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6901 > Neuro > Flashcards

Neuro Flashcards

1
Q

Main CNS inhibitory neurotransmitter

A

GABA

  • Opens Cl channels
  • Reduces excitability of neurons by hyperpolarizing them
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2
Q

Main CNS excitatory neurotransmitter

A

Glutamate

  • Activates NMDA receptor (opens Na channel)
  • When activated it depolarizes neurons, making them more likely to fire action potentials
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3
Q

3 classification actions of neurons

A

Sensory (afferent, toward posterior root)
Motor (efferent, away from anterior root)
Interneuron

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4
Q

Gyri vs Sulci

A

Gyri: Outer 3mm area of cerebral structure that is convoluted to increase surface area
Sulci: Grooves that separate Gyri

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5
Q

4 cerebral structure lobes and their functions

A 
Frontal
-Motor, thought
Parietal
-Pain, pressure, temperature, touch
Temporal
-Hearing, smelling, recognition, memory
Occipital
-Visual
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6
Q

Brainstem: Midbrain, Pons, and Medulla

A

Contain reticular activating system
-Consciousness, arousal, alertness
Pons: connects midbrain and medulla oblongata
Medulla: Respiratory and cardiovascular centers

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7
Q

3 meningeal layers and spaces in between them

A

Cover brain and spinal cord

  • Epidural space is above dura
  • Dura: thickest, providers structural support
  • Subdural space
  • Arachnoid: thin cobweb like, major pharmacologic barrier (BBB), avascular
  • Subarachnoid space, contains CSF
  • Pia: thin, highly vascular
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8
Q

Cranial nerve pneumonic and sensory/motor pneumonic

A 
Olfactory:On:Some
Optic:Occasion:Say
Oculomotor:Our:Money
Trochlear:Trusty:Matters
Trigeminal:Truck:But
Abducens:Acts:My
Facial:Funny:Brother
Vestibulocochlear:Very:Says
Glossopharyngeal:Good:Big
Vagus:Vehicle:Brains
Accessory:Any:Matter
Hypoglossal:How:More
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9
Q

2 main arteries to brain

A

Carotid arteries: Anterior portion of brain

Vertebral arteries: Posterior portion

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10
Q

Circle of Willis

A

Anastomosis formed by arteries giving blood supply to the brain

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11
Q

Cerebral blood flow (normal ml/g/min and percentage of cardiac output the brain receives)

A

50mL/100g/min of brain tissue
-700-750mL/min
15-20% of CO
-Disproportionately large b/c high metabolic rate, inability to store energy

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12
Q

Cerebral Perfusion Pressure calculation and normal number, ICP where CPP/CBF compromised

A

MAP-ICP/CVP
-ICP vs CVP=whichever is higher (CVP at ear canal)
Normally 10-15 mmHg
>30 even if MAP is normal CPP/CBF can be compromised

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13
Q

Cerebral metabolic rate of oxygen

A

CMRO2
Glycolysis -> ATP =90% aerobic process
-Parallels glucose consumption
-Influences CBF directly

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14
Q

How long cellular injury can occur in without oxygen stores/ATP store depletion

A

3-8 minutes

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15
Q

What CPP/MAP that CBF will remains constant with

A

50-150mmHg

-Can shift in chronic hypertension

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16
Q

O2/CO2 effect on CBF

A

O2 has little effect unless its <50mmHg
CO2=Most important regulator
-CBF changes 3% for every 1mmHg change in PaCO2

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17
Q

Steal phenomenon

A

Hypoventilation/hypercarbia -> increased CBF to normal areas

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18
Q

Temperature effect on CBF

A

1C decrease -> 5-7% decrease in CBF

-also decreased CMRO2

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19
Q

Blood viscosity impact on CBF

A 
Increased viscosity (Hct) -< decreased CBF
Optimal Hct for O2 delivery to brain =30%
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20
Q

Autonomic influence on CBF

A

Sypathetic -> Vasoconstriction/decreased CBF

Parasympathetic -> Vasodilation/increased CBF

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21
Q

CSF (where produced, rate of production, total volume present at a time, normal CSF pressure)

A
  • Produced at choroid plexus, secreted by ependymal cells there
  • Produced at 30mL/hr
  • 150mL present at a time (recycles every 3-4 hours)
  • Normal CSF pressure: 5-15mmHg
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22
Q

Brain percentages of brain vs blood vs CSF

A

Brain: 80%
Blood: 12%
-ICF, ECF
CSF: 8%

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23
Q

ICP level considered intracranial HTN

A

> 15mmHg

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24
Q

Cushing reflex

A

HTN, bradycardia, respiratory irregularities

  • Brain ischemia if ICP is too high
  • Increases MAP to compensate but then CPP falls further -> more ischemia
  • Last ditch effort by the body to maintain homeostasis in the brain (usually ends up making things worse)
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25
Q

