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Anesthesia Pharmacology > Lecture 14 (Exam 3 Nondepolarizing NMBD) > Flashcards

Lecture 14 (Exam 3 Nondepolarizing NMBD) Flashcards

1
Q

Selection of Non-depolarizing NMBD is influenced by what factors?

A

Onset
Duration of action
Rate of Recovery
Metabolism

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2
Q

What is the MOA of Non-depolarizing NMBD?

A

Act at pre-junctional sites to block ACh release.
Also acts on BOTH alpha subunits of the post-junctional nAChR.
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 in twitch response with non-depolarizing NMBD?

A

Fade suggest some fibers are contracting while some are blocked. Some receptors are more susceptible to NMBD than others.

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6
Q

What happens if you intubate with Vecuronium and you give Rocuronium for maintenance?

A

The two non-depolarizing NMBDs can potentiate each other and prolong the duration of the recovery period.

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7
Q

The cardiovascular effects of non-depolarizing NMBD are due to what factors?

A

Release of histamine
Effects on cardiac muscarinic receptors
Effects on nAChRs at autonomic ganglia

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8
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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9
Q

Most NMBDs have a __________ autonomic margin of safety.

A

Wide

Vec, Roc, Cis

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10
Q

What non-depolarizing NMBD has the same dose for ED95 and autonomic nervous system stimulation?

What is the side effect of this drug?

A

Pancuronium (sympathomimetic) will result in tachycardia at the ED95 dose. This can be offset by giving a narcotic.

Be mindful in administering pancuronium in patients with coronary artery disease, aortic stenosis, cardiac issues, etc…

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11
Q

What is critical illness myopathy?

A

Skeletal muscle weakness occurs weeks to months after the NMBD drip is discontinued.

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12
Q

Factors that contribute to critical illness myopathy included:
Patients with __________ who were ventilated for six days.
__________ prior to NMBD may enhance risk.
_________ (chemical classification) blocker

A

Multi-System Organ Failure
Glucocorticoids
Aminosteroid Blocker

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13
Q

If patients have predosing factors leading to critical illness myopathy, what actions must be taken?

A

Nerve monitoring (continuous)
More Sedation
More Analgesia
Small Doses of NMBD

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14
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

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15
Q

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

A

Enhance or prolong the blockade d/t depression of cholinesterase activity. Most of these drugs also decrease ACh release.

clarified by Dr. Kane

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16
Q

______ is dosed on ACTUAL body weight.

______ is dosed on IDEAL body weight.

A

Succinylcholine (Depolarizing NMBD)

Non-depolarizing NMBD

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17
Q

What is the altered response if a non-depolarizing NMBD is given with magnesium?

MOA?

A

The blockade will be enhanced.

MOA: Decreases prejunctional release of ACh and decreases sensitivity to the postjunctional membrane.

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18
Q

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

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

A

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

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

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19
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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20
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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21
Q

Acute hypokalemia with NMBD
________ cell membrane.
Resistance to ___________
Increased sensitivity to _________

A

Acute hypokalemia with NMBD
Hyperpolarize cell membrane.
Resistance to depolarizing NMBD
Increased sensitivity to non-depolarizing NMBD

Hypokalemia will increase the concentration gradient of the K+, and caused more K+ to move out of the cell, increasing resting membrane potential (making the resting membrane potential more negative). This will make the cell harder to depolarize, which is why there is resistance to depolarizing NMBD.

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22
Q

Acute hyperkalemia with NMBD.
There will be a partially ___________ cell membrane.
Increases effect of __________
Resistance to ___________

A

Acute hyperkalemia with NMBD.
There will be a partially depolarized cell membrane.
Increases effect of depolarizing NMBD
Resistance to non-depolarizing NMBD

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23
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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24
Q

NMBD on stroke patients.
Paretic Arm
Unaffected Side
MOA

A

Paretic Arm: Resistance compared to the unaffected side
Unaffected Side: Resistance compared to normal patients
MOA: Proliferation of extrajunctional nAChRs

25
Q

Which NMBD is more prone to allergic reactions?

A

Succinylcholine

26
Q

NMBD may have cross-sensitivity to other ___________ groups.

A

quaternary ammonium (soaps and cosmetics)

27
Q

Women are more sensitive to nondepolarizing NMBD (less muscle mass in women):
Need _____% less vecuronium
Need _____% less rocuronium

The duration of the block is greater in women.

A

22% LESS VEC
30% LESS ROC

28
Q

What is our long-acting NMBD?
What chemical group is the drug?

A

Pancuronium (Pavulon)
Aminosteroid

29
Q

What is the intubating dose of Pancuronium?
Onset:
Duration:

A

Pancuronium
Dose: 0.1 mg/kg
Onset: 3-5 minutes
Duration: 60-90 minutes

30
Q

What percentage of Pavulon is eliminated in the urine?

31
Q

Pancuronium in renal failure:
_______ % (range) decreased plasma clearance

A

30-50% decrease in plasma clearance

32
Q

Pancuronium in liver disease:
Increase ______
______ initial dose is needed.
_______ elimination time.

