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N934 Advanced Principles of Anesthesia II > Neuro > Flashcards

Neuro Flashcards

1
Q

anterior circulation to the brain

A

internal carotid artery

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2
Q

posterior circulation to the brain

A

vertebral arteries

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3
Q

two vertebral arteries

A
  • branches of subclavian
  • enter skull through foramen magnum and run along the medulla
  • join in pons to form basilar artery
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4
Q

basilar artery

A

branches at the midbrain into 2 posterior cerebral arteries which supply the occipital lobes of the brain

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5
Q

internal carotid branches

A
  • enter through the base of the skull and pass through the cavernous sinus
  • divided into anterior and middle cerebral artery
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6
Q

circle of willis

A
  • located at base of brain and forms an anastomotic ring that includes vertebral (basilar) and internal carotid flow
  • provides collateral flow if one portion becomes obstructed
  • major site of aneurysm and atherosclerosis (especially MCA)
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7
Q

cerebral blood flow in adults

A
  • varies with metabolic activity
  • averages 750 mL/min
  • about 15-20% of cardiac output
  • 50 mL/100g/min
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8
Q

gray matter blood flow

A

80 mL/100g/min

more blood flow here vs white matter because more activity

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9
Q

white matter blood flow

A

20 mL/100g/min

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10
Q

EEG cerebral impairment

A

20-25 mL/100g/min

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11
Q

EEG flat

A

15-20 mL/100g/min

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12
Q

EEG irreversible brain damage

A

below 10 mL/100g/min

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13
Q

CBF monitoring

A
  • transcranial doppler (TCD) = ultrasound MCA
  • brain tissue oximetry = bolt with a clark electrode oxygen sensor
  • intracerebral microdialysis = assesses brain tissue chemistry
  • near infrared spectroscopy (NIRS)
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14
Q

NIRS

A
  • receptors detect the reflected light from superficial and deep structures
  • largely reflects absorption of venous hemoglobin
  • NOT pulsatile arterial flow
  • more of a TREND, good to put it on to go to sleep so you can get a baseline
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15
Q

neuro events + NIRS

A

rSO2 < 40%

change in rSO2 of > 25% from baseline

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16
Q

CPP Formula

A

CPP = MAP - ICP

*CVP must be substituted for ICP if CVP is higher

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17
Q

ICP normal value

A

10-15 mmHg

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18
Q

CPP normal value

A

80-100 mmHg

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19
Q

CPP slowing of EEG

A

<50 mmHg

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20
Q

CPP flat EEG

A

25-40 mmHg

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21
Q

CPP irreversible brain damage

A

<25 mmHg

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22
Q

autoregulation

A
  • myogenic regulation (originating in vascular smooth muscle)
  • cerebral vasculature rapidly (10-60s) adapts to changes in CPP
  • increase CPP = cerebral vasoconstriction (limit CBF)
  • decrease CPP = cerebral vasodilation (increase CBF)
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23
Q

myogenic response

A

intrinsic response of smooth muscle in cerebral arterioles

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24
Q

metabolic response

A
  • metabolic demands determine arteriolar tone
  • tissue demand > blood flow
  • release of tissue metabolites causes vasodilation = increase flow
  • once thought to be hydrogen ions, but likely other things too
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25
Q

CBF remains constant between MAP of what?

A
  • 60-160 mmHg
  • variation between patients and based on source you look at
  • CBF remains constant between these MAPs, beyond these limits, blood flow becomes pressure dependent
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26
Q

MAP >150-160 mmHg

A

this can disrupt the BBB and may result in cerebral edema and hemorrhage

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27
Q

chronic hypertension and autoregulation

A

right shifted in patients with chronic hypertension

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28
Q

factors effecting CBF

A
  • PaCO2
  • PaO2
  • temperature
  • viscosity
  • autonomic influences
  • age
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29
Q

PaCO2 effect on CBF

A
  • most important extrinsic influence on CBF
  • CBF directly proportionate to PaCO2 between tensions 20-80 mmHg
  • blood flows changes 1-2 mL/100g/min per 1 mmHg change in PaCO2
  • immediate and secondary changes in the pH of CSF and cerebral tissue
  • attenuated at PaCO2 < 25 mmHg (ceiling effect)
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30
Q

does HCO3- change CBF

A
  • ions do NOT passively cross the BBB so bicarb DOES NOT acutely affect CBF
  • acute metabolic acidosis has little effect on CBF
  • in 24-48 hours CSF HCO3- compensates (active transport) for change in PaCO2
  • effects of hypo and hypercapnia are diminished
  • BOTTOM LINE = HCO3- compensation probably happens in the ICU not the OR
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31
Q

