Mivacurium Atracurium

Kim KS, Chun YS, Choi SU, Suh IK. Neuromuscular intemction between cisatracurium and mivacurium, atracurium, vecurcnium or rocuronium administered in combination. Anaesthesia (1998) 53, 872-8. 

The rate of non-lgE-mediated immediate hypersensitivity reactions usually varies between 20 and 50% [1-7, 9], They are assumed to result from direct non-specific mast cell and basophil activation, which causes direct histamine release [19], Histamine release is predominantly found with the use of the benzylisoquinoUnes d-tubocurarine, atracurium and mivacurium, and the aminosteroid rapacuronium. Severe bronchospasm related to rapacuronium administration has been reported in children and adults. It might be related to the higher affinity of rapacuronium for M2 versus M3 muscarinic receptors [20]. Rapacuronium has been withdrawn from the market in the USA. 

Avoid drugs that cause histamine release (e.g., morphine sulfate, codeine, atracurium, metocurine, mivacurium, and tubocurarine)... 

Vecuronium Rocuronium Pancuronium Atracurium Cis-atracurium Mivacurium Gallamine Tubocurare... 

Nondepolarizing Blockers d-Tdbocurarine, Atracurium, Mivacurium, Pancuronium, Vecuronium, Rocuronium, and Rapacuronium... 

Mivacurium chloride (Mivacron) is a newer agent that is chemically related to atracurium. The primary mechanism of inactivation is hydrolysis by plasma cholinesterase. Although it is useful for patients with renal or hepatic disease, some caution is warranted, since these individuals may have reduced plasma cholinesterase as a result of the disease. Mivacurium has an onset of action (1.8 minutes) and duration of effect (20 minutes) only twice that of succinylcholine, and in this respect, it is the most similar to succinylcholine of all of the nondepolarizing agents. 

Agent Tubocuranine Pancuronium Vecuronium Atracurium Rocuronium Cisatracurium Mivacurium Cis-trans isomer Trans-trans isomer C/s-c/s isomer... 

Mivacurium has onset of action similar to that of atracurium, but recovery from blockade is more rapid making mivacurium useful for short surgical procedures. Drug is hydrolyzed by plasma cholinesterase. 

By competition with acetylcholine (atracurium, cisatracurium, mivacurium, pancuronium, rocuro-nium, vecuronium). These drugs are competitive antagonists of acetylcholine. They do not cause depolarisation themselves but protect the endplate from depolarisation by acetylcholine. The result is a flaccid paralysis. 

Mivacurium belongs to the same chemical family as atracurium. It is the only nondepolarisng neuromuscular blocker that is metabolised by plasma cholinesterase. It is comparatively short acting (10-15 minutes), depending on the initial dose. Mivacurium can cause some h5rpotension because of histamine release. 

Ah HH, Savarese JJ, Embree PB, Basta SJ, Stout RG, Bottros LH, Weakly JN. Clinical pharmacology of mivacurium chloride (BW B1090U) infusion comparison with vecuronium and atracurium. Br J Anaesth 1988 61(5) 541-6. 

Caldwell JE, Heier T, Kitts JB, Lynam DP, Fahey MR, Miller RD. Comparison of the neuromuscular block induced by mivacurium, suxamethonium or atracurium during nitrous oxide entanyl anaesthesia. Br J Anaesth 1989 63(4) 393-9. 

Clinically important, potentially hazardous interactions with aminophylline, atracurium, cisatracurium, doxacurium, epinephrine, ergometrine, mivacurium, non-depolarizing muscle relaxants, oxprenolol, oxytocin, pancuronium, rapacuronium, rifampin, vecuronium, xanthines... 

NMBAs are further differentiated by their duration of action during anesthesia. Succinylcholine and mivacurium are common ultra-short-acting competitive NMBAs (5-10 min). An intermediate duration of action (30-45 min) is maintained with the use of atracurium, cisatracurium, rocuronium and vecuronium. A long-lasting duration of action (90-100 min) is observed with d-tubocurarine, doxacurium, metocurine, pancuronium and pipecuronium. 

The skeletal muscle reiaxants provide muscle relaxation and/or immobility via N-receptor interactions. Most including d-tubocurarine, pancuronium, atracurium, and mivacurium, are competitive and nondepolarizing and can be reversed by AChE inhibitors. Succinylcholine is a depolarizing, noncompetitive agonist. 

Atracurium, doxacurium, pancuronium, pipecuronium, d-tubocurarine, mivacurium. and metocurine are examples of nondepolarizing blockers. 

Fentanyl, ketamine, midazolam, > propofol, thiopental Depolarizing succinylcholine Nondepolarizing atracurium, mivacurium, tubocurarine... 

Lidocaine, bupivacaine, mepivacaine, 1 procaine, cocaine Depolarizing succinylcholine Nondepolarizing D-tubocurarine, atracurium, mivacurium... 

Pharmacokinetics All agents are given parenterally. Drugs that are metabolized (eg, mivacurium, by plasma cholinesterase) or eliminated in the bile (eg, vecuronium) usually have shorter durations of action than those eliminated by the kidney (eg, doxacurium, pancuronium, tubocurarine). Atracurium clearance involves spontaneous breakdown (Hofmann elimination) to form laudanosine and other products is largely independent of hepatic or renal function. 

Autonomic effects and histamine release Autonomic ganglia are stimulated by succinylcholine and blocked by tubocurarine. Succinylcholine also stimulates cardiac muscarinic receptors, while vecuronium is a moderate blocking agent. Tubocurarine is the most likely of these agents to cause histamine release, but it may also occur to a sUght extent with atracurium, mivacurium. and succinylcholine. A summary of these autonomic effects is shown in Table 27-3. 

Spontaneous or plasma ChE, intermediate-short duration Atracurium Cisatracurium Mivacurium... 

ChE cholinesterase. (Atracurium breaks down spontaneously mivacurium is metabolized by plasma ChE.)... 

The inhalational anaesthetics increase the effects of the neuromuscular blockers to differing extents, but nitrous oxide appears not to interact significantly. Ketamine has been reported to potentiate the effects of atracurium. Propofol does not appear to interact with mivacurium or vecuronium. Xenon is reported not to interact with mivacurium or rocuronium, and has less effect than sevoflurane on vecuronium neuromuscular blockade. Bradycardia has been seen in patients given vecuronium with eto-midate or thiopental. Propofol can cause serious bradycardia if it is given with suxamethonium (succinylcholine) without adequate antimuscarinic premedication, and asystole has been seen when fentanyl, propofol and suxamethonium were given sequentially. 

Anticipate the need to use more (possibly up to twice as much) doxacu-rium, metocurine, pancuronium, pipecuronium, rocuronium and vecuronium in patients who have taken these antiepileptics for more than a week, and expect an accelerated recovery. The effects on tubocurarine and atracurium appear only to be small or moderate, whereas mivacurium appears not to interact. 

Naguib M, Abdulatif M, Al-Ghamdi A, Selim M, Seraj M, El-Sanbary M, Ivkigboul MA. Interactions between mivacurium and atracurium. BrJAnaesth (1994) 73,484-9. 

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