by ependymal cells

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69
Q

how much csf is produced

A

21 mL/hr, 500 mL/day
total volume 150 mL
replaced 3-4x per day

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70
Q

role of csf

A

protect the CNS from trauma

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71
Q

formation of csf

A

involves active secretion of sodium in the choroid plexuses = isotonic fluid despite lower K+, bicarb, and glucose concentration

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72
Q

csf production is inhibited by

A

carbonic anhydrase inhibitors (Acetazolamide), corticosteroids, spironolactone, furosemide, isoflurane, and vasoconstrictors

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73
Q

csf absorption

A

translocation from arachnoid granulations into cerebral sinuses

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74
Q

the monro-kellie hypothesis states that

A

the cranial compartment is incompressible and the volume inside the cranium is a fixed volume
so any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another to prevent a rise in ICP

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75
Q

brain composition in the cranial vault

A

80%

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76
Q

blood composition in the cranial vault

A

12%

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77
Q

csf composition in the cranial vault

A

8%

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78
Q

major compensatory mechanisms with intracranial elastance

A

initial displacement of csf from the cranial to spinal compartment, increase in csf absorption, decrease in csf production, decrease in total cerebral blood volume

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79
Q

provider goals for a closed cranium

A

maintain CPP, prevent herniation

80
Q

provider goals for an open cranium

A

facilitate surgical access, reverse ongoing herniation

81
Q

causes of intracranial hypertension

A

expanding tissue or fluid mass, interference with csf absorption, excessive csf production, systemic disturbances promoting edema

82
Q

signs and symptoms of increased ICP

A

HA, N/V, papilledema, focal neurological deficit, decrease LOC, seizures, coma, cushing triad: irregular respirations, HTN, bradycardia

83
Q

where do we mainly see herniation

A

cerebellotonsillar

84
Q

signs and symptoms of uncal and central herniation

A

decrease LOC, pupils sluggish, cheyne stokes respirations, posturing

85
Q

signs and symptoms of cerebellar tonsillar herniation

A

no specific manifestations, arched stiff neck, paresthesias in shoulder, decrease LOC, respiratory abnormalities, pulse rate variations

86
Q

treatment of intracranial hypertension

A

brain tissue - surgical removal of mass
csf - no effective pharmacological manipulation so need a drain
fluid - steroids, osmotics/diuretics
blood - decrease arterial flow or increase venous drainage
reduce PaCO2
CMR suppression

87
Q

inhaled anesthetics affect CMRO2, CBF, ICP

A

decrease CMRO2
increase CBF
increase ICP

88
Q

iv anesthetics affect CMRO2, CBF, ICP

A

all decrease

89
Q

LA affect CMRO2, CBF, ICP

A

all decrease

90
Q

ketamine affect on CMRO2, CBF, ICP

A

+/- CMRO2, increase CBF and ICP

91
Q

opioids affect on CMRO2, CBF, ICP

A

+/- for all

92
Q

nitrous oxide

A

34 x more soluble than nitrogen in blood

increases everything but can be inhibited by barbs, benzos, narcotics, and propofol

93
Q

intracranial tumors with 66% N2O average ICP increases

A

13 to 40 mmhg

94
Q

alpha 1 agonists on CBF

A

bolus - transiently change CBF and cerebral SaO2

continuous infusion - little effect

95
Q

alpha 2 agonists on CBF

A

decreases CBF up to 25-30%

results from reduced CMRO2 leading to reduced CBF

96
Q

beta agonists on CBF

A

small doses- little effect
large doses + physiologic stress - increased CMRO2 and CBF
ex. large dose epi is >0.05 mcg/kg/min
response exaggerated with BBB defect

97
Q

beta blockers on CBF

A

little to no effect on CBF and CMRO2

98
Q

ACE inhibitors and ARBs on CBF

A

little to no effect on CBF and CMRO2

autoregulation is maintained

99
Q

barbiturates on CBF

A

dose dependent reduction until isoelectric EEG (max 50%)
effective in lowering ICP
robin hood/reverse steel phenomenon (CBF to ischemic areas)
CMR is decreased more than CBF (supply > demand)
anticonvulsant

