6901 Neuro Part II Flashcards

1
Q

Low doses of volatile agents do what to CBF?

A

it’s either unchanged or increased

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2
Q

Low doses of volatile agents do what to CBF?

A

it’s either unchanged or increased

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3
Q

What happens to CBF in higher doses of volatile agent?

A

increases bc of the vasodilator effect

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4
Q

Autoregulation is impaired with what MAC?

A

> 1

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5
Q

Least and worst problematic inhalational agent?

A

sevo; halothane

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6
Q

Vasodilator influence of volatile agents is opposed by?

A

decreased CMRO2

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7
Q

Coupling includes what 2 values?

A

CBV and CMRO2

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8
Q

Coupling occurs at what MAC value?

A
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9
Q

What do volatile agents do to the coupling effect?

A

alter the coupling effect by redistributing the blood flow

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10
Q

Uncoupling is when?

A

CBF increases and CMR does not

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11
Q

What is circulatory steal?

A

increase in blood flow to normal areas but in ischemic areas vessels are maximally dilated and blood is redistributed away from ischemic area

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12
Q

Only what type of brain tissue can constrict?

A

normal

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13
Q

What happens to CBF in higher doses of volatile agent?

A

increases bc of the vasodilator effect

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14
Q

Autoregulation is impaired with what MAC?

A

> 1

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15
Q

Least and worst problematic inhalational agent?

A

sevo; halothane

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16
Q

Vasodilator influence of volatile agents is opposed by?

A

decreased CMRO2

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17
Q

Coupling includes what 2 values?

A

CBV and CMRO2

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18
Q

Coupling occurs at what MAC value?

A

less than 1

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19
Q

What do volatile agents do to the coupling effect?

A

alter the coupling effect by redistributing the blood flow

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20
Q

Uncoupling is when?

A

CBF increases and CMR does not

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21
Q

What is circulatory steal?

A

increase in blood flow to normal areas but in ischemic areas vessels are maximally dilated and blood is redistributed away from ischemic area

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22
Q

Only what type of brain tissue can constrict?

A

normal

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23
Q

What do volatile agents do to the coupling effect?

A

luxury perfusion which is when increased CBF causes decreased CMRO2

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24
Q

What type of MACs cause luxury perfusion/uncoupling?

A

higher

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25
Q

What is Robin Hood phenomenon?

A

vasoconstriction in normal vessels in the brain (decrease flow to normal area and increase flow to ischemic area)

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26
Q

Barbs cause what?

A

vasoconstriction

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27
Q

Effects of CBF last how long with all volatile agents?

A

2-5 hours

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28
Q

Which volatile agent causes the least vasodilation?

A

Iso

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29
Q

Which volatile agent causes biggest reduction in CMRO2?

A

Iso

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30
Q

Does N20 interfere with MEPs?

A

yes

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31
Q

What is the consensus about use of N20 in intracranial surgery?

A

controversial

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32
Q

N20 has been shown to increase what 3 things?

A

ICP, CBF, CMRO2

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33
Q

What’s significant about use of N20 with hypocapnia and IV anesthetics?

A

no change in CBF

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34
Q

Does Iso or Sevo increase the CBV more?

A

Iso

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35
Q

What does propofol do to CBF and CMRO2?

A

dose dependent decrease

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36
Q

Can you use propofol for MEP monitoring?

A

yes

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37
Q

What relaxes the brain better than volatile anesthetics?

A

propofol

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38
Q

What does etomidate do to CBF, CMRO2, and ICP?

A

decrease

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39
Q

The only agent that dilates cerebral vasculature and increases CBF by 60-80%?

A

ketamine

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40
Q

What type of effect do opioids have on CBF, CMRO2, and ICP?

A

minimal

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41
Q

What do benzos do to CBF, CMRO2?

A

decrease them to a lesser extent than barbs

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42
Q

What type of drug decreases CMRO2 the most?

A

barbs

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43
Q

What type of drugs decrease CBF the most?

A

propofol

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44
Q

Drug that is useful for awake craniotomy and carotid endarectomy?

A

dexmetomidine

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45
Q

Why is dexmetomidine a good drug for smokers?

A

their airways are really reactive and this allows for a smoother emergence

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46
Q

What does precedex do to CBF and CMRO2?

