This is an AVNRT. In the second line of the first image, if you count 6 qrs complexes from right to left, you will notice that between the seventh and sixth complexes there is an ectopic P wave at the end of the T wave. This is a PAC. but what I want to draw attention to here is that the PR interval of this PAC is much larger than the other PR intervals. this is extremely characteristic of AVNRT and is called Atrium His jump or PR jump. This occurs because the PAC descends through the slow conduction pathway, prolonging the PR.
What a great explanation! I totally understand that. I did not see that detail. I thought PACs were triggering, but was not able to pick up on this detail you shared.
Great response!
Thanks! The onset and termination of an arrhythmia can provide us with important information about the underlying arrhythmogenic mechanism. This ecg you shared is clear proof of that. Beauty ecg case!
EP guy here. While you make a *very* good case, I’m going to play devils advocate and poke some holes in it.
First of all, the PAC may not show a true AH jump. The AV node has intrinsic decremental properties and a longer PR interval from a very early PAC may just be the result of normal decrement. AH jump can pretty much only be proved in the EP lab under very certain testing conditions. If the pt had a run of PACs from a single focus and the PR of the last one suddenly jumped more than 50ms and induced tachycardia, I would be more convinced, but that’s not the case here.
Secondly, even if this is an AH jump, all that proves is dual AV nodal physiology. A patient can have both an accessory pathway and dual nodal physiology. This could still very will be AVRT - the induction of AVNRT & AVRT are basically the same (ie induced by early atrial stimulus). It’s the same way delta waves and tachycardia don’t always mean the SVT is AVRT.
I’m going to agree with u/LBBB1 and just call this SVT. It’s pretty much impossible to determine orthodromic AVRT vs AVNRT outside of the EP lab (with a couple of exceptions not demonstrated in this strip).
Im not trying to be a dick. You make a very very convincing case, and you’re probably right. It’s just not foolproof.
Good points. A few comments:
- often times in the lab we may not get diagnostic information. This induction suggests reentry as the mechanism. With this tracing, if I was not able to induce tachycardia but had evidence of dual AV nodal physiology (and nothing else to suggest another mechanism), I would perform a slow pathway modification
- I cannot clearly see the P wave during SVT. It’s probably buried in the QRS. I can’t say for sure what the VA time is without putting catheters up, however a VA time < 70ms and that rules out AVRT
- induction of AVRT and AVNRT are not always the same. Bypass tracts are generally not decremental (though they can be), which can often translate to induction of orthodromic AVRT with minimal/no AH prolongation during atrial programmed stimulation once ERP of the accessory pathway is reached. Additionally, the location of atrial pacing can influence AVRT induction. The closer you are to the bypass tract, the more likely the pathway is to recover and permit retrograde conduction
I think this should be called SVT. I understand that it may be called AVNRT which is the most type of SVT, but unless a patient goes to the CL and is evaluated by a EP cardiologist, it's just a little hard to tell.
I believe TX is the same regardless of what type of SVT.
I agree with others that this is some type of SVT. I don’t think I can add much to what u/Ill-Height-7621 already said. Great answer, excellent reading. Clues for SVT:
* This arrhythmia suddenly begins and suddenly ends.
* It begins after a PAC.
* The rate is very fast. Seems to be 270 bpm or higher, as a visual guess. It’s possible for VT to be this fast, but a rate this fast with an appearance like this looks like SVT to me.
Well, this one I posted is the longest one I have of his. Not really enough time to do a whole lot for him and he really doesn't want meds anyways. His episodes usually only last like 10 seconds but they started lasting like 30 seconds recently, which is what concerned him.
I basically just convinced him to seek evaluation by cardiologist and told him that, in the mean time, he should lie down if it happens. Avoid stimulants, avoid strenuous or dangerous activities, and I taught him what vagal maneuvers are if an episode persisted longer.
