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2024 Pharm II > Inhaled Anesthetics Part 2 (Exam III) > Flashcards

Inhaled Anesthetics Part 2 (Exam III) Flashcards

1
Q

What are the purposes of the anesthesia circuit? (3)

A
  • Delivery of O₂ and inhaled anesthetics
  • Maintenance of temperature & humidity
  • Removal of CO₂ and exhaled drugs
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2
Q

What types of gas delivery systems are there?

A
  • Rebreathing (Bain system)
  • Non-rebreathing (BVM system)
  • Circle systems (Anesthesia machine)
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3
Q

What type of system is depicted below?
Where is the aPL valve located on this system?

A
  • Bain Circuit
  • Blue circle depicts aPL below.
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4
Q

In the figure below, what portion of the anesthesia circle system is indicated by 1?

A

Inspiratory Unidirectional Valve

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5
Q

In the figure below, what portion of the anesthesia circle system is indicated by pink arrow?

A

Fresh Gas Inlet (O₂ & medical air)

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6
Q

In the figure below, what portion of the anesthesia circle system is indicated by 2?

A

CO₂ Absorber

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7
Q

In the figure below, what portion of the anesthesia circle system is indicated by 3?

A

Bag/Ventilator Selector Switch

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8
Q

In the figure below, what portion of the anesthesia circle system is indicated by 4?

A

APL Valve

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9
Q

In the figure below, what portion of the anesthesia circle system is indicated by 5?

A

Expiratory Unidirectional Valve

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10
Q

In the figure below, what portion of the anesthesia circle system is indicated by 6?
8?

A

6 = Expiratory Limb
8 = Inspiratory Limb

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11
Q

In the figure below, what portion of the anesthesia circle system is indicated by 7?

A

Y-Piece

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12
Q

When fresh gas flow (FGF) exceeds V̇T then you have _________________.

A

High Flow Anesthesia

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13
Q

When V̇T exceeds fresh gas flow (FGF) then you have _________________.

A

Low Flow Anesthesia

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14
Q

When would one see lack of rebreathing, wasteful volatile use, and cool dried air?

A

High flow anesthesia

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15
Q

When would one see lower volatile use, less cooling/drying of air, and slow changes in anesthetics?

A

Low flow anesthesia

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16
Q

Do volatiles cause bronchoconstriction or bronchodilation?

A

Bronchodilaton

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17
Q

How do volatiles cause bronchodilation?

A
  • Blockage of VG Ca⁺⁺ channels
  • Depletion of SR Ca⁺⁺
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18
Q

Is the bronchodilatory effect of volatiles still present in someone with reactive airway disease?

A
  • No (or very little effect). Bronchodilatory effects of volatiles require an intact epithelium, normal inflammatory processes, etc.
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19
Q

Will volatiles cause bronchospasm on their own (in a patient with no history of bronchospasm)?

A

No

Histamine release or vagal afferent stimulation needed to cause spasm.

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20
Q

In a patient without history of bronchospasm, how much would you anticipate PVR to change with 1-2 MAC?

A

PVR would be unchanged in patient with no history of bronchospasm.

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21
Q

What risk factors increase risk of bronchospasm? (4)

A
  • COPD
  • Coughing w/ ETT in place
  • <10 years old
  • URI
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22
Q

What anesthetic is generally the best at bronchodilating?

A
  • Sevoflurane
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23
Q

Which anesthetic can function as a pulmonary irritant (especially in smokers)?

A

Desflurane

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24
Q

Which volatile anesthetic in the graph below caused the greatest increase in airway resistance?
Lowest?

A
  • Desflurane = ↑ airway resistance
  • Sevoflurane = ↓ airway resistance
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25
Q

Inhaled anesthetics provide a dose-dependent skeletal muscle relaxation. T/F?

A

True

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26
Q

Which volatile gas has no effect on the relaxation of skeletal muscles?

A

N₂O

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27
Q

Will volatiles potentiate or inhibit NMBD’s? How?

A

Potentiate via sensitization of nACh receptors at NMJ.

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28
Q

How do volatile anesthetics cause skeletal muscle relaxation as a solo agent?

A

Volatiles cause skeletal muscle relaxation via enhancement of glycine at the spinal cord.

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29
Q

What is ischemic preconditioning?

