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Primary Conduction Abnormality Driven Autonomically


cardiactec
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just thought this was an interresting case....this woman had a supine HR of 100 on tilt, but with upright position, her rates shot to 200. at first diagnosed she was diagnosed with pots, but when they looked more carefully at her ecg, they noticed it wasnt sinus tachy in origin in upright position. this goes to show that some people, posturally driven tachycardia's might not necessarily mean a PRMARY autonomically mediated abnormality, but perhaps more of a conduction system abnormality..

just interresting seeing the possibilty of posturally driven tachycardia's where the underlying issue isnt necessarily autonomic imbalance, but moreso a conduction issue...autonomic factors was the SECONDARY issue with this woman, influencing the PRIMARY conduction abnormality that existed.

http://europace.oxfordjournals.org/cgi/con...full/7/3/231#F1

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Thank you for posting this. I wonder how many cardios missed the extra P wave (per your earlier thread on how many opinions each of us has gotten).

I have two questions for you, "Prof". One is what does the flecainide do? The other is do you have a theory or knowledge about why posture affected the conduction block?

Thanks again.

OLL

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hey there,

basically flecainide is used to slow nerve impulses to the heart so that cardiac tissue becomes less sensitive....

ah, my theory. :unsure:) to tell you the truth, a posturally driven primary conduction tachyarrhythmia i thought was highly unlikely, but when i read that case report on that woman, it shocked me. it had crossed my mind that this could occur though, since dealing with my own tachy issues when upright and thinking for a long time that there was something other than a primary autonomic dysregulation causing the tachy......

cardiac cells have what is called an action potential. basically what that means is an electrical charge of a single cardiac cell. when cells exchange certain ions into and out of the cell, it causes the cell to become more electrically charged, creating a voltage difference across the cell, which causes the cell's to start depolarizing and repolarizing (depolarizing leads to contraction of the heart muscle, repolarizing causes relaxation of cardiac muscle). throughout the heart, the action potentials are of different shape and size. the sinus node has ions that depolarize the cell sooner than other cells can depolarize (this is a normal phenomenon called automaticity). so in a normal heart, the SA node overpowers all the other action potentials throughout the heart from firing before it (the sinus node).

electrical propagation through the av node when there is high electrical discharge from the sa node (as in this case what they referred to a "2:1", a 2:1 means that the sinus node/atria were firing two impulses to the av node instead of one,) depends on a certain part of the action potential of the cells in the av node called the refractory period (this is the time electrically, where the cell cannot be ''restimulated'' until the electrical charge finishes helping the cells to repolarize (relax).

when someone stands up it can cause a decrease in the refractory state (resting state) of the av nodal cells, causing a decrease in the time alloted for cells to finish repolarizing ("resting") causing the block of impulse in the atria, seen as the 2:1 (one of the 2 beats is being blocked because the cells in the av node are trying to finish repolarizing their cells before accepting any more from the sinus node.....it's like a baseball pitcher throwing three balls to one catcher. the catcher only has two hands so the third ball ends up not getting caught, but instead lost in the bushes behind him. the 2nd impulse ends up not being picked up by the av node.

hopes this makes some sort of sense. it's very tough info to both comprehend and explain and of course is only one potential cause of why this woman had an underlying atrial tachy that was driven autonomically/posturally.

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That is interesting. I remember that this seemed to be your interest earlier, too.

Doctors performing tilt table tests are supposed to monitor the HR during- that's the reason for the EKG. Most POTS cases will go into sinus tachycardia, which is what they expect, and I have been told that a doctor who looks at my EKG may think there's atrial fibrillation, but it's not, and with the POTS it's "normal". So, a doctor OUGHT to recognize what type of tachycardia is occuring upon a tilt, and seeing anything out of the range of what he or she would expect, ought to look into that. There are a few on this board who have additional heart complications other than MVP that cause other arrhythmias, related or not, and hopefully they are being properly treated.

We know that there are patients for whom POTS is secondary, which you can see in various articles including Dr. Grubb's more recent ones... Hopefully they'll look into this particular issue more carefully and may know more what they're looking at. It seems to me, though, that POTS that is related to dysautonomia is what most of us are here for, and something that looks like POTS and smells like POTS but isn't quite POTS might find more answers in further studies, soon hopefully.

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Guest tearose

Can some of these electrical/conduction abnormalities be "short term" and not permanent?

Can there be a "cold or virus" in the conduction system so to speak in that make mixed messages happen and then things turn around come to a better baseline?

I am starting to think when we "capture" things during testing of these systems there are more variables than we now have an understanding of.

Was the medication she was on helping or hindering her body from finding a better balance?

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Interesting read. Thanks for linking it.

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Very interesting. Where do you see the second p wave on the 2nd ekg? Right after the qrs, the little bump? Would only be considered an a-tach if it is a consistent extra p-wave, meaning could not movement during an ekg etc, change the pattern? What if you see a "bump" in one wave but the rest are fine, considered artifact?

I'm interested(if you can't tell) on reading ekgs. :unsure:

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Thanks, Cardiactec, for taking the time to explain your theory. Back to my two questions if you don't mind (the lady is old....)

My neurology training was that when you slow down nerve conduction velocity to tissue, the target tissue will become more sensitive. It is a compensation to keep it firing or acting as action potentials to it decrease (either temporally or spatially). If you cannot answer, I will get my lazy self to look up the drug. I only ask because maybe it will help us need fewer beta blockers, or a reduced dose, or make them work more effectively.

Your answer makes me also wonder...when oxygen to any tissue is decreased it also causes it to become more sensitive (eg., tingling in hypoxia). Maybe posture changes respiration reducing oxygen to the heart or perhaps through other means increases its sensitivity. Pooling may alter cardiac oxygen or electrolyte supply. I am going to think more about this one.

Thanks again.

Please share any other interesting cases with us.

OLL

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Cardiactec,

Thanks for sharing this! It is very interesting (though I have to admit that I think some of the information in the article is confusing to ME because I am not well informed on the heart and how to read the tests).

I do think it is worth showing my doc though, just in case!

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