Neuromuscular Agents

Question 1

What are neuromuscular agents?

NB used in isolation?

Answer 1

Drugs that paralyse patients that are undergoing surgery or need venitlation and act at the neuromuscular junction.

They are not sedatives, amnesic or analgesics.

Not used in isolation, part of balanced anaethesia

Question 2

What is the clinical use of NMBA’s?

Answer 2

• Facilitate intubation of the trachea (intra operative ventilation)
• Facilitate surgical exposure (e.g abdomen relaxed)
• Prevent deleterious movement during surgery
• Intensive Care: ventilation, decrease O2 consumption etc

Question 3

What two enzyme will NMNA’s act on primarily?

Answer 3

Nicotinic acetylcholine receptors. @ bind to alpha 1 subunits.

Acetylcholinesterase on basal lamina made by muscle cells.

Question 4

Mechanism of action and example of depolarising NMBA

Answer 4

Succinylcholine (SCh).

Mimics ACh acts as an agonist. 1 molecule binds to both alpha subunits.
Biphasic response. Causes contractions followed by relaxation. Is not broken down by AChE.

Acts until kidney elimination or broken down

Question 5

What are some features of Succinylcholine?

Answer 5

Fast(est) acting (<60s)
Duration of action short
broken down by pseudocholinesterase

Question 6

Side effects/ Disadvantages of Succinylcholine

Answer 6

Cannot be reversed
Fasciculations can cause postop muscle pain
cardiac dysryhtmias

Question 7

Mechanism of non depolarising NMBA’s

NB benzylisoquinolones and aminosteroids

Answer 7

They are positively charged ammonium compounds that attach to 1 or both alpha subunits of the AChR.

Competitive interaction between NMBA and ACh.

Block acquired when 70% receptors occupied.

Question 8

Atracurium: onset; excretion; CV effects; Acting

Answer 8

Onset: 3-5 mins
Excretion indepenedent of liver and kidney
CV effects: transient skinrash, hypotension
Acting: Intermediate (25-45 mins)

Question 9

Mivacurium: Potency; onset; Acting; degradation

Answer 9

Potency: 3 times that of atracurium
Onset: 3-4 mins
Acting: Short acting (20-25mins)
Degradation: pseudocholinesterase (irreversible?)

Question 10

Rocuronium: Onset: Acting; potency

Answer 10

Onset: fast due to large dose (low potency)
Acting: Intermedate 40

Question 11

Vecuronium: onset; acting; excretion;

Answer 11

Onset: slower onset
Acting: intermediate acting
Excretion: kidney

Question 12

Pancuronium: potency; onset; acting; CV effects; excretion

Answer 12

Potency: high
Onset: slow
Long Acting 1.5-2 hours (good for long cardiac surgeries)
increases BP and HR
Excretion liver and kidneys

Question 13

How can we reverse NMBA’s note only for non depolarising

Answer 13

Titrate perfectly

Accelerate reversal- increase ACh at NMJ or decrease plasma NMBA

Question 14

What are some drugs that causes reversals?

Answer 14

Anticholinesterases, to stop ACh breakdown. Tilts competiton for AChR

Eg Neostigmine/ pryidostigmine

Question 15

What is the problem with NMBA’s reversers?

How are these combatted?

Answer 15

Act at all cholinergic receptors causing side effects.

Parasympathetic activity altered causing bradycardias, ssalviations.

Combat: combined with atropine or an antimucarinic drug to stop this

Question 16

Sugammadex

Answer 16

Binds to rocuronium and take sit into the plasma where it is excreted. Expensive

Question 17

What is a TOF?

fade?

Answer 17

Train of four is 4 stimuli done on a peripheral nerve every 0.5s.
TOF count is number of twitches seen.
TOFR is ratio of the 4th twitch to the 1st twitch. Complete NM block has a ratio of 0 and count of 0
Fade shows deficiency of NM transmission

Use adductor pollicis as surrogate, diaphragm less senstive.

Question 18

What is the danger of a residual block from NMBA’s?

When will a reversal drug given?

Answer 18

The ventilatory response to hypoxia is impaired until a TOFR of 0.9. Hard to measure this. Pharyngeal muscles at 0.8

When count is at 4 to prevent reparalysis