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Anesthesia Pharm 1 Sp 25' > NMBDs: Non-depolarizing (Exam III) > Flashcards

NMBDs: Non-depolarizing (Exam III) Flashcards

1
Q

What are the main causes of differences between all of the non-depolarizing muscle blockers?

A
  • Onset;
  • Duration of action;
  • Rate of recovery;
  • Metabolism
  • Comorbidities
  • Surgery Duration
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2
Q

What is the MoA of non-depolarizing blockers?

A
  • Pre-junctional sites → block ACh release;
  • Post junctional → Compete with ACh at nACh-R for alpha subunits → no conformational change
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3
Q

What sites do NDNMBDS attach to on the receptor.

A

Alpha

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4
Q

Which type of neuromuscular blocking drug will cause a conformational change of the nicotinic ACh receptor?

A

By definition, Succinylcholine causes a conformational change

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5
Q

What are the characteristics of a non-depolarizing block?

A
  • ↓ twitch response to a single stimulus;
  • Unsustained response (fade) to continuous stimulus;
  • TOF ratio < 0.7;
  • Post-tetanic potentiation;
  • Potentiation of other non-depolarizing drugs;
  • Antagonism by anticholinesterase drugs;
  • No fasciculations during onset
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6
Q

Why would you not give an intubating dose of rocuronium and then give vecuronium as the rocuronium starts to offset?

A

Non-depolarizing neuromuscular blockers will potentiate (enhance) each other’s effects.

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7
Q

When would you use a priming dose of a non-depolarizing paralytic?

A

ONLY with succinylcholine to avoid its side effects (fasciculations, eye weakness, etc.)

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8
Q

What is fade?

A

Fade suggestssomefibers are contracting while some are blocked (muscle contraction is all or nothing)

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9
Q

What causes the adverse CV effects of non-depolarizing blockers?

A
  • Release of histamine;
  • Effects at cardiac muscarinic receptors;
  • Effects on nACh-R at autonomic ganglia
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10
Q

Why do the adverse CV effects of non-depolarizing blockers vary between patients?

A
  • Underlying diseases
  • Pre-op meds
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11
Q

What is the “Autonomic Margin of Safety”?

A

Essentially Therapeutic Index

Difference between dose thatproducesblockade (ED95) and dose thatcreatescirculatory effects.

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12
Q

Which non-depolarizing blocker has a required dose that both causes blockade and adverse CV effects, also known as the “autonomic margin of safety”?

A

Pancuronium

Essentially no therapeutic index

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13
Q

What adverse event have non-depolarizing blockers been shown to have in critically ill patients?
When does this occur?

A
  • Critical Illness Myopathy
  • Weeks to months after NMBD discontinuation
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14
Q

Who is most often affected by critical illness myopathy?

A
  • Had MODS for > 6 days;
  • Usually had an aminosteroid NMBD;
  • Administered Glucocorticoids prior to NMBD
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15
Q

Why is critical illness myopathy thought to occur?

A

Possible ↓ clearance or active metabolites

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16
Q

Which volatile gasses exhibit a dose-dependent enhancement of NMBDs?
Why is this?

A
  • Desflurane > Sevoflurane > Isoflurane
  • Thought to occur due to solubility allowing rapid movement into muscular partition/compartment.
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17
Q

What drug classes and/or drugs will enhance or prolong neuromuscular blockade?

A
  • Diuretics
  • Corticosteroids
  • Metoclopramide
  • Local Anesthestics
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18
Q

How does Magnesium affect non-depolarizing blockers and SCh?
Why is this thought to occur?

A

Enhances blockade

  • ↓Release of ACh and
  • ↓sensitivity to ACh
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19
Q

T/F Magnesium enhances a blockade (paralytic)

A

True true true

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20
Q

How will sympathomimetics such as Ephedrine or EPI affect NMBDs?

A

↓ onset time (Drug works faster)

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21
Q

How will sympatholytics such as ESMOLOL (beta blocker) affect NMBDs?

A

↑ onset time (Drug works slower)

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22
Q

How does Hypothermia affect non-depolarizing blockers?
Does this occur for CYP450 metabolism or hoffman elimination?