A

decreases CBF w/out decrease in CMRO2

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47
Q

Downfall to precedex?

A

may limit adequate cerebral oxygenation

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48
Q

Should you avoid suxxs when rapid paralysis is desired?

A

no

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49
Q

What is suxxs effect on CBF, CMRO2, ICP? What can you do to blunt that response?

A

increases prob d/t the fasciculations; give nonfasciculating dose

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50
Q

NMDAs effect on CBF, CMRO2, ICP?

A

little

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51
Q

Do you need to avoid NMDAs for cranial nerve monitoring?

A

yes

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52
Q

What about NMDAs may cause increased CBF?

A

histamine release that leads to dilation

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53
Q

What may NMDAs interact with?

A

seizure meds like phenytoin

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54
Q

If pt is on a lot of meds with hepatic enzyme induction what does that mean for suxxs and NMDAs?

A

rapidly metabolized and don’t last long; may need larger dose

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55
Q

These drugs are preferred for control of HTN after intracranial procedures?

A

Esmolol, Labetolol

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56
Q

What effect do Esmolol and Labetolol have on CBF and CMRO2?

A

none

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57
Q

Caution with use of these antiHTN drugs that impair autoregulation and dilate cerebral vessels and cause increased CBF and ICP?

A

nipride, nitro, hydralazine

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58
Q

Drug used to prevent vasospasm after subarachnoid bleed?

A

nimodipine

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59
Q

Adenosine is used for aneurysm clip surgeries why?

A

a lot easier to place clip if heart brady or stopped

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60
Q

Drug used during Na thiopental admin to offset hypotension?

A

phenylephrine

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61
Q

Most widely used drugs for decreasing CMR, with objective of causing coupled reduction in CBF and CBV?

A

barbs

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62
Q

What’s the end point for maximal brain protection?

A

burst suppression

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63
Q

Another drug that may cause coupled reduction in CBF and CBV?

A

propofol

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64
Q

How do glucocorticoids work for brain surgery?

A

penetrate the BBB and decrease edema associated with lesions

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65
Q

Most commonly used glucocorticoid regimen during intracranial surgery?

A

dexamethasone 4mg q6h

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66
Q

How long does it take to see effects from glucocorticoids in decreasing ICP?

A

several hours; so a lot are started 48 hours before surgery

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67
Q

A drug that is given prophylactically to decrease cortical irritation?

A

dilantin

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68
Q

These type of diuretics produce general diuresis and decrease the rate of CSF production and decrease cerebral edema?

A

loop diuretics

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69
Q

These type of diuretics decrease the water content of the brain?

A

osmotic

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70
Q

Do osmotic diuretics decrease ICF or ECF water?

A

both

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71
Q

Why do you give mannitol slowly?

A

may produce rapid vasodilation (hyperosmolarity), increased CBF, a transient rise in ICP, and increase in CBV

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72
Q

How quickly should you give mannitol and what should you monitor during it?

A

15 min; ICP

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73
Q

Dose of mannitol?

A

0.25-1g/kg

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74
Q

What do you have to do to prevent edema in prolonged surgeries if you have given mannitol during intracranial surgery?

A

check serum Na levels on regular basis

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75
Q

3 times fent, lido, prop should be given during intracranial surgery to blunt SNS response?

A

intubation, suctioning, skull pin application

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76
Q

Great risk of ICP spikes and brain herniation if midline shift >?

A

5cm

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77
Q

S/s increased ICP?

A

N/V, HTN, bradycardia, personality change, altered LOC, papilloedema, seizures, neuro deficits, resp pattern

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78
Q

How high should HOB be elevated to help with venous drainage?

A

15-30

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79
Q

How soon should intracranial surgery be delayed after balloon angioplasty, BMS, and DES?

A

> 2 weeks angioplasty, 4-6 BMS, 12 mos DES

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80
Q

Why do you use benzos and opioids with caution as premedication in brain surgery?

A

respiratory depression and increased ICP

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81
Q

In patients with midline shift and abnormal ventricular size what should you do with premedication?

A

omit

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82
Q

What 3 things should you avoid in neurosurgical patients?

A

hypotension, HTN, prolonged apnea

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83
Q

How should you treat hypotension in neurosurgical pts?

A

gentle volume and alpha adrenergic agonist

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84
Q

Which surgery do you need to be particularly mindful in preventing HTN with DL?