100
Q

benzos on CBF

A

dose dependent reduction (less than barbiturates, propofol, and etomidate but more than narcotics)
Midazolam is agent of choice
may prolong emergence
anticonvulsant

101
Q

propofol on CBF

A

dose dependent reduction in CBF and CMR
anticonvulsant
short elimination half life
commonly used for maintenance phase of anesthesia for neuro cases/intracranial hypertension

102
Q

etomidate on CBF

A

decreases CMR, CBF, and ICP
myoclonic movements on induction
has been used to treat seizures (not first choice though)
small doses can activate seizure foci in patients with epilepsy

103
Q

What is the only IV anesthetic that dilates cerebral vasculature and increases CBF?

A

Ketamine by 50-60%

104
Q

Ketamine

A

increases CBF and ICP (potentially if they have decreased intracranial compliance)
can be blunted if given with other anesthetics
CMR does not change (debatable)

105
Q

Ketamine and CMR debate

A

In 1997: subanesthetic doses (0.2-0.3 mg/kg) can INCREASE global CMR by 25%
In 2005: subanesthetic and anesthetic doses increased CBF without altering CMRO2

106
Q

what may be appealing about ketamine in neuroanesthesia?

A

NMDA antagonist - neuroprotective

107
Q

NMDA antagonist

A

dissociates the thalamus from limbic cortex
thalamus - relays sensory impulses from the reticular activating system to cerebral cortex-limbic cortex
limbic cortex -involved with the awareness of sensation
increases HR, BP, CO, and secretions
analgesic and hallucinogenic properties

108
Q

NMDA antagonism in brain injury patients may be protective against

A

neuronal cell death

109
Q

opioids on CBF

A

minimal effects on CBF, CMR, and ICP (unless increase PaCO2)
avoid Morphine - poor lipid solubility, slow onset and long DOA
avoid Meperidine- active metabolite can cause seizures especially in renal patients

110
Q

hyperventilation and PaCO2 blunts increase of CBF/ICP from

A

ketamine and volatile agents

111
Q

in general, anesthetic agents ____ the CMR with exception of ___ and ____

A

suppress; ketamine; nitrous oxide

112
Q

control and manipulation of ____ are central to the management of ICP

A

CBF

113
Q

when does CBF not parallel with cerebral blood volume?

A 
cerebral ischemia - CBV increases but CBF decreases
normal BP (MAP 70-150 mmHg) - autoregulation intact
initial increases in CBV doesn't increase CBF - compensatory responses from venous blood shifting to extracerebral vessels and CSF shifting to spinal compartment
114
Q

CBV is ___ mL/___g of brain

A

5mL/100g (70mL)

115
Q

types of intracranial neurosurgeries

A

craniotomy, interventional radiology, trauma

116
Q

types of functional neurosurgeries

A

epilepsy, movement, pain

117
Q

types of spine neurosurgeries

A

anterior, posterior, and transoral

118
Q

preoperative neurological assessment includes

A

always get a baseline!

  • LOC
  • reflexes
  • motor/sensory function
  • evaluate for S/S of increased ICP
  • document pre-existing neurological deficits
119
Q

preoperative considerations for medications

A

anticonvulsants (frequency, continue intraop)
antibiotics (vanc and ancef)
diuretics
steroids

120
Q

hypothermia ____ amplitude of EEG tracing

A

suppresses

121
Q

MEP neuromonitoring

A

used in surgeries where motor tract is at risk
more sensitive to ischemia than SSEP by 15 minutes and degree detection
difficult to obtain due to pre-existing conditions or anesthetic conditions

122
Q

SSEP neuromonitoring

A

Most common method
stimulation of peripheral sensory nerve
mapping in spinal cord and sensory cortex
ischemia detection in cortical tissue
reduce risk of spinal cord/brainstem insults

