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Muscle

Relaxants
dr. Boby Suryawan

Triad of Anaesthesia
Analgesia
Pain control w/ opioid and non-opioid analgesics
Hypnosis
Drug induced sleep
Muscle Relaxation
To minimize patient movement and/or facilitate
ventilation

Muscle Relaxation
Relaksasi Otot dapat dicapai dengan:
Mendalamkan anestesia umum
inhalasi
Melakukan blokade saraf regional
Pemberian pelumpuh otot

Muscle Relaxants

Depolarizing Muscle Relaxants


Non-depolarizing Muscle
Relaxants

What is a Muscle Relaxer?


Amuscle relaxer, also
known as a muscle
relaxant,is a drug
which affectsskeletal
musclefunction and
decreases themuscle
tone. It may be used to
alleviate symptoms
such as musclespasms,
pain.

History of Muscle Relaxers

The earliest known use of muscle relaxant drugs dates back


to the 16th century, when European explorers encountered
natives of the Amazon were usingpoison-tippedarrows that
produced death by skeletal muscle paralysis.By 1943,
neuromuscular blocking drugs became established as
muscle relaxants in the practice ofanesthesia andsurgery.

Muscle Relaxers and the


Nervous System
Muscle
relaxers refer
to two major
therapeutic
groups:
neuromuscula
r blockers
andspasmolyt
ics

Two Therapeutic Muscle


Relaxers
Neuromuscular BlockersSpasmolytics

Neuromuscular blockers act by interfering with


transmission at the neuromuscular end plate and
have nocentral nervous system activity. They are
often used during surgical procedures and
inintensive careandemergency medicine to cause
temporaryparalysis.

Spasmolytics, also known as "centrally acting" muscle


relaxants, are used to alleviate musculoskeletal pain and
spasms and to reducespasticity in a variety of neurological
conditions.

Neuromuscular Blockers
Most neuromuscular blockers function by blocking transmission at the end
plate of the neuromuscular junction.
Normal end plate function can be blocked by two mechanisms. Non
depolarizing agents, such as tubocurarine, block the agonist, acetylcholine,
from binding to nicotinic receptors and activating them, thereby preventing
depolarization.
Alternatively, depolarizing agents, such as succinylcholine, are nicotinic
receptor agonists which mimic Ach, block muscle contraction by depolarizing
to such an extent that it desensitizes the receptor and it can no longer initiate
an action potential and cause muscle contraction.
Both of these classes of neuromuscular blocking drugs are structurally similar
to acetylcholine, the endogenous ligand, in many cases containing two
acetylcholine molecules linked end-to-end by a rigid carbon ring system, as
in pancuronium (a nondepolarizing agent).

Depolarizing Muscle
Relaxants
Depolarizing Muscle Relaxants bekerja seperti acetylcholine, tetapi tidak dapat
dirusak oleh cholinesterase di celah saraf.

Depolarizing Muscle Relaxants menyebabkan depolarisasi yang ditandai oleh


fasikulasi yang disusul oleh relaksasi otot lurik.

Termasuk golongan pelumpuh otot depolarisasi adalah succinylcholine dan


decamethonium.

Durasi kerja succinylcholine sangat pendek


Succinylcholine dimetabolisme oleh enzim plasma cholinesterase
(pseudocholinesterase) di pembuluh darah.

Depolarizing Muscle
Relaxants
Efek samping succinylcholine adalah:
Nyeri otot, terjadi pada 90% kasus, dapat dikurangi dengan memberikan
pelumpuh otot non-depolarisasi dosis kecil sebelumnya.
Peningkatan tekanan intraokular
Peningkatan tekanan intrakranial
Peningkatan tekanan intragastrik
Peningkatan kadar kalium plasma (hiperkalemia)
Aritmia jantung
Salivasi
Alergi, anafilaksis
Malignant hyperthermia

Non-depolarizing Muscle
Relaxants
Non-depolarizing muscle relaxants
berikatan dengan muscarinic
cholinergic receptors, sebagai inhibitor
acetylcholine, sehingga acetylcholine
tidak dapat bekerja dan tidak terjadi
depolarisasi.

