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N926: Pharmacology > Inhalation Agents II > Flashcards

Inhalation Agents II Flashcards

1
Q

Nitrous oxide molecular formula

A

N2O

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2
Q

Nitrous oxide blood:gas coefficient

A

0.46

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3
Q

Nitrous oxide oil:gas partition coefficient

A

1.4

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4
Q

Nitrous oxide vapor pressure

A

38,700

Gas

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5
Q

Nitrous oxide boiling point

A

-88 C

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6
Q

Nitrous oxide molecular weight

A

44

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7
Q

Nitrous oxide MAC

A

104

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8
Q

Isoflurane molecular formula

A

C3H2CIF5O

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9
Q

Isoflurane blood:gas coefficient

A

1.46

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10
Q

Isoflurane oil:gas coefficient

A

91

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11
Q

Isoflurane vapor pressure

A

238

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12
Q

Isoflurane boiling point

A

49 C

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13
Q

Isoflurane molecular weight

A

184

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14
Q

Isoflurane MAC

A

1.17

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15
Q

Desflurane molecular formula

A

C3H2F6O

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16
Q

Desflurane blood:gas partition coefficeint

A

0.42

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17
Q

Desflurane oil:gas partition coefficient

A

19

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18
Q

Desflurane vapor pressure

A

669

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19
Q

Desflurane boiling point

A

24 C

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20
Q

Desflurane molecular weight

A

168

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21
Q

Desflurane MAC

A

6

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22
Q

Sevoflurane molecular formula

A

C4H3F7O

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23
Q

Sevoflurane blood:gas partition coefficient

A

0.65

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24
Q

Sevoflurane oil:gas partition coefficient

A

47

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25
Q

Sevoflurane vapor pressure

A

157

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26
Q

Sevoflurane boiling point

A

59 C

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27
Q

Sevoflurane molecular weight

A

200

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28
Q

Sevoflurane MAC

A

2

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29
Q

Halothane molecular formula

A

C2HBrClF3

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30
Q

Halothane MAC

A

0.75

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31
Q

Halothane blood:gas partition coefficient

A

2.54

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32
Q

Halothane oil:gas partition coefficient

A

224

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33
Q

Halothane vapor pressure

A

244

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34
Q

Halothane boiling point

A

50.2 C

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35
Q

Halothane molecular weight

A

197

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36
Q

Xenon MAC

A

71

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37
Q

Xenon blood:gas partition coefficient

A

0.115

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38
Q

Xenon oil:gas partition coefficient

A

1.9

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39
Q

Xenon boiling point

A

-108 C

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40
Q

FI-Factors affecting inspiratory concentration

A

Fresh gas flow
Breathing system volume
Machine absorption

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41
Q

FA-Factors affecting alveolar concentration

A

Blood solubility of the agent
Alveolar blood flow
Partial pressure between alveoli and venous blood

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42
Q

Fa-Factors affecting arterial concentration

A

Alveolar and arterial anesthetic partial pressures are considered equal
Fa is less than end-tidal level would predict
-Venous admixture
-Alveolar dead space
-Non-uniform distribution

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43
Q

What anesthetic gas is metabolized the most?

A

Sevoflurane

5-8%

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44
Q

What are factors that effect the absorption of anesthetic gases?

A

Temperature
Solubility
Ventilation
Cardiac output

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45
Q

What are factors that effect the distribution of gases?

A

Lipid solubility
Tissue related factors
Metabolism

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46
Q

Where in the CNS does amnesia occur?

A

Brainstem

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47
Q

Where in the CNS does analgesia occur?

A

Thalamic tract

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48
Q

Where in the CNS does areflexia occur?

A

Spinal cord

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49
Q

Which solubility coefficient is the indicator of the speed of uptake and the elimination of the drug?

A

Blood:gas coefficient

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50
Q

Which solubility coefficient determines how efficiently the anesthetic gas is going to move through the blood to the tissues to the target?

A

Oil:gas coefficient

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51
Q

What is unique about Desflurane?

A

Low blood:gas solubility

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52
Q

What is unique about Isoflurane?

A

Potent

High oil:gas solubility

53
Q

What do you do if you want to get your gas on more quickly?

A

Increase flow

54
Q

What can you do to increase rate of rise of FA/Fi?

A 
Increase concentration (over pressure)
Second gas effect
Increase minute ventilation*
Decrease CO*
Decrease solubility*
55
Q

Where do anesthetic gases go first?

A

Vessel rich group

Includes brain

56
Q

What percentage of cardiac output goes to the vessel rich group?

