Muscle Relaxants

Question 1

Succinylcholine

1. MOA
2. Dosage; Onset; Duration
3. Side effects

Answer 1

1. DEPOLARIZING: Essentially two ACh molecules connected by an ester bond that mimics the action of ACh by binding the alpha subunits of the cholinergic nicotinic receptor at the NMJ (also autonomic ganglia, heart, secretory glands, smooth muscle) → depolarization of the NMJ and then flaccid paralysis
2. .6mg/kg -> onset 45-60 seconds-> duration 8-15 minutes
3. • Negative inotropic and chronotropic effects at low doses, high dose = tachycardia
     - With kids → dysrhythmias, bradycardia, etc.
     - Hyperkalemia
     - Increased intra-ocular pressure, intra-gastric pressure, ICP
     - Myalgias, Masseter spasm
     - MH

Question 2

D-Tubocurarine

1. Class
2. MOA

Answer 2

1. Benzylisoquinolinium Non-Depolarizing Muscle Relaxant
2. Competitively bind with one of the two alpha subunits on the post junctional nicotinic cholinergic receptor and prevent interaction of the receptor with ACh → inhibits the opening of the ion channel preventing depolarization of the membrane.

As long as there is more NDMR at the NMJ, no contraction.

Question 3

Metocurine

1. Class
2. MOA

Answer 3

1. Benzylisoquinolinium Non-Depolarizing Muscle Relaxant
2. Competitively bind with one of the two alpha subunits on the post junctional nicotinic cholinergic receptor and prevent interaction of the receptor with ACh → inhibits the opening of the ion channel preventing depolarization of the membrane.

As long as there is more NDMR at the NMJ, no contraction.

Question 4

Atracurium

1. Class
2. MOA

Answer 4

1. Benzylisoquinolinium Non-Depolarizing Muscle Relaxant
2. Competitively bind with one of the two alpha subunits on the post junctional nicotinic cholinergic receptor and prevent interaction of the receptor with ACh → inhibits the opening of the ion channel preventing depolarization of the membrane.

As long as there is more NDMR at the NMJ, no contraction.

Question 5

Cis-atracurium

1. Class
2. MOA
3. Why is this commonly used?

Answer 5

1. Benzylisoquinolinium Non-Depolarizing Muscle Relaxant
2. Competitively bind with one of the two alpha subunits on the post junctional nicotinic cholinergic receptor and prevent interaction of the receptor with ACh → inhibits the opening of the ion channel preventing depolarization of the membrane.
   As long as there is more NDMR at the NMJ, no contraction.
3. Virtually no CV side effects because devoid of histamine release

Question 6

Doxacurium

1. Class
2. MOA

Answer 6

1. Benzylisoquinolinium Non-Depolarizing Muscle Relaxant
2. Competitively bind with one of the two alpha subunits on the post junctional nicotinic cholinergic receptor and prevent interaction of the receptor with ACh → inhibits the opening of the ion channel preventing depolarization of the membrane.

As long as there is more NDMR at the NMJ, no contraction.

Question 7

Pancuronium

1. Class
2. MOA

Answer 7

1. Aminosteroidal Non-Depolarizing Muscle Relaxant
2. Competitively bind with one of the two alpha subunits on the post junctional nicotinic cholinergic receptor and prevent interaction of the receptor with ACh → inhibits the opening of the ion channel preventing depolarization of the membrane.

As long as there is more NDMR at the NMJ, no contraction.

Question 8

Vecuronium

1. Class
2. MOA

Answer 8

1. Aminosteroidal Non-Depolarizing Muscle Relaxant
2. Competitively bind with one of the two alpha subunits on the post junctional nicotinic cholinergic receptor and prevent interaction of the receptor with ACh → inhibits the opening of the ion channel preventing depolarization of the membrane.

As long as there is more NDMR at the NMJ, no contraction.

Question 9

Rocuronium

1. Class
2. MOA

Answer 9

1. Aminosteroidal Non-Depolarizing Muscle Relaxant
2. Competitively bind with one of the two alpha subunits on the post junctional nicotinic cholinergic receptor and prevent interaction of the receptor with ACh → inhibits the opening of the ion channel preventing depolarization of the membrane.

As long as there is more NDMR at the NMJ, no contraction.

Question 10

Pipercuronium

1. Class
2. MOA

Answer 10

1. Aminosteroidal Non-Depolarizing Muscle Relaxant
2. Competitively bind with one of the two alpha subunits on the post junctional nicotinic cholinergic receptor and prevent interaction of the receptor with ACh → inhibits the opening of the ion channel preventing depolarization of the membrane.

As long as there is more NDMR at the NMJ, no contraction.

Question 11

What are the reversal agents for:

1. Succinylcholine
2. Benzylisoquinoliniums
3. Aminosteroids

Answer 11

1. None
2. Anticholinesterases
3. Anticholinesterases OR suggamadex

Question 12

Edrophonium

1. CV Effects
2. What do you use edrophonium with? Why?
3. Dose and onset

Answer 12

1. Weak muscarinic effect → less slowing of HR than Neo
2. Atropine (.001-.014 mg/kg) due to onset time
3. .5-1 mg/kg -> onset 45-120 seconds

Question 13

Neostigmine

1. CV Effects
2. What do you use Neo with? Why?
3. Why do we normally use this?
4. Dose and onset

Answer 13

1. Profound bradycardia due to vagal ACh stimulation
2. Glycopyrrolate (.2mg/mg) → onset matches
3. Better for DEEP blockade reversal; Better for DEEP blockade reversal
4. .04-.08 mg/kg -> onset 5 minutes, peak at 10 min

Question 14

Pyridostigmine

1. CV effects
2. What do you use with pyridostigmine?
3. Dose and onset

Answer 14

1. Profound bradycardia due to vagal ACh stimulation
2. Glycopyrrolate (.05mg/mg) → onset matches
3. .1-.25mg/kg -> onset 10-15 minutes

Question 15

Suggamadex

1. MOA
2. Dosage

Answer 15

1. Modified gamma-cyclodextrin = selective relaxant binding agent → electrostatically binds to rocuronium or vecuronium
   * *Irreversible binding of STEROIDAL only (-oniums) NOT (-uriums)
   * *NO INHIBITION of acetylcholinesterase ⇒ NO ACh build up (don’t need anti-muscarinic like glyco or atropine)
2. 2-16 mg/kg based on TOF count and %