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Final_Brain Flashcards

1
Q

CPP

A

= MAP - ICP

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2
Q

Autoregulation

A

ability of brain to maintain CBF at constant levels despite changes in CPP

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3
Q

When CPP is increased, arterial ____ occurs

A

constriction

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4
Q

When CPP is decreased, arterial ____ occurs

A

dilation

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5
Q

rapid lowering of BP in HTN patients can cause

A

cerebral ischemia

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6
Q

Changes in CMRO2 usually leads to _____

A

same direction changes in CBF

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7
Q

VA effect on CBF and CMRO2

A

CBF: dose-dependent increase
CMRO2: decrease
*different from norm “CBF-CMRO2 coupling”

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8
Q

VA effect on ICP: most to least

A

Increases ICP

Des > Sevo, Iso

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9
Q

VA effect on CBF: most to least

A

Increases CBF

Des > Sevo > Iso

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10
Q

VA effect on CMRO2: most to least

A

Decreases CMRO2

Iso > Des/Sevo

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11
Q

How to offset VA effect on CBF?

A

Arterial hypocapnea helps to minimize increases in CBF

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12
Q

Normal CPP

A

50-150 mmHg

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13
Q

poor mans way to calculate CPP

A

substitute ICP for CVP

CPP=MAP-CVP

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14
Q

Brain receives how much cardiac output

A

15%

or 750 mL/min

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15
Q

CMRO2 of brain

A

3mL O2/g brain tissue/min

  • 50mL/min
  • 18-23% of total body O2 consumption
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16
Q

Hypocapnea can effect cerebral blood flow how?

A

acutely decrease: CBF, CBV, ICP

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17
Q

1 mmHg increase in PaCO2 = ______ CBF

A

15 mL/min

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18
Q

As _____ returns to normal, hypocapnea is no longer effective at decreasing CBF, CBV, ICP

A

CSF pH

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19
Q

PaO2 effect on CBF?

A

Decreased PaO2:
-Increases cerebral vasodilation + CBF
Only effects CBF when PaO2 < 50 mmHg

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20
Q

Nitrous Oxide effect on brain

A

increases ICP

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21
Q

Ketamine effect on brain

A

cerebral vasodilator

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22
Q

Propofol effect on brain

A

cerebral vasoconstrictor

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23
Q

Opioid effects on brain

A

cerebral vasoconstrictor

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24
Q

NDMR effects on brain

A

prevent coughing = avoid acute increase in ICP

25
Q

When to decrease ICP

A

Tx sustained ICP > 20

26
Q

Methods to decrease ICP

A 
Elevate HOB
Hyperventilate
CSF drainage
Surgical decompression
hyperosmotic Rx
Diuretics
Corticosteroids
Cerebral vasoconstricting agents
27
Q

Fastest intervention to decrease ICP

A

hyperventilation

28
Q

Cerebral vasoconstriction results in

A

reduced CBF/CBV

29
Q

Hyperventilation to decrease ICP: goal

A

PaCO2 25-35

30
Q

Hyperosmotic Rx

A 
Mannitol 
-0.25-0.5mg/kg: removes 100mL h2O from brain 
-decreased ICP seen w/in 30min
U/O up to 1-2L
Hypertonic Saline
-CVL, caution w/ rapid admin
-1-2mL/kg of 3% over 5min
*check serum Na prior! (hold if Na>160)
31
Q

Sux effect on brain

A

increased in ICP, CBF

32
Q

When to use lasix vs. mannitol

A

Lasix: good for pt who cannot tolerate transient increase in intravasc volume

33
Q

Corticosteroids effect on ICP

A

Decreases - for localized vasogenic cerebral edema/pseudomotor cerebri

34
Q

Effective treatment to decrease ICP in acute head injury pts

A

Barbiturates

35
Q

Anesthetic considerations for intracranial tumors

A
  • Identify if increased ICP present
  • sensitive to sedation/opioids
  • combo: NO, VAs, opioids, barbiturates, propofol
36
Q

Intraop goals for increased ICP

A
  • pre-treat for increased ICP
  • control BP thru induction
  • deep before induction
  • profound muscle relaxation: DL/intubation
  • Euvolemia, avoid dextrose
  • rapid emergence
37
Q

Induction agents - increased ICP

A

Propofol + barbiturates

38
Q

Special monitoring for intracranial tumors

A

PIV, A-line, EEG

39
Q

Delay of elective surgery post stroke

A

Elective surgery should be delayed for up to 9 months (allow return of cerebral autoregulation)

40
Q

periop stroke associated with

A

8x increase risk of death within 30 days of surgery

41
Q

Sitting position does what to CPP?

A

Decreases CPP by ~ 15%

42
Q

Advantages of sitting position

A

Surgical exposure, enhanced venous drainage, minimize EBL, decreases ICP

43
Q

Disadvantages of sitting position

A

HOTN, decreased CO, risk of VAE

44
Q

How does HOB elevation effect hemodynamics?

A

1mmHg drop in MAP per 1.25 cm increase in HOB elevation

45
Q

supratentorial tumor resection is done in which position?

46
Q

When could a VAE occur?

A

When exposed veins are above the level of the heart

47
Q

Why does a VAE occur?

A

Veins:

  • don’t collapse when cut d/t attachment to bone/dura
  • are sub-atmospheric pressure
48
Q

VAE: Air into RA

A

interferes with R-sided co + pulm arterial blood flow –> bronchoconstriction/pulm edema

49
Q

VAE: Air Lock

A

R-sided output failure, acute cor pulmonale, hypoxemia

50
Q

VAE: caution with who?

A

R-L shunt (paradoxical air embolism: obstruction of coronaries with air= vfib/death)

51
Q

S/S VAE

A

Sudden decrease in ETCO2
Gasp reflex
Millwheel murmur

TEE

Late: HOTN, tachycardia, dysrhythmias, cyanosis

52
Q

Tx: VAE

A

CRNA

  • Notify surgeon/Call for help ASAP
  • Aspirate RAC
  • d/c N2O, admin. 100% FiO2

Surgeon

  • flood site with fluid
  • apply occlusive material to bone edges
53
Q

SAH: Tx

A
  • MRI/MRA localization
  • percutaneous radiology techniques (control bleed: via coil/clip)
  • outcome optimal w/in 72h of bleed
54
Q

Day 3-15 after SAH, risk of

A

cerebral vasospasm
goal: HTN, hypervolemia, hemodilution
Tx: Nimodipine CCB day 1-21

55
Q

SAH clipping: anesthetic management

A

induction: avoid increasing ICP
Maintenance: A-line, CVP, PA catheter or TEE (CV dx), EP monitoring (detect ischemia)

56
Q

Goals of SAH clipping aesthetic management

A
  • Depth of anesthesia appropriate to level of stimulation
  • Facilitate surgical exposure: brain relaxation
  • Maintain CPP
  • Reduce aneurysm transmural pressure
  • Prompt awakening of pt post-procedure
  • Drugs, fluids, blood must be immediately available in event of rupture
57
Q

Biggest risk during AVM intraop

A

severe/rapid hemorrhage

58
Q

AVM anesthetic considerations

A
  • pre-induction A-line
  • tight BP control
  • fluid/blood readily available

Anesthesia & Coexisting Disease (23 decks)

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