Wide QRS complex tachycardias
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(Redirected from Differential Diagnosis of Tachycardia with a Wide QRS Complex)
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Differential Diagnosis of Tachycardia with Wide QRS Complex
- A regular tachycardia with a rate of 120 to 200 BPM with a QRS duration of .12 seconds or longer may be due to:
- Paroxysmal VT
- Supraventricular tachycardia with abnormally wide QRS
- Sinus tachycardia
- SA nodal reentrant tachycardia
- Paroxysmal atrial tachycardia
- Intraatrial reentrant tachycardia
- Atrial flutter with 2:1 conduction and occasional 1:1 conduction
- AV nodal reentrant tachycardia
- Automatic junctional tachycardia
- AV reentrant tachycardia using a bypass tract
Differential Diagnosis of Wide QRS Complexes
- Aberrant ventricular conduction
- Preexisting left or right bundle branch block
- Preexisting nonspecific IVCD
- Antegrade conduction through the bypass tract in patients with WPW
Clues to the Diagnosis of VT
- Morphology of Premature Beats During Sinus Rhythm:
- Previous EKG may show preexisting IVCD.
- If PVCs are present, and if the morphology of the arrhythmia is the same, then it is likely to be ventricular in origin.
- If there are PACs with aberrant conduction, then the origin of the arrhythmia may be supraventricular.
- Onset of the Tachycardia:
- Diagnosis of SVT made if the episode is initiated by a premature P wave.
- If the paroxysm begins with a QRS then the tachycardia may be either ventricular or junctional in origin.
- If the first QRS of the tachycardia is preceded by a sinus p wave with a PR interval shorter than that of the conducted sinus beats, the tachycardia is ventricular.
- AV Dissociation:
- Although is highly suggestive of VT, it may also be seen in junctional tachycardias with retrograde block.
- Morphology of the QRS Complexes and QRS Axis:
- 80 to 85% of aberrant beats have a RBBB pattern, but ectopic beats that arise from the LV have a similar morphology.
- The finding of a positive or negative QRS complex in all precordial leads is in favor of ventricular ectopy.
- A QRS duration of > .14 seconds (A Wellens criterion)
- Left axis deviation (A Wellens criterion)
- A monophasic or biphasic RBBB QRS complex in V1. But none of their patients with SVT had a preexisting RBBB. Therefore, this finding is of limited importance. (A Wellens criterion)
- Akhtar studied 150 patients with a wide complex tachycardia. The following were helpful in the diagnosis of VT:
- all patients with VT had a QRS duration > 120 msecond.
- QRS > .14 with a RBBB, QRS > .16 with LBBB.
- V1 - V6 all show a positive deflection.
- QRS axis between -90 and + 180 degrees.
- The QRS complexes have a LBBB but the QRS axis is rightward.
- In patients with preexisting bundle branch block, there is a change in the QRS pattern during the tachycardia.
- Capture beats:
- Rare, but one of the strongest pieces of evidence in favor of VT.
- Aberrancy rarely follows a beat of such short cycle length.
- Fusion beats:
- Rare but also strongly suggests VT.
- Vagal Stimulation:
- VT is not affected by vagal stimulation.
- May terminate reentrant arrhythmias
- Atrial pacing:
- A pacing wire is placed in the RA and the atrium is stimulated at a rate faster than the tachycardia.
- If ventricular capture occurs and the QRS is normal in duration, then one can exclude the possibility of aberrant conduction.
- His bundle recording:
- In SVT, each QRS is preceded by a His bundle potential.
- In VT there is no preceding His deflection.
- The retrograde His deflection is usually obscured by the much larger QRS complex.
| example | regularity | atrial frequency | ventricular frequency | origin (SVT/VT) | p-wave | effect of adenosine | |
|---|---|---|---|---|---|---|---|
| Wide complex (QRS>0.12) | |||||||
| Ventricular Tachycardia | 
| regular (mostly) | 60-100 bpm | 110-250 bpm | ventricle (VT) | AV-dissociation | no rate reduction (sometimes accelerates) |
| Ventricular Fibrillation | 
| irregular | 60-100 bpm | 400-600 bpm | ventricle (VT) | AV-dissociation | none |
| Ventricular Flutter | 
| regular | 60-100 bpm | 150-300 bpm | ventricle (VT) | AV-dissociation | none |
| Accelerated Idioventricular Rhythm | 
| regular (mostly) | 60-100 bpm | 50-110 bpm | ventricle (VT) | AV-dissociation | no rate reduction (sometimes accelerates) |
| Torsade de Pointes | 
| regular | 150-300 bpm | ventricle (VT) | AV-dissociation | no rate reduction (sometimes accelerates) | |
| Bundle-branch re-entrant tachycardia* | 
| regular | 60-100 bpm | 150-300 bpm | ventricles (VT) | AV-dissociation | no rate reduction |
| *) Bundle-branch re-entrant tachycardia is extremely rare | |||||||
Differential Diagnosis of Wide QRS Complex Tachycardia
- The following favor the diagnosis of VT:
- AV dissociation
- RBBB with QRS > .14, or LBBB with QRS > .16
- QRS axis in RUQ between -90 and +180 degrees
- Positive QRS in all the precordial leads (V1-V6)
- LBBB with a rightward axis
- LBBB with the following QRS morphology
- R wave in V1 or V2 > 0.03 second
- any Q wave in V6
- Onset of the QRS to nadir of the S wave in V1 > 0.06 seconds
- Notching of the S wave in V1 or V2
- Capture beats, fusion beats
- QRS morphology identical to that of premature ventricular beats during sinus rhythm
Clinical Correlation
- Most patients with VT have organic heart disease.
- Post MI VT is associated with a doubling of the risk of death.
- This was an a risk factor independent of poor LV function.
- VT can be seen with reperfusion, but an accelerated idioventricular rhythm is more common.
- Digoxin intoxication is a common cause. Other antiarrhythmics, phenothiazines, TCAs, and pheochromocytoma may also cause this.
- Cardiac catheterization, DC countershock, following repair of congenital lesions, and the hereditary QT prolongation are all associated with VT.
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