PaCO2 < 20 mmHg

A
  • marked hyperventilation shifts the oxygen hemoglobin dissociation curve to the LEFT and with changes in CBF, may result in EEG changes suggestive of cerebral impairment even in normal individuals
  • LEFT = LOVE
  • alkalosis causes increased affinity of Hgb for O2 and therefore decreased release of O2
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32
Q

restoration of normal PaCO2 after surgery/hyperventilation

A
  • acute restoration of normal PaCO2 value will result in significant CSF acidosis after sustained period of hyperventilation and hypocapnia
  • CSF acidosis results in increased CBF
  • increased CBF results in increased ICP
  • SLOWLY increase to normal PaCO2
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33
Q

PaO2 effect on CBF

A
  • 50 to 300 mmHg little influence on CBF

- <50 mmHg rapidly increases CBF

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34
Q

PaO2 <50-60 mmHg

A
  • vasodilation mediated by various things
  • release of neuronal nitric oxide
  • open ATP dependent K+ channels
  • rostral ventrolateral medulla (RVM)
  • brains O2 sensor stimulation = increase CBF, but not CMRO2
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35
Q

rostral ventrolateral medulla

A

also known as the pressor area of the medulla, is a brain region that is responsible for basal and reflex control of sympathetic activity associated with cardiovascular function

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36
Q

temperature effect on CBF

A
  • CBF changes 5-7% per 1 degree celcius
  • CMR decreases 6-7% per 1 degree celcius
  • CMRO2 decreases by 7% per 1 degree celcius
  • CMRO2 decreased by decreasing temperature
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37
Q

viscosity effect on CBF

A
  • hematocrit determines viscosity
  • viscosity and CBF inversely proportional
  • decrease in HCT decreases viscosity and increases CBF
  • decrease in HCT also decreases oxygen carrying capacity
  • impaired oxygen delivery to brain tissue
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38
Q

what is optimal cerebral oxygen delivery

A

occurs at a hematocrit of about 30%

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39
Q

autonomic influence on CBF

A
  • SNS = vasoconstricts and decreases CBF

- PSNS = vasodilates and increases CBF

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40
Q

age influence on CBF

A
  • progressive loss of neurons with aging
  • loss of myelinated fibers, loss of white matter
  • loss of synapses
  • CBF and CMRO2 decrease by 15-20% at 80 years
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41
Q

CMRO2

A
  • brain normally consumes 20% of total body oxygen
  • 60% used to generate ATP
  • CMRO2 is 50 mL/min
  • oxygen mostly consumed in the gray matter
  • interruption of cerebral perfusion = unconsious in 10 seconds
  • oxygen not restored in 3-8 minutes = depletion of ATP = irreversible cellular injury
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42
Q

which areas of the brain are most sensitive to hypoxic injury

A
  • hippocampus

- cerebellum

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43
Q

glucose and the brain

A
  • glucose primary energy source
  • brain glucose consumption 5 mg/100g/min
  • 90% aerobically O2 metabolized
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44
Q

hypoglycemia

A

means brain injury

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45
Q

hyperglycemia

A

may exacerbate hypoxic injury

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46
Q

blood brain barrier

A
  • PAUCITY OF PORES are responsible for the blood brain barrier
  • cerebral blood vessels are unique in vasculature
  • vascular endothelial cell junctions are nearly fused
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47
Q

lipid barrier of brain what can pass

A
  • lipid-soluble substances freely pass
  • ionized molecules restricted
  • large molecules restricted
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48
Q

determinants of what can pass the BBB

A
  • size
  • charge
  • lipid solubility
  • plasma protein binding
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49
Q

what freely crosses the BBB

A
  • O2
  • CO2
  • Lipid soluble molecules (most anesthetics)
  • H2O
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50
Q

what is restricted to cross the BBB

A
  • ions (electrolytes like Na+)
  • plasma proteins
  • large molecules (mannitol)
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51
Q

what disrupts the BBB

A
  • HTN
  • tumor
  • trauma
  • stroke
  • infection
  • marked hypercapnia
  • hypoxia
  • sustained seizure
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52
Q

where is CSF made

A
  • formed in choroid plexus
  • formed by ependymal cells
  • involves active secretion of sodium in the choroid plexus
  • result is fluid that is isotonic with the plasma (even though there is lower concentrations of potassium, bicarb and glucose)
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53
Q

how much CSF do adults make?

