Dear Soren,

I am not a cardiologist, but it makes sense. Normal levels of K+ in the serum is around 3.5 to 5 mM (compared to intracellular levels of ~140 mM), and this level is very important for excitability of the action potential producing cells including cardiac cells and neurons. Increasing extracellular K increases excitability by bringing resting membrane potential closer to action potential firing threshold, in contrast decreasing extracellular K in contrast decreases excitability. The extracellular and intracellular levels of K are maintained by the Na-K-ATPase. I guess even having mild hypokalemia can hyperpolarize the membranes away from the action potential firing threshold, and also make the Na-K-ATPase work harder.

best wishes,

Refik

Dear Refik,

You are absolutely right about the mechanism, but it is still odd that the importance has not been described by others who make resuscitation research on animals, even the slightest decrease in K seems to by important. We will try to maintain a normokalemic state for the next line of experiments.

Kind regards, Søren. 

Hi Soren,

It may have been described 100 years ago but then forgotten over time. I remember from my BVSc years that the lactating cows can get hypokalemia due to loss of K with milk, and show signs of muscle weakness. Regardless, you should put something together and publish your results. Though you may need to do a proper dose-response for external K and identify the critical concentration when the resuscitation becomes impossible. Are there any cases or situations in humans when hypokalemia may occur? Also keep in mind that excessive extracellular (serum) K will also result in undesired conditions by over depolarizing the membranes to the level that can result in depolarization block, stopping action potential firing due to inactivation of voltage-gated Na and Ca currents and lack of hyperpolariozation.

regards, Refik