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Anesthesia Pharm (Spring '24) - B > Lecture 14 (Exam 3) - Non-depolarizing Muscle Relaxants > Flashcards

Lecture 14 (Exam 3) - Non-depolarizing Muscle Relaxants Flashcards

1
Q

What is the only Short-Acting non-depolarizing NMBD (that is not used anymore)?

A

Mivacurium (Mivacron)

(slide 37)

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2
Q

Which receptor do Non-Depolarizing muscle relaxants work on?

A

Nicotinic Acetylcholine Receptors

Slide 3

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3
Q

What is Mivacurium(Mivacron):
Intubating dose:
Onset:
DOA:

With it’s DOA, what has to be considered?

A

0.15mg/kg
2-3 min
12-20min

Since its DOA is so short, may have to give supplemental doses.

(slide 37)

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4
Q

True or False:
Non-depolarizing drugs only bind to one alpha-subunit

A

False - They compete for both alpha-subunits. 💁🏻‍♀️

Slide 3

ChatGPT:
False. Non-depolarizing drugs can bind to the nicotinic acetylcholine receptors at the neuromuscular junction, and while effective blockade can occur by binding to one of the alpha subunits, these drugs do not exclusively bind to only one alpha subunit. They can bind to either of the alpha subunits, and their mechanism of action involves competing with acetylcholine for its binding sites on the alpha subunits. This blockade prevents acetylcholine from binding to both alpha subunits, which is necessary for the receptor to activate and for muscle contraction to occur.

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5
Q

With Mivacurium(Mivacron) what airway conditions/side effects are less desirable?

And why does this drug have these?

A

Still causes s/e like coughing and spitting with inductions

Due to this drug being less “dense” of a block - remember not so deep sedation causes these reflexes to occur.
AKA “move-a-cron”

(slide 37)

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6
Q

Since there is no conformational change in the nicotinic acetylcholine receptor, there are no shifts in which electrolytes?

A

Sodium and Potassium
Slide 3

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7
Q

TOF ratio of _________ is indicative of a successful Non-Depolarizing NMBA block.

A

< 0.7

Slide 4

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8
Q

What is the only Long-acting NMBD that we have to know/use?

What class of drug is it considered?

What properties does it have?

Induction dose:
Onset:
Duration:

A

Pancuronium (Pavulon)

Class: Bisquaternary aminosteroid

Properties: Vagolytic (inhibits actions of the vagus nerve)

Induction dose: 0.1 mg/kg
Onset: 3-5 mins
Duration: 60-90 mins

(slide 20)

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9
Q

How many stereoisomers does Mivacurium (Mivacron) have and what are they? Which ones actually have neruomuscular blocking activity?

A

3 stereoisomers:
Cis-cis
*Cis-trans
*Trans-trans

*NM blocking ability

(slide 38)

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10
Q

You give your patient Rocuronium for intubation, which drug should you give to maintain the paralysis?

What will occur if you give a different NMBD?

A

Rocuronium - non-depolarizing drugs potentiate the action of other non-depolarizing drugs so both duration and recovery are long if you give a different drug

Slide 4

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11
Q

How is Mivacurium(Mivacron) cleared?

A

by plasma cholinesterase

(slide 38)

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12
Q

Does Mivacurium (Mivacron) release histamine?
And what additional vascular detail or symptoms are seen about your answer?

A

Yes it can.

But only at doses that are >3X ED95 (this is never done- almost OD)

Would see:
- Transient MAP drop (histamine causes vasodilation)
- More common with rapid, large doses
- MAP drop more in HTN pts than non-HTN pts

(slide 39)

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13
Q

Pancuronium primarily is eliminated how?

By how much percent?

A

80% eliminated unchanged in the urine

(slide 21)

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14
Q

This term is used to suggest that some fibers are contracting while some are still blocked…

A

Fade

Slide 5

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15
Q

CV adverse effects are due to what three things?

A
  1. Release of histamine
  2. Effects on cardiac muscarinic receptors
  3. Effects on nACh-Rs at autonomic ganglia

Slide 7

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16
Q

Difference between dose that produces blockade (ED95) and the dose that creates circulatory effect.