A

21 mL/hr or 500 mL/day

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54
Q

total volume of CSF

A

150 mL

1/2 in cranium and 1/2 in spinal canal

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55
Q

CSF facts

A
  • replaced 3-4x per day
  • found in cerebral ventricles and cisterns and subarachnoid space surrounding the brain and spinal cord
  • protects the CNS from trauma
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56
Q

what inhibits production of CSF

A
  • Carbonic anhydrase inhibitors (acetazolamide)
  • corticosteroids
  • spironolactone
  • furosemide
  • isoflurane
  • vasoconstrictors
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57
Q

absorption of CSF

A

-translocation from arachnoid granulations into cerebral sinuses

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58
Q

monro kellie doctrine/hypothesis

A
  • cranial compartment is incompressible and the volume inside the cranium is a fixed volume
  • the cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that 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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59
Q

cranial vault components

A
  • brain 80%
  • blood 12%
  • CSF 8%
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60
Q

ICP

A
  • supratentorial CSF pressure measured in the lateral ventricles or over the cerebral cortex
  • small increases in volume in one component are initially well compensated
  • 5-15 mmHg
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61
Q

normal ICP

A

< 10 mmHg

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62
Q

intracranial elastance compensatory mechanisms

A
  • initial displacement of CSF from the cranial to spinal compartment
  • an increase in CSF absorption
  • a decrease in CSF production
  • a decrease in total cerebral blood volume
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63
Q

> 20 mmHg ICP

A
  • anything over 20 mmHg for greater than 5 mins creates ISSUES
  • a point is eventually reached at which further increases produce precipitous rises in ICP
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64
Q

ICP provider goals for closed crainium

A
  • maintain CPP

- prevent herniation

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65
Q

ICP provider goals for open cranium

A
  • facilitate surgical access

- reverse ongoing herniation

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66
Q

intracranial hypertension

A

sustained increase in ICP about 20-25 mmHg

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67
Q

causes of intracranial HTN

A
  • expanding tissue or fluid mass
  • interference with CSF absorption
  • excessive CSF production
  • systemic disturbances promoting edema
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68
Q

S/S increased ICP

A
  • HA
  • nausea/emesis
  • papilledema
  • decreased LOC
  • focal neurological deficit
  • seizures
  • coma
  • cushings triad
69
Q

cushing’s triad

A
  • irregular respiration
  • HTN
  • bradycardia
70
Q

herniation areas

A
  • cingulate gyrus under falx cerebri
  • central
  • uncal (transtentorial)
  • cerebellar tonsils through foramen magnum
  • upward herniation of cerebellum
  • transcalvarial
71
Q

most common area of herniation

A

-cerebellar tonsils through foramen magnum

72
Q

S/S cingulate gyrus herniation

A

-little known

73
Q

uncal and central herniation S/S

A
  • decrease LOC
  • pupils sluggish –> fixed and dilated
  • cheyne stokes respirations
  • decorticate –> decerebrate posturing
74
Q

cerebellar tonsillar herniation S/S

A
  • no specific clinical manifestations
  • arched stiff neck
  • paresthesias in shoulder
  • decreased LOC
  • respiratory abnormalities
  • pulse rate variations
75
Q

transcalvarial herniation S/S

A

-may occur during surgery

76
Q

treatment of intracrainial HTN

A
  • brain tissue = surgical removal of mass (lobectomy or removal of bone flap)
  • CSF = no effective pharmacological manipulation, only practical management is drain
  • Fluid = steroids, osmotics/diuretics
  • blood = most amenable to rapid alteration; decrease arterial flow or increase venous drainage with patient position
  • reduction of PaCO2 (to no less than 23-35 mmHg
  • CMR suppression with barbiturates, propofol and hypothermia)
77
Q

nitrous oxide effect on brain

A
  • 34x more soluble than nitrogen in blood
  • increases CMRO2, CBF, CBV, and ICP (more dramatic change if sole agent)
  • sympathoadrenal stimulating effect
  • second stage arousal phenomenon
  • increase is attenuated by barbiturates, benzos, narcotics, and propofol
  • intracranial tumors with 66% N2O increased ICP 13 mmHg to 40 mmHg
78
Q

