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mdubb342 mdubb342 (New Member)

Ca++ and Threshold potential

CRNA   (693 Views 5 Comments)
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Hey everyone I have a calcium question:

In patients with hyperK+, Ca++ blocks the Na+ leak channels reducing the rate of depolarization and may also decrease VRM (please correct me if I am wrong). However, we learned in physiology that Ca++ can be beneficial in early hyperK+ by increasing threshold potential. I've searched high and low (googleing), and I cannot find the mechanism for how this works. Can anyone help a brotha out?

Thanks in advance!

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Hey everyone I have a calcium question:

In patients with hyperK+, Ca++ blocks the Na+ leak channels reducing the rate of depolarization and may also decrease VRM (please correct me if I am wrong). However, we learned in physiology that Ca++ can be beneficial in early hyperK+ by increasing threshold potential. I've searched high and low (googleing), and I cannot find the mechanism for how this works. Can anyone help a brotha out?

Thanks in advance!

What the heck does VRM mean?

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In hyperK, the resting membrane potential rises, which brings it closer to the threshold potential. This means that a much smaller stimulus is needed to trigger an action potential, which can lead to arrhythmias. Ca raises the threshold potential without raising the resting membrane potential. This restores the difference between resting and threshold potentials and makes it harder to trigger an AP.

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In hyperK, the resting membrane potential rises, which brings it closer to the threshold potential. This means that a much smaller stimulus is needed to trigger an action potential, which can lead to arrhythmias. Ca raises the threshold potential without raising the resting membrane potential. This restores the difference between resting and threshold potentials and makes it harder to trigger an AP.

To the OP, you mention early hyperkalemia and calcium, which our resident resident nicely broke down for us, but you mention early, and thus imply late, or worseneing hyperkalemia effects of benefits of giving calcium.

You see this in the widening of the QRS (conduction delay) as hyper K progresses because it is the value of the RMP at the moment of depolarization that determines the number of sodium channels available for impulse conduction. The more positive the RMP, the less sodium channels available and the slower the conduction and the wider the QRS.

So while calcium does affect irritability of cardiac myocytes as described by Pres, it won't stop the dreaded "sine wave" EKG pattern leading to asystole. To do that you need to drop the serum potassium and get the RMP more negative.

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Yes. Ca can "buy you some time" by maintaining the difference between RMP and threshold, but it will not keep badness from happening. This is true of most "treatments" like bicarb, hyperventilation, insulin/glucose, albuterol, etc which only shift K instead of getting rid of it.

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