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APEX Pharmacology > PHARMACOLOGY-Inhaled anesthetics PD > Flashcards

PHARMACOLOGY-Inhaled anesthetics PD Flashcards

1
Q

How does nitrous oxides solubility compare to nitrogen.

Why is this significant

A

N2O is 34 times more soluble than nitrogen

For every 1 N molecule that leaves a space, 34 N2O take it’s place

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2
Q

What effect does N2O have on a compliant air space

examples

A

It increases the volume of the space

ie blebs, bowel, air bubbles in blood

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3
Q

What effect does N2O have in a fixed airspace

examples

A

It increases pressure in the space

i.e. middle ear, eye during retinal detachment surgery, brain during intracranial surgery

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4
Q

What effect can N2O have on anesthesia equipment

A
  1. ETT cuff volume increasing pressure on trachea
  2. LMA cuff increased volume/pressure
  3. Balloon-tipped PA cath
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5
Q

What effect does N2O have on B12. Why is this significant

A

Irreversibly inhibits vitamin B12, which inhibits methionine synthase. This enzyme is required for folate metabolism and myelin production

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6
Q

What effect can nitrous oxide have on the middle ear

A
  1. Increases pressure which can damage tympanic membrane grafts
  2. Discontinuation can quickly decrease middle ear pressure leading to serous otitis
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7
Q

What effect does nitrous oxide have during retinal detachment surgery

A

N2O can expand the bubble that is being used as a retinal splint during detachment surgery

Retinal perfusion can become compromised causing permanent blindness

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8
Q

When should N2O be avoided with SF6 use in eye surgeries (Before vs after)

A

Before: d/d N2O at least 15 minutes prior to bubble placement

After: avoid N2O for 7-10 days

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9
Q

How long should N2O be avoided after injection of the following types of bubbles
Air=
Perfluoropropane=
Silicone oil=

A

Air= 5 days
Perfluoropropane= 30 days
Silicone oil= no CI

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10
Q

What is the significance of B12 inhibition by N2O and possible side effects

A

Significance:
Decreases methionine synthase which is needed for folate metabolism and myelin production

Side effects:

  1. Immunocompromised
  2. Decreased DNA synthesis
  3. Neuropathy
  4. Megaloblastic anemia from marrow suppression
  5. Homocysteine accumulation
  6. Possible teratogenicity
  7. Possible risk of SBA
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11
Q

What 4 factors increase risk of complications with B12 and N2O

A 
Prolonged exposure
Pts w/ pre-existing B12 deficiency
-pernicious anemia
-alcoholism
-strict vegan
-recreational N2O use
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12
Q

Fire risk with N2O use

A

It is not flammable but it does support combustion

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13
Q

Compare the potency of N2O, Des, Iso, and Sevo from greatest to least

A

Iso&raquo_space; Sevo&raquo_space;> Des > N2O

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14
Q

What does MAC measure

A

Potency

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15
Q

Define MAC

A

Minimum alveolar concentration is the concentration of inhalational anesthetic that prevents movement following painful stimulus in 50% of the population

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16
Q 
What percentage equals 1 MAC for each anesthetic
Iso=
Sevo=
Des=
N2O=
A 
Iso= 1.2%
Sevo= 2.0%
Des= 6.6%
N2O= 104%
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17
Q

What are 5 effects produced by general anesthetics

A
  1. amnesia
  2. loss of consciousness
  3. Immobility
  4. Modulation of autonomic function
  5. Some analgesia
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18
Q

Level for…
MAC-awake induction
MAC-awake on emergence
MAC-bar

A

MAC-awake induction = 0.4-0.5 MAC
MAC-awake on emergence = 0.15 MAC
MAC-bar = 1.5 MAC

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19
Q

Movement is prevented in 95% of the population at what MAC

A

1.3 MAC

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20
Q

Awareness and recall are prevented at what MAC

A

0.4 - 0.5 MAC

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21
Q

What is MAC compared to for systemic drugs

A

ED50

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22
Q

5 Factors that increase MAC

A
  1. Chronic etoh consumption
  2. Increased CNS neurotransmitter activity
  3. Hypernatremia
  4. Infants 1-6 months
  5. Hyperthermia
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23
Q

8 drugs that decrease MAC

A
  1. Acute etoh intoxication
  2. IV anesthetics
  3. N2O
  4. Opioids
  5. a-2 agonist
  6. Lithium
  7. Lidocaine
  8. Hydroxyzine
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24
Q

