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APEX > Unit 4 - Inhaled Anesthetics > Flashcards

Unit 4 - Inhaled Anesthetics Flashcards

1
Q

3 groups of inhaled anesthetics

A

ethers alkanes gases

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2
Q

inhaled anesthetics - ethers

A

Desflurane

Isoflurane

Sevoflurane

Enflurane

Methoxyflurane

Ether

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3
Q

inhaled anesthetics - alkanes

A

Halothane

Chloroform

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4
Q

inhaled anesthetics - gases

A

Nitrous oxide

Cyclopropane

Xenon

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5
Q

relationship between fluorination and potency

A

tends to reduce potency

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6
Q

type & number of halogens in isoflurane

A

5 fluorine atoms

1 chlorine atom

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7
Q

type & number of halogens in desflurane

A

6 fluorine atoms (fully fluorinated)

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8
Q

type & number of halogens in sevoflurane

A

7 fluorine atoms

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9
Q

inhaled anesthetics that have a chiral carbon

A

desflurane

isoflurane

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10
Q

what is vapor pressure

A

pressure exerted by a vapor in equilibrium with its liquid or solid phase inside a closed container

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11
Q

relationship between vapor pressure and temperature

A

directly proportional

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12
Q

what is boiling point

A

vapor pressure = atmospheric pressure

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13
Q

what is evaporation

A

process where compound transitions from liquid to gas at temp below its boiling point

vapor pressure < atmospheric pressure

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14
Q

relationship between atmospheric pressure and boiling point

A
  • ↑ atmospheric pressure = ↑ boiling point (ex. Hyperbaric O2 chamber)
  • ↓ atmospheric pressure = ↓ boiling point (high altitude)
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15
Q

what is partial pressure

A

fractional amount of pressure a single gas exerts within a gas mixture

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16
Q

what is Dalton’s law of partial pressures

A

total gas pressure in a container is equal to the sum of the partial pressures exerted by each gas

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17
Q

what determines the depth of anesthesia

A

partial pressure of anesthetic agent in the brain

NOT the volumes percent (set on vaporizer dial)

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18
Q

partial pressure of 6% Desflurane at sea level vs. in Denver (1 mile above sea level)

A

sea level = 45.6 mmHg

Denver = 37.2 mmHg

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19
Q

inhaled anesthetics that can become unstable in dessicated soda lime

what can they produce

A

desflurane

isoflurane

can produce carbon monoxide (des > iso)

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20
Q

vapor pressure of sevo

A

157 mmHg

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21
Q

vapor pressure of des

A

669 mmHg

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22
Q

vapor pressure of iso

A

238 mmHg

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23
Q

vapor pressure of N2O

A

38,770 mmHg

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24
Q

boiling point of des

A

22 dec C

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25
Q

molecular weight of sevo

A

200 g

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26
Q

molecular weight of des

A

168 g

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27
Q

molecular weight of iso

A

184 g

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28
Q

molecular weight of N2O

A

44 g

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29
Q

inhaled anesthetic that is unstable in hydrated CO2 absorbent

A

sevo

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30
Q

inhaled anesthetic that is stable in dehydrated CO2 absorber

A

N2O

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31
Q

what is solubility of an anesthetic agent

A

ability of anesthetic agent to dissolve in blood & tissues

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32
Q

which is more soluble in a hydrophilic solvent - polar or nonpolar solute?

A

polar

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33
Q

what describes the relative solubility of a solute in 2 different solvents

A

partition coefficient

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34
Q

describes relative solubility of an inhalation anesthetic in blood vs. in alveolar gas when partial pressures between compartments are equal

A

blood:gas partition coefficient

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35
Q

how is b:g partition coefficient calculated

A

anesthetic dissolved in blood / anesthetic inside alveolus

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36
Q

anesthetic implications of a low b:g

A

faster onset, faster speed of emergence

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37
Q

anesthetic implications of a higher b:g

A

slower onset, slower speed of emergence,

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38
Q

b:g of sevo

A

0.65

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39
Q

b:g of des

A

0.42

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40
Q

b:g of iso

A

1.46

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41
Q

b:g of N2O

A

0.46

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42
Q

what is FA/FI

A
  • Concentration of agent inside alveoli is proportional to concentration inside blood, which is proportional to anesthetic inside brain
  • Alveolar partial pressure ~ blood partial pressure ~ brain partial pressure
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43
Q

what is FA?