A

Brief periods of ischemia preparing the heart for longer periods of ischemia.

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30
Q

Ischemic preconditioning with volatile anesthetics can occur as low as ______ MAC.

A

0.25

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31
Q

Why does ischemic preconditioning happen?

A
  • ↑ PKC activity
  • Phosphorylation of ATP sensitive K⁺ channels
  • Production of ROS (Reactive Oxygen Species)
  • Better regulation of vascular tone.
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32
Q

What molecule mediates ischemic preconditioning?

A

Adenosine

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33
Q

What does ischemic preconditioning prevent? (4)

A
  • Reperfusion injuries
  • Cardiac dysrhythmias
  • Contractile dysfunction
  • Delays MI’s in CAD patients.
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34
Q

At what MAC does volatile depression of CMRO₂ begin?

A

0.4 MAC

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35
Q

At what MAC would we see EEG burst suppression?
What about total electrical silence?

A
  • 1.5 MAC = burst suppression
  • 2 MAC = EEG silence
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36
Q

Which volatile causes the most EEG suppression?

A

Trick question. They all affect EEG’s the same.

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37
Q

Which volatiles have anticonvulsant activity?

A

Des, Sevo, & Iso at high concentrations & with hypocarbia.

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38
Q

Which volatile is a proconvulsant?

A

Enflurane

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39
Q

Give an example of a somato-sensory evoked potential (SSEP).

A

Stimulation of the foot evoking an electrical response in the CNS.

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40
Q

Give an example of a motor-evoke potential (MEP).

A

Direct stimulation of the brain eliciting a twitch response in the hand.

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41
Q

You have a case where SSEPs and MEPs need to be monitored, what general anesthetics options do you have?

A
  • TIVA
  • N₂O 60% and 0.5 MAC volatile.
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42
Q

What specific effects will volatile agents have on SSEPs and MEPs? At what MAC?

A

Dose-dependent (0.5 - 1.5MAC):

  • ↓ amplitude
  • ↑ latency (delayed frequency)
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43
Q

What occurs with cerebral blood flow with volatile administration?

A

Dose dependent:

  • ↑ CBF due to vasodilation ⇒ ↑ ICP
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44
Q

At what MAC would you expect to start to see an increase in CBF due to volatile administration?

A

At > 0.6 MAC

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45
Q

Which volatile has less cerebral vasodilatory effects?

A

Sevoflurane

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46
Q

Which volatiles have the greatest effect on increasing CBF? (and thus ICP)

A

Halothane and N₂O

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47
Q

Which volatile is the best for neuro cases? Why?

A

Sevoflurane

(preserves autoregulation mechanism up to 1 MAC & minimal cerebral vasodilation).

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48
Q

What patient population is most at risk due to the ICP increasing effects of volatile agents?

A

Patients with CNS occupying tumor/lesion.

49
Q

What average ICP increase is seen with volatile use?

A

7mmHg

50
Q

At what volatile dosage does ICP increase?

A

> 0.8 MAC

51
Q

What do volatiles do to the respiratory system?

A

Dose dependent:

  • Tachypnea
  • ↓ VT
52
Q

How do volatiles cause their respiratory effects?

A
  • Direct depression of medullary ventilatory center.
  • Interference with intercostal muscles.
53
Q

At what volatile dosage would apnea be seen?

A

1.5 - 2 MAC

54
Q

All volatiles will blunt the hypercarbic response. T/F?

A

False. N₂O does not blunt the hypercarbic response.

55
Q

All volatiles will blunt the hypoxic response. T/F?

A

True

56
Q

How can the hypercarbic response be preserved whilst using volatile anesthetic gasses?

A
  • Use N₂O and volatile together.
57
Q

What effect is seen in the graph below?

A

Volatile effects on CO₂
minimal effects with N₂O

58
Q

What is hypoxic pulmonary vasoconstriction?

A

Contraction of pulmonary arteries to shunt blood away from poorly ventilated portions of the lung.

59
Q

When is the blunting of HPV most concerning?

A

When one lung ventilation is being utilized.

60
Q

How fast is the HPV response?

A

Fast: within 5 minutes regional blood flow is ½ of normal.

61
Q

50% depression of HPV occurs at ___ MAC.

A

2

62
Q

Which volatile(s) does not cause cardiac depression?

