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Anesthesia Made Easy > Neuromuscular Blocking Agents > Flashcards

Neuromuscular Blocking Agents Flashcards

1
Q

Succinylcholine advantages

A

Most rapid onset
Shortest duration
RSI

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2
Q

Succinylcholine disadvantages

A

Contraindicated in burn and stroke
Can cause lethal hyperkalemia due to extrajunctional Ach receptors
MH!!!

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3
Q

Succinylcholine dose

A

1-2mg/kg
Typically we give 100 in the OR
This might not be enough for larger patients

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4
Q

Vecuronium dose

A

0.1 mg/kg

We typically give 10 mg

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5
Q

Rocuronium advantages

A

Best alternative to sux for RSI

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6
Q

Rocuronium dose

A
  1. 6 mg/kg

1. 2 mg/kg for RSI

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7
Q

Cisatracurium advantages

A

Used is renal and liver disease patients

Does not rely on liver or kidney for metabolism or excretion

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8
Q

Cis dose

A

0.2 mg/kg

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9
Q

Cis onset and duration

A

2 min

1 hour

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10
Q

Neostogmine MOA

A

Anticholinesterase that increases the amount of acetylcholine throughout the body
This reverses the blockade

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11
Q

Neostigmine dose

A

0.07 mg/kg up to 5 mg

Can be decreased depending on TOF

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12
Q

Glycopyrrolate use

A

Offsets the bradycardia caused by acetylcholine

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13
Q

Glycopyrrolate dose

A

0.2 for every mg of neostigmine given

For quick calculation you can just draw up the same volume of glyco as neo

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14
Q

Nondepolarizing NMBDs MOA

A

Compete with ACh for alpha subunit of the nicotinic receptor

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15
Q

Describe the characteristics of sux phase I and phase II blocks

A

I: depolarized, TOF ratio is 1. No further contractions
II: receptor available sux defused away, but still not a normal response to stimulation, TOF ratio has a fade

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16
Q

Calcium dependent presynaptic release of ACh

Effects of calcium and magnesium levels

A

High magnesium inhibits (OB)

High calcium increase ACh release, so the patient will need more muscle relaxant

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17
Q

What is the structure of the postjunctional ACh receptor?
Where is acetylcholinesterase located?
How does the structure of extra junction all ACh receptor differ?

A

5protein units
2 alpha units where NMBs bind
Postjunctional membrane, near the receptor
Gamma subunit, stays open longer

18
Q

Name the enzyme that breaks down sux

A

Butyrylcholinesterase AKA pseudocholinesterase
Remi is broken down by nonspecific cholinesterase
esmolol is broken down by RBC cholinesterase

19
Q

Is sux contraindicated in CP?

A

No

20
Q

Renal failure and its effects of panc, vec/roc, cis, and mica/sux

A

Pancuronium starts with a P, excreted in the pee, so longest
Vec and roc are intermediate
Cisatracurium is spontaneously degraded by Hoffman elimination

21
Q

Is sux contraindicated in liver disease?

A

No, but you may need a higher dose because of extra water space and higher Vd
The block may last longer because liver makes plasma cholinesterase

22
Q

Which part of the NMJ is affected in Eaton lambert?

Which NMBs are they more sensitive to? Why?

A

Presynaptic Ca channel

Both depoland non depol because there are more ACh receptors and less synaptic ACh to compete with

23
Q

How does myasthenia gravis affect the pt response to NMB?

A

Less postjunctional ACh receptors

Therefore resistance to Sux and sensitive to ND

24
Q

How does myotonic dystrophy affect contraction?

A

Dystrophin is messed up, so contraction happens normally, but relaxation takes WAY longer
For this reason, you should avoid SCh
Response to ND is normal, but it does not relieve contracture

25
Q

Which ion channel causes potassium fluctuations in periodic paralysis?
How do you treat it?

A

Na

Acetazolamide

26
Q

Which form of periodic paralysis should you avoid SCh?

A

Hyperkalemic (duh)

27
Q

What does the dibucaine number tell you?

If someone has a dinucaine number <80, which drugs could be prolonged?

A

Quality of pseudocholinesterase
SCh, mivacurium, and ester LAs
NOT remi or esmolol

28
Q

Cyclophosphamide and echothiophate inhibit and inactivate which enzyme?
How would you treat prolonged recovery due to these drugs?

A

Pseudocholinesterase

ABC, FFP if necessary

29
Q

Which NMB is vagolytic?

Which NMB causes bradycardia?

A

Pancuronium

SCh (cholinergic at muscarinic receptor)

30
Q

Mac dose rationale of neostigmine

A

Ceiling: excess ACh can cause a depolarizing block like SCh

31
Q

After reversal and extubation, a pt has laryngospasm and is give SCh for reintubation. You notice that they remained paralyzed for longer than usual with SCh. Why?

A

Neostigmine inhibits pseudocholinesterase

32
Q

Both botulism and tetanus block presynaptic release of a ACh. So why then are tetanic pts contracted?

A

Tetanus toxin block inhibitory neurons

33
Q

Nerve gases and organophosphate do what?

A

Block acetylcholinesterase

34
Q

TOF >0.9 could still mean poor swallow and risk of aspiration

A

Remember that

35
Q

Which drugs does butyrylcholinesterase act on?

A

SCh
Ester anesthetics
Mivacurium

36
Q

What is the MOA of donepezil?

A

Acetylcholinesterase inhibitor

Reversible!

It is a central inhibitor it crosses the blood brain barrier

37
Q

How does Aricept interact with SCh?

Nondepolarizers?

A

Donepezil can also cross over and Inhibit pseudocholinesterase which will prolong the action of succinylcholine

Because donepezil inhibits acetylcholinesterase there will be increased acetylcholine in the cleft which could possibly require higher doses to maintain blockade with a non-depolarizer

Manufacturers recommend withholding Aricept at least two weeks prior to scheduled surgeries

38
Q

Are skeletal muscles nicotinic or muscarinic

A

Nicotinic

39
Q

Will hypocalcemia attenuate or prolong presynaptic release of acetylcholine?

A

Attenuate, the presynaptic neuron needs to influx calcium in order to release acetylcholine

Under these conditions you will need less NMB

40
Q

What affect does lithium have on NMB?

A

Lithium potentiates both nondepolarizer’s and depolarizers

It also decreases Mac

Anesthesia Made Easy (8 decks)

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