A

aneurysmal subarachnoid hemorrhage bc it can prevent recurrent hemorrhage from the aneurysm

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85
Q

Why should you prevent apnea in neurosurgical pt?

A

it causes increase in PaCO2 and corresponding cerebral vasodilation and decreases CPP

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86
Q

How can you blunt the effects of induction in neurosurgical pt?

A

fentanyl and lido 1.5 mg/kg

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87
Q

What does a flexed head impede?

A

jugular venous drainage and so it increases ICP

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88
Q

Why should you make sure all circuit connections are tight in neurosurgical pt?

A

bed is rotated 90-180 degrees

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89
Q

Cervical collar placement makes for a difficult what and therefore?

A

intubation; very sensitive to hypotension and HTN

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90
Q

2 contraindictions for suxxs use?

A

weakness or paralysis

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91
Q

2 conditions in which suxxs can only be used for the 48 hours following the injury? And why is that?

A

acute stroke or spinal cord injury; up regulation of the K receptors leading to hyperkalemia

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92
Q

Most IV agents (3) are indirect cerebral vasoconstrictors and decrease CBF, CMR leading to preserved autoregulation and CO2 activity?

A

propofol, thiopental, etomidate

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93
Q

Does dexmetomidine interfere with electrophysiological mapping?

A

no

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94
Q

What MAC of volatile agent should be used with SSEP monitoring and brain relaxation?

A
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95
Q

The 3 primary considerations in neurosurgery?

A

type of neuromonitoring planned, optimal brain relaxation, balance between adequate analgesia and ability to assess neuro function at the end of the surgical procedure

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96
Q

3 things to do to maintain brain relaxation?

A

o2/air infusion

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97
Q

4 ways to decrease ICP for optimal brain relaxation?

A

mannitol, hypertonic saline, TIVA, hypocapnia

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98
Q

One way to offset cerebral vasodilation from inhalation agents?

A

hypocapnia

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99
Q

MEP monitoring gets optimal signal with what type of anesthesia?

A

TIVA

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100
Q

A benefit of propofol infusion is that it provides better relaxation by further decreasing?

A

CBV

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101
Q

How does muscle relaxation facilitate venous drainage?

A

relaxes chest wall which decreases intrathoracic pressure and facilitates venous drainage

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102
Q

Some considerations with hyperventilation in neurosurgery?

A

cerebral vasoconstriction maintains decreased CBF and CBV, has a potential for causing or exacerbating cerebral ischemia, avoid in all pts with TBI, maintain PaCO2 between 30 and 35

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103
Q

What’s the exception for avoiding hyperventilation in all TBI pts?

A

if there is an acute increase in ICP hyperventilation can be done

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104
Q

A PaCO2 less than what should be discussed with the surgeon?

A

30

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105
Q

The goal for CVP in intracranial surgery?

A

euvolemia/ normal CVP

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106
Q

Fluid management in intracranial surgeries: pt should be kept (3)?

A

isovolemic, isotonic, and isooncotic

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107
Q

Fluid rate for intracranial surgery?

A

0.5-1 mL/kg/h

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108
Q

Should pre and intraop fluid and blood loss be replaced in intracranial pt?

A

yes

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109
Q

Is BBB subject to water movement?

A

yes

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110
Q

How does hypertonic saline reduce ICP?

A

osmotic effect and ability to remain outside of effective BBB

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111
Q

2 side effects of hypertonic saline?

A

electrolyte abnormalities, cardiac failure

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112
Q

What type of fluids should you avoid in intracranial pts?

A

dextrose containing

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113
Q

Why is it important to maintain normoglycemia in pts undergoing brain surgery?

A

high glucose levels may exacerbate neuro injury during ischemia

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114
Q

Target blood sugar in brain surgery?

A

140-180

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115
Q

When should you check glucose levels if pt having brain surgery?

A

definitely preop and check them frequently (q30 min) after

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116
Q

Intraop hyperglycemia is common in those undergoing?

A

emergent/urgent craniotomy following TBI

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117
Q

Increased variability in blood glucose can lead to?

A

increased osmotic shifts

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118
Q

How does hypoglycemia effect the brain?

A

it lowers brain tissue glucose concentration and the precipitation of brain energy crisis

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119
Q

Once the dura has been closed where do you maintain the BP?

