Friday, November 9, 2012

Wide Complex Tachycardia. What is the Diagnosis?

A man in his 40's with a h/o coronary disease complained of sudden dizziness and chest pain.  Medics found him with a high pulse, and rhythm strip and prehospital 12-lead (not shown) had a wide complex at a consistent rate of 135.

On arrival, here is his initial ED ECG, and is identical to the prehospital ECG and at the same rate:

There is a regular, wide complex.  No p-waves are seeen.  The wide complex has a right bundle branch and left anterior fascicular block morphology.  No flutter waves are apparent.

So this is most likely SVT (PSVT) with aberrancy (RBBB) because: a) the typical RBBB pattern makes VT unlikely b) the absence of p-waves and the constancy of the rhythm makes sinus tach unlikely and c) flutter should have something that could be construed as flutter waves in leads II and/or V1.

Alternatively, it could be posterior fascicular ventricular tachycardia.

Therefore, adenosine was given: the patient responded with several seconds of asystole.  No underlying flutter waves were uncovered and no p-waves either.  The rhythm gradually returned to its baseline at a rate of 135.  So it is not VT, but it was still puzzling.  Either the PSVT was broken and restarted, or there is sinus tachycardia.

Having remembered Christopher Watford's post on EMCrit about the Lewis lead, I Googled "Christopher Watford" and found the post.

Just as it describes, I then:

  1. Placed the Right Arm electrode on the patient’s manubrium.
  2. Placed the Left Arm electrode on the 5th intercostal space, right sternal border.
  3. Placed the Left Leg electrode on the right lower costal margin.
  4. Monitored Lead I.
This is the rhythm strip that resulted:
Now p-waves are obvious (and large!)

 By changing the lead orientation, one can detect atrial activity with much higher sensitivity.  Our electrophysiologist learned of this age-old technique (first described by Sir Thomas Lewis in 1931) technique from his mentor, and also uses it in wide complex tachycardia to detect atrioventricular dissociation (when you see AV dissociation in wide complex tachycardia, it is diagnostic of ventricular tachycardia).

The link to Christopher's interview provides all the resources you need to learn more about the Lewis Lead.

Some Final Comments:

I have added this because of some comments/questions of whether I might treat with verapamil because this looks like verapamil sensitive idiopathic VT:

While this does look like verapamil sensitive idiopathic VT, it does have a typical bifascicular block pattern.  The only thing atypical about it is the T-waves in V2 and V3, but the QRS pattern is typical for RBBB + LAFB.

The patient's baseline ECG looks exactly the same, except that it is slower (93) and the p-waves are obvious.  The Lewis leads proved that it was indeed sinus tach.  And with time and fluids and anxiolytics, the rate did trend down.

Sinus tach is usually compensatory to some underlying illness.  Maybe the patient has dehydration, sepsis, hemorrage, or PE.  If you were to give verapamil to someone with sinus tach secondary to underlying pathology, you would harm them and perhaps provoke hypotension and shock.

Thus, I would be very careful about giving verapamil to someone with such an ECG until you have proven that it is not sinus tach.

In fact, this is what we did.  My resident wanted to treat the presumed SVT with verapamil because it had apparently recurred after adenosine.  I expressed my concerns as above, and that is when we did the Lewis leads.


The etiology of the patient's sinus tachycardia was not discovered.  He later returned to the hospital for recurrent bouts of idiopathic sinus tach.

Here is his ECG 24 hours later, at a rate of 118:

P-waves at this slower rate are now clearly visible.
The QRS morphology is identical, confirming that this rhythm had to be supraventricular.
The supraventricular rhythm was sinus

Here is an ECG from 2 weeks later:
Again, this is clearly sinus rhythm with RBBB and LAFB.

Learning Point:

When SVT with aberrancy or VT are suspected, both may be ruled out by diagnosis of sinus tachycardia using Lewis Leads.  These are simple and fast.


  1. Dr. Smith, the morphology of the qrs complex in V1 (bbdx) and qrs in the inferior leads DII, DIII, aVF, with an axis deviated to the left (anterior fascicular block type) suggests a fascicular ventricular tachycardia (verapamil-sensitive)
    It would have been proper and safe (obviously if the patient is unstable recourse to electrical cardioversion synchronized) administration of verapamil?
    (drug classically avoided in wide complex tachycardia)
    Vittorio Masciulli

  2. Interesting case Dr. Smith. Look like idiopathic fascicular LV tachycardia to me. If this is tipical RBBB, could you explain or post some cases of atipical RBBB to make DD. thanks

  3. Dr. Smith,

    Thanks for presenting this marvellous case and reminding this precious tool. But, I am curious where does this definition of the Lewis lead come from. Is this a modification of the Lewis lead which had been shown to be better than the original definition ? I am not sure why Lewis lead is defined by the referenced page as described above, since Sir Thomas Lewis used this lead as

    Placed the Right Arm electrode on the 2nd intercostal space, right sternal border
    Placed the Left Arm electrode on the 4th intercostal space, right sternal border
    The Leg electrodes remained the same.
    Monitored Lead I.

    The referenced page cites two papers, both of which used the original Lewis definition. I only find this placement in Wikipedia, which references Goldman's Principles of Clinical Electrocardiography 1982.

    Any comment for clarifying this issue would be really appreciated.

    Thanks in advance

    1. Emre,
      I got it from Christopher Watford:
      I asked him where he got it from and here is his answer:

      "I learned the "S5" lead, which apparently was a Marriott choice from the original Lewis leads (perhaps an apocryphal story of Marriott's teaching, as I wasn't there). Lewis described a number of leads, the most popular of which is simply called the Lewis Lead where they're much closer together than the "S5 lead". Truly I have no clue why it is called the S5 lead."


  4. But why after the adenosine the p waves were not obvious? Also how do you explain the dominant R wave in aVR?I am bit confused.

    I am a big fan of your ecg blog. You have taught me so many things. Sincerely thank you sir!

    1. Adenosine causes sinus arrest, so P-waves disappear with adenosine. Flutter waves do not.
      Thank you for the kind words!
      Steve Smith

  5. NICE case! In addition to RBBB/LAHB morphology — the rapid (ie, narrow) initial part of the QRS deflection in most leads on this tracing during the initial tachycardia support a supraventricular etiology — though as per Dr. Smith, one can’t completely rule out the possibility of posterior fascicular tachycardia based solely on the initial tracing. It almost looks like sinus P waves may be present at the end of what looks to be a long QT in each of the inferior leads. That said, lead V1 typically shows atrial activity when the rhythm is sinus — and such atrial activity is strangely absent from the initial 12-lead. Even with underlying (hidden) sinus P waves — the QT during the initial tachycardia looks prolonged, suggesting possible electrolyte imbalance (low K+/Mg++) as a possible contributing factor. Use of Lewis Leads is a excellent suggestion here. I was especially interested in the post-conversion 12-lead (done 24 hours later) — which still made me wonder why no atrial activity was seen in V1 on the initial tracing … That said, this is an excellent case illustrating the benefit of using Lewis Leads to help assess problematic arrhythmias.

    1. All good points, Ken. One correction: he never "converted", just slowed down. Same sinus rhythm on all EKGs.

  6. I've been using that lead for over 40 years Henry Marriott taught it to us. He always called it the S5 lead.


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