ion concept questions

[Medicman13]

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Can somebody please explain why tetany occurs with hypocalcemia?
Also, why does hypokalemia enhances cardiac automaticity and delays ventricular repolarization?
Thanks for your help

 

[Bernoull]

Can somebody please explain why tetany occurs with hypocalcemia?
Also, why does hypokalemia enhances cardiac automaticity and delays ventricular repolarization?
Thanks for your help

hypocalemia lowers AP threshold thus --> increased excitability.
Maybe some else can expound on it.

I'm not sure about the the hypokalemia question but increasing automaticity AND delaying repolarization seem antithetical, doesn't the membrane need to repolarize b4 firing another AP, how does delaying the repolarization increase rate of AP firing?

 

[hrain]

I'm not sure about the hypokalemia question, either, but here's my take on the hypocalcemia part:

Calcium stabilizes the voltage-gated Sodium channels' "closed state." So, low calcium makes the NaV channels hyperexcitable, causing muscle spasms and tetany.

I hope that makes sense...

 

[hrain]

Here's the best explanation that I've found. Hope it helps.

There is increased excitability of nerve and muscle with decreased calcium ions (hypocalcemia), because the threshold for activation of an action potential moves closer to the resting membrane potential without changing the level of the resting membrane potential. The reason for this is that there are negative charges on the outside of the membrane that are normally screened by the calcium ions. When Ca is low, the screening is decreased. The Na+ channels then see the negative charge outside and act as if the membrane were depolarized by opening even though the resting membrane potential is unchanged.

 

[hrain]

And as for the Hypokalemia part, I'll try to reason it out but I'm not entirely certain that I'm correct, so take it with a grain of salt.

Automaticity is the ability of the cardiac muscle to DEpolarize without any external influence. I believe that hypokalemia should bring the membrane potential closer to 0 (ie a little closer to the Na+ Nernst potential and further away from the K+ Nernst potential of -95mV). So, the muscle can be DEpolarized more easily, because it's already not as polarized.

Meanwhile, ventricular REpolarization is caused by the Calcium channels closing and the K+ rectifier channels opening up to allow outflow of K+. If there's less Potassium, the ventricles would take longer to fully repolarize, because there's simply less K+ to flow out through the channels.

I hope that makes sense and that I'm not saying it wrong. Like I said, this is just me trying to reason through it, and I'm not going by any book, so I'm sorry if it's not right!