A

Hypothermia will DOUBLE NMBD duration
ESPECIALLY VEC AND PANC

This occurs whether the process is CYP450 dependent or hoffman elimination dependent

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23
Q

What is Hoffman elimination and what paralytic is associated with it?

A

It is a temperature-dependent metabolism of Cisatricurium where the patient must be normothermic in order for the drug to be metabolised, otherwise the DOA is prolonged.

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24
Q

How doesacute hypokalemiaaffect non-depolarizing blockers?

A

↓ Vᵣₘ decreased resting membrane potential

  • Resistance to depolarizing NMBDs
  • Sensitivity to non-depolarizing NMBD’s
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25
Q

How does acute hyperkalemia affect non-depolarizing blockers?

A

↑ Vᵣₘ increased resting membrane potential

  • Sensitivity to depolarizing NMBDs;
  • Resistance to non-depolarizing NMBDs

With ↑K⁺ we are sensitive to succs & resistant to roc

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26
Q

How do burns affect non-depolarizing blockers?

A

Burns patients within the 10 - 60 day time from burn will have a resistance to NMBDs.

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27
Q

What percentage of the body needs to be affected by burns to cause altered response to non-depolarizing blockers?

A
  • 30% BSA or >
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28
Q

For a patient with burns needing intubation, how can we offset the resistance to non-depolarizing blockers the burn causes?

A

1.2 mg/kg dose of Rocuronium

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29
Q

What is the dose for “high dose Rocuronium”?
What does this high dose act like, but without the hyperkalemia response?

A

1.2 mg/kg
It acts like Succs but the high-dose Roc doesn’t lead to an increase of potassium by 0.5

30
Q

What is a pro and con of using Roc like Succs?

A

Its a fast response, but they stay paralyzed longer.

31
Q

Explain how paresis/paralysis will affect neuromuscular blocking drugs effects.

A

The more “paralyzed” = more resistant

Ex. Paralyzed leg (most resistant) > unaffected side of a person who suffered a stroke > person who never had a stroke or any paresis whatsoever.

32
Q

Which depolarizing/non-depolarizing blocker is the most likely to cause allergic reactions? Which is least likely to cause reaction?

A

SCh (most) > Pancuronium, Vecuronium, Rocuronium > Cisatracurium (least)

33
Q

What organic functional group makes a cross sensitivity reaction possible for depolarizing/non-depolarizing blockers?

A
  • Quaternary ammonium group
34
Q

How can a patient get an allergic reaction from a depolarizing/non-depolarizing blocker on their 1st exposure?

A

Due to prior sensitization →Soaps/cosmetics (women > men)

35
Q

How does Gender affect non-depolarizing blockers? MoA?

A
  • Women more sensitive (need 22% less Vec or 30% less Roc) and have greater drug duration.
  • MoA: likely muscle mass
36
Q

What is the most common long acting NMBD?

A

Pancuronium (Pavulon)

37
Q

What is the intubating dose, onset and duration of Pancuronium?

A
  • Dose: 0.1mg/kg;
  • Onset: 3-5 minutes;
  • Duration: 60-90 minutes
38
Q

How is the majority of Pancuronium eliminated?

A
  • 80% eliminated unchanged in urine
39
Q

What patients would you not want to use pancuronium on?

A

Liver and Kidney cases (prolonged elimination and metabolism).

40
Q

What changes in metabolism of Pancuronium do we see with a liver disease patient?

A
  • Increased VD
  • Larger initial dose is needed
  • Prolonged E½ time
41
Q

What CV effects do we see with Pancuronium?

A

Sympathomimetic:/ Vagolytic (lyses the vagal response)

  • ↑ HR;
  • ↑ MAP;
  • ↑ CO;
42
Q

What occurs with norepinephrine after pancuronium administration?

A
  • ↑NE release
  • ↓NE reuptake
43
Q

Does Pancuronium (pavulon) have an active metabolite?

A

Yes, and it is still even 1/2 as strong as panc

44
Q

What are the bread and butter of NMBDs?

A

Intermediate-acting NMBDs

45
Q

Compared to pancuronium, what duration of action do intermediate-acting NMBDS have?

