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NA 3 > Neuro Quizlet > Flashcards

Neuro Quizlet Flashcards

1
Q

Brain usually consumes _ % of total body O2, and _mL/100g/min is the normal CMRO2 ( ~ _ mL/min)

A

20%
3.8mL/100g/min
~ 50mL/min

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2
Q

CMRO2 is greatest in _ matter of the cerebral cortex at _ mL/100g/min

A

gray
80mL/100g/min

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3
Q

2 areas of the brain most sensitive to hypoxic injury of the brain:

A

-hippocampus
-cerebellum

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4
Q

Primary source of energy for neuronal cells and how much is consumed:

A

glucose
5mg/100g/min

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5
Q

T/F Most glucose in the brain is metabolized anaerobically

A

false
aerobic

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6
Q

Normal CBF
-mL/100g/min
-total mL/min
-%CO

A

50mL/100g/min
750mL/min
15-20% CO

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7
Q

Regional CBF parallels metabolic activity and can vary from _ to _ mL/100g/min

A

10-300mL/100g/min

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8
Q

Gray matter receives _ mL/100g/min of CBF and white matter receives _mL/100g/min

A

gray: 80mL/100g/min
white: 20mL/100g/min

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9
Q

Which CBF will you see EEG slowing, flattening, and irreversible damage?

A

slowing: 20-25mL/100g/min
flattening: 15-20mL/100g/min
damage: <10-15mL/100g/min

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10
Q

Transcranial doppler measures the _ CBF in the _ artery

A

velocity
MCA

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11
Q

Normal CBF velocity on transcranial doppler:
-what does it mean if number is high?

A

55mm/sec
>120 can mean vasospasm

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12
Q

Which artery has a higher velocity flow when measured with a transcranial doppler, MCA or ICA?

A

MCA (3x)

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13
Q

Does infrared spectroscopy reflect cerebral arterial or cerebral venous O2 sat?

A

venous

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14
Q

Which receives more CBF, cortical or subcortical region of the brain?

A

cortical

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15
Q

5 determinants of CBF:

A

-CMRO2
-CPP
-Venous pressure
-PaCO2
-PaO2

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16
Q

Is more CMRO2 used for electrical or cellular integrity?

A

Electrical

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17
Q

Brain autoregulates between CPP of _ - _ and a MAP of _ - _

A

CPP 50-150
MAP 60-160

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18
Q

What happens below the lower limit of cerebral autoregulation? Above the upper limit?

A

Below lower limit: vessels become maximally dilated and risk hypoperfusion and ischemia

Above upper limit: vessels are maximally constricted and risk cerebral edema and hemorrhage

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19
Q

CMRO2 drops by _ % for every 1*C drop in temperature.

A

7%

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20
Q

EEG suspension occurs at _ - _ *C

A

18-20

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21
Q

Hyperthermia beyond _ *C destroys neurons and denatures proteins

A

42*C

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22
Q

What controls cerebral vascular resistance?

A

pH of CSF around the arterioles

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23
Q

_ has a linear relationship with CBF

A

PaCO2

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24
Q

At a PaCO2 of 40, CBF is _ mL/100g/min. For every _ mm increase or decrease in PaCO2, CBF will increase/decrease by _ mL/100g/min

A

50mL/100g/min

1-2mL/100g/min

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25
Q

Max vasodilation occurs when PaCO2 is at _ - _ and max vasoconstriction occurs at _

A

80-100 vasodilation
25 vasoconstriction

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26
Q

Effects on CBF:
-resp. acidosis

A

increases CBF

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27
Q

Effects on CBF
-resp alkalosis

A

decreases CBF

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28
Q

Effects on CBF
-met acidosis

A

no effects

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29
Q

PaO2 < _ - _ causes cerebral vasodilation and increases CBF

A

50-60

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30
Q

PaO2> 60 does not affect CBF

A

60

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31
Q

Normal ICP

A

5-15mmHg

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32
Q

Avg brain wt, blood volume, CSF volume

A

brain wt: 1350g
blood volume: 50mL
CSF: 75mL

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33
Q

T/F Brain has a large O2 reserve

A

false

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34
Q

LOC in < _ sec without O2, ATP stores deplete in _ minutes.

A

10 sec
3-8min

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35
Q

CPP formula and normal value

A

CPP = MAP - ICP or CVP (whichever is greater)
CPP (n) = 80-100 mmHg

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36
Q

At which CPP will you see EEG slowing, flattening, and irreversible damage of the brain?

