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Nondepolarizing NMBDs - test 3 Flashcards

1
Q

Selection for nondeloparizing NMBDs is influenced by what factors?

A
  • Onset
  • duration of action
  • Rate of recovery
  • Metabolism
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2
Q

MOA for non-depolarizing NMBDs:

A
  • Act at prejunctional sites to block Ach release
  • Compete for alpha subunits of post-junctional nAchRs with Ach
  • No conformational change
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3
Q

Characteristics of Non-depolarizer Blockade.
-Decrease twitch response to _________.
-__________ response to a continuous stimulus.
- TOF ratio _________

A

-Decrease twitch response to single twitch.
- Unsustained (fade) response to a continuous stimulus.
- TOF ratio <0.7

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4
Q

Characteristics of Non-depolarizer Blockade.
Post-tetanic potentiation
Potentiation of other ___________.
Antagonism by ___________
No _________ during onset.

A

Potentiation of other non-depolarizing drugs.
Antagonism by anticholinesterase
No fasciculations during onset.

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5
Q

Why is there a fade with non-depolarizing NMBDs?

A

Suggests that SOME fibers are contracting while some are blocked
- some are more susceptible to NMBDs

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6
Q

What causes the cardiovascular effects in non-depolarizing NMBDs?

A
  • release of histamine
  • effects at cardiac muscarinic receptors
  • effects on nAchRs at autonomic ganglia
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7
Q

Cardiovascular effects from non-depolarizing NMBD are __________ clinically significant.

A

rarely

The patient often is already on drugs to counter the cardiovascular effects. Fentanyl to counter the tachycardic effects of histamine or pressors to treat the hypotension.

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8
Q

What is the autonomic margin of safety for NMBDs?

A
  • Difference between dose that produces blockade (ED95) and dose that creates circulatory effects
  • Same dose for pancuronium (the dose you give is also the dose that causes CV effects)
  • Very different dose for vec, roc, cis
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9
Q

What is critical illness myopathy?

A

Skeletal muscle weakness that occurs weeks to months after NMBD is discontinued

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10
Q

What are some risk factors for critical illness myopathy?

A
  • Patients with MSOF who were ventilated > 6 days
  • Usually an aminosteroid blocker
  • Glucocorticoids prior to NMBD
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11
Q

What are some things that could be beneficial for patients with critical illness myopathy?

A
  • Nerve monitoring
  • Sedation
  • Analgesia
  • Small doses of NMBD beneficial?
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12
Q

What is the altered response if a non-depolarizing NMBD and a volatile anesthetics are concurrently used?

What is the MOA?

A

There will be a dose-dependent enhancement to the NMBD.
(Desflurane will have the most enhancement > Sevo > Iso)

MOA: Dose-dependent inhibition nAChR - not completely understood

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13
Q

What is the altered response if a non-depolarizing NMBD was given concurrently with loop diuretics, corticosteroids, metoclopramide, and local anesthetics?

A

Enhances or antagonizes blockade
- Increase acetylcholine release
- Depression of cholinesterase activity
- Depression of nerve conduction

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14
Q

What is the altered response if a NMBD or sux is given with magnesium?

A
  • Enhances blockade
  • MOA for non-depol: decreases prejunctional release of Ach, decreases sensitivity to postjunctional membranes
  • MOA for sux is unclear
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15
Q

What is the altered response if a non-depolarizing NMBD is given with ephedrine (SNS drug)?

A

Faster onset time d/t increased CO and skeletal muscle flow.

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16
Q

What is the altered response if esmolol is given before induction with a non-depolarizing NMBD?

A

If esmolol is given before induction, there will be a delayed onset.

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17
Q

What altered response in non-depolarizing NMBD if there is hypothermia?

MOA?

A

Even with mild hypothermia, Vec and Pancuronium will double in duration.

MOA: Temperature slows down hepatic enzyme activity.

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18
Q

Which non-depolarizing NMBD is not metabolized by the liver but is pH and temperature dependent?

What is the MOA?

A

Atracurium and Cisatracurium

MOA: temperature-dependent elimination process through Hoffman elimination (need normal temperature and pH) and ester hydrolysis

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19
Q

Acute hypokalemia with NMBDs:

A
  • Hyperpolarizes cell membrane (increased transmembrane potential)
  • Resistance to depolarizing NMBDs
  • Increased sensitivity to non-depolarizing NMBDs
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20
Q

Acute hyperkalemia with NMBDs:

A
  • Decreases membrane potential (partially depolarizes cell membrane)
  • Increases effects of depolarizing NMBDs
  • Resistance to non-depolarizing NMBDs
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21
Q

Burns are resistant to non-depolarizing NMBD ______ days post-injury.

When does the resistance go away?

What non-depolarizing drug is the exception to burns, and what is the dose?

A

Ten days

Resistance goes away in 60 days.

Rocuronium 1.2mg/kg

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22
Q

MOA for altered responses of NMBDs with burn patients:

A
  • Altered affinity of nAchRs?
  • Not related to altered density (# of receptors)
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23
Q

NMBD on stroke patients:
Paretic Arm
Unaffected Side
MOA

A

Paretic arm: Resistance compared to unaffected side

Unaffected side: Resistance compared to normal patients

MOA: Proliferation of extrajunctional nAChRs

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24
Q

Which NMBD is more likely to cause an allergic reaction?

A

Succinylcholine

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25
Q

Which NMBD is least likely to cause an allergic reaction?

A

Cisatracurium

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26
Q

What group is it possible to have cross-sensitivity with NMBDs?

A

Quaternary ammonium group

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27
Q

Altered responses: Gender and NMBDs

A
  • Women are more sensitive
  • Need 22% less vec
  • Need 30% less roc
  • Duration of block greater in women
28
Q

What is the long acting NMBD?
What groups is it?

