Suxamethonium Quinidine

The place of the dmg in dentistry [153 4] and in electro-convulsive therapy [ 154] (with a description of a technique to surmount difficulties arising from the concurrent use ot suxamethonium) has been evaluated. A refined radio telemetric technique has enabled a detailed study [155] of the cardiovascular effects of propanidid to be made, resulting in strong evidence for a transient procainamide- or quinidine-like depression of myocardial conductive tissue. The above publications [150-5] quote a large number of relevant references. 

Cuthbert MF. The effect of quinidine and procainamide on the neurom uscular blockii action of suxamethonium. BrJ Anaesth (1966) 38,775-9. 

The effects of both depolarising neuromuscular blockers (e.g. suxamethonium (succinylcholine)) and competitive neuromuscular blockers (e.g. tubocurarine) can be increased by quinidine. Re-curarisation and apnoea have been seen in patients when quinidine was given during the recoveiy period from neuromuscular blockade. 

Not fully understood, but it has been shown that quinidine can inhibit the enzyme (choline acetyltransferase), which is concerned with the synthesis of acetylcholine at nerve endings. Neuromuscular transmission would be expected to be reduced if the synthesis of acetylcholine is reduced. Quinidine also inhibits the activity of plasma cholinesterase, which is concerned with the metabolism of suxamethonium. ... 

The interaction between quinidine and neuromuscular blockers is an established interaction of clinical importance, but the documentation is limited. The incidence is uncertain, but it was seen in one report cited to a greater or lesser extent in 5 of the 6 patients studied.- It has only been reported clinically with metocurine, tubocurarine and suxamethonium, but it occurs in animals with gallamine, and it seems possible that it could occur clinically with any depolarising or non-depolarising neuromuscular blocker. Be alert for increased neuromuscular blocking effects during and after surgery. 

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