A

slowing: CPP < 50
flat: CPP 25-45
damage: CPP < 25

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37
Q

Cerebral autoregulation curve is shifted to the _ in patients with HTN

A

right

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38
Q

What is the myogenic mechanism of cerebral autoregulation?

A

Intrinsic response of smooth muscle cells in cerebral arterioles to changes in MAP

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39
Q

What is the metabolic mechanism of cerebral autoregulation?

A

cerebral metabolic demands determine the arterial tone
-when demand > CBF metabolites are released > vasodilation and increases CBF

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40
Q

Hypotonicity moves water (in/out of) the brain, where hypertonicity moves water (in/out)

A

hypo - into
hyper- out of

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41
Q

When the resting CBF is low, the reduction of CBF from hypocapnia is (more/less) effective

A

less

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42
Q

Why is the decreased CBF from hypocapnia not sustained

A

pH of CSF normalizes with 6-8hr from dissociation of HCO3 from H2CO3

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43
Q

What effect will an abrupt increase in CO2 have on CBF?

A

increased CBF and ICP, will also cause CSF acidosis

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44
Q

What effect will an abrupt decrease in CO2 have on CBF?

A

potential ischemia
-decreased CBF
-also causes CSF alkalosis

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45
Q

Effect on CBF?
-hypoxia (PaO2 <60)

A

causes rapid increase

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46
Q

What is the target Hct for ideal CBF and what happens if blood viscosity increases?

A

30-33% Hct
increased viscosity = decreased CBF

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47
Q

What happens in “steals” and what conditions can precipitate this?

A

vessels that supply ischemic areas in the brain lose their tone and become maximally dilated so that when cerebral vasodilation occurs, vessels that still have tone will vasodilate and “Steal” perfusion from the ischemic areas
-hypercapnia, hypoventilation, vasodilators

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48
Q

What happens in “inverse steal”?

A

hyperventilation is used to constrict cerebral vessels that supply healthy tissue, allowing flow to redistribute to ischemic regions

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49
Q

Another term for “steal”

A

luxury perfusion

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50
Q

Most important chemical regulator of CBF

A

PaCO2

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51
Q

CMRO2 decreases by _ % for every 10 degree in temp decrease

A

50%

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52
Q

CSF:
-total volume
-spec grav
-pH

A

Volume: 150mL
SG: 1.002-1.009
pH: 7.32

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53
Q

Normal CSF production is _mL/hr or _mL/day and it is replaced every _ hrs

A

21mL/hr
500mL/day
Q 3-4hr

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54
Q

Path of CSF flow:

A
  1. Lateral ventricles
  2. Intraventricular foramen of munro
  3. 3rd ventricle
  4. Aqueduct of Sylvius
  5. 4th ventricle
  6. Foramen of magendie, formaen of luschka
  7. Cisterna Magna
  8. SA space
  9. Arachnoid granulations of hemispheres
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55
Q

Name 6 drugs/types of drugs that decrease CSF production:

A
  1. acetazolamide (carbonic anhydrase inhibitors)
  2. corticosteroids
  3. spironolactone
  4. furosemide
  5. isoflurane
  6. vasoconstrictors
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56
Q

3 electrolytes that are higher in CSF than in plasma?

A

Na, Cl, Mg

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57
Q

Normal supratentorial ICP:

A

10mmHg

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58
Q

What is intracranial elastance and what determines it?

A

determined by measuring changes in ICP in response to volume change
-normally small changes in volume are well compensated for but eventually elastance decreases and ICP increases more

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59
Q

4 compensatory mechanisms of the intracranial vault:

A

-displacement of CSF from cranial to spinal compartment
-increase CSF absorption
-decrease CSF production
-decrease in total CBV

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60
Q

CBV increases by _ mL/100g per 1mmHg increase in PaCO2

A

0.5mL/100g

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61
Q

Which IA (sevo, iso, des) decreases CMR?

A

all of them

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62
Q

Which IA (sevo,iso,des) increases CSF absorption and which decreases it?

A

increased absorption : Iso
decreased absorption: Des

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63
Q

Which IA (sevo, iso, des) increases CBV the most?

A

Iso

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64
Q

What effect does IA(sevo/iso/des) have on ICP

A

increases ICP

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65
Q

What effect do all the IAs and N2O have on CBF?

A

increases it slightly

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66
Q

What does ketamine do to CSF absorption

A

decreases

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67
Q

When used alone, what effect does N2O have on CBF, CMR, and ICP?