A

partial pressure of anesthetic inside the alveoli (surrogate for measurement of anesthetic inside the brain)

Anesthetic washes into alveoli & establishes a partial pressure

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44
Q

what is FI

A

concentration of anesthetic exiting vaporizer

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45
Q

how are anesthesia gases transferred from machine to the patient’s brain (4 steps)

A
  1. machine to fresh gas
  2. fresh gas to alveoli
  3. alveoli to arterial blood
  4. arterial blood to brain
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46
Q

what is speed of induction a function of?

A

solubility

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47
Q

opposes buildup of anesthetic partial pressure in alveoli

A

continuous uptake of agent into blood

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48
Q

3 factors that have the most significant impact on anesthetic uptake into the blood (determinants of removal from alveoli)

A
  1. b:g
  2. CO
  3. partial pressure difference between alveolar gas and mixed venous gas
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49
Q

how does low solubilty affect speed of induction

A

↓ uptake into blood = ↑ rate of rise = faster equilibration of FA/FI = faster onset

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50
Q

how does high solubility affect speed of induction

A

↑ uptake in blood = ↓ rate of rise = slower equilibration of FA/FI = slower onset

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51
Q

what does the FA/FI curve show us?

A

the speed at which alveolar partial pressure equilibrates with partial pressure leaving the vaporizer

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52
Q

fastest to slowest rate of rise of FA/FI

A

N2O > des > sevo > iso > halothane

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53
Q

6 determinants of gas delivery to alveoli

A
  1. setting on vaporizer
  2. FGF
  3. time constant of delivery system
  4. anatomic dead space
  5. alveolar ventilation
  6. FRC
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54
Q

3 determinants of tissue uptake of gas

A
  1. tissue:blood solubility
  2. tissue blood flow
  3. partial pressure difference between arterial blood and tissue
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55
Q

what must happen for FA/FI to increase

A

there must be greater wash in or reduced uptake

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56
Q

what must happen for FA/FI to decrease

A

there must be either a reduced wash in or an increased uptake

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57
Q

5 factors that increase wash in and therefore increase FA/FI

A
  • high FGF
  • high alveolar ventilation
  • low FRC
  • low time constant
  • low anatomic dead space
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58
Q

3 factors that decrease uptake and therefore increase FA/FI

A
  1. low solubility
  2. low CO
  3. low Pa-Pv difference
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59
Q

5 factors that decrease wash in and therefore decrease FA/FI

A
  1. low FGF
  2. low alveolar ventilation
  3. high FRC
  4. high time constant
  5. high anatomic dead space
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60
Q

3 factors that increase uptake and therefore decrease FA/FI

A
  1. high solubility
  2. high CO
  3. high Pa-Pv difference
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61
Q

body mass for VRG, muscle, fat, and vessel-poor groups

A
  • VRG = 10%
  • muscle = 50%
  • fat = 20%
  • vessel poor = 20%
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62
Q

CO received by VRG, muscle, fat, and vessel-poor groups

A
  • VRG = 75% CO
  • muscle = 20%
  • fat = 5%
  • vessel poor = < 1%
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63
Q

organs in vessel rich group

A
  • brain
  • heart
  • kidneys
  • liver
  • endocrine glands
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64
Q

what is contained in the muscle group

A

skeletal muscle & skin

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65
Q

contained in vessel-poor group

A

bone, tendon, cartilage

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66
Q

what 3 things is the rate of anesthetic uptake into tissues dependent on?

A
  1. tissue blood flow
  2. solubility coefficient
  3. arterial blood:tissue partial pressure gradient
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67
Q

first to equilibrate with FA

A

VRG - These organs receive most of the anesthetic agent during induction,

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68
Q

uptake of N2O by different body compartments

A

uptake minimal in all groups; partitions the same to all compartments

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69
Q

3 ways inhaled anesthetics are eliminated

A
  1. Elimination from alveoli (primary mechanism)
  2. Hepatic biotransformation (secondary)
  3. Percutaneous loss (minimal, not clinically significant)
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70
Q

hepatic biotransformation of inhaled anesthetics

A
  • N2O = 0.004%
  • des = 0.02
  • iso = 0.2
  • sevo = 2-5
  • halothane = 20
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71
Q

why does desflurane undergo a greater degree of elimination from the lungs than other anesthetics

