Lecture 7/10

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 depolarizing neuromuscular agent(s) is/are used?

Answer 6

Succinylcholine

Question 7

What is sux’s duration of action?

Answer 7

4-10 minutes+ depending on dose/pt.

Question 8

What’s the time of onset for sux?

Answer 8

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

Question 9

What enzyme metabolizes succinylcholine?

Answer 9

Plasma cholinesterase

Question 10

What are the life-threatening complications of sux?

Answer 10

“-severe hyperkalemia (in vulnerable pts)

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

Question 11

Who is at risk of hyperkalemia with sux administration?

Answer 11

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

Question 12

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

Answer 12

“-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 13

What chemical structures make up a succinylcholine?

Answer 13

Two acetylcholines

Question 14

How do nondepolarizing neuromuscular blockers work?

Answer 14

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

Question 15

Where do nondepolarizing muscle relaxants work?

Answer 15

Neuromuscular junction, post-synaptic region

Question 16

List some nondepolarizing neuromuscular blockers.

Answer 16

“Think ““onium”” and ““urium”” drugs

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

Question 17

What is the onset of vecuronium?

Answer 17

Several minutes

Question 18

What is the half time of vecuronium?

Answer 18

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

Question 19

How is vecuronium cleared by the body?

Answer 19

Redistribution, hepatic excretion, renal excretion, some metabolism

Question 20

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

Answer 20

Reversal/antagonism

Question 21

What is used to reverse nondepolarizing neuromuscular blockers?

Answer 21

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 22

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

Answer 22

“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 23

How do anticholinesterase drugs work?

Answer 23

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 24

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

Answer 24

“-cholinergic crisis

-bradycardia”

Question 25

What should ALWAYS be given with an anticholinesterase drug?

Answer 25

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

Question 26

Why is vecuronium a good nondepolarizing muscle relaxant?

Answer 26

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 27

How does sugammadex work?

Answer 27

“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 28

What is Hoffman elimination?

Answer 28

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

Question 29

Which two drugs are eliminated via Hoffman elimination?

Answer 29

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

Question 30

Why is Hoffman elimination useful?

Answer 30

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

Question 31

Which NMBD is not metabolized at all?

Answer 31

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

Question 32

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

Answer 32

Electrical stimulation twitch response.