Does potassium level or gender affect MAC potency

A

No

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25
Q

Electrolyte and other physiologic abnormalities that can decrease MAC

A
  1. Hyponatremia
  2. Older age (dec MAC 6% per decade after 40 yrs)
  3. Extremes of age
  4. Hypothermia
  5. Metabolic acidosis
  6. Pregnancy
  7. HoTN
  8. Hypoxia
  9. Sever hypercarbia
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26
Q

6 drugs that increase MAC

A
  1. Chronic ETOH
  2. Acute meth intoxication
  3. Acute cocaine intoxication
  4. MAOIs
  5. Ephedrine
  6. Levodopa
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27
Q

What is the Meyer-Overton rule

A

That lipid solubility is directly proportional to the potency of an inhaled anesthetic

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28
Q

Define the unitary hypothesis

A

All anesthetics share similar mechanisms of action, but each may work at different sites

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29
Q

General anesthesia is produced by what mechanism at which sites

A

Mechanism=membrane-bound protein interactions

Site=Brain and spinal cord

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30
Q

How do volatile anesthetics affect inhibitory vs stimulatory receptors

A

stimulate inhibitory receptors

inhibit stimulatory receptors

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31
Q

What is the most important site of volatile anesthetic action in the brain

A

GABA-A receptors

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32
Q

What are the most important receptor sites of volatile anesthetic action in the spinal cord (3)

A

glycine receptor stimulation
NMDA receptor inhibition
Na+ channel inhibition

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33
Q

What 2 receptors do N2O and xenon target

A

NMDA receptor antagonism

K+ 2P-channel stimulation

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34
Q

How is immobility produced by volatile anesthetics

A

Action at receptor sites in the ventral horn of the spinal cord

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35
Q

Unconsciousness if produced by volatile anesthetics due to interacting with which 3 parts of the brain

A
  1. Cerebral cortex
  2. Thalamus
  3. reticular activating system
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36
Q

Amnesia is produced via what location of the brain (2)

A
  1. amygdala

2. hippocampus

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37
Q

Autonomic effects are produced via which parts of the brain

A
  1. Pons

2. Medulla

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38
Q

Analgesia is produced via what tract

A

Spinothalamic tract

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39
Q

Immobility is due to anesthetic action at what location

A

Ventral horn of the spinal cord

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40
Q

The hippocampus and amygdala produce what effect with volatile anesthetic

A

Amnesia

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41
Q

The pons and medulla produce what effect with volatile anesthetics

A

Autonomic effects

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42
Q

The reticular activating system produces what effect with volatile anesthetics

A

loss of consciousness (arousal)

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43
Q

The ventral horn in the spinal cord produces what effect with volatile anesthetics

A

Immobility

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44
Q

The spinothalamic tract produces what effect with volatile anesthetics

A

Analgesia

Ascending nociceptive signals are inhibited

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45
Q 
What effect do halogenated anesthetics have on
MAP
Contractility
SVR
HR
A 
MAP = decrease
Contractility = decrease
SVR =decrease
HR:
-iso/des=increase
-sevo=no effect
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46
Q

What effect does N2O have on MAP and SVR

A

It increases MAP and SVR by SNS activation

47
Q

What physiologic effect do volatile anesthetics have on cardiac and vascular smooth muscle

A
  • Reducing Ca++ influx in the sarcolemma
  • Decreasing Ca++ release from the SR
  • Modulate NO release
  • Inhibit Ach-induced vasodilation
  • Impair Na+/Ca++ pump
48
Q

What is the mechanism of MAP decrease by volatile anesthetics

A

Decreased Ca++ in vascular smooth muscle causes vasodilation which decreases SVR and VR

Myocardial depression d/t decreased Ca++ in the cardiac myocyte. This decreases inotropy

49
Q

How do volatile anesthetics affect cardiac conduction

A
  1. decreased SA node automaticity
  2. Decreased conduction velocity via AV node, His-Purkinje system and ventricular conduction pathways
  3. Increased duration of myocardial repolarization
  4. Altered baroreceptor function
50
Q

How is conduction affected by volatile anesthetics

A

It is decreased through the AV node, His-Purkinje system, and ventricular conduction pathways

51
Q

How is cardiac repolarization affected by volatile anesthetics and why

A

Increased duration of repolarization due to impaired outward K+ current

This increases the action potential duration and prolongs QT interval

52
Q

Explain the increase in HR caused by Iso and Dex

A

SNS activation from respiratory irritation

Pulmonary irritation leads to SNS activation. Increase norepi release and beta-1 stimulation

