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For Class 1c drugs, FA states that it doesnt increase the APD/ERP in ventricular tissue(ventricular AP), but in the AV node and accessory tracts(im assuming WPW and such) it prolongs the ERP, but it doesnt have the diagram for it, and i did pharm from kaplan and they didnt mention it. So is this an important point, bc FA didnt draw the diagram in.
 

Nabin

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For Class 1c drugs, FA states that it doesnt increase the APD/ERP in ventricular tissue(ventricular AP), but in the AV node and accessory tracts(im assuming WPW and such) it prolongs the ERP, but it doesnt have the diagram for it, and i did pharm from kaplan and they didnt mention it. So is this an important point, bc FA didnt draw the diagram in.
I think its something to do with the use-dependence of class IC drugs. They have high affinity to non-resting Na channels. This would mean they are more effective in constantly depolarizing tissues. They are rather slow to dissociate from the channel and when heart is firing rapidly it also gives it less time to dissociate from the channel make it more effective. This is the 'Use-dependence' phenomenon. Its kind of proarrythmic in this regard, and the reason you don't give this to Post-MI patients.
 
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Nabin

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Also how do Class IV's increase the ERP?
I guess this is due to the less intracellular Calcium available for the fast-response tissues. This would slow the plateau phase (phase 2). So, ultimately ERP will be prolonged.
 
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less calcium would shorten the plateau, bc of the continued K efflux, so the duration if anything would be shortened. your first explanation is spot on, saw that in a UW concept too.
 

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less calcium would shorten the plateau, bc of the continued K efflux, so the duration if anything would be shortened. your first explanation is spot on, saw that in a UW concept too.
Less intracellular calcium meaning that less calcium will enter inside the ventricular myocyte due to blockage of the Ca++ receptors during the plateau phase. This means it takes longer for the phase 2 to complete. This will ultimately increase the time the cell stays in its ERP.

EDIT: Sorry for bad english!
 
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that still doesnt make sense, bc ca2+ would promote depolarization, the K efflux is promoting towards repolarization, if you lose the calcium coming in, you'll repolarize faster, and shortened plateau. ALso w/tthe use dependance, the use dependance thing is cool, but if its overall effect isnt to increase ERP, why would it do it in the av node's and bypass tracts? unless its Na channel blocking effect is increased w/use dependance, therefore prolonging phase 4 of the funny current.
 

Nabin

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that still doesnt make sense, bc ca2+ would promote depolarization, the K efflux is promoting towards repolarization, if you lose the calcium coming in, you'll repolarize faster, and shortened plateau. ALso w/tthe use dependance, the use dependance thing is cool, but if its overall effect isnt to increase ERP, why would it do it in the av node's and bypass tracts? unless its Na channel blocking effect is increased w/use dependance, therefore prolonging phase 4 of the funny current.
I think this is due to the nature of the delayed rectifier potassium channels (Ik). These channels are slow to open and their opening is activated by a preceding depolarization. Like in this case, increasing Ca++ influx drive the K+ efflux that occurs via this channels, without that they are even slower to open.

Class IC increase the refractoriness of the cells to subsequence depolarizations. They are use-dependent in the sense that they bind with high affinity to Na channels when they are open. After depolarization has finished, the drug (like Flecainide) doesn't dissociate from the Na-channel very easily, and it will thus prevent any reentrant circuit from passing through it again. The higher the rate of depolarizations, the more the Na channels open, the more the drug binds and doesn't let go. That is also why these drugs are effective against tachys and not much against bradys.

I will go with this info. My exam is in 12 days. :p :p
This area of step 1 (including ethics and biostats) gives me nightmares!
 
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so by not letting go, it keeps the channels in a depolarized state, preventing it to go through the entire AP again?(class 1c) Biostats itself doesnt give me nightmares, but whenever i see a question, my eyes roll back and forth hoping that its not an actual biostats question lmao.
 