CBF and alpha 1 agonists

A
  • bolus may transiently (2-5 min) change CBF and cerebral SaO2
  • continous infusion has little effect on CBF and cerebral SaO2
  • does not have adverse effect on brain
79
Q

CBF and alpha 2 agonists

A
  • decreases CBF up to 25-30%

- results from reduced CMRO2 leading to a reduced CBF

80
Q

CBF and beta agonist

A
  • small dose = little effect on CBF
  • large doses + physical stress leads to increase in CMRO2 and CBF
  • large dose increases MAP
  • may increase CMRO2 and CBF up to 20%
  • beta 1 receptor mediated effects
  • response exaggerated with BBB defect
81
Q

antagonists effects on CBF

A
  • b blockers –> little to no effect on CBF and CMRO2

- ACE-inhibitors and ARBs –> little to no effect on CBF and CMRO2, autoregulation maintained

82
Q

barbiturates effect on brain

A
  • dose dependent reduction in CBF and CMR until isoelectric EEG
  • maximum reductions in CBF and CMR of nearly 50% (flat EEG)
  • highly effective in lowering ICP
  • robin hood (reverse steal effect) –> CBF redistributed from normal to ischemic areas of brain
  • CMR decreased more than CBF
  • anticonvulsant (all except methohexital which is used for ECT)
83
Q

benzodiazepines effect on brain

A
  • dose-dependent reduction in CMR and CBF
  • greater reduction in CMR and CBF than narcs
  • less reduction than barbiturates, propofol or etomidate
  • moderate reduction in CBF
  • midaz is benzo of choice in neuro due to short half life
  • may prolong emergence so consider this when there is need for post-op neuro exam
  • anitconvulsant
84
Q

propofol + brain

A
  • dose dependent reduction in CBF and CMR
  • decrease in CBF may exceed that in metabolic rate
  • anticonvulsant
  • short elimination half-life neuroanesthesia
  • commonly used for maintenance of anesthesia in patients with or at risk of intracranial HTN
  • most common induction agent for neuroanesthesia
85
Q

etomidate + brain

A
  • decreases CMR, CBF and ICP
  • myoclonic movements on induction, but not associated with seizure activity on the EEG
  • has been used to treat seizures, but not a first choice anticonvulsant
  • small dose can activate seizure foci in patient with epilepsy
86
Q

ketamine + brain

A
  • only IV anesthetic that dilates cerebral vasculature and increases CBF
  • can potentially increase ICP markedly if decreased intracrainial compliance
  • selective activation of certain areas (limbic and reticular) is particularly offset by depression of other areas (somatosensory and auditory)
  • CMR does not change (debated)
  • ketamine as sole agent can increase ICP
87
Q

NMDA Antagonist

A
  • functionally dissociates the thalamus from the limbic cortex
  • thalamus - relays sensory impulses from the reticular activating system to the cerebral cortex
  • limbic cortex - involved with awareness of sensation
  • increases HR, BP, CO, and secretions
  • analgesic, hallucinogenic effects
  • NMDA antagonism in brain injury patient may be protective against neuronal cell death
88
Q

opioids

A

-minimal effects on CBF, CMR, and ICP unless increase PaCO2

89
Q

intracranial surgeries

A
  • craniotomy
  • interventional radiology
  • trauma
90
Q

functional surgeries

A
  • epilepsy
  • movement
  • pain
91
Q

spine surgeries

A
  • anterior
  • posterior
  • transoral
92
Q

MEP

A
  • motor evoked potentials
  • used in surgeries where motor tract is at risk
  • direct and scalp electrodes
  • more sensitive to ischemia than SSEP by 15 minutes and degree detection
  • difficult to obtain due to pre-existing conditions or anesthetic conditions
93
Q

SSEP

A
  • most commonly monitored
  • stimulation of peripheral sensory nerve
  • mapping in spinal cord and sensory cortex
  • ischemia detection in cortical tissue
  • reduce risk of spinal cord/brainstem
  • mechanical or ischemic insults
  • does have some motor but not as specific as MEPs, may not sense deficits as sensitively
  • hyperthermia - suppresses amplitude
  • hypothermia - increases latency
94
Q

