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Neuromuscular Blocking Agents > NonDepolarizing Muscle Relaxants > Flashcards

NonDepolarizing Muscle Relaxants Flashcards

1
Q

How do non-depolarizing muscle relaxants work?

A

Competitively bind with one of the 2 alpha subunits on the postjunctional nicotinic cholinergic receptor & prevent interaction with ACh- prevents opening of ion channel. As long as NMDR>ACh - muscle spindle cannot contract

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2
Q

2 groups of non-depolarizing muscle relaxants

A

Benzylisoquinolinium & aminosteroid

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3
Q

Benzylisoquinolinium non-depolarizing muscle relaxants

A

dTc, atracurium, cis-atracurium

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4
Q

Aminosteroid compound non-depolarizing muscle relaxants

A

Pancuronium, vecuronium, rocuronium, pipercuronium

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5
Q

How do non-depolarizing muscle relaxants bind to the nACHr

A

They are quaternary ammonium chemical compounds with at least 1 positively charged nitrogen atom that binds to the alpha subunit

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6
Q

What is typical dosing for NMBAs?

A

1.5-2 times the ED95 to ensure that patients who may be resistant to effects of the relaxant develop at least 90% blockade

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7
Q

Ideal body weight

A

5 foot person should be 100 pounds, women get 5 pounds per inch, men get 7 pounds per inch - doses based on this

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8
Q

What happens to the speed of onset as potency of a non-depolarizing muscle relaxants increases? Side effects?

A

As potency increases, speed of onset decreases, side effects decrease

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9
Q

Benzylisoquinolinium & vagolytic/histamine properties?

A

No vagolysis, increases histamine release - may cause bronchospasm in reactive airway or significant hypotension (dependent upon total dose & speed of injection)

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10
Q

Benzylisoquinolinium excretion

A

Most by Kidneys - BUT (Cis)Atracurium - Hofmann elimination (at normal temp & pH) & ester hydrolysis by non-specific esterases (do not need functional liver or kidney)

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11
Q

Atracurium ED 95, onset, duration

A

0.25 mg/kg, onset 3-5 minutes, duration 30-45 minutes (if give 2x ED95- speed of onset decreases to 2-3 minutes, increases duration to 60 minutes). Can redose throughout surgery with no buildup.

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12
Q

Atracurium metabolism

A

Ester hydrolysis & Hofmann elimination (higher temp & pH eliminate faster.. decreases muscle relaxation time).. this will create the metabolite Laudanosine

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13
Q

What is Laudanosine

A

Metabolite produced by Hofmann reaction with atracurium, CNS stimulant, can increase MAC of inhaled anesthetic used (may accumulate during infusion)

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14
Q

Atracurium side effects

A

2.5-3x ED95- may cause hypotension & tachycardia from histamine release- may be decreased by admin of H1 or H2 antagonist

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15
Q

Cis-Atracurium potency versus Atracurium

A

4 times as potent, no histamine release at typical dose = no CV side effects at intubating dose

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16
Q

Cis-Atracurium metabolism

A

Hofmann elimination, produces much less laudanosine because 1/4 of the dose is required for muscle relaxation, not organ specific

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17
Q

Cis-Atracurium ED95, onset, duration, intubating dose

A

0.05 mg/kg, onset 3-5 minutes, duration 20-35 minutes, intubating dose 0.1-0.2 mg/kg but lasts 60-70 minutes

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18
Q

Pancuronium potency

A

Highly potent

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19
Q

Pancuronium side effects

A

Tachycardia (vagolysis)

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20
Q

Pancuronium ED95, onset, duration, intubating dose

A

0.07 mg/kg, onset 3-5 minutes, duration 60-90 minutes, intubating: 0.08-0.1 mg/kg due to tachycardia

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21
Q

What causes the vagolytic activity of steroidal NMBAs?

A

Action at muscarinic receptor in ANS & inhibition of catecholamine reuptake at SNS terminals.. tachycardia from selective blockade of cardiac muscarinic receptors in SA node

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22
Q

What is pancuronium good for?

A

Long cases where a little tachycardia wouldn’t hurt (high dose opioids or beta blockers)

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23
Q

Pancuronium metabolism & elimination

A

Eliminated by the kidneys - clearance decreases up to 50% in renal failure. 10-20% of panc is metabolized to active metabolite - has 1/2 the duration of pancuronium, also eliminated by the kidney

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24
Q

Vecuronium potency

A

More potent than panc

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25
Q

Vecuronium ED95, duration, typical intubating dose

A

0.03-0.05 mg/kg, 25-40 minutes with intubating dose, 0.2-0.2 mg/kg is intubating dose (can go as high as 4x ED95 with no CV effects but will last longer!)