A

at baseline

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120
Q

Signs of needing to delay extubation d/t upper airway edema?

A

facial edema and absence of cuff leak

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121
Q

3 considerations for prior to closure of dura?

A
  1. BP parameters should be set 2. PaCO2 should be allowed to return to normal; BP raised 120% above baseline 3. ability of brain to withstand such challenges can be directly assessed by the surgeon
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122
Q

Why may normal autoregulation not exist after brain surgery?

A

BBB leakage= hemorrhage and edema

123
Q

Late emergence may mask a problem such as?

A

hematoma or hydrocephalus

124
Q

There is a relationship between HTN and what formation during emergence?

A

hematoma

125
Q

3 goals of emergence after brain surgery?

A

avoid coughing or straining (with lido), sudden emergence may lead to uncontrolled BP, titrate short acting HTNives such as esmolol and labetolol

126
Q

Intraop monitoring for most intracranial procedures includes?

A

7 ASA monitors, 2 IVs, a line 0ed at level of external auditory meatus, foley, nerve stimulator, neurologic monitors (EEG), maybe central line

127
Q

7 things which influence ICP?

A

MAP/autoregulation, PaCO2, PaO2, viscosity, CMR (arousal, pain, seizures, temp), anesthetics, vasoactive agents

128
Q

Probably most common reason for neuro surgery?

A

surgery for tumors

129
Q

Common presentation for supratentorial surgery?

A

seizures, HA, endocrine abnormalities, aphasia, cognitive decline

130
Q

Common presentation for infratentorial surgery?

A

altered consciousness, nystagmus, abnormal ?

131
Q

Tentorium divides?

A

cerebral hemispheres from hind brain/cerebellum

132
Q

Tumors leading to intracranial HTN are at risk for?

A

cerebral ischemia and herniation

133
Q

3 devastating complications from brain tumor surgery?

A

brainstem injury-quadraplegia, VAE, pneumocephalus

134
Q

5 considerations for brain tumor surgery?

A

may be in unusual position, adequate relaxation of the brain optimizes surgical conditions, CV effects, avoid complications from surgery, assess preop LOC and CT

135
Q

Neck flexion can lead to what with the ETT?

A

kinking and right mainstem intubation

136
Q

4 ways to promote adequate brain relaxation?

A

sub MAC or TIVA, mild to moderate hyperventilation, minimizing tumor edema (dexamethasone, mannitol, HTS), preventing fullness from venous congestion (minimize excessive rotation of neck)

137
Q

Why do you have to pay meticulous attention to the EEG and a line in brain surgery?

A

brainstem is involved in systemic HDs

138
Q

What part of brain contains major motor and sensory pathways, CV and resp centers, RAS, and cranial nerves?

A

posterior fossa

139
Q

What part of the brain is involved in systemic hemodynamics and can cause rapid alterations in BP and HR?

A

brainstem

140
Q

What do you do if your patient starts having rapid changes in BP and HR during brain surgery?

A

let the surgeon know

141
Q

What position increases the likelihood of pneumocephalus? And why?

A

sitting position; air can readily enter subarachnoid space as CSF is lost

142
Q

When does tension pneumocephalus occur?

A

when brain expands so much and compresses the brain

143
Q

3 things pneumocephalus can cause?

A

delayed emergence, CV collapse, neuro deficits

144
Q

VAE usually occurs when surgical site is how much above the heart?

A

20 cm

145
Q

When do you particularly have to watch for VAE?

A

turning of brain flap and bone work

146
Q

What increases risk of VAE?

A

when open vessels cannot collapse

147
Q

Air is entrained thru what in VAE?

A

venous sinuses

148
Q

Massive air embolism produces?

A

major HD changes

149
Q

Incidence of VAE during craniotomy? And during cervical laminectomies?

A

40-45%; 10-15%

150
Q

What happens in venous air embolism?

A

airlock w/in the right ventricle leads to RHF which leads to decreased LV filling pressures which leads to decreased CO/BP and dysrhythmias. vascular obstruction increases dead space, nitrogen increases before ETCO2 decreases and SaO2 decreases

151
Q

What is a paradoxic air embolism?

A

air enters thru venous circulation and travels thru patent foramen ovale to the arterial side. it may present as CVA or coronary event

152
Q

Where do you place the precordial doppler to listen for VAE? And how much air can it detect?

A

between the 3rd and 6th ICS on the right sternal border; 0.25 mL air

153
Q

The greater the air embolus, the greater the drop in?

A

ETCO2

154
Q

Most sensitive monitor for VAE?

A

TEE

155
Q

End tidal gas monitoring in VAE shows?

A

decrease in ETCO2 and presence of end tidal nitrogen

156
Q

Where do you want the tip of the right atrial catheter to aspirate VAE?

A

junction between the SVC and right atrium

157
Q

Sensitivity for detection of VAE?

A

TEE > doppler > PAP and ETCO2 > CVC > BP > EKG

158
Q

Treatment of VAE?

A

tell surgeon, will flood field, 100 % FiO2 and turn of N2O, aspirate RA catheter, support BP with ephedrine and fluids, compress jugular veins to minimize air entrapment, can add PEEP if BP will tolerate, left lateral position or operative site lower than right atrium, CV support as needed, supine

159
Q

S/s pituitary tumor?

A

neuro, visual, and hormonal changes

160
Q

What’s the major visual change that happens when pt has pituitary tumor?

A

2 nasal sides of the field get cut out

161
Q

7 symptoms of pituitary tumor?

A

amenorrhea, galactorrhea, Cushings (increased ACTH), acromegaly (increased GH), hyperthyroidism, panhypopituitarism (hormone replacement requiring cortisol, levothyroxine, possibly DDAVP), DI

162
Q

Intracranial approach for pituitary surgery is used for?

A

tumors > 10 cm

163
Q

Some benefits of the transphenoidal approach to pituitary surgery?

A

reduced morbidity and mortality d/t decreased blood loss and less manipulation of brain tissue, panhypopituitarism and DI reduced

164
Q

Monitoring for pituitary surgery?

A

glucose and lytes

165
Q

Common complication from pituitary surgery?

A

DI

166
Q

Is DI temporary or permanent?

A

can be both

167
Q

DI is loss of what hormone production?

A

ADH

168
Q

Some descriptions of DI?

A

may occur intra or post op, diuresis as evidenced by urine osmo of

169
Q

Treatment of DI?

A

DDAVP 0.5-1 microgram IV or SQ

170
Q

Most patients with an aneurysm have a normal ICP unless?

A

it has ruptured

171
Q

S/s of a cerebral aneurysm?

A

severe HA, focal neurological deficits, lethargy, coma

172
Q

Peak age for rupture of a cerebral aneursym?

A

55-60 years

173
Q

Leading cause of subarachnoid hemorrhage?

A

rupture of saccular aneurysm

174
Q

Type of aneurysm that is usually d/t an infection?

A

mycotic

175
Q

Type of aneurysm usually caused by cervical neck trauma?

A

traumatic aneurysm

176
Q

Type of aneurysm where plaque starts crumbling and force of heart pumping starts dissecting vascular wall away from plaque

A

atherosclerotic aneurysm

177
Q

What % of ppl with SAH die or have neurologic disabilities?

A

50%

178
Q

Type of aneurysm that looks like a pouch?

A

saccular

179
Q

What’s the classification scale for SAH?

A

Hunt and Hess Classification

180
Q

Hunt and Hess classification where there is drowsiness, confusion, or mild focal deficits?

A

3

181
Q

Hunt and Hess classification where pt is in deep coma, decerebrate rigidity, and moribound appearance?

A

5

182
Q

How are aneurysms repaired?

A

surgical or endovascular intervention

183
Q

Some complications pts with SAH are at risk for?

A

cardiac dysfunction, neurogenic or cardiogenic pulmonary edema, hydrocephalus, hemorrhage

184
Q

Some anesthetic considerations for aneurysm repair?

A

control HDs (prevent SNS during DL and placement of Mayfield collar w narc and lido), TIVA or sub MAC VA, mild to mod hyperventilation, mannitol (0.5 to 1 g/kg), lumbar drain or external ventricular to drain CSF,

185
Q

What do you have to keep in mind with brain relaxation and SAH?

A

brain relaxation may be difficult to achieve

186
Q

Complications of cerebral aneurysm repair?

A

rebleeding,

187
Q

How much of a chance is there of rebleeding the first few days following SAH?

A

50%

188
Q

Is rebleeding of a previously ruptured SAH life threatening?

