Suxamethonium Neuromuscular blockers, competitive

The competitive (non-depolarising) neuromuscular blockers and depolarising neuromuscular blockers mentioned in this section are listed in Table 5.2 , (p.91). The modes of action of the two types of neuromuscular blocker are discussed in the monograph Neuromuscular blockers + Neuromuscular blockers , p.l28. It should be noted that mivacurium (a competitive blocker) and suxamethonium (a depolarising blocker) are hydrolysed by cholinesterase, so share some interactions in common that are not relevant to other competitive neuromuscular blockers. 

The neuromuscular blockade due to suxamethonium (succinyl-choline) can be increased and prolonged by lidocaine, procaine and possibly procainamide. These local anaesthetics all have some neuromuscular blocking activity and may theoretically also enhance the block produced by competitive neuromuscular blockers. Increased toxicity occurred when mivacurium and prilocaine were given together for regional anaesthesia. 

Anticholinesterases oppose the actions of competitive neuromuscular blockers (e.g. tubocurarine) and can therefore be used as an antidote to restore muscular activity following their use. Conversely, anticholinesterases increase and prolong the actions of the depolarising neuromuscular blockers (e.g. suxamethonium (succinylcholine)). Anticholinesterases used to treat Alzheimer s disease may also interact with neuromuscular blockers. 

An in vitro study found that the acute neuromuscular effects of carbamazepine reduced the concentrations required for 50% paralysis with both a depolarising neuromuscular blocker (suxamethonium (succinylcholine)) and a competitive neuromuscular blocker (atracurium) by about 30%. ... 

The effects of cisatracurium, mivacurium, pancuronium, rocuro-nium, tubocurarine, vecuronium, and probably other competitive neuromuscular blockers can be increased and prolonged by magnesium sulfate given parenterally. There is some evidence that magnesium may interact similarly with suxamethonium (succinylcholine), but also evidence from well-controlled trials that it does not. 

Suxamethonium and decamethonium would be expected to antagonise competitive neuromuscular blockers due to their opposite mechanisms of action (suxamethonium and decamethonium exert a receptor agonist-type activity whereas competitive blockers exhibit receptor antagonism). However, the depolarising blockers may also reverse a competitive block by enhancing the effect of acetylcholine postsynaptically. ... 

Paralysis is preceded by muscular fasciculation, and this may be the cause of the muscle pain experienced commonly after its use. The pain may last 1-3 days and can be minimised by preceding the suxamethonium with a small dose of a competitive blocking agent. Suxamethonium is the neuromuscular blocker with the most rapid onset and the shortest duration of action. Tracheal intubation is possible in less than 60 seconds and total paralysis lasts up to 4 min with 50% recovery in about 10 min (t / for effect). It is particularly indicated for rapid sequence induction of anaesthesia in patients who are at risk of aspiration — the ability to secure the airway rapidly with a tracheal tube is of the utmost importance. If intubation proves impossible, recovery from suxamethonium and resumption of spontaneous respiration is relatively rapid. Unfortunately, if it is impossible to ventilate the paralysed patient s lungs, recovery may not be rapid enough to prevent the onset of hypoxia. 

The depolarising blockers (such as suxamethonium (succinylcholine)) act like acetylcholine to depolarise the motor endplate, but unlike acetylcholine, they are not immediately removed by cholinesterase. The anticholinesterase drugs increase the concentration of acetylcholine at the neuromuscular junction, which enhances and prolongs this type of blockade, and therefore anticholinesterases cannot be used as an antidote for this kind of blocker. Care should be taken if an anticholinesterase has been given to antagonise a competitive neuromuscular block prior to the use of suxamethonium, as the duration of the suxamethonium block may be prolonged. ... 

The manufacturer warns that irinotecan could possibly prolong the neuromuscular blocking effects of suxamethonium (succinylcholine) and antagonise the neuromuscular blockade of competitive (non-depolarising) drugs. This is based on the fact that irinotecan has anticholinesterase activity (see also Neuromuscular blockers + Anticholinesterases , p. 114, for an explanation of this mechanism). 

It has been suggested that depolarising neuromuscular blockers such as decamethonium and suxamethonium may have a presynaptic action resulting in reduced acetylcholine output. Although not always clinically significant, be aware that a reduction in the dose of competitive blocker may be necessary following the use of a depolarising neuromuscular blocker. 

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