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Principles III > neurosurgical anesthesia > Flashcards

neurosurgical anesthesia Flashcards

1
Q

what occupies the closed, non-expandable cranial vault?

A
  • brain tissue (80%)
  • blood (12%)
  • CSF (8%)
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2
Q

what are challenges of craniotomy procedures?

A
  • space-occupying lesions and increased intracranial volume in an enclosed space (increased pressure; something displaced, usu. blood)
  • altered vasoreactivity and autoregulation
  • control of CBF, CBV, CPP, ICP and brain swelling
  • unfamiliar monitoring
  • HOB away from the anesthetist
  • access to airway is not readily available
  • varying levels of noxious stimuli (intense at beginning and end; little in the middle)
  • flow and metabolism are coupled
  • blood loss and hemodynamics can change rapidly
  • head ROM is fixed d/t cranial pinning
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3
Q

what are the varying levels of noxious stimuli during craniotomy?

A
  • scalp, skull, dura elicit increased noxious stimuli (sawing open)
  • brain tissue almost free from nociceptive nerve tissue (once in, may see a drop in BP d/t decreased stimulation)
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4
Q

what is cushing’s reflex?

A

with an increased ICP will see a reflex systemic HTN and decreased HR
*increased ICP can lead to brain damage (ischemic neurological tissue)

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5
Q

what is the use of epinephrine soaked gauze and what is the AI?

A
  • used by surgeon to stop bleeding by immediate vasoconstriction where it is placed
  • as it is absorbed systemically will see beta 2 effects causing systemic vasodilation and a decrease in BP
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6
Q

since hemodynamics can change rapidly w/ craniotomies, what is best practice?

A

-vasoconstrictors AND vasodilators inline and ready for immediate titration (both are hung and titrated as needed to keep hemodynamics at optimal level)

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7
Q

what is the anesthetic goal during craniotomies?

A

keep the brain “relaxed” not “tight”

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8
Q

describe metabolism of the brain

A
  • glucose is the primary substrate of metabolism
  • hypoglycemia worsens hypoxic injury
  • metabolic rate of the brain is measured in O2 consumption
  • cerebral metabolic rate of oxygen consumption (CMRO2)
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9
Q

what does “flow and metabolism are coupled” in the brain mean?

A

high brain metabolic activity causes high CBF

*flow and metabolism are proportional

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10
Q

how much of the CO does the brain utilize?

A

650-700 ml out of 5000 total of CO

*15-20% of CO

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11
Q

what is the average cerebral blood flow (CBF)?

A

avg. 50 ml/100 gm/min

* can vary from 30-300 ml/100 gm/min

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12
Q

what EEG changes are seen with decreases in CBF?

A
  • less than 25 ml/100 gm/min: slowing of EEG
  • 15-20 ml/100 gm/min: isoelectric EEG
  • less than 10 ml/100 gm/min: irreversible injury
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13
Q

what parts of the brain are more sensitive to hypoxic brain injury?

A
  • hippocampus (memory)

- cerebellum (coordination; movement)

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14
Q

how is cerebral perfusion pressure determined?

A

CPP equal to MAP-ICP or CVP (whichever is higher)

*since ICP/CVP is small, CPP essentially equal to MAP

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15
Q

at what MAP is CBF autoregulated?

A

50-150 torr

*autoregulation diminished below 50 torr

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16
Q

what EEG changes are seen with decreases in CPP?

A
  • CPP less than 50 torr: EEG changes

- CPP less than 25 torr: irreversible damage

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17
Q

what is CBF proportional to?

A

PaCO2

*when Vm doubles (CO2 dropped), CBF decreases by half

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18
Q

how does temperature effect CBF?

A

CBF increases 5-7% for every 1 degree C temp

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19
Q

how do volatile agents affect the brain?

A
  • all decrease cerebral vascular resistance: cerebral vascular dilation
  • dose dependent impairment of autoregulation
  • increases CBV, CBF, and ICP
  • decrease CMRO2 and abolishes cortical activity
  • *neuroprotective at high doses
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20
Q

with volatile agents what must be done to offset the increase in ICP?

A

hyperventilate

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21
Q

how does nitrous oxide affect the brain?

