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*Pharmacology > Apex- Volatile Anesthetics- Pharmacodynamics > Flashcards

Apex- Volatile Anesthetics- Pharmacodynamics Flashcards

1
Q

What is the blood:gas partition coefficient of Nitrogen?

A

0.014

  1. you know that nitrous oxide is 34x more soluble than nitrogen
  2. You know the blood:gas coefficient for N20 is 0.46
  3. 0.46 / 34 = 0.014

And that somehow = the blood:gas coefficient of nitrogen ::shrugs::

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2
Q

For every 1 molecule of nitrogen that leaves a closed space, ____ molecules of nitrous oxide enter to take it’s place

A

34

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3
Q

Is nitrous oxide flammable?

A

No, but it supports combustion

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4
Q

Nitrous oxide irreversibly inhibits what? Why is this an issue

A

Vitamin B12

Issue bc vitamin b12 promotes methionine synthase (the enzyme required for folate metabolism and myelin production) so your also inhibiting this

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5
Q

What is the gas bubble called they use for retinal detachment surgery that gets placed over the retinal break as a “splint” to hold the retina in place while healing occurs.

Why can’t you use N20?

A

Sulfur hexafluoride (SF6)

-Nitrous oxide is to be avoided bc it can diffuse into the bubble faster than the other gasses in the bubble can diffuse out > bubble expands > compromised rental perfusion > permanent blindness

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6
Q

When to avoid N20 with a SF6 bubble (2)

A

Before SF6 is placed > discontinue N20 at least 15 mins before placement
After SF6 is placed > avoid N20 for 7-10 days

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7
Q

When to avoid N20 in retinal bubbles other than SF6: Air, perfluropropane , silicone oil

A

Air - 5 days
Perfluopropane- 30 days (propane bill comes q30 days)
Silicone oil - no contraindication

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8
Q

Populations to avoid n20 in due to the risk of complications associated with inhibition of vitamin B12 (4)

A
  1. Pernicious anemia
  2. ETOHism
  3. Strict vegan diet
  4. Recreational use of N20
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9
Q

Example of when N2O can pose a fire risk

A

During laparoscopy with pneumoperitoneum if electrocautery is used

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10
Q

7 potential side effects of prolonged expose to N20 secondary to vitamin B12 inhibition

A
  1. Megaloblastic anemia
  2. Neuropathy (mylin destruction)
  3. Immunocompromise
  4. Impaired DNA synthesis
  5. Possible teratogenicity (data lacking)
  6. Risk of spontaneous abortion (avoid in first 2 trimesters)
  7. Homocysteine accumulation (data lacking)
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11
Q

MAC values of ISO, sevo, des, nitrous

A

ISO- 1.15%
SEVO- 2%
DES- 6.6%
N20- 104%

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12
Q

General anesthetic produce what 5 effects

A

LIMAS

Loss of consciousness
Immobility
Modulation of autonomic function
Amnesia
Some analgesia
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13
Q

T/F: MAC is additive

A

True

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14
Q

MAC “awake” during induction/emergence

A

Induction ~ 0.4-0.5 MAC awake

Emergence ~ 0.15 MAC awake

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15
Q

MAC BAR

A

1.5 MAC

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16
Q

1.3 MAC: movement is prevented in ____% of the population

A

95%

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17
Q

Awareness and recall are prevented at ___ - _____ MAC

A

0.4-0.5 MAC

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18
Q

The essential triad of anesthetic action includes what 3 things:

A

Amnesia
Loss of consciousness
Immobility

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19
Q

Define MAC BAR

A

The alveolar concentration required to block autonomic response following a supra-maximal painful stimulus (1.5 MAC)

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20
Q

What is MAC a measure of? (1 term)

A

Potency

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21
Q

Arrange inhalational agents from most to least potent

A

ISO > Sevo > DES > N20

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22
Q

If volatile anesthetic potency is decreased by something, does that increase or decrease MAC

A

Increase

Ie) volatile anesthetic potency is decreased by chronic ETOH consumption and red hair (you need more, so your MAC increases)

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23
Q

Drugs that increase MAC (6)

A
  1. Chronic ETOH consumption

[increased CNS neurotransmitters]

  1. Acute amphetamine intoxication
  2. Acute Cocaine intoxication
  3. MAOi’s (MAO helps break down catecholamines so if you inhibit their break down, they will be circulating)
  4. Ephedrine (increase NT- NE)
  5. Levodopa
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24
Q

Drugs that decrease MAC (8)

A
  1. Acute ETOH intoxication
  2. IV anesthetic
  3. N20
  4. Opioids
  5. Lidocaine
  6. Alpha-2 Agonists (precedex, clonidine)
  7. Lithium
  8. Hydroxyzine
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25
Q

Does Lithium increase or decrease MAC

A

Decrease

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26
Q

How do sodium levels affect MAC? Potassium? Mag?

