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anesthesia pharm II > inhalational agents: effects on neuro, hepatic, renal, and metabolism > Flashcards

inhalational agents: effects on neuro, hepatic, renal, and metabolism Flashcards

1
Q

what are the effects of volatile agents on skeletal muscle?

A
  • dose-dependent relaxation of skeletal muscle (not N2O)
  • higher the MAC multiple, the greater the fad on tetanus
  • can be used instead of NMB or to enhance the effect of NMB
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2
Q

what is the effect of N2O on skeletal muscle?

A

muscle rigidity

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3
Q

what MOA causes inhalation agents to enhance NMB?

A

may be from pre- or post-junctional effects
-pre: decreased release of ACh
-post: decreased sensitivity to ACh
or may be a direct effect on spinal motor neurons

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4
Q

what are the benefits of inhalational skeletal muscle relaxation

A
  • may decrease dose of nondepolarizing NMB
  • decrease frequency of re-dosing (or may not need to)
  • can avoid NMB all together (myasthenia gravis)
  • pts. w/ hepatic or renal impairment
  • also may reduce dose of neostigmine required to reverse NMB, leading to less PONV
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5
Q

describe the duration of rocuronium when combined w/ different volatile agents

A
  • longer duration depending on agent
  • desflurane most effect: 90 min
  • sevoflurane: 59 min
  • isoflurane: 35 min
  • propofol only prolongs to 35 min
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6
Q

if recovery is prolonged from NMB and volatile concentration is still maintained, what should be done?

A
  • blow off volatile to help get twitches back
  • to maximize recovery from NMB at the end of a case, be sure volatile is off
  • increased age is a factor prolonging recovery from NMB w/ volatile
  • always check w/ peripheral nerve stimulator to maintain 1 twitch on TOF
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7
Q

does volatile agents enhance effect of neostigmine on reversing NMB?

A

NO

  • once volatile concentration is down, no longer provides enhanced skeletal muscle relaxation
  • no lower doses are required to reverse
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8
Q

which agent prolonged blocks w/ cisatracurium and rocuronium?

A

sevoflurane

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9
Q

with vecuronium, which agents prolonged block?

A
  • sevoflurane

- isoflurane

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10
Q

what are the effects of isoflurane and nitrous oxide on succinylcholine?

A
  • potentiates SCh

- isoflurane causes more rapid shift from phase I to phase II block w/ SCh infusion

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11
Q

what does the amount of enhancement on NMB by volatiles depend on?

A
  • time dependent
  • sevo for 30 min. delayed recovery from vecuronium 89%
  • sevo for 60 min. delayed recovery 100%
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12
Q

since volatiles enhance skeletal muscle relaxation, what are the effects on reversal of nondepolarizing NMB?

A
  • can impair reversal (not b/c it effects Neostigmine, just causes more relaxation)
  • *carefully administer NMB, using twitch monitor and consider using relaxant effect of volatile instead of NMB if possible
  • *check twitches, not time, d/t pt. variability
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13
Q

what are the effects of volatile agents on uterine smooth muscle?

A
  • dose-dependent relaxation of the uterine smooth muscle
  • 0.5 MAC modest relaxation
  • greater than 1 MAC, significant relaxation
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14
Q

what are advantages and disadvantages of uterine smooth muscle relaxation by volatiles?

A
  • positive: desirable relaxation for removal of retained placenta
  • negative: contribute to increased blood loss w/ uterine atony
  • may prefer to have uterine contractions after C-section or d&c to minimize blood loss
  • reason C section high risk for awareness, don’t want much volatile on board; just explain up front
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15
Q

what are the effects of volatiles on malignant hyperthermia?

A
  • all agents can trigger (even w/o SCh)
  • Halothane most potent trigger
  • N2O much weaker trigger
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16
Q

describe pathophysiology of malignant hyperthermia

A
  • exposure to triggering agents cause the ryanodine receptor to release calcium from the sarcoplasmic reticulum to enter the muscle cell
  • muscle contraction occurs d/t interaction of actin and myosin
  • both aerobic and anaerobic muscle metabolism increase producing massive amounts of heat, carbon dioxide, and lactate (hypermetabolic state)
  • muscle membrane permeability allows leakage
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17
Q

what are early signs of malignant hyperthermia?