Blood brain barrier (how it’s formed, what passes through well vs not well)

A

Formed from tight junctions between endothelial cells
Passes through well: Lipid soluble molecules
Not well: Large, highly charged, water soluble

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26
Q

Intra vs extracranial causes of HTN

A 
Intracranial
-Brain tumor
-Trauma
-Intracerebral hemorrhage
-Stroke
-Hydrocephalus
Extracranial
-Hypercarbia
-Hypoxia
-HTN
-Hyperpyrexia
-Venous outflow obstruction (jugular pressure, intrathoracic pressure)
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27
Q

Compensatory mechanisms for increased ICP

A
  • Decreased CSF production/increase reabsorption
  • Translocate CSF to spinal column
  • Decrease CBF
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28
Q

Gold standard for ICP monitoring

A

Intraventricular catheter

-Also allows for drainage of CSF

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29
Q

Volatile agent effect on CBF/CMRO2

A 
Low dose
-CBF unchanged or slightly increased
Higher dose
-Vasodilated -> increased CBF
*Autoregulation impaired at 1MAC
-Decreased CMRO2
-Iso increases the most, sevo the least
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30
Q

Coupling CBF and CMRO2

A

In normal patients:
<1 MAC = coupling
-CMRO2 decreases along with CBF (coupled reductions)
>1 MAC = uncoupling
-CBF increases but CMRO2 doesn’t
-Volatile agents alter the coupling effect (don’t disengage it) by redistributing the blood flow

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31
Q

Robin Hood vs Circulatory Steal Phenomenon

A

How volatile agents change coupling effect (normal brain tissues can vasoconstrict, ischemic tissue can’t)

  • Circulatory Steal: Increased blood flow in normal areas but ischemic areas are dilated so blood flow is redistributed away from the ischemic area
  • Robin Hood: Normal parts of brain vasoconstrict to decrease flow to normal area to give to ischemic area
  • Barbiturates will cause this vasoconstriction
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32
Q

Which inhaled anesthetic increases CBF the least

A

Isoflurane, also decreases CMRO2 the most

Then sevo

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33
Q

N2O use in neurosurgery

A

Controversial

-Increases ICP, CMRO2, CBF (but this doesn’t happen when its used with IV anesthetics or hypocapnea)

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34
Q

Propofol use in neurosurgery

A

Decreases CBF and CMRO2 (dose dependent)

“Relaxes brain”

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35
Q

Etomidate use in neurosurgery

A

Decreases CMRO2, CBF, ICP

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36
Q

Ketamine use in neurosurgery

A

Dilates cerebral vasculature and increases CBF 60-80%

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37
Q

Opioid use in neurosurgery

A

Have minimal effect on CBF, CMRO2, and ICP

38
Q

Benzo use in neurosurgery

A

Decreases CBF and CMRO2 (to a lesser extent than barbiturates)

39
Q

Precedex use in neurosurgery

A

Decreases CBF without a decrease in CMRO2 (could limit adequate cerebral oxygenation)

40
Q

Muscle relaxant use in neurosurgery

A

Succs
-May increase ICP, CBF, CMRO2 (increased muscle spindle activity)
-Nonfasciculating dose of NMDA will help blunt this increase
NMDAs
-No effect on ICP, CBF, CMRO2
-Histamine release may cause vasodilation -> increased ICP
-Can’t do if cranial nerve monitoring is needed

41
Q

Vasoactive agent use in neurosurgery

A

Labetalol/Esmolol
-No effect on CBF, CMRO2
Nipride/Nitro/Hydralazine
-Dilate cerebral vessels -> increased CBV/ICP
Phenylephrine
-Possibly causes decreased CBF, some studies don’t support this

42
Q

IV agent that dilates cerebral vasculature

A

Ketamine

43
Q

Anti-seizure medication effect on NDMRs

A

Patients on phenytoin and anti-seizure medications have hepatic enzyme induction

  • Rapidly metabolize NDMRs
  • Need increased dose and will have a decreased DOA
44
Q

Barbiturate use in neurosurgery

A

Decrease CMRO2 - coupled with reducing CBF/CBV

45
Q

End point for maximal brain protection

A

Burst suppression

46
Q

Steroid use during neurosurgery

A

Dexamethasone 4mg q6h
Decrease edema associated with lesions/tumors
-Penetrate BBB

