SDN Members don't see this ad. (About Ads) A friend mentioned the use of a defasciculating dose of a nondepolarizing muscle relaxant to eliminate the fasciculations that come with using Succinylcholine (in this case they wanted no fascic. to prevent transient rises in ICP for a neuro case). After discussing it I decided that I didn't understand the mechanism for how this would work. I can see how depolarizers work: mimic ACh to cause the endplate to generate an action potential, but whereas ACh releases the receptor, Sux. holds on and maintains end-plate depolarization. Which means the muscle contracts then becomes flaccid... So... if you give a "defasciculating dose" of Roc or Vec or whatever, it will competitively inhibit sux from binding, which means that you'll have to an increased dose of Sux... Which seems to leave you in the same situation - overriding ACh (and now Roc as well) in order to create an endplate depolarization... and fasciculations? Clearly I'm missing something. The only thing I can think of is that by using a nondepolarizing muscle relaxant first you paralyze some muscles fibers through nondepolarization, then others through depolarization. Since you give a larger dose of Sux, it ultimately outcompetes the Roc, but over a longer time which creates smaller/less fasciculations?