This month’s ECG comes courtesy of Scott Walton, arrhythmia afficionado and regular contributor to our discussions on this page. This is a 32-second extract from a Holter recording from an elderly male who had suffered a stroke and was being screened for paroxysmal atrial fibrillation. I am happy to admit that I don’t know exactly what is happening here. Concentrating on the middle section, I can see that the rhythm is mostly irregular, although fast and regular towards the end, and that there are some obvious P waves, but I can’t work out the relationship, if any, between P waves and QRS complexes and why the rate is mostly irregular.

What do you think is happening?




NOTE: Answer added 19.02.24

The provider of this month’s ECG, Scott Walton, has supplied us with a detailed explanation of what he thinks is happening. Do you agree with it? Do you have an alternative explanation or anything further to add? I haven’t made up my mind yet but will add a few comments of my own in a few days’ time.

Dave Richley

Apart from the QRS morphology, everything about this is consistent with a short ventricular arrhythmia, particularly having independent and entirely uninterrupted atrial rhythm. If this had been detected by a pacemaker or ICD it would be discriminated as ventricular simply as there are more V’s than A’s. The irregular onset followed by acceleration and stabilisation is a pretty typical pattern for NSVT with a fibrotic/scar substrate, and in pacing clinics we see this regularly. Just like:

The complete lack of retrograde conduction would be unusual for a supraventricular arrhythmia. AV conduction of sinus P-waves is also barely affected, implying the AV node is not involved with propagating or sustaining the arrhythmia.

We don’t often think about narrow complex ventricular arrhythmias, as they contradict one of the first things we learn: VT has a broad QRS. Some studies indicate that almost 5% of VT is actually narrow QRS ( My feeling is that the prevalence in practice isn’t really this high, but I could be wrong, or perhaps just assumed they were all SVTs with some degree of intraventricular aberration.

There are plenty of mechanisms that could explain the pattern seen here, as almost any imaginable variant of accessory pathways exist, alongside a micro-re-entrant scars and fascicular re-entry. The most comparable case study I found was this:,the%20very%20rare%20upper%20septal

Although the QRS of conducted sinus complexes is narrow, it isn’t necessarily normal (relatively deep S-wave, although of course I have no idea where the ECG electrodes have been placed), and therefore could represent a hemi-block, which could represent either a substrate for arrhythmia, or a conduit for ventricular rhythms to enter the intraventricular conduction system by the same pathway as anterograde supraventricular activity, by travelling retrogradely up the “blocked” fascicle, then anterogradely down the normally conducting fascicles.

There are also slight morphological QRS differences between those beats which are normally conducted and the ectopic complexes, although they are not particularly telling, or even consistent. I’ve included a couple of the other narrow complex isolated premature beats found on this recording, both of which display characteristics consistent with ventricular ectopy, although they do have a slightly slurred/notched initial deflection which is only partly seen in the actual arrhythmia towards the end as the rate accelerates. One of these isolated ectopic beats also displays complete retrograde conduction, whereas the interpolated complex has incomplete retrograde conduction, which is the same as the arrhythmia.

To summarise my theory, I think there is an area of scar with at least two possible micro-re-entrant circuits, which is either alongside the His bundle, or is able to conduct retrogradely up one anterogradely blocked fascicle to then conduct through the other bundle branches in virtually the same way sinus complexes do. The only way to confirm the pathways involved would be a full electrophysiology study, however this arrhythmia is not sustained or symptomatic, so invasive investigations are not indicated or justified to clarify the mechanism involved.

Scott Walton



NOTE: Added to site 22.02.24

I find this one difficult, but there are a few things that I think I can be confident of, so let’s start with those and then try to work out what might be happening with the rest of the ECG. There is an underlying sinus bradycardia and this continues through the periods of ventricular irregularity as well as the regular tachycardia. This means that whatever the source of the non-sinus beats, there must be retrograde block so that the sinus node can continue to function without interruption. It is very possible, even likely, that during the arrhythmias at least some of the sinus P waves are conducted, but it’s difficult to be sure exactly which are conducted and which just happen to occur before a QRS of ectopic origin.

So, what is the origin of the non-sinus beats and what might be the mechanism(s) behind their appearance? The non-sinus QRS complexes are narrow and of almost identical shape to the sinus complexes, so are almost certainly of AV junctional origin. However, the AV junction is generally understood to comprise the AV node and the bundle of His, perhaps including also tissue immediately adjacent to the AV node, so identifying the origin as junctional doesn’t really pinpoint it precisely. Towards the end of strip A and for the first 17 beats of strip B there are complexes that are not preceded by P waves. The coupling intervals vary, making the heart rate irregular. Are these irregularities due to sinus rhythm with multiple, random premature discharges from an ectopic junctional site, or could they be due to an irregular, automatic junctional tachycardia that shows a ‘warming-up’ phenomenon before it evolves into the faster and more regular tachycardia that is seen from beat 18 to beat 28?

Maybe, as Scott suggests, this is a rare narrow-QRS re-entrant ventricular arrhythmia due to myocardial scarring – I just don’t know. Alternatively, could there be an automatic junctional tachycardia with retrograde block and variable exit block, such that not all the junctional impulses emerge from the focus, perhaps associated also with variable AV block, to explain the irregularities of rate? Again, I don’t know but I have created a laddergram to show how this might provide an explanation for what we see. This is highly speculative, and quite likely to be completely wrong, but it shows a junctional site discharging at a rate of about 150 bpm, but with initially many impulses failing to propagate to the ventricles because they fail to conduct out of the junctional focus (exit block) or through the AV node (AV block). There is also entrance block, meaning that the junctional focus is immune from depolarisation from the sinus impulses, so that it continues to depolarise at a regular(ish) rate. This, as suggested by Arron Pearce, would be a parasystolic mechanism. In this explanation, some of the sinus impulses manage to conduct through to the ventricles and some of them don’t, which explains some of the ventricular irregularity.

There are probably other plausible – and better – explanations. I have previously quoted the legendary arrhythmia expert, the late Dr Mauricio Rosenbaum, and I make no apology for doing so again: “Every complex arrhythmia has at least 3 different explanations!”.

I wish to thank everyone who has participated in the discussion, but particularly Scott Walton, who not only supplied the ECG but also provided a detailed, referenced explanation. Further contributions are welcome.