53
Q

How can the increase in HR from Iso and Des be countered

A

Opioids
Alpha-2 agonist
Beta-1 antagonist

54
Q

Which anesthetic agent reduces SVR the LEAST

A

Sevoflurane

55
Q

What effect doe volatile agents have on coronary blood flow

A

INCREASE CBF in excess of myocardial O2 demand

This dilates small cardiac vessels

56
Q

Compare the potency of coronary artery vasodilation with volatile agents from greatest to least

A

Iso > des > sevo

57
Q

How do volatile anesthetics affect PaCO2 (5)

A
  1. Hypercapnia thru depressed central chemoreceptors and respiratory muscles
  2. Decreased Vt and increased RR
  3. Increased apneic threshold
  4. Relaxed upper airway muscle tone causing obstruction
  5. Bronchodilation
58
Q

How much does minute ventilation change with increased PaCO2

A

For every 1 mmHg PaCO2 increase above baseline, Vm increases 3 L/min

59
Q

How are respiratory mechanics altered by volatile anesthetics
Effects on PaCO2

A

Dose-dependent depression of central chemoreceptors and respiratory muscle contribute to hypercarbia

Impaired motor neuron output and muscle tone to upper airway and thoracic muscles

60
Q

How is the respiratory pattern altered by volatile anesthetics
Effects on PaCO2

A

Reduced Vt
Compensates with increase RR
Smaller, faster breaths increase dead space and PaCO2

61
Q

How is dead space altered by volatile anesthetics

A

It’s increased due to smaller Vt and increase in RR

62
Q

What does the slope of the CO2 response curve represent

A

The sensitivity of the entire respiratory apparatus to PaCO2

63
Q

What are causes of left shift in the CO2 response curve (7)

A 
Anxiety
Surgical stimulation
Metabolic acidosis
Increased ICP 
Salicylates
Aminophylline
Dozpram
64
Q

What effect does a left shift of the CO2 curve have on ventilation

A

Stimulates ventilation

Breathe off CO2

65
Q

What are causes of a right shift in the CO2 response curve (4)

A

General anesthetics
Opioids
Metabolic alkalosis
Denervation of peripheral chemoreceptors

66
Q

What effect does a right shift of the CO2 curve have on ventilation

A

Depresses ventilation

Retain CO2

67
Q

What is the significance of a right shift in the CO2 response curve

A
  1. Decrease response to CO2

2. Increased apneic threshold (PaCO2 level that stimulates respiration)

68
Q

What upper airway muscles lose tone with anesthetic agents, causing upper airway obstruction

A 
Genioglossus (oropharynx obstruction)
Tensor palatine (nasopharyngeal obstruction)
Geniohyoid? (hypopharynx obstruction)
69
Q

How do anesthetic agents affect airway patency

A

Impairment of airway dilator muscles (genioglossus and tensor palatine)

70
Q

How is FRC affected by anesthetic agents

A

FRC is decreased d/t impaired pulmonary muscles

71
Q

What effect do halogenated agents have on airway diameter

A

Most volatiles are bronchodilators

Des can cause bronchoconstriction in asthmatics

72
Q

Where is hypoxemia monitored peripherally

A

In the peripheral chemoreceptors of the carotid bodies

73
Q

What is the PaO2 threshold for hypoxic drive

A

<60 mmHg

74
Q

What is the response to stimulation of the hypoxic ventilatory response

A

When PaO2<60 mmHg minute ventilation increases to restore arterial O2

75
Q

How are afferent impulses from the carotid and aortic bodies.

A

Carotid bodies = glossopharyngeal nerve (CN 9)

Aortic bodies = vagus nerve (CN 10)

76
Q

What changes stimulate the carotid bodies

A

Changes in arterial gas tension of PaO2, PaCO2, H+ concentration

77
Q

What changes stimulate the aortic bodies

A

Changes in BP

78
Q

How long can volatile agents impair peripheral chemoreceptors

A

Up to several hours after anesthesia

79
Q

At what MAC can the response to acute hypoxia be impaired

A

0.1 MAC

80
Q

What cells in the carotid bodies sense decreased PaO2

How do anesthetics affect this cell

A

Glomus type 1 cells

Anesthetics may create a reactive O2 species that impairs the glomus type 1 cells

81
Q

Compare the ability to inhibit hypoxic drive for volatile agents, from greatest to least

A

Sevo > Iso > Des

82
Q

Which anesthetic impairs the hypoxic drive the most and why

A

Halothane, because it undergoes the most biotransformation

Sevo

83
Q

Which anesthetic agent may be best for patients who rely on hypoxic drive to breathe

