Atrium Drug Interactions

As with other non-depolarising neuromuscular blocking agents, the magnitude and/or duration of atracurium's effects may be increased as a result of an interaction with the following agents.
Inhalation anesthetics: atracurium is potentiated by isoflurane, desflurane, sevoflurane and enflurane anesthesia, and only marginally potentiated by halothane anesthesia.
Antibiotics: including the aminoglycosides, polymyxins, spectinomycin, tetracyclines, lincomycin, clindamycin and vancomycin.
Anticonvulsants (acute administration only): phenytoin, carbamazepine.
Antiarrhythmic drugs: local anaesthetics such as lidocaine, procainamide, quinidine.
Beta-blockers: propranolol, oxprenolol.
Antirheumatic drugs: chloroquine, d-penicillamine.
Calcium channel blockers: diltiazem, nicardipine, nifedipine, verapamil.
Diuretics: furosemide, thiazides, acetazolamide and possibly mannitol.
Ganglion blocking agents: trimetaphan, hexamethonium.
Others: dantrolene, parenteral magnesium sulphate, chlorpromazine, steroids, ketamine, lithium salts and quinine.
Rarely, some of the previously mentioned drugs may aggravate or unmask latent myasthenia gravis or actually induce a myasthenic syndrome. In these situations a consequent increased sensitivity to atracurium would be expected.
The administration of combinations of non-depolarising neuromuscular blocking agents in conjunction with atracurium may produce a degree of neuromuscular blockade in excess of that which might be expected were an equipotent total dose of atracurium administered. Any synergistic effect may vary between different drug combinations.
A depolarising muscle relaxant such as suxamethonium chloride should not be administered to prolong the neuromuscular blocking effects of non-depolarising blocking agents such as atracurium, as this may result in a prolonged and complex block which can be difficult to reverse with anticholinesterase drugs.
The prior use of suxamethonium reduces the onset (to maximum blockade) by approximately 2 to 3 minutes and may increase the depth of neuromuscular blockade induced by atracurium. Therefore, the initial atracurium dose should be reduced and the reduced dose should not be administered until the patient has recovered from the neuromuscular blocking effects of suxamethonium.
The use of intravenous corticosteroids with neuromuscular blocking agents has been reported to antagonise neuromuscular blockades. In addition, prolonged co-administration of these agents may increase the risk and/or severity of myopathy resulting in prolonged flaccid paralysis following discontinuation of the neuromuscular blocking agent. The myopathy is usually reversible with recovery in several months.
The onset of neuromuscular blockade is likely to be lengthened and the duration of blockade shortened in patients receiving chronic anticonvulsant therapy (e.g. carbamazepine, phenytoin). However, if the anticonvulsants are given acutely, the neuromuscular blocking effects may be increased.
In principle, maintaining neuromuscular monitoring until complete reversal of neuromuscular blockade should permit detection of most interactions. Nevertheless, recurrence of neuromuscular blockade may occur, for example, upon treatment with post surgical antibiotics.