123
Q

EMG neuromonitoring

A

records muscle electrical activity using needle pairs

used to detect nerve irritation, nerve mapping, assess nerve function, and monitor cranial nerves

124
Q

what do we use to assess posterior corticospinal tract

A

MEP and SSEp

125
Q

etomidate and ketamine ___ amplitude of neuromonitoring tracing

A

increase

126
Q

stereotactic neurosurgery

A

applies rules of geometry to radiologic images to allow for precise localization within the brain, providing up to 1mm accuracy
allows surgeons to perform certain intracranial procedures less invasively
interferes with pulse ox

127
Q

craniotomy medications

A

cleviprex, mannitol, keppra, phenylephrine sticks, precedex, epi

propofol gtt at 40-100 mcg/kg/min ABW
remifentanil gtt at 0.2 mcg/kg/min IBW
phenylephrine gtt at 0.2 mcg/kg/min

induction: fentanyl, propofol, rocuronium

128
Q

craniotomy meds to decrease ICP

A

10mg decadron
50-100mg mannitol (0.25-0.5 mg/kg)
lasix

129
Q

antiepileptics for craniotomy

A

1g keppra

vimpat

130
Q

awake craniotomy specific drugs

A

caffeine (adenosine receptor antagonist)

physotigmine (Anticholinesterase)

131
Q

types of intracranial mass lesions

A

congenital, neoplastic, infectious, and vascular

132
Q

typical presentation of an intracranial mass lesions

A

HA, seizures, focal neurological deficits, sensory loss, cognitive dysfunction

133
Q

frontal supratentorial intracranial mass lesion

A

personality changes, increased risk taking, difficulty speaking (damage to Broca’s area)

134
Q

parietal supratentorial intracranial mass lesion

A

sensory problems

135
Q

temporal supratentorial intracranial mass lesion

A

problems with memory, speech perception, and language skills

136
Q

occipital supratentorial intrcranial mass lesion

A

difficulty recognizing objects, an inability to identify colors, and trouble recognizing words

137
Q

cerebellar dysfunction infratentorial/posterior fossa intracranial mass lesion

A

ataxia, poor balance, nystagmus, dysarthria, cannot perform rapid alternating movements, loss of muscle coordination

138
Q

brainstem compression infratentorial/posterior fossa intracranial mass lesion

A

cranial nerve palsy, altered LOC, abnormal respiration, edema, obstructive hydrocephalus at 4th ventricle

139
Q

primary intracranial tumor locations

A

glial cells, ependymal cells, supporting tissues

140
Q

glial cell primary tumor

A

astrocytoma, oligodendroglioma, glioblastoma

141
Q

ependymal cell primary tumor

A

ependymoma

142
Q

supporting tissue primary tumor

A

meningioma, schwannoma, choroidal papilloma

143
Q

major considerations for intracranial mass lesions

A

tumor location - determines position, EBL, risk for hemodynamic changes intraop
growth rate and size- slow growing tumors are often asymptomatic
ICP elevated

144
Q

anesthetic goals for intracranial mass lesion

A

control ICP
maintain CPP
protect from position related injuries
rapid emergence for neuro assessment

145
Q

intraoperative considerations for monitoring for intracranial mass lesion

A 
standard monitors
a line
foley
\+/- central line
PNS
\+/- ventriculostomy
neuromonitoring potentially
146
Q

where do you zero for a ventriculostomy?

A

at the external auditory meatus

147
Q

why do we not monitor PNS on hemiplegic side of patients?

