The source of increased plasma potassium following succinylcholine.
Increases in plasma potassium following succinylcholine have been reported by many workers. In the present studies, these are greater when Althesin is used as the induction agent than after thiopental, and the rise is particularly marked in patients given halothane, occurring earlier in patients having electroshock therapy, and being reduced by the prior administration of a small dose of tubocurarine. These findings suggest that  the rise in potassium is due to muscle trauma indiced by the relaxant during the period of fasciculation, and this is confirmed by an increase in creatine phosphokinase enzyme activity. Althesin and halothane are best avoided with succinylcholine in chronic catabolic states where an excessive rise in plasma potassium could lead to dangerous cardiac dysrhythmias.
D003402:Creatine Kinase / Q000097:blood; D004597:Electroshock; D005260:Female; D006801:Humans; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009132:Muscles / Q000201:enzymology; D011188:Potassium / Q000097:blood*; D013268:Stimulation, Chemical; D013390:Succinylcholine / Q000008:administration & dosage / Q000494:pharmacology*; D013997:Time Factors
D003402:Creatine Kinase; D013390:Succinylcholine; D011188:Potassium