Inhaled Anesthetics 2 Flashcards

1
Q

Name places N20 will have fast equilibrium

A

pulmonary blebs
air bubbles in blood
gas bubble in the eye

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2
Q

name places N20 will have slow equilibrium

A

bowel
pneumoperitoneum

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3
Q

How can N20 affect the middle ear?

A

can increase pressure in middle ear and damage tympanic membrane graft.

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4
Q

if N20 is discontinued quickly how can it impact the ear?

A

quickly decrease middle ear pressure leading to serous otitis

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5
Q

What is an SF6 Bubble? How is it used?

A

sulfur hexafluoride bubble

used in retinal detachment surgery to hold retina in place while it heals

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6
Q

Risk of N20 use with SF6 bubble?

A

N20 can increase pressure in the bubble leading to retinal compression and permanent blindness.

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7
Q

N20 guidelines for SF6 bubbles. How soon to DC before and how soon safe to use after?

A

Must stop it 15min before placement

need to avoid for 7-10 days afterwards

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8
Q

N20 guidelines for other bubbles besides SF6

A

Air: avoid N20 for 5 days
perfluoropropane: avoid for 30 days
silicone oil: no CI to N20

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9
Q

How does N20 affect Vit B12 and what does this cause?

A

N20 irreversibly inhibits Vit B12 > inhibited methioine sythase > impaired folate metabolism and impaired myelin production

this can cause:
decreased DNA synthesis
neuropathy
megaloblastic anemia (bone marrow suppression)
immunocompromise

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10
Q

what conditions increase the associated risks of N20 use?

A

pernicious anemia
alcoholism
vegan diet
recreational N20 use

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11
Q

MAC awake?

A

0.4-0.5 during induction
0.15 during recovery

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12
Q

MAC level to prevent movement in 95% of patients?

A

MAC 1.3

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13
Q

MAC level required to prevent awareness and recall?

A

assumed to be MAC 0.4-0.5

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14
Q

What factors increase MAC?

A

chronic Etoh use
^ CNS neurotransmitters
acute amphetamine intoxication
acute cocaine intoxication
MAOIs
Ephedrine
Levodopa
Hypernatremia
1-6mo of age
Hyperthermia
Red hair by 19% (science is questionable)

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15
Q

drugs that can decrease MAC?

A

acute etoh intoxication
lithium
lidocaine
hydroxyzine
IV anesthetics

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16
Q

What can decrease MAC other than drugs?

A

hyponatremia
prematurity
Age > 40
hypothermia
MAP < / = 50
hypoxia
anemia < 4.3 ml O2 / dL blood
CPB
metabolic acidosis
hypo-osmolarity
pregnancy
24-72 hrs post partum
PaCO2 > 95

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17
Q

do thyroid levels affect MAC?

A

no not directly

but sever hypothyroidism > decreased CO > slower onset of anesthetics > easy to accidentally overdose patient

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18
Q

do you get more HoTN from VA + N20 or VA alone?

A

from VA alone. N20 doesn’t drop BP as much

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19
Q

which inhaled agents can increase HR?

A

Des, Iso, and N20.

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20
Q

how does N20 affect SNS?

A

it activates SNS and ^ HR

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21
Q

how does inhaled anesthetics affect cardiac contractility?

A

slight decrease, except for N20. N20 has no affect on contractility alone.

N20 with opioids though will cause myocardial depression

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22
Q

which volatile agent decrease SVR the least?

A

Sevo

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23
Q

which volatiles cause the most coronary dilation? can volatiles lead to cardiac ischemia?

A

Iso > Des > Sevo

historical concern for coronary steal syndrome but VAs actually precondition myocardium and protect against ischemia.

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24
Q

What is the Myer-overton rule?

A

lipid solubility is directly proportional to the potency of inhaled anesthetics

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25
Q

what is the unitary hypothesis?

A

all volatile anesthetics have simillar mech of action but work on different sites

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26
Q

what is the old-school assumed mech of action of VAs

A

assumed to be on the lipid bilayer of neurons

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27
Q

Newer understanding about VAs mech of action?

A
  1. stimulate inhibitory receptors
  2. inhibit stimulatory receptors
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28
Q

inhibitory pathways VAs work on

A

GABA-A R
glycine R
potassium channels

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29
Q

stimulatory pathways VAs work on?

A

NMDA receptor
nicotinic R
sodium channels
dendritic spine function and motility

30
Q

on what receptor do VAs work in the brain? what kind of receptor is it?

A

GABA-A
ligand gated chloride channel

31
Q

where do VAs work in the spinal cord? What do they cause?

A

provide immobility in the ventral horn of spinal cord by inhibiting:
glycin R
NMDA R
Na channel

32
Q

In what part of the brain do VA produce amnesia?

A

amygdala & hippocampus

33
Q

In what part of the brain do VA produce autonomic effects?

A

pons and medulla

34
Q

where do VA produce analgesia?

A

spinothalamic tract

35
Q

where do VAs produce immobility?

A

ventral horn of spinal cord

36
Q

N20 and Xenon mech of action

A

NMDA antagonism
Potassium 2P channel stimulation

do not stimulate GABA-A Receptor

37
Q

where are central chemo receptors found? What do they control?

