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NUNA 681(pharm) > Inhalational Agents: Effects on MSK, Neuro, Hepatic, Renal, and Metabolism > Flashcards

Inhalational Agents: Effects on MSK, Neuro, Hepatic, Renal, and Metabolism Flashcards

1
Q

____ cause a dose dependent relaxation skeletal muscle

A

inhaled volatile agents

nitrous oxide has no effect

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2
Q

the higher the MAC multiple, the greater the ___

A

fade on tetanus

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3
Q

volatile agents can be used instead of ___ or to __

A

NMB

enhance the effect of NMB

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4
Q

the enhanced effect of NMB may be from __ or __ effects or from effects on ___- inhibit nicotinic receptors ____

A

pre- or post-junctional

spinal motor neurons

incompletely at MAC

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5
Q

practical application of inhaled anesthetics enhancing effect of NMB

A
  1. decrease dose of nondep NMB 25%
  2. decrease frequency of redosing
  3. myasthenia gravis patients- give no NMB
  4. patient with hepatic or renal impairment
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6
Q

__ has a longer duration depending on the volatile agent interaction:
desflurane-
sevoflurane-
isoflurane-
propofol-

A

rocuronium

desflurane- 90 min
sevoflurane- 59 min
isoflurane- 35 min
propofol- 35 min

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7
Q

prolonged recovery from NMB when __ is maintained

A

volatile concentration

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8
Q

must maintain __ on TOF

A

one twitch

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9
Q

__ is also a factor in prolonging recovery from NMB with volatile agents

A

increased age

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10
Q

as the % concentration of volatile was decreased when vecuronium infusion was maintained, __ increased

A

the twitch height

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11
Q

different results with different agents may be explained by

A

methodology of study

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12
Q

different results with different agents- with cisatracurium and rocuronium, ___ caused prolonged block, but ___ didn’t

A

sevoflurane

isoflurane

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13
Q

different results with different agents- with vecuronium, __ and __ both prolonged block

A

sevo and iso

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14
Q

all volatile agents are additive effect with

A

succinylcholine

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15
Q

iso causes more rapid shift from ___ to ___ block with succ infusion

A

phase I to phase II

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16
Q

volatiles cause a __ dependent enhancement of nondep NMB (recovery of ToF 1 twitch)

A

time

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17
Q

volatile agents can cause impairment of __ of nondepolarizing NMB

A

reversal

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18
Q

carefully administer ___, use ___, and consider using ___ in lieu of NMB if possible

A

NMB

twitch monitor

relaxant effect of volatile

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19
Q

volatile anesthetics cause ___ relaxation of the uterine smooth muscle

A

dose-dependent relaxation

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20
Q

__ MAC causes __ relaxation of uterine smooth muscle

A

0.5

modest

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21
Q

__ MAC causes significant relaxation of uterine smooth muscle

A

> 1

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22
Q

positive implication of uterine smooth muscle

A

desirable relaxation for removal of retained placenta

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23
Q

negative implication of uterine smooth muscle

A

contribute to increased blood loss with uterine atony

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24
Q

__ does not alter uterine contractility in doses used to provide analgesia during vaginal delivery

A

nitrous oxide

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25
Q

nitrous oxide can be useful to __ and __ during vaginal delivery

A

decrease volatile

avoid benzodiazepines, opioids

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26
Q

volatiles decrease in __ blood flow

A

maternal uterine

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27
Q

to avoid decreases in maternal uterine blood flow maintain MAC

A

< 1.5

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28
Q

can have amnesia with no neonatal distress at __ MAC with __ N2O

A

0.5

50%

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29
Q

consider avoiding ___ in presence of fetal distress

A

N2O

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30
Q

volatile cross __ rapidly

A

placenta

exhaled rapidly by neonate

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31
Q

all volatile agents can trigger

A

MH (even without succinylcholine)

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32
Q

__ is the most potent trigger of MH

A

halothane

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33
Q

__ is a much weaker trigger of MH and is considered ___

A

nitrous oxide

on the “safe list” of MHAUS

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34
Q

MH causes a pathologic change in

A

muscle; hypermetabolic state

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35
Q

with MH, exposure to triggering agents cause the __ receptor to release ___ from the __ to enter the muscle cell

A

ryanodine

calcium

sarcoplasmic reticulum

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36
Q

with MH, muscle contraction occurs due to

A

interaction of actin and myosin

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37
Q

in MH, __ and __ metabolism increase producing massive amounts of __, __, and ___