A

Autonomic Margin of Safety

Slide 7

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17
Q

The “autonomic margin of safety” for Pancuronium is the ________ dose

A

Same as ED95 dose

Slide 7

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18
Q

Pancuronium produces ___________ (r/t heart) at ED95 dose

A

Tachycardia ❤️‍🩹

Slide 7

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19
Q

Skeletal muscle weakness that occurs weeks to months after NMBDs are discontinued…

A

Critical Illness Myopathy

Slide 8

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20
Q

Giving what drugs prior to NMBD may enhance risk for critical illness myopathy?

A

Glucocorticoids

Slide 8

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21
Q

What two things would you want to give patients with critical illness myopathy?

A

More sedation
More analgesia

Slide 8

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22
Q

In the presence of LIVER DX, what would we expect when considering the administration of Pavulon?

_________ volume distribution
______ initial dose needed
Prolonged ___________ ___ time

A

D/t deficient protein production, fluid leaks out grossly throughout the body, thereby causing the following:

⬆️ VD
Larger initial dose is needed
Prolonged elimination 1/2 time

(slide 21)

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23
Q

Which NMB chemical classification normally causes critical illness myopathy?

A

Aminosteroid blocker (roc, vec, panc)

Slide 8

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24
Q

Would 75-year-old Pee-paw be a good candidate for receiving Pancuronium?

Why or why not?

A

No!

Pee-paw has seen more moons than most and thus has a ⬇️ plasma clearance d/t ⬇️ renal function.

(slide 21)

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25
Q

You give Pavulon to your pt undergoing a sloppabotomy (i.e., irrelevant procedure). What cardiovascular effects would you expect to see?

Why?

Where does this medication affect most often?

Will the BP ⬆️ or ⬇️?

A

⬆️ in HR, MAP, and CO

d/t vagal blockade (remember it’s a vagolytic)

occurs mostly at the SA node

BP increases d/t HR

(slide 22)

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26
Q

CV effects of Pavulon continued.

Why else might we see an ⬆️ in HR, MAP, and CO? (we already said vagal blockade in a prev card)

What does that mean?

Does this mean we’ll have changes in the SVR or inotropy?

A

d/t SNS activation

This means that we’ll have release of NE presynaptically AND a simultaneous blockade of NE reuptake

No, there will not be changes in SVR or inotropy

(slide 22)

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27
Q

T/F: Pancuronium will cause histamine release

A

False

(slide 22)

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28
Q

When comparing Intermediate-acting NMBDs with Long-acting NMBDs, we would see a similar _____ of maximum ________.

Intermediate NMBDs would also have a _____ of the duration of Long-acting NMBDs.

Would CV effects be minimal or profound with Intermediate NMBDs?

What type of drugs could antagonize the intermediate NMBDs?

How long before this drug-mediated antagonism would take place?

A

onset; blockade

1/3

minimal/absent CV effects with Intermediate NMBDs

Anticholinesterase drugs would antagonize Intermediate NMBDs (b/c Ach would be there longer at the NMJ)

would take ~20 mins after giving a full induction/intubation dose before antagonism would occur

(slide 24)

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29
Q

List the 4 Intermediate-acting NMBDs.

A

Vecuronium
Rocuronium
Cisatracurium
Atracurium

(slide 23)

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30
Q

How does acute hypokalemia alter response to NMBD?

A
  1. Acute hypokalemia hyperpolarizes cell membrane (inside of cell becomes more negative if more K moves out of cell to achieve equilibrium; increased transmembrane potential)
  2. Resistance to depolarizing NMBDs.
  3. ↑ sensitivity to non-depolarizing NMBDs (Hyperpolarization + NDNMB).

Slide 14

31
Q

How does acute hyperkalemia alter the response to NMBD?

A
  1. Acute hyperkalemia decreases membrane potential (partially depolarizes cell membrane)
  2. ↑ effects of depolarizing NMBDs.
  3. Resistance to non-depolarizing NMBDs.

Slide 14

32
Q

When do you see NMBD resistance in Burn patients?

A

Resistance to NMBD begins approx. 10 days post-injury and declines after 60 days.
And 30%BSA or > burn( she didn’t explain very well)
(if pt with bad burn comes to ER, you use a regular dose to intubate)

Slide 15

33
Q

Vecuronium(Norcuron)

Is it an Aminosteroid?
Intubation dose?
Onset?
Duration?

A

Yes

Intubating Dose: 0.1 mg/kg

Onset: 3-5 minutes

Duration: 20-35 minutes

(Slide 25)

34
Q
  1. Where is Vecuronium(Norcuron) metabolized?
  2. What is the metabolite pathway?
A
  1. The liver! Principle organ of elimination (*70% metabolized in liver).
  2. Vecuronium is metabolized to 3-desacetylvecuronium [50-80% as potent].
    3-desacetylvecuronium is then rapidly converted to metabolite with 1/10 the effects!

