Although not directly related to the original question, as someone with extensive electrophys background, I just want to correct a common misunderstanding involving hyperkalemia and RMP, i.e. the thinking that hyperkalemia causes the resting membrane potential (RMP) to be more negative and therefore the heart less excitable.
This explanation, although seemingly very intuitive, is actually false, and can cause problems down the line when trying to explain other arrhythmias that occur with electrolyte abnormalities. Therefore, I think it's important to clarify this point: hyperkalemia causes the RMP to actually be more positive (in fact, it's HYPOkalemia that causes the RMP to be more negative; see attached image). Weird, I know, but bear with me.
The reason for this is because electrical charge across membranes is determined by the flow (or more accurately, the INCENTIVE to flow) of ions across membranes, not the concentrations of ions themselves. For example, K+ is a mostly intracellular ion (140 mM inside vs. 5 mM outside) that carries a positive charge. Therefore, based on the default RMP of -90 mV in the heart, the direction that K+ naturally likes to flow is out of the cell. Since K+ is a positive ion, the more it wants to flow out of the cell, the more negative the intracellular space will become. Therefore, if you look at how RMP is affected by K+ based on how much INCENTIVE it has to flow out of the cell, how hyper- and hypokalemia respectively affect the RMP becomes clear.
So let's look at hyperkalemia. In hyperkalemia, the extracellular K+ concentration increases to >5 mM. Assuming the intracellular K+ stays largely unchanged at 140 mM due to how strictly cells regulate their potassium, the concentration gradient of intracellular vs. extracellular K+ will decrease. This decreased gradient in turn reduces the incentive for K+ to flow out of the cell (i.e. more K+ wants to stay inside the cell now). And since K+ is a positive ion, the decreased incentive to flow out makes the inside of the cell more positive compared to the outside, hence raising the RMP. The reverse is true for hypokalemia.
Does these minute details matter? Yes, because knowing that hyperkalemia makes the RMP more positive can help explain why a lot of patients with hyperkalemia (particularly mild hyperkalemia) experience cardiac hyperexcitability and palpitations (because the RMP is now closer to the cardiac action potential threshold). Interestingly however, more severe hyperkalemia will have the paradoxical effect of decreasing cardiac excitability due to the progressive inactivation of sodium channels at RMPs higher than -70, which counteracts the effect of the RMP being close to the action potential threshold. In summary, hyperkalemia has an fascinating biphasic effect on the heart depending on how severe it is: mild hyperkalemia causes the heart to go into overdrive, while more severe hyperkalemia will cause QRS prolongation (because of sodium channel inactivation) and dampen overall heart function.