mivacurium
TRANSCRIPT
MIVACURIUMVerdah SabihHouse officerAnesthesiology dept. HFH
ROAD MAP INTRODUCTION STRUCTURE MODE OF ACTION PHARMACOKINETICS DOSAGE INDICATIONS SIDE EFFECTS INTERACTIONS WITH OTHER DRUGS
INTRODUCTION: non-depolarizing/competitive neuro
muscular-blocking drug or skeletal muscle relaxant.
Fast onset & short duration(10-20 mins). no sedative or analgesic effects. not considered to trigger malignant
hyperthermia. not associated with vagolytic activity or
ganglionic blockade.
STRUCTURE Belong to
benzylisoquinolinium group non-depolarizing skeletal muscle relaxants.
Symmetrical molecule.
PHARMACOKINETICS Onset time : 2-4 mins Duration :12-18 mins Elimination by plasma cholinesterase. Hepatic impairment reduce dose in severe
impairment Renal impairment clinical effect prolonged in
renal failure—reduce dose according to response ED95 of mivacurium is 0.08 mg/kg. mean elimination half-life : 1.7 to 2.6 min Poor lipid solubility does not enter CNS Highly polar,inactive when given by mouth
only intravenous route avaliable.
MODE OF ACTION
1.resting:
2.active:Na Ca
K
ACh
ACh
Normal transmission Non depolarizing neuromuscular blockade
Low doses: •competitive antagonist of Ach•Action reversed by Ach esterase inhibitors
Large doses:•Ion channel is blocked•More weakness of neuromuscular transmission•Action could not be reversed by Ach esterase inhibitors
Other actions:Can block pre-junctional sodium channels and interfere with mobilization of Ach at nerve endings
MODE OF REVERSAL cholinesterase
inhibitors as neostigmine and pyridostigmine by:
1- increasing the availability of acetylcholine at the motor end plate
2- to a lesser extent, neostigmine and pyridostigmine increase release of transmitter from the motor nerve terminal
The deeper the level of neuromuscular block at reversal, the longer the time required for recovery of neuromuscular function and the greater the dose of anticholinesterase agent required. Because spontaneous recovery after mivacurium is rapid, routine reversal may not always result in a clinical. benefit
DOSAGE AND ADMINISTRATION By intravenous injection:
ADULT 70–250 mg/kg; maintenance 100 mg/kg every 15 min;
CHILD 2–6 months initially 150 mg/kg, 7 months–12 years initially 200 mg/kg; maintenance (CHILD 2 months–12 years) 100 mg/kg every 6–9 minutes
By intravenous infusion ADULTafter initial bolus intravenous dose, maintenance
of block, 8–10 mg/kg/min, adjusted if necessary every 3 min by 1 mg/kg/minto usual dose of 6–7 mg/kg/min;
CHILD 2 months–12 years, usual dose 11–14 mg/kg/min Resistance can develop in patients with burns, who
may require increased doses; low plasma cholinesterase activity in these patients requires dose titration for mivacurium.
INDICATIONS Skeletal muscle relaxation during
surgery Mechanical Ventilation Endotracheal Intubation
CONTRAINDICATIONSNo documented contraindications except in
such conditions; Allergy Myasthenia Gravis Asthma
CLINICAL SIDE EFFECTS histamine release, which can cause skin
flushing, hypotension, tachycardia, bronchospasm,
anaphylactoid reactions (rare). Acute myopathy
INTERACTIONS WITH OTHER DRUGS Inhaled anesthetics: augment the
neuromuscular blockade produced by nondepolarizing muscle relaxants because
1) CNS depression 2) peripheral vasodilatation larger
fraction of the injected muscle relaxant to reach the neuromuscular junction
3) decreased sensitivity of the postjunctional membrane to depolarization.
Aminoglycosides: augment the neuromuscular blockade produced by nondepolarizing muscle relaxants by decreasing release of Ach
Local Anesthetics enhance the neuromuscular block produced by both nondepolarizing and depolarizing.
Calcium Channel Blockers synergistic effect.
Interactions between Nondepolarizing Blocking Drugs synergistic/additive.
Depolarizing relaxants antagonistic.