A

medulla and control PaCO2

for every 1mmHg ^ in PaCO2 ventilation ^ by 3ml/min

38
Q

how do VA cause resp depression?

A

depress central chemo receptors
depress resp muscles including: uppper airway m. diaphragm, intercostal m.

39
Q

How do VA affect normal breathing?

A

decrease tidal volumes

body tries to compensate by increasing RR but this is not enough to offset rise in PaCO2

40
Q

how doe VA shit CO2 response curve?

A

down and to the right

41
Q

where is the apneic threshold?

A

typically 3-5mmHg below PCO2 that is maintaned during spontaneous ventilation

42
Q

how do VA affect airway diameter?

A

halogenated agents are bronchodilators but this is minimal unless there is increased airway resistance.

Exception: Des can induce bronchospasm in asthmatics

43
Q

where are peripheral chemo receptors? what do they monitor?

A

carotid body
measure PaO2

44
Q

what is the PaO2 trigger level for pheripheral chemo receptors ot stimulate ^minute ventilation?

A

PaO2 < 60 causes stimulation to increase minute ventilation

45
Q

what are carotid bodies most sensitive too? what are aortic bodies most sensitive to?

A

carotid bodies: changes in PaO2, PaCO2, H+

aortic bodies: changes in BP

46
Q

pathway for afferent info from carotid bodies to resp center?

A

via glossopharyngeal n.

47
Q

pathway for afferent infrom for aortic bodies to resp center?

A

vagus nerve

48
Q

how doe VAs affect peripheral chemo receptors? for how long?

A

impair them for several hours after anesthesia

49
Q

what MAC level impairs response to actue hypoxia but not PaCO2

50
Q

what cells in carotid body provide sensory arm to hypoxic drive?

A

glomus cells

51
Q

what is the mech of action for VA inhibiting the hypoxic drive? when is this clinically relevant?

A

theory is reactive oxygen species from VA metabolism impair glomus type I cells.

agents with the most biotransformation inhibit the hypoxic drive the most (sevo>iso>des)

clincial relevance: important for pts that rely on hypoxic drive to breath. I.E. emphysema or sleep apnea. Des is best for these patients.

52
Q

does N20 affect carotid bodies response to hypoxia? how?

A

yes, but in different way than VAs

53
Q

how do pain and surgical stimulation affect the bodies response to CO2 and the hypoxic ventilatory drive?

A

reverse depression of response to CO2

do not reverse depression of hypoxic ventilatory drive

54
Q

How do VA affect CMRO2 and CBF?

A

decrease CMRO2 and ^ CBF causing uncoupling.

this obviously increases CBV and ICP

55
Q

at what MAC level can you get isoelectric state?

A

1.5-2.0 MAC

56
Q

how does N20 affect CMRO2 and CBF?

A

increases both CMRO2 and CBF

57
Q

describe the paradoxical effect VAs have on CMRO2 and CBF. Waht is the one downside?

A

typically decreased CMRO2 causes vasoconstriction to decrease CBF, but VA cause CMRO2 and vasodilation… so what really happens? vasodilation or constriction?

Bottom line: at MAC > 0.5 VA increase CBF even though they decrease CMRO2

VA increase ICP from the increased CBF

58
Q

what VA can cause seizures at 2.0 MAC?

59
Q

Waht conributes to CMRO2? what are VA actually decreasing when they decrease CMRO2?

A

CMRO2
1. electrical activity 60%
2. cellular homeostasis 40%

VA only decrease CMRO2 by decreasing electrical activity. Once isoelectric VAs can not decrease CMRO2 any further.

60
Q

name each type of evoked potential

A

SSEP
MEP
VEP
BAEP

61
Q

what part of spinal cord does SSEP monitor? what perfuses this region?

A

monitor integrity of dorsal column (medial lemniscus) whish is perfused by post. spinal arteries

62
Q

what part of spinal cord do MEPs monitor? what perfuses this region of spinal cord?

A

corticospinal tract perfused by ant. spinal artery

63
Q

how often are BAEP and VEP used?

A

very rarely

64
Q

what changes on evoked potential warrant concern about ischemia?

A

if amplitude decreaes by about 50% or latency increases by about 10%

65
Q

best anesthetic method to conserve evoked potentials?

A

TIVA without N20

66
Q

which evoked potentials are most sensitive to anesthetic agents?

A

visual evoked potentials

67
Q

which evoked potentials are most resistant to effects of anesthetics?

A

BAEP. you can use any drugs with BAEP monitoring.

68
Q

how does ketamine affect evoked potentials?

A

enhances the signals

69
Q

what are some things besides meds that can affect evoked potentials?

A

hypoxia
hypercarbia
hypothermia

70
Q

what to do if evoked potentials decrease during surgery

A
  1. have surgeon investigate surgical cause

anesthetic mgmt:
increase persusion
^ BP
volume expansion
transfusion (if anemic)

71
Q

what is the wake up test?

A

old school technique now abandonded for SSEP and MEP monitoring

I think used in scoliosis surgery??

they would wake people up in the middle of surgery

if they can omve hands but not fet surgeon needs to decrease distraction (stretching) on spinal column

72
Q

risk of wake up test

A

extubation
losing lines
air embolism
awareness
pain
damage to surgical instrumentation