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Anesthesia pharm > Nondepolarizing NMBDs - test 3 > Flashcards

Nondepolarizing NMBDs - test 3 Flashcards

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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
Which NMBD is least likely to cause an allergic reaction?
Cisatracurium
26
What group is it possible to have cross-sensitivity with NMBDs?
Quaternary ammonium group
27
Altered responses: Gender and NMBDs
- Women are more sensitive - Need 22% less vec - Need 30% less roc - Duration of block greater in women
28
What is the long acting NMBD? What groups is it?
Pancuronium Bisquaternary aminosteroid
29
Pancuronium Dose: Onset: Duration:
Intubating dose = 0.1 mg/kg Onset = 3-5 minutes Duration = 60-90 minutes
30
How is pancuronium metabolized?
80% eliminated unchanged in the urine
31
How does metabolism for pancuronium change in renal failure?
- 30-50% decreased plasma clearance - 10-14% desacetylpancuronium metabolite 1/2 as active (by liver)
32
How does metabolism for pancuronium change in liver disease?
- Increased Vd - Larger initial dose is needed - Prolonged elimination 1/2 time
33
How does metabolism for pancuronium change with aging?
Decreased plasma clearance d/t renal function
34
What causes increased heart rate, MAP, and CO with pancuronium?
Vagal blockade - mostly at SA node - BP increase d/t HR SNS activation - Release of NE presynaptically - Bloackade of NE reuptake
35
What are other CV effects of pancuronium?
- No changes in SVR or inotropy - No histamine release
36
What are the 4 intermediate acting NMBDs?
- Vecuronium - Rocuronium - Cisatracurium - Atracurium
37
How do intermediate NMBDs compare to long acting?
- 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
What group is Vec in?
Aminosteroid
39
Vecuronium dose: Onset: Duration:
Intubating dose = 0.1 mg/kg Onset = 3-5 minutes Duration = 20-35 minutes to be reversible (not completely out of your system)
40
Metabolism of Vecuronium:
Hepatic metabolism - Principle organ of elimination - 3-desacetylvecuronium 50-80% as potent (but rapidly converted to metabolite with 1/10 the effects)
41
Excretion of vecuronium:
Renal excretion - approx 30% appears unchanged (70% metabolized in liver) - Renal dysfunction = eliminated 1/2 time prolonged
42
Why isn't vecuronium used as a drip very often?
It has cumulative effects - d/t metabolite 3-desacetylvecuronium 50 to 80% as potent
43
How does metabolism for vec change in the elderly?
- Decreased volume of. distribution (less muscle mass) - Decreased plasma clearance (less hepatic flow) - Single dose mechanics unchanged - Delayed recovery with infusions
44
How does metabolism of vecuronium change in obstetrics?
- Insignificant effects to fetus - Increased clearance in 3rd trimester (progesterone) - Prolonged duration early postpartum (give IBW)
45
Acid base changes with vecuronium:
Dependent on when the acid-base status changes - Prior to NMBD = no prolonged blockade - Following NMBD = prolongs blockage
46
Respiratory acidosis with vecuronium:
- Activity inversely proportional to bound drug - acidosis increases bound amount - Changes in ionization at receptor increases attachment time - Concern postop with hypoventilation
47
Are there any CV effects with vecuronium? Histamine release?
- Essentially no CV effects - No histamine release
48
What group is Rocuronium?
Aminosteroid
49
Rocuronium Dose: Onset: Duration:
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
Metabolism of Rocuronium:
- 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
CV effects for rocuronium:
- No histamine release - No cardiac effects - slight vagolytic effects?
52
What group is cisatracurium?
Benzylisoquinolone
53
Cis dose: Onset: Duration of action:
Intubating dose = 0.1 mg/kg Onset = 3-5 minutes Duation of action = 20-35 minutes
54
Is recovery from a cis infusion affected by time?
NO
55
Cistatracurium is a cis- isomer of what??
Atracurium
56
How is Cis degraded?
Hoffman elimination (temperature dependent) - Doesn't use non-specific plasma cholinesterase as much as atracurium
57
Metabolism of Cis for elderly: Obese patients:
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
CV effects for Cis:
- No histamine release - CV stability
59
What is the only clinically useful short acting non-depolarizer? What group is it?
Mivacurium - Benzylisoquinolone
60
Mivacurium Dose: Onset: Duration of action:
Intubating dose = 0.15 mg/kg Onset = 2-3 minutes - conditions less desirable Duration of action = 12-20 minutes
61
What are the 3 stereoisomers of mivacurium?
- Cis-cis - Cis-trans** - Trans-trans** ** = NM blocking ability
62
How is mivacurium cleared?
Cleared by plasma cholinesterase
63
Is mivacurium currently on the market?
Nope
64
CV effects of mivacurium:
Minimal effects
65

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