Pancuronium in aging:
_______ plasma clearance d/t renal functions.

A

Pancuronium in liver disease:
Increase Vd
Larger initial dose is needed.
Prolonged elimination time.

Pancuronium in aging:
Decreases plasma clearance d/t renal functions.

33
Q

What are the cardiovascular effects of pancuronium?

A

Increase HR, MAP, and CO.
Release NE presynaptically and blocks the reuptake of NE.
No histamine release.

34
Q

Compared with long-acting NMBD.

Intermediated NMBD have a _______ onset of maximum blockade.

______ duration of action compared to long-acting NMBD.

_________ CV effects

Antagonized by anticholinesterase drugs in ______ mins.

A

Compared with long-acting NMBD.

Intermediated NMBD have a similar onset of maximum blockade.

1/3 duration of action compared to long-acting NMBD.

Minimal/absent CV effects

Antagonized by anticholinesterase drugs in 20 mins.

35
Q

Name your 4 intermediated non-depolarizing NMBD.

A

Vecuronium
Rocuronium
Cisatracurium
Atracurium

36
Q

What chemical group does vecuronium belong to?

A

Aminosteroid

37
Q

Vecuronium
Intubating Dose:
Onset:
Duration:

A

Vecuronium
Intubating Dose: 0.1 mg/kg
Onset: 3-5 minutes
Duration: 20-35 minutes

38
Q

Where is Vec metabolized and excreted?

A

Metabolized in the liver (70%), excreted in the kidneys.

Liver and/or kidney disease will result in the drug being in the system longer.

39
Q

Repeat doses or infusions of vecuronium will have ______ effects.

A

cumulative

d/t active metabolite 3-desacetylvecuronium 50 to 80% as potent.

40
Q

Describe the metabolism of vecuronium in the elderly.

A

Decrease Vd (less muscle mass)
Decrease plasma clearance (less hepatic flow)
Delayed recovery with infusion.

41
Q

Describe the metabolism of vecuronium in obstetrics.

A

No effect on the fetus.
Increase clearance in 3rd trimester (progesterone)
Prolonged duration in early postpartum (give IBW)

42
Q

Acid-base changes when you give vecuronium is dependent on what?

A

When you gave the drug related to when the acid-base change occurred.

If there is respiratory acidosis prior to NMBD, there will be no prolonged blockade.

If there is respiratory acidosis following NMBD, there will be a prolonged blockade.

43
Q

What are the cardiovascular effects of vecuronium?

A

None and no histamine release.

44
Q

What chemical group is Rocuronium in?

A

Aminosteroid

45
Q

Rocuronium
Normal intubating dose:
Onset:
Duration:

A

Rocuronium
Normal intubating dose: 0.6 mg/kg
Onset: 3-5 minutes
Duration:20-35 minutes

46
Q

Rocuronium
RSI dose:
Onset:
Duration of action:

A

Rocuronium
RSI dose: 1.2 mg/kg
Onset: 1-2 minutes
Duration of actions: 40-70 minutes

47
Q

How is rocuronium excreted?

What conditions will result in a longer duration of action for rocuronium?

A

Excreted unchanged in the bile. 10-30% excreted in the kidneys.

Liver failure and elderly patients

48
Q

Cardiovascular effects of rocuronium.

A

No histamine release.

Slight vagolytic effect, slows the HR a little bit.

49
Q

What is the chemical group of cisatracurium?

A

Benzylisoquinolone

50
Q

Cisatracurium
Intubating Dose:
Onset:
Duration:

A

Cisatracurium
Intubating Dose: 0.1 mg/kg
Onset: 3 -5 minutes
Duration: 20 - 35 minutes

51
Q

Cisatracurium is a cis-isomer of _________.

Recovery of cisatracurium infusion is not affected by ________.

How is cisatracurium degraded?

A

Atracurium

Time

Hoffman elimination (pH and temperature dependent), does not use plasma cholinesterase to degrade.

52
Q

What is the metabolism of cisatracurium in the elderly and obese?

A

Elderly: Slight delay in onset d/t CO

Obese: Duration of action is prolonged if dosed at actual bodyweight d/t high Vd (use IBW).

53
Q

Cardiovascular effects of Cisatracurium

A

No histamine effect
CV stability

54
Q

Cardiovascular effect of Atracurium

A

There is histamine effect

55
Q

What chemical group is mivacurium?

A

Benzylisoquinolone

56
Q

Mivacurium
Intubating Dose
Onset:
Duration of Action

A

Mivacurium
Intubating Dose: 0.15 mg/kg
Onset: 2-3 minutes (patient moves)
Duration of Action: 12-20 minutes

57
Q

What are the three stereoisomers of mivacurium?
Which ones are involved in neuromuscular blocking activity?

A

Cis-cis
Cis-trans blocking activity
Trans-trans blocking activity

58
Q

How is mivacurium broken down?

A

Plasmacholinesterases

59
Q

Cardiovascular effects of mivacurium?

A

Histamine release with 3x ED 95 dose

Anesthesia Pharmacology (20 decks)

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