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Anesthesia Basics > Pharm: Inhaled Anesthetic Drugs > Flashcards

Pharm: Inhaled Anesthetic Drugs Flashcards

1
Q

Isoflurane (Flurane) vapor pressure

A

238

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2
Q

Isoflurane (Flurane) MAC

A

1.15

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3
Q

Isoflurane (Flurane) B:G coefficient

A

1.4

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4
Q

Isoflurane (Flurane) O:G coefficient

A

90-99

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5
Q

Isoflurane (Flurane) chemical structure

A

1-chloro-2,2,2-trifluroethyl difluoromethyl ether

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6
Q

Isoflurane (Flurane) vapor pressure

A

238

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7
Q

Isoflurane (Flurane) pharmacodynamics

A

Pharmacodynamics
- Cardiac = maintain CO, vasodilation, HR increases @ MAC >1,
dose-dependent arterial BP decrease, prolong QT
- Respiratory = less tachypnea, respiratory irritant, resp
depression, breath holding, laryngospasm
- Neurologic = may decrease intellectual function 2-3 days,
decrease CMR, does not evoke seizure activity
- Neuromuscular = potentiates muscle relaxant, moderate
muscle relaxation, malignant hyperthermia
- Renal = transient increase Cr and BUN, no renal metabolites
- Liver = metabolized 0.2%

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8
Q

Isoflurane (Flurane) adverse effects

A

Shivering
N/V
Ileus
Transient elevation in WBC

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9
Q

Isoflurane (Flurane) clinical advantage

A

moderate muscle relaxation
decrease CMR
minimal biotransformation
no significant systemic toxicity
inexpensive
possible neurologic and cardia protection

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10
Q

Isoflurane (Flurane) clinical disadvantages

A

pungent odor
airway irritant
trigger for MH
slower induction and emergence

**

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11
Q

Isoflurane (Flurane) inspired concentration and surgical anesthesia

A

concentration 1.5-3% produce surgical anesthesia in 7-10min

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12
Q

Desflurane (Suprane) vapor pressure

A

669

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13
Q

Desflurane (Suprane) MAC

A

5.8-6

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14
Q

Desflurane (Suprane) B:G coefficient

A

0.42

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15
Q

Desflurane (Suprane) O:G coefficient

A

18.7

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16
Q

Desflurane (Suprane) chemical structure

A

1,2,2,2, - tetrafluoroethyl difluoromethyl ether (6 fluorides)

totally fluurinated methyl either inset

low solubility

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17
Q

Desflurane (Suprane) vaporizer type

A

Tech 6 Vaporizer
- high VP of 669
- heated to 39 C, approx. 2 atms
- dual-gas blended vaporizer (heated and pressurized)
- does not account for altitude changes
- blended with FGF to dilute
- concentration dial: 1-18%

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18
Q

Desflurane (Suprane) pharmacodynamics

A

-Cardiac = >1 MAC increase HR, dose-dependent in MAP & CO,
minimal predisposition to PVCs w/ epi
-Respiratory = Airway irritant when >6%, dose-related resp depression, bronchodilation, increase upper airway events in peds
Neurologic = increased ICP, give < 0.8 MAC
Neuromuscular = synergistic with NMBD, trigger for MH
-Renal = urinary metabolites less than 0.02%
-Liver = minimally bio transformed in liver

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19
Q

Desflurane (Suprane) delivery

A

-low FGF rates are beneficial with less soluble anesthetics (allows for better control and less depletion of anesthetic from inspired gas)
-frequent starting concentration = 3% ().5 MAC)
-Increased 0.5-1% every 2-3 breaths until desire depth
-maintenance 2.5-8.5%

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20
Q

Desflurane (Suprane) adverse effects

A

N/V
respiratory irritant
CO production with desiccant absorbent

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21
Q

Desflurane (Suprane) clinical advantages

A

rapid wash-in/wash-out
stable molecular structure
no sig systemic toxicity
possible neurologic and cardiac protection

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22
Q

Desflurane (Suprane) clinical disadvantages

A

carbon monoxide production possible with CO2 absorbents
not recommended for pediatrics d/t upper airway events
caution if concern for for increase HR and BP
Resp irritant

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23
Q

Sevoflurane (Ultane) Vapor pressure

A

157

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24
Q

Sevoflurane (Ultane) MAC

A

1.8-2.0

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25
Q

Sevoflurane (Ultane) B:G coefficient

26
Q

Sevoflurane (Ultane) O:G coefficient

27
Q

Sevoflurane (Ultane) pharmacodynamics

A

Cardiac = dose-related depression, no inc HR < 2 MAC
- Respiratory = dose-related resp depression, bronchodilation
- Neurologic = slight increase in CBF, if MAC > 1.5
autoregulation affected
- Neuromuscular = synergistic with NMBD, trigger for MH
- Renal = slight dec RBF & GFR, fluoride HL prolonged in renal
-Liver = dec portal vein flow, inc hepatize artery flow, metabolized by CYP450 to hexafluoro isopropanol, 5% metabolized

28
Q

Sevoflurane (Ultane) warnings

A

-proteinuria & glycosuria noted with admin exceeding 2 MAC-hours and at FGF rates of <2L/min
-FGF rates <1L/min are NOT recommended
-Degradation of sevoflurane to compound A & B

29
Q

Sevoflurane (Ultane) clinical advantages

A

rapid uptake and elimination
excellent for inhalation induction
bronchodilation
cardidovascular effects comparable to iso

30
Q

Sevoflurane (Ultane) clinical disadvantages

A

reacts with soda-lime = compound A
trigger for MH
some biotransformation
emergence delirium & agitation

