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2-Anesthesia Pharm Exam 2 > The inhaled anesthetic agents & physiological effects > Flashcards

The inhaled anesthetic agents & physiological effects Flashcards

1
Q

What IA is rate of emergence most rapid?

A

with the least soluble inhaled anesthetics (nitrous oxide, desflurane, sevoflurane)

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2
Q

What happens when inhaled anesthetic administration is abruptly stopped?

A

skeletal muscle & fat don’t initially release the anesthetic back into the bloodstream for degradation in the liver

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3
Q

More soluble inhaled agents = ___________ emergence

A

slower/longer

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4
Q

What does elimination of inhaled anesthetics depend on?

A

Length of administration,
Blood-gas solubility of the inhaled anesthetic

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5
Q

What is important with inhaled anesthetics for long period of time ?

A

Context-sensitive half time important with administration

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6
Q

What is floods example of context sensitive half time?

A

If an anesthetic is 3-4 hrs duration, then about 30 min before the end of the case, turn off sevoflurane and replace it with 70% N2O

(This gives sevoflurane adequate time to decrease 90% & rapid recovery once N2O is DCd at end of surgery)

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7
Q

Review context sensitive half time.

A

Slide 47

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8
Q

What effect does the greater the uptake of the anesthetic have? (3)

A

the greater the difference between inspired and alveolar concentrations, and the slower the rate of induction.

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9
Q

What effect does low-output states have?

A

predispose patients to overdosage with soluble agents, as the rate of rise in alveolar concentrations will be markedly increased.

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10
Q

What are some key factors that speed induction & recovery? (6)

A
  • Elimination of rebreathing, high fresh gas flows
  • Low anesthetic-circuit volume
  • Low absorption by the anesthetic circuit
  • Decreased solubility
  • High cerebral blood flow
  • Increased ventilation
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11
Q

What is the Blood: Gas Partition Coefficient of methoxyflurane?

A

12

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12
Q

What is the Blood: Gas Partition Coefficient of halothane?

A

2.54

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13
Q

What is the Blood: Gas Partition Coefficient of enflurane?

A

1.90

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14
Q

What is the Blood: Gas Partition Coefficient of isoflurane?

A

1.46

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15
Q

What is the Blood: Gas Partition Coefficient of Nitrous oxide?

A

0.46

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16
Q

What is the Blood: Gas Partition Coefficient of Desflurane?

A

0.42

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17
Q

What is the Blood: Gas Partition Coefficient of Sevoflurane?

A

0.69

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18
Q

What is the Blood: Gas Partition Coefficient of Xenon?

A

0.115

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19
Q

What are intermediately soluble agents?

A

Halothane, Enflurane & Isoflurane

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20
Q

What are intermediately poor soluble agents?

A

Nitrous oxide, desflurane, sevoflurane and xenon

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21
Q

What is the smell properties of nitrous oxide?

A

Odorless, sweet smelling

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22
Q

What is true about the solubility of nitrous oxide?

A

poor blood solubility that results in rapid alveolar and brain partial pressures

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23
Q

Nitrous OXIDE: Mostly used in _________ with other agents (except dental)

A

Conjunction

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24
Q

What is the flammability of nitrous oxide?

A

Not flammable but is an oxidizing agent that WILL SUPPORT COMBUSTION

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25
Q

What is true about the storage of nitrous oxide?

A

Only “nonvolatile” inhaled anesthetic, an inorganic gas in gas state at room temp (liquified under pressure and stored in blue tanks)

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26
Q

What is the principle characteristic of nitrous oxide?

A

Rapidly expands closed air spaces (readily crosses lipid membranes diffuses 35 times faster into closed air spaces than nitrogen can diffuse out)

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27
Q

When is nitrous oxide contraindicated? (8)

A

venous or arterial air embolism, pneumothorax, acute intestinal obstruction w/bowel distension, intracranial air/pneumocephalus, pulmonary air cysts, intraocular air bubbles, tympanic membrane grafting

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28
Q

What is true about nitrous oxide and tracheal cuffs?

A

Will also diffuse into tracheal tube cuffs increasing the pressure against the tracheal mucosa

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29
Q

What is the MOA of nitrous oxide?