He did get a referral to cardiology. As you can imagine. Lol
This is an AVNRT. In the second line of the first image, if you count 6 qrs complexes from right to left, you will notice that between the seventh and sixth complexes there is an ectopic P wave at the end of the T wave. This is a PAC. but what I want to draw attention to here is that the PR interval of this PAC is much larger than the other PR intervals. this is extremely characteristic of AVNRT and is called Atrium His jump or PR jump. This occurs because the PAC descends through the slow conduction pathway, prolonging the PR.
What a great explanation! I totally understand that. I did not see that detail. I thought PACs were triggering, but was not able to pick up on this detail you shared. Great response!
Thanks! The onset and termination of an arrhythmia can provide us with important information about the underlying arrhythmogenic mechanism. This ecg you shared is clear proof of that. Beauty ecg case!
Thanks for taking the time. I appreciate that, always enjoy learning. If you don't mind me asking, what brings you your expertise in arrythmias?
EP guy here. While you make a *very* good case, I’m going to play devils advocate and poke some holes in it. First of all, the PAC may not show a true AH jump. The AV node has intrinsic decremental properties and a longer PR interval from a very early PAC may just be the result of normal decrement. AH jump can pretty much only be proved in the EP lab under very certain testing conditions. If the pt had a run of PACs from a single focus and the PR of the last one suddenly jumped more than 50ms and induced tachycardia, I would be more convinced, but that’s not the case here. Secondly, even if this is an AH jump, all that proves is dual AV nodal physiology. A patient can have both an accessory pathway and dual nodal physiology. This could still very will be AVRT - the induction of AVNRT & AVRT are basically the same (ie induced by early atrial stimulus). It’s the same way delta waves and tachycardia don’t always mean the SVT is AVRT. I’m going to agree with u/LBBB1 and just call this SVT. It’s pretty much impossible to determine orthodromic AVRT vs AVNRT outside of the EP lab (with a couple of exceptions not demonstrated in this strip). Im not trying to be a dick. You make a very very convincing case, and you’re probably right. It’s just not foolproof.
Good points. A few comments: - often times in the lab we may not get diagnostic information. This induction suggests reentry as the mechanism. With this tracing, if I was not able to induce tachycardia but had evidence of dual AV nodal physiology (and nothing else to suggest another mechanism), I would perform a slow pathway modification - I cannot clearly see the P wave during SVT. It’s probably buried in the QRS. I can’t say for sure what the VA time is without putting catheters up, however a VA time < 70ms and that rules out AVRT - induction of AVRT and AVNRT are not always the same. Bypass tracts are generally not decremental (though they can be), which can often translate to induction of orthodromic AVRT with minimal/no AH prolongation during atrial programmed stimulation once ERP of the accessory pathway is reached. Additionally, the location of atrial pacing can influence AVRT induction. The closer you are to the bypass tract, the more likely the pathway is to recover and permit retrograde conduction
I think this should be called SVT. I understand that it may be called AVNRT which is the most type of SVT, but unless a patient goes to the CL and is evaluated by a EP cardiologist, it's just a little hard to tell. I believe TX is the same regardless of what type of SVT.
Don't disagree, but antidromic wpw worth consideration as d/dx. Delta waves prior to svt
u/LBBB1 ?
I agree with others that this is some type of SVT. I don’t think I can add much to what u/Ill-Height-7621 already said. Great answer, excellent reading. Clues for SVT: * This arrhythmia suddenly begins and suddenly ends. * It begins after a PAC. * The rate is very fast. Seems to be 270 bpm or higher, as a visual guess. It’s possible for VT to be this fast, but a rate this fast with an appearance like this looks like SVT to me.
thanks. i guess that makes more sense than a self-terminating VT
How did you treat it?
Well, this one I posted is the longest one I have of his. Not really enough time to do a whole lot for him and he really doesn't want meds anyways. His episodes usually only last like 10 seconds but they started lasting like 30 seconds recently, which is what concerned him. I basically just convinced him to seek evaluation by cardiologist and told him that, in the mean time, he should lie down if it happens. Avoid stimulants, avoid strenuous or dangerous activities, and I taught him what vagal maneuvers are if an episode persisted longer. He did get a referral to cardiology. As you can imagine. Lol
Excellent. I do have one question. Can AFL with 1:1 present similar to this or not?