A

increases them

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68
Q

Which is greater with the use of N2O, the increase in CBV or the increase in CBF?

A

CBF increases more

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69
Q

Which IA produces the greatest depression of CMRO2?

A

Iso

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70
Q

T/F At normocarbia, volatile agents, dilate cerebral vessels and impair autoregulation in a dose-dependent manner

A

true

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71
Q

Which volatile agent produces the LEASE cerebral vasodilation?

A

sevo

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72
Q

T/F Volatile agents impair CO2 responsiveness of cerebral vasculature

A

false

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73
Q

_ can blunt the increase in CBV associated with volatile agents

A

hypocapnia

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74
Q

T/F VAs uncouple the relationship between CBF and CMRO2

A

false- they alter it but don’t uncouple it

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75
Q

The net effect of volatile agents on ICP (increase it) is the result of what 3 things:

A
  1. immediate changes in CBV
  2. delayed alterations of CSF dynamics
  3. arterial CO2 tension
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76
Q

What are the two VAs of choice in patients with decreased intracranial compliance?

A

Iso and Sevo

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77
Q

CBF vs CBV: changes are larger

A

CBF

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78
Q

CBF vs CBV: does NOT reliably predict increases in ICP

A

CBF

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79
Q

CBF vs CBV: responds to PaCO2

A

both but CBV less so

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80
Q

T/F there is a direct 1:1 relationship between CBF and CBV?

A

false it is direct but not 1:1

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81
Q

How do NDMRs affect cerebral physiology?

A

no effect unless histamine is released

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82
Q

T/F Both barbs and lidocaine reduce CBF via increasing cerebral vascular resistance

A

true

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82
Q

T/F Ketamine increases CMRO2

A

False CMRO2 is unchanged (everything else increased - CBF, CSF, ICP)

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83
Q

What is the only type of vasodilating agent that has little or no effect on CBF and CBV

A

ganglionic blocker (Trimethaphan)

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84
Q

What effect does remifentanil have on CBF and CMR alone vs as an adjunct?

A

alone: increases CBF and CMR
adjunct: no effect

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85
Q

Does fentanyl have any effect on CBF and CMR?

A

no

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86
Q

Lidocaine effects on CMR and CBF?

A

decreases

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87
Q

T/F: IV induction agents cause parallel decreases in CMR and CBF but preserve flow-metabolism coupling, autoreg, and CO2 responsiveness

A

true

88
Q

T/F: Propofol reduces CMRO2 and CBF the same degree as barbiturates

A

true

89
Q

All vasodilators cause _ _ but catecholamine agonists only effect CBF/CMR when the _ is disrupted

A

cerebral vasodilation
BBB

90
Q

Which 2 agents may elicit seizures?

A

ketamine
etomidate

91
Q

T/F Benzos have no effect on CMR/ CBF

A

false; moderate reduction

92
Q

How do inhaled agents differ from IV agents at >1 MAC?

A

they increase ICP and CBF and abolish autoreg but they also decrease CMRO2 (uncoupling)

93
Q

Which primarily determines ICP, CBF or CBV?

A

CBV

94
Q

Patients having an ischemic stroke can have tPA within _ hrs of symptom onset

A

3hr

95
Q

HTN is common after a CVA; a target pressure should be < _ / _

A

185/110

96
Q

Altered area of brain after an ischemic CVA is called the _ _

A

ischemic penumbra

97
Q

Hypothermia is good for which type of ischemia?

A

global/complete

98
Q

for protective hypothermia, body temp is reduced to _ *C for 24hr

A

32-34

99
Q

In incomplete ischemia, where should MAP be maintained? How long should surgery be delayed?

A

MAP 70-80

delay for 6wks

100
Q

Effect on EEG: MAC <1

A

activation

101
Q

Effect on EEG: barbs, benzos and etomidate

A

dose dependent

102
Q

Effect on EEG: opioids

A

depression

103
Q

Effect on EEG: propofol

A

depression

104
Q

Effect on EEG: N2O

A

activation

105
Q

Effect on EEG: hypercapnia

A

activation

106
Q

Effect on EEG: hypothermia

A

depression

107
Q

Effect on EEG: early v late hypoxia

A

early: activation
late: depression

108
Q

Which IA produces an isoelectric EEG at high doses (1-2MAC)

A

Iso

109
Q

Which IAs produce burst suppression but not electrical silence at high clinical doses?

A

Des and Sevo

110
Q

How does N2O impact EEG?

A

increases BOTH frequency and amplitude

111
Q

What are the only agents capable of producing burst suppression AND electrical silence at high doses (3)?

A

Propofol
Barbs
Etomidate

112
Q

How does ketamine affect EEG?

A

unusual activation consisting of a rhythmic high-amplitude theta activity followed by very high amp gamma and low amp beta

113
Q

What is cushings triad and what causes it?

A

HTN
Bradycardia
Cheyne-Stokes respirations

caused by SNS outflow from brainstem compression

114
Q

Define intracranial HTN

A

sustained increase in ICP >15

115
Q

What is intracranial compliance? What does it mean if ICP is increasing?

A

compliance is the ability of the compartment to accommodate increased volume without major changes in pressure

increased ICP = decreased compliance

116
Q

What is cushings response?

A

periodic increases in MAP with reflex slowing of the HR lasting 1-15 min

117
Q

Tx of intracranial HTN and cerebral edema

A

corticosteroids control BG
decrease swelling: fluid restriction, osmotic agents, loop diuretics
Moderate hyperventilation (PaCO2 30-33) can help with exposure IV agents

118
Q

T/F hyperventilation should be used universally

A

false

119
Q

VAE s/s

A

decrease in EtCO2 of SpO2 (before hemodynamic changes), ETN2, sudden HoTN, ST changes, decreased CO, changes in BP and heart sounds are LATE SIGNS

120
Q

VAE can cause acute _ - sided HF

A

right

121
Q

Tx of VAE in neurosurgery:

A
  1. tell surgeon and flood field
  2. 100% FiO2, no N2O
  3. Aspirate 60mL from multi orifice CVC
  4. IVF to increase CVP
  5. Valsalva 5-10 sec
  6. head down, left tilt position
122
Q

True or false: mayfield pins should be removed while patient is in sitting position

A

false VAE risk

123
Q

Risk of VAE is higher during spontaneous or mechanical ventilation? why?

A

spontaneous - negative inspiratory pressure

124
Q

What is a paradoxical air embolism and who is at risk?

A

develops with air entry into systemic circulation
people with connections between right and left heart (PFO)
when R>L pressure, systemic air may enter arterial circulation

125
Q

If patients who are going to have surgery in the sitting position have a murmur, what should be done pre-op to minimize VAE risk?

A

An echo, if a PFO is present, then surgery should be done in a different position

126
Q

What is the standard of care for VAE detection?

A

precordial doppler, ETCO2 monitoring

127
Q

Where is precordial doppler placed?

A

right of sternum, 3rd-6th intercostal (over RA)

128
Q

What is the most sensitive test of VAE that can detect presence of a paradoxical embolus in presence of a pFO?

A

TEE

129
Q

Symptoms of VAE develop at >____mL of air

A

50mL

130
Q

What is the most sensitive NON-INVASIVE monitor for VAE?

A

pre-cordial doppler

131
Q

Which is a more sensitive detector of VAE, PA catheter or EtCO2?

A

PA catheter

132
Q

Cerebral aneurysms typically occur where?

A

Bifurcation of the large arteries at the base of the brain i the ANTERIOR circle of willis

133
Q

What is the most common cause of SAH

A

rupture of saccular aneurysm

134
Q

What is the hallmark symptom of cerebral aneurysm rupture?

A

sudden severe headache (without focal deficit)

135
Q

What EKG changes may you see with cerebral aneurysm rupture?

A

ST depression, T wave inversion

136
Q

What is the most common symptoms and sign of an UNRUPTURED aneurysm?

A

Symptom: headache
Sign: third-nerve palsy

137
Q

Aneurysm rupture is most likely to occur at what points during repair?

A

Dissection and clipping

138
Q

Transmural pressure calculation? What does it mean if it’s increased?

A

MAP - ICP
increased risk of rupture

139
Q

In aneurysm repair, arterial line should be placed when?

A

before induction

140
Q

Where should you keep MAP during aneurysm repair and why?

A

high normal to maintain perfusion and avoid vasospasm

141
Q

What is the leading cause of morbidity and mortality in patients with SAH after rupture, and what happens physiologically?

A

Vasospasm; delayed and sustained contraction of cerebral arteries causing decreased blood flow and lower CPP

142
Q

Neuro deterioration after SAH peaks when and resolves when

A

peak: 13-14th day
resolve: 2-3 weeks

143
Q

What is the only medication known to decrease vasospasm?

