Origin of A-Fib

[Simusid]

So I'm a basic with aspirations. When the call is low-ish priority I like to try and look at the LP15 before the medic. I can usually correctly make some of the simpler observations like A-Fib (and really if I can't see that I can't see a normal sinus rhythm). Friday we had an A-Fib patient and for the rest of the quiet evening I was reading about a-fib trying to learn more about what causes it and not just the symptoms.

What I learned, which fascinated me, was that a very large percent (I want to say 90% but I don't have the reference right in front of me now) of the ectopic a-fib activity occurs where the 4 pulmonary veins join the left atrium. This video shows an ablation procedure http://www.youtube.com/watch?v=_D-PXK2NvCM, again fascinating.

So, what I get from that is that there is something very different about the morphology of the cells at that interface. The wiki says that a "structural abnormality" can lead to a-fib. What kind of structural (mechanical?) changes could be occuring there? Does it lead to changes in the typical action potential? Is this the interface where some cardiac cells are contracting but the cells of the pulmonary veins are not?

Sorry I'm sounding like the medical student equivalent of a "whacker"!

 

[stemi]

From a basic to another basic, I'm not sure if there's a physical morphology change to cardiac muscle cells that would cause A Fib. Conditions such as HCM might increase the risk of A Fib, but from what I know, it is the automaticity (or self-pacing property) of individual cardiac muscle cells that changes (pathologically), which is the most common cause. Every cell in the heart has the ability to depolarize by itself, its just that the SA node is in control, because its cells reach full depolarization more often than other cells in the heart. However, pathologically, other cells may depolarize prematurely, before the SA Node depolarizes, causing the premature and irregular contractions of A fib. This can occur at a single point/cell (one ectopic focus), which will typically manifest as A Flutter, but more often than not, A Flutter soon degrades to full on A Fib where there are several or many points/cells that all become ectopic foci.

As you said, most of the time, the ectopy originates from where the pulmonary veins enter the left atrium. I dont believe these cells actually contract, but they are capable of having their own automaticity in A fib/flutter. The cells at the entrance of the pulmonary veins are just like the cells of the SA node, which are also located in a non-contracting part of the heart, the superior vena cava.

In other cases, the ectopy may arise from areas outside of the pulmonary veins. From what I've seen at my old job, a lot post-ablation patients still have significant atrial ectopy, but not at a rate fast enough to cause atrial flutter and not significant enough to cause a fib.

Not sure if I answered your question, but feel free to let me know if you have any others and I will try my best to answer them.

 

[Simusid]

The cells at the entrance of the pulmonary veins are just like the cells of the SA node, which are also located in a non-contracting part of the heart, the superior vena cava.

In other cases, the ectopy may arise from areas outside of the pulmonary veins. From what I've seen at my old job, a lot post-ablation patients still have significant atrial ectopy, but not at a rate fast enough to cause atrial flutter and not significant enough to cause a fib.

It didn't occur to me that those cells would be similar to the superior vena cava and non-contracting.

The circular ablation and the box lesion procedure, plus the name of the older procedure ("maze lesion") made me think that the ablation wasn't stopping the ectopy, but rather was trapping it and stopping it from progressing past the scar tissue.

 

[JPINFV]

Good job on the A-fib (microreentry arrhythmia generally centered in the left atrium or the ends of the pulmonary veins).

For A-Flutter, the pathophsyiology is slightly different. In general, it's caused by a macroreentry circuit (multiple cells) that ring the tricuspid valve. Basically, a loop of cells are resetting just enough to keep a depolarization circuit going around the valve like a car going around a round-a-bout (hence the flutter waves) that can end a signal down the AV node once the AV node resets.

 

[stemi]

The circular ablation and the box lesion procedure, plus the name of the older procedure ("maze lesion") made me think that the ablation wasn't stopping the ectopy, but rather was trapping it and stopping it from progressing past the scar tissue.

I'm not sure exactly how it works, so you could be right about that.

 

[stemi]

For A-Flutter, the pathophsyiology is slightly different. In general, it's caused by a macroreentry circuit (multiple cells) that ring the tricuspid valve. Basically, a loop of cells are resetting just enough to keep a depolarization circuit going around the valve like a car going around a round-a-bout (hence the flutter waves) that can end a signal down the AV node once the AV node resets.

Interesting, I saw there was very little info on A flutter when I first read wikipedia a while back. Are there any good books that explain the pathophysiology of arrhythmia's? I've read through part of Lange's cardiovascular phys, but didnt find much on arrhythmia's there.

 

[JPINFV]

Interesting, I saw there was very little info on A flutter when I first read wikipedia a while back. Are there any good books that explain the pathophysiology of arrhythmia's? I've read through part of Lange's cardiovascular phys, but didnt find much on arrhythmia's there.

Shrug... Harrisons?

 

[stemi]

Thanks for the explanation as well. Hopefully I can learn more about it.

 

[JPINFV]

...and to be clear, I'm not trying to be cheeky with referring to Harrisons, but that's where I got it from.

 

[stemi]

...and to be clear, I'm not trying to be cheeky with referring to Harrisons, but that's where I got it from.

No worries, I didnt even know what Harrisons is. Had to look it up.:rofl:

But I do hope to be in your shoes someday.

 

[mycrofft]

My cardiologist, plus online searches (I'm a RN and former EMT), yield the following:

1. Success rates for ablation of A-fib (recovery for at least a year postop, or some such, and certainly surviving the procedure) are quite variable for most approaches. There are several approaches (in contrast to something like, say, appendectomy or cholelithectomy), and the success rate for each is variable between practitioners, institutions, etc., suggesting the mechanism's physical origins are not well understood or very hard to detect specifically. Not to mention it is no cakewalk to thread a little catheter to the heart and do anything, it's an art and every patient is different. (Also, remember most a-fib pts went into it having some degree of hypertension, but not necessarily malignantly high).


2. He did say that pt's who have A-fib for long have a chance of cardioversion plus meds reversing it which decreases the longer it has gone on and presumably made physical changes to the organ.

PS: been cardioverted twice after having it underdiagnosed for about five years. First time: back to normal with meds, in fact more normal than for a long time, but it only gave me a summer. Second time: lasted a couple weeks. We await improvements in reliability of therapies before I undergo anything like ablation.

 

[Doczilla]

I'll explain my understanding of basic arrythmias (patho) when I actually get to a computer. More to follow.

 

[mycrofft]

Holding breath:mellow: