How do CCBs increase ERP?

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ChessMaster3000

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If they block calcium channels, this would decrease the length of the plateau (phase II), so I dont understand how the ERP is increased. Any thoughts?

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that's because they act on pacemaker tissue(SAN, AVN), not ventricular muscle. Hence they decrease the slope of phase 0(Ca2+ influx is slowed) leading to increased ERP.
 
No. I looked up the same thing, maybe youll have better luck, but I was expecting find a clear cut answer (eg 2 different receptors with different names etc) but it just became way to confusing to be beneficial.
Like someone on another thread mentioned. Class I and III = atrial/ventricle, Class II and IV = nodal tissue. If you find a good answer be sure to share
 
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Calcium-channel blockers reduce the slope of phase 4, thereby decreasing the rate of spontaneous depolarization, which reduces the rate of pacemaker firing. These drugs also decrease the slope of phase 0, which slows conduction velocity within the AV node. The AV nodal ERP is also lengthened by calcium-channel blockers.Potassium-channel blockers delay phase 3 repolarization, thereby lengthening the action potential duration and ERP.
CV Pharmacology: Cardiac Action Potentials
I get what your saying in that I don't really know what an longer ERP means in nodal tissue but this dude says there is
 
so phase 3 is not affected in nodal tissue?

Phase 3 in the nodal AP is not due to calcium, it is due to potassium. Phase 0 is the upstroke, which is due to calcium. Block calcium = nodal cells depolarize even slower = increased ERP.
 
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You're right, it makes sense that they would have one, but I had a hard time imaginging how that plays out on nodal tissue phases. google image search helped
avnerp_1.png%3Fw%3D600
 
Can anyone explain why CCBs prolong repolarization at the AV node? If this because they extend the ERP (I thought the ERP was in reference to phase 0 not the funny current)
upload_2014-2-18_2-57-54.png
 
If they block calcium channels, this would decrease the length of the plateau (phase II), so I dont understand how the ERP is increased. Any thoughts?

Can anyone explain why CCBs prolong repolarization at the AV node? If this because they extend the ERP (I thought the ERP was in reference to phase 0 not the funny current)
View attachment 178572

This should be a fairly simple concept from what I can tell. So I think its a matter of syntactical confusion.

First, ERP needs to be defined. Effective refractory period is the time when NO stimulation can cause another AP. Why is this the case? this is because the AP has not sufficiently decreased enough to open the gates for the funny Na current involved in phase 4. These currents only open up when the AP has sufficiently decline enough to some level. This extends from the minute phase zero begins and all the way to when phase 4 is ending.

Thus, the ERP is not necessarily during the repolarization phase but the phases before that including the slow rise of the AP.

CCB prolong repolarization not because they necessarily affect the repolarization phase itself but by lengthening the entire AP - this is because they slow the rate at which the phase zero current opens. Because of the decreased slope of phase zero the entire AP is stretched out- as a result the reploarization phase also is pushed farther out (though its slope may not be affected)- thus this causes an increase in the overall repolarization.

Finally, the biggest confusion seems to be what CCBs actually do. They do NOT completely block calcium channels. I know weird right. They only slow them down. As a result, they delay the action potential slope and lengthen int instead of closing it entirely. If they completley blocked then yes the AP would be shortened and the ERP would be shortened. but instead, they merely slow the calcium movement....this causes the slope to be longer.
 
This should be a fairly simple concept from what I can tell. So I think its a matter of syntactical confusion.

First, ERP needs to be defined. Effective refractory period is the time when NO stimulation can cause another AP. Why is this the case? this is because the AP has not sufficiently decreased enough to open the gates for the funny Na current involved in phase 4. These currents only open up when the AP has sufficiently decline enough to some level. This extends from the minute phase zero begins and all the way to when phase 4 is ending.

Thus, the ERP is not necessarily during the repolarization phase but the phases before that including the slow rise of the AP.

CCB prolong repolarization not because they necessarily affect the repolarization phase itself but by lengthening the entire AP - this is because they slow the rate at which the phase zero current opens. Because of the decreased slope of phase zero the entire AP is stretched out- as a result the reploarization phase also is pushed farther out (though its slope may not be affected)- thus this causes an increase in the overall repolarization.

Finally, the biggest confusion seems to be what CCBs actually do. They do NOT completely block calcium channels. I know weird right. They only slow them down. As a result, they delay the action potential slope and lengthen int instead of closing it entirely. If they completley blocked then yes the AP would be shortened and the ERP would be shortened. but instead, they merely slow the calcium movement....this causes the slope to be longer.

Thanks for that! So your saying that the CCBs decrease the slope of phase 0 and everything else (phase 3,4) is basically shifted right due to that while their respective slopes remain the same?
 
Got it. Class IV = extend the ERP by slowing Ca+ conduction of phase 0. So Class IA and III in contrast extend the ERP by prolonging repolarization in non pacemaker cells, i.e. phase 3?
 
I think so. not so great with cardiac pharm atm- I did cards like 2 months ago gottta rereview.
 
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