A

the greater the hepatic metabolism, the less is eliminated from the lungs

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72
Q

how are halogenated agents metabolized

A

P450 system

primarily CYP2E1

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73
Q

primary mechanism for immune-mediated hepatic dysfunction

A

Trifluoroacetic acid (TFA)

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74
Q

metabolites of des & iso

A

inorganic fluoride ions

TFA

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75
Q

what is concentration effect

A

the higher the concentration of inhalation anesthetic delivered to alveolus (FA), the faster its onset of action (overpressurizing)

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76
Q

concentration effect is probably only clinically relevant for what inhaled anesthetic

A

N2O

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77
Q

which is more affected by concentration effect - higher or lower solubility gases

A

higher

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78
Q

N2O is ____ x more soluble in the blood than nitrogen

A

~34

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79
Q

why does N2O acheive the fastest rate of rise of FA/FI even though des is less soluble?

A

concentration effect

  • When N2O introduced in lung, volume of N2O going from alveolus to pulmonary blood is much higher than amount of Nitrogen moving in opposite direction - alveolus shrinks - reduction in alveolar volume causes relative increase in FA
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80
Q

what is the augmented gas inflow effect

A
  • Concentrating effect temporarily reduces alveolar volume
  • Subsequent breath - concentrating effect causes increased inflow of tracheal gas containing anesthetic agent to replace lost alveolar volume
  • Increases alveolar ventilation, augments FA
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81
Q

what is ventilation effect

A

describes how changes in alveolar ventilation can affect rate of rise of FA/FI

Greater alveolar ventilation = greater rate of rise of FA/FI

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82
Q

how does ventilation effect minimize risk of anesthetic overdose

A

In spontaneously ventilating patient, as anesthetic deepens alveolar ventilation decreases - reduced anesthetic input to alveolus

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83
Q

what is the 2nd gas effect

A

consequences of concentration effect when a second gas is co-administered

  • When N2O and the second gas are introduced into alveolus, rapid uptake of N2O causes alveolus to temporarily shrink
  • Reduction in alveolar volume and augmented tracheal inflow = relative increase in concentration of 2nd gas
  • Partial pressure of alveolar O2 also increases when alveolus shrinks (transient)
  • End result: alveolar concentration of the other gases is higher vs. admin alone
  • More meaningful benefit with agents of higher b:g (iso > seo > des)
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84
Q

how does R-L shunt affect FA/FI

A
  • causes some deoxygenated blood leaving R heart to bypass lungs
  • Results in reduced PaO2
  • Results in slower rate of rise, reduction in partial pressure of anesthetic in arterial blood
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85
Q

examples of conditions that cause a R-L shunt

A

ToF, PFO, Eisenmenger’s syndrome, tricuspid atresia, Ebstein’s anomaly

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86
Q

are gases of high or low solubility more affected by R-L shunt

why

A

lower

Less soluble agents undergo very little uptake by blood (effect of dilution unchecked)

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87
Q

inhaled anesthetic FA/FI curves affected the most and least by R-L shunt

A

most = des (lowest b:g)

least = iso (highest b:g)

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88
Q

how is IV induction affected by R-L shunt

A

faster induction (blood bypasses lungs and travels to brain faster)

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89
Q

what is MAC

A

concentration that prevents nociceptive withdrawal reflex following painful stimulus in 50% of population

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90
Q

potency of inhaled anesthetics from most to least

A

isoflurane > sevoflurane > desflurane > N2O

higher MAC = lower potency

91
Q

what is MAC-awake

A

alveolar concentration where a pt opens eyes (~0.4-0.5 during induction, as low as ~0.15 during recovery)

92
Q

what is MAC-bar

A

alveolar concentration required to block ANS response following painful stimulus (~1.5 MAC)

93
Q

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

A

~ 1.3

94
Q

awareness and recall generally assumed to be prevented at what MAC

A

0.4-0.5

95
Q

what is MAC-hour

A

one times the MAC that prevents movement in response to a noxious stimulus in 50% of subjects administered for 1 hour

