How to differentiate between Ventricular Tachycardia (VT) and Supraventricular Tachycardia (SVT) with aberrancy in the Emergency Room (ER)?

Differentiating VT from SVT with Aberrancy in the Emergency Room

Critical First Principle

When you cannot definitively prove SVT, treat the patient as if VT is present—administering calcium channel blockers (verapamil or diltiazem) for presumed SVT when the rhythm is actually VT can precipitate hemodynamic collapse or ventricular fibrillation. 1, 2, 3

Initial Assessment Algorithm

Step 1: Assess Hemodynamic Stability

• Unstable patients (altered mental status, ischemic chest pain, acute heart failure, hypotension, or shock) require immediate synchronized cardioversion regardless of the underlying rhythm 3, 4
• Stable vital signs do NOT distinguish SVT from VT—patients with VT can remain hemodynamically stable 1, 2

Step 2: Obtain 12-Lead ECG During Tachycardia

• This is essential for accurate diagnosis and should be obtained immediately in stable patients 3
• Attach cardiac monitor, establish IV access, and evaluate blood pressure 3

Step 3: Determine QRS Width

• Narrow QRS (<120 ms): Almost always indicates SVT 2
• Wide QRS (≥120 ms): Could be VT or SVT with aberrancy—presume VT until proven otherwise 2

ECG Criteria for Diagnosing VT (Wide Complex Tachycardia)

Pathognomonic Features (100% Specific for VT)

• AV dissociation with ventricular rate faster than atrial rate—look for independent P waves 1, 2, 3
• Fusion or capture beats—represent merger between conducted sinus impulses and ventricular depolarization 1, 2, 3

Physical Examination Clues for AV Dissociation

• Irregular cannon A waves in jugular venous pulse 1, 3
• Variable intensity of first heart sound 1, 3
• Variability in systolic blood pressure 1

Highly Suggestive ECG Features for VT

• QRS width >140 ms with RBBB pattern or >160 ms with LBBB pattern 1, 2
• QRS concordance (all precordial leads V1-V6 show either all positive or all negative deflections) 2, 3
• Absence of RS complexes in all precordial leads (Brugada criteria) 2
• RS interval >100 ms in any precordial lead (Brugada criteria) 2
• R-wave peak time ≥50 ms in lead II 2
• Initial R wave or Q wave >40 ms in lead aVR (Vereckei algorithm) 2
• Notch on descending limb of predominantly negative QRS (Vereckei algorithm) 2

Clinical History Strongly Favoring VT

• Prior myocardial infarction (>95% positive predictive value for VT) 5
• History of congestive heart failure (>95% positive predictive value for VT) 5
• Recent angina pectoris (>95% positive predictive value for VT) 5
• Age >35 years (85% positive predictive value for VT) 5

Features Suggesting SVT with Aberrancy

Narrow Complex Tachycardia Patterns

• Pseudo-R wave in V1 or pseudo-S wave in inferior leads (suggests AVNRT with hidden P waves) 2
• Visible P waves in ST segment separated from QRS by ≥70 ms (suggests AVRT) 2
• Short RP interval (RP < PR): typical of AVNRT or AVRT 2
• Long RP interval (RP > PR): typical of atypical AVNRT, PJRT, or atrial tachycardia 2

Response to Vagal Maneuvers

• Termination or slowing with vagal maneuvers (Valsalva, carotid massage) suggests SVT where AV node is part of reentrant circuit 3
• VT will not respond to vagal maneuvers 3

Diagnostic Use of Adenosine

Adenosine can be used diagnostically in stable, regular, monomorphic wide-complex tachycardia of uncertain origin 3, 4

Cautions with Adenosine:

• May precipitate ventricular fibrillation in patients with coronary artery disease 3, 4
• Can accelerate ventricular rate in pre-excited atrial fibrillation/flutter 3, 4
• Do NOT use for irregular or polymorphic wide-complex tachycardia 3

Interpretation of Adenosine Response:

• Termination of tachycardia: strongly suggests SVT 2
• Transient AV block revealing underlying atrial activity: suggests atrial tachycardia or flutter 2
• No response: suggests VT (though some VTs may respond) 2

Critical Pitfalls to Avoid

Never Assume These Indicate SVT:

• Hemodynamic stability—VT can present with stable vital signs 1, 2
• Prior history of SVT—patients can develop VT later, especially with structural heart disease 5
• Younger age alone—while age ≤35 years has 70% positive predictive value for SVT, 30% still have VT 5

Dangerous Medication Errors:

• Never give calcium channel blockers (verapamil/diltiazem) for undiagnosed wide-complex tachycardia—can cause hemodynamic collapse in VT 1, 2, 3, 4
• Avoid AV nodal blocking agents in pre-excited atrial fibrillation—can accelerate ventricular response 3, 4

Confounding Scenarios:

• Pre-existing bundle branch block can make SVT appear as wide-complex tachycardia 2, 3
• SVT with accessory pathway conduction (antidromic AVRT) presents with wide QRS 1, 2, 3
• Class Ia or Ic antiarrhythmic drugs can widen QRS in SVT to >140-160 ms 1

Management Based on Diagnosis

If VT is Confirmed or Suspected:

• Unstable: Immediate synchronized cardioversion 3, 4
• Stable: Amiodarone 150 mg IV over 10 minutes 3, 4
• Alternative: Procainamide (if no severe heart failure or acute MI) 4

If SVT with Aberrancy is Confirmed:

• Unstable: Immediate synchronized cardioversion 3, 4
• Stable: Adenosine 6 mg rapid IV push, followed by 12 mg if needed 3, 4
• Alternative: Beta-blockers or non-dihydropyridine calcium channel blockers 3, 6

When Diagnosis Remains Uncertain:

Default to treating as VT—this is the safest approach given the higher morbidity and mortality risk 1, 2, 3

Role of Electrophysiology Study

• Consider cardiology referral for electrophysiology study when diagnosis remains uncertain despite ECG analysis, especially in patients being considered for ICD placement 7
• Recent data shows that up to 95% of patients with presumed VT referred for ICD had SVT with aberrancy confirmed by EPS, allowing successful ablation and avoiding unnecessary ICD implantation 7