A

Desflurane

84
Q

What effect do pain and surgical stimulation have on the hypoxic ventilatory drive

A

None

Unlike their ability to affect the ventilatory response of CO2

85
Q 
What neurophysiologic effects do volatile anesthetics have on the following
CMRO2
ICP
CBF
Cerebral blood volume
EEG
A 
Dose-dependent effects
CMRO2 = reduction
ICP = increase
CBF = increase
Cerebral blood volume = increase
EEG = isoelectric at 1.5-2.0 MAC
86
Q

What 2 factors is CMRO2 dependent on

A
  1. Electrical activity

2. Cellular homeostasis

87
Q

At what MAC is an isoelectric state induced

A

1.5 - 2.0 MAC

88
Q

Which agent can induce seizures at high concentrations

A

Sevo

At >2.0 MAC

89
Q

What effect do anesthetic agents have on cerebral vasculature

A

Vasodilation

90
Q

How do anesthetic agents affect the coupling of CMRO2 and CBF

A

They are uncoupled by volatile anesthetics

CBF is increased while CMRO2 is decreased at concentrations >0.5 MAC

91
Q

How can ICP be addressed in patients receiving volatile anesthetics

A

Mild hyperventilation to PaCO2<35 mmHg

Concurrent use of propofol, opioids and barbiturates to decrease MAC needs

92
Q

What effect does N2O have on CBF and CMRO2

A

Both CBF and CMRO2 are increased

93
Q

What effect do volatile anesthetics have on cerebral autoregulation

A

It is attenuated, especially and moderate to high doses

The MAP changes based on CBF (whereas, normally, the MAP can be maintained with altered CBF within a range)

94
Q

How do volatile agents impact CSF production
Iso
Des
Sevo

A 
Iso= no change
Des= no change to possibly increased
Sevo= decreased
95
Q

How do volatile agents impact CSF absorption
Iso
Des
Sevo

A 
Iso= increased
Des= no change
Sevo= unknown
96
Q

What does SSEP monitor

A 
The integrity of the DORSAL column (medial lemniscus)
SENSORY tract (posterior)
97
Q

What arteries perfuse the areas monitored by SSEP

A

The posterior spinal arteries

98
Q

What does MEP monitor

A 
The integrity of the corticospinal tract
MOTOR tract (anterior)
99
Q

What arteries perfuse the areas monitored by MEP

A

The anterior spinal artery

100
Q

When is nerve ischemia concerning in evokes

A

Amplitude DECREASED >50%

Latency INCREASE >10%

101
Q

What impact do volatile anesthetics have on evoke potential monitoring

A

Decrease amplitude

Increase latency

102
Q

What is the best anesthetic technique to preserve evoke potential monitoring

A

TIVA without N2O

No NMBD

103
Q

What are recommendations for volatile agent use when evoked potentials are being monitored

A

<0.5 MAC supplemented with IV agents

No N2O

104
Q

What type of evoked potentials are most sensitive to the effects of volatile agents

A

Visual evoked potentials

105
Q

Which type of evoked potential are most resistant to the effects of volatile anesthetics

A

Brain auditory evoked potentials

106
Q

What is the purpose of evoked potential monitoring

A

To monitor the integrity of neural pathways

107
Q

What are 4 types of evoked potentials that are monitored

A

Somatosensory (SSEP)
Motor (MEP)
Visual (VEP)
Brainstem auditory (BAEP)

108
Q

How are SSEP produced

A

Applying current to a peripheral nerve

109
Q

In evoked potentials, what do amplitude and latency measure

A 
Amplitude = strength of nerve response (voltage)
Latency = speed of nerve conduction (time)
110
Q

What are the guidelines for muscle relaxant use when evokes are monitored

A

They should not be used for maintenance

Short-acting NMB use during induction but should metabolized ore reversed by the time potentials are monitored

111
Q

What effect does ketamine have on evoked potentials

A

Enhances signal

112
Q

What does loss of the evoked potential signal suggest

A

Ischemia to the neural pathway being monitored

113
Q

What are 4 interventions anesthesia can perform to aid in the loss of evoked potential signal

A
  1. Improve neural tissue perfusion by increasing BP
  2. Volume expansion
  3. Transfusion if anemic
  4. Normalize gas tension (PaO2/PaCO2)
114
Q

What physiologic alterations can impact evoke potential amplitude or latency

A

Hypoxia
Hypercarbia
Hypothermia

APEX Pharmacology (8 decks)

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