96
Q

what is the essential triad of anesthetic action

A

amnesia, loss of consciousness, immobility

97
Q

drugs that increase MAC

A
  • Chronic ETOH
  • Acute amphetamine intox
  • Acute cocaine intox
  • MAOIs
  • Ephedrine
  • Levodopa
98
Q

how does sodium level affect MAC

A

hypernatremia = increased MAC

hyponatremia = decreased mAC

99
Q

how does age affect MAC

A
  • increased in infants 1-6 (sevo is the same for infants & neonates)
  • decreased in prematurity, older age

MAC ↓ 6% per decade after 40 years

100
Q

how does core temp affect MAC

A

hyperthermia = increased MAC

hypothermia = decreased MAC

101
Q

how does red hair affect MAC

why

A

~19% increase

presumably d/t mutations in menalocute-stimulating hormone receptor and ↑ pheomelanin

102
Q

drugs that decrease MAC

A
  • Acute ETOH intox
  • IV anesthetics
  • N2O
  • Opioids (IV & neuraxial)
  • Alpha-2 agonists
  • Lithium
  • Lidocaine
  • Hydroxyzine
103
Q

misc. things that decrease MAC

A
  • MAP < 50
  • Hypoxemia
  • Anemia (< 4.3 mL O2/dL blood)
  • CPB
  • Metabolic acidosis
  • Hypo-osmolarity
  • 24-72 hrs postpartum
  • PaCO2 > 95
104
Q

how does HTN affect MAC

A

no effect

105
Q

how do electrolytes affect MAC

A

only Na affects

106
Q

what is the Meyer-Overton rule & what does it imply

A
  • states that lipid solubility is directly proportional to the potency of an inhaled anesthetic
  • Implies that depth of anesthesia determined by # anesthetic molecules dissolved in brain, not necessarily particular agent used
107
Q

what is the unitary hypothesis

A

Implies that depth of anesthesia determined by # anesthetic molecules dissolved in brain, not necessarily particular agent used

108
Q

how is general anesthesia produced?

A
  • produced by membrane-bound protein interactions in the brain & spinal cord
  • Stereoselectivity of anesthetic potency suggests chiral binding site
  • Probably affect specific areas of cell membrane
109
Q

how do volatiles affect inhibitory and stimulatory receptors

A

1) stimulate inhibitory receptors

2) inhibit stimulatory receptors

110
Q

inhibitory pathways stimulated by inhaled anesthetics

A
  • GABA-A
  • glycine channels
  • K+ channels
111
Q

stimulatory pathways inhibited by inhaled anesthetics

A
  • NMDA receptors
  • nicotinic receptors
  • Na+ channels
  • dendric spine function & motility
112
Q

most important site of volatile action in the brain

A

GABA-A receptor (ligand-gated chloride channel)

likely increase duration chloride channel remains open

113
Q

effect of GABA-A stimulation in the brain

A

increased chloride influx, hyperpolarized neurons

impairs ability of neurons to fire

114
Q

how do volatiles produce immobility

A

ventral horn of spinal cord

important sites of action: glycine receptor stim, NMDA inhibition, Na+ inhibition

115
Q

pathways affected by N2O & Xenon

A

NMDA antagonism

K+ 2-P channel stimulation

116
Q

sites of anesthetic function responsible for amnesia

A

amygdala

hippocampus

117
Q

sites of anesthetic function responsible for autonomic modulation

A

pons & medullla

118
Q

sites of anesthetic function responsible for unconsciousness

A

cerebral cortex

thalamus

RAS

119
Q

sites of anesthetic function responsible for analgesia

A

spinothalamic tract

120
Q

function of the amygdala

A

emotion

response to pain

formation of stress response

121
Q

function of hippocampus

A

memory formation

122
Q

function of thalamus

A

relay station of sensory and motor input to cortex

123
Q

function of RAS

A

influences consciousness & arousal

124
Q

function of ventral horn of spinal cord

A

upper and lower motor neurons synapse

125
Q

function of spinothalamic tract

A

inhibit nociceptive signals along ascending pain pathway

126
Q

how do volatiles affect cardiac and vascular smooth muscle

A

↓ Ca2+ influx in sarcolemma & ↓ Ca2+ release from sarcoplasmic reticulum

causes systemic vasodilation, decreased SVR/VR

127
Q

primary mechanism of dose-dependent MAP decrease with volatiles

A

↓ intracellular Ca2+ in vascular smooth muscle = systemic vasodilation = decreased SVR & venous return

