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Special Pops II > 2b. Intracranial Pressure & Spinal Cord Blood Supply > Flashcards

2b. Intracranial Pressure & Spinal Cord Blood Supply Flashcards

1
Q

normal ICP

A

5-15 mm Hg in adults

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2
Q

intracranial HTN

A

sustained increase in ICP above 20-25 mm Hg

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3
Q

causes of intracranial HTN (4)

A
  • obstructed CSF absorption
  • brain edema
  • expanding mass
  • elevated CBF
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4
Q

one of the first signs of increasing ICP is?

A

nausea and vomiting

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5
Q

other s/s of inc ICP

A
  • changes in LOC
  • headache
  • seizures
  • eyes: impaired movement, papilledema, pupillary changes
  • changes in speech
  • posturing
  • changes in VS
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6
Q

cushing’s triad

A
  • increased SBP
  • decreased HR
  • irregular respiratory pattern
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7
Q

gold standard for ICP monitoring

A

intraventricular catheter- ventriculostomy

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8
Q

complication of ICP monitoring

A

infection

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9
Q

patients that need ICP monitoring

A

TBI
GCS <9
abnormal CT scan
Normal CT with two of the following:
- > 40 years old
- Uni or bilat posturing
- SBP<90 mm Hg

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10
Q

3 components of ICP waveform

A
  • heart pulse waves
  • respiratory waves
  • slow vasogenic waves
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11
Q

true or false: steroids are contraindicated in TBI

A

true

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12
Q

arterial blood delivered to spinal cord va:

A

75% anterior spinal artery
25% posterior spinal arteries

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13
Q

major source of blood to the lower 2/3 of the spinal cord is via the…

A

artery of adamkiewicz

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14
Q

interruption of blood flow through the artery of adamkiewicz can l/t…

A

paraplegia

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15
Q

what comprises cranial volume?

A

blood
brain
CSF

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16
Q

ICP may be decreased by reduction of any of the following…

A

CBF
CSF
cerebral edema
cerebral mass

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17
Q

how does PaCO2 affect CBF?

A

hyperventilation decreases PaCO2 which causes vasoconstriction, this decreases CBF and therefore ICP

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18
Q

PaCO2 30-35 causes…

A

vasoconstriction of cerebral vessels

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19
Q

PaCO2 < 30 …

A

danger zone

risk of cerebral ischemia

(b/c O2 offloading is reduced)

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20
Q

Rx that reduce CMRO2

A

Propofol, Thiopental

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21
Q

what happens when BP surpasses upper limit of autoregulation?

A

cerebral edema

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22
Q

ways to promote CBF reduction via venous drainage

A

HOB 30º
head and neck midline to avoid JV compression
Keep PEEP at physiologic levels

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23
Q

position to avoid to promote venous drainage

A

Trendelenburg

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24
Q

to promote CBF reduction, what agents to avoid?

A

strong vasodilating agents: NTG, SNP

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25
Q

PaO2 below what increases CBF?

A

50

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26
Q

what is used for chronic treatment of CSF reduction?

A

VP or ventriculoatrial shunt

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27
Q

Rx to reduce CSF and treat idiopathic intracranial hypertension

A

Acetazolamide & furosemide

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28
Q

mainstays of cerebral edema treatment (3):

A
  • diuretics (loop + osmotic)
  • corticosteroids
  • hypertonic saline (not common)

*be mindful of hypovolemia

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29
Q

why are corticosteroids contraindicated in TBI?

A

cause elevated serum glucose, which can produce poor outcomes when cerebral ischemia is present

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30
Q

what are ways to reduce cerebral mass?

A
  • surgical debulking of cerebral tumors
  • mass reduced when cellular water is reduced with osmotic diuretics
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31
Q

intracranial aneursym

A

focal protrusion arising from weakened arterial walls at major bifurcations of the arteries at the base of the brain

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32
Q

how are aneurysms most commonly treated

A

endovascular coiling (>50%) or microsurgical clip ligation

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33
Q

what is the most common cause of SAH

A

aneurysm rupture into the subarachnoid space

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34
Q

explain T = P x r

A

T = circumferential wall tension
P = transmural pressure
r = mean vessel radius

increased blood pressure > increased tension stress > progressive vessel dilatation + weakening of vessel wall > enlargement of aneurysm

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35
Q

which law defines enlargement of aneurysms until rupture?

A

Law of Laplace: wall tension is proportional to vessel radius

36
Q

when does aneurysm rupture occur?

A

when mechanical stress on wall exceeds strength of wall tissue

37
Q

what scale is used for prognostic clinical outcome for SAH?

A

Hunt-Hess Grading System

38
Q

Hunt-Hess score 0

A

unruptured, asymptomatic aneurysm

39
Q

Hunt-Hess score 1

A

ruptured aneurysm
minimal headache
no neurologic deficits

40
Q

Hunt-Hess score 2

A

moderate to severe headache
no deficit other than cranial nerve palsy

41
Q

Hunt-Hess score 3

A

drowsiness, confusion
mild focal motor deficit

42
Q

Hunt-Hess score 4

A

stupor, significant hemiparesis
early decerebration

43
Q

Hunt-Hess score 5

A

deep coma
decerebrate rigidity

44
Q

what Hunt-Hess scores require intubation?

A

4 and 5

45
Q

s/s SAH

A

worst HA of my life
LOC (50%)
nausea and vomiting
fever
photophobia

46
Q

morbidity from SAH results from…

A

vasospasm!!!
rebleeding
obstructive hydrocephalus (if bleeding blocks outflow of CSF)

47
Q

leading cause of morbidity and mortality following SAH

A

vasospasm
may lead to cerebral infarct

48
Q

amount of bleeding in SAH is directly proportional to…

A

incidence of vasospasm

49
Q

vasospasm occurs how many days after SAH?