31
Q

What is Compound A

A

vinyl ether - nephrotoxic with exposure of 1-3 hours

32
Q

Sevoflurane (Ultane) chemical structure

A

fluoromethyl and 1,1,1,3,3,3-hexafluoroisopropyl as the two alkyl groups

33
Q

Halothane (Fluothane) vapor pressure

34
Q

Halothane (Fluothane) MAC

35
Q

Halothane (Fluothane) B:G coefficient

36
Q

Halothane (Fluothane) O:G coefficient

37
Q

Halothane (Fluothane) Pharmacodynamics

A

Cardiac = dose-related depression, slowing of SA node,
decrease HR, increased arrhythmogenic effect of epi
- Respiratory = dose-related resp depression, bronchodilation
- Neurologic = slight increase in CBF, autoregulation affected
- Neuromuscular = synergistic with NMBD, trigger for MH
- Renal = slight dec RBF & GFR, and UOP
- Liver = cellular dysfn, hepatotoxicity, metabolized 12-25%

38
Q

Nitrous Oxide MAC

39
Q

Nitrous Oxide B:G coefficient

40
Q

Nitrous Oxide O:G coefficient

41
Q

Nitrous Oxide Pharmacodynamics

A
  • Cardiac = no change in BP, CO, and HR
  • Respiratory = inc RR, dec TV, dec hypoxic drive
  • Neurologic = Inc CBF, inc CBV, and ICP
  • Neuromuscular = no muscle relaxation, not a trigger for MH
  • Renal = slight dec RBF, inc renal vascular resistance
  • Liver = midl decrease in blood flow
42
Q

Nitrous Oxide contraindications

A

-air embolus
- pneumothorax
- acute bowel obstruction
- intracranial air
- intra-ocular gas bubble (perfluoropropane or sulfur
hexafluoride)
- tympanic membrane

43
Q

Nitrous Oxide clinical advantages

A

-analgesia, anxiolysis
- rapid uptake and elimination
- second gas effect
- decrease MAC requirements
- minimal resp or cardiac depression
- nonpungent

44
Q

Goal of inhaled anesthetics

A

Establish a constant optimal partial pressure of anesthetic in CNS
CNS partial pressure = blood partial press= alveolar partial press

Produce:
1.Amnesia
2.Unconscious
3.Immobility

45
Q

Challenges of inhaled anesthetics

A
  • Airway irritation
  • SNS stimulation
  • Compound A (sevoflurane)
  • CO production with CO2 absorbent
  • Complex desflurane vaporizer
  • Perioperative hyperkalemia
  • Cost
46
Q

Advantages of inhaled anesthetics

A
  • Rapid induction
  • Precise control of end tidal concentrations during maintenance of anesthesia
  • Prompt recovery at end of case
47
Q

Stages of anesthesia: One

A

Begins with Induction of anesthesia & ends with loss of consciousness. Pain perception threshold not lowered

48
Q

Stages of anesthesia: two

A

Uninhibited excitation. Agitation, delirium, irregular breathing pattern including breath-holding, dilated & divergent pupils. Noxious stimuli can cause HTN, ↑HR, laryngospasm, vomiting, uncontrolled movements

49
Q

Stages of anesthesia: three

A

Target anesthesia depth: painful stimulation does not elicit somatic reflexes & autonomic responses. Central eye gaze, constricted pupils, regular respirations

50
Q

Stages of anesthesia: four

A

Includes hypotension, dilated & nonreactive pupils, onset of apnea

51
Q

MOA: Meyer-Overton (traditional)

A
  • lipid solubility is proportional to potency
  • thought general anesthetics work by binding directly to proteins
  • revised: anesthetics have a polar and nonpolar side
52
Q

MOA: Enhanced inhibitory receptors

A
  • GABAa, glycine, NMDA receptors
  • sodium channels, calcium channels, potassium channels, 5HT3
53
Q

MOA: Inhibitory effect on excitatory channels

A

neuronal nicotine & glutamate receptors

54
Q

Sites of action producing unconsciousness, amnesia, analgesia, immobility

A

Sites of action:
-supraspinal (sedation, amnesia)
-spinal (immobility)
- suppress withdrawal effect in dorsal horn

Unconscious = cortex, thalamus, and brainstem

Amnesia = amygdala, hippocampus

Analgesia = spinothalamic tract

Immobility = spinal cord

55
Q

MAC

A

MAC = minimum alveolar concentration at equilibrium (1 atm) in which 50% of subjects will not respond to a painful stimulus (such as skin incision)
🡺 Mirrors brain partial pressure

56
Q

MAC-awake

A

minimum alveolar concentration at which 50% of persons will follow the command to “open your eyes”
🡺 0.3-0.4 MAC associated with awakening from anesthesia
🡺 Loss of awareness & recall approx. 0.4-0.5 MAC

57
Q

MAC-Bar

A

exceeds requirements for ablation of skeletal muscle movement with surgical stimuli. Blunts hemodynamic responses (heart rate, MAP) to incision
🡺 Roughly 1.3 MA

58
Q

MAC-Bar for desflurane, sevoflurane, isoflurane

A
  • Des 7.8 MAC
  • Sevo 2.6 MAC
  • Iso 1.5 MAC
59
Q

Loss of recall: desflurane, sevoflurane, isoflurane

A

-Des 2.4-3.0 MAC
-Sevo 0.8-1.0 MAC
-Iso 0.46-0.57 MAC

60
Q

Halogenated ethers

A
  • Isoflurane (Forane)
  • Sevoflurane (Ultane)
  • Desflurane (Suprane)
61
Q

Halogenated Hydrocarbons

A

Halothane (fluothane)

62
Q

Impact of drugs halogenated with fluorine

A

are less soluble in blood -> allows for faster induction & emergence

Anesthesia Basics (7 decks)

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