A

75%

57
Q

What percentage of cardiac output goes to the muscle?

A

19%

58
Q

What percentage of cardiac output goes to fat?

A

6%

59
Q

What would expect if ETT only goes into right mainstem?

A

Right side of lung is being ventilated and perfused.

Left side of the lung is being perfused.

VQ mismatch

60
Q

Ventilation/perfusion mismatch

A

Right bronchial intubation or PFO

Overall effect is increase in alveolar partial pressure (highly soluble agents like isoflurane) and decrease in arterial partial pressure (low solubility agents)

61
Q

Most likely targets of anesthetic gases

A 
NMDA receptors 
Tandem pore K+ channels 
VG NA+ channels 
Glycine receptors
GABA receptors
62
Q

Meyer Overton theory

A

Also called critical volume hypothesis
Lipophilicity equates potency (increasing oil:gas coefficient)
Says that if you administer a large volume of anesthetic gas, eventually will hit critical volume threshold where the drugs will cross lipid bilayer

Says effect some ion channels but does not specify

63
Q

How do anesthetic gases effect CMRO2

A

Decreased

64
Q

How do anesthetic gases effect cerebral blood flow?

A

Cerebral blood flow (CBF) increased (dose-dependent)

Increases ICP

65
Q

What phenomenon describes the increase of CBF?

Which anesthetic gas causes this the most?

A

Uncoupling

Sevoflurane

66
Q

How does nitrous gas effect CMRO2 and CBF?

A

Increases CMRO2

Increases CBF

67
Q

How do you decrease ICP?

A

Mild hyperventilation

30-35 mmHg

68
Q

How do anesthetic gases effect evoked potentials?

A

Decrease amplitude and increase latency

69
Q

What is burst suppression?

A

Term used to describe an EEG pattern associated with high-voltage, mixed frequency, slow wave activity, along with periods of electrical suppression that lasts several seconds.

70
Q

Burst suppression occurs at:

A

1.5 MAC of Desflurane

2 MAC with Isoflurane and sevoflurane

71
Q

What type of anesthetic would you use if you are doing any neuromonitoring case?

A

TIVA

72
Q

Postoperative cognitive dysfunction

A

Greater concern in the elderly

No clinically significant association between major surgery and anesthesia with long-term POCD

73
Q

Emergence delirium in children

A

More common with sevoflurane and desflurane

74
Q

How do inhalation agents effect cardiac output?

A

Reduce cardiac output and index in dose-dependent fashion

75
Q

What happens to CI and HR as MAC hours increase?

A

Slight increase

76
Q

Inhalation agents effect on MAP

A

Reduced MAP secondary to SVR reduction

Nitrous oxide used in combination with anesthetics reduces this

77
Q

Heart rate decreases with

A

Halothane

78
Q

Heart rate increases with

A

Isoflurane
Desflurane (tachycardia)
Sevoflurane

79
Q

Volatile agents and nitrous oxide induce HR changes via

A

Unknown exactly, could be:
SA node antagonism
Modulation of baroreflex activity
SNS activity

80
Q

All inhalation agents produce some vasodilation

A

True
Decrease SVR, leads to decrease in MAP
EXCEPT for nitrous oxide

81
Q

Reverse Robin Hood or Coronary Steal

A

Seen the most with isoflurane
Response to hypotension
If body is having ischemic area in cardiac tissues, body will shunt blood away from those tissues.

Perfuses good tissue, not perfusing ischemic areas.

82
Q

What is preconditioning?

A

A phenomenon in which the heart is exposed to a cascade of intracellular events that protect it from ischemic and reperfusion insult

83
Q

What is sensitization?

A

Volatile agents reduce the quantity of catecholamines necessary to evoke arrhythmias

84
Q

How is PVR effected by nitrous oxide?

A

Slight increase
Other volatile agents have no effect
Worsens in pts with pulmonary HTN

85
Q

How do volatile agents effect pulmonary artery pressure?

A

Decrease

86
Q

Hypoxic pulmonary vasoconstriction

A

Mildly depressed
Isoflurane has the greatest effect
Normal physiologic response of body to vasoconstrict areas that are not being oxygenating, this response is depressed.

87
Q

Respiratory effects of inhalation agents

A

Decrease in tidal volume: compensated by increase in RR (but not sufficient to offset TV)
Responsiveness to hypoxemia
Responsiveness to CO2
-increases apneic threshold
-exacerbated by co administration of opioid
Relax airway muscle and produce bronchodilation

88
Q

Airway irritant

A

Desflurane

Don’t use for induction

89
Q

What happens to the CO2 response curve?

