There seems to be a lot of confusion with regard to wide complex tachycardias.
For some reason, health care providers of all ranks and stripes forget the most basic rule.
If it's a wide complex rhythm (fast or slow) it's ventricular until proven otherwise!
Reasonable people can disagree as to what constitutes "proof" but you need to start somewhere, and the place to start is not "it's SVT with aberrancy (or a bundle branch block) until proven otherwise."
That's how patients get killed.
A little bit of knowledge can be a dangerous thing, and I'm not a huge fan of Wellens' Criteria or Brugada's Criteria. In the wrongs hands, these algorithms do more harm than good.
When they "rule in" VT, they're fine. When they (wrongly) suggest SVT, they're dangerous.
There are several reasons these algorithms might wrongly suggest SVT. No algorithm is perfect. In addition, mistakes are made when using the algorithms, and the algorithms are sometimes used in ways they were not designed to be used.
For example, with modified leads MCL-1 and MCL-6.
Wellens' Critera and Brugada's Criteria are not the same, and the former is part of the latter, so I don't mean to oversimplify here. But in my experience, a far more valuable tool is to recognize the typical patterns. In other words, typical RBBB, typical LBBB, typical bifascicular block (RBBB/LAFB), and typical bifascicular block (RBBB/LPFB).
Having said that, just because the ECG shows a typical pattern, that doesn't mean the ECG shows SVT!
VT can mimic virtually all typical patterns on the 12 lead ECG.
I remember when I was a cardiac monitoring technician on the Critical Care Stepdown (CCSD) unit of a medium-sized (about 400 beds) community hospital with 2 cath labs and an open heart program on the west side of Cleveland, Ohio.
Our unit could handle 32 patients, and we were always full. That translates into 4 monitors, each with 8 different heart rhythms, and it was my job to watch them.
The technology has since been licensed to Philips Healthcare.
The system is ideal for stepdown units (where hooking a patient up to continuous 12 lead ECG monitoring isn't practical), holter monitors (where the morphology of an arrhythmia might help the cardiologist), NASA astronauts, and so on.
Much of what I know about 12 lead ECGs stems from my experience comparing the "derived" 12 lead ECG to the standard 12 lead ECG in the patient's chart, and asking cardiologists lots of questions.
The EASI lead system has many advantages, but it has a couple of drawbacks. It is very dependent upon proper lead placement. I mean no disrespect to my nurse colleagues (they were very competent and I enjoyed working with them), so let's just say their self esteem did not depend on lead placement precision.
The other main drawback (for a stepdown unit) is simple. Where is the surgical wound for an open heart patient? Right down the middle of the sternum. Where do you have to place the electrodes for Channel 1 in the EASI lead system? On the top and bottom of the sternum. Since that's not possible for an open heart patient, you have to:
1.) place the electrodes off to the side (which is what we did 99.9% of the time),
2.) use standard lead placement, or
3.) use some type of modified lead placement.
The whole advantage of the EASI lead system is that it gives you the opportunity to view arrhythmias in 12 leads. It's a lot easier to figure out what those FLBs (funny little beats) are when you can look at the limb leads and the precordial leads. So what's the next best thing?
If we had a set of leads that allowed the limb leads plus one precordial lead, that would have been a good alternative. But since we didn't, I decided to place a post-CABG patient in MCL-1 and MCL-6.
I had read (and this was validated by a discussion with a cardiologist) that you could differentiate wide complex tachycardias using these leads, since they mimic leads V1 and V6, and those are the relevant leads for Wellen's Criteria.
Wouldn't you know it? The patient cooperated and experienced a wide complex tachycardia!
The arrhythmia lasted about 12 seconds. The patient was totally asymptomatic.
I was thrilled! To an ECG dork, the opportunity to view a brand new wide complex tachycardia in MCL-1 and MCL-6 is quite a treat.
It didn't take me long to decide that the "right bunny ear" was taller than the "left bunny ear" in lead MCL-1 (surrogate for lead V1). Yup, this was typical RBBB. SVT with aberrancy all the way!
The cardiologist agreed, and wrote down in the chart that the patient experienced a short run of atrial fibrillation with "rate activated RBBB".