A

NMDA receptor antagonist

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30
Q

What is the elimination and uptake of nitrous oxide?

A

Rapid

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31
Q

What is the effects on skeletal muscles with nitrous oxide? What can it cause at high concentrations?

A

Minimal skeletal muscle relaxation & Causes skeletal muscle rigidity at high concentrations

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32
Q

What are the cardiac physiology of nitrous oxide? Why do you not see these?

A

Myocardial depressant, it has Mild sympathomimetic

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33
Q

What does nitrous oxide have on MAC?

A

Reduces MAC of potent volatile inhaled anesthetics

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34
Q

What is the respiratory effects of nitrous oxide?

A

Pulmonary vascular smooth muscle constriction/ increases pulmonary vascular resistance

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35
Q

What CNS effect occurs from Nitrous oxide?

A

Increases CBF, CBV, & CMRO2

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36
Q

What is true about analgesia and nitrous oxide?

A

Concentrations below MAC may provide analgesia (dental surg, labor, minor surg procedures) – analgesia ends once N2O admin. ceases

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37
Q

How does nitrous oxide increase the risk of PONV?

A

Increases risk of PONV d/t activation of the chemoreceptor trigger zone & vomiting center in medulla

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38
Q

What does nitrous oxide inactivate by the oxidation of cobalt?

A

vitamin B12 (methionine & thymidylate synthetase enzyme)

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39
Q

What is the importance of methionine synthetase?

A

converts homocysteine to methionine which is crucial in DNA, RNA, myelin, catecholamines.

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40
Q

What can a decrease of methionine result in?

A

in both genetic and protein abnormalities (concerns with repeated exposures within 3 days)

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41
Q

What changes occur from the inactivation of B12 by nitrous oxide?

A

Megaloblastic changes in bone marrow & Peripheral neuropathy

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42
Q

Who is most vulnerable for the inactivation of vitamin b12 by nitrous oxide?

A

Extremes in age are most vulnerable

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43
Q

What occurs when nitrous oxide is abruptly stopped?

A

Diffusion Hypoxia

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44
Q

What occurs with diffusion hypoxia?

A

discontinued which leads to reversal of partial pressure gradients such that nitrous oxide leaves the blood to enter the alveoli

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45
Q

Describe the relationship of diffusion hypoxia and nitrous oxide?

A
  • PAO2 is diluted with N2O so that PaO2 decreases
  • Also dilution of the PACO2 = decreases the stimulus to breath
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46
Q

When is diffusion hypoxia from nitrous oxide is of greatest concern?

A

Of greatest concern during the first 1-5 minutes after its discontinuation of nitrous oxide

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47
Q

What is the treatment of NO diffusion hypoxia?

A

Increase oxygen flows at end of the anesthetic once nitrous oxide is discontinued

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48
Q

What is the chemical property of halothane?

A

Halogenated alkane

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49
Q

What is true about the use of halothane in the US?

A

Not used in the US any longer

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50
Q

What is halothane susceptible to decomposition to?

A

Susceptible decomposition to HCl & hydrobromic acid (used thymol preservative)

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51
Q

What agent is associated with used thymol perservative?

A

Halothane

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52
Q

What is the smell properties of halothane?

A

Sweet and nonpungent

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53
Q

What is halothane most commonly used with? What has it been replaced with?

A

Used with pediatric inhalational inductions along with nitrous (replaced with Sevoflurane)

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54
Q

What is true about the induction of halothane?

A

Unlike SEV- had to slowly increase concentration delivered to induce: could not do a 1-2 breath induction

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55
Q

What are the cardiac effects of halothane? (2)

A

Direct myocardial depression & slowing of sinoatrial node conduction

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56
Q

What are two arthymias associated with halothane?

A

May result in junctional rhythm & bradycardia

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57
Q

Halothane is associated with Dose-dependent ________ in cardiac output

A

decrease

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58
Q

What effect does halothane have with epinephrine?

A

Sensitizes heart to arrhythmogenic effects of epinephrine

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59
Q

What effect does halothane have on blood flow in the CNS?

A

Lowers cerebral vascular resistance, increase CBF, blunts autoregulation

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60
Q

What effect does halothane have on hypoxic drive? What cellular effect can be seen?