A
  • expands closed gas spaces

- increases CBF, ICP, and CMRO2

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22
Q

when should N2O be avoided in craniotomies?

A
  • presence of intracranial air such as during a recent craniotomy, repeat craniotomy or cranial trauma
  • evoked potential signal is inadequate
  • evidence of increased ICP
  • tight brain
  • *just don’t use
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23
Q

how do barbiturates (thiopental) affect the brain?

A
  • decreases CBF, ICP, and CMRO2
  • inhibit excitatory neurotransmitter receptors
  • slowing of EEG
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24
Q

how does propofol affect the brain?

A
  • dose dependent decrease in CBF, CMRO2
  • isoelectric EEG at 500 mcg/kg/min
  • neuroprotective
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25
Q

how does etomidate affect the brain?

A
  • decreases CBF, ICP, and CMRO2

* *but can cause seizures in pts. w/ seizure history (spikes CMRO2 up; don’t want to risk)

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26
Q

how do opioids affect the brain?

A
  • dose dependent decreases in CBF, CMRO2

* Demerol metabolite, normeperidine, can cause seizures

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27
Q

how do benzodiazepines affect the brain?

A
  • anticonvulsants
  • decreases in CBF, CMRO2
  • respiratory depression limits use (increased CO2 leads to increased CBF)
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28
Q

how does ketamine affect the brain?

A
  • dissociative effects
  • increased ICP (more than 80%)
  • increased CBF
  • avoid
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29
Q

how do muscle relaxants affect the brain?

A
  • depolarizers (SCh): increased ICP, CBF, CMRO2
  • contraindicated in denervated muscle, CVA, motor neuron lesions
  • nondepolarizers: effects are small
  • anticonvulsants like Dilantin are enzyme inducers and cause and increased dosage requirement of nondepolarizers (constantly monitor nerve stimulator)
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30
Q

describe fluid management considerations for craniotomy

A
  • avoid dextrose containing solutions
  • limit volume of LR
  • use colloid and NS for volume resuscitation
  • limit hetastarch to 1-1.5 L to avoid coagulopathy
  • maintain hct at 30-35%
  • mild volume expansion for aneurysm clipping may help reduced vasospasm
  • keep pts. isovolemic, isotonic, and isooncotic
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31
Q

describe monitoring including during a craniotomy

A
  • EKG
  • direct arterial BP
  • ETCO2, pulse ox, ABGs
  • peripheral nerve stimulation
  • CVP
  • body temp (usu. keep cold)
  • urinary output
  • EEG or SSEP
  • cerebral oximetry
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32
Q

how do volatiles affect SSEP?

A
  • increase in latency
  • decrease in amplitude
  • IV anesthetics affect SSEP less than inhaled anesthetics
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33
Q

how do etomidate and ketamine affect SSEP?

A

increase in amplitude

34
Q

how do opioids affect SSEP?

A

no effect on amplitude

35
Q

how does N2O affect SSEP?

A

60% N2O: decreased amplitude

-no effect on latency

36
Q

how does CBF affect SSEP?

A

reductions in blood flow decrease SSEP

37
Q

what is important to remember if pt. has SSEP monitoring?

A
  • GA inhibits neurotransmission
  • regulate hemodynamics w/ non-anesthetic agents b/c its important to maintain a constant anesthetic level throughout the procedure so they can know if changes in SSEP are d/t nerve damage
38
Q

what is the purpose of EEG monitoring?

A

detects decreases in perfusion and ultimately ischemia based on reductions in electrical brain activity

39
Q

how does the EEG detect decreases in perfusion?

A
  • CBF for electrical failure is still higher than that needed to maintain cell integrity
  • will see an EEG change before any cell damage occurs
40
Q

what other factors can affect the EEG?

