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Muscle Relaxant

The document discusses muscle relaxants, including their uses, mechanisms of action, types (depolarizing vs. nondepolarizing), examples of specific drugs, and how their effects are reversed. It focuses on drugs that act at the neuromuscular junction to facilitate intubation and mechanical ventilation or optimize surgical conditions by reducing muscle tone.

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Ari Puji Astuti
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323 views

Muscle Relaxant

The document discusses muscle relaxants, including their uses, mechanisms of action, types (depolarizing vs. nondepolarizing), examples of specific drugs, and how their effects are reversed. It focuses on drugs that act at the neuromuscular junction to facilitate intubation and mechanical ventilation or optimize surgical conditions by reducing muscle tone.

Uploaded by

Ari Puji Astuti
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT, PDF, TXT or read online on Scribd
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Muscle

Relaxants
I Wayan Sumardika
Pharmacology Department
Faculty of Medicine, Udayana
University
Muscle Relaxants
 Facilitate intubation of the
trachea
 Facilitate mechanical ventilation

 Optimized surgical working

conditions
 Reduce abnormally elevated tone

by neurologic or muscle end plate


diseases
Muscle Relaxants
 Muscle relaxants must not be
given without adequate dosage
of analgesic and hypnotic drugs

 Inappropriately given : a patient


is paralyzed but not anesthetized
Muscle Relaxants
 Mechanism of Action
 Neuromuscular junction
 Nerve terminal
 Motor endplate of a muscle
 Synaptic cleft
 Nerve stimulation
 Release of Acetylcholine (Ach)
 Postsynaptic events
Neuromuscular Junction
(NMJ)
Binding of Ach to receptors on muscle end-
plate
Neuromuscular
Blocking Drugs
 Depolarizing muscle relaxant
 Succinylcholine
 Nondepolarizing muscle
relaxants
 Short acting
 Intermediate acting
 Long acting
Depolarizing Muscle
Relaxant
 Succinylcholine
 Pharmacokinetics
 Metabolized by plasma cholinesterase
 Not metabolized locally at NMJ
 Physically resemble Ach
 Rapid onzet of action
 Mechanism of Action
 Act like nicotinic agonist and depolarize the
neuromuscular end plate
 Initial depolarization: twicthing and fasciculations
 Continuous end-plate depolarization causes
muscle relaxation
Neuromuscular
Blocking Drugs
 Reversal of Blockade
 Action of Non depolarizing blockers reversed by
increasing the cooncentration of transmitter at
the receptor
 Accomplised by administration of cholinesterase
inhibitors (neostigmine, pyridostigmine)
 Paralysis produced by depolarizing blockers
increased by cholinesterase inhibitors during
phase I. During phase II, the block produced by
succinilcholine is ussually reversible by
cholinesterase inhibitors
Neuromuscular
Blocking Drugs
 Toxicity
 Respiratory paralysis Mechanical
ventilation
 Autonomic effect and histamine release
 Specific effect of succinylcholine
hypercalemia
 Interaction

Inhaled anesthetics, potentiate and prolong
neuromuscular blockade

Aminoglycoside and antiarrhytmic drugs
Nondepolarizing Muscle
Relaxants
 Long acting
 Pancuronium
 Intermediate acting
 Atracurium
 Vecuronium
 Rocuronium
 Cisatracurium
 Short acting
 Mivacurium
Nondepolarizing Muscle
Relaxants
 Pharmacokinetic
 Agents that metabolized or eliminated in the bile have shorter
duration of action than those eliminated by the kidney.
 Mechanism of Action
 Compete with Ach at the binding sites
 Do not depolarized the motor endplate
 Act as competitive antagonist
 Excessive concentration causing channel blockade
 Act at presynaptic sites, prevent movement of Ach to
release sites
Nondepolarizing Muscle
Relaxants
 Pancuronium
 Aminosteroid compound
 Onset 3-5 minutes, duration 60-90
minutes
 Intubating dose 0.08-0.12 mg/kg
 Elimination mainly by kidney (85%),
liver (15%)
 Side effects : hypertension, tachycrdia,
dysrhythmia,
Nondepolarizing Muscle
Relaxants
 Vecuronium
 Analogue of pancuronium
 much less vagolytic effect and shorter
duration than pancuronium
 Onset 3-5 minutes duration 20-35 minutes
 Intubating dose 0.08-0.12 mg/kg
 Elimination 40% by kidney, 60% by liver
Nondepolarizing Muscle
Relaxants
 Atracurium
 Metabolized by
 Ester hydrolysis

Hofmann elimination
 Onset 3-5 minutes, duration 25-35 minutes
 Intubating dose 0.5 mg/kg
 Side effects :
 histamine release causing hypotension, tachycardia,
bronchospasm
 Laudanosine toxicity
Nondepolarizing Muscle
Relaxants
 Cisatracurium
 Isomer of atracurium
 Metabolized by Hofmann elimination
 Onset 3-5 minutes, duration 20-35
minutes
 Intubating dose 0.1-0.2 mg/kg
 Minimal cardiovascular side effects
 Much less laudanosine produced
Nondepolarizing Muscle
Relaxants
 Rocuronium
 Analogue of vecuronium
 Rapid onset 1-2 minutes, duration 20-
35 minutes
 Onset of action similar to that of
succinylcholine
 Intubating dose 0.6 mg/kg
 Elimination primarily by liver, slightly
by kidney
Antagonism of
Neuromuscular
Blockade
Effectiveness of anticholinesterases depends
on the degree of recovery present when they
are administered
 Anticholinesterases
 Neostigmine
 Onset 3-5 minutes, elimination halflife 77

minutes
 Dose 0.04-0.07 mg/kg

 Pyridostigmine
 Edrophonium
Antagonism of
Neuromuscular
Blockade
 Mechanis of action
 Inhibiting activity of acetylcholineesterase
 More Ach available at NMJ, compete for
sites on nicotinic cholinergic receptors
 Action at muscarinic cholinergic receptor
 Bradycardia
 Hypersecretion
 Increased intestinal tone
Antagonism of
Neuromuscular
Blockade
 Muscarinic side effects are
minimized by anticholinergic
agents
 Atropine

Dose 0.01-0.02 mg/kg
 Scopolamine
 glycopyrrolate
SPASMOLYTIC DRUGS
 Diseases of the CNS (cerebral palsy,
multiple sclerosis)
 Abnormal high reflex activity in the neural
pathways that control skeletal muscle
 Painful spasm
 Therapy: reduction of excessive sceletal
muscle tone without reduction of strength.
Drugs for Chronic Spasm
 Act in the CNS or in the sceletal
muscle cell rather than at the NMJ
 Diazepam
 Baclofen
 Tizanidine
 Dantrolene
 Mechanism of Action
 Diazepam---facilitates GABA-mediated
presynaptic inhibition
 Baclofen---acts as a GABA agonist causing
membrane hyperpolarization via increased K+
conductance
----decrease the release of excitatory
neurotransmiter
 Tizanidine---significant Alpha 2 agonist activity,
reinforce both presynaptic and postsynaptic
inhibition in the cord
 Dantrolene---reduce the release of
activator calcium from the
sarcoplasmic reticulum
 Effective in the treatment of
malignant hypertermia (massive
calcium release from the
sarcoplasmic reticulum of skeletal
muscle)
Drugs for Acute Muscle
Spasm
 Treatment of acute spasm resulting
from muscle injury
 Sedative or act in the brain stem or
spinal cord
 Cyclobenzaprine
 Antimuscarinic actions
 Cause confusion and visual hallucination

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