Why is repolarization delayed in class II, IV antiarrhythmics?

[OphthLover]

FirstAid states that in both class II and IV antiarrhythmics, repolarizations are delayed in nodal cells, but I am having difficulty understanding why. Isn't the repol done by opening potassium channels? How does blocking Ca2+ influx into the cell delay K+ channel-led repolarization? Is it because when there is less Ca2+ current flowing into the cell, there'd be less electrical repulsion to pump K+ out of the cell? I'd appreciate very much your help. Thank you.

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[wjs010]

Part of the funny currents are calcium right? Someone correct me if I'm wrong. So if you delay these funny (calcium) currents, that phase would be delayed.

 

[EmetyreUSMLEStep1Tutor1]

Part of the funny currents are calcium right? Someone correct me if I'm wrong. So if you delay these funny (calcium) currents, that phase would be delayed.

No, its not a part of If channels. Na and K are.

Mate, you confused me too

 

[wjs010]

No, its not a part of If channels. Na and K are.

Mate, you confused me too

sorry, I have it in my notes that there's a small bit of calcium in the I(f) channels, which is why things like class 1c drugs affect the nodal refractory rate (prolong)...i'll look it up for clarification

 

[wjs010]

sorry for the confusion: BRS says that I(f) are mainly Na+, so I guess I cannot answer OP's question.

 

[worldbeater]

I am pretty sure repolarization is affected only by potassium efflux in phase 3 (and by class 3 antiarrhythmics), for both the atrium and ventricle. So the original statement doesn't really make any sense to me.

 

[Entadus]

FirstAid states that in both class II and IV antiarrhythmics, repolarizations are delayed in nodal cells, but I am having difficulty understanding why. Isn't the repol done by opening potassium channels? How does blocking Ca2+ influx into the cell delay K+ channel-led repolarization? Is it because when there is less Ca2+ current flowing into the cell, there'd be less electrical repulsion to pump K+ out of the cell? I'd appreciate very much your help. Thank you.

Class II are Beta-blockers (beta adrenoceptor antagonists). Since the end effect of NE is not only accelerated depolarization through funny sodium currents but also quicker repolarization... So by blocking Beta receptors you would be lengthening the time required to hyperpolarize(repolarize). They will also decrease the rate of spontaneous depolarization (If )Na+ channels by decreasing the effects of sympathetic input.

Class IV is Ca++ channel blockers.... since you're asking about nodal cells, these drugs would prolong the action potential duration (reduced slope of phase zero through Ca++ channels NOT sodium like in ventricular cells). As a result, they will slow the rate of AV conduction in pts with re-entry arrhythmias (but also prolong QT). Examples include Diltiazem and Verapamil

I know K+ blockers (Class III) will prolong(delay) repolarization as well.

 

[Brorthopedic]

When talking about nodal cells, you are referring to slow response AP.

Calcium channel blockers reduce the AP amplitude which reduces the conduction speed.

 

[seminoma]

FirstAid states that in both class II and IV antiarrhythmics, repolarizations are delayed in nodal cells, but I am having difficulty understanding why. Isn't the repol done by opening potassium channels? How does blocking Ca2+ influx into the cell delay K+ channel-led repolarization? Is it because when there is less Ca2+ current flowing into the cell, there'd be less electrical repulsion to pump K+ out of the cell? I'd appreciate very much your help. Thank you.

Don't know if it's accurate science, but I've always thought of it as CCBs block calcium influx = relatively higher extracellular Ca2+ = reduced charge gradient = reduced K+ efflux.