Berdasarkan susunan molekul, non-depolarizing muscle relaxants digolongkan


menjadi:

Benzylisoquinol : tubocurarine,
metocurine,
inium
doxacurium, mivacurium
Steroid

: pancuronium, vecuronium,
rapacuronium, rocuronium

Phenol ethers

: Gallamine

Nortoxiferine

: Alcuronium

atracurium,
pipecuronium,

Nondepol long-acting
1. Tubocurarine

Duras

Dosis

Dosis

awal

rumatan

(mg/kg)

(mg/kg)

Efek Samping

(meni
t)

0.40-0.60

0.10

30-60

Histamin +, hipotensi

(tubarin)

0.08-0.12

0.015-0.020

30-60

Vagolitik,

2.

Pancuronium

0.20-0.40

0.05

40-60

tensi

3.

Metocurine

0.05-0.12

0.01-0.015

40-60

Histamin -, hipotensi

4.

Pipecuronium

0.02-0.08

0.005-0.010

45-60

Kardiovaskular stabil

5.

Doxacurium

0.15-0.30

0.05

40-60

Kardiovaskular stabil

6.

Alcuronium

Vagolitik, takikardia

(alloferin)
Nondepol intermediate acting
1. Gallamine (flaxedil)
2.
3.

4-6

0.5

30-60

Histamin , hipotensi

Atracurium

0.5-0.6

0.1

20-45

Aman

(tracrium)

0.1-0.2

0.015-0.02

25-45

ginjal

Vecuronium

0.6-1.0

0.10-0.15

30-60

0.15-0.20

0.02

30-45

(norcuron)
4.

takikardi,

untuk

hepar,

Isomer atrakurium

Rocuronium
(esmeron)

5. Cistacuronium
Nondepol short acting
1. Mivacurium
(mivacron)
2. Ropacuronium
Depol short acting

0.20-0.25

0.05

10-15

1.5-2.0

0.3-0.5

15-30

Histamin +, hipotensi

Muscle Relaxants
1. Pilihan
muscle
relaxants
Gangguan
faal : Atracurium, vecuronium
ginjal

: Atracurium

2. Gangguan faal hati : Jika dibutuhkan, dosis 1/10 atracurium


3. Miastenia gravis

: Atracurium, rocuronium, mivacuronium

4. Bedah singkat

: Semua dapat digunakan kecuali gallamine

5. Kasus obstetri

Tanda-tanda kekurangan pelumpuh otot


Cegukan (hiccup)
Dinding perut kaku
Ada tahanan pada inflasi paru

Antidotum
Neuromuscular Blocker
Penawar pelumpuh otot atau acetylcholinesterase inhibitor (anti-cholinesterase)
bekerja pada neuro-muscular junction untuk mencegah acetylcholinesterase.

Anti-cholinesterase yang paling sering digunakan adalah neostigmine


(prostigmin), piridostigmin, dan edrophonium.

Penawar pelumpuh otot bersifat muscarinic sehingga menyebabkan hipersalivasi,


keringatan, bradikardia, kejang bronkus, hipermotilitas usus, dan pandangan
kabur.

Pemberian obat penawar pelumpuh otot harus disertai oleh obat


vagolytic

Antidotum
Neuromuscular Blocker

Dosis obat-obatan penawar muscle relaxants

neostigmine adalah 0,04-0,08 mg/kg;

pyridostigmine 0,1-0,4 mg/kg;

edrophonium 0,5-1,0 mg/kg;

dan physostigmine 0,01-0,03 mg/kg.

Dosis obat-obatan vagolytic

atropine dosis 0,01-0,02 mg/kg atau

glycopyrrolate dosis 0,005-0,01 mg/kg sampai 0,2-0,3 mg pada dewasa.

Spasmolytics
Spasmolytic agents generally work by either enhancing the level of
inhibition, or reducing the level of excitation.
Inhibition is enhanced by mimicking or enhancing the actions of
endogenous inhibitory substances, such as gamma-Aminobutyric acid
(GABA).
GABA is the chief inhibitory neurotransmitter in the mammalian central
nervous system. It plays a role in regulating neuronal excitability
throughout the nervous system. In humans, GABA is also directly
responsible for the regulation of muscle tone.
Spasmolytics are referred to as centrally acting muscle relaxants
because they can be used to target specific regions of the body such as
low back and neck.

