Clocked at 352 beats per minute (at it's fastest), this is a recording from a event recorder I saw today (used with permission). Note the small inverted triangle is a marker denoting when the patient pushed the button on the event recorder. The patient was a "little lightheaded" when this occurred:
Click to enlarge
So, what is this?
"So, what is it?": Extreme vtach?!
Interference? Someone tapping on the leads?
Clue: It's not noise or interference...
afib conducted aberrantly when it really gets going
It almost looks like runs of vfib with runs a afib with aberrancy.
Wouldn't that be strange to have both rhythms simultaneosly?
a flutter 1:1 with aberrant conduction
Agree with anonymous. Too fast for v tach; native rate of atrial flutter is usually around 350 as is seen here. Rate-related conduction delay would explain the wide complexes.
Looks like afib with a bypass tract conducting antegrade to me. Would love to see a twelve lead in sinus rhythm. I'm surprised no one else has guessed this already. Am I the only electrophysiologist who reads this site?????
I'm going with WPW, not because that's what I think it is, but because I've always wanted to use WPW as an answer on a test.
Thanks to all who've chimed in so far. Just so others "across the pond" can view this, I'll post my interpretation here tomorrow AM...
Jay said: "Looks like afib with a bypass tract conducting antegrade to me."
Then a-fib with WPW would fit that definition, correct?
Because that's what I was going to say...
Take a young individual with atrial fibrillation, add some wet packed snow, and have ‘em work real hard, and you can get what’s seen here. (Incidentally, this occurred the same day I strained my back!)
This telemetry strip is rapidly-conducted atrial fibrillation via the AV node. All of this patient’s EKGs failed to demonstrated evidence of pre-excitation. This person was shoveling snow, became lightheaded, stopped shoveling, held still, and pressed the event recorder button. The tracings demonstrated are a continuous recording from that event. The patient had complained of intermittent lightheadedness, but had never demonstrated rapid ventricular rates previously.
This is a good example of “Ashman’s phenomenon,” described by Gouaux and Ashman in 1947 in atrial fibrillation where the distal conduction system has a longer refractory period than the proximal conduction system, and develops block, or “aberrant conduction” via the alternate bundle branch.
There is a suggestion in the earlier portions of this recording that the patient may have a brief period of catecholamine-induced polymorphic ventricular tachycardia precipitated by the rapidly-conducting atrial fibrillation. It is not difficult to imagine that such a tracing could precipitate sudden death in an athlete. Gratefully, that was not the case here. But applying Ockham's razor, most likely this is all just rapidly-conducting atrial fibrillation.
What would you think about giving a shot of adenosine in sinus rhythm to exclude latent preexcitation? If the patient is young and has enhanced AV nodal conduction, the delta wave may not be apparent on a resting ECG. That strip seems a little too fast for AV nodal conduction to me (unless your patient is actually a hummingbird).
I guess if you have afib recorded on other occasions at rest without fast rates this may be unnecessary. Your note above was not clear on this matter.
Wow! I wonder how many ER visits are SNOW SHOVELING related? Whether it be cardiac events like this one, hip fractures from falling on the ice, or the dreaded back strain from heavy lifting of the snow.
On another note, do you have any comment on Baxter's Heparin supply?
An article is on the front page of the Chicago Tribune 3/6/8. Thanks!
do you see narrow qrs complexes at slower rates and then wider complexes at higher rates in preexcited afib? i can understand why pathways may not conduct at higher rates than lower rates, but i am not sure why the reverse should occur? why would the pathway suddenly start to conduct?
In preexcited Afib, all QRS complexes need not be wide.
Consider that both the AV node and the accessory pathway are barraged by rapid stimuation. Each of these conducting pathways have their own block cycle and not every impulse will get through. If the pathway happens to block at a time that the AV node conducts, the resultant complex will be narrow.
In addition conduction down the AV node could cause concealed retrograde penetration up the pathway, rendering it refractory for a time (a process called "linking") This could cause multiple consecutive complexes to be narrow.
In the case of a young patient with enhanced AV nodal conduction who is exercising, the AV node may conduct very rapidly, approaching the conduction time of the accessory pathway (which is generally insensitive to catacholamine stimulation). In this case prexcitation may be effectively "latent." That is, conduction occurs down the pathway, but the majority or all of myocardial activation is through the AV node, and the complex is narrow (or prexcitiation minimal and not apparant on a single lead Holter strip).
Here's an ECG of preexited afib I found through a Google image search --
The original article is at - -
Note the presence of consecutive narrow QRS complexes along with the wide complexes.
That's my take on the situation. I'm not sure how well it would withstand peer review, but I think it's probably academic enough for Wes's blog.
(I'm Director of Cardiac Electrophysiology at Christ Hospital in Cincinnati, OH)
Wow, I'm getting so excited by all of this EP-speak! Thanks, Jay and anony!
One thing I have learned in medicine is "never say 'never'." I just don't know at this point if the AV node in this patient can physiologically conduct this fast or not. I have seen very rapid conduction in our EP labs with healthy young patients on Isuprel, but I agree with Jay that this rate de novo in the real world is unusual (especially if no accessory pathway conduction exists). Certainly, the speed of these tracings got my attention (and hence why I thought they would garner interest).
The full story is not in yet. The patient has yet to be cardioverted (currently rate-controlled as anticoagulation is initiated). Once in sinus rhythm, adenosine administration might demonstrate pre-excitation if an anterogradely-conducting accessory pathway exists. I agree with anony that it is unusual that pre-excitation has never been seen on prior Holters, even at slow rates. (One would think we'd see this as the refractory period of the AV node prolongs, usually more than the accessory pathway). But, accessory pathways ARE sometimes sensitive to adrenaline and may not conduct at all at the resting state in some individuals, yet conduct rapidly in the presence of catecholamines.
Administration of adenosine is a simple, non-invasive test that can establish the presence of an accessory pathway by blocking the AV node and "exposing" the accessory pathway conduction. It can also re-induce atrial fibrillation due to the shortened atrial effective refractory period, but hey, what's another cardioversion among friends?
I love posts like these. Reminds me why EP is so much fun.
-EP/Cath Lab Tech
Post a Comment