A

Pancuronium

Bisquaternary aminosteroid

29
Q

Pancuronium Dose:
Onset:
Duration:

A

Intubating dose = 0.1 mg/kg
Onset = 3-5 minutes
Duration = 60-90 minutes

30
Q

How is pancuronium metabolized?

A

80% eliminated unchanged in the urine

31
Q

How does metabolism for pancuronium change in renal failure?

A
  • 30-50% decreased plasma clearance
  • 10-14% desacetylpancuronium metabolite 1/2 as active (by liver)
32
Q

How does metabolism for pancuronium change in liver disease?

A
  • Increased Vd
  • Larger initial dose is needed
  • Prolonged elimination 1/2 time
33
Q

How does metabolism for pancuronium change with aging?

A

Decreased plasma clearance d/t renal function

34
Q

What causes increased heart rate, MAP, and CO with pancuronium?

A

Vagal blockade
- mostly at SA node
- BP increase d/t HR

SNS activation
- Release of NE presynaptically
- Bloackade of NE reuptake

35
Q

What are other CV effects of pancuronium?

A
  • No changes in SVR or inotropy
  • No histamine release
36
Q

What are the 4 intermediate acting NMBDs?

A
  • Vecuronium
  • Rocuronium
  • Cisatracurium
  • Atracurium
37
Q

How do intermediate NMBDs compare to long acting?

A
  • Similar onset maximum blockade (except high dose roc)
  • Approximately 1/3 duration of action
  • Minimal/absent CV effects
  • Antagonized by anticholinesterase drugs in about 20 minutes
38
Q

What group is Vec in?

A

Aminosteroid

39
Q

Vecuronium dose:
Onset:
Duration:

A

Intubating dose = 0.1 mg/kg
Onset = 3-5 minutes
Duration = 20-35 minutes to be reversible (not completely out of your system)

40
Q

Metabolism of Vecuronium:

A

Hepatic metabolism
- Principle organ of elimination
- 3-desacetylvecuronium 50-80% as potent (but rapidly converted to metabolite with 1/10 the effects)

41
Q

Excretion of vecuronium:

A

Renal excretion
- approx 30% appears unchanged (70% metabolized in liver)
- Renal dysfunction = eliminated 1/2 time prolonged

42
Q

Why isn’t vecuronium used as a drip very often?

A

It has cumulative effects - d/t metabolite 3-desacetylvecuronium 50 to 80% as potent

43
Q

How does metabolism for vec change in the elderly?

A
  • Decreased volume of. distribution (less muscle mass)
  • Decreased plasma clearance (less hepatic flow)
  • Single dose mechanics unchanged
  • Delayed recovery with infusions
44
Q

How does metabolism of vecuronium change in obstetrics?

A
  • Insignificant effects to fetus
  • Increased clearance in 3rd trimester (progesterone)
  • Prolonged duration early postpartum (give IBW)
45
Q

Acid base changes with vecuronium:

A

Dependent on when the acid-base status changes
- Prior to NMBD = no prolonged blockade
- Following NMBD = prolongs blockage

46
Q

Respiratory acidosis with vecuronium:

A
  • Activity inversely proportional to bound drug - acidosis increases bound amount
  • Changes in ionization at receptor increases attachment time
  • Concern postop with hypoventilation
47
Q

Are there any CV effects with vecuronium?
Histamine release?

A
  • Essentially no CV effects
  • No histamine release
48
Q

What group is Rocuronium?

A

Aminosteroid

49
Q

Rocuronium Dose:
Onset:
Duration:

A

Dose = 0.6 mg/kg or 1.2 mg/kg
- larger doses parallel onset of Sux but offset of pancuronium

Onset = 3-5 minutes; 1-2 minutes

Duration = 20-35 minutes; 60-90 minutes

50
Q

Metabolism of Rocuronium:

A
  • Excreted unchanged in bile - longer duration of action in liver failure and eldery
  • d/t decreased clearance and an increased Vd
  • 10-30% renal excretion - only marginally affected in renal failure
51
Q

CV effects for rocuronium:

A
  • No histamine release
  • No cardiac effects - slight vagolytic effects?
52
Q

What group is cisatracurium?

A

Benzylisoquinolone

53
Q

Cis dose:
Onset:
Duration of action:

A

Intubating dose = 0.1 mg/kg
Onset = 3-5 minutes
Duation of action = 20-35 minutes

54
Q

Is recovery from a cis infusion affected by time?

55
Q

Cistatracurium is a cis- isomer of what??

A

Atracurium

56
Q

How is Cis degraded?

A

Hoffman elimination (temperature dependent)
- Doesn’t use non-specific plasma cholinesterase as much as atracurium

57
Q

Metabolism of Cis for elderly:
Obese patients:

A

Elderly = slight delay (1 min) in onset d/t CO

Obese = Duration of action prolonged if dosed at actual body weight d/t Vd

58
Q

CV effects for Cis:

A
  • No histamine release
  • CV stability
59
Q

What is the only clinically useful short acting non-depolarizer?
What group is it?

A

Mivacurium
- Benzylisoquinolone

60
Q

Mivacurium Dose:
Onset:
Duration of action:

A

Intubating dose = 0.15 mg/kg

Onset = 2-3 minutes - conditions less desirable

Duration of action = 12-20 minutes

61
Q

What are the 3 stereoisomers of mivacurium?

A
  • Cis-cis
  • Cis-trans**
  • Trans-trans**

** = NM blocking ability

62
Q

How is mivacurium cleared?

A

Cleared by plasma cholinesterase

63
Q

Is mivacurium currently on the market?

64
Q

CV effects of mivacurium:

A

Minimal effects

Anesthesia pharm (15 decks)

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