A 
HYPERnatremia = INCREASES Mac
Hyponatremia = decreases Mac

K and MAG levels do NOT affect MAC

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27
Q

Premise: increased or decreased MAC

A

Decreased

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28
Q

What age group has increased MAC requirements?

A

Infants 1-6 months (sevo same for infants and neonates)

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29
Q

How much does MAC decrease after 40?

A

6% every decade after 40

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30
Q

How does temperature effect MAC?

A 
HYPERTHERMIA = increased MAC
Hypothermia = decreased Mac (cold, holding onto blankets/that anesthetic/doesn’t want to give it up)
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31
Q

how much does red hair increase MAC requirements?

A

By 20%

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32
Q

Why do pts with red hair have increased Mac requirements?

A

Due to mutations in the melanocytes stimulating hormone receptor and an increase production of phenomelanin

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33
Q

Increased or decreased MAC: CPB

A

Decreased

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34
Q

Increased or decreased Mac or no change:
Hypotension
Hypoxia
Anemia

A

Hypotension - decrease
Hypoxia- decrease
Anemia- decrease

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35
Q

Increased or decreased Mac or no change:

Metabolic acidosis

A

Decreased MAC

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36
Q

Increased or decreased Mac or no change:

Hypo-osmolarity (SIADH)

A

Decreased MAC

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37
Q

Increased or decreased Mac or no change:

Pregnancy
Postpartum

A

Decreased pregnancy > postpartum 24-72 hrs

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38
Q

Increased or decreased Mac or no change:

PaCO2 > 95

A

Decreased MAC

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39
Q

Increased or decreased Mac or no change:

Hyper/Hypothyroidism

A

NO DIRECT CHANGE; however changes in CO can affect MAC

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40
Q

Increased or decreased Mac or no change:

HTN

A

No change

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41
Q

Increased or decreased Mac or no change:

Gender

A

No change

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42
Q

MAC is unchanged with a PaCO2 between what?

A

15-95mmHg

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43
Q

What rule states that lipid solubility is directly proportional to potency

A

The Meyer-Overton rule

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44
Q

What theory suggest that a inhalational anesthetic interact with stereo selective receptors

A

Modern anesthetic theory

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45
Q

What states that all anesthetic share a similar MOA but each may work at a different site

A

Unitary hypothesis

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46
Q

The Meyer-Overton rule states that lipid solubility is (directly/inversely) proportional to the potency and (directly/inversely) proportional to MAC of an inhaled anesthetic

A

Directly proportional to potency (increased lipid solubility = increased potency)
Inversely proportional to MAC (increased lipid solubility = decreased MAC)

47
Q

Do volatile anesthetic most likely exert their effects by stimulating and inhibiting a variety of stereoselective receptors or disrupting the integrity of the phospholipid bilayers

A

By inhibiting a variety of steroselective receptors

48
Q

What are the primary targets of volatile anesthetic in the spinal cord? (2)

A

Stimulating glycine channels (inhibitory)

& inhibiting NMDA receptors and sodium channels (stimulatory)

49
Q

Where do volatile anesthetic produce immobility?

A

In the ventral horn of the spinal cord

50
Q

Where do upper and lower MOTOR neurons synapse?

A

In the VENTRAL horn of the spinal cord

51
Q

What is the primary target of halogenated agents in the brain?

A

The GABA-A receptor

52
Q

T/F: volatile anesthetic produce immobility by the GABA-A receptor in the spinal cord

A

FALSE

53
Q

Does nitrous oxide stimulate the GABA-A receptor?

A

No- it antagonizes the NMDA receptor and stimulates potassium 2P channels

54
Q

Where do volatile anesthetics produce unconsciousness (3) places

A
  1. Reticular activating system (RAS- in brain stem - responsible for consciousness and arousal)
  2. Thalamus - relay station of sensory and motor input into the cortex
  3. Cerebral cortex - Higher order cerebral functions
55
Q

Where do volatile anesthetics produce amnesia (2)?

A
  1. Hippocampus (temporal lobe: learning and memory)

2. Amygdala (emotional, response to pain, formation of stress response)

56
Q

Where do volatile anesthetics produce analgesia?

A

Spinothalmic tract (nociceptive signals along the ascending pathway are inhibited)

57
Q

Where do volatile anesthetics produce autonomic modulation? (2)

A

Pons & Medulla (control center for autonomic reflexes)

58
Q

What are the most important sites of VA action in the spinal cord (3)?