A

yes

189
Q

Where is a cerebral aneurysm clip placed?

A

right at neck of aneurysm

190
Q

What cardiac and pulmonary issues are common during SAH?

A

ST changes, dysrhythmias, elevated troponin, cardiogenic shock

191
Q

When should surgical clipping of ruptured aneurysm be delayed?

A

hemodynamically unstable pt

192
Q

When repairing a cerebral aneurysm, when is the risk of recurrent hemorrhage removed?

A

once secured with an aneurysm clip

193
Q

Reactive narrowing of cerebral arteries following SAH repair is called?

A

vasospasm

194
Q

What causes vasospasm after cerebral aneurysm repair?

A

breakdown products of Hg from the blood that has accumulated around the vessels of the circle of willis

195
Q

Leading cause of morbidity and mortality after SAH?

A

vasospasm

196
Q

What 3 negative effects does vasospasm have?

A

impairs circulation and leads to ischemia and may lead to infarction

197
Q

What’s the ratio of patients with SAH who develop vasospasm?

A

1/4

198
Q

In 60% of pts vasospasm can be detected with?

A

angiography (and only half develop symptoms)

199
Q

Vasospasm peaks how many days after surgery?

A

4-9 days

200
Q

Vasospasm treatment depends on?

A

maintaining CPP

201
Q

Triple H treatment for vasospasm is?

A

HTN, hypervol, hemodilution

202
Q

Most commonly employed pressors for vasospasm?

A

phenylephrine and dopamine

203
Q

2 meds which decrease the morbidity of ischemia occurring after SAH?

A

nimodipine (po) and nicardipine

204
Q

Can angioplasty treat vasospasm?

A

yes

205
Q

Why does vasospasm depend on CPP?

A

ischemic areas have impaired autoregulation and CBF depends on CPP

206
Q

When treating vasospasm with HTN what parameters do you want to follow?

A

SBP 160-200 and MAP 20-30 mm above baseline

207
Q

How does an endovascular treatment of an aneurysm work?

A

intra arterial catheter deploys coils in to the aneurysm that cause it to thrombose

208
Q

Complications after endovascular repair of aneurysm?

A

hemorrhage, stroke, vessel dissection

209
Q

4 anesthetic considerations during endovascular repair of aneurysm?

A

general anesthesia; patient movement is devastating (muscle relaxation), hyperventilation should be avoided because it decreases CBF and makes access more challenging, heparin/protamine

210
Q

A congenital abnormal vascular connection between the arterial and venous circulation is?

A

AVM

211
Q

2 bad characteristics of AVM?

A

bypasses the walls of the capillaries and the vessel walls are thin and can easily rupture

212
Q

Gold standard for cerebral AVM diagnosis?

A

cerebral angiography

213
Q

3 sx of AVM?

A

bleeding, seizures, focal neuro deficits

214
Q

2 types of surgeries to cure AVM?

A

open surgery or radiosurgery

215
Q

Why is autoregulation of blood flow missing in AVM repair?

A

vasogenic edema and hemorrhage

216
Q

Anesthetic problems for AVM?

A

similar to those of aneurysm, the operation is more complicated and there is more blood loss

217
Q

What do you have to aggressively control in AVM pts during surgery?

A

HTN

218
Q

Immediate post op neuro exam after what type of surgery?

A

AVM

219
Q

2 types of surgery where want pt awake to assess neuro status?

A

awake crani and epilepsy surgery

220
Q

Contraindications to awake brain surgery?

A

anxiety, claustrophobia, pysch disorders, difficult airway, OSA, orthopnea, high BMI

221
Q

Intraop considerations for awake crani?

A

keep direct visual contact and calm quiet environment, comfortable room temp, talk to pt, use prop and dex 0.3-0.6 ug/kg/min

222
Q

Preferred method for epilepsy surgery and tumor resection?

A

asleep awake asleep

223
Q

What type of anesthesia is used for AAA brain surgery?

A

general with local infiltration

224
Q

When does pt emerge for AAA surgery?

A

middle of surgery

225
Q

Why does neurosurgeon apply electrical stimulation mapping in AAA surgery?

A

allows for maximal tumor resection while minimizing neuro deficits

226
Q

What meds should you avoid during AAA and why?

A

benzos; interferes with electrocorticography

227
Q

Airways to use for AAA?