A

N₂O

63
Q

How do volatiles cause hypotension?

A
  • Direct myocardial depression by altering Ca⁺⁺ entry and SR function.
64
Q

Volatiles will cause a dose-dependent decrease in ______ , ______ , and CO.

A

contractility ; SV

65
Q

When is volatile depression of cardiac function most concerning?

A

With pathologic hearts (particularly pathologies of ↓ contractility)

66
Q

What volatile can cause significant tachycardia with overpressurization?

A

Desflurane

67
Q

When will sevoflurane begin to cause increases in heart rate?

A

Only at > 1.5 MAC

68
Q

What variables confound the tachycardic effect of volatiles? (↑ and ↓)

A

Increase tachycardia:

  • Anxiety
  • Vagolytics

Might help reduce Tachycardia:

  • Concurrent opioids
  • β blockade
69
Q

What volatile is slightly sympathomimetic, causing a slight increase in CO?

A

N₂O

70
Q

Is the coronary steal effect of volatiles clinically significant?

A

Nope

71
Q

What electrocardiac effect do volatiles have?

A

QT prolongation via inhibition of K⁺ currents ⇒ risk of Torsade’s

72
Q

Which volatile has minimal pro-arrhythmic activity?

A

N₂O

73
Q

What volatile is the gas of choice for EP ablations? Why?

A
  • Sevoflurane
  • Other volatiles increase refractoriness of accessory pathways making identification of arryhthmia location difficult.

Sevo gang.

74
Q

Volatile neuroendocrine modulation will cause a perioperative surge in _______, _______, and _______.

A

catecholamines; ACTH; & cortisol

75
Q

Volatiles will suppress what important immune system components?

A

Volatiles suppress monocytes, macrophages, and T-cells.

76
Q

What does the total neuroendocrine profile of volatile anesthetics suggest for cancer patients undergoing surgery?

A

Neuraxial anesthesia is likely better than GA for cancer patients.

77
Q

What hepatic blood flow changes are seen with volatile administration? At what MAC might you see these changes?

A

Portal vein dilation = ↑ portal vein flow (at 1-1.5 MAC).
Maintained total hepatic flow.

78
Q

Which volatile is the only one that decreases hepatic flow?

A

Halothane (likely contributes to halothane hepatitis)

79
Q

What causes volatile hepatotoxicity?
When is it a concern?

A
  • Inadequate oxygenation of liver cells via ↓ blood flow and ↑ O₂ demand.
  • Concern for patients with preexisting liver disease.
80
Q

What is Type 1 Volatile hepatotoxicity?

A
  • Direct toxicity or free radical effect 1-2 weeks post surgically with N/V & fever in 20% of patients.
81
Q

What is Type 2 Volatile Toxicity?

A
  • Immune-mediated response caused with previous exposure to volatile with eosinophilia, fever, and higher mortality rate from hepatitis and necrosis.
82
Q

Which volatile is the choice anesthetic for severe liver disease? Why?

A

Sevoflurane: broken down to vinyl halide and won’t stimulate antibody production causing a Type II reaction.

Sevo the GOAT gas fr

83
Q

What volatiles are metabolized into acetyl halides? What is the significance of this?

A

Enflurane > Iso > Des

  • Acetyl halides can cause antibody reactions especially with previous exposure to halothane or enflurane.
84
Q

What are the renal effects of volatile anesthetics?

A

Dose dependent decrease in RBF, GFR, and UO from CO depression.

85
Q

How can the renal effects of volatile anesthetics be counteracted?

A

Hydration (both pre-operative and intra-operative).

86
Q

What other organ (besides the heart) undergoes protective ischemic preconditioning from volatile anesthetics?

A

Kidneys

87
Q

What toxic metabolites of volatiles can cause nephrotoxicity?
Why is this not an issue typically?

A
  • Fluoride metabolites
  • Newer volatiles are exhaled prior to being metabolized and eliminated renally.
88
Q

What volatile is 70% metabolized and can cause fluoride metabolite nephrotoxicity more than any of the other volatiles?

A

Methoxyflurane

89
Q

What measure is utilized in CO₂ absorbents today to help prevent the formation of compound A?

A

75% or greater concentrations of calcium hydroxide.