A
  • hypothermia
  • tumors
  • anesthesia
  • *crucial to maintain the same level of anesthesia throughout the surgical procedure
41
Q

describe sensory evoked potentials

A
  • assess the integrity of sensory pathway
  • stimulation of peripheral nerve sends electrical signal to brain, where electrodes sense response
  • damage to the pathway will display a decreased signal amplitude and an increased latency
  • SSEP: median and posterior tibial nerves stimulus recorded at spinal or cortical sites
  • BAEP: clicking sends auditory nerve sensory signal; indicated for surgery in posterior fossa to assess integrity of CN8
42
Q

describe motor evoked potentials

A
  • better assessment for spinal surgery b/c anterior (motor) cord is at greatest risk than posterior (sensory)
  • stimulus above the surgical site via transcranial or direct stimulation of spinal cord
  • electrical potentials measured below the surgical site by monitoring nerve or muscle potentials
  • anesthesia affects transcranial greater than direct spinal
  • MEP usefulness still under discussion
  • EMG: monitors motor response to nerve stimulation; used to assess facial nerve integrity
  • *avoid paralytic agents when MEP used
43
Q

what are goals of induction for a craniotomy?

A
  • smooth induction
  • avoid increase in ICP or compromising CBF
  • avoid HTN (increases CBF and ICP)
  • avoid hypotension (decreased CPP)
  • maximize venous drainage: avoid excessive neck flexion; HOB up greater than 15 degrees
  • hyperventilation during apnea time or preoxygenation period
  • opioids can blunt SNS outflow
  • adequate muscle relaxant to prevent bucking/coughing
44
Q

what are goals of emergence for a craniotomy?

A
  • slow, smooth and controlled!!
  • neurological function intact prior to extubation
  • prevent straining, coughing, or bucking on ETT (increased ICP, re-bleeds, hematoma, etc)
  • fentanyl
  • HOB returned to machine and CRNA
  • rapid awakening promotes neuro assessment
45
Q

when should spontaneous breathing be re established?

A

prior to skin closure and pin removal

*once pins (noxious stimuli) removed, then return of spontaneous ventilation may be delayed

46
Q

what categories are masses divided into based on location on the brain?

A
  • supratentorial (cerebrum): above the tentorium

- infratentorial (cerebellum): below the tentorium (worse d/t vital respiratory and cardiac centers)

47
Q

what symptoms are seen w/ supratentorial mass lesions?

A
  • HA
  • seizures
  • hemiplegia
  • aphasia
48
Q

what symptoms are seen w/ infratentorial mass lesions?

A
  • cerebellar dysfunction (ataxia, nystagmus)

- brain stem compression (altered mental status or altered respirations)

49
Q

what are intracranial mass symptoms present based on?

A
  • growth rate: slow typically asymptomatic; fast acute neurological deficits
  • location: deficits align w/ location of masses
  • ICP: intracranial HTN is common
50
Q

what are common neurological symptoms usually present w/ intracranial mass?

A
  • reduced cognitive function
  • HA
  • focal neurological deficits
51
Q

what type of mass of majority of intracranial mass surgeries for?

A

supratentorial

52
Q

what are AIs for mass lesions?

A
  • all types have same anesthetic implications
  • brain edema and midline shift may be evident on CT
  • evaluate and document neurologic deficits (or will sue you for them)
  • many times are on anticonvulsants (enzyme induction), steroids (need coverage; abnormal glucose), and diuretics (hypovolemic; abnormal electrolytes)
  • present w/ HA, seizures, reduced cognitive and neuro functions, focal neuro deficits
53
Q

what should be done to avoid ICP?

A
  • avoid benzos and opioids pre-op (resp. depression leads to increased PaCO2 and increased ICP)
  • raise HOB 15-30 degrees to control ICP
54
Q

what are signs and symptoms of elevated ICP?

A
  • HA
  • N/V
  • papilledema
  • focal neuro deficits
  • altered mental status (AMS)
55
Q

what can contribute to poor outcomes after ischemic events?

A

increased blood glucose
increased brain temp
increased CPP
**neuroprotection: anesthetic induced suppression of electrocortical activity allows brain to tolerate disruption of metabolic substrate delivery

56
Q

how is ICP treated?