A

Shifts to the right

Decrease response to CO2

90
Q

Effect of inhalation agents on GFR and UO

A

Decreases

91
Q

Which inhalation agent effects renal function the least?

A

Desflurane

92
Q

Which inhalation agent effects renal function the most?

A

Sevoflurane because of degradation that leads to increase of fluorine ions that can cause renal injury

To counter this: should not exceed 2 MAC hours at flows <2L/min

93
Q

Halothane hepatitis

A

Why we don’t use it anymore

Most likely caused by trifluoracetyl-containing metabolites binding to proteins and
forming anti-trifluoroacetyl protein antibodies

Re-exposure of the patient to halothane these antibodies mediate massive
hepatic necrosis that can result in death

94
Q

THE IDEAL ANESTHETIC AGENT

A
  • Non-irritating to the respiratory tract
  • Rapid induction and emergence
  • Chemically stable (non-flammable)
  • Produce amnesia, analgesia and areflexia
  • Potent
  • Not metabolized and excreted by respiratory tract**
  • Free of toxicity and allergic reactions
  • Minimal systemic changes
  • Uses a standardized vaporizer
  • Affordable
95
Q

Neuromuscular effects

A

All volatile agents produce a dose-dependent relaxation on
skeletal muscle
• Additive effect on non-depolarizing NMBDs
• Can be reduced 25-50% of dose when compared to TIVA
• Delay recovery from non-depolarizing NMBDs

96
Q

Vapor pressure

A

Pressure exerted inside a container between liquid and vapor
At room temperature most volatile agents have a vapor pressure below atmospheric
pressure
As long as liquid is present, vapor pressure is independent of volume
Directly proportional with temperature

97
Q

Boiling point

A

Temperature at which vapor pressure exceeds atmospheric pressure in an open
container

98
Q

Partial pressure

A

Fraction of pressure within a mixture (Dalton’s Law)

99
Q

Solubility

A

Tendency of a gas to equilibrate with a solution (Henry’s Law)
• Anesthetic gases administered to the lungs diffuse into the blood until the partial
pressures of the alveoli and blood are equal
• Equalizing of blood and target tissues occurs similarly; however there is no gas phase

100
Q

MAC

A

The definition of MAC is the minimum alveolar concentration
(%) required to produce anesthesia (lack of movement) in
50% of the population (ED50)

101
Q

MAC ‘awake’

A

the MAC in which 50% of the population opens eyes to command

102
Q

MAC ‘BAR’

A

MAC ‘BAR’ – the MAC necessary to block adrenergic response to
stimulation
Usually 1.3 of MAC value
Can be reduced by administering a narcotic prior to incision

103
Q

What happens to MAC with age?

A

Decreases with age
• 6% decline each decade after the age of 40
• MAC relatively unaffected by gender, duration of anesthesia,
comorbidities
• Red-haired females?

104
Q

Additive effect

A

• 0.5 MAC of nitrous oxide + 0.5 MAC of isoflurane = 1 MAC sevoflurane

105
Q

Factors that increase MAC

A
  • Hyperthermia
  • Drug-induced increases in CNS activity
  • Hypernatremia
  • Chronic alcohol abuse
106
Q

Factors that decrease MAC

A
  • Hypothermia
  • Increasing age*
  • Alpha -2 agonists
  • Acute alcohol ingestion
  • Pregnancy
  • Hyponatremia
107
Q

Isoflurane

A

Halogenated methyl ethyl ether
• Most potent of the current volatile agents**
• Slower onset and recovery from anesthesia
Cardiovascular
• Minimal cardiac depression; preserves carotid baroreceptors
• Dilates coronary arteries; concern for ‘reverse-Robin Hood’
Respiratory
• Pungent; not used for inhalational induction
• Tachypnea less pronounced

108
Q

Vaporizers

A

The delivery device for volatile agents
• Facilitate the movement of anesthetic from the machine to the patient
through
• Fresh gas flow
• Pressure
• Temperature
• Vaporizers are calibrated for specific agents

109
Q

Desflurane

A

Least potent of the volatile agents
• Quicker induction and emergence
• Potential to boil at room temperature

Cardiovascular
• Rapid increases in desflurane lead to increases
in HR and BP
• Attenuated with fentanyl, esmolol, clonidine

Respiratory
• VERY pungent; can cause airway irritation,
increased salivation, breath holding, coughing,
laryngospasm
• Avoid in patients with reactive airway disease

