How to differentiate ventricular tachycardia (VT) from atrioventricular (AV) dissociation with a ventricular rhythm in an adult patient with potential pre-existing heart conditions?

Differentiating Ventricular Tachycardia from AV Dissociation with Ventricular Rhythm

The key distinction is that AV dissociation with a ventricular rate faster than the atrial rate IS diagnostic of ventricular tachycardia—these are not separate entities to differentiate, but rather AV dissociation is a pathognomonic feature proving VT. 1

Understanding the Core Concept

The question reflects a common misconception. AV dissociation where the ventricles beat faster than the atria is not an alternative diagnosis to VT—it is a defining characteristic that confirms VT. 1 When you observe independent atrial and ventricular activity with the ventricular rate exceeding the atrial rate during a wide-complex tachycardia, you have proven the rhythm originates from the ventricles. 1

Diagnostic Approach to Wide-Complex Tachycardia

Step 1: Identify AV Dissociation (The Gold Standard)

AV dissociation is visible in only ~30% of VT cases but is highly specific when present: 1, 2

On ECG:

• Look for P waves marching through the QRS complexes at a slower rate than the ventricular rate 1
• Fusion complexes (pathognomonic for VT): Represent merger of conducted supraventricular impulses with ventricular depolarization 1, 2
• Capture beats: Occasional narrow QRS complexes from supraventricular conduction 1

On Physical Examination (often overlooked but valuable):

• Irregular cannon A waves in the jugular venous pulse 1, 2
• Beat-to-beat variability in the intensity of the first heart sound 1, 2
• Variable systolic blood pressure 1, 2

Clinical Pearl: If P waves are not visible on surface ECG, use esophageal pill electrodes or perform carotid massage to bring out retrograde VA block. 1

Step 2: Apply Morphologic ECG Criteria (When AV Dissociation Not Visible)

Brugada Criteria (ACC/AHA/HRS endorsed): 1

• Absence of RS complexes in all precordial leads V1-V6 → VT 1, 2
• RS interval >100 ms (onset of R to nadir of S) in any precordial lead → VT 1, 2

Vereckei aVR Algorithm: 1

• Initial R wave in aVR → VT 1
• Initial R or Q wave >40 ms in aVR → VT 1
• Notch on descending limb of predominantly negative QRS in aVR → VT 1

Additional Morphologic Features: 1

• QRS width >140 ms with RBBB pattern or >160 ms with LBBB pattern → favors VT 1
• Positive or negative concordance (all QRS complexes in same direction) in precordial leads → VT 1
• R-wave peak time ≥50 ms in lead II → suggests VT 1
• QR complexes indicate myocardial scar (present in ~40% of post-MI VT) 1

Step 3: Consider Clinical Context

History of prior myocardial infarction with first wide-complex tachycardia after the infarct strongly indicates VT. 1 This clinical context alone should shift your presumption heavily toward VT. 3

Age matters: VT accounts for >80% of wide-complex tachycardias in adults, particularly those with structural heart disease. 3

Critical Management Principle

If you cannot definitively prove the rhythm is supraventricular, treat it as VT. 1, 2 This is the ACC/AHA/ESC consensus recommendation because:

• Treating VT as SVT (particularly with verapamil or diltiazem) can precipitate hemodynamic collapse 1
• Treating SVT as VT is safer 1, 2
• Most wide-complex tachycardias are VT 2, 3

Common Pitfalls to Avoid

Hemodynamic stability does NOT differentiate VT from SVT. 1 Patients can have stable vital signs with VT, so never use blood pressure or consciousness level as your primary diagnostic criterion.

The differential diagnosis of wide-complex tachycardia includes: 1, 2

• SVT with pre-existing bundle branch block
• SVT with rate-related aberrant conduction
• SVT with conduction over accessory pathway (pre-excitation)
• Antiarrhythmic drugs causing QRS widening (Class Ia, Ic) 1
• Hyperkalemia or severe heart failure 1

QRS width criteria become less specific in patients on antiarrhythmic medications or with severe electrolyte abnormalities. 1