A
  • hyperventilation (PaCO2 30-35 mmHg)
  • admin. diuretics (mannitol or Lasix)
  • cerebrospinal fluid drainage if available
  • avoid over hydration; target normovolemia
  • elevate head; position to improve cerebral venous return; avoid neck vein compression
  • intracranial pressure monitor
  • optimize hemodynamics (MAP, CVP, PCWP, HR, CPP); consider antihypertensive
  • corticosteroids (decadron)
  • surgical decompression; consider decompressive craniectomy if hematoma is present
  • cerebral vasoconstriction (thiopental, propofol)
  • consider mild hypothermia
57
Q

what are concerns w/ posterior fossa surgery (infratentorial)?

A
  • vital brain stem centers in close proximity: circulatory and respiratory centers; RAS, ANS and some cranial nerves
  • infratentorial masses can obstruct CSF at 4th ventricle and lead to obstructive hydrocephalus
  • spontaneous ventilation is a form of monitoring respiratory center damage
  • sitting position is most preferred
58
Q

describe venous air embolism (VAE) risk w/ posterior fossa surgery

A
  • increased risk w/ open venous system subatmospheric
  • can occur in any position where wound is above heart
  • highest incidence (over 20%) during sitting craniotomy
  • dependent on volume and rate of entry
  • small air bubble diffuse into pulmonary system; large air bubbles can impede pulmonary flow leading to increased RV afterload and decreased CO
  • N2O enhances the air embolus
59
Q

what clinical presentation is seen with VAE?

A
  • decreased ETCO2 (flattens)
  • decreased oxygen saturation
  • sudden hypotension
  • circulatory arrest (obstructing RV outflow)
  • increased ET nitrogen d/t absorption through alveoli (nitrogen in the air that is entrained large enough to be captured on sensor in lungs)
  • precordial Doppler (most sensitive non-invasive): sporadic roaring sound
  • TEE (most sensitive invasive): o.25 ml air detected
  • precordial stethoscope: mill wheel
60
Q

describe treatment for VAE

A
  • notify surgeon on detection (will flood surgical field w/ saline and wax bone edges to close off “open system”)
  • dc N2O admin and admin 100% O2
  • perform valsalva maneuver or compression of jugular veins (close pop off and give breath and hold)
  • aspirate air from atrial catheter
  • support BP w/ volume and vasopressors
  • reposition in left lateral decubitus w/ 15 degree head down tilt if BP continues to drop
  • modify anesthetic as needed to optimize hemodynamics
61
Q

describe paradoxical air embolism

A
  • air enters the systemic circulation
  • patent foramen ovale (PFO) or atrial or ventricular septal defect
  • PFO exists in 30-35% of population (unknown)
  • further evaluation should be initiated for those suspected of having intracardiac defects (murmur)
  • surgical positioning may need to be altered to lessen the risks of air entrainment (prone rather than sitting)
62
Q

what is a cerebral aneurysm?

A

dilated intracranial arteries

-many types exist

63
Q

what are complications of aneurysms

A
  • subarachnoid hemorrhage (SAH)
  • bleeding
  • vasospasm (need to dilute cell mass and irritating factors)
64
Q

what is the leading cause of SAH (non traumatic)?

A

saccular aneurysm rupture

  • peak rupture age 55-60 y/o
  • females greater than males
65
Q

what vessels are mostly affected by aneurysms?

A
  • internal carotid bifurcation

- anterior cerebral artery

66
Q

what are signs of SAH?

A
  • intense HA (85%)
  • transient LOC (45%)
  • N/V (most often seen)
67
Q

what are complications of cerebral aneurysms?

A
  • SAH
  • HTN develops which can worsen SA bleed
  • autoregulation impaired (dropping BP not good option)
  • ECG: T and ST changes (non ischemic in origin, no adverse effect)
  • 50% of previously ruptured aneurysms re-bleed w/ 80% mortality
  • cerebral vasospasm (30%) 4 days post-op rupture is major cause of mortality and morbidity
68
Q

when is surgical intervention usu. done w/ cerebral aneurysms?

A

if greater than 7mm

69
Q

what are coiling procedures?

A
  • pt. put to sleep and paralyzed
  • enters through groin to fix aneurysm w/o cutting skull open
  • have been successful
70
Q

what correlates best w/ CPP?

A

BP transducer at the level of the external auditory meatus and tragus

  • estimates CPP at Circle of Willis
  • lower pressure than level of heart d/t vertical column and hydrostatic pressure difference
71
Q

how does the distance from the heart to circle of willis compare in mmHg of pressure?

