Neuromuscular Blocking Agents Flashcards
Succinylcholine advantages
Most rapid onset
Shortest duration
RSI
Succinylcholine disadvantages
Contraindicated in burn and stroke
Can cause lethal hyperkalemia due to extrajunctional Ach receptors
MH!!!
Succinylcholine dose
1-2mg/kg
Typically we give 100 in the OR
This might not be enough for larger patients
Vecuronium dose
0.1 mg/kg
We typically give 10 mg
Rocuronium advantages
Best alternative to sux for RSI
Rocuronium dose
- 6 mg/kg
1. 2 mg/kg for RSI
Cisatracurium advantages
Used is renal and liver disease patients
Does not rely on liver or kidney for metabolism or excretion
Cis dose
0.2 mg/kg
Cis onset and duration
2 min
1 hour
Neostogmine MOA
Anticholinesterase that increases the amount of acetylcholine throughout the body
This reverses the blockade
Neostigmine dose
0.07 mg/kg up to 5 mg
Can be decreased depending on TOF
Glycopyrrolate use
Offsets the bradycardia caused by acetylcholine
Glycopyrrolate dose
0.2 for every mg of neostigmine given
For quick calculation you can just draw up the same volume of glyco as neo
Nondepolarizing NMBDs MOA
Compete with ACh for alpha subunit of the nicotinic receptor
Describe the characteristics of sux phase I and phase II blocks
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
Calcium dependent presynaptic release of ACh
Effects of calcium and magnesium levels
High magnesium inhibits (OB)
High calcium increase ACh release, so the patient will need more muscle relaxant
What is the structure of the postjunctional ACh receptor?
Where is acetylcholinesterase located?
How does the structure of extra junction all ACh receptor differ?
5protein units
2 alpha units where NMBs bind
Postjunctional membrane, near the receptor
Gamma subunit, stays open longer
Name the enzyme that breaks down sux
Butyrylcholinesterase AKA pseudocholinesterase
Remi is broken down by nonspecific cholinesterase
esmolol is broken down by RBC cholinesterase
Is sux contraindicated in CP?
No
Renal failure and its effects of panc, vec/roc, cis, and mica/sux
Pancuronium starts with a P, excreted in the pee, so longest
Vec and roc are intermediate
Cisatracurium is spontaneously degraded by Hoffman elimination
Is sux contraindicated in liver disease?
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
Which part of the NMJ is affected in Eaton lambert?
Which NMBs are they more sensitive to? Why?
Presynaptic Ca channel
Both depoland non depol because there are more ACh receptors and less synaptic ACh to compete with
How does myasthenia gravis affect the pt response to NMB?
Less postjunctional ACh receptors
Therefore resistance to Sux and sensitive to ND
How does myotonic dystrophy affect contraction?
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
Which ion channel causes potassium fluctuations in periodic paralysis?
How do you treat it?
Na
Acetazolamide
Which form of periodic paralysis should you avoid SCh?
Hyperkalemic (duh)
What does the dibucaine number tell you?
If someone has a dinucaine number <80, which drugs could be prolonged?
Quality of pseudocholinesterase
SCh, mivacurium, and ester LAs
NOT remi or esmolol
Cyclophosphamide and echothiophate inhibit and inactivate which enzyme?
How would you treat prolonged recovery due to these drugs?
Pseudocholinesterase
ABC, FFP if necessary
Which NMB is vagolytic?
Which NMB causes bradycardia?
Pancuronium
SCh (cholinergic at muscarinic receptor)
Mac dose rationale of neostigmine
Ceiling: excess ACh can cause a depolarizing block like SCh
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?
Neostigmine inhibits pseudocholinesterase
Both botulism and tetanus block presynaptic release of a ACh. So why then are tetanic pts contracted?
Tetanus toxin block inhibitory neurons
Nerve gases and organophosphate do what?
Block acetylcholinesterase
TOF >0.9 could still mean poor swallow and risk of aspiration
Remember that
Which drugs does butyrylcholinesterase act on?
SCh
Ester anesthetics
Mivacurium
What is the MOA of donepezil?
Acetylcholinesterase inhibitor
Reversible!
It is a central inhibitor it crosses the blood brain barrier
How does Aricept interact with SCh?
Nondepolarizers?
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
Are skeletal muscles nicotinic or muscarinic
Nicotinic
Will hypocalcemia attenuate or prolong presynaptic release of acetylcholine?
Attenuate, the presynaptic neuron needs to influx calcium in order to release acetylcholine
Under these conditions you will need less NMB
What affect does lithium have on NMB?
Lithium potentiates both nondepolarizer’s and depolarizers
It also decreases Mac