EMG

A
  • records muscle electrical activity using needle pairs
  • continuous recording
  • triggered responses
  • uses –> detect nerve irritation, nerve mapping, assess nerve function, monitoring cranial nerves
95
Q

stereotactic neurosurgery

A
  • applies rules of geometry to radiologic images to allow for precise localization within the brain, provides up to 1mm accuracy
  • less invasive intracranial surgery
  • small markers (fudicials) affixed to scalp and forehead
  • IMPORTANT fudicials do not move
  • in OR patient’s head is appropriate positioned and the locations of the fudicials are entered into a computer
  • computer calculates the position of the pointer with respect to the patient and display images front he scan on the monitor
  • smaller brain biopsies may be done under local/MAC
  • GETA for larger resections
96
Q

crani bag

A
  • cleviprex
  • mannitol
  • keppra
  • phenyl
  • precedex
  • epi
97
Q

drips for crani

A
  • propofol 40-100 mcg/kg/min [max 40 mcg/kg/min for asleep motor mapping and awake crani]
  • remifentanil 0.2 mcg/kg/min [titrate up as needed]
  • phenylephrine 0.2 mcg/kg/min [titrate up as needed]
98
Q

induction meds for crani

A
  • fentanyl
  • propopfol
  • rocuronium (not always redosed, but may redose for aneurysm or pituitary tumor because those surgeries are VERY stimulating)
  • sometimes succ if performing MEPs RIGHT away
99
Q

meds to decrease ICP for crani

A
  • decadron 10 mg
  • mannitol 50-100g (or 0.25-0.5 g/kg)
  • +/- lasix
100
Q

antiepileptic meds for crani

A
  • keppra

- vimpat (have to order in preop because usually really hard to get)

101
Q

antibiotics for crani

A
  • vancomycin

- ancef

102
Q

analgesics for crani

A
  • tylenol (within 30 min of wakeup)

- narcotic (dilaudid or fentanyl)

103
Q

specific drugs for awake crani

A
  • caffeine (adenosine receptor antagonist; CNS stimulant, 60 mg in 3 mL)
  • physostigmine (anticholinesterase; crosses BBB; antagonizes CNS depressants; 0.5-1 mg/kg Q2-10min)
104
Q

types of intracranial mass lesions

A
  • congenital
  • neoplastic (benign vs malignant)
  • infections (abscess or cyst)
  • vascular (hematoma or AVM)
105
Q

typical presentation of intracranial mass lesions

A
  • HA (50-60%)
  • seizures (50-80%)
  • focal neurological deficits (10-40%)
  • sensory loss
  • cognitive dysfunction
106
Q

supratentorial intracranial mass lesions

A
  • seizures, hemiplegia, aphasia
  • fronta - personality changes, increased risk taking, difficulty speaking
  • parietal - sensory problems
  • temporal - problems with memory, speech perception, and language skills
  • occipital - difficulty recognizing objects, an inability to identify colors, and trouble recognizing words
107
Q

infratentorial/posterior fossa intracranial mass lesions

A
  • cerebellar dysfunction - ataxia/poor balance, nystagmus, dysarthria, cannot perform rapid alternating movements, loss of muscle coordination
  • brainstem compression - cranial nerve palsy, altered LOC, abnormal respiration
  • edema, obstructive hydrocephalus at fourth ventricle
108
Q

tentorium

A

-fold of the dura mater that separates and forms partition between the cerebrum and cerebellum

109
Q

primary tumors

A
  • glial cells = astrocytoma, oligodendroglioma, glioblastoma
  • ependymal cells = ependymoma
  • supporting tissues = meningioma, schwannoma, choroidal papilloma
110
Q

major considerations for intracranial mass lesion

A
  • tumor location = determines position, EBL, risk for hemodynamic changes intraoperatively
  • growth rate and size = slow growing tumors are often asymptomatic
  • ICP elevated
111
Q

anesthetic goals for intracranial mass lesion

A
  • control ICP
  • maintain CPP
  • protect from position related injuries
  • rapid emergence for neuro assessment
112
Q

monitoring for intracranial mass lesion

A
  • standard monitors
  • arterial line
  • foley
  • +/- central line
  • PNS - do not monitor on hemiplegic side because you may end up overdosing paralytics
  • +/- ventric for ICP monitoring (zero at external auditory meatus)
  • possible IONM
113
Q

positioning for intracranial mass lesion

A
  • anticipate turning HOB 90-180 degrees
  • insure ability to access all vital equipment
  • adequate IV line extension
  • long breathing circuit
  • PNS often on LEs
  • HOB often elevated 10-15 degrees
  • patient may be supine, lateral, prone or sitting (sitting falling out of favor)
  • anticipate sympathetic response with placement of mayfield head pins
114
Q