A

aerobic and anaerobic muscle

heat, carbon dioxide, and lactate

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38
Q

in MH, ___ allows leakage

A

muscle membrane permeability

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39
Q

time to onset of MH with desflurane trigger only

A

260 min

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40
Q

time to onset of MH with isoflurane trigger only

A

140 minutes

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41
Q

time to onset of MH with halothane trigger only

A

35 minutes

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42
Q

cerebral metabolic oxygen requirements (CMRO2) decrease at approximately

A

0.4 MAC as the patient moves toward unconsciousness

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43
Q

reduction in CMRO2 is

A

dose dependent

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44
Q

once ___ is produced, further increases in the agent concentration do not further decrease CMRO2

A

an isoelectric EEG

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45
Q

CRMO2 =

A

electrical activity 60% + cellular homeostasis 40%

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46
Q

CMRO2 decreases normal response with no volatile anesthesia

A

brain matches (couples) its blood flow with its metabolic requirements

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47
Q

when metabolic demands decrease, blood vessels ___ and CBF ___

A

constrict (CVR increases)

decreases

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48
Q

two opposing factors with volatile anesthetics and CMRO2

A
  1. vasoconstriction from reduction of CMRO2
  2. vasodilation from anesthetic agent directly
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49
Q

CRMOs decrease has no uncoupling if

A

less than or equal to 1 MAC of iso or des

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50
Q

uncoupling can occur at

A

higher doses

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51
Q

N2O causes increased __ and __ however there is still uncoupling due to __

A

CMRO2 and CBF

the greater increase in CMRO2 than CBF

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52
Q

uncoupling is

A

decreased CRMO2 at the same time that CBF is increased- paradoxical (they supply the brain with more blood flow than it needs)- CBV increases

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53
Q

if uncoupling does not occurs, it is said that

A

flow-metabolism coupling mechanism is preserved

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54
Q

affects change in CBF

A
  1. dose of volatile
  2. other drugs administered (propofol, opioids, barbiturates, nitrous)
  3. rate of change of concentration of volatile
  4. ventilation (hyper)
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55
Q

dose dependent __ in CBF

A

increase

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56
Q

normocarbia with > 0.6 MAC causes

A
  1. cerebral vasodilation
  2. decreased cerebral vascular resistance
  3. increased CBF (potential increased ICP)
  4. decreased CMRO2 (uncoupling should result in decreased CBF)
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57
Q

cerebral vasodilation agents

A

iso = des > sevo

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58
Q

increase CBF occurs within

A

minutes of administration of inhaled agents

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59
Q

increase CBF is independent of

A

MAP

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60
Q

increase of CBF is sustained for

A

as long as 4 hours during anesthetic

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61
Q

lower metabolism of isoflurane =

A

less CO2 production, less vasodilation

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62
Q

des, sevo, and iso maintain the cerebral vascular reactivity to

A

carbon dioxide at less than 1 MAC

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63
Q

iso 1 MAC preserves

A

autoregulation of CBF

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64
Q

__ eliminates autoregulation

A

halothane

65
Q

at 1.5 MAC, sevo preserves ___ better than iso- as dose increase above 1 MAC, __ is affected

A

autoregulation

autoregulation

66
Q

uncoupling at higher dose (>1 MAC) =

A

CBF is maintained (unchanged or higher) and CMRO2 is decreased (iso>halothane)

67
Q

isoflurane may blunt __ processes results from cerebral ischemia due to transient ___ during carotid endarterectomy

A

necrotic

regional ischemia

(cerebral oxygen supply-demand balance is improved)

68
Q

cerebral vasodilation and increased CBF raise risks of

A

increased ICP

69
Q

hyperventilation to decrease PaCO2 to ___ counters the increased ICP

A

30 mmHg

70
Q

to counter increased ICP, start hyperventilation at ___ with iso, sevo, des

A

start of agent

71
Q

to counter increased ICP, start hyperventilation at ___ with halothane

A

before agent is started

72
Q

isoflurane does not change production of CSF but

A

decreases resistance to reabsorption (increases reabsorption)

73
Q

the result of iso not producing CSF is

A

only minimal increases in ICP even if CBF increases

74
Q

des may ___ CSF production

A

increase or not change

75
Q

sevo __ CSF production

A

deceases

76
Q

N2O ___ in CSF production

A

causes no increase in

77
Q

cerebral vasculature normal response to hypocarbia

A

vasoconstriction (goal PaCO2 30-35 mmHg- effective 4-6 hours)