A

Nimodipine

144
Q

3 signs of SEVERE vasospasm

A
  1. increased flow velocity >200 cm/sec
  2. lindegaard ratio >3
  3. brain tissue O2 tension <20mm Hg
145
Q

How do you treat patients with symptomatic vasospasm who have an inadequate response to nimodipine, IV expansion, and induced HTN?

A

Triple H therapy!
-induce HTN
-hypervolemia (fluids)
-hemodilution

146
Q

What does “triple H” therapy consist of?

A

Hypervolema, hemodilution, HTN

147
Q

Hypervolemia = CVP>_______, PAWP>_______

A

12;14

148
Q

SSEP vs. MEP: measures electrical CNS responses to peripheral electrical stimuli

A

SSEPs

149
Q

SSEP vs. MEP: tests peripheral motor response to transcranial stimuli

A

MEPs

150
Q

SSEP vs. MEP: measures dorsal horn of spinal cord

A

SSEP

151
Q

SSEP vs. MEP: measures anterior horn of spinal cord

A

MEP

152
Q

SSEP vs. MEP: muscle relaxants restricted

A

MEP

153
Q

SSEP vs. MEP: more sensitive to anesthetic agents

A

MEP

154
Q

SSEP vs. MEP: electrodes placed over median and posterior tibial nerves

A

SSEP

155
Q

SSEP vs. MEP: require bite block

A

MEP

156
Q

SSEP vs. MEP: amplitude and latency change indicate potential spinal cord injury

A

SSEP

157
Q

How does midazolam affect SSEPs?

A

increased latency

158
Q

How does Diazepam affect SSEPs?

A

decreased amplitude

159
Q

How does Etomidate affect SSEPs?

A

decreases latency AND amplitude

160
Q

How does an Opioid bolus affect SSEPs?

A

may interefere, avoid during critical monitoring

161
Q

What induction agent is acceptable with SSEPs?

A

propofol

162
Q

How doe IHA and N2O affect SSEPs?

A

Depress them in a dose-dependent manner

163
Q

How does hypothermia of 2-3 degrees impact SSEPs? What about hyperthermia

A

hypothermia: increases latency
Hyperthermia: suppresses amplitude by 85%!

164
Q

EMG monitors which cranial nerves

A

3, 4, 10, 11, 12

165
Q

CNS is made up of the _____ and ______; PNS is made up of _______ and __________.

A

brain and spinal cord
cranial/spinal nerves and their receptors

166
Q

CNS is derived from 2 cell types, what are they?

A

neurons and glial cells

167
Q

Stimulation of multiple dendrites in the _______mater produce an impulse towards the cell body, and then conduction away from the cell body via the _______.

A

gray ; axon

168
Q

A single axon (_______ mater) emerges from the cell body and branches to form collateral nerves

A

white

169
Q

Multipolar vs. Pseudounipolar: motor neurons

A

Motor neurons

170
Q

Multipolar vs. Pseudounipolar: sensory neurons

A

pseudounipolar

171
Q

Multipolar vs. Pseudounipolar: interneurons

A

pseudounipolar

172
Q

Where are unipolar cell bodies found?

A

Lower vertebrae

173
Q

Where are bipolar cell bodies found?

A

retina, ear, olfactory mucosa

174
Q

The majority of CNS neurons are ______polar

A

multi

175
Q

Glial cells support the neuron function in what 4 ways

A
  1. creating healthy ion environment
  2. modulating nerve conduction
  3. controlling re-uptake of neurotransmitters
  4. repairing neurons following neuronal injury
176
Q

Name that glial cell type: most abundant, regulates metabolic environment and repairs neurons after injury

A

astrocytes

177
Q

Name that glial cell type: involved in CSF production, concentrated in the roof of the 3rd and 4th ventricles

A

ependymal cells

178
Q

Name that glial cell type: form myelin sheath of CNS, increase conduction velocity

A

oligodendrocytes

179
Q

Name that glial cell type: act as macrophages and phagocytize neuronal debris

A

microglia

180
Q

True or false: glial cells participate in neuronal signaling

A

false

181
Q

In an unmyelinated axon (PNS), in order to double the speed of impulse conduction, what must happen?

A

axon must double in size

182
Q

Brain blood supply originates from ________ arteries for anterior circulation, and ________ arteries from posterior circulation.

A

Internal carotid; vertebral

183
Q

Vasospasm is thought to be caused by the breakdown of products of _______ that has accumulated around the vessels of the circle of willis after SAH

A

Hgb

184
Q

Which lobe of the brain has motor control?

A

frontal

185
Q

Which lobe of the brain has pain and touch?