A

4-9

50
Q

why is it important to maintain CPP during vasospasm?

A

ischemic areas depend on pressure to receive blood flow

51
Q

triple H therapy for vasospasm

A

Hypertensive (higher CPP; use pressors)
Hypervolemic (crystalloids, colloids)
Hemodilution (Hct 27-32%; blood less viscous)

52
Q

what can be used for daily monitoring of vasospasm?

A

transcranial doppler

53
Q

Rx for vasospasm

A

nimodipine

54
Q

how does nimodipine treat cerebral vasospasm compared to other CCBs?

A

Nimodipine primarily targets L-type calcium channels in cerebral arteries, which are associated with vasospasm after subarachnoid hemorrhage (SAH).

Unlike other calcium channel blockers, nimodipine has a more selective effect on cerebral vessels, making it suitable for preventing and treating cerebral vasospasm.

55
Q

what is the gold standard for detection of intracranial aneurysms?

A

digital subtraction angiography

56
Q

23% of patients with intracranial aneurysm have…

A

neurogenic pulmonary edema

57
Q

EKG changes with intracranial aneurysm

A

PVCs
T wave inversion
ST depression

58
Q

induction for craniotomy for intracranial aneurysm

A
  • goal = smooth induction
  • decrease CBF by inducing cerebral vasoconstriction
  • pressors (CPP) i.e. phenylephrine during and after induction
  • pts may benefit from moderate hyperventilation during induction
59
Q

anesthetic maintenance for craniotomy for intracranial aneurysm

A

Iso or Sevo 0.5 MAC (if EP monitoring)
Avoid N2O
Propofol gtt (↓ CMRO2)

60
Q

other maintenance for craniotomy for intracranial aneurysm

A

BP control (aline preop)

Substantial HTN = rebleeding, rupture, permanent neuro deficits or death

Substantial hypoTN = cerebral ischemia and infarct

61
Q

emergence for craniotomy for intracranial aneurysm:
Hunt-Hess I-III

A

extubate
titrate BBlockers and vasodilators

62
Q

emergence for craniotomy for intracranial aneurysm:
Hunt-Hess IV-V

A

remain intubated + sedated postop
avoid coughing
HOB elevated 30º on transport

63
Q

Intra-op Concerns for AVM intubation

A

fiberoptic awake
(if arrives with stereotactic frame)

64
Q

Intra-op Concerns for AVM: complication

A

VAE

place central line

65
Q

Intra-op Concerns for AVM: msc

A

Aline
mild hypothermia
brain relaxation

66
Q

strategies for brain relaxation

A

↓ PaCO2 (dec cerebral vascular volume)

mannitol/furosemide (monitor K+ and Na+)

67
Q

mild hypothermia at what ºC can ↓ CMRO2 and to ↓ susceptibility to ischemia?

A

Mild hypothermia (33–34°C)

(CMRO2 decreases ~30% @ 33°C)

68
Q

effective and safe induction agents for AVM

A

Barbiturates, propofol, and etomidate

69
Q

methods to blunt stimulation of laryngoscopy & Mayfield placement

A

+Deepen with VAA
+Esmolol
+Lido
+Short acting opioids
+Dexmedetomidine

70
Q

NMBs for AVM induction

A

non-depolarizing agents, avoid sux

71
Q

emergence for AVM

A

close regulation of BP = key
suppress cough = lidocaine IV
HOB elevated 20-30º

72
Q

treat increases in BP for AVM

A

B-blockers or vasodilators

73
Q

monitors for tumor craniotomy when sitting or beach chair position and why?

A

precordial doppler,
CVP monitoring, or
TEE on standby

d/t risk of VAE

74
Q

induction for tumor craniotomy

A

DEEP anesthesia
complete skeletal muscle paralysis to avoid ↑ICP

75
Q

anesthesia maintenance for tumor craniotomy

A

maintain CPP
maintain euvolemia and eucapnia (consider mannitol)
consider mild hyperventilation
HOB 20-30 degrees
may require CSF drain

76
Q

tumor craniotomy emergence

A

goal = rapid awakening
avoid bucking, coughing (lidocaine)
treat BP w/ BBs and vasodilators

77
Q

what MAP may a surgeon require to test hemostasis after tumor is resected during craniotomy?

A

transient increase to 90-100 mm Hg

78
Q

awake craniotomy indications

A

epilepsy
tumors involving motor or speech (eloquent cortex)
patients with full understanding only

79
Q

induction for awake crani

A

LMA
Mayfield headrest
cranium removal
patient positioning

80
Q

awake crani premapping

A

mannitol slow infusion
Precedex
scalp block
aline
foley

81
Q

preop management for ventricular shunt

A

assess for cushing’s triad
HA w/ ICP > 15 mm Hg
no preop med required

82
Q

goals for ventricular shunt

A

normocarbia and normovolemia

83
Q

how does hyperventilation and hypocarbia affect ventricular shunt maintenance

A

makes cannulation of vessel difficult

maintain PeCO2 35-40 mm Hg

84
Q

how does seizure activity during GA manifest?

A

abrupt changes in HR and BP
increased CO2 production

85
Q

termination of seizures

A

propofol, barbiturates, benzos

other: surgeon may apply cold saline to brain surface

86
Q
A

Special Pops II (6 decks)

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