High levels of Potassium hydroxide and Sodium hydroxide not used anymore.

90
Q

What volatile is predisposed to starting fires? Why?

A
  • Sevoflurane
  • Reacts with dried absorbant to produce methanol and formaldehyde causing a heat reaction and eventual combustion.
91
Q

How is sevoflurane fire avoided?

A
  • Addition of H₂O to Sevo
  • Check temp of absorbent cannister
  • Exchange exhausted absorbents
92
Q

Which volatile anesthetics are emetogenic?

A

All

93
Q

What rate of PONV is seen with two triggering agents? (ex. desflurane and fentanyl)

A

25 - 30% PONV

94
Q

When is N₂O emetogenic?

A

At greater than 50% or 0.5 MAC

95
Q

Why is N₂O administration in a pregnant patient with B12 deficiency dangerous?

A

N₂O will oxidize the cobalt ion in B12 thus inhibiting methionine synthase = inhibition of DNA synthesis.

96
Q

Which volatile anesthetic can cause bone marrow suppression?

A

N₂O

97
Q

What is the result from increases in plasma homocysteine levels from N₂O administration?

A

If the patient also has low B vitamins and atherosclerosis, then N₂O increases risk of myocardial events.

98
Q

What is/are the obstetric effects of volatile anesthetics? And at what MAC?

A

Dose-dependent (0.5 - 1.0 MAC) decrease in uterine smooth muscle contractility. (relaxation)

99
Q

When would a decrease in uterine muscle tone be useful?

A

With retained placenta

100
Q

What is a downside to decreased uterine muscle contractility with volatile use?

A

Uterine atony (worsen blood loss)

101
Q

Why is N₂O useful in mom’s post delivery?

A

Swiftly increases analgesia without opioid/benzo’s (use as the spinal starts to wear off).

102
Q

Which volatiles have a sweeter smell?

A
  • Halothane
  • Sevoflurane
103
Q

What is the only real benefit of halothane?

A

↓ N/V

104
Q

What are the four major concerns of halothane?

A
  • Catecholamine-induced arrhythmias
  • Hepatic necrosis
  • Pediatric bradycardia
  • Decomposing into HCL acid.
105
Q

Which two volatiles can’t be used for induction due to their pungency?

A
  • Isoflurane
  • Desflurane
106
Q

Which volatile does not degrade, even after 5 years of storage?

A

Isoflurane

107
Q

If a vaporizer has a heating element, then the gas for that vaporizer can be assumed to be ____________.

A
  • Desflurane
108
Q

List the order in which volatiles will degrade into carbon monoxide if the absorbent becomes dehydrated.

A

Desflurane (worst) > Enflurane
> Isoflurane > Sevoflurane (trivial)

109
Q

Which volatile anesthetic would be the choice for inhalation induction? Why?

A
  • Sevoflurane
  • Least airway irritation & not pungent.
110
Q

Which volatile causes the least increase in ICP?

A

Sevoflurane

111
Q

How does N₂O produce skeletal muscle relaxation?

A

Trick question. It does not.

112
Q

What are the benefits of N₂O? (2)

A
  • Good analgesia
  • 2nd gas effect
113
Q

What are the major cons of N₂O ? (3)

A
  • Significant N/V @ 0.5 MAC
  • ↑ PVR
  • No surgeries with air filled spaces
114
Q

At what MAC would cerebral autoregulation be lost with halothane?
Sevo?
Iso/Des?

A
  • Halothane lost by 0.5 MAC
  • Sevo lost by 1 MAC
  • Iso/Des lost by 0.5-1.5 MAC
115
Q

Why is hypercarbia seen with volatiles?

A

↓VT, increased rate insufficient to maintain PaCO₂

116
Q

At what MAC would you see 100% depression of hypoxic response?
50-70% depression?

A

1.1 MAC ⇒ 100%

0.1 MAC ⇒ 50-70%

117
Q

What effect do volatiles have on CO?

A

dose dependent ↓CO but offset by mild ↑HR

Halothane has significant ↓CO

N₂O can cause mild ↑CO

118
Q

How do you prepare for an expected Malignant Hyperthermia case?

A
  • Remove Vaporizers
  • Do case first in the day
  • Run machine cycle according to instructions
  • Replace components

2024 Pharm II (32 decks)

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