(Slide 26)

35
Q

How is Vecuronium(Norcuron) excreted from the body?

A

Through the kidneys! [Approx 30% appears unchanged (*70% metabolized in liver)]

(Slide 26)

36
Q

Why should you be cautious in giving your renal dysfunction patient Vecuronium(Norcuron)?

A

Renal excretion: 30% appears unchanged. Renal dysfunction - Elimination ½ time prolonged

(Slide 26)

37
Q

What offsets the resistance of NMBD in burn patients?

A

Using 1.2mg/kg dose of rocuronium

Slide 15

38
Q

What is the proposed mechanism behind the resistance of NMBD in burn patients?

A

Burns alter the affinity of nACH receptors. Not related to altered density (or number or receptors)

Slide 15

39
Q

Why do Repeated doses or infusion of Vecuronium(Norcuron) cause cumulative effects?

A

Due to the cumulative effects from the active metabolites!!!

(Slide 26)

40
Q

Why do we need to be cautious when using Vecuronium(Norcuron) with the elderly?

A
  1. Decreased volume of distribution (less muscle mass) (dehydration from ACE inhibitors)(Low CO and low blood flow)
  2. Decreased plasma clearance (less hepatic flow)
    *Single dose mechanics unchanged
    *Delayed recovery with infusions

(Slide 27)

41
Q

Why do we need to be cautious when using Vecuronium(Norcuron) with obstetrics?

A

**Insignificant effects to fetus*

  1. Increased clearance time in 3rd trimester (Due to progesterone)
  2. Prolonged duration early postpartum (give IBW)

(Slide 27)

42
Q

How does pH effect Vecuronium(Norcuron)?

A
  1. If you give your patient Vecuronium when they are already acidotic then there is no change in the duration of the drug!
  2. If you give your patient Vecuronium and then your patient become acidotic, then you will prolong the duration of Vecuronium.
    [Concern postop with hypoventilation]
    *Acidosis decreases bound amount
    *Change in ionization at receptor increases attachment time

(Slide 28)

43
Q

In terms of resistance to NDNMBD, the Paretic arm (weakened or paralyzed) has _____resistance compared to the unaffected arm.

A

Higher

(so you want to use TOF on both side of the arms to compare in stroke patients.)

Slide 16

44
Q

In terms of NMBD resistance, the unaffected side of the stroke patient still has _____resistance compared to normal people who do not have a stroke.

A

greater
(Stroke patients: greater resistance in affected side than unaffected side and greater resistance in unaffected side than normal people)

Slide 16

45
Q

What is the proposed MOA of NMBDs on paresis or hemiplegia?

A

Due to the proliferation of extra junctional nACh receptors. ( more drugs needed to block the affected side)

Slide 16

46
Q

Cardiovascular concerns with Vecuronium(Norcuron)?

A

Essentially none

No histamine release

(Slide 29)

47
Q

What NMBDs are more likely to have allergic reaction to and less likely to have allergic reaction to?

What is the name of the NMBD that is least likely to have allergic reaction to?

A

More likely –> Succinylcholine

Less likely –> Pavulon, Vecuronium, Rocuronium (Aminosteroids)

Least likely –> Cisatricurium (Benz)

Slide 17

48
Q

What group of drugs is it possible to see cross sensitivity with?

A

Quaternary ammonium group

Slide 17

49
Q

Can you develop allergic reaction to quaternary ammounium group NMBD if you are allergic to soaps and cosmetics that contain quaternary ammonium?

A

Yes.
Slide 17

50
Q

Rocuronium (Zemuron) is an _________ acting ND-NMBA.

Is it an aminosteroid or benzylisoquinolone?

*bonus: will Sugammedex work reverse this?

A

Intermediate acting

Aminosteroid

Sugammadex should work to reverse!

slide 30

51
Q

Which gender is more sensitive to NMB, men or women? And why?

A

Women. They have less muscle mass than men (more fat).
Slide 18

52
Q

You give ___ less vecuronium and ___ less rocuronium to women than men.

A

22% less vec
30% less roc
Slide 18

53
Q

Rocuronium (Zemuron)

Dose:
Onset:
Duration:

What is the double dose of this med and what does it mimic? What would the onset be?
What is the risk of doing this?