preop for intracranial mass lesion

A
  • determine presence of elevated ICP
  • document LOC and neuro deficits
  • review PMH and general health status
  • review med regime (esp anticonvulsants, diuretics)
  • review lab findings
  • review radiological studies
  • premedication (avoid benzos and narcs; continue corticosteroids and anticonvulsants)
115
Q

intraoperative for intracranial mass lesion

A
  • maintenace = no preferred anesthetic technique, hyperventilation, avoid excessive PEEP (<10)
  • fluid management = glucose free crystalloids or colloids; replace blood loss with blood/colloids
  • ICP control = EVD/lumbar drain, increases in cerebral blood flow
116
Q

emergence for intracranial mass lesion

A
  • must be slow and controlled, straining or bucking can cause ICH or worsen cerebral edema
  • aggressive BP management (SBP <140 or <160); risk for hemorrhage or stroke, clevidipine, labetalol, esmolol
  • surgical team will do neuro exam immediately after extubation, prior to OR departure
117
Q

postoperative for intracranial mass lesion

A
  • admit to ICU for obs
  • transport with HOB elevated (30 degrees)
  • manage HTN
  • O2 for transport
  • minimal pain post crani
  • observe for seizures, neuro deficits, or increased ICP
118
Q

awake-awake crani

A
  • no infusions until closing

- propofol bolus for pins

119
Q

asleep-awake crani

A
  • start under GA with LMA or ETT
  • wake the patient up once tumor is exposed
  • propofol drip 40 mcg/kg/min ABW
  • remi drip 0.2-0.4 mcg/kg/min IBW
120
Q

asleep crani

A
  • TIVA if IONM or asleep motor mapping

- GETA if no IONM

121
Q

why are awake craniotomies done?

A
  • used for epilepsy surgery and resection of tumors in frontal lobes and temporal lobes when speech and motor are to assessed intraop
  • patient considerations = airway, temperature, anxiety
  • asleep with LMA for exposure
  • awake for cortical mapping and tumor resection
  • sedated for iMRI (to evaluate the resection)
  • when tumor resection complete use appropriate anesthetic to keep comfortable
122
Q

MRI safety hazards for personnel

A
  • magnetic field strength
  • cold hazards
  • acoustic noises
123
Q

monteris medical (“LITT”)

A
  • epilepsy
  • glioblastomas
  • recurrent brain metastases
  • radiation necrosis
124
Q

MR Thermography

A
  • uses phase change to calculate real time (8 second delay) temperature data at and around probe
  • thermal dose confirmed in real time using bio thermodynamic theory
  • basically burns the tumor or eliptogenic focus
125
Q

contents of posterior fossa

A
  • cerebellum = movement and equilibrium
  • brainstem = ANS, CV and respiratory centers, RAS, motor/sensory pathways
  • CN I-XII
  • large venous sinuses
126
Q

trigeminal nerve stimulation

A

cushing’s reflex

bradycardia and hypertension

127
Q

glossopharyngeal or vagus nerve stimulation

A

bradycardia and hypotension

128
Q

brainstem injuries

A
  • respiratory centers may be damaged and necessitate mechanical ventilation postoperatively
  • tumors around glossopharyngeal and vagus nerves may impair gag reflex and increase risk of aspiration
  • CN IX, X, and XI control pharynx and larynx
129
Q

posterior fossa periop considerations

A

-same considerations as intracranial lesions

130
Q

posterior fossa positioning considerations

A

-may be sitting, modified lateral, or prone

131
Q

sitting position advantages

A
  • improved surgical exposure
  • less retraction and tissue damage
  • less bleeding
  • less cranial nerve damage
  • better resection of lesion
  • access to airway, chest, extremities
132
Q

sitting position disadvantages

A
  • postural hypotension
  • arrhythmias
  • venous pooling
  • pneumocephalus
  • nerve injuries (ulnar, sciatic, lateral peroneal, brachial plexus)
133
Q

Pneumocephalus

A
  • open dura –> CSF leak –> air enters –> VAE
  • after dural closure, air can act as a mass lesion as CSF reaccumulates
  • usually resolves spontaneously
  • tension pneumocephalus - burr holes to relieve
  • symptoms include delayed awakening, HA, lethargy, confusion
  • if using N2O discontinue before dural closure
134
Q