A

LMA, ETT, none

228
Q

Goal with head trauma?

A

secure ETT quickly without moving neck

229
Q

How is axial cervical stabilization done?

A

one anesthetist puts traction on angle of mandible and the other inserts

230
Q

What may help to prevent displacement of cervical fractures?

A

bimanual application

231
Q

5 clinical criteria to clear spine in conscious trauma pts?

A

no posterior midline cervical spine tenderness, alert, not intoxicated, no painful distracting injuries, no focal deficits

232
Q

Components of GCS?

A

eye opening, verbal, best motor response

233
Q

3 criteria r/t GCS that require intubation?

A

hypoventilation, absence of gag, GCS

234
Q

When cerebral autoregulation is impaired it is dependent on?

A

CPP

235
Q

Some considerations for head trauma surgery pts?

A

avoid HTN, hypotension; cerebral autoregulation may be impaired after TBI, fluid (isotonic fluid, blood, colloids) use is controversial, albumin should not be used unless hypoalbuminemic

236
Q

Goal is to maintain CPP in what for head trauma pt?

A

50-70

237
Q

Why do you have to be careful about rapid restoration of intravascular volume in head trauma pts?

A

cerebral edema can result

238
Q

Does moderate hypothermia improve outcomes in head injury pt?

A

no

239
Q

Goals for PaO2, ETCO2, and O2 sat in head injury pt?

A

PaO2> 60, ETCO2 30-35, O2 sat >90%

240
Q

Fluids to use for head trauma surgery pt?

A

mannitol, HTS

241
Q

When can you use barbs in head trauma pts?

A

when HD stable and adequately resuscitated; don’t use if MAP and CPP can’t be maintained

242
Q

TIA’s happen when carotid is stenosed > __ %?

A

60%

243
Q

Types of anesthesia for carotid surgery?

A

general, regional, angioplasty, stenting, superficial or deep cervical plexus block

244
Q

What should the goal be with BP for carotid surgery and what makes it difficult to control?

A

keep baseline; infuse lido before start so it makes it difficult to control

245
Q

In carotid surgery, before clamping the ICA a perfusion pressure (stump) is measured and if it’s less than ___=___ then shunt may be used to prevent ischemia or rely on collateral flow?

A

20-40

246
Q

When are heparin and protamine given during carotid surgery?

A

heparin: just before clamping; protamine: prior to skin closure

247
Q

Intraop considerations for carotid surgery?

A

control BP, BP >180 may be associated with CVA, cerebral oximetry may be used, EEG, SSEPs may be used, maintain SBP and MAP 20% over baseline especially if shunt is used (phenyl drip), prevent coughing and large swings in BP, treat HTN to avoid cerebral edema, foley, central line, rapid emergence

248
Q

Normal cerebral oximetry value?

A

60-80

249
Q

Caution w foley and cl in carotid surgery?

A

can cause HTN especially in men

250
Q

Potential complications of CEA?

A

CVA, MI, nerve injuries, wound hematomas, infection

251
Q

Most common nerve injuries in CEA?

A

hypoglossal, SL, RLN

252
Q

Assessment for wound hematoma in CEA? And what is wound hematoma usually precipitated by?

A

tracheal deviation; BP goes up

253
Q

Carotid artery stenting is done in what type of patients?

A

those who are poor candidates for surgery

254
Q

What type of anesthesia is carotid stenting performed under?

A

sedation and converted to general if risk of comorbidities

255
Q

What do you have to be prepared for during carotid stent placement?

A

HD changes- brady, asystole during balloon angioplasty of internal carotid artery bc it sits next to vagal

256
Q

What do you not want to use to pretreat for prevention of brady/asystole in carotid pts and why?

A

atropine bc tachycardia not desirable in these pts

257
Q

What should be immediately available intraop for those pts with vascular lesions?

A

blood

258
Q

Do craniotomy pts have severe pain?

A

no

259
Q

In general, what 2 gasses have way more effect on motor and sensory evoked potentials than IV agents?

A

nitrous and volatile agents

260
Q

EEG is used to assess what 3 things?

A

cerebral perfusion, metabolism, and anesthetic depthg

261
Q

Cerebral ischemia produces similar level of changes on the EEG as what type of anesthesia?