110
Q

Sevoflurane

A

Fluorinated methyl isopropyl ether
Moderate potency
• Rapid induction and emergence

Cardiovascular
• May prolong QT interval; clinical significance?
• Cardiac output is less maintained than other volatile agents
• HR not increased

Respiratory
• Non-pungent; preferred volatile for inhalational induction

111
Q

Sevoflurane Metabolism

A
  • CYP-450 2E1 metabolizes 5-8% of sevoflurane
  • Increase in inorganic fluoride(F-) ions
  • However, never shown to result in nephrotoxicity
112
Q

Sevoflurane renal effects

A

Soda lime can degrade sevoflurane into Compound A:
Increased gas temperature, low flow anesthesia, high sevoflurane concentrations
and prolonged surgeries
Nephrotoxic in rats, not humans

For safety: Calcium hydroxide absorbent, flows 2 lpm, avoid in patients with renal dysfunction

113
Q

Nitrous oxide

A

Not a volatile anesthetic; colorless and odorless
• Gas at room temperature
• Kept as a liquid under pressure (745 psi)
• Nonexplosive and nonflammable
• However, it does support combustion like oxygen
• NMDA receptor antagonist
• May lower risk chronic pain after surgery

114
Q

Nitrous oxide decreasing in popularity?

A

Chronic exposure can lead to inactivation of vitamin B12 cofactor for enzyme synthesis, disrupting DNA synthesis leading to teratogenic, bone marrow and immunosuppression effects

115
Q

Nitrous oxide CV

A
  • Stimulates sympathetic nervous system

* BP, HR, CO unchanged or slightly elevated

116
Q

Nitrous oxide respiratory

A
  • Increases respiratory rate

* Decreases hypoxic drive

117
Q

Nitrous oxide cerebral

A

• Increases CMRO2 and CBF

Don’t use for gas filled spaces because N2O is 34 times more soluble than nitrogen (ENT, bowel cases)

118
Q

Nitrous oxide GI

A

• Increases the risk of PONV

119
Q

Nitrous oxide absolute contraindications

A

Methionine synthase pathway deficiency

• Expansion of gas-filled space

120
Q

Nitrous oxide relative contraindications

A
  • PONV
  • First trimester of pregnancy
  • Increased ICP
  • Pulmonary hypertension
  • Prolonged surgery (> 6 h)
121
Q

Xenon

A

Noble gas with known anesthetic properties
• Odorless, colorless, non-explosive naturally occurring
• Inert, does not form chemical bonds

Actions via NMDA and glycine receptor binding sites

Minimal cardiovascular, hepatic or renal effects
• Neuroprotective?

No effect on the ozone layer

Cost and limited availability have prevented widespread use
Favors air bubble expansion

122
Q

Malignant hyperthermia is triggered by

A 
• Volatile anesthetics
-nitrous oxide is considered acceptable 
• Succinylcholine
• Stress
Ryanodine receptor gene mutation (chromosome 19)
123
Q

MH signs and symptoms

A
  • Increase in carbon dioxide production
  • Muscle rigidity
  • Metabolic acidosis
  • High temperature (late sign)
  • Muscle rigidity
  • Increase in ETCO2
  • Increase in body temperature
  • Urine color darkens
  • Tachycardia
  • Tachypnea
124
Q

MH treatment

A 
• Dantrolene sodium – muscle relaxant
• 1mg/kg (supplied in 70 mL vials containing 20 mg of Dantrolene, 3000 mg of
Mannitol and sodium hydroxide)
• Administer until symptoms subside
• Up to 10 mg/kg

Ryanodex
• New IV formulation of dantrolene for the prevention and treatment of MH
• Requires fewer dials and less reconstitution
• Shorter half-life
• Requires supplementation of mannitol

125
Q

Halothane CV

A

More likely to induce arrhythmias
Alkyl halide
Susceptible to degradation, stored in amber bottles

126
Q

Pregnancy

A

Between 0.2-0.75% of pregnant patients may require general
anesthesia
• Most common appendectomy, cholecystectomy, ovarian or trauma
Some clinicians avoid nitrous oxide due to teratogenic effects
• Elective surgery should be delayed until after delivery
• Non-urgent surgery should be performed in the second trimester

127
Q

Obesity causes

A

Delayed emergence

128
Q

Measure depth of anesthesia

A

Pbrain

129
Q

Does nitrous oxide cause skeletal muscle relaxation?

A

No

N926: Pharmacology (4 decks)

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