VT or SVT?

In the chapter on VTs, we stated that in the routine clinical setting, for safety reasons every wide complex tachycardia must be considered a ventricular tachycardia until proven otherwise. In this chapter, we want to show you how to distinguish between SVT and VT!

Why is this important? It is because their clinical impact and therapies are very different.

Patients with sustained VT must remain on an intensive care unit or receive intermediate care with continuous cardiac monitoring. After the initial diagnosis, invasive coronary angiography is more or less obligatory to rule out the most common cause, namely myocardial ischemia secondary to coronary artery disease. The subsequent diagnostic procedures and therapeutic approaches are also rather complex, and some involve risks for the patient.

So, it is very important to appreciate the consequences of assigning a diagnosis of true VT. We need to be aware of the alternative differential diagnoses that can lead to a wide complex tachycardia.

What are the differential diagnoses of wide complex tachycardia?

In principle, these are all tachycardias of supraventricular origin and pre-existing or tachycardia-induced bundle branch block.

A further differential that must be considered is the antidromic AVRT in WPW-syndrome. You will find more information about AVRT in the chapter about supraventricular tachycardias.

Differentiation between a ventricular and a supraventricular tachycardia is a frequent and time-consuming task in clinical practice. It is particularly difficult if the ECG tracing was only made on the monitor display and not in a 12-lead ECG format. The reason for this is that in order to evaluate certain criteria for the differentiation between the two disorders, we need to see the tracings of all chest wall leads.

For the correct differential diagnosis of wide complex tachycardias, we have to go a little deeper into the depths of ECG diagnostic skill. But don’t panic: there are a few simple tricks that are easy and quick to apply!

As a first approach to differential diagnosis of wide complex tachycardia let’s use a tool you already know from the narrow complex tachycardias: regularity.

First, let’s have a look at irregular wide complex tachycardia.

Irregular wide complex tachycardias are rare, and if you see one, in most cases there is underlying atrial fibrillation with aberrancy or bundle branch block.

Polymorphic VT on the other hand looks so different that you will usually recognize it at once.

The only truly confusing situation is atrial fibrillation, which is conducted via an accessory pathway in WPW syndrome, and is thus wide and irregular. This is so rare, classic, and dangerous, that a nice acronym has been developed for it: FBI, which stands for "fast, broad, irregular". In contrast to the AV node, the accessory pathway does not necessarily slow down the rate. This means that the ventricular rates can be identical to those of the atria, which is life-threatening!

There are several differentials for regular wide complex tachycardias.

Simply put, if the origin of the tachycardia is not the ventricles, then it must be the atria.

If we deal with an SVT with regular ventricular beats, there must be an association between the excitation of the atria and the ventricles. Depending on the activity of the AV node, the association between the atrium and the ventricle may look very different. Usually, the AV node slows down very fast impulses from the atria. We see certain patterns, such as a 2 to 1 conduction, meaning that there will be two excitations of the atrium followed by one excitation of the ventricles. In the corresponding ECG, we see two P waves followed by one QRS complex. The classical example of this is atrial flutter. Unfortunately, however, P waves tend to be so poorly visible that this criterion is sometimes difficult to apply in practice.

As you already know, we are dealing with an SVT if there is a clear association between atrial and ventricular excitation. As always, however, there is one exception: VT with retrograde conduction to the atria via the AV node.

This means that a ventricular excitation in a healthy AV node can also be conducted "backwards" into the atrium. There is approximately the same time delay as in the case of an antegrade conduction. If retrograde VA conduction is possible, we may see excitation of the atria after each QRS complex, as represented by a negative P wave in leads II, III, and aVF.

However, if retrograde VA conduction is blocked, the sinus node excites the atrial myocardium completely, and the atria and the ventricles are activated independently of each other. This phenomenon is called AV dissociation. In the ECG, the interval between two P waves is in this case completely independent of the interval between two R waves, and will be the same throughout the ECG strip.

If you are fortunate enough to be dealing with a long ECG strip showing regular rhythm before the VT, followed by the VT, and another longer strip with regular rhythm after the VT, then you will be able to measure P to P-intervals. The distance between the first visible P wave after the tachycardia and the last visible P wave before the tachycardia will be a multiple of one P to P-interval. This makes a lot of sense, since the sinus node and the atria keep on going while the ventricles are busy with their VT. This criterion is a sure sign of a VT. For this purpose, the entire episode of tachycardia should be documented from beginning to end, and the patient must be in sinus rhythm. As you can imagine, however, we rarely have the luxury of this scenario in routine clinical practice, but it is still a useful concept in terms of understanding VTs. And then, of course, we have to consider the fact that if the distance does not fit to our little mathematical calculation, this does not necessarily mean that it is definitely an SVT, since the sinus node is also influenced by the sympathetic nervous system. The sinus node is therefore likely to be activated during a longer lasting VT, since this is not exactly a relaxing situation for our patient.