A

may end up overdosing on paralytics

148
Q

awake-awake for craniotomy for tumor

A

no infusions until closing

prop bolus for pins

149
Q

asleep-awake for craniotomy for tumor

A

start under GA with LMA/ETT
wake the patient up once tumor is exposed
prop gtt 40 mcg/kg/min ABW
remi gtt 0.2-0.4 mcg/kg/min IBW

150
Q

asleep craniotomy for tumor

A

TIVA with neuromonitoring

GETA with no neuromonitoring

151
Q

awake craniotomies are useful for

A

epilepsy and resection of tumors in frontal lobes and temporal lobes when speech and motor are to be assessed intraop

152
Q

types of cases for iMRI

A 
awake tumor resection
laser ablation
cytokine delivery
ROSA
clearpoint
153
Q

monteris medical LITT interventions for

A

epilepsy, glioblastomas, recurrent brain metasstases, and radiation necrosis

154
Q

MR thermography

A

uses phase change to calculate real time temperature data at and around probe
thermal dose confirmed in real time using bio thermodynamic theory
white line - 43 C - 60 min (vaporized)
blue line - 43 C - 10 min (dead)
yellow line- 43 C - 2 min (recoverable)

155
Q

contents of posterior fossa

A

cerebellum- movement and equilibrium
brainstem - autonomic nervous system, CV and respiratory centers, RAS, motor/sensory pathways
cranial nerves I - XII
large venous sinuses

156
Q

brainstem injuries

A

bradycardia and hypertension - trigeminal nerve stimulation (Cushing’s reflex)
bradycardia and hypotension - glossopharyngeal or vagus nerve stimulation
respiratory centers may be damaged and necessitate mechanical ventilation postop
tumors around glossopharyngeal and vagus nerves may impair gag reflex and increase risk of aspiration
cranial nerves IX, X, and XI control pharynx and larynx

157
Q

advantages of sitting position

A

improved surgical exposure, less retraction and tissue damage, less bleeding, less cranial nerve damage, better resection of the lesion, access to airway, chest, and extremities

158
Q

disadvantages of sitting position

A
  1. CV compromise - postural hypotension, arrhythmias, venous pooling
  2. pneumocephalus- open dura (CSF leak, air enters), after dural closure air can act as a mass lesion as CSF reaccumulates, usually resolves spontaneously, tension pneumocephalus = burr holes, symptoms (delayed awakening, HA, lethargy, confusion)
  3. nerve injuries - ulnar compression, sciatic nerve stretch, lateral peroneal compression, brachial plexus stretch
  4. venous air embolism
159
Q

venous air embolism signs and symptoms

A

decreased EtCO2, decreased PaO2, decreased SaO2, spontaneous ventilation, mill wheel murmur, detection of ET nitrogen, increased PaCO2, hypotension, dysrhythmias

160
Q

monitoring for VAE

A

capnography, CVP/PA line, precordial doppler

do not rely on one monitor!

161
Q

most sensitive to detecting VAE to least sensitive

A

TEE –> precordial doppler –> etco2 –> PAP –> CVP –> PaCO2 –> MAP

162
Q

VAE treatment

A

100% O2, notify surgeon to flood field or pack wound, call for help, aspirate from CVP line with 30-60 mL syringe, volume load, inotropes/vasopressors, jugular vein compression, PEEP, position left lateral decubitus and trendelenburg, CPR

163
Q

craniocervical decompression (chiari malformation)

A

cerebellum protrudes through foramne magnum compressing brainstem and cervical spinal cord
types 1-4
syringomyelia

164
Q

deceleration injuries

A

coup and contrecoup lesions

165
Q

linear skull fracture

A

subdural or epidural hematomas

166
Q

basilar skull fracture

A

CSF rhinorrhea, penumocephalus, and cranial nerve palsies (battle’s sign, racoon/panda eyes)
depressed skull fracture

167
Q

primary head injury

A

biomechanical effect of forces on the brain at time of insult
contusion concussion, laceration, hematoma

168
Q

secondary head injury

A

represents complicating processes related to primary injury

intracranial hematoma, increased ICP, seizures, edema, vasospasm

169
Q

glasgow coma scale

A

classifies severity of head injury
prognosis (type of lesion, age, and severity of injury)
mortality = initial GCS score