A

Approximately 1/3 duration of action

46
Q

Compared to pancuronium, what cardiovascular effects do intermediate-acting NMBDS have?

A

Minimal/absent cardiovascular effects

47
Q

After administering any intermediate-acting neuromuscular blocker, when you be able to reverse its effects via an cholinesterase-inhibitor?

A

Approximately 20min post administration

48
Q

What does that last answer mean?

A

It means that you cant just reverse a paralytic whenever, you have to wait until it is within its duration window to start to reverse it, and the shortest duration is approx 20-35 mins.

49
Q

What is the intubating dose, onset, and duration of Vecuronium?

A
  • Intubating Dose: 0.1 mg/kg
  • Onset: 3-5 minutes
  • Duration: 20-35 minutes
50
Q

What is the main way Vecuronium is metabolized?

A
  • CYP450’s
  • 3-desacetylvecuronium 50-80% as potent (but rapidly converted to metabolite with 1/10 the effects)
51
Q

How does metabolism of Vecuronium change with the elderly?

A
  • ↓ volume of distribution (less muscle mass);
  • ↓ plasma clearance (less hepatic flow / delayed recovery with infusions)
52
Q

Is vecuronium a great drug for those with liver or kidney problems?

A

Nope

  • Hepatic metabolism
  • Renal dysfunction = ↑E½
53
Q

How does metabolism of Vecuronium change with an obstetric patient?

A
  • Insignificant effects to fetus;
  • ↑ clearance in 3rd trimester (progesterone);
  • ↑ duration early postpartum (give IBW)
54
Q

What will respiratory acidosis post administration of vecuronium do?

A

Prolong NMJ blockade DOA

55
Q

When is respiratory acidosis that occurs after Vecuronium administration a concern?

A

With post-operative hypoventilating patients (ex. post-opioid administration)

56
Q

What is the normal intubating dose, onset and duration of Rocuronium?

A
  • Dose: 0.6 mg/kg
  • Onset: 3-5 minutes
  • Duration: 20-35 minutes
57
Q

What is the RSI intubating dose, onset and duration of Rocuronium?

A
  • Dose: 1.2 mg/kg
  • Onset: 1-2 minutes
  • Duration: 60-90 minutes
58
Q

How is Rocuronium excreted?

A

Unchanged in bile

59
Q

Why will Rocuronium have a longer DoA in the elderly or with liver failure patients?

A

Due to ↓ clearance and ↑ Vd

60
Q

What percentage of Rocuronium is excreted renally?

A

10-30% → only marginally affected by renal failure

Roc is good for CKD patients?

61
Q

What is the intubating dose, onset and duration of Cisatracurium?

A
  • Intubating Dose: 0.1 mg/kg;
  • Onset: 3-5 minutes;
  • Duration of action: 20-35 minutes
62
Q

What is unique about the metabolism of Cisatracurium?

A

Recovery from infusion is NOT affected by time.

63
Q

How is cisatracurium metabolized?

A

Hoffman Elimination

64
Q

What is Hoffman elimination again?

A

A temperature-dependent metabolism of a drug that requires the patient to be normothermic.

65
Q

What changes occur in Cisatracurium when used in an elderly patient? What changes occur in an obese patient?

A
  • Elderly: Slight delay in onset d/t CO;
  • Obese:Duration of action prolonged IF dosed at actual body weight d/t ↑ Vd
66
Q

What changes occur in Cisatracurium when used in an obese patient?

A

Duration of action prolonged IF dosed at actual body weight d/t ↑ Vd

67
Q

What is the intubating dose, onset and duration of Mivacurium?

A
  • Intubating Dose: 0.15 mg/kg;
  • Onset: 2-3 minutes (Conditions less desirable);
  • Duration: 12-20 minutes
68
Q

What was ok about Mivacron?

A

It didn’t work well long-term but it was great for surgeries under 5 mins.

69
Q

How is mivacurium cleared from plasma?

A

Via Plasma cholinesterases

70
Q

Which two NMBDs cause histamine release?

A
  • Atracurium
  • Mivacurium (with massive overdoses)

Anesthesia Pharm 1 Sp 25' (20 decks)

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