VAE when does it happen

A
  • pressure in a vein is subatmospheric
  • level of incision is > 5 cm higher than heart
  • patients with PFO can have air enter circulation
135
Q

VAE incidence

A
  • potentially lethal
  • mortality rate 1%
  • sitting position = 25-50%
  • prone, lateral, supine = 12%
136
Q

paradoxical air embolism

A
  • air enters L side of heart and travels to systemic circulation
  • occurs when right heart pressure is greater than left
  • common in patients with PFO
137
Q

VAE S/S

A
  • decreased ETCO2
  • decreased PaO2
  • decreased SaO2
  • Spontaneous ventilation
  • mill-wheel murmur (late sign)
  • detection of ET nitrogen
  • increased PaCO2
  • hypotension
  • dysrhythmias
138
Q

monitoring for VAE

A
  • capnography
  • CVP/PA line
  • precordial doppler
  • DO NOT rely on one monitor to diagnose VAE, use monitors with different sensitivities to confirm
139
Q

monitors for VAE from greatest to least sensitivity

A
  • TEE (5-10x more sensitive than doppler, detects 0.25 mL of air)
  • precordial doppler
  • ETCO2 (decreases with 15-25 mL of air)
  • PAP (increases with 20-25 mL of air)
  • CVP
  • PaCO2
  • MAP
140
Q

VAE treatment

A
  • 100% O2, discontinue N2O
  • notify surgeon to flood the field or pack wound
  • call for HELP
  • aspirate from CVP line with stopcock and 30-60 cc syringe
  • volume load
  • inotropes/vasopressors
  • Jugular vein compression (valsalva)
  • PEEP
  • position patient in durant (L lateral decubitus with slight trendelenburg)
  • CPR if necessary
141
Q

craniocervical decompression (chiari malformation)

A
  • cerebellum protrudes through foramen magnum
  • compresses brainstem and cervical spinal cord
  • types I-IV
  • syringomyelia (CSF abnormally located in spinal cord)
142
Q

chiari malformations anesthetic considerations

A
  • position prone or sitting
  • EBL - large venous sinuses
  • vital sign instability due to brainstem manipulation
  • postop = pain management
143
Q

decelerations injuries

A

coup and contrecoup lesions

144
Q

skull fractures

A
  • linear = subdural or epidural hematomas
  • basilar = CSF rhinorrhea, pneumocephalus, and cranial nerve palsies (battles sign, racoon/panda eyes)
  • depressed = brain contusion
145
Q

primary head injury

A
  • biomechanical effect of forces on the brain at time of insult
  • contusion
  • concussion
  • laceration
  • hematoma
146
Q

secondary head injury

A
  • represents complicating process related to primary injury (minutes, hours, days after primary injury)
  • intracranial hematoma, increased ICP, seizures, edema, vasospasm
147
Q

pituitary non functioning tumors

A
  • arise from growth of transformed cells of anterior pituitary
  • generally well tolerated until 90% of gland is non-functional
148
Q

pituitary functioning tumors

A
  • cushings
  • acromegaly
  • prolactinomas
  • TSH adenomas
149
Q

cerebral aneurysm

A
  • leading cause of non-traumatic intracranial hemorrhage
  • incidence of cerebral aneurysm is 2% in north america
  • commonly located in anterior circle of willis
  • aneurysm fills with blood and can rupture, spilling blood into the subarachnoid space, creating a subarachnoid hemorrhage
  • can lead to permanent brain damage, disability or death
150
Q

unruptured aneurysm

A
  • HA
  • unsteady gait
  • visual disturbances (loss, diplopia, photophobia)
  • facial numbness
  • pupil dilation
  • drooping eyelid
  • pain above or behind eye
151
Q

ruptured aneurysm

A
  • sudden extremely severe HA (worst of life)
  • N/V
  • LOC, prolonged coma
  • focal neural deficits
  • hydrocephalus
  • seizure
  • S/S increased ICP
152
Q

vasospams

A
  • causes ischemia or infarction
  • exact mechanism not known
  • accounts for 14% M/M
  • digital subtraction angiography is the gold standard for diagnosis (not detectable until 72 hours after SAH)
  • clinically significant occurrence (20-30%)
  • calcium channel blockers
153
Q

rebleeding

A
  • rebleeding following initial SAH peaks seven days post incident
  • major threat during delayed surgery
  • accounts for 8% of M/M
  • antifibrinolytic therapy
154
Q