A
  • a rapid increase in ETCO2, unable to correct w/ increased ventilation
  • increase in HR
  • *increase in temp is a late sign
  • stop triggering factor and treat quickly w/ Dantrolene
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18
Q

describe times to onset of MH w/ various sole volatile agent triggers

A
  • desflurane: 260 min
  • isoflurane: 140 min
  • halothane: 35 min
  • *times much faster if combined w/ SCh
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19
Q

what are the effects of volatile agents on cerebral metabolic oxygen requirements (CMRO2)?

A
  • all but N2O cause dose-dependent decrease in CMRO2 starting at approx. 0.4 MAC, as the pt. moves toward unconsciousness
  • once an isoelectric EEG is produced, further increases in agent concentration does not further decreased in CMRO2
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20
Q

what are the effects of N2O on CMRO2 and cerebral blood flow (CBF)?

A
  • increases both CMRO2 and CBF

* but still uncoupling d/t a greater increase in CMRO2 than CBF

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21
Q

describe effects of volatiles on CMRO2 compared to effects on CBF

A
  • CMRO2 decreases
  • CBF may increase, remain unchanged, or decrease
  • if vascular resistance decreases: increased CBF, CBV, CSFP, ICP
  • uncoupling: paradoxical decrease in CMRO2 at same time of increase in CBF
  • no uncoupling (imbalance of supply and demand) if less than 1 MAC of halothane or isoflurane
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22
Q

what factors affect the changes in CBF?

A
  • dose of volatile
  • other drugs administered (propofol, N2O)
  • rate of change of concentration of volatile
  • animal used in study
  • w/ pentothal, cerebral vasoconstriction offset volatile dilation
  • N2O decreases cerebral vascular resistance significantly
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23
Q

describe effects of CBF in a normocarbic pt. w/ volatile greater than 0.6 MAC

A
  • dose dependent increase in CBF
  • cerebral vasodilation
  • decreased cerebral vascular resistance
  • increased CBF (potential increased ICP)
  • but still decreased CMRO2
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24
Q

in what order do agents increase cerebral vasodilation from greatest to least?

A

isoflurane and desflurane greater than sevoflurane

*clinically wont see much difference

25
Q

how rapid does increased CBF occur?

A

within minutes of administration of inhaled agent

  • independent of MAP
  • sustained for as long as 4 hours during anesthetic
26
Q

how do agents affect cerebral vascular reactivity to carbon dioxide?

A
  • desflurane, sevoflurane, and isoflurane maintain reactivity to CO2 at less than 1 MAC
  • can still hyperventilate to decrease CBF
27
Q

describe agents affects on autoregulation of CBF

A
  • isoflurane, desflurane, and sevoflurane at 1 MAC preserve autoregulation of CBF
  • can hyperventilate to vasoconstrict after giving agent
  • at 1.5 MAC, sevo preserves better than iso
  • halothane eliminates autoregulation
  • must hyperventilate PRIOR to giving agent to help keep down CBF
28
Q

describe cerebral protectant effects of volatile agents

A
  • CBF is maintained, CMRO2 is decreased (iso greater than halothane)
  • once EEG is isoelectric, increasing agent concentration will not decrease CMRO2 any more
  • *isoflurane may blunt necrotic processes resulting from cerebral ischemia d/t transient regional ischemia during carotid endarterectomy (protection does not apply to global ischemia like w/ cardiac arrest)
29
Q

describe effects of agents on ICP

A
  • cerebral vasodilation and increased CBF raise risks of increased ICP
  • hyperventilation to decrease PaCO2 to 30 mmHg counters the increased ICP
  • isoflurane, sevoflurane, and desflurane- start hyperventilation w/ start of agent
  • halothane- start hyperventilation before agent is started
  • *pt. w/ VP shunts
30
Q

