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23 terms

Neuromuscular Blockers

WVSOM Maloney
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What are the clinical uses for NMB
1. Relax skeletal muscle for surgical procedures and tracheal intubation
2. Prevent fractures and dislocations associated with ECT
3. Control muscle spasms of tetanus
4. Sustained neuromuscular blockade in critically ill patients
Name the NMB agents
Tubucurarine
Atracurium
Cisatracurium
Mivacurium
Pancuronium
Rocuronium
Vecuronium
Succinylcholine (only depolarizing drug listed)
What is the mechanism of action for the non depolarizing blockers
competitive antagonist of the nAChR in the NMJ
What is the sequence of paralysis of muscles
Eyes (first)
Face (first)
Limbs
Abdominal
Intercostals
Diaphragm (last)

- function is recovered in reverse order
How can you reverse the effects of pancuronium
...
3 important notes about ALL NMB
Do not enter CNS
Do not affect sensory neurons
are not anesthetic or analgesic
What is succinylcholine
A depolarizing blocker
What do you notice about the chemical composition of succinylcholine
...
What is the mechanism of action for succinylcholine
- acts like ACh but it produces a longer effect at the NMJ

- Resistant to hydrolysis by AChE in the NMJ
- Metabolized by butrylcholinesterase in liver
(two phases of Block)
Name the 2 phases of succinylcholine block
Phase I (depolarizing)
- prolonged depolarizing
a. Fasciculations
b. Can't repolarize
c. E-C coupling requires endplate repolarization and repetitive firing to maintain muscle tension
d. End result flaccid paralysis

Phase II (desensitizing)
- Continued exposure causes the membrane to gradually depolarize, but is also desensitized. It can not easily be depolarized again
- Later in Phase II it begins to act like a non depolarizing blocker
Will neostigmine reverse the effects of succinylcholine phase I block
Resistant to ACh Esterase inhibitors
Will neostigmine reverse the effects of succinylcholine phase II block
Cholinesterase inhibitors may reverse
What are the ultrashort and short acting NMBs
Succinylcholine (~5 minutes)
Mivacurium (~10-20 minutes)

- both are eliminated by plasma cholinesterase
What are the intermediate acting NMB's
Atracurium (~30-60 minutes)
- Spontaneous and plasma esterase elimination
Cisatracurium (~30-60 minutes)
- mostly spontaneous elimination
Rocuronium (~30-60 minutes)
- Eliminate by liver metabolism
Vecurium (~60-90 minutes)
- Eliminate by liver metabolism
What are the long acting NMBs
Tubocurarine (~80-120 minutes)
Pancuronium (~120-180 minutes)

- both are renal eliminated
What are some adverse non depolarizing NMB's
Histamine Release
Block autonomic ganglia
Block muscarinic receptors

- variable dependent on the agent used
What effect can histamine have on the CV system
...
What effect can histamine have on the lungs, especially for an asthmatic
...
What effect can ganglionic blockades have on the CV system
...
What effect can muscarinic blockade have on the CV system
...
What are the adverse effects of succinylcholine
1. Rapidly metabolized by plasma and liver butyrylcholinesterase
- genetic variants or poisoned enzyme may give prolonged effects
2. Bradycardia
3. Post-op muscle pain
4. Stimulates histamine release
5. Hyperkalemia
- can be severe and fatal in select patient
a. Occurs more often in patients with: Burns, severe muscle trauma, upper or lower motor neuron denervation and prolonged ICU care
b. This causes upregulation of the nicotinic acetylcholine receptors which results in, not only an increase in their density, but also they spread over the muscle surface outside the motor endplate area.
c. There is a change in the subunit type
d. This is called denervation supersensitivity
Describe the actions in at the NMJ for healthy muscle.
1. When the nAChR opens, it allows the passage of K and Na ions across the membranes
2. This generates Na and K currents, but since the Na current predominates, an excitatory postsynaptic potential is generated.
What are the considerations for hyperkalemia when dealing with adverse effects of Succinylcholine
1. can be severe and fatal in select patient
- Occurs more often in patients with: Burns, severe muscle trauma, upper or lower motor neuron denervation and prolonged ICU care
2. This causes upregulation of the nicotinic acetylcholine receptors which results in, not only an increase in their density, but also they spread over the muscle surface outside the motor endplate area.
3.There is a change in the subunit type
4. This is called denervation supersensitivity
5. When the NMJ is exposed to succinylcholine, more ion channels become available to release K during depolarization
6. When large muscle groups are involved, there can be a massive efflux of K ions from the muscle cells causing marked hyperkalemia.
7. This precipitates severe cardia events including cardiac arrest
8. Be careful with heart failure patients on digoxin or diuretics
9. Limits its use primarily to short term procedures
10. Malignant hyperthermia: triggered most often by a combination of anesthetics and succinylcholine
11. Excessive calcium release from the SR
12. Treat symptomatically and with dantrolene