A

Dose: 0.6mg/kg
Onset: 3-5 mins
Duration: 20-35 mins

Double dose: 1.2mg/kg
-will mimic SCh with an onset of 1-2 mins but it will last as long as Pancuronium.

slide 30

54
Q

Where is Rocuronium metabolized?

10-30% is excreted where?

A

Liver
⚠️ in liver failure & elderly pt’s (⬆ Vd)

Excreted via kidneys.

slide 31

55
Q

What are the cardiovascular effects of Rocuronium (Zemuron)?

A

No significant effects…lolz

-slight vagolytic effect BUT this is hard to tell bc of the Fentanyl and Prop you just gave.

slide 32

56
Q

Does Rocuronium (Zemuron) release histamine?

A

Not that we know of 😁

slide 32

57
Q

What effect does volatile gases have on NMB’s?

A

Dose dependent enhancement

Slide 9

58
Q

In what order do the volatile gases enhance NMB effect? (From greatest to least)

A

Des > Sevo > Iso

Slide 9

59
Q

What effects do diuretics, reglan, local anesthetics, and corticosteroids have on a NMB?

A

Prolonged or enhanced effect of the NMB.

Slide 10

60
Q

What effect does magnesium have on non-depolarizing agents? and how?

A

Magnesium enhances the blockade by decreasing prejunctional release of ACh (so less ACh, less competition between NMB and ACh for receptors) and decreasing sensitivity to postjunctional membranes.

Slide 11

61
Q

What effect does magnesium have on depolarizing agents? and how?

A

Magnesium enhances the blockade of SCh. We dont know for sure.

**Mg sits its big ass in the way of Ca++ (all i remember from Schmidtty)

Slide 11

62
Q

What effect does an SNS stimulating drug have on a NMB?

A

Faster onset time of the NMB d/t increase in CO and skeletal muscle flow.

Slide 12

63
Q

What effect does an SNS inhibiting drug have on a NMB?

A

Delays onset of the NMB d/t decrease in CO and skeletal muscle flow.

Slide 12

64
Q

What effect does temperature have on Vecuronium and Pancuronium?

A

Mild hypothermia can double the duration.

Decreased temperature = decrease hepatic enzyme activity = decrease in drug metabolism.

Slide 13

65
Q

Dose, onset, duration, and chemical class of cisatracurium?

A

Dose: 0.1 mg/kg
Onset: 3 - 5 min
Duration: 20 - 35 min
Benzylisoquinoline
(Slide 33)

66
Q

Cisatracurium vs Atracurium- which is cleared more by plasma cholinesterase?

A

Atracurium = cleared via plasma cholinesterase.

Cisatracurium = cleared via Hoffman elimination (temp and pH dependent)
(Slide 34)

67
Q

Does onset change in the elderly with cisatracurium administration?

A

Yes, but onset delayed only by one minute. (🫥)
(Slide 35)

68
Q

How should dosing of cisatracurium be changed with obese patients?

A

Dosing should be done on IBW. Per slide blockade will be prolonged if dose is based on ABW.

Per lecture , obese pts will have prolonged duration of action –> Kane emailed and said its actually on IBW

(Slide 35)

69
Q

CV effects of Nimbex/cisatracurium?

A

CV stable and no histamine release.
(Slide 36)

70
Q

How does atracurium differ from cisatracurium?

A

Atracurium does cause a histamine release and is eliminated primarily via plasma cholinesterase. (Written on slide 36 during lecture)

71
Q

Will it take a long time to recover once a Nimbex drip is stopped?

A

No! The beauty of nimbex/cisatracurium is that it is eliminated quickly via Hoffman elimination, so not dependent on organs for clearance. Therefore, recovery from infusion is not affected by time.
(Slide 34)

72
Q

In the presence of RENAL FAILURE, what should we expect when considering administering Pavulon?

__-__% ⬇️ plasma clearance

A

Would expect much longer duration of effects of Pavulon

Renal failure:

  • 30-50% ⬇️ plasma clearance
  • 10-40% Deasacetylpancuronium metabolite 1/2 as active (by liver)

(slide 21)

73
Q

Pancuronium

A

Intubating Dose: 0.1 mg/kg
ED95: 0.08 mg/kg
Time to Maximum Block: 2.9 minutes
Clinical Duration of Response: 86 minutes

Anesthesia Pharm (Spring '24) - B (20 decks)

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