78
Q

cerebral vasculature normal response to hypercarbia

A

vasodilation

79
Q

HTN patients cerebral vasculature effects

A

1 MAC iso with 67% nitrous was more effective than 1 MAC sevo with 67% nitrous in controlling vascular resistance with PaCO2 manipulation

80
Q

diabetic patients effects on cerebral vasculature

A

impaired control of vascular resistance with PaCO2 manipulation with both 1 MAC of iso and sevo with 67% nitrous

81
Q

__ changes to EEG

A

dose-dependent

82
Q

less than 0.4 MAC will have __ and __ on EEG

A

increased frequency and voltage

83
Q

at 0.4 MAC, EEG change are

A

activity shifts to anterior portions of the brain (transition from excitement to unconsciousness)

84
Q

EEG changes at 1 MAC

A

increased voltage and decreased frequency (bigger, slower waves)

85
Q

EEG changes at 1.5 MAC

A

deeper level of anesthesia- burst suppression occurs

86
Q

EEG changes at 2 MAC

A

possibly flat

87
Q

__ does not produce burst suppression at clinical levels

A

halothane

88
Q

des, iso, and sevo can ___ seizure activity related to drugs like lidocaine

A

suppress

89
Q

__ has been associated with seizure activity

A

sevo

90
Q

increased incidence of seizures with

A
  1. higher concentration of sevo (2 MAC)
  2. hypocarbia
  3. repeated auditory stimulation
  4. pre-existing seizure disorder
91
Q

evoked potentials monitor

A

the transmission of the impulse from the periphery to/through the cord

92
Q

evoked potentials are typically utilized with

A

spinal fusion for scoliosis- monitoring to protect the spinal cord

93
Q

___ depress SSEP

A

all potent inhaled anesthetics

94
Q

volatiles cause ___ reduction in evoke potential

A

dose-dependent

95
Q

__ evoked potential is the most sensitive and __ is the most resistant

A

visual

brainstem

96
Q

__ or __ are indication of ischemia OR can be related to the volatile agent with evoked potential monitoring

A

an increase in latency (time of stimulus in periphery and onset of EP recorded by scalp electrode)

decrease in amplitude

97
Q

evoked potentials are monitored at __ MAC

A

0.5-0.7

98
Q

for research on evoke potential, __ can be utilized at 1.3 MAC

A

sevo

99
Q

for research on evoke potential, __ can be utilized at 0.5-1 MAC

A

isoflurane

100
Q

for research on evoke potential, __ can be utilized at 0.5-0.7 MAC

A

halothane

101
Q

nitrous oxide effects on evoked potentials

A

may profoundly decrease amplitude so AVOID

102
Q

volatile anesthetics do not cause __ amnesia

A

retrograde

103
Q

__ MAC of iso prevent awareness and __ MAC of nitrous oxide required to prevent awareness

A

0.4

> 0.5-0.6

104
Q

learning may be altered at

A

low concentration (0.2 MAC)

105
Q

__ may increase the concentration required to prevent awareness

A

surgical stimulation

106
Q

volatile cause impairment of cerebral regulation of

A

temperature control

107
Q

inhaled agents reset the threshold for

A

regulation of temperature control to a lower level

108
Q

nitrous oxide has __ of an effect on temperature regulation

A

less

(substitution of N2O impairs the threshold less)

109
Q

volatiles cause the center for temp regulation to permit

A

a lower range of temperatures to exist before cutaneous vasoconstriction occurs

110
Q

volatiles permit a lower temperature before

A

the body attempts to regulate heat loss and heat production

111
Q

temperature regulation is __ dependent

A

dose

112
Q

__ can also lead to temperature loss

A

vasodilation

113
Q

heat is transferred from __ to __ which causes

A

core to periphery

a decrease in core temp of 0.5-1 degree C in the first half-hour of anesthesia

114
Q

__ have greater inhibition of temperature regulation than others

A

the elderly

115
Q

neuroapoptosis causes neurotoxicity in animals- ___, ___, and ___ contributing to remodeling of neuronal circuitry and development remodeling

A

altered neurogenesis

neurite growth

synapse formation

116
Q

neurotoxicity in animals led to

A
  1. cognitive deficits, delayed learning
  2. impaired memory formation and retention
  3. altered motor and behavioral development
117
Q

FDA issues a safety announcement advising that

A

repeated or lengthy exposures to anesthetic and sedative drugs prior to age 3 years have the potential to harm the development of children’s brains

