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Spr24 Pharm II > NMBDs: Non-depolarizing (Exam III) Stephen's Cards > Flashcards

NMBDs: Non-depolarizing (Exam III) Stephen's Cards Flashcards

1
Q

What are the 4 main differences between all of the non-depolarizing muscle blockers?

A
  • Onset;
  • Duration of action;
  • Rate of recovery;
  • Metabolism
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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

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

A

Succinylcholine

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4
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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5
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 each others effects.

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6
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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7
Q

What does fade suggest?

A

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

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8
Q

What generally 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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9
Q

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

A
  • Underlying diseases
  • Pre-op meds
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10
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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11
Q

Which non-depolarizing blocker has a required dose that both causes blockade and adverse CV effects?

A

Pancuronium

Essentially narrow/no therapeutic index

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12
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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13
Q

Who is most often affected by critical illness myopathy?

A
  • Had MODS and ventilated > 6 days;
  • Usually had an aminosteroid NMBD;
  • Administered Glucocorticoids prior to NMBD
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14
Q

Why is critical illness myopathy thought to occur?

A

Possible ↓ clearance or active metabolites

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15
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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16
Q

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

A
  • Diuretics
  • Corticosteroids
  • Metoclopramide
  • Local Anesthestics
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17
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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18
Q

How will sympathomimetics such as ephedrine or epinephrine affect NMBDs?

A

↓ onset time (Drug works faster d/t ↑CO)

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19
Q

How will sympatholytics such as esmolol affect NMBDs?

A

↑ onset time (Drug works slower)

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20
Q

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

A

Hypothermia will increase NMBD duration

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

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21
Q

How does acute hypokalemia affect D-NMBs and non-depolarizing blockers?

A

↓ Vᵣₘ (hyperpolarizes)

  • Resistance to D-NMBDs
  • Sensitivity to ND-NMBD’s
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22
Q

How does acute hyperkalemia affect non-depolarizing blockers?

A

↑ Vᵣₘ

  • Sensitivity to D-NMBDs;
  • Resistance to ND-NMBDs

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

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23
Q

How do burns affect non-depolarizing blockers?

A

Burns patients within the 10 - 60 days post-burn will have a resistance to NMBDs.

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24
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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25
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

26
Q

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

A

The more “paralyzed” = more resistant d/t proliferation of extrajunctional nAChRs

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

27
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)

28
Q

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

A
  • Quaternary ammonium group
29
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)

30
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
31
Q

What is the most common (only used) long acting NMBD?

A

Pancuronium (Pavulon)

32
Q

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

A
  • Dose: 0.1mg/kg;
  • Onset: 3-5 minutes;
  • Duration: 60-90 minutes
33
Q

How is the majority of Pancuronium eliminated?

A
  • 80% eliminated unchanged in urine
34
Q

What patients would you not want to use pancuronium on?

A

Liver and Kidney cases (prolonged elimination and metabolism).

35
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
36
Q

What CV effects do we see with Pancuronium?

A

Sympathomimetic: from vagal blockade

  • ↑ HR;
  • ↑ MAP;
  • ↑ CO;
37
Q

What occurs with norepinephrine after pancuronium administration?

A
  • ↑NE release
  • ↓NE reuptake
38
Q

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

A

Approximately 1/3 duration of action

39
Q

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

A

Minimal/absent cardiovascular effects

40
Q

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

A

Approximately 20min post administration

41
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
42
Q

What is the main way Vecuronium is metabolized? Excreted?

A
  • 70% Hepatic metabolism
  • 3-desacetylvecuronium 50-80% as potent (but rapidly converted to metabolite with 1/10 the effects)
  • 30% unchanged excreted in kidneys
43
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)
44
Q

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

A

Nope

  • Hepatic metabolism
  • Renal dysfunction = ↑E½
45
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)
46
Q

What will respiratory acidosis post administration of vecuronium do?

A

Prolong NMJ blockade

47
Q

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

A

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

48
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
49
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
50
Q

How is Rocuronium primarily excreted?

A

Unchanged in bile

51
Q

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

A

Due to ↓ clearance and ↑ Vd

52
Q

What percentage of Rocuronium is excreted renally?

A

10-30% → only marginally affected by renal failure

Roc is better than Vec for CKD patients?

53
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
54
Q

What is unique about the metabolism of Cisatracurium?

A

Recovery from infusion is NOT affected by time.

55
Q

How is cisatracurium metabolized?

A

Hoffman Elimination (pH and temp dependent)

56
Q

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

A
  • Elderly: Slight delay in onset d/t CO
57
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

58
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
59
Q

How is mivacurium cleared from plasma?

A

Via Plasma cholinesterases

60
Q

Which two NMBDs cause histamine release?

A
  • Atracurium
  • Mivacurium (with massive overdoses)

Spr24 Pharm II (32 decks)

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