A short presentation about the different types of muscle relaxants and their mechanism of action.

1. S
Skeletal muscle relaxants

2. Skeletal muscle relaxants
They are groups of drugs which affects skeletal muscle
function and decreases the muscular tone. Thus, cause the
muscle to relax.

3. Muscle Relaxants Agents
Neuromuscular
Blockers
Non
Depolarizing
Blockers
Spasmolytic
Depolarizing
Blockers

4. Neuromuscular blocking agents
S Drugs can block neuromuscular transmission either by
acting presynaptically to inhibit ACh synthesis or release,
or by acting postsynaptically, the latter being the site of
action of all the clinically important drugs (except for
botulinum toxin

5. Neuromuscular blocking agents
S Clinically, neuromuscular block is used only as an adjunct
to anaesthesia, when artificial ventilation is available; it is
not a therapeutic intervention.
S The drugs that are used all work postsynaptically, either
(a) by blocking ACh receptors (or in some cases the ion
channel) or (b) by activating ACh receptors and thus
causing persistent depolarization of the motor endplate.
They fall into two categories: 1.non-depolarising blocking
agent agents 2.depolarising blocking agents

6. Non Depolarizing neuromuscular blockers

7. How do muscles contract?

8. Mechanism of action:

9. Action
S It starts with the smaller muscles in the eyes and face and then
moves to the larger muscle groups in the tongue, neck and
shoulder, and finally to the respiratory muscles: the intercostal, the
larynx and diaphragm.
S Recovery from neuromuscular blocking drugs occurs in the reverse
order.

10. Pharmacokinetics:
S Neuromuscular-blocking agents are used mainly in anaesthesiato produce muscle
relaxation
S They are given intravenously but differ in their rates of onset and recovery
S Most of the non-depolarising blocking agents are metabolised by the liver or
excreted unchanged in the urine, exceptions being atracurium, which hydrolyses
spontaneously in plasma, and mivacurium, which, like suxamethonium), is
hydrolysed by plasma cholinesterase.
S Atracurium was designed to be chemically unstable at physiological pH (splitting
into two inactive fragments by cleavage at one of the quaternary nitrogen atoms),
although indefinitely stable when stored at an acid pH. It has a short duration of
action, which is unaffected by renal or hepatic function

11. Examples of competitive neuromuscular
blockers

12. S Tubocurarine (curare):
S It is a plant alkaloid that has slow onset of action (> 5 min) and longer
duration(1-2 h). It also affect autonomic ganglia.
S The main side effects is Bronchoconstriction and hypotension. In
addition to other side effects related to its ganglion blocking activity
( blurred vision , urine retention , constipation and male impotence)

13. S Gallamine (Flaxedil):
S It is synthetic compound has less potent NM blocking activity than
curare ( 1/5 potency)
S It has shorter onset (2-3 min) and longer duration ( > 2h) than d-tubocurarine.
S It is execrated unchanged mainly by kidney. It is contraindicated in
renal failure
S Main side effect is “tachycardia” due to an atropine-like action and
stimulation of NA release from adrenergic nerve endings.

14. S Mivacurium:
S It is new drug that is chemically-related to Atracurium. It has Fast
onset (∼2 min) and short duration (∼15 min).
S It is metabolized by plasma pseudocholinesterases (Longer duration
in patient with liver disease or genetic cholinesterase deficiency).
S Transient hypotension is the main side effect.

15. S Pancuronium:
S It is the first steroid-based compound that is more potent than curare
( 6 times ). It has Intermediate onset (2-3 min) and slight long
duration (>2h)
S Excreted mainly by the kidney ( 80 % ).
S Tachycardia is the main side effect (due to an atropine-like action
and stimulation of NA release from adrenergic nerve endings).

16. S Vecuronium:
S It is more potent NMBs than curare (6times) with Intermediate
onset (2-3 min) and Intermediate duration (30-40 min)
S It is metabolized mainly by liver. It has few side effects (no
histamine release, no ganglion block and no antimuscarinic action).
Occasionally causes prolonged paralysis, probably owing to active
metabolite
S It is widely used.

17. Depolarizing neuromuscular blockers

18. Mechanism of action:
S Depolarization at the endplate region of the muscle fiber 
Fasciculation (twitching) because the developing endplate
depolarization initially causes a discharge of action potentials in
the muscle fiber Paralysis because re-polarization doesn’t
occur.

19. Examples:
S Decamethonium :
 Was used clinically but has the disadvantage of too long a duration of action.
S Suxamethonium :
 The only depolarising blocking drug currently used.
 Closely related in structure to both decamethonium and ACh (consisting of two
ACh molecules linked by their acetyl groups).
 Its action is brief, because it is quickly hydrolysed by plasma cholinesterase.
When given intravenously, however, its depolarising action lasts for long
enough to cause the endplate region of the muscle fibres to become inexcitable.

20. Unwanted effects and dangers of
suxamethonium:
S Bradycardia
S Increased intraocular pressure
S Prolonged paralysis
S Malignant hyperthermia

21. Comparison of non-depolarising and
depolarising blocking drugs:
S Anticholinesterase drugs are very effective in overcoming
the blocking action of competitive agents (non
depolarizing).
S The fasciculations seen with suxamethonium as a prelude to
paralysis do not occur with competitive drugs (non-depolarizing).
S Tetanic fade is increased by non-depolarising blocking
drugs, compared with normal muscle.

22. Thank You!
S Lama Al Jlayl.
S Alaa Assiri
S Esraa Sebieh
S Sarah Abu El Asrar