A
  1. Glycine receptor stimulation
  2. NMDA receptor inhibition
  3. Sodium channel inhibition
59
Q

How do VA effect cardiac conduction cycle?

A

Prolong the QT

  • they increase the duration of myocardial depolarization by impairing an outward K+ current, which prolonged the QT interval
60
Q

How is the HR effected by Iso, Des, Sevo, N20

A

Iso, Des, and N20- HR increases

SEVO- no change

61
Q

By what mechanism does N20 increase MAP and SVR?

A

By SNS activation

62
Q

Which VA decreases SVR the least?

A

Sevo

63
Q

What is the primary and secondary methods by which halogenated agents decrease MAP

A

Primary: decreased intracellular calcium in VSM > vasodilation > decreased SVR & venous return

Secondary: decreased intracellular calcium in the cardiac monocytes > myocardial depression > decreased inotropy

64
Q

What are the effects on HR by ISO and DES and why?

A

Increases HR 5-10% from baseline - likely do to SNS activation from respiratory irritation
SNS activation > increased NE release > beta 1 stimulation

65
Q

Of the volatile agents, which one reduces SVR the least?

A

Sevo

66
Q

Potency of coronary artery vasodilation from most potent to least

A

Iso > Des > Sevo

Why they use Iso in heart rooms I’m assuming

67
Q

Hearts extraction ratio of O2

A

75%

68
Q

How do halogenated agents affect minute ventilation?

A

Decrease tidal volume and increase RR > increase in dead space ventilation

69
Q

What maintains tight control of PaCO2?

A

The central chemoreceptors in the medulla

70
Q

For every 1mmHg increase in PaCO2 above baseline, minute ventilation will increase by ________L/min

A

3L/min

71
Q

How do halogenated agents affect the CO2 response curve?

A

Shifts down and right

72
Q

A (left/right) shift in the CO2 response curve results in a minute ventilation that is greater than predicted, causing a respiratory (acidosis/alkalosis)

A

Left - Alkalosis

73
Q

Causes of right shifts in the CO2 response curve (4) What does this imply

A

GA’s, opioids, metabolic alkalosis, denervation of peripheral chemoreceptors

*implies that for a given PaCO2, the minute ventilation is less than predicted, creating a resp acidosis

74
Q

How do volatile anesthetics lead to upper airway obstruction?

A

By impairing the airway dilator muscles such as the genioglossus or tensor palatine muscles

75
Q

Which volatile agent can induce bronchoconstriction in asthmatics?

A

Desflurane

76
Q

The carotid bodies relay afferent input to the respiratory center via which cranial nerve?

A

IX - Glossopharyngeal

CG - Cover Girl - Carotid bodies, Glossopharyngeal

77
Q

The aortic bodies relay afferent input via which cranial nerve?

A

X - vagus

AV - AV node - Aortic bodies - Vagus

78
Q

Halogenated agents decrease tidal volume and increase RR leading to what?

A

Increased deadspace ventilation

79
Q

What receptors maintains tight control of PaCO2? Where are they located?

A

Central chemo receptors in the medulla

80
Q

Every 1mmHg increase in PaCO2 above baseline will increase minute ventilation by ____L/min

A

3L/min

81
Q

What does a left shift in the CO2 response curve imply?

A

That for a given PaCO2, the minute ventilation would me MORE than predicted
>creating a resp alkalosis

82
Q

Causes of left shift in PaCO2 response curve (7)

A
  1. Anxiety
  2. Surgical stimulation
  3. Metabolic acidosis
  4. ICP (body trying to blow off CO2 to decrease it)
  5. Salicylate
  6. Doxapram
  7. Aminophylline

(think what would make someone breathe faster)

83
Q

What does a right shift of the PaCO2 response curve imply?

A

That for a given PaCO2, the minute ventilation would be LESS than predicted
>results in a resp acidosis

84
Q

Things that cause right shift of the PaCO2 response curve (depresses ventilation) (4)

A
  1. Volatile anesthetics
  2. Opioids
  3. Metabolic alkalosis
  4. Denervation of peripheral chemoreceptors
85
Q

What kind of receptors monitor for hypoxemia? Where are they located?

A

Peripheral chemoreceptors in the Carotid bodies

86
Q

PaO2 < ________mmHg is a stimulus to increase minute ventilation in an effort to restore arterial oxygenation

A

60mmHg

87
Q

What are carotid bodies vs aortic bodies more sensitive to?

A

Carotid bodies - change in arterial gas tensions (PaO2, PaCO2) & H+ concentration

Aortic bodies- change in BP

88
Q

How long do volatile anesthetics impair the peripheral chemoreceptors for?