vasopasm treatment

A
  • triple H therapy (goal is to treat ischemia with an increased CPP)
  • hypertension (SBP 160-200 mmHg)
  • hemodilution (Hct ~33% provides balance between O2 carrying capacity and viscosity)
  • hypervolemia (aggressive IV infusion of colloids and crystalloids for CVP >10 mmhg or PCWP 12-20 mmHg)
155
Q

interventional radiology endovascular coiling

A
  • GETA with complete muscle paralysis
  • control CPP
  • minimal narcotic needs since minimally invasive
  • aline preferred
  • minimal to no blood loss
  • heparin may be used for ACT 200-250
  • same post op concerns with clipping
156
Q

aneurysm coiling

A
  • guglieimi detachable coil inserted into aneurysm
  • standard arteriogram is performed to locate aneurysm
  • catheter is passed often through femoral vessels and coil is advanced
  • advantages - shorter stay, less anesthetic requirements, uncomplicated positioning, minimally invasive
  • complications –> aneurysm rupture/subarachnoid hemorrhage, vasopasm, CVA, incomplete coiling
157
Q

cerebral aneurysm operating room

A
  • most commonly treated by microsurgical clip ligation
  • crani approach, parent vessel giving rise to aneurysm is identified
  • aneurysm neck is isolated and clip is placed across the neck, excluding it from circulation
  • deep circulatory arrest may be necessary with giant aneurysm
158
Q

cerebral aneurysm intraoperative management

A
  • maintain optimum CPP
  • decrease CPP rapidly if rupture occurs during surgical clipping
  • maintain transmural pressure (MAP-ICP)
  • decreased intracranial volume (blood and tissue); provide slack brain
  • minimize CMRO2
159
Q

cerebral aneurysm preinduction

A
  • limit sedation
  • a line
  • 2 large bore IVs
  • type and cross 2-4 units
  • remember HOB turned 90-180 degrees
160
Q

cerebral aneurysm induction

A
  • smooth induction

- aggressive BP and HR control (narcotics, beta blockers, deepen anesthetic)

161
Q

cerebral aneurysm maintenance

A
  • may use TIVA or anesthetic gases
  • temporary occlusion of a cerebral artery
  • maintain BP 15-20% below baseline to prevent vasospasm, decrease EBL and allow for better exposure and visualization
  • employ methods for cerebral protection and to reduce ICP if necessary
162
Q

cerebral aneurysm fluid management

A
  • run patient dry
  • expand blood volume with colloids
  • have PRBCs available
  • no glucose containing solutions
163
Q

cerebral aneurysm control of BP

A
  • control of BP is critical to successful outcome of case
  • increased BP = increased TMP across aneurysmal wall = rupture of aneurysm
  • surgeon may ask for temporary increase in MAP to 80-100 mmHg to provide for collateral flow if a feeder vessel is clamped for a short period to allow for clipping of aneurysm
  • post clipping, MAP usually kept 80-100 mmHg
164
Q

likely times of intraop aneurysm rupture

A
  • dural incision
  • excessive brain retraction
  • aneurysm dissection
  • during clipping or releasing of clip
165
Q

treatment of intraop aneurysm rupture

A
  • immediate, aggressive fluid resuscitation and replacement of blood loss
  • propofol bolus for brain production, to decrease MAP, and decrease blood loss
  • decrease MAP to 40-50 mmHg (clevidipine, labetalol, esmolol)
  • surgeon may apply temporary clip on parent vessel to control bleeding, restore BP after clipping to improve collateral flow
166
Q

AVM

A
  • congential abnormality that involves direct connection from an artery to a vein nidus without a pressure modulating capillary bed
  • most common presentation intracranial hemorrhage
  • treatment includes intravascular embolization, surgical excision, or radiation
  • preop considerations are same as with aneurysm
  • potential for significant blood loss is much higher (upwards of 3L)
167
Q

cranial nerve decompression

A
  • treats disorders of cranial nerves (trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia)
  • unilateral
  • usually caused by compression of a vascular structures
168
Q

cranial nerve decompression anesthetic considerations

A
  • position = lateral, prone, supine
  • monitoring = facial nerve, brainstem auditory evoked response, EMG
  • anesthesia = TIVA, brain relaxation
  • PONV = multimodal

N934 Advanced Principles of Anesthesia II (17 decks)

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