A

10 cmH2O equals 7.5 mmHg

72
Q

describe treatment for vasospasm

A
  • no perfusion distal to site; promote perfusion
  • maintain CPP
  • augment BP and CO
  • admin inotropic agents (dopamine, dobutamine)
  • admin Ca+ channel blockers (nimodipine, nicardipine)
  • intravascular volume expansion
  • hemodilution (hct less than 32%)
  • correct hyponatremia
  • transluminal angioplasty
  • *triple H: hemodilution, hypervolemia, HTN**
73
Q

describe arteriovenous malformation (AVM)

A
  • progressively grow w/ time
  • intracerebral hemorrhage (not SA)
  • present at an earlier age (10-30) w/ bleeding
  • HA and seizures often present
74
Q

describe surgical Rx of AVMs

A
  • if neuroradiology Rx fails, then surgical resection
  • extensive blood loss compared w/ aneurysms
  • hyperventilation and mannitol facilitates surgical resection of AVMs or any mass
  • same techniques apply to AVM as for aneurysms
75
Q

describe pituitary surgery considerations

A
  • 20-50% are non-secretory
  • hypersecretory tumors can lead to acromegaly and hyperglycemia
  • difficult intubations may be a factor (enlarged facial features, laryngeal hypertrophy, enlarged tongue)
  • resection is usu. transphenoidal (may be intracranial)
  • cushing’s disease may be present
  • diabetes insipidus may occur post-op
76
Q

what are the benefits of transphenoidal resection for pituitary tumors?

A
  • less blood loss

- less mortality and morbidity

77
Q

what are presenting symptoms of cushing’s disease?

A
  • HTN
  • diabetes
  • osteoporosis
  • obesity
  • friability of skin
78
Q

what are anesthetic implications peri-op w/ transphenoidal resection?

A
  • remember, airway is shared w/ surgeon (ETT placed to left side and secured to chin)
  • upper lip free
  • thorough airway assessment
  • lubricate eyes to prevent fluids from entering
  • avoid N2O
  • *avoid hyperventilation as it causes pituitary to retract into sella, hindering resection
  • *raise ETCO2 to force the pituitary into view
  • be prepared for blood loss as carotid arteries lie in close proximity
79
Q

describe stereotactic procedures

A
  • usu. undertaken w/ MAC and light sedation
  • uncomfortable procedures are securing the halo w/ pins and drilling a hole in the skull, both of which are performed following local anesthetic infiltration
  • since halo preclude, direct laryngoscopy care must be taken not to obliterate respirations w/ sedation or compromise the pts. ability to maintain airway
  • an alternate airway plan for oxygenation and ventilation should be in place
  • greater airway control may be needed; fiberoptic bronchoscopy as head is in fixed position in pinned head frame
  • or just intubate from the start
80
Q

describe Arnold-Chiari malformation

A
  • malformation where medulla protrudes through foramen magnum
  • CSF outflow obstruction, hydrocephalus
  • more common in females
  • Rx: decompressive pressure relief
  • AIs: same as for posterior fossa surgery
81
Q

what are challenges w/ head trauma?

A
  • other traumatic injuries accompany
  • hypotension, hemodynamic instability
  • pulm. contusions, 70% have hypoxemia
  • assumed to have cervical spine injury
  • varying degrees of consciousness
  • increased ICP
  • brain contusion, deceleration injuries
  • hemorrhage, hematomas, epidural/subdural bleed
  • airway challenges: facial fracture, full stomach
  • primary neuro insult and secondary insult
  • *ketamine a good choice for trauma
82
Q

what are AIs w/ head trauma?

A
  • avoid N2O
  • treat HTN w/ increased agent, hyperventilation (avoid too much hyperventilation as it decreases CBF)
  • treat hypotension w/ alpha agonist
  • maintain CPP at 70-110 mmHg
  • treat enhanced vagal tone w/ atropine
  • avoid PEEP until after dura is opened b/c of increased ICP
  • may have to leave intubated and paralyzed until increased ICP is resolved

Principles III (6 decks)

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