Neuromuscular blockers depolarising

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. 

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 interaction between competitive (non-depolarising) neuromuscular blockers and parenteral magnesium is established. Magnesium may decrease the time to onset (vecuronium but not rocuronium), prolong the duration of action and reduce the dose requirement of competitive neuromuscular blockers. Be alert for an increase in the effects of any compet-... 

Combinations of competitive (non-depolarising) neuromuscular blockers may have additive or synergistic effects. Structural differences between the interacting neuromuscular blockers may have an effect it has been suggested that structurally similar neuromuscular blockers tend to produce an additive response, whereas structurally different blockers may be synergistic. For example, additive effects have been found between the structurally similar combinations of ... 

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. 

A double-blind placebo-controlled study of 30 patients undergoing elective surgery found that intravenous ondansetron 8 or 16 mg given over 5 minutes had no effect on subsequent neuromuscular blockade with atracurium. No special precautions would therefore seem necessary. The authors suggest that no interaction is likely with other non-depolarising neuromuscular blockers, but this needs confirmation. 

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. 

Fig. 7. Effect of calcium and acetylcholine on histamine release (means standard errors) by alcuronium in a patient with idiosyncrasy to non-depolarising neuromuscular blockers. Broken /me=control e/re/ej=without Ca " diamondsCa triangles—W ih Ca " and 10 pg/ml acetylcholine...

Non-depolarising neuromuscular blockers (NMBs) in normal doses act by competitive inhibition of the interaction between acetylcholine and nicotinic receptors. In higher doses, they are thought to block the ion channel as well, which explains the decreased effectiveness of AChE inhibitors in treating non-depolarising neuromuscular blocker toxicity. 

The duration of action of non-depolarising neuromuscular blockers is basically dependent on their metabolism, with agents excreted by the kidney being the longer acting. Here, we should take into consideration that patients under surgery have different liver and kidney functions from aware patients, as do elderly and young patients. 

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