118
Q

in iso, des, and sevo had maintained ___ blood flow and __ or increased __

A

total hepatic

hepatic artery blood flow

portal vein blood flow

119
Q

halothane effect on hepatic blood flow

A

hepatic artery vasoconstrictor so decreased

120
Q

metabolism % or desflurane

A

0-0.02

121
Q

metabolism % of isoflurane

A

0-0.2

122
Q

metabolism % of sevoflurane

A

5-8

123
Q

metabolism % of halothane

A

15-40%

124
Q

N2O metabolism

A

not at all in the liver; 0.004% in the gut from normal flora

125
Q

determinants of metabolism

A
  1. chemical structure
  2. hepatic enzyme activity
  3. blood concentration
126
Q

chemical structure is __ or __

A

ether bond or carbon-halogen bond

127
Q

hepatic enzyme activity effecting metabolism

A
  1. cytochrome P450 induced or depressed
  2. obese- increased fluoride concentrations
128
Q

blood concentration effects on metabolism

A

< 0.1 MAC undergoes extensive metabolism in the liver (less soluble- quicker out via lungs)

129
Q

__ are metabolized

A

all inhaled anesthetics just to varying degrees

130
Q

the concern of metabolism is

A

the fluoride

131
Q

the metabolites of concern with metabolism are

A

trifluoroacetic acid (TFA) and inorganic fluoride

132
Q

metabolic pathways are __ for des, iso, sevo

A

oxidative

133
Q

metabolism of halothane

A

principally oxidation by cytochrome P-450 enzymes when oxygen is present, but reductive metabolism when hepatocyte PO2 decreases

134
Q

trifluoroacetic acid (TFA) produced by

A

the biodegradation of has, iso, and des

135
Q

trifluoroacetic acid causes

A

acetylation of proteins on the surface of hepatocytes to form antigens to which antibodies form

136
Q

with TFA, there is a connection between

A

its hepatic production and hepatotoxicity via an immune pathway

137
Q

inorganic fluoride is produced by

A

biodegradation of sevo in the liver and only minimally in the kidney; thus little negative effect on the kidneys

138
Q

same level of inorganic fluoride produced as with methoxyflurane which causes ____ but no evidence of ____ with sevo

A

renal failure

renal injury

(even in patients with pre-existing renal damage)

139
Q

infrarenal production of inorganic fluoride (methoxyflurane) is a bigger problem for __ than ____

A

nephrotoxicity

inorganic fluoride produced from hepatic metabolism (sevo)

140
Q

inorganic fluoride historically, has no renal effects when

A

peak plasma fluoride concentrations < 40 mcm/L

141
Q

inorganic fluoride historically, has subconical toxicity when

A

50-80 mcm/L

142
Q

inorganic fluoride historically, has clinical toxicity when

A

> 80 mcm/L

143
Q

level of __ is the indicator that renal toxicity may occur however __

A

50

no renal damage even with levels exceeding this level

144
Q

__ and __ are less soluble and exhaled more and less metabolized

A

enf and sevo

145
Q

high output renal failure (unresponsive to vasopressin) is the inability to

A

concentrate urine, polyuria, hypernatremia, hyperosmolatiry, increased plasma creatinine

146
Q

studies have shown no renal necrosis after

A

sevo

147
Q

have been cases of transient impairment of __ and __ in patient exposed to sevo and with peak plasma inorganic fluoride levels > 50 mcm/L

A

renal concentrating ability

increased excretion of beta-N-acetylglucosaminidase (NAG)

148
Q

NAG is

A

an indicator of acute proximal renal tubular injury

149
Q

renal effects show no

A

elevation in BUN or creatinine

150
Q

with preexisting renal disease show

A

no increased risk for damage

151
Q

renal effects

A
  1. renal blood flow is reduced (may effect urine output intraoperatively)
  2. decreased glomerular filtration rate
  3. decreased urinary output
152
Q

renal effects are due to

A

the decrease in CO and systemic BP

153
Q

__ attenuates renal effects

A

preop hydration

154
Q

___ causes release of ADH

A

surgical stress, not inhaled anesthestics

155
Q

___ might also cause ADH release to contribute to decreased urine output

A

fluid status changes

156
Q

___ may cause inability to concentrate urine causing high output and decreased response to vasopressin

A

Compound A

157
Q

__ have been seen with compound A

A

proteinuria, glucosuria, enzymuria

no renal necrosis

158
Q

to decrease the risk of compound A

A
  1. minimum flow of 2 L/min if case longer than 2 hours (1 L/min is less than 2 hours)
  2. lower concentrations of sevo
  3. avoid KOH and NaOH in CO2 absorbent
  4. avoid increased temp in CO2 absorbent

NUNA 681(pharm) (12 decks)

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