A

deep anesthesia

262
Q

EEG is a summation of excitatory and inhibitory responses produced where?

A

cerebral cortex

263
Q

Can an EEG detect cerebral ischemia?

A

yes

264
Q

Des and Sevo produce burst suppression at what doses?

A

Des >1.2; Sevo > 1.5 MAC

265
Q

Inhalational agents produce EEG activation at what MAC?

A

subanesthetic

266
Q

Small doses of barbs cause what EEG changes and regular doses cause what?

A

small: activation; regular: depression

267
Q

Benzos in small doses cause what EEG changes and opioids cause what changes?

A

benzos: activation; opioids: depression

268
Q

etomidate in small doses causes what EEG changes? What ab propofol?

A

small doses of etomidate: activation; propofol: depression

269
Q

Etomidate in regular doses causes what EEG changes?

A

depression

270
Q

N2O causes what type of EEG changes?

A

activation

271
Q

What does ketamine do to EEG changes?

A

activation

272
Q

What do hypocapnia, mild hypercapnia, and marked hypercapnia do to EEG changes?

A

hypocapnia: depression; mild hypercapnia: activation; marked hypercapnia: depression

273
Q

What do sensory stimulation and hypothermia do to EEG?

A

sensory stimulation: activation; hypothermia: depression

274
Q

What do early, late hypoxia, and ischemia do to EEG?

A

early hypoxia: activation; late hypoxia: depression; ischemia: depression

275
Q

What 3 drugs produce a similar EEG pattern?

A

barbs, propofol, etomidate

276
Q

Only agents capable of producing burst suppression and electrical silence at high doses?

A

IV agents

277
Q

SSEPs test the integrity of?

A

dorsal spinal columns, ascending tracts, sensory cortex, supplied by posterior spinal artery

278
Q

3 surgeries where SSEPs are useful?

A

spinal surgery, CEA, aortic surgery

279
Q

This has the greatest effect causing dose dependent decrease in amplitude and increase in latency?

A

volatile agents

280
Q

An increase in latency and decrease in amplitude can mean?

A

ischemia

281
Q

4 physiologic factors which influence SSEPs?

A

temp, PaO2, PaCO2, SBP

282
Q

Do muscle relaxants effect SSEPs? Do all anesthetics?

A

no; yes

283
Q

Sensory tracts in dorsal spinal columns go which way and are found where?

A

afferent or towards and found in posterior root of spinal column

284
Q

Motor tracts in dorsal spinal columns go which way and are found where?

A

efferent, away and in anterior root of spinal column

285
Q

Brainstem auditory evoked response tests what?

A

8th cranial nerve and auditory pathways above the pons

286
Q

Visual evoked potentials are used to measure what?

A

optic nerve and occipital cortex during resections of large pituitary tumors

287
Q

Fentanyl in large doses does what to BAER?

A

does not effect

288
Q

BAER are used for what surgeries?

A

acoustic tumor surgery and pts at risk of brainstem

289
Q

Do IV or inhalational agents effect BAER readings more?

A

inhalational

290
Q

MEPs assess ftn of?

A

motor cortex and descending tracts supplied by anterior spinal artery

291
Q

SSEPs travel where?

A

along posterior tracts of spinal cord

292
Q

What surgeries may use MEPs?

A

aortic surgery to assess spinal cord perfusion

293
Q

These 3 things suppress MEP response? So what is recommended for use with MEPs?

A

volatiles, N20, NMDAs; TIVA

294
Q

This is the recording of electrical activity of muscle that is irritated or injured?

A

EMG

295
Q

Purpose of EMG?

A

identify nerves and test their integrity

296
Q

Nerve that is most often monitored with EMG?

A

facial; VII

297
Q

What type of anesthesia may mimic neuronal imitation with EMG?

A

light anesthesia

298
Q

Where are electrodes placed for EMG monitoring?

A

subdermally over muscle

299
Q

Standard of care for acoustic tumor surgery or when increased risks of facial nerve functioning?

A

EMG

300
Q

Can you use NMDA with EMG monitoring?

A

yes, but should be maintained at light level

301
Q

EEG is often used for what type of surgery?

A

carotid endarectomy

302
Q

This type of neuro monitoring is used to detect inadequate spinal cord flow?

A

SSEP

303
Q

Nerves EMG monitors?

A

VII, III, IV, V, XI