Nondepolarizers and electrolytes

[hotroddin]

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Recently I was reading through some text that didn't quite make sense regarding potassium and NM blockers. In big Miller 6th edition, it states hypocalcemia potentiates the actions of nondepolarizers which reasoning I think I understand. However it doesn't comment on potassium that I could find. However, in big blue it states that low potassium as well as hypocalcemia potentiate NM blockers. This seems a little counterintuitive as we use hyperkalemia to induce cardioplegia. So one would think that high potassium would potentiate NM blockers, not HYPOkalemia. Any help with this concept is appreciated.
Hotroddin

 

[Mman]

NMBs have nothing to do with cardiac myocytes, at least as far as I can remember and I wouldn't even attempt to use information from potassium values with NMBs and correlate it with how cardioplegia works.

 

[Gern Blansten]

Stoelting's Coexisting Disease Text, 4th Edition, Pg 382. Also, the product insert for succinylcholine warns of the risk. Also, search Hypokalemic Periodic Paralysis for some more interesting information that is peripherally related.

 

[Planktonmd]

As you know, potassium is mainly an intracellular electrolyte, actually 98% of it is intracellular and only 2% is extracellular.
Maintenance of high intracellular potassium and high extracellular sodium is essential for the membrane to have a polarization that would allow depolarization / repolarisation action.
Low serum potassium reflects low extracellular potassium which could be caused by two different things:
1- Potassium shift from extracellular to intracellular (relative low potassium) like the one caused by alkalosis for example, this should not affect skeletal muscles too much unless there is also low magnesium and low calcium (frequent).
2- True low potassium, (intracellular), which could cause extracellular hypokalemia as well. This is usually chronic, and will cause profund decrease in the membrane polarization in the muscles, and the neuro-muscular junction as well, the result will be lower amplitude of the action potential, and weaker muscle contraction. This will strengthen the effect of non depolarizing relaxants and possibly increase their duration.