A number of drugs may influence neuromuscular transmission and thus interfere with the action of both competitive and depolarizing neuromuscular blockers, resulting in potentiation or antagonism of neuromuscular block. Some interactions may be advantageous, such as the reversal of competitive neuromuscular block by anticholinesterases. In general, adverse reactions are potentially more serious in patients with impaired neuromuscular function.
Drug interactions affecting neuromuscular blockers of either type (competitive and depolarising) as well as those specific for competitive neuromuscular blockers.
Lidocaine, procainamide, quinidine and verapamil all have same neuromuscular blocking activity and may enhance the block produced by neuromuscular blockers. Large doses of lidocaine may reduce the release of acetylcholine and act directly on the muscle membrane.
Quinidine has a curare-like action at the neuromuscular junction and depresses the muscle action potential. If given during recovery from neuromuscular block, it can result in muscle weakness and apnoea and it should be avoided, if possible, in the immediate postoperative period.
Some antibacterials in very high concentration can produce a muscle paralysis that may be additive to or synergistic with that produced by neuromuscular blockers. The neuromuscular block produced by antibacterials may be enhanced in patients with intracellular potassium deficiency, low plasma-calcium concentration, neuromuscular disease, or a tendency to a high plasma-antibacterial concentration, for example after large doses or in renal impairment. The interaction appears to be more important for competitive neuromuscular blockers.
The antibacterials most commonly implicated are aminoglycosides, lincosamides, polymyxins and more rarely, tetracyclines.