Spasmolytics

Spasmolytic drugs
Definition of muscle spasm
(spasticity):
1. Increased muscle tone
2. together with muscle weakness
It is often associated with cerebral palsy,
multiple sclerosis, and stroke.

Centrally acting
spasmolytic drugs
Drug

Mechanism

1-

Diazepam

GABA receptor

2-

Baclofen

GABA receptors causing


hyperpolarization by increasing
potassium conductance
Adverse effects: drowsiness and
increased seizure activity

3-

Tizanidine

2 adrenoreceptor agonist

4-

Gabapentin

DIAZEPAM
Benzodiazepines facilitate the action of -

aminobutyric acid (GABA) in the central nervous


system.
Diazepam acts at GABAA synapses, and its action
in reducing spasticity is at least partly mediated in
the spinal cord
Although diazepam can be used in patients with
muscle spasm of almost any origin (including
local muscle trauma), it produces sedation at the
doses required to reduce muscle tone.

BACLOFEN
Baclofen (p-chlorophenyl-GABA) was designed

to be an orally active GABA-mimetic agent, its


spasmolytic activity at GABAB receptors, this
result in:
hyperpolarization, probably by increased K+
conductance.
inhibition of reducing calcium influx
This will reduce excitation of spinal cords and
reduce pain in patients with spasticity,
perhaps by inhibiting the release of substance
P (neurokinin-1) in the spinal cord.
Baclofen is at least as effective as diazepam in
reducing spasticity while producing less
sedation. In addition, baclofen does not reduce
overall muscle strength as much as dantrolene.

Adverse effects:
Drowsiness, tolerant to the sedative
effect with chronic administration.
Increased seizure activity has been
reported in epileptic patients.

Therefore, withdrawal from baclofen


must be done very slowly.

TIZANIDINE
Adverse effects, including
drowsiness, hypotension, dry mouth,
and asthenia.

OTHER CENTRALLY ACTING


SPASMOLYTIC DRUGS
Gabapentin
It is an antiepileptic drug that has shown considerable

promise as a spasmolytic agent in several studies


involving patients with multiple sclerosis.
Pregabalin
is a new analog of gabapentin that may also prove
useful. Progabide and glycine have also been found in
preliminary studies to reduce spasticity. Progabide is a
GABAA and GABAB agonist and has active metabolites,
including GABA itself. Glycine is another inhibitory
amino acid neurotransmitter. It appears to possess
pharmacologic activity when given orally and readily
passes the blood-brain barrier.
Idrocilamide and riluzole
They are newer drugs for the treatment of amyotrophic
lateral sclerosis that appear to have spasm-reducing
effects, possibly through inhibition of glutamatergic
transmission in the central nervous system.

Peripheraly acting spasmolytic drugs


Dantrolene:
Mechanism of action:
Dantrolene reduces skeletal muscle strength by interfering
with excitation-contraction coupling in the muscle fibers
Normal contraction involves release of calcium from its
stores in the sarcoplasmic reticulum through a calcium
channel
Dantrolene interferes with the release of calcium through
this sarcoplasmic reticulum calcium channel.
Cardiac muscle and smooth muscle are depressed only
slightly, perhaps because the release of calcium from their
sarcoplasmic reticulum involves a different process.

Dantrolene:
Indications:
1- Muscle spasticity
2- Malignant hyperthermia:
o Patients at risk for this condition have a hereditary impairment in
the ability of the sarcoplasmic reticulum to sequester calcium.
o Following administration of one of the triggering agents (general
anesthetics or succinylcholine) there is a sudden and prolonged
release of calcium, with massive muscle contraction, lactic acid
production, and increased body temperature.
Treatment of malignant hyperthermia:
1. control acidosis and body temperature
2. Reduce calcium release with intravenous dantrolene

. Major adverse effects

are generalized muscle weakness, sedation, and occasionally hepatitis.

THANKS