128
Q

secondary mechanism of dose-dependent MAP decrease with volatiles

A

↓ intracellular Ca2+ in cardiac myocyte = myocardial depression = decreased inotropy

129
Q

how do volatiles affect NO, ACh, and Na/Ca pump

A

modulate NO release, inhibit ACh-induced vasodilation, & impair Na+/Ca+ pump (↓ intracellular Ca2+ concentration)

130
Q

how do volatiles affect HR

A
  • ↓ SA node automaticity
  • ↓ Conduction velocity through AV node/His-Purkinje/ventricular conduction pathways
  • ↑ Duration myocardial repolarization by impairing outward K+ current = increases AP duration (prolongs QT interval)
  • Altered baroreceptor function
131
Q

which 2 volatiles increase HR 5-10% above baseline

A

des and iso

132
Q

how do volatiles affect contractility

A

small dose-dependent decrease in baseline

myocardium remains preload responsive

133
Q

how do volatiles affect SVR

which affects it the least

A

↓ intracellular Ca2+ in vascular smooth muscle = systemic vasodilation = ↓ SVR

Of volatiles, sevoflurane decreases the least

134
Q

how do volatiles affect coronary vascular resistance

A
  • Volatiles ↑ coronary blood flow in excess of myocardial O2 demand
  • Preferentially dilate small cardiac vessels (20-50 micrometers diameter)
135
Q

Potency of coronary dilation:

A

isoflurane > desflurane > sevoflurane

136
Q

respiratory effects of volatiles

A

↑ apneic threshold

↓ vent. Response to CO2

Airway obstruction

Bronchodilation

↓ Vt

↑ RR

↓ FRC

137
Q

physiologic control of PaCO2

A

central chemoreceptor in medulla

138
Q

every 1 mmHg increase in PaCO2 above baseline will increase Vm by:

A

3 L/min

139
Q

how do volatiles imapact central chemoreceptors and respiratory muscles

A

dose-dependent depression

140
Q

3 mechanisms of volatiles that contribute to hypercarbia

A
  1. altered resp pattern
  2. impaired response to CO2
  3. impaired motor neuron output & muscle tone to upper airway and thoracic muscles
141
Q

how do volatiles affect Vt

A

decrease

142
Q

how does the body try to compensate for reduced Vt from volatiles

A
  • Body attempts to compensate with ↑ RR (not enough to prevent ↑ PaCO2)
  • Smaller, faster breaths increase dead space to Vt ratio
143
Q

what does the slope of the CO2 response curve represent

A

sensitivity to PaCO2

144
Q

what happens to the CO2 response curve with decreased response to CO2

A

curve shifts down and to the right

145
Q

what is the apneic threshold

A

PaCO2 at which a patient is stimulated to breathe

usually 3-5 mmHg below PaCO2 maintained during spontaneous ventilation (if ventilation is assisted below threshold, pt won’t breathe)

146
Q

what does a right shift of the CO2 response curve imply

A
  • Implies Vm is < predicted for given PaCO2 - respiratory acidosis
  • depressed ventilation
147
Q

what can cause a right shift of the CO2 response curve

A
  • GA
  • opioids
  • metabolic alkalosis
  • denervation of peripheral chemoreceptors
148
Q

what does left shift of CO2 response curve mean

A

implies Vm is > predicted for given PaCo2 - respiratory alkalosis

stimulates ventilation

149
Q

causes of CO2 response curve left shift

A
  • anxiety
  • surgical stimulation
  • increased ICP
  • salicylates
  • aminophylline
  • doxapram
150
Q

how do volatiles depress ventilation

A

by inhibiting muscle function in upper airway, diaphragm, & intercostals

151
Q
A
152
Q

what PaO2 stimulates carotid bodies to increase Vm to restore arterial oxygenation

A

< 60 mmHg

153
Q

where do carotid bodies relay afferent input

A

respiratory center via CN 9

154
Q

how do aortic bodies relay afferent traffic

A

via CN 10

155
Q

what is the sensory arm of the hypoxic drive

A

glomus type 1 cells in carotid bodies

hypothesized that volatiles create reactive O2 species that impairs these cells

156
Q

source of reactive O2 species that impair glomus cells

A

anesthetic metabolism

157
Q

what determines how much a volatile inhibits hypoxic drive

A

agents that undergo the most biotransformation inhibit hypoxic drive the most (sevo > iso > des)

