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Neuromuscular Blocking Agents > NonDepolarizing Muscle Relaxants > Flashcards

NonDepolarizing Muscle Relaxants Flashcards

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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
Vecuronium ED95, duration, typical intubating dose
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!)
26
Vecuronium infusion rate
2-8 mcg/kg/min
27
Vecuronium metabolism/elimination
30-40% eliminated unchanged in bile, 25% renal excretion, metabolite will accumulate in renal failure and has 80% of potency
28
Rocuronium ED95, onset, duration & intubating dose
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
Rocuronium metabolism/elimination
Eliminated unmetabolized by liver & kidneys (30%), renal and/or liver failure will increase duration of action
30
Rocuronium side effects
Mild vagolytic properties, rare increase in heart rate
31
Reversal drugs for NMDRs work how?
They are anti-cholinesterase, so they inhibit acetylcholinesterase from breaking down ACh at the receptor site and it will build up creating competition
32
Fastest to slowest onset AChE inhibitors in a patient with medium residual paralysis
Edrophonium, neostigmine, pyridostigmine
33
Max dose of Neostigmine
0.06-0.08 mg/kg or total of 5 mg
34
Max dose of Edrophonium
1-1.5 mg/kg
35
When reversing NMDAs what other aspect of anesthesia do you need to think about (in regards to other medications)
Lowering the level of inhaled agents prior to giving reversal is recommended - not as much of a problem with lower solubility agents
36
Edrophonium - chemical structure & how it works
Quaternary amine, attracted to anionic site of AChE, forms an electrostatic bond - concentration dependent, more easily broken, shorter acting reversible competitor of AChE
37
Neostigmine & Pyridostigmine mechanism of action
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
Edrophonium benefits
Fast onset, weaker muscarinic effect
39
Edrophonium typical dose
0.5-1 mg/kg, must be given with atropine or glycopyrrolate
40
Atropine typical dose due with edrophonium, onset & duration
15 mcg/kg, onset 1-2 minutes, lasts 1-2 hours
41
Edrophonium CV effects
Weak muscarinic- less slowing of HR
42
Edrophonium excretion
Renal 75%, half life will almost double with renal failure -- onset/duration not affected by aging alone.
43
Neostigmine benefts
Longer duration than edrophonium, better for deep blockade reversal
44
Neostigmine onset, peak, & duration
onset is 5 minutes, peak is 10 minutes, duration is 60+ minutes
45
Neostigmine dose
0.04-0.08 mg/kg
46
Glycopyrrolate dose with neostigmine
0.2 mg/mg neo (25-75 mcg/kg)
47
Atropine with neostigmine
Can be used at 0.02-0.03 mg/kg but will have greater tachycardia
48
Neostigmine CV effects
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
Neostigmine Respiratory effects
Bronchoconstriction (ACh causes bronchodilation), increases oral secretions
50
What happens if you give too much neostigmine?
>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
Neostigmine & GI effects
Increases motility & gastric secretions, may increase PONV
52
Neostigmine half life
80 minutes (180 minutes with renal failure)
53
Neostigmine clearance
Renal 50%
54
How neostigmine works
Inhibits both AChE & pseudocholinesterase
55
Pyridostigmine benefits
Slightly longer with less muscarinic side effects
56
Pyridostigmine onset
10-15 minutes
57
Pyridostigmine duration
>2 hours (good for reversal of deep blockade by long acting NMDRs)
58
Pyridostigmine dose
0.1-0.25 mg/kg with 0.05 mg glyco/mg pyridostigmine
59
Pyridostigmine CV effects
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
Pyridostigmine elimination
Renal 75%
61
Pyridostigmine half life
90-110 minutes with normal renal function (>350 minutes with renal failure)
62
Glycopyrrolate dose
10-20 mcg/kg
63
Glycopyrrolate onset
2-3 minutes
64
Glycopyrrolate duration
2-4 hours
65
Atropine dose
15 mcg/kg
66
Atropine onset
1-2 minutes
67
Atropine duration
1-2 hours

Neuromuscular Blocking Agents (2 decks)

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