A

parietal

186
Q

Which lobe of the brain has the auditory cortex?

A

temporal

187
Q

Which lobe of the brain has the visual cortex?

A

occipital

188
Q

Which lobe of the brain is separated from the frontal and parietal lobes by the sylvian fissure?

A

temporal

189
Q

Walk through the anterior circulation of the brain from aorta to cerebrum?

A

Aorta - carotid arteries - internal carotid - circle of willis - cerebral hemispheres

190
Q

Walk through the posterior circulation of the brain from aorta to spinal cord?

A

aorta- subclavian artery - vertebral artery - basilar artery - posterior fossa structures and cervical spinal cord

191
Q

Name the arteries of the circle of willis

A
  1. ant. communicating
  2. ant. cerebral
  3. middle cerebral
  4. post. communicating
  5. post. cerebral
  6. basilar artery
  7. vertebral arteries
192
Q

All venous blood exits the brain via the _______ veins

A

jugular

193
Q

Pons contains which cranial nerves

A

V and VII

194
Q

Medulla contains which cranial nerves

A

8,9,10,11,13

195
Q

________ separates the cerebral hemispheres, while _______ separate the occipital lobe and the cerebellum

A

falx cerebri; tentorium cerebellum

196
Q

Distance from skin to epidural space

A

3-8 cm

197
Q

Gray matter is enlarged in what 2 areas of the spinal cord?

A

C5-C7 (upper extremities)
L3-S2 (lower extremities)

198
Q

Dorsal white matter is composed of _________fiber tracts, while lateral and ventral white matter contains ________ tracts.

A

ascending sensory; descending motor

199
Q

Order these fibers from fastest to slowest: A-beta, A-gamma, A delta, A alpha, C fibers, B fibers

A
  1. a alpha
  2. a beta
  3. a gamma
  4. a delta
  5. b
  6. c
200
Q

Which 3 cranial nerves are only sensory?

A

Olfactory CN I
Optic CN II
Vestibulocochlear CN VIII

201
Q

Spinal cord receives blood from ________ (1/2) anterior spinal artery(s) and ________(1/2) posterior spinal artery(s)

A

1;2

202
Q

Where does the artery of adam-whatever enter the cord and what does it supply?

A

T7; lumbosacral segment

203
Q

Excitatory neurotransmitters increase the permeability of ________, inhibitory neurotransmitters increase the permeability of ________.

A

Sodium; chloride

204
Q

What are the 3 inhibitory neurotransmitters?

A

GABA, glycine, dopamine

205
Q

Which CN is responsible for taste to the anterior 2/3 of the tongue?

A

Facial CN VII

206
Q

Eye movement is controlled by which 3 CNs? What about vision?

A

Vision = Optic CN II
Eye movement = CN III, IV, VI

207
Q

Which CN is responsible for somatic sensation to the anterior 2/3 of the tongue

A

Trigeminal CN V

208
Q

What is autonomic hyperreflexia?

A

Stimulation below the level of a SCI triggers SNS reglex causing vasoconstriction below the injury and vasodilation above the injury

209
Q

What happens to HR in autonomic hyerreflexia?

A

slows due to baroreceptor reflex

210
Q

SCI lesions above ________ are at risk for autonomic hyperreflexia?

A

T5-T8

211
Q

Which happens first, spinal shock or autonomic hyperreflexia?

A

Spinal shock lasting 1-3 weeks

212
Q

How do you treat autonomic hyperreflexia?

A
  1. remove the stimulus
  2. deepen the anesthsia
  3. administer direct vasodilators
213
Q

ICP Waveform: what’s the first peak correspond to?

A

Percussion wave - SBP

214
Q

ICP Waveform: what’s the second peak correspond to?

A

Tidal wave - dicrotic notch

215
Q

ICP Waveform: whats the third wave correspond to?

A

dicrotic wave - will surpass P1 as ICP increases

216
Q

What do plateau waves indicate on ICP waveform?

A

critically low intracranial compliance thought to be caused by brief episodes of decreased CPP leading to exaggerated cerebral vasodilation, and then increased CBV

217
Q

First tier vs. second tier treatment for increased ICP

A

First tier: controlled hypocapnia (PaCO2 35), hyperosmolar therapy
Second tier: forced hyperventilation (PaCo2 25), barb coma, induced hypothermia, emergent surgery

218
Q

What is an appropriate bolus dose of 3% saline?
Mannitol?

A

250mL
0.25-1mg/kg

NA 3 (8 decks)

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