Lecture 7 Neuromuscular Blockers

Question 1

What is the post-synaptic receptor for the neuromuscular junction?

Answer 1

nicotinic cholinergic receptors

Question 2

Where do neuromuscular blockers work?

Answer 2

at the post-synaptic nicotinic cholinergic receptors

Question 3

When do we use neuromuscular blockers?

Answer 3

“-facilitating intubation
-facilitation of surgical exposure (stops muscle tone in abdominal, thoracic, orthopedic, or spine surgery)
-blunting muscle artifact
-prevention of movement during life threatening event (if no other options available)
-prevention of movement that interferes with delicate surgery
“

Question 4

What are the two classes of neuromuscular blockers?

Answer 4

Depolarizing and non-depolarizing

Question 5

What do the two classes of muscle relaxants have in common?

Answer 5

“-Both can kill

-both work at the post-synaptic junction”

Question 6

What’s the time of onset for sux?

Answer 6

30-60 seconds (fast onset). Can look for fasiculations for action confirmation if you haven’t given a de-fasiculating agent.

Question 7

What enzyme metabolizes succinylcholine?

Answer 7

Plasma cholinesterase

Question 8

What are the life-threatening complications of sux?

Answer 8

“-severe hyperkalemia (in vulnerable pts)

• cardiac arrest 2/2 bradycardia
• malignant hyperthermia (MH)”

Question 9

Who is at risk of hyperkalemia with sux administration?

Answer 9

"-spinal cord injury pts 
-pts w/ neuromuscular dz 
-severe burn pts 
-severe trauma pts 
-bedridden pts -
pts w/ high potassium levels already"

Question 10

What are the non-life-threatening side FX of sux?

Answer 10

“-myalgias,

• non-fatal cardiac dysrhythmias (bradycardia, junctional rhythm)
• myoglobinuria
• fasiculations
• trismus (jaw muscle spasm that keeps jaw closed)
• increased intraocular pressure
• increased intragastric pressure”

Question 11

What chemical structures make up a succinylcholine?

Answer 11

Two acetylcholines

Question 12

How do nondepolarizing neuromuscular blockers work?

Answer 12

Reversible, competitive inhibition of acetylcholine. They bind to the nicotinic cholinergic receptors and prevent skeletal muscle activation

Question 13

Where do nondepolarizing muscle relaxants work?

Answer 13

Neuromuscular junction, post-synaptic region

Question 14

List some nondepolarizing neuromuscular blockers.

Answer 14

“Think ““onium”” and ““urium”” drugs

• Vecuronium (will be the example drug for this class)
• Pancuronium
• Rocuronium
• Atracurium
• Cisatracurium
• Mivacurium”

Question 15

What is the onset of vecuronium?

Answer 15

Several minutes

Question 16

What is the half time of vecuronium?

Answer 16

Less than an hour (despite this, even small amounts can cause airway obstruction and respiratory failure, esp. in the setting of premature extubation)

Question 17

How is vecuronium cleared by the body?

Answer 17

Redistribution, hepatic excretion, renal excretion, some metabolism

Question 18

How can we protect patients from the residual effects of nondepolarizing neuromuscular blockers?

Answer 18

Reversal/antogonism

Question 19

What is used to reverse nondepolarizing neuromuscular blockers?

Answer 19

Anticholinesterase drugs like Neostigmine, Pyridostigmine, Edrophonium. All of these enhance the levels of ACH present, with the resultant drop in heart rate. Remember that Parasympathetic Nervous System predominately decreases HR, and has little (if any) effect on cardiac contractility.

Question 20

What is the “danger time” if not enough neostigmine is used?

Answer 20

“Any time from extubation to 30 minutes later in the PACU. The residual nondepolarizing muscle relaxant could impair airway integrity.
Factors that contribute to adverse events in the PACU: Obesity, opioids, long duration of surgery, emergency surgery, and abdominal surgery”

Question 21

How do anticholinesterase drugs work?

Answer 21

They prevent the breakdown of ACh by acetylcholinesterase->acetylcholine storm->competition w/ neuromuscular blocker for receptor->antagonism of the blocker effect until the drug is eliminated

Question 22

What are some side effects of the “acetylcholine storm”?

Answer 22

“-cholinergic crisis

-bradycardia”

Question 23

What should ALWAYS be given with an anticholinesterase drug?

Answer 23

An anti-muscarinic drug (anti-cholinergic drug) such as atropine or glycopyrrolate. This is done to counter the drop in HR that occurs with Acetylcholineesterase inhibitors.

Question 24

Why is vecuronium a good nondepolarizing muscle relaxant?

Answer 24

It doesn’t cause hypotension by dumping histamine (like atracurium), nor does it cause an atropine-like effect (increased HR, MAP, and CO like pancuronium).

Question 25

How does sugammadex work?

Answer 25

“It antagonizes steroidal NMBDs (esp rocuronium) by encapsulating and inactivating them. There is no action on the neuromuscular junction itself.
-Complete reversal in 2-3 minutes.
-No cardiovascular effects, so no Atropine or Glycopyrolate needed when Sugammadex is used.
“

Question 26

What is Hoffman elimination?

Answer 26

Spontaneous, non-enzymatic degradation of drug at body temperature and pH. This non-enzymatic, spontaneous degradation occurs with Atracurium and cisatracurium.

Question 27

Which two drugs are eliminated via Hoffman elimination?

Answer 27

Atracurium (along w/ plasma ester hydrolysis) and cisatracurium (only method for eliminating this drug)

Question 28

Why is Hoffman elimination useful?

Answer 28

These drugs can be used in the presence of renal and hepatic failure (organ-independent metabolism).

Question 29

Which NMBD is not metabolized at all?

Answer 29

Rocuronium. It’s excreted into the hepatobiliary system and then excreted renally

Question 30

What’s the most reliable way to monitor the effects of NMBDs?

Answer 30

Electrical stimulation twitch response.