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Regular Wide Complex Tachycardia. What is the Diagnosis?

Posted Feb 05 2013 11:32am
A male in his 40's with no previous heart history presented with palpitations.  There were no symptoms or evidence of hypoperfusion.  A 12-lead was recorded during the tachycardia
There is a regular, wide complex tachycardia at rate of 170 bpm, with QRS duration of 124 ms.  There are no p-waves, no AV dissociation, no concordance (QRS in precordial leads are not all in the same direction).  There is inferior axis (all positive in II, III, aVF, and all negative in lead aVR.  There is an initial wide septal r-wave in V1 and V2 (greater than 40 ms).  There is a left bundle branch block morphology, except that the initial r-wave is wider than 40 ms.
What is the diagnosis?

The tachycardia resolved on its own with no therapy.  The post conversion ECG is below. 
There is lead reversal, making it appear as if there are Q-waves in leads I and aVL.  Otherwise it is normal.

Had it not spontaneously converted, what therapy would be appropriate?

Answer: this is RVOT, right ventricular outflow tract ventricular tachycardia, and it is usually sensitive to adenosine.  (I have been waiting for a case of this for years, and here it is!)  This is one of the "idiopathic" (though no longer actually idiopathic) VT types that occur in the absence of structural heart disease.  They generally have a relatively narrow QRS, less than 140 ms, whereas most VT has a QRS greater than 140 ms.  Here is a fine article discussing these and other types of VT in the absence of structural heart disease .

Adenosine would be appropriate here, as it generally is for regular, monomorphic, wide complex tachycardia, as long as you recognize that not all wide complex tachycardia that converts with adenosine is SVT with aberrancy.  This is the exception to that rule. In other words, conversion with adenosine does not prove SVT.  

The 12-lead ECG in RVOT VT has

1. LBBB pattern
2. wide septal r-wave
3. Inferior axis. 
4. The transition from S-wave to R-wave in the precordial leads depends on how far anterior (RV outflow tract vs. LV outflow tract) the origin of the VT is.

Here is a short quote from the article:

"Patients may be asymptomatic but often present with palpitations, chest pain, dyspnea, presyncope, and even syncope. In general, Outflow Tract Arrhythmia occur more frequently with exertion or emotional stress, and may have a diurnal variation. Women may have an increase in symptoms related to changes in hormonal status. In general, the prognosis of truly idiopathic OTA is benign.  Long-term follow-up studies have provided evidence that the vast majority of patients do not develop structural heart disease or SCD. However, as already noted, a small percentage of patients with very frequent VAs may have LV dysfunction over time, and rare reports have documented cardiac arrest and Polymorphic VT in patients who were initially thought to have “benign” Outflow Tract Arrhythmia."

Here are 2 more relevant posts, which include the approach to wide complex tachycardia: 1)  SVT with aberrancy   2) verapamil-sensitive posterior fascicular VT

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