170
Q

blind nasal intubation is contraindicated in presence of

A

basilar skull fracture

171
Q

head injury anesthetic consideration

A

hypotension, bradycardia, maintain Hct >30%, seizure prophylaxis, DIC with severe injuries (treat with plts, FFP, cryo), pituitary dysfunction (DI, SIADH), remains intubated

172
Q

nonfunctioning/nonsecretory pituitary tumors

A

arise from growth of transformed cells of anterior pituitary

generally well tolerated until 90% of gland is nonfunctional

173
Q

functioning/secretory pituitary tumors

A

cushing’s disease (ACTH)
acromegaly (GH)
prolactinomas (prolactin)
TSH adenomas

174
Q

macroadenoma

A

> 1 cm

175
Q

microadenoma

A

<1 cm

176
Q

transsphenoidal approach necessitates

A

HOB elevated 10-20 degrees

177
Q

intraop considerations for pituitary surgery

A

avoid hyperventilation (reduction in ICP result in retraction of pituitary into teh sella tursica)
use oral RAE or reinforced ETT
potential for mass hemorrhage as the carotid arteries lie adjacent to the suprasellar area
mouth and throat pack
avoid positive pressure upon extubation

178
Q

preop eval of pituitary surgery

A 
visual field evaluation
S/S of increased ICP
endocrine labs
electrolytes
steroids?
179
Q

postop management after pituitary surgery

A

DI is common and is usually self limiting (resolves in one week)
treat with vasopressin or DDAVP
SIADH

180
Q

cerebral aneurysm is the leading cause of

A

nontraumatic intracranial hemorrhage

181
Q

cerebral aneurysm is commonly located in

A

the anterior circle of willis

182
Q

how can a cerebral aneurysm lead to subarachnoid hemorrhage

A

aneurysm fills with blood and can rupture, spilling blood into the subarachnoid space, creating the subarachnoid hemorrhage

183
Q

unruptured cerebral aneurysm

A

HA, unsteady gait, visual disturbances, facial numbness, pupil dilation, drooping eyelid, pain above or behind eye

184
Q

ruptured cerebral aneurysm

A

sudden, extremely severe HA, NV, LOC, prolonged coma, focal neuro deficits, hydrocephalus, seizure, S/S of increased ICP

185
Q

vasospasm

A

causes ischemia or infarction
digital subtraction angiogrpahy is gold standard
(not detectable until 72 hours after SAH)
use calcium channel blockers

186
Q

rebleeding following initial SAH

A

peaks 7 days post incident
major threat during delayed surgery
antifibrinolytic therapy

187
Q

vasospasm treatment

A 
triple H therapy
hypertension (SBP 160-200)
hemodilution (hct 33%) 
hypervolemia
intended to increase CBF in ischemic brain areas
188
Q

endovascular coiling

A 
GETA with complete muscle paralysis
control CPP
minimal narcotics
a line
minimal to no blood loss
heparin may be used for ACT 200-250
189
Q

advantages of endovascular aneurysm coiling

A

shorter stay, less anesthetic requirements, uncomplicated positioning, minimally invasive

190
Q

complications of endovascular aneurysm coiling

A

aneurysm rupture/SAH
vasospasm
CVA
incomplete coiling

191
Q

cerebral aneurysm in the OR

A

most commonly treated by microsurgical clip ligation

deep circulatory arrest may be necessary for large aneurysms

192
Q

likely times of rupture intraoperatively

A

dural incision, excessive brain retraction, aneurysm dissection, during clipping or releasing of clip

193
Q

treatment of intraop aneurysm rupture

A

immediate aggressive fluid resuscitation, replace blood loss, propofol bolus, decrease MAP to 40-50mmHg

194
Q

AVM treatment

A

intravascular embolization, surgical excision, or radiation

195
Q

cranial nerve decompression treats disorders of which cranial nerves

A

trigeminal, hemifacial, glossopharyngeal

N934 Advanced Principles II - Christine (3 decks)

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