A

Hypoxic drive depressed (decrease alveolar ventilation, increase resting Paco2)

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61
Q

What is the respiratory effects of halothane?

A

Potent bronchodilator by inhibiting intracellular Ca++ influx

62
Q

What hepatic effect can be see by halothane?

A

decreased hepatic blood flow

63
Q

Describe the variation in metabolism by the CYP450 of halothane, desflurane, sevoflurane and isoflurane.

A

Metabolism: HAL (20%) > SEV (5%) > ISO (2%) > DES (0.02): All by CYP450 system

64
Q

What does metabolism of halothane result in?

A

oxidative process that results in trifluoroacetyl halide and an immune response

65
Q

What are two important liver effects of halothane?

A

Hepatotoxicity & Halothane hepatitis

66
Q

What side effect is most implicated with halothane?

A

Hepatotoxicity, but can involve any of the volatile agents

67
Q

What predisposes someone to hepatotoxicity by halothane?

A

Predisposition with liver disease will increase likelihood

68
Q

What is the physiological pathology hepatotoxicity by halothane?

A

Inadequate hepatocyte oxygenation due to ↓ alveolar ventilation (hepatic hypoxia) or ↓ hepatic blood flow

69
Q

What can increase the risk of heptatotoxicity?

A

Enzyme induction (i.e., with phenobarbital) lead to production of hepatotoxic end products of metabolism & increased risk of hepatotoxicity

70
Q

What are the characteristics of halothane hepatitis?

A
  • extremely rare, 1:30,000, results from changes in hepatic blood flow
  • Resembles acute hepatitis
  • Antigen-antibody interaction (immunoglobulin G)
71
Q

What is the risk factors of halothane hepatitis? (3)

A

female, middle age, obesity, prior exposure to halothane

72
Q

What are the symptoms associated with halothane hepatitis?

A

fever, rash, arthralgia, eosinophilia

73
Q

What is another inhaled anesthetic no longer used in anesthesia?

A

Enflurane, No longer used in the US

74
Q

What effect does enflurane have on seizures?

A

Decreased the threshold for seizures

75
Q

How is enflurane oxidized?

A

Oxidized in the liver to inorganic nephrotoxic fluoride (physiological effects)

76
Q

What activity is enflurane tide to?

A

Tied to EEG seizure activity

77
Q

What is the chemical storage of isoflurane?

A

Clear, nonflammable liquid at room temp (isomer to enflurane)

78
Q

What is the solubility of isoflurane?

A

Intermediate solubility (more soluble than sevoflurane and desflurane so induction and emergence are slower)

79
Q

What is the smelling properties of isoflurane? What does this mean for induction?

A

Pungent odor/airway irritant – poor choice for inhalation induction

80
Q

What is isoflurane is characterized by?

A

Characterized by extreme physical stability (no deterioration with prolonged storage, does not interact with CO2 absorber or sunlight)

81
Q

What is the cost of isoflurane?

A

Cheap

82
Q

What is the cardiac effect of isoflurane?

A

Minimal LV depression

83
Q

What can be cause by rapid increases in concentration of isoflurane?

A

Rapid increase in concentration may lead to transient incr. in HR & BP

84
Q

What respiratory effect can be seen with isoflurane?

A
  • Decrease in alveolar ventilation causes rise in resting Paco2 & depresses ventilatory response to increase Paco2
  • bronchodilation
85
Q

What CNS effects can be see with Isoflurane?

A
  • Increases CBF and ICP at > 1MAC (reversed by hyperventilation)
  • Reduces CMRO2
86
Q

What is the CNS protective effects of isoflurane?

A

May offer degree of cerebral protection

87
Q

What is isoflurane metabolized too?

A

Metabolized to trifluoroacetic acid – may cause rise in serum fluoride levels

88
Q

What is rare with isoflurane?

A

nephrotoxicity rare

89
Q

What are the chemical properties of desflurane?

A

Fluorination rather than chlorination increases its vapor pressure, enhances stability, decreases potency

90
Q

Which inhaled anesthetic has the highest vapor pressure?

A

Desflurane (Suprane) (660 mmHg at 20 degrees C)

91
Q

What is the storage of desflurane?

A

Liquid would boil at room temperature

92
Q

What is required by desflurane do to its high vapor pressure?