A

Several hours after surgery

89
Q

Which cells in the carotid bodies provide the sensory arm of the hypoxia drive?

A

Globules type 1 cells

90
Q

Reactive oxygen species impair glomulus type 1 cells (provide sensory arm for hypoxic drive)

  • anesesthetic metabolism is a source of reactive oxygen species
  • list the volatile agents that inhibit the hypoxic drive from most to least

*What patient population is this a consideration for?

A

Halothane > Sevo > Iso > Des
20% metabolism > 2% > 0.2% > 0.02%

*Important for pts who rely on hypoxic drive to breathe > emphysema/COPD > Des is best for these pts then iso then sevo

91
Q

Mechanism by which volatile anesthetics increase cerebral blood flow

A

VA’s uncouple metabolism from cerebral blood flow > meaning they supply the brain with more blood flow than it actually needs —> since more blood is delivered to the brain per minute, cerebral blood volume increases

92
Q

What is CMRO2 dependent on (2)?

A
  1. Electrical activity (60%)

2. Cellular hemostasis (40%)

93
Q

Do volatile anesthetics decrease CRMO2?

A

Yes, but only to the extent that they decrease electrical activity — once the brain is iso-electric, VA’s cannot reduce CMRO2 any further

94
Q

What MAC is required to produce an isoelectric state?

A

MAC 1.5-2

95
Q

Which VA, in high concentrations (2 MAC) can produce seizure activity?

What is this exacerbated by and in when is it more commonly seen?

A

Sevo

—exacerbated by hypocapnea
— more common is pediatric inhalational induction

96
Q

The cerebral vascular use continuously adjusts vessel diameter to maintain a constant cerebral perfusion pressure of what?

A

50-150mmHg

97
Q

When metabolic demand increases, blood vessels (constrict/dilate) and cerebral vascular resistance (increases, decreases)

A

Vessels dilate and CVR decreases

98
Q

When metabolic demand decreases, blood vessels (constrict/dilate) and resistance (increases/decreases)

A

Vessels Constrict, resistance increases

99
Q

Volatile anesthetics result in vasoconstriction from reduction in CRMO2 + vasodilation from the anesthetic agent . What is the net effect of this? (3)

How is nitrous oxide different?

A

Increased CBF, increased CBV, increased ICP

Nitrous oxide increases both CMRO2 and CBF

100
Q

Which agents have what effects on CSF production and CSF absorption? Iso, Des, Sevo

A

Iso - increased CSF absorption (no production so it just increases absorption instead)
Des- increased/no change CSF production (no effect on absorption)

Sevo- DECREASED CSF production, ?effect on absorption

101
Q

What are evoked potentials used to monitor?

A

Integrity of a neural pathway

102
Q

What do SSEPs monitor the integrity of?

What perfuses this region of the spinal cord?

A

The dorsal medial lemniscus column

-the posterior spinal arteries

103
Q

What do MEPs monitor the integrity of?

What perfuses this region of the spinal cord?

A

The corticospinal tract

-The anterior spinal artery

104
Q

What is the best technique to preserve evoked potentials?

A

TIVA w/o N20

105
Q

If you use a volatile agent during evoked potential monitors, what should you keep MAC below?

A

0.5 MAC

106
Q

What drug enhances evoked potential signals?

A

Ketamine

107
Q

What type of evoked potentials are the most resistant to anesthetics and any technique can be used?

A

Brain auditory evoked potentials

108
Q

Which evoked potentials are most sensitive to anesthetics and are rarely used?

A

Visual EPS

109
Q

Evoked potentials: What is amplitude vs latency?

A

Amplitude: The strength of the nerve response
Latency: The speed of nerve conduction

110
Q

Evoked potentials: As a general rule, you should be concerned about nerve ischemia when amplitude decreases by ____ % or latency increases by _______%

A

Amplitude decreases by 50% or more

Latency increases by 10% or more

111
Q

What do volatile anesthetics due to amplitude and latency on evoked potentials?

What factors exaggerate this? (4)

A

Decrease amplitude and increase latency

> addition of N20
hypoxia
hypercarbia
hypothermia

112
Q

What should happen if EPS diminish or go away?

A

The surgeon should investigate a mechanical cause. Anesthetic goals are directed towards improving neural tissue perfusion by:

Increasing BP, volume expansion, transfusion if anemic, normalizing gas tensions

113
Q

At what MAC is the response to hypoxia impaired? Is the CO2 response impaired at this level?

A

0.1 MAC; no

*Pharmacology (25 decks)

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