describe correlations of PaCO2 and CBF

A
  • linear
  • PaCO2 increased, increases CBF
  • hyperventilate to decrease CBF
  • lowest PaCO2 that will decrease CBF is 25 mmHg, no changes in CBF once under PaCO2 of 25
  • *for every 1 mmHg drop in PaCO2, you decrease CBF 1-2
31
Q

describe normal cerebral vascular response to CO2

A
  • hypocarbia: vasoconstrict
  • goal PaCO2 30-35 mmHg; effective 4-6 hrs.
  • hypercarbia: vasodilate, increased CBF
  • resp. depression and volatiles inhibit reaction to increased CO2 (used mech. ventilation)
  • response altered in HTN and diabetic pts.
32
Q

describe EEG changes seen w/ volatiles

A
  • dose-dependent changes
  • at 0.4 MAC, increased frequency and voltage, but activity shifts to anterior portions of the brain
  • 1 MAC, increased voltage and decreased frequency (bigger, slower waves)
  • 1.5 MAC, burst suppression (less than 1.5 MAC iso)
  • 2.0 MAC, flat EEG (isoflurane)
  • *halothane does not produce burst suppression at clinical levels
  • *N2O has little effect on EEG at 1 atm., substitution for portion of MAC of volatile decreases EEG suppression
33
Q

what are the effects of volatiles on seizure activity?

A
  • des, iso, sevo suppress seizure activity r/t drugs like lidocaine (LA toxicity induced seizures)
  • sevo has been associated w/ seizure activity (unknown MOA)
34
Q

what increases the risk of seizure activity with sevoflurane?

A
  • higher concentrations
  • hypocarbia (doubles)
  • repeated auditory stimulation
  • pre existing seizure disorder
  • *also an increased incidence of emergence delirium (possible link w/ seizure tendency)
  • *cautious w/ kids
35
Q

describe somatosensory evoked potentials and use of monitoring

A
  • monitoring the transmission of the impulse from the periphery to/through the cord
  • typically utilized w/ spinal fusions for scoliosis-monitoring to protect the spinal cord
36
Q

how do volatiles effect somatosensory evoked potentials(SSEP)?

A
  • dose dependent reduction in evoked potentials
  • visual EP is most sensitive; brainstem EP is most resistant
  • increase in latency and decrease in amplitude can be caused by ischemia or volatiles
37
Q

what concentrations of volatiles are best to use when SSEP monitoring is occurring?

A
  • sevoflurane and desflurane can use 1.3 MAC
  • isoflurane 0.5-1 MAC
  • halothane 0.5-0.7 MAC
  • N2O may decrease amplitude of EP so AVOID
38
Q

describe volatile effects on awareness and amnesia

A
  • do not cause retrograde amnesia
  • agents are not equal in effectiveness of preventing awareness
  • 0.4 MAC isoflurane prevents awareness
  • greater than 0.5 MAC N2O required (approx. .68 MAC)
  • learning may be altered at low concentration (up to 0.2 MAC)
  • surgical stimulation may increase the concentration required to prevent awareness (GO WELL ABOVE MACE AWAKE)
39
Q

how do volatiles effect cerebral regulation of temperature control?

A
  • impair regulation
  • expands the vasoconstriction-to-shivering range of temperatures
  • alters set point where vasoconstriction occurs and also the ability to vasoconstrict d/t vasodilation
  • N2O affects less, so substitution impairs less
40
Q

how do volatiles reset threshold for temperature regulation?

A
  • reset threshold for regulation of temperature control to a lower level
  • causes center for temp regulation to permit a broader range of temperatures to exist before cutaneous vasosconstriction occurs (at lower temps)
  • permits a lower temperature before the body attempts to regulate heat loss and heat production
  • *dose related
  • *elderly have greater inhibition of temp regulation
  • *must actively warm pts.
41
Q

along w/ decreased temp. regulation, what also leads to heat loss?

A
  • vasodilation
  • heat transferred from core to periphery
  • causes a decrease in core temperature of 0.5-1 degree C in the first half hour of anesthesia
42
Q

how do volatiles affect cerebrospinal fluid production?