47
Q

Anticonvulsant use during neurosurgery

A

Dilantin: Usually administered prophylactically

-Acute irritation of cortical surface can result in seizures

48
Q

Diuretic use during neurosurgery

A 
Loop diuretics
-Decrease CSF production/cerebral edema
Osmotic diuretics
-Decrease water content of brain
-Mannitol: Rapid admin may produce vasodilation/increased CBF/increase ICP. *Administer 0.25-1g/kg slowly over 10-15 mins
-Check Na levels regularly
49
Q

Preop eval for neurosurgery: Cardiac risks

A
  • Delay surgery 2 weeks after simple balloon angio
  • Delay 4-6 weeks after bare metal stent placement
  • Delay 1 year after drug eluting stent
50
Q

Preop eval for neurosurgery: meds/premeds

A
  • Meds: Know anticonvulsant plan and last dose
  • Premeds: Caution with benzos/opioids. Respiratory depression -> increased ICP
  • No premeds in patients with midline shift or abnormal ventricular size
51
Q

Paralysis or weakness with succs use

A
  • In acute stroke/SCI succs is OK

- After 48-72 hours AcH receptors are upregulated -> hyperkalemia -> cardiac arrest

52
Q

IV anesthetic that doesn’t interfere with electrophysiological (EP) mapping

A

Precedex

-Also provides hemodynamic stability

53
Q

Anesthesia maintenance during neurosurgery

A

< 1 MAC with Propofol and narcotic

  • Mannitol, hypertonic saline, TIVA
  • Hypocapnea offsets cerebral vasodilation from inhalation agents
54
Q

Hyperventilation in neurosurgery

A

Causes cerebral vasoconstriction/brain relaxation

  • But can potentially exacerbate cerebral ischemia
  • Avoid in TBI patients unless briefly necessary to manage acute increase in ICP
  • gPaCO2=30-35
55
Q

IVF in neurosurgery

A

Goal=euvolemia
Hypertonic saline
-Osmotic effect -> reduced ICP
-Low side effects but may cause electrolyte abnormalities/cardiac failure
Dextrose containing fluids
-Avoid
High glucose levels may exacerbate neurological injury during ischemia

56
Q

Target blood sugar during neurosurgery

A

Normoglycemia or 140-180
Check q30mins
Variability in blood glucose can cause cerebral osmotic shifts

57
Q

Neurosurgery emergence before/after closing dura

A 
Before
-PaCO2 allowed to return to normal
-BP raised 120% above baseline so surgeon can assess the ability to withstand challenges
After
-Maintain BP at baseline
58
Q

Where to zero A-line for neurosurgery

A

External auditory meatus

-Same as circle of willis

59
Q

Overall methods to provide adequate brain relaxation

A
  • Sub-MAC volatile anesthesia and/or TIVA
  • Mild-moderate hyperventilation
  • Minimize tumor edema with mannitol, dexamethasone, HTS
  • Maximize venous drainage/minimize congestion/avoid excessive neck rotation
60
Q

Venous air embolism often occurs when surgical site is ____

A

20cm above the heart

61
Q

Paradoxic air embolism

A

If air enters venous circulation and travels through patent foramen ovale to arterial side
-May present as acute cerebral vascular or coronary event

62
Q

Most sensitive monitor to detect VAE

A

TransEsophageal Echocardiography (TEE)

63
Q

Pituitary

A 
Tumors are rarely metastatic
S/Sx: Neuro, *visual, hormonal changes
-Amenorrhea
-Galactorrhea
-Cushins (increased ACTH)
-Acromegaly (increased GH)
-Hyperthyroid
-Panhypopituitarism (hormone replacement with cortisol, levothyroxine, DDAVP)
-Diabetes insipidus
64
Q

Pituitary surgery transphenoidal vs craniotomy

A

Intracranial only when tumor>10mm

Transphenoidal=reduced morbidity and mortality

65
Q

Diabetes insipidus associated with pituitary surgery

A

Common complication

  • No ADH production, temporary or permanent, intraop or post op
  • Tx: DDAVP
66
Q

Hunt & Hess Classification

A

What surgeons use for SAH to indicate mortality rate

  • Score 0-5
  • 3=Mortality rate 5-10%
  • 5=Mortality rate 30-40%
67
Q

Rebleeding after SAH

A

50% chance of occurring in the first few days, life threatening
-Typically wait 2 weeks to do elective repair

68
Q

Postponing surgical clipping of ruptured aneurysm

A

Shouldn’t be postponed unless hemodynamically unstable patient
-Once it’s done the risk of recurrent hemorrhage is gone

69
Q

Vasospasm after SAH

A

Leading cause of morbidity and mortality after SAH (1/4 will get it)

  • Reactive narrowing of cerebral arteries, impairs circulation -> ischemia and infarction
  • Detected with angiography
  • Peak 4-9 days postop
70
Q