158
Q

when does impaired response to acute hypoxia begin with volatiles

A

at 0.1 MAC

(does not impair response to PaCO2)

159
Q

what 2 things is CMRO2 dependent on

A

1) electrical activity & 2) cellular homeostasis

160
Q

what determines total brain O2 consumption

A

electrical activity is 60%

cellular homeostasis is 40%

161
Q

MAC required to produce isoelectric state

A

1.5-2 MAC

162
Q

how do volatiles affect CMRO2

A

↓ (only to the extent that they reduce electrical activity - can’t reduce any further once isoelectric)

163
Q

volatile that can produce seizure activity in high concentrations (> 2 MAC)

how can this effect be exacerbated

A

sevo

exacerbated by hypocapnia & more common with inhalation induction

164
Q

how does the body adjust for increased CMRO2

A

vasodilation to ↓cerebrovascular resistance, ↑ CBF

165
Q

how does the body adjust for decreased CMRO2

A

vasoconstriction to ↑ cerebrovascular resistance

166
Q

how do volatiles affect CBF & CMRO2

A

cause uncoupling

concentrations > 0.5 MAC increase CBF even though CMRO2 is decreased

167
Q

downside of volatiles causing uncoupling of CBF and CRMO2

A

increases ICP

168
Q

upside of volatiles causing uncoupling of CBF and CRMO2

A

favorable cerebral O2 supply-demand ratio

169
Q

how can cerebral vasodilation from volatiles be partially offset

A
  • mild hyperventilation (PaCO2 < 35)
  • propofol, opioids, barbiturates
170
Q

sensitivity of evoked potentials to volatiles

A

VEP > SSEPs ~ MEPs > brainstem

171
Q

how are SSEPs produced

A
  • by applying current to a peripheral nerve
  • Most commonly tibial or ulnar n.
172
Q

what do SSEPs monitor

A
  • integrity of dorsal column (medial lemniscus)
  • posterior spinal a. perfusion
173
Q

what do MEPs monitor

A
  • integrity of corticospinal tract
  • anterior spinal a. perfusion
174
Q

what is amplitude of an evoked potential

A

strength of nerve response

175
Q

what is latency of an evoked potential

A

speed of nerve conduction

176
Q

when are there concerns for ischemia with evoked potentials

A

amplitude ↓ > 50% or latency ↑ > 10%

177
Q

best anesthesia technique to preserve evoked potentials

A

TIVA without N2O

178
Q

maximum MAC if volatiles used with evoked potentials

A

0.5

179
Q

how does ketamine affect evoked potentials

A

enhanced signal

180
Q

how do volatiles affect evoked potentials

A

Des, sevo, & iso = dose-dependent ↓ amplitude, ↑ latency (signal is not as strong & slower to conduct)

181
Q

when does an evoked potential suggest ischemia

A

loss of signal

182
Q

goals if evoked potential signal disappears or diminishes

A

improve neural tissue perfusion (↑ BP, volume expansion, transfusion if anemic)

183
Q

how do hypoxia, hypercarbia, and hyperthermia affect evoked potentials

A

can affect amplitude

184
Q

chemical name of desflurane

A

difluoromethyl 1,2,2,2-tetrafluoroethyl ether

185
Q

which 2 volatiles are nearly identical

A

des & iso

des - chlorine atom replaced by fluorine (fully fluorinated)

186
Q

effects of fluorination

A
  • ↓ potency (↓ oil:gas solubility) = ↑ MAC
  • ↑ vapor pressure (↓ intermolecular attraction)
  • ↑ resistance to biotransformation (↓ metabolism) = ↓ trifluoroacetate makes an immune-mediated hepatitis extremely unlikely
187
Q

methods to minimize tachycardia with rapid increase in des

A

opioids, alpha 2 agonists, beta 1 antagonists

188
Q

volatile that can cause bronchoconstriction in asthmatics

A

desflurane

189
Q

which anesthetic agent impairs hypoxic drive the least

A

des

190
Q

how does des affect CSF

A

↑ or no change in CSF production

191
Q

chemical name of sevoflurane

A

fluoromethyl 2,2,2-trifluoro-1-(trifluoromethyl) ethyl ether

192
Q

why is sevo more potent than des with regards to fluorination

A

most likely d/t bulky propyl side chain

193
Q

which volatile is unstable in hydrated soda lime

A

sevo

194
Q

minimum FGF requirements for sevo

A
  • 1 L/min for up to 2-MAC hours
  • 2 L/min after 2-MAC hours
  • <1 L/min not recommended at any time
195
Q

