A wide complex tachycardia

Submitted by Van Wall M.D., Written by Pendell Meyers

Let's go back to the basics for a common and classic scenario.

A middle-aged patient presents with shortness of breath and palpitations. The patient was stable without signs of low cardiac output or distress. Her ECG is shown below (first see what you think without using the baseline): 

What do you think?

There is a (minimally) wide complex, regular monomorphic tachycardia at a little faster than 150 bpm. I measure the QRS duration at almost exactly 120 ms. The differential would include ventricular tachycardia, any cause of narrow complex regular tachycardia plus added conduction aberrancy (such as a bundle branch block), or other causes of QRS widening like hyperkalemia or sodium channel blockade. Of course, the interpreter should always start by assuming that a wide complex monomorphic tachycardia is due to ventricular tachycardia and/or life threatening hyperkalemia, until proven otherwise.

This demonstrates why it is so important to be able to recognize RBBB, LBBB, and paced rhythms (pacer spikes) so quickly. This ECG has perfect RBBB morphology, one of the rare times that we can be confident that a regular wide complex rhythm is not classic ventricular tachycardia. 

For more discussion on features of SVT vs. VT, see these prior posts:

Wide Complex Tachycardia: Ventricular Tachycardia or Supraventricular Tachycardia with Aberrancy?

Wide Complex Tachycardia and Cyanosis

A prior baseline showing identical RBBB morphology during sinus rhythm would prove this definitively. 


Here is the prior baseline ECG on file:

This shows the same RBBB morphology in sinus rhythm.

They applied Lewis leads to see if they could get a better look at the atrial rhythm:

I can't say that I see clear atrial activity.

They gave 12 mg adenosine (a perfectly reasonable and guideline-endorsed option for any rhythm that is regular and monomorphic, regardless of QRS width):

Flutter waves are revealed.

The rhythm soon returned to 2:1 atrial flutter, of course. The patient was then rate controlled and did well.

Learning Points:

Assume that wide complex regular tachycardia is VT and/or hyperkalemia. Then work backwards and prove that assumption false, if possible. VT is more likely statistically, and the likelihood of VT increases further with age, cardiac pathology, and QRS duration.

Recognizing classic RBBB or LBBB morphology may enable the diagnosis of SVT with aberrancy. This can be basically definite if the morphology is shown to be identical to prior known RBBB or LBBB morphology on baseline ECG.

Adenosine is contraindicated in irregular or polymorphic QRS complex rhythms. It is not contraindicated for wide complex regular monomorphic tachycardia, and is very reasonable in this scenario.