Vasospasm treatment

A 
Triple H method: 
-HTN (MAP 20-30 above baseline)
-Hypervolemia
-Hemodilution (Hct ~30%)
Nimodipine PO decreases morbidity from cerebral ischemia
71
Q

Anesthesia for endovascular treatment of aneurysms

A
  • Patient movement is devastating: *keep relaxed

- Avoid hyperventilation! (makes access more challenging)

72
Q

Awake epilepsy surgery or awake craniotomy anesthetic considerations

A

Pt is sedated but able to respond

  • Done to facilitate monitoring of the region of the brain the surgeon is operating on
  • Contraindications: anxiety, claustrophobia, psych disorders, difficult airway, OSA, orthopnea
  • Propofol or precedex drip
73
Q

Asleep awake asleep technique

A

Used for epilepsy and tumor resection surgery
General with LA infiltration on skull
Pt emerges in middle of surgery
-Neurosurgeon applies electrical stimulation to map which allows for maximal tumor resection and minimizes neurologic deficits
*Preop pt education of what to expect

74
Q

Head trauma goal

A

Secure the airway rapidly and efficiently with minimal/no neck movement

  • Increases difficulty of intubation
  • Incorrectly applied CP may displace cervical fractures
75
Q

Glascow coma scale possible scores and categories

A

3 (bad) - 15
Eye opening 1-4
Verbal response 1-5
Motor response 1-6

76
Q

Cerebral autoregulation after head trauma (and goal CPP)

A

Impaired
-Avoid hypotension (->ischemia) and HTN (->hemorrhage)
-Albumin -> higher mortality rate/unfavorable outcomes. Don’t use it unless pts are hypoalbuminemic
-Can cause cerebral edema
-Use mannitol or hypertonic saline
Goal CPP 50-70

77
Q

Goal PaO2 ETCO2 and temp in head trauma with increased ICP patients

A

PaO2 >60 SpO2>90
ETCO2 30-35
Moderate hypothermia (controversial, some studies say no benefit)

78
Q

Barbiturate use in head trauma/elevated ICP patients

A

Only if they’re hemodynamically stable and have been adequately volume resuscitated
-Not if MAP and CPP can’t be maintained

79
Q

Normal cerebral oximetry (SctO2)

A

60-80%

80
Q

BP goal during carotid endarterectomy (CEA)

A

Controlled 20% over baseline
-Usually with phenylephrine drip
SBP>180 may be associated with CVA

81
Q

Nerve injuries or hematoma after carotid endarterectomy

A

Nerve injury: Hypoglossal, sublingual, or RLN (hoarseness)
Wound hematoma: Worry about tracheal deviation, immediate action required (secure airway in OR)
-Usually precipitated by HTN in PACU

82
Q

Carotid artery stenting typical anesthesia and complication/what to do

A

Performed under sedation, done for patients who are poor surgical candidates
Near vagal nerve, may get bradycardia or asystole during balloon angioplasty of internal carotid artery
-Don’t give atropine-don’t want tachycardia
-Have surgeon infiltrate lidocaine-will prevent

83
Q

EEG: Deep anesthesia vs cerebral ischemia

A

Both produce similar changes

84
Q

Meds/labs that cause EEG activation

A 
Inhalation agents
-subanesthetic
Barbiturates
-small dose
Benzos
-small doses
Etomidate
-small doses
N2O
Ketamine
Mild hypercapnia
Stimulation
Hypoxia
-early
85
Q

Meds/labs that cause EEG depression

A 
Inhalation agents
-1-2MAC
Barbiturates
Opioids
Propofol
Etomidate
Hypocapnia
Marked hypercapnia
Hypothermia
Hypoxia
-Late
Ischemia
86
Q

Somatosensory evoked potentials (SSEP)

A

Test the integrity of the dorsal spinal column, ascending tract, and sensory cortex supplied to posterior spinal artery
-Used for spinal, CEA, and aortic surgery

87
Q

Anesthetic effect on SSEPs

A

Volatile agents have greatest effect

-Influenced by all anesthetics except MRs

88
Q

Motor evoked potentials (MEPs)

A

Assess function of motor cortex/descending tracts supplied by anterior spinal artery (vs SSEP=posterior/ascending tract)

89
Q

Anesthetic effect on MEPs

A

Volatiles, N2O, and NMDAs all suppress the response

-TIVA recommended

90
Q

Electromyography (EMG)

A

Recording of electrical activity of muscle that is irritated or injured

  • Identifies nerves and tests their integrity
  • Assesses motor function of facial nerve and CN III, IV, X, XI

6901 (9 decks)

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