I’d like to thank everyone for the great comments on the most recent “rhythm challenge”. This turned out to be a more interesting rhythm strip that I thought!
I’m going to break this down using some standardized steps that I follow for difficult rhythm strips.Â When I look at a strip, the first thing I ask is, “What is the underlying rhythm?”
What do I mean by that and how do I make that determination?
I mentally remove the abnormalities to see if there is a “normal” rhythm underneath!
How would that work for Rhythm Challenge #4?
In my mind, I make the rhythm strip look like this:
Now I can see the “underlying rhythm” which appears to be sinus rhythm with a normal PR-interval and LBBB morphology.
The next thing I noticed about this rhythm strip is that it’s “regularly irregular”.
It shows a fairly elaborate repeating pattern (repeated at least once anyway).
Next I zero in on the premature complexes with identical QRS morphology to the underlying rhythm.
We know these aren’t PVCs because the QRS morphology doesn’t change. So these must be either PACs or PJCs.
In the field I don’t bother taking the analysis any farther because it doesn’t change anything. But when I worked inside the hospital we would indulge ourselves by trying to solve the mystery!
At first glance, they appear to be PJCs because there are no obvious ectopic P-waves. However, a careful examination of the preceding T-waves tells the tale.
This is what it means to develop a “trained eye” in electrocardiography.
In lead II, you can see a “bump” on the T-wave and in lead V1 the apex of the T-wave is narrower and slightly taller. The most likely explanation is that an ectopic P-wave is “buried” in there, which makes these premature complexes PACs.
Next I move on to the “abnormal” QRS complexes (abnormal QRS morphology in comparison to the underlying rhythm).
Initially, I just assumed these were PVCs (perhaps fusion complexes since they are preceded by a P-wave).
However, some very interesting comments here and on the facebook fan page have made me consider other possibilities.
I still think these might be PVCs, but it’s also at least remotely possible that these abnormal-looking QRS complexes are the result of Ashman’s phenomenon or an accessory pathway.
Statistically speaking, an accessory pathway is the least likely (in my opinion), but it’s interesting that the PR-interval is “short” and QRS complex in lead V1 shows a slurred upstroke consistent with a delta wave. Good eye, Adam!
I was also fascinated by Peter Shin’s comments on the facebook fan page. He raised the possibility that these complexes represent aberrant conduction secondary to Ashman’s phenomenon. I hadn’t considered that possibility, because I normally associate Ashman’s phenomenon with atrial fibrillation.
For those who have never heard of Ashman’s phenomenon (or need a refresher) it’s abnormal ventricular conduction that follows a sudden “long” cardiac cycle. As you can see, these abnormal complexes follow a “long” cycle.
Consider this quote from the Ashman’s Phenomenon article at WebMD’s emedicine:
Ashman phenomenon is an aberrant ventricular conduction due to a change in QRS cycle length. In 1947, Gouaux and Ashman reported that in atrial fibrillation, when a relatively long cycle was followed by a relatively short cycle, the beat with a short cycle often has right bundle-branch block (RBBB) morphology.1 This causes diagnostic confusion with premature ventricular complexes (PVCs). If a sudden lengthening of the QRS cycle occurs, the subsequent impulse with a normal or shorter cycle length may be conducted with aberrancy.
The only thing creating cognitive dissonance for me is the part about RBBB aberrancy. If Ashman’s phenomenon occurs in a patient with baseline LBBB, shouldn’t the result be a “dropped” QRS complex? After all, if left bundle branch is blocked, and the right bundle branch is still refractory, what’s left to conduct the impulse to the ventricles?