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26
Q

Vecuronium infusion rate

A

2-8 mcg/kg/min

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27
Q

Vecuronium metabolism/elimination

A

30-40% eliminated unchanged in bile, 25% renal excretion, metabolite will accumulate in renal failure and has 80% of potency

28
Q

Rocuronium ED95, onset, duration & intubating dose

A

0.3 mg/kg, 3-5 minutes, lasts 18-30 minutes (at 0.3).. intubating dose is 0.4-0.6 mg/kg in about 3 minute window but lasts 25-45 minutes. You CAN get 50 second intubating conditions with 1.2 mg/kg but this will cause a 60-120 minute duration

29
Q

Rocuronium metabolism/elimination

A

Eliminated unmetabolized by liver & kidneys (30%), renal and/or liver failure will increase duration of action

30
Q

Rocuronium side effects

A

Mild vagolytic properties, rare increase in heart rate

31
Q

Reversal drugs for NMDRs work how?

A

They are anti-cholinesterase, so they inhibit acetylcholinesterase from breaking down ACh at the receptor site and it will build up creating competition

32
Q

Fastest to slowest onset AChE inhibitors in a patient with medium residual paralysis

A

Edrophonium, neostigmine, pyridostigmine

33
Q

Max dose of Neostigmine

A

0.06-0.08 mg/kg or total of 5 mg

34
Q

Max dose of Edrophonium

A

1-1.5 mg/kg

35
Q

When reversing NMDAs what other aspect of anesthesia do you need to think about (in regards to other medications)

A

Lowering the level of inhaled agents prior to giving reversal is recommended - not as much of a problem with lower solubility agents

36
Q

Edrophonium - chemical structure & how it works

A

Quaternary amine, attracted to anionic site of AChE, forms an electrostatic bond - concentration dependent, more easily broken, shorter acting reversible competitor of AChE

37
Q

Neostigmine & Pyridostigmine mechanism of action

A

Bind to anionic & esteratic site on AChE, binding at esteratic site creates carbamylated enzyme that has a half-life of about 30 minutes - ACh builds up at the receptor site. Allows competitive inhibition between ACh & NMDR

38
Q

Edrophonium benefits

A

Fast onset, weaker muscarinic effect

39
Q

Edrophonium typical dose

A

0.5-1 mg/kg, must be given with atropine or glycopyrrolate

40
Q

Atropine typical dose due with edrophonium, onset & duration

A

15 mcg/kg, onset 1-2 minutes, lasts 1-2 hours

41
Q

Edrophonium CV effects

A

Weak muscarinic- less slowing of HR

42
Q

Edrophonium excretion

A

Renal 75%, half life will almost double with renal failure – onset/duration not affected by aging alone.

43
Q

Neostigmine benefts

A

Longer duration than edrophonium, better for deep blockade reversal

44
Q

Neostigmine onset, peak, & duration

A

onset is 5 minutes, peak is 10 minutes, duration is 60+ minutes

45
Q

Neostigmine dose

A

0.04-0.08 mg/kg

46
Q

Glycopyrrolate dose with neostigmine

A

0.2 mg/mg neo (25-75 mcg/kg)

47
Q

Atropine with neostigmine

A

Can be used at 0.02-0.03 mg/kg but will have greater tachycardia

48
Q

Neostigmine CV effects

A

Profound bradycardia (vagal ACh stimulation), dysrhythmias & arrest have been noted, glyco blocks muscarinic effects of ACh, stimulation of autonomic ganglia & release of epinephrine from adrenal medulla results in increased HR & BP

49
Q

Neostigmine Respiratory effects

A

Bronchoconstriction (ACh causes bronchodilation), increases oral secretions

50
Q

What happens if you give too much neostigmine?

A

> 0.08 mg/kg or 5 mg total can create muscular weakness due to excessive pseudocholinesterase at the NMJ, may result in cholinergic crisis

51
Q

Neostigmine & GI effects

A

Increases motility & gastric secretions, may increase PONV

52
Q

Neostigmine half life

A

80 minutes (180 minutes with renal failure)

53
Q

Neostigmine clearance

A

Renal 50%

54
Q

How neostigmine works

A

Inhibits both AChE & pseudocholinesterase

55
Q

Pyridostigmine benefits

A

Slightly longer with less muscarinic side effects

56
Q

Pyridostigmine onset

A

10-15 minutes

57
Q

Pyridostigmine duration

A

> 2 hours (good for reversal of deep blockade by long acting NMDRs)

58
Q

Pyridostigmine dose

A

0.1-0.25 mg/kg with 0.05 mg glyco/mg pyridostigmine

59
Q

Pyridostigmine CV effects

A

Profound bradycardia (vagal ACh stimulation), dysrhythmias & arrest have been noted, glyco blocks muscarinic effects of ACh, stimulation of autonomic ganglia & release of epinephrine from adrenal medulla results in increased HR & BP

60
Q

Pyridostigmine elimination

A

Renal 75%

61
Q

Pyridostigmine half life

A

90-110 minutes with normal renal function (>350 minutes with renal failure)

62
Q

Glycopyrrolate dose

A

10-20 mcg/kg

63
Q

Glycopyrrolate onset

A

2-3 minutes

64
Q

Glycopyrrolate duration

A

2-4 hours

65
Q

Atropine dose

A

15 mcg/kg

66
Q

Atropine onset

A

1-2 minutes

67
Q

Atropine duration

A

1-2 hours

Neuromuscular Blocking Agents (2 decks)

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