Muscle Relaxants

(Neuromuscular
Blocking Drugs)

dr. Ristiawan Muji L, SpAn.

Departement of Anesthesiology & Reanimation

Dr Saiful Anwar Hospital, Brawijaya University
Malang
 Muscle Relaxants
"The principal pharmacologic effect of
neuromuscular blocking drugs is to interrupt
transmission of nerve impulses at the
neuromuscular junction".

- Cause a flaccid paralysis of skeletal

musculature
- Binding to motor endplate
cholinoceptors
- Blocking neuromuscular transmission
- As adjuncts to general anesthetics
(Chatzung,2006
 How it works At rest, ion
Na+ flow through
the central
pore or
channel is
prevented by
Gate K+ a narrowing
(gate).
When acetylcholine binds to its binding site,
there is a disturbance in the subunit structure so
that the gate opens, allowing ions to pass.
Cholinoceptors Types with Documented or Probable
Effects
on Peripheral Autonomic Effector Tissue
Mechanism of Action
Non-depolarizers:
competitive block
prevent binding of Ach to receptor
No structural alteration of ACh receptor, no initial
depolarisation, but competing with ACh on binding site
insufficient to trigger contraction
> 75% receptors have to be blocked to have effect

Depolarizers :
mimic action of Ach
excitation followed by block
Mechanism of Action
Depolarizers :
Mimic action of Ach
Succinylcholine chloride binds to the -subunits of
receptorwhich lead to depolarization of endplate
Because SCh is not degraded as quickly as
Ach,persistent endplate depolarization inhibits the
inward flow of sodium ions,and there is
inexcitability of the perijunctional muscle
membrane muscle relaxation
 Key Concepts

Muscle relaxation does not ensure

unconsciousness, amnesia, or
analgesia.
Depolarizing muscle relaxants act as
acetylcholine (ACh) receptor
agonists, whereas
nondepolarizing muscle relaxants
function as
competitive antagonists.
Depolarizing muscle relaxants are
hydrolyzed in
the plasma and liver by
 Key
Concepts
Succinylcholine is considered
contraindicated
in the routine management of
children and
adolescents because of the risk of
hyperkalemia,
rhabdomyolysis, and cardiac arrest in
children
with undiagnosed myopathies.
Succinylcholine-induced depolarization
to
 Key
Concepts
Atracurium and cisatracurium undergo degradation by
organ-independent Hofmann elimination

monoquaternary acrylate and laudanosine

no intrinsic neuromuscular blocking

effects.

Pancuronium caused Hypertension and

tachycardia by
the combination of vagal
blockade and
catecholamine release from
Rocuronium (0.91.2 mg/kg) has an onset
of action that approaches succinylcholine
(6090 s), making it a suitable alternative
for rapid-sequence inductions, but at the
cost of a much longer duration of action.

Depolarizing and Nondepolarizing Muscle
Relaxants.
Drug
Interactions
?