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We’ve already discussed the use of CRM devices to monitor and manage arrhythmias, but what about using the leads to gain more information about the root cause of the problem?

We can use the information from the separate leads during, for example, a tachycardic event to analyse and really find out what’s happening to the patient. This is good for the patient as it can mean avoiding further invasive EP studies, and helpful for us because we can make a more informed and timely decision about treatment routes. One of the first things we’re taught when learning to interpret EKGs is not to trust the machine’s report without checking it out for ourselves (STEMI or LVH, anyone?); maybe we should take that a little further and make sure we agree with our CRM devices!

Let’s start with an example – the arrhythmia report (from a Boston Scientific Implanted Cardiac Defibrillator (ICD) here tells us we’re looking at an episode of VT, but we notice that the atrial and ventricular rates are around the same rate – 144/145bpm. The A-sensed lead and V-sensed lead show that we start off with A-paced beats followed closely by V-paced beats… all good so far.

Then we see that the episode of tachycardia starts with a premature atrial beat – and we know that VT typically starts with a ventricular premature beat. Is this really VT? Could it be SVT? Then we see a run of atrial premature beats, each followed – eventually – by a ventricular beat. So it looks like we’re seeing an atrial rhythm with a very – VERY – slow pathway. Our atrial premature beat did have a V-paced beat afterwards, but the conduction pathway is so slow… could the premature beat have blocked the fast pathway, forcing conduction through a slow pathway with retrograde fast pathway conduction? So we now have a slow-fast SVT; typical of atrio-ventricular nodal re-entry tachycardia (AVNRT). With AVNRT we have a re-entry circuit going round the AV node.

Now, this patient has a device with an atrial electrode and a ventricular electrode, and these devices have the capacity to do basic EP studies without any further invasive procedures. So we can use this device alone to further our understanding of the patient’s needs, with none of the risks or costs associated with traditional EPS.

Wonderful!

Here we have a report from a St. Jude’s/Abbott dual chamber pacemaker in a female patient who was admitted to hospital with serious symptomatic palpitations and pre-syncope. We had been unable to catch one of these episodes on a 12-lead EKG, but they were convincingly cardiac, at high risk of causing injury to the patient, and so we really needed to consider treatment. Should we do EP studies with a view to finding a source of arrhythmia and ablating? Traditional EP studies, although generally very safe, are not without their risks. It’s an invasive procedure where we introduce tubes through a blood vessel into the heart. There’s a risk of bleeding at the insertion site, and a risk of trauma anywhere en route to or within the heart. Although they’re done in aseptic conditions we can’t rule out the possibility of infection, and in this case the patient had a known blood-borne virus which always increases the risks to the staff involved in her care.

Luckily, we knew that this woman had a dual-chamber pacemaker, with an atrial and a ventricular lead. In this case we were able to use her pacemaker to do an atrial drive at 700milliseconds – we can see two beats conducted from the atrium to the ventricles… then we initiate a premature atrial beat which actually triggered 8 beats of SVT – supra-ventricular tachycardia. At this point the patient confirmed that this had reproduced her symptoms of palpitations and feeling pre-syncopal. So we were able to make a diagnosis, based only on EP studies conducted through her already implanted device, of AVNRT. We can see that her premature atrial beats took a long time to conduct, so we think they’re going down a slow pathway to the ventricle, then with a dual nodal pathology - following a refractory phase - are returning to the atrium via the fast pathway and looping round until terminated. We could also consider the possibility of an atrial tachycardia, but we know that atrial tachycardia doesn’t typically terminate in the atrium unless with an ectopic premature atrial beat. What we have here terminates with an normal atrial beat with a usual morphology complex - unlikely to be an atrial tachycardia.

What could we do in the EP  lab to help confirm our diagnosis and plan management?

We need to reinduce the tachycardia and try pacing it from the ventricle slightly faster than the atrial tachycardia had been. Once we stop pacing the ventricle, we can see a V-beat… then an A-beat… then a V-beat. Such a V-A-V response, according to Morady is most likely to be AVNRT or AVRT – atrioventricular re-entry tachycardia involving an accessory pathway, such as in Wolff-Parkinson-White syndrome. If we’d been looking at atrial tachycardia we’d expect to see V-A then another A then V. We’d see the drive for the tachycardia coming truly from the atria so we’d see more atrial than ventricular beats sensed.

How can we tell from this whether it’s an AVNRT or an AVRT’s accessory pathway? We need to measure the PPI – the post-pacing interval. If we take the time between the last paced beat in the ventricle to the next beat in the ventricle and subtract it from the tachycardia cycle length (TCL) we’ll see the distance our entrainment location is from the tachycardia. The distance of this PPI minus TCL tells us more about what we’re seeing: if it’s less than 110 milliseconds, it’s most likely an accessory pathway – the ventricle is involved in the tachycardia, close to the circuit in the accessory pathway. However if its above 110milliseconds, it’s likely to be AVNRT; we’re further from the tachycardia circuit as the circuit is within the atria/AV node so when we pace from the ventricle we’re waiting for the impulse from our pacemaker-initiated ventricular beat to penetrate the atrial-nodal circuit. In this example we have a PPI of 541, minus a TCL of 360 – well above the 110, and far away from the tachycardia circuit. When we paced from the ventricle we were entraining the tachycardia, but we were pacing from a point in the conduction system far away from the tachycardia initiation point.

We also used a few other techniques to help our diagnosis: we did incrementally faster pacing from the ventricle, and also from the atrium, and we saw that the conduction from the atrium to the ventricle, and the conduction from the ventricle to the atrium, as we increased the speed, was decremental; both the AV delay AND the VA delay grew longer. This indicates that the patient is unlikely to have an accessory pathway – in an accessory pathway the conduction is not decremental as it’s the AV node that slows down the conduction from the atria to the ventricle and vice-versa. There are some other pathways which could be considered, and we’ll discuss these another time.

This is a great example of getting some really sophisticated EPS and making a clear diagnosis using already-implanted dual chamber devices. We followed this with a typical AVNRT ablation which ended up being a really simple procedure based on the information we already had from her pacemaker.

It’s uncommon, in our experience, to use already-implanted devices to perform fully diagnostic EP studies. Does your department use this method? If you have any experience or comments about this, if you have any thoughts about the benefits or limits of these methods, we’d love to hear from you!

Copy Editor: Elaine Francis

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COMING UP: Next few weeks, we're gonna be talking about EP. With some really interesting case studies Fresh From The EP Lab - Our first case is called “4th Time Lucky”.

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