Tugas Anestesi Muscle Relaxan

MUSCLE RELAXANTSOleh :

Agnes Christiani (0710113)

Ferry Yulianto (0710101)

Lani Oktaviani (0710080)

Pembimbing :

dr.Christin.,

SMF AnestesiologiFakultas Kedokteran

Universitas Kristen Maranatha Rumah Sakit Immanuel

Bandung2011

Indikasi Fasilitasi intubasi trachea Fasilitasi ventilasi mekanik Optimalisasi kondisi bedah

Relaksasi Otot Skelet didapatkan dengan cara :

Dosis tinggi anestetik inhalasi

Anesthesia regional Neuromuscular blocking agents

Proper patient positioning on the operating table

Muscle relaxants tidak boleh diberikan tanpa dosis obat analgesik & hipnotik adekuat

Inappropriately given : pasien paralisis tanpa teranestesi

Muscle Relaxants

Neuromuscular junction Nerve terminal Motor endplate of a muscle Synaptic cleft

Nerve stimulation Release of Acetylcholine (Ach) Postsynaptic events

Muscle relaxant bekerja di:

Impuls sarafmotor nerve terminalinflux Caexocytosis synaptic vesicles containing ACHdiffuses across synaptic clefthydrolysed by AchE/bind nicotinic receptors on the motor end plate

The binding of two ACH moleculesconformational change opens sodium-potassium channel of the nicotinic receptor. Na+ & Ca2+ ions to enter the cell & K+ ions leave the cell depolarization of the end platemuscle contraction

Neuromuscular Junction (NMJ)

Following depolarization, the acetylcholine molecules are then removed from the end plate region and enzymatically hydrolysed by acetylcholinesterase

Neuromuscular Junction (NMJ)

Neuromuscular Junction (NMJ)

Binding of Ach to receptors on muscle end-plate

Depolarizing muscle relaxant Succinylcholine

Nondepolarizing muscle relaxants Short acting Intermediate acting Long acting

Muscle Relaxants dibagi menjadi:

Succinylcholine Mekanisme kerja:

Secara fisik mirip dengan Ach Berperan sebagai acetylcholine receptor

agonist Tidak dimetabolisme secara lokal di NMJ Dimetabolisme oleh pseudocholinesterase

dalam plasma Masa depolarisasinya lebih panjang dari Ach Depolarisasi terus menerus menyebabkan

relaksasi otot

Depolarizing Muscle Relaxant

Succinylcholine Penggunaan secara klinis:

Paling sering digunakan untuk fasilitasi intubasi

Dosis succinylcholine untuk intubasi: 1-1.5 mg/kg Onset 30-60 detik, durasi 5-10 menit

Depolarizing Muscle Relaxant

Efek Succinylcholine Cardiovascular Fasciculation Muscle pain Increase intraocular pressure Increase intragastric pressure Increase intracranial pressure Hyperkalemia Malignant hyperthermia

Depolarizing Muscle Relaxant

Mekanisme kerja: Kompetisi dengan Ach pada binding sites Tidak terjadi depolarisasi pada motor

endplate Berperan sebagai competitive antagonist Konsentrasi berlebih menyebabkan channel

blockade Berperan di presynaptic sites, mencegah

berpindahnya Ach ke release sites

Nondepolarizing Muscle Relaxants

Long acting Pancuronium

Intermediate acting Atracurium Vecuronium Rocuronium Cisatracurium

Short acting Mivacurium

Nondepolarizing Muscle Relaxants

Pancuronium Aminosteroid compound Onset 3-5 menit, durasi 60-90 menit Dosis intubasi 0.08-0.12 mg/kg Eliminasi terutama di ginjal (85%), hepar

(15%) Efek samping: hypertension, tachycrdia,

dysrhythmia

Nondepolarizing Muscle Relaxants

Vecuronium Analogue of pancuronium Efek vagolytic lebih sedikit dan durasi lebih

singkat daripada pancuronium Onset 3-5 menit, durasi 20-35 menit Intubating dose 0.08-0.12 mg/kg Eliminasi di 40% ginjal, 60% hepar

Nondepolarizing Muscle Relaxants

Atracurium Dimetabolisme oleh

Ester hydrolysis Hofmann elimination

Onset 3-5 menit, durasi 25-35 menit Dosis intubasi 0.5 mg/kg Efek samping:

histamine release causing hypotension, tachycardia, bronchospasm

Laudanosine toxicity ( kejang )

Nondepolarizing Muscle Relaxants

Cisatracurium Isomer of atracurium Dimetabolisme oleh Hofmann elimination Onset 3-5 minutes, duration 20-35 minutes Intubating dose 0.1-0.2 mg/kg Minimal cardiovascular side effects Produksi laudanosine lebih sedikit

Nondepolarizing Muscle Relaxants

Rocuronium Analogue of vecuronium onset cepat 1-2 minutes, duration 20-35

minutes Onset of action mirip dengan

succinylcholine Intubating dose 0.6 mg/kg Eliminasi terutama di hepar, sebagian di

ginjal

Nondepolarizing Muscle Relaxants

Temperature Acid-base balance Electrolyte abnormality Age Penyakit penyerta Drug interactions

Respon obat tergantung pada:

Penyakit penyerta: Neurologic diseases Muscular diseases

Myasthenia gravis Myasthenic syndrome (Eaton-Lambert

synrome) Liver diseases Kidney diseases

Alteration of responses

Drug interactions Inhalation agents Intravenous anesthetics Local anesthetics Neuromuscular locking drugs Antibiotics Anticonvulsants Magnesium

Alteration of responses

Fraction of receptor occupied by

nondepolarizing muscle relaxant

Response to nerve stimulator

Whole body signs

99-100 No response Flaccid, extreme relaxation

95 Posttetanic facilitation present

Diaphragm moves, hiccough possible

90 One of four twitch of TOF present

Abdominal relaxation adequate for most prcedure

75 Four twitch of TOF present, TOF ratio 0.7

Tidal volume and vital capacity normal

50 100-Hz tetanus sustained

Passes inspiratory pressure test

30 200-Hz tetanus sustained

Head lift and hand-grip sustained

Hierarchy 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

Mekanisme kerja: Inhibisi aktivitas acetylcholineesterase Ach semakin banyak di NMJ, berkompetisi

menduduki nicotinic cholinergic receptors Bekerja di muscarinic cholinergic receptor

Bradycardia Hypersecretion Increased intestinal tone

Antagonism of Neuromuscular Blockade

Efek Muskarinik diminimalisasi oleh anticholinergic agents Atropine

Dose 0.01-0.02 mg/kg Scopolamine glycopyrrolate

Antagonism of Neuromuscular Blockade

Tujuan : terjadinya spontaneous respiration dan kemampuan untuk mencegah aspirasi

Reversal of Neuromuscular Blockade