In conclusion, when AV dissociation is clearly documented, it’s a very reliable sign for VT, with a specificity of over 98%.

If there is no retrograde VA conduction, we have complete AV dissociation, and two further criteria may be visible in the ECG: the capture beat and the fusion beat.

If atrial excitation, for example, is conducted randomly into the ventricles at exactly the same time as the cycle of the VT ends and the ventricular myocardium is no longer refractory, the excitation coming from the atria can completely capture the VT. In this case, we suddenly see a single normal excitation cycle in between the regular wide QRS complexes. This one beat shows normal QRS width and morphology. This is called "capture beat".

The "fusion beat" is related to the capture beat. Here, atrial excitation only partially captures the VT, that is, a region of the ventricle is excited via the Tawara branches, while the rest is excited by the ventricular origin of the VT. A fusion beat has the mixed morphology of an intrinsic QRS complex and the QRS complex of the VT.

A further independent and easy-to-remember criterion, is the so-called R wave to peak time. The concept is extremely simple: in lead II, we measure the time from the beginning of the QRS complex to the tip of the R wave or the Q wave. If the time is 50 ms or more, then it is very likely to be a VT.

The specificity in a study with 167 subjects was 82.7%. Unfortunately, only 60% of patients with true VT have an R-wave-to-peak-time of more than 50 ms, so you should check further criteria if this criterion is not fulfilled.

Another useful criterion for detecting a VT is a change in the electric heart axis during ventricular tachycardia.

A change of the heart axis, also called a "vector change", is always suggestive of VT. A heart axis during tachycardia in “no-man’s-land“, which is far beyond the borders to an extreme left or right axis deviation, is also suggestive. When looking at the Cabrera circle, this means a heart axis that is more negative than minus 30° or more positive than 120°, or more specifically, a vector in the "north-west region", meaning, minus 90° to minus 180°.

Many different algorithms have been developed to differentiate between an SVT and a VT. During this course, we will refer to the so-called Brugada-criteria.

1. As already mentioned in the basic chapters of this course, we see many different variations of the QRS complex. There is not always a Q, an R, and an S. Sometimes we find only an R wave and an S wave, which is then called an RS complex.

Alternatively, we see only one negative amplitude without a positive R wave.

This constellation is called a QS complex. QR complexes also occur. Now, let’s look at the chest leads. The first Brugada criterion for a VT is the absence of RS complexes in leads V1 to V6. In other words, we only find QR or QS complexes. The specificity for the presence of a VT is almost 100%. Furthermore, this criterion is largely consistent with that of the so-called "negative concordance", meaning all chest leads show a negative vector.

2. If RS complexes are seen in V1 to V6, we look for the chest lead in which the time from the beginning of the R wave to the lowest point of the S wave is the longest. If it is 110 ms or more, we have diagnosed a VT with a specificity of 98%.

3. The third Brugada criterion is AV dissociation, which we already explained in detail before.

4. The fourth and fifth Brugada criteria refer to he morphology of the QRS complex in leads V1 or V2 and in V6.

If there is a left bundle branch block configuration, the following criteria are indicative of a VT:

a) The duration of the R wave in V1 or V2 is 40 ms or longer.

b) The downwards leg of the S wave is notched.

c) If a QS complex is present in v1 or v2, the time from the beginning of the Q wave to the lowest point of the QS complex is more than 60 ms.

d) A Q or a QS complex is present in V6.

In the case of a right bundle branch block configuration, the following criteria are suggestive of a VT:

a) A QR complex or only one monophasic R is seen in V1. That is, the typical Mconfiguration of the right bundle branch block cannot be seen in V1.

b) R is greater than R’ in V1. Thus, the upper point of change comes earlier. This is also called a "rabbit ear".

c) An rS configuration is seen in V6. In other words, the R/S ratio is less than 1 in V6.

By combining these criteria, we can diagnose a VT with a sensitivity of almost 90%.

The most important requirement, of course, is a 12-lead ECG tracing.

Unfortunately, implementation of this set of complex criteria is not exactly easy in an emergency. We don’t usually see 12-lead-VTs on a daily basis, and who would want to memorize them all?

Please do remember this one rule: If your patient is doing badly, there is only one option: terminate the arrhythmia, and preferably immediately, by medical or electrical cardioversion.

And what about the previously mentioned diagnostic path for VTs? Often, it’s sufficient to only know a few of the named criteria, because VT is very likely if you find at least one of them positive!

With practice, you will correctly diagnose every wide complex tachycardia in the 12-lead ECG. To help you practice, we have collected numerous tracings from our ECG library and you can work through them using our ECG trainers.