We were both wrong.
No, the patient didn't die, or experience an adverse outcome. At least, I don't think s/he did. But then again, I don't know for sure. It wasn't until years later that I realized this ECG shows VT.
Let me prove it to you.
Take a good look at the circled QRS complex. I didn't notice it right away (okay, until years later) but it's wider than the previous QRS complexes. There is also a change in amplitde.
There's something different about this QRS complex, all right. It's a fusion complex. In other words, it's a hybrid.
A "fusion" QRS complex is the result of ventricular depolarization happening through two different mechanisms at the same time. In this case, "normal" ventricular depolarization through the AV node/His/Purkinje system, and spontaneous ventricular depolarization from a PVC (most likely triggering the run of VT that follows).
Still aren't sure?
Look at the PR interval of the underlying rhythm, and the PR interval of the fusion complex. The PR interval of the fusion complex is slightly shorter (thank you Tom G.).
If this evidence isn't compelling enough (and I think it is), look at the following image.
If you march out the P waves, AV dissociation is present.
Point, game and match.
I know what you're thinking. Brugada's Criteria would have caught this run of VT! Sure. If you are skilled enough to identify AV dissociation at the point of patient contact and decision making.
My point is simple. Your default diagnosis should be VT anyway! In my opinion, QRS morphology is insufficient evidence that a wide complex tachycardia is SVT with aberrancy.
That's all I wanted to establish for Part I.
Differential diagnosis of wide complex tachycardias – Part I
*** UPDATE ***
I recently discovered this article from the March 2006 issue of Emergency Medical Services. In it, the author states:
With the introduction of new pharmacological interventions that target specific areas of the cardiac conduction system, it has become increasingly important for EMS providers to make an accurate interpretation of an ECG. Though most paramedics have no difficulty distinguishing VT from narrow complex supraventricular tachycardia (SVT), some might fall victim to the "wide + fast = VT" trap when looking at SVT with aberrant conduction. Although VT and SVT with aberrant conduction look similar, they vary greatly in terms of origin, pathophysiology and treatment. Mislabeling dysrhythmias can have severe consequences. Improper identification of VT could place a patient in grave danger by delaying indicated pharmacological and electrical interventions.
"Wide and fast = VT" is not a trap! It's a rule of thumb that exists to protect you and your patient!
The author continues:
A common aphorism among advanced practitioners is, "When in doubt whether a WCT is VT or SVT, treat patients as if they are experiencing VTs." This stems from a statistic showing that approximately 80% of all WCTs are VT. Though this aphorism is generally a good rule of thumb, it is also important to acknowledge that one in five WCTs is not VT and therefore requires different treatment regimens. One must possess the proper diagnostic tools and knowledge to decide whether a WCT is VT or SVT with aberrant conduction. EMS providers should be able to differentiate VT and SVT with aberrant conduction with confidence and a high degree of certainty.
They do not require different treatment regimens!
Unstable SVT is treated the same as unstable VT! Anyone disagree?
It's debatable whether or not a stable wide complex tachycardia should be treated in the field at all, but if you do reach for an antiarrhythmic, it better be one that works for SVT and VT (i.e., amiodarone or procainamide).
Note: With the 2010 AHA ECC Guidelines adenosine is once again an option for undifferentiated regular wide complex tachycardia.
If you give a calcium channel blocker to a wide complex tachycardia without knowing with 100% certainty that it's SVT with BBB (or aberrancy) you are a fool.
The article also contains outright errors. Here's one of the most disturbing.
SVTs with aberrancy will produce either a right or left axis deviation. If the aberrancy is conducted in a RBBB pattern, right axis deviation will be present. If the aberrancy is conducted in a LBBB pattern, left axis deviation will be present. In almost all VT, the axis will be in the extreme right quadrant.
This is nonsense!
In the first place, RBBB and LBBB aberrancy can both show a normal axis. RBBB aberrancy in particular can show a normal axis, right axis deviation, or left axis deviation (bifascicular patterns).
Most cases of VT present with an other-than-extreme axis.
See what I mean about a little bit of knowledge being dangerous?
*** End update ***