K+ out of cells should lead to hyper polarization. If I stated otherwise, that is likely a mistake. Can you tell me where in the article this was?

I really love this breakdown – definitely helps me understand some of the basic principles!

I have an issue with the potassium channels increasing to increase K+ out which causes depolarization, however. Specifically, I have an issue with it because adenosine causes K to leave which hyperpolarizes the cell – this directly conflicts with your etiology detailed here stating that more K out causes depolarization of the cell membrane. Any explanation for that?

Hi Wisdom Seeker.  Wow, lots to address here.  First, my understanding is that you want to give Ca++ NOT to control nodal tissue, per se, but because the arrhythmias that will kill you are the ones that start in the ventricle (V-Fib, V-Tach).  In other words, you want to decrease the risk of ventricular arrhythmias, and Ca++ can reduce the excitability of ventricular myocytes.  You are correct that hyperkalemia can cause weakness, but the main reason you want to treat K+ is because it can be fatal (I had a close family member who passed away recently, presumably because of an arrhythmia, so this is very real, and quite deadly).  Thanks again for the feedback – I look forward to hearing from you on other/future articles!

Hyperkalemia (↑ extracell K+) bc resting membrane potential is determined by potassium — although it raises the membrane potential, this sustained depolarization actually causes the slow responding Na+ inactivation gates to remain closed– making it unlikely/impossible for AP to occur in SKELETAL & non-nodal cardiac muscle (correct?) — causing weakness
BUT in nodal cardiac muscle — bc it doesn’t depend on voltage Na+ inactivation/activation gate mechanism, rather only Ca++ conductance– by raising the membrane potential & perhaps passing the depolarization threshold potential w/ hyperkalemia you are MORE likely to get arrhythmia

vs

Hypercalcemia (↑ extracell Ca++) bc has little influence on the membrane potential just raises the depolarization threshold potential (I’m guessing bc there is no conductance Ca++ just a bigger concentration gradient difference) you are LESS likely to have AP in SKELETAL & non-nodal cardiac muscle (same as hyperkalemia)– causing weakness too
BUT in nodal cardiac muscle– bc resting membrane potential is still dependent on K+– you won’t get arrhythmias with hypercalcemia bc you are just raising the depolarization threshold potential making it still less likely for AP to occur

So giving calcium is just to prevent the most dangerous part of hyperkalemia in its effects on the heart? Bc otherwise, you would want to reduce potassium levels to get the resting membrane potential back to normal for the effects on skeletal muscle and non-nodal cardiac tissue.

Thank you! Hope you can help clear this up.

Hi FemmeFatale,

Thank you so much for your feedback, and for your great questions. You are correct – hyperkalemia would raise the membrane potential, moving it closer to the depolarization threshold. Thus, hyperkalemia would make it EASIER to set off an action potential. Calcium has the ability to raise the depolarization threshold, thus making it harder to depolarize.

Simply put, hyperkalemia makes it easier to set off an action potential, so we give calcium to people to make it harder to get an action potential again, since ventricular arrhythmias are very dangerous.

Hope this helps!
Alec

1. “Ca++ is thought to raise the threshold for depolarization” – Make it harder for depolarization?
2. “hyperkalemia ↑ membrane potential” – Make it easier for depolarization?
3. “give Ca++ to ↑ the action potential threshold” – Make it harder for depolarization?

Thanks for the positive feedback!! Glad it helped!!!