theoretical concern of sevo biotransformation

A
  • Biotransformation results in liberation of inorganic fluoride ions
  • Theoretical concerns of fluoride-induced high output renal failure
196
Q

s/s high-output renal failure with sevo

A
  • typically unresponsive to vasopressin
  • polyuria
  • hypernatremia
  • hyperosmolarity
  • ↑ plasma creatinine
  • inability to concentrate urine
197
Q

how does sevo affect CSF

A

decreased production

198
Q

chemical name of isoflurane

A

1-chloro 2,2,2-trifluoroethyl difluoromethyl ether

199
Q

why is iso more potent than sevo and desflurane

A

Addition of heavier chlorine atom

200
Q

how does addition of chlorine atom affect isoflurane

A
  • more potent than sevo (2x) and des (5x)
  • increases blood and tissue solubility
201
Q

volatile that is the most potent coronary vasodilator

A

iso

202
Q

what is coronary steal

A
  • Thought is that ↑ myocardial O2 demand = dilation of healthy vessels, heart increases its own flow to satisfy O2 requirement
  • diseased vessels may not be able to dilate further
  • coronary blood flow would be preferentially directed to healthy tissue
203
Q

chemical name of halothane

A

2-bromo-2-chloro-1,1,1-trifluoroethane

204
Q

which volatile has a bromine atom and no ether bridge

A

halothane

205
Q

important metabolic byproduct of halothane metabolism

A

TFA

may cause halothane hepatitis

206
Q

N2O is ___ times more soluble than nitrogen

A

34

207
Q

Gas-containing areas of the body can absorb up to __ L N2O within first __ hours of admin.

A

30L

2 hours

208
Q

how does N2O cause decreased stimulus to breathe

A

Can temporarily dilute alveolar oxygen & CO2 = diffusion hypoxia & hypocarbia

209
Q

b:g of nitrogen

A

0.014

210
Q

rate of pressure change inside space with N2O

A

compliance of space, partial pressure of N2O, perfusion of surrounding tissue, and time

211
Q

what happens in a compliant air space filled with N2O

A

volume ↑, pressure unchanged

212
Q

what happens in a noncompliant air space filled with N2O

A

pressure ↑, volume unchanged

213
Q

negative effect of discontinuing N2O in middle ear surgery

A

can quickly decrease middle ear pressure & lead to serous otitis

214
Q

N2O use with SF6 bubble

A

d/c at least 15 min prior to placement

avoid for 7-10 days after

215
Q

avoid N2O for how long with these ocular gas bubbles:

air bubble

perfluoropropane

silicone oil

A

air = 5 days

perf = 30 days

silicone = no contraindications

216
Q

how does N2O affect vitamin B12

A
  • irreversibly inhibits B12
  • Inhibits methionine synthesis (required for folate metabolism, myelin)
217
Q

side effects of vitamin B12 inhibition from N2O

A
  • immune compromise
  • homocysteine accumulation
  • possible risk of spontaneous abortion
  • megaloblastic anemia (bone marrow suppression)
  • neuropathy
  • ↓ DNA synthesis
218
Q

increases risk of vitamin b12 inhibition with N2O

A
  • prolonged exposure
  • pre-existing B12 deficiency (alcoholism, pernicious anemia, strict vegan diet, recreational use)
219
Q

complications of N2O vitamin B12 inhibition

A
  • megaloblastic anemia (bone marrow suppression)
  • immune compromise
  • neuropathy
220
Q

CV effects of N2O

A
  • Increased HR
  • BP increased/unchanged
  • CO decreased
  • SVR increased
  • Doesn’t meaningfully ↓ contractility by itself; may ↓ combined with opioid
  • May increase CVP & PAP
221
Q

neuro effects of N2O

A

Increases CBF as a function of increased CMRO2

222
Q

2 classes of ethers

A
  1. methyl isopropyl ether (sevo)
  2. methyl ethyl ether (des, iso)
223
Q

best agent to use in a pt with hx of halothane hepatitis

A

sevoflurane

(metabolism doesn’t produce TFA)

APEX (54 decks)

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