Depolarising Muscle Relaxants eLFH

Question 1

What does acetylcholine bind to on post synaptic membrane?

Answer 1

2 alpha subunits of nicotinic acetylcholine receptor.

Question 2

What percentage of NAChR’s need to be activated to allow the end plate to depolarise?

Answer 2

Only 10% of the NAChRs need to be activated to allow the endplate to depolarise from -70 to -50 mV,

(sufficient to allow voltage-gated sodium channels on the muscle fibre to open and a wave of depolarisation to initiate the contractile response.)

Question 3

Under normal conditions, how long is ACh present in the synaptic cleft?

Answer 3

less than 10 ms

because it is rapidly metabolised by acetylcholinesterase.

Question 4

What happens when acetylcholinesterase is inhibited irreversibly by organophosphates?

Answer 4

When acetylcholinesterase is inhibited irreversibly by organophosphates, ACh remains in the synaptic cleft and flaccid paralysis ensues.

Question 5

Is succinylcholine lipid soluble?

Answer 5

NO

With two permanently charged nitrogens, SCh is water soluble but not lipid soluble.

Does not cross BBB/ or placenta.

Question 6

What are the two phases of neuromuscular blockade seen with Succinycholine?

Answer 6

Phase I block, which occurs during normal use.

Phase II block, which occurs after infusion or multiple doses of SCh.

Question 7

Phase 1 Block:
1. When do fasciculations stop?

2. How is the TOF response affected, ?fade
3. Can it be reversed/ increased?

Answer 7

Fasciculation stops when depolarisation of the post-synaptic membrane occurs due to activation of nicotinic receptors.

The train-of-four (TOF) response SUSTAINED - depolarising block

Phase I block cannot be reversed by the use of anticholinesterases, such as neostigmine, and the block may be increased.

Question 8

What is the ‘desensitisation block’?

Answer 8

Once activated, NAChRs transition to a desensitized state in which they are unresponsive to agonists. In the presence of SCh or high concentrations of ACh, the proportion of NAChRs in the desensitized state increases.

Return to the responsive state is time-dependent.

Question 9

What is visualised in Phase 2 Block?

Answer 9

The block is characterised by:

1. fade in the TOF
2. tetanic response
3. post-tetanic potentiation

all of which are seen with non-depolarising neuromuscular blockers.

Question 10

What is the T4:T1 ratio of non-depolarising blocks?

Answer 10

< 0.7

Question 11

List problems associated with Succinylcholine usage?

Answer 11

Bradycardia and arrhythmias
Hyperkalaemia
Myalgia
A rise in intraocular pressure
A rise in intragastric pressure
A rise in intracranial pressure
Pharmacogenetic variation in response
Allergic reactions
Malignant hyperthermia
Masseter spasm

Question 12

Dose of Succinylcholine in neonates, children and adults?

Answer 12

Neonate - 2

Infant and young child - 1.5

Older child and adult - 1

Question 13

How does induction with Sux affect potassium levels?

Answer 13

After a normal intubating dose, a rise in plasma potassium concentration up to 0.5 mmol/L may occur.

Question 14

How can you reduce the incidence of myalgia post induction with suxamethonium?

Answer 14

Pre-treatment with a small dose of non-depolarising muscle relaxant, such as 0.1 mg/kg of rocuronium given 60 seconds before propofol administration, can prevent fasciculations and reduce the incidence of myalgia.

Lidocaine 1.5 mg/kg is also effective at reducing the incidence of these unpleasant muscle pains.

Question 15

Which muscle relaxant has highest risk of anaphylaxis?

Answer 15

> > Succinylcholine

and of the NDM Rocuronium.

Question 16

How do you test for allergy to anaesthetic agents?

Answer 16

Investigation involves measuring serum tryptase, histamine and NMBA-specific IgE in a sample taken 1 hour after the onset of the reaction.

If positive, then cutaneous testing should be undertaken 6 weeks later.

Question 17

What inheritance is malignant hyperthermia?

Answer 17

autosomal dominant familial - ryanodine receptor gene.

Question 18

What is the treatment for malignant hyperthermia?

Answer 18

Treatment is with dantrolene, 1 mg/kg initially, repeated as necessary, and supportive sedation and ventilation.

Question 19

What is the recovery time from Succinylcholine?

Answer 19

Recovery begins at about 3 minutes after a single dose of SCh and is complete within 12-15 minutes.

Paralysis is potentiated by the volatile agents.

Question 20

How is succinylcholine metabolised?

Answer 20

• plasma cholinesterase

SCh is metabolised to succinylmonocholine (SMCh) and choline, and then to succinic acid and a second choline molecule.

SMCh has some neuromuscular blocking properties, although it contributes little to the overall effect of SCh.

Question 21

Cause of sux apnoea?

Answer 21

deficiency of plasma cholinesterase

Question 22

TOF monitoring: what maybe seen if there is sux apnoea?

Answer 22

phase II block may appear after a single dose of SCh because levels remain high in the synaptic cleft.

Question 23

What are acquired causes of acetylcholine deficiency?

Answer 23

Chronic infection
Renal disease
Liver disease
Malnutrition
Carcinoma

Question 24

What is Myasthenia Gravis?

Answer 24

Myasthenia gravis is an autoimmune condition in which autoantibodies to the nicotinic receptor at the NMJ reduce the effectiveness of acetylcholine.

Question 25

Treatment for Myasthenia Gravis?

Answer 25

Treatment is with an anticholinesterase: specifically one that can inhibit acetylcholinesterase. Pyridostigmine is commonly used to block acetylcholinesterase at the NMJ.

Question 26

Which condition should SCh be avoided in?

Answer 26

1. Guillian Barre Syndrome.
2. Day 10 ICU admission with severe sepsis.
3. Patients with proliferation of extra-junctional receptors.