A
  • isoflurane (des, sevo) does not change production of CSF, and decreases resistance to reabsorption
  • results in minimal increases in ICP (but still will see ICP effects d/t CBF)
43
Q

how much of halothane is metabolized?

A

15-40% (greatest metabolism)

44
Q

how much of sevoflurane metabolized?

A

5-8%

45
Q

how much of isoflurane metabolized?

A

0.2%

46
Q

how much of desflurane metabolized?

A

0.02%

47
Q

how much of nitrous oxide is metabolized, and where?

A

0.004% undergoes reductive metabolism to nitrogen in the GI tract

48
Q

what is the concern of inhaled agent metabolism?

A

fluoride metabolites

  • trifluroacetic acid
  • inorganic fluoride
49
Q

what is the metabolic pathway for des, iso, and sevo?

A

-oxidative (aerobic)

50
Q

what is the harm of metabolism of halothane?

A
  • principally oxidative by C-P450 enzymes when O2 is present*
  • reductive metabolism when hepatocyte PO2 decreases
  • trifluoroacetic acid: hepatotoxicity (halothane hepatitis)
51
Q

describe halothane hepatitis

A
  • d/t trifluoroacetic acid produced in liver w/ reductive metabolism of halothane (can see with others but metabolism % so low much less likely)
  • immune mediated w/ an antigen-antibody reaction
  • halothane hepatitis seen often w/ pts. re exposed to halothane within 20-30 days
52
Q

describe trifluoroacetic acid

A
  • produced also by biodegradation of halothane, iso and des

* significant difference in percentage metabolized of des and iso vs. halothane

53
Q

describe inorganic fluoride

A
  • produced by biodegradation of sevo in the liver* (minimal in kidney, so little negative effect on kidneys)
  • same level of inorganic fluoride produced w/ methoxyflurane (50mcgmol/L) which causes renal failure BUT no evidence of renal injury w/ sevo (even in pts. w/ existing renal damage)
  • infrarenal production of inorganic fluoride seen w/ methoxyflurane is a bigger problem for nephrotoxicity than inorganic fluoride produced from hepatic metabolism w/ sevo
54
Q

what levels of inorganic fluoride are considered toxic?

A
  • no renal effects w/ peak plasma fluoride concentration less than 40 mcgmol/L
  • subclinical toxicity when 50-80 mcm/L
  • clinical toxicity when greater than 80 mcm/L
  • level of 50 is used to indicate that renal damage may occur, but no renal damage even w/ levels exceeding 50
55
Q

do inhalation agents cause renal impairment?

A
  • no renal impairment after sevo
  • cases of transient impairment of renal concentrating ability and increased excretion of NAG in pt. exposed to sevo and w/ peak plasma inorganic fluoride levels greater than 50 (theoretical, but don’t risk w/ transplant)
  • NAG considered an indicator of acute proximal renal tubular injury
  • no elevation of BUN or creatinine
  • no increased risk for damage w/ preexisting renal disease
56
Q

what are renal effects of inhalation agents?

A
  • renal blood flow reduced d/t decreased CO; may effect UOP intra-op
  • decreased GFR
  • decreased UOP
  • pre-op hydration attenuates renal effects
  • surgical stress (not inhaled agents which decrease) cause release of ADH; fluid status may also cause release to further add to decreased UOP
  • still shoot for UOP 0.5 ml/kg/hr
57
Q

describe effects of compound A

A

nephrotoxic

  • may cause inability to concentrate urine, causing high output and decreased response to vasopressin
  • no renal necrosis
  • proteinuria, glucosuria, and enzymuria have been seen
58
Q

how is compound A formed?

A

-w/ sevo degradation, a fluoride is lost from the chemical structure resulting in a double carbon bond (compound A)

59
Q

how should you decrease the risk of compound A?

A
  • minimum flows of 2 l/m if case longer than 2 hrs
  • lower concentrations of sevo
  • avoid KOH and NaOH in CO2 absorbent
  • avoid increased temperature in CO2 absorbent (don’t want dry absorbent)
  • *increased flows reduces the rebreathing of compound A by washing it out and reduces the temperature of absorbent

anesthesia pharm II (5 decks)

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