A

Requires a special electrical vaporizer that is heated and pressurized (39 degrees C at 2 atm)

93
Q

What is true about desflurane’s blood:gas solubility?

A

Its lower blood:gas solubility (0.42) allows for rapid onset/offset

94
Q

What is the smell properties of desflurane?

A

Is very pungent & an airway irritant

95
Q

Why are the characteristics that make desflurane a poor choice for inhalation induction?

A

airway irritant (breath holding, coughing, laryngospasm, can increase airway resistance in patients w/ reactive airways

96
Q

What can desflurane cause in smokers?

A

bronchoconstriction

97
Q

What is the respiratory effects of desflurane?

A

Decrease in alveolar ventilation causes rise in resting Paco2 & depresses ventilatory response to increase Paco2

98
Q

What can rapid increases in concentration in desflurane? Who is this contraindicated in?

A

Rapid increases in concentration lead to transient elevation in HR, BP, & catecholamine levels can last several minutes (undesirable in patients with CAD)

99
Q

What can increase in HR/BP can be seen by Increasing DES concentration from 4% to 8% over < 1 min?

A

incr. HR/BP up to 2x baseline

100
Q

What are the potential cause of the increased HR/BP effects of desflurane?

A

rapidly adapting airway receptors, renin-angiotensin system activation, or central adrenergic stimulation

101
Q

What can attenuate the cardiac effects of desflurane?

A

response w/ fentanyl, esmolol, or clonidine

102
Q

What CNS effect can be seen with desflurane?

A

Increases CBF, CBV, & ICP / decreases CMRO2

103
Q

What can desflurane produce? How?

A

CO production with desiccated CO2 absorber/interaction with strong base in CO2 absorer - Desflurane the greatest for CO production:

104
Q

What does CO production of desflurane cause?

A

carboxyhemoglobin

105
Q

What are potential causes of CO production from desflurane?

A
  • High fresh gas flows through AGM left on high when not in use
  • High temperature of CO2 absorber from low gas flows & long case
  • Type of CO2 absorbent
106
Q

What are the two types of CO2 absorbents that can interact with Desflurane?

A

sodium & potassium hydroxide, barium hydroxide soda lime

107
Q

What is another side effect associated with Desflurane?

A

CO poisoning: difficult to dx under general anesthesia

108
Q

What are the signs associated with CO poisoning?

A
  • Carboxyhemoglobin level: ABG
  • Lower than expected pulse oximetry readings (but still falsely high)
109
Q

What is important to note about desflurane and the AGM?

A

turn off fresh gas flows on the AGM between cases and at the end of the day (consider turning AGM off at end of day unless OR is on standby for an emergency case)

110
Q

What is sevoflurane halogenated with?

A

Halogenated w/fluorine (desflurane is too)

111
Q

What is the blood:gas solubility of sevoflurane? What does this allow?

A

Blood:gas solubility (0.69) slightly higher than desflurane (allows fast onset/offset)

112
Q

What is the smell of sevoflurane?

A

Nonpungent

113
Q

What is the preferred agent for inhalational inductions for adults and children?

A

Sevoflurane

114
Q

What do the properties of sevoflurane allow for?

A

able to deliver a high concentration from the onset to increase PA (“turn up the dial”); induction is smooth & rapid

115
Q

What is the characteristics of inhalation induction with 4%-8% sevoflurane?

A

in a 50% mixture of nitrous oxide and oxygen can be achieved within 1 min.

116
Q

What is the respiratory effects of Sevoflurane?

A

Decreases CO2 drive, Bronchodilation

117
Q

Sevoflurane is least likely to _______________.

A

react with CO2 absorber to form CO

118
Q

What can occur with sevoflurane at a MAC of 1.5-2?

A

Apnea

119
Q

What are some isolated incidents that have occurred between sevoflurane and AGMs?

A

Isolated incidents of fire in the respiratory circuits of AGMs w/desiccated CO2 absorbents (***turn off fresh gas flows in-between cases and at end of the day!)

120
Q

What does sevoflurane react with? What does this produce?

A

Reacts with bases in barium hydroxide lime or soda lime CO2 absorbers (containing barium, sodium, or potassium hydroxide) to form Compound A (a vinyl ether

121
Q

What is Compound A toxic too?