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Nabin

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so by not letting go, it keeps the channels in a depolarized state, preventing it to go through the entire AP again?(class 1c)
Its blocking the Na channels and preventing it go back to its closed, deactivated state when it can be further excited again, so essentially prolonging the ERP. The cell cannot be excited again with a conducted AP unless the drug stops binding the channel. And because it has the property of dissociating slowly, it makes it even harder for another AP to conduct through the Na channel. All of those class I agents have this membrane stabilizing effect and only differences are when they bind to the channels, their affinities and their effects on APD. I tried to understand this even more but then the electrode mafia showed up and I asked myself if I were a physics student. :D :D
If you have time, you can look into it. I saw plenty of articles of them doing those freaky electrode experiments. I just snapped out of it in no time..


Biostats itself doesnt give me nightmares, but whenever i see a question, my eyes roll back and forth hoping that its not an actual biostats question lmao.
That was one of the funniest things I've heard in a while. lmao.
 
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what controls conduction velocity? a table in FA mentions that class 1 a, c, slow conduction velocity, while other anti-arrh dont.
 

Nabin

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what controls conduction velocity? a table in FA mentions that class 1 a, c, slow conduction velocity, while other anti-arrh dont.
Really? But even CCBs would affect conduction velocity. Conduction velocity has mostly to do with the slope of phase 0 in fast-response tissues, and the slopes of phase 4 and 0 in slow-response tissues. CCBs would decrease the slope of both phase 4 and 0, and decrease conduction velocity in the AV node. Could you tell me where that table is? I can't seem to find it.
 
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well if so, that makes total sense, b class 1a and C both delay phase 0 of the ventricular AP. QID 899
 
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Mar 5, 2014
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also any idea why bicuspid aortic valve's cause Aortic regurg? unless the LVHT a/c with stenosis somehow causes aortic root dilation
 

Nabin

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also any idea why bicuspid aortic valve's cause Aortic regurg? unless the LVHT a/c with stenosis somehow causes aortic root dilation
BAV disease can go either way. It could cause aortic stenosis due to early dystrophic calcification changes, or even regurgitation due to the failure of valve closure since its cusps are fused, maybe there is some intrinsic connective tissue defect in the valve. I don't know the exact mechanism behind it but its definitely to do with the valve abnormality.
 
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also side ?, since making an own post about this is useless since we seem to be discussing topics well, on pg 348 in FA, why does it say anorectal varices but not internal hemorrhoids?
 

Nabin

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also side ?, since making an own post about this is useless since we seem to be discussing topics well, on pg 348 in FA, why does it say anorectal varices but not internal hemorrhoids?
My UW has expired already :D

Varices would be SPECIFIC for portal hypertension. Hemorrhoids are just veins that prolapse and though they prolapse due to increased pressure (or may be lack of proper support), it can be attributed to many factors.
 

Nabin

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also side ?, since making an own post about this is useless since we seem to be discussing topics well, on pg 348 in FA, why does it say anorectal varices but not internal hemorrhoids?
When is your exam?
 
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lol another pharm question, but why dont b blockers work on the Ventricular AP? muscle fibers do have B1 receptors? bc UW states b blockers prolong p-r interval, but no effect on QRS(bc they dont effect the ventiruclar AP, but i think they should work on it.
 

Nabin

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lol another pharm question, but why dont b blockers work on the Ventricular AP? muscle fibers do have B1 receptors? bc UW states b blockers prolong p-r interval, but no effect on QRS(bc they dont effect the ventiruclar AP, but i think they should work on it.
I had read in that cvsphysiology site that beta-blockers do decrease action potential duration in the ventricular muscles. (I think its because of their effect in the plateau phase since beta-agonists increase calcium influx during that phase so the opposite must be true as well). They don't affect the QRS wave though. Note that the QRS wave begins following Na influx during phase 0 and ends when the transient K repolarisation of phase 1 has finished i.e. QRS ends just at the beginning of the plateau phase before Ca++ influx has started to occur. So, no change in QRS wave.
 
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