Tugas Anestesi Muscle Relaxan
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Transcript of 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