A

Renal toxic

122
Q

What increases the risk of compound A? (5)

A

Risk increases with increased respiratory gas temperature, low-flow anesthesia, dry barium hydroxide absorbent (Baralyme), high sevo concentrations, & anesthetics of long duration

123
Q

What was discontinued in 2004 because of compound A and sevoflurane?

A

Barium hydroxide absorbers

124
Q

When is gas flows not an issue for compound A production?

A

Not an issue with gas flows of at least 2 lpm which reduces accumulation

125
Q

Absorbers containing ________ do not degrade sevoflurane.

A

calcium hydroxide

126
Q

_______________ do not degrade sevoflurane

A

Newer CO2 absorbers (i.e., lithium)

127
Q

What is sevoflurane metabolism more vulnerable to?

A

to inorganic fluorides – no association with peak fluoride levels following sevoflurane and any clinically significant renal dysfunction

128
Q

What is xenon?

A

Noble gas/inert element

129
Q

What is the characteristics of xenon?

A

Nonexplosive, nonpugnent, odorless, no metabolism, low toxicity

130
Q

Why is Xenon not used as often?

A

Expensive (must be purified from the atmosphere). #54 on periodic table

131
Q

What is the MOA of Xenon?

A

Anesthetic effects mediated by NMDA inhibition by competing w/glycine at glycine binding site

132
Q

What is the MAC of Xenon?

A

MAC 0.71

133
Q

What is the blood: gas solubility of Xenon?

A

Lowest blood:gas solubility (0.115)

134
Q

What is the nitrous oxide effect on MH?

A

Not a triggering agent of MH

135
Q

What is the evoke effects of inhaled anesthetics?

A

inhaled anesthetics produce dose-dependent decrease in amplitude & increased latency in evoked potential monitoring (somatosensory, motor, brainstem, auditory, and visual)

136
Q

What are some surgeries that monitor evoke potentials?

A

spinal cord/neuro surgeries & neurophysiologic monitoring

137
Q

Visual-evoked potentials _________

A

Most sensitive

138
Q

Brainstem-evoked potentials _________

A

most resistant

139
Q

What are the general CNS effects of inhaled anesthetics? (4)?

A

Produce cerebral vasodilation, decreased cerebral vascular resistance, increased CBF, decreased CMRO2

140
Q

What inhaled anesthetic has the most myocardial depression?

A

Halothane

141
Q

What inhaled anesthetics decrease SVR?

A

isoflurane, desflurane, sevoflurane

142
Q

What Cardiac effect is most common with inhaled anesthetics?

A

Decreased MAP: isoflurane, desflurane, & sevoflurane via decreased SVR; halothane via decreased cardiac output

143
Q

What causes ventilatory depression and decreased PaO2?

A

depression of medullary ventilatory centers - occurring with spontaneous vent; this effect offset with mechanical/controlled ventilation

144
Q

What ventilatory response can be seen with inhaled anesthetics?

A

Depressed ventilatory response to hypoxemia (normally mediated by carotid bodies) & hypercarbia

145
Q

What tidal volume response can be seen with inhaled anesthetics?

A

Decreased tidal volume with spontaneous ventilation: rapid & shallow pattern of breathing

146
Q

What temperature effect can be seen with inhaled anesthetics?

A

Increased cutaneous blood flow results in loss of body heat (central inhibition of temperature regulation)

147
Q

What is true regarding inhaled anesthetics besides nitrous oxide?

A

All inhaled anesthetics (except nitrous oxide) are triggers for malignant hyperthermia

148
Q

What is the receptor associated with malignant hyperthermia?

A

ryanodine receptor [RYR1] plays important role in Ca ++ release from sarcoplasmic reticulum)

149
Q

Inhaled anesthetics potentiate ________

A

nondepolarizing NMBDs

150
Q

What are possible effects of inhaled anesthetics?

A

Possible neuro and cardiac protection (iso, sevo, & des)

151
Q

What is true about inhaled anesthetics and skeletal muscle relaxation?

A

Incompletely inhibit skeletal muscle nicotinic receptors leads to skeletal muscle relaxation (incomplete)

2-Anesthesia Pharm Exam 2 (6 decks)

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