Last month’s ECG was quite simple, so to make up for it this month’s is perhaps a bit tricky. Once again, it’s the rhythm I’m interested in, so what exactly is going on? Any answer should account for the ventricular irregularity and the relationship, if any, between P waves and QRS complexes.


First of all, this is not THE answer, it is AN answer. Despite much examination and analysis, and the comments of others, I’m still not sure what is going on here. I have modified my original explanation as a result of comments posted by Scott Walton and Arron P, and private exchanges also with Arron.

I have constructed a laddergram, on which I have displayed my measurements of the RR intervals (black), some PP intervals (green) and RP intervals (purple), in the hope (probably forlorn) that they might reveal some sort of pattern. I propose that there are dual AV nodal pathways and I have represented the fast pathway conduction with a dotted line, and the slow pathway conduction with an unbroken line. I have shown what I postulate may be the refractory period of the ventricular tissue with a pink parallelogram.

First, the basics. There is sinus rhythm with an atrial rate of about 80 bpm. There is also left anterior fascicular block and right bundle branch block, slight ST depression in I, II and aVL, with slight ST elevation in II and aVR. Additionally, there are very small Q waves in V2 and V3, with very small initial R waves, and dominant S waves, from V4 to V6. The T waves are inverted in V4 and V5.

But let’s concentrate on the rhythm and atrioventricular conduction, which are not straightforward. I think that what we may be seeing is basically sinus rhythm with 2:1 AV block and long PR intervals, complicated by non-conducted atrial premature beats (APBs). The RBBB and LAFB tell us that there is disease of the bundle branch system; the long PR intervals suggest that there is concomitant AV nodal disease and it is difficult to be sure at what level the problem lies when atrial impulses fail to conduct at all.

I’ll go through the ECG beat by beat, explaining what I think may be happening, but then admit the weaknesses in my theory and consider an alternative hypothesis.

It’s difficult to say much about QRS1 because we can’t see enough of what precedes it.

P1, visible only as a small defection merging with the start of QRS1, is a sinus impulse that fails to conduct because it arrives at the ventricles when they still in their refractory state. P2 is an APB and also fails to propagate to the ventricles. P3-P9 are all sinus impulses. P3 is able to conduct to the ventricles and is therefore followed by QRS2. P4, which is almost completely masked by QRS2, arrives at the ventricles while they are refractory and therefore does not elicit a QRS. P5 does conduct all the way to the ventricles and results in QRS3. P6, visible as a small deflection merging with the start of QRS3, is blocked because the ventricles have had insufficient recovery time. P7 succeeds in conducting, producing QRS4. P8 is blocked, but P9 conducts and results in QRS5. P10 is an APB, which blocks in the AV node and although QRS5 follows P10, there is no connection between the two events. P11, another sinus impulse, conducts, resulting in QRS6. P12 and P13 are both APBs, and they fail to conduct through the AV node. P14, the final sinus impulse, conducts with a normal PR interval, resulting in QRS 7.

Why should P14 conduct with a normal PR interval when all the other sinus impulses that manage to conduct do so with a very prolonged PR interval? I think the answer is provided by the preceding PP interval of 960 ms, which is the longest on the ECG. So far in this ECG the fast AV nodal pathway has not been able to conduct because the atrial rate is too fast: its refractory period is just too long, so the sinus impulses conduct instead down the slow pathway, hence the long PR interval. But after a PP interval of 960 ms the fast pathway is able to conduct, as suggested by Scott, and the impulse whizzes down to the ventricles. When it reaches the bottom of the AV node it starts to conduct retrogradely up the slow pathway, where it meets the impulse travelling down it and the impulses block each other.

The main weakness of this explanation is that the PR intervals of what I assume are conducted beats are not constant: they vary between 680 and 800 ms. If there is 2:1 block, the PR intervals should be constant. PR intervals can vary as a result of a changing atrial rate: shorter PP intervals are sometimes followed by longer PR intervals, but I don’t see evidence of this here. Perhaps there are other factors at play which I have not been able to identify.

Arron P’s alternative explanation is that this is essentially high-grade AV block with a junctional escape rhythm and one conducted beat, which results in QRS2. This would explain the varying PR intervals, because if the explanation is correct there is AV dissociation for most of the ECG. However, if the blocking of P2 creates a pause which allows P3 to conduct to the ventricles, it is not clear to me why other sinus impulses, eg P11, do not succeed in conducting also. It is also not clear why a junctional escape beat does not intervene before QRS2, since the RR interval to QRS2 is by far the longest on the ECG. Also, although most of the remaining RR intervals are pretty constant at 1420-1460 ms, supporting the concept of an escape rhythm, the 2nd RR interval is significantly longer at 1560 ms, which argues against it.

So, I’m still not sure what is going on and would welcome further opinions.

This is my last ‘ECG of the Month’, because I have finally run out of suitable material. Thanks to everyone who has contributed to this feature over the last 2 or 3 years. Most of the ECGs have been challenging to interpret – that was the intention! –  but I hope that some people have learnt something from some of the discussions: I certainly have.

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