These ECGs (figures 1 and 2) were recorded during an exercise tolerance test on a man who was being investigated for an episode of collapse and paroxysmal tachycardia. What is the explanation for the transient change in QRS morphology?
I wish to thank Debbie Wilson and Klara Powell of Mid Yorkshire Teaching Trust for sharing this case with me.
The ECG begins with sinus rhythm at a rate of 94 bpm with first degree AV block, the PR interval approximately 300 ms. After a few beats the QRS broadens and the PR interval shortens. Why? Let’s have a close look at the first few seconds to work out exactly what’s happening.
Beats 1 and 2 in figure 3 show sinus rhythm (RR interval 640 ms) with a long PR interval. Let’s ignore beat 3 for now and go straight to beat 4. The QRS is now broad, the PR interval has shortened considerably and the ventricular rate has increased slightly, the RR interval having shortened to 540 ms. For beat 5 the PR interval has shortened further and the RR interval remains at 540 ms. This is because there is now a VT or accelerated idioventricular rhythm with a rate very close to 100 bpm, and there is AV dissociation – the sinus impulses no longer conduct to the ventricles. It’s not that there is any AV block, it’s just that the ventricular focus discharges before the sinus impulses get the chance to conduct. From beat 6 the ventricular rhythm slows slightly and becomes a little irregular, but even though the sinus node discharge rate is now almost exactly the same as the ventricular rate, there are no conducted beats because the long AV conduction time means that the ventricular rhythm continues to be determined by the ventricular focus discharge rate.
Eventually, the ventricular rhythm stops spontaneously and sinus rhythm with AV conduction resumes. But let’s go back to beat 3: here the QRS is intermediate in shape compared to beat 2, a conducted sinus beat, and beat 4, which is of ventricular origin. This is because beat 3 is a fusion beat: the ventricular focus discharges at exactly the same moment that the sinus impulse reaches the ventricles. This beat alone is very strong evidence that the broad-QRS rhythm that follows is of ventricular origin.
Why can’t this be a supraventricular rhythm with right bundle branch block aberrancy? Because of the shorter and variable PR interval and the fusion beat, indicating AV dissociation, and because there is not a RBBB morphology: the first R wave in V1 is taller than the second, which is the opposite of what is typically seen in RBBB. The QRS morphology and left axis deviation of the broad-QRS rhythm indicate that it probably originates in the left posterior fascicle.