How can I differentiate supraventricular tachycardia (SVT) from ventricular tachycardia (VT) and what are the acute management strategies for stable and unstable patients?

Differentiating SVT from VT and Acute Management

When in Doubt, Treat as VT

If you cannot definitively prove a wide-complex tachycardia is supraventricular in origin, you must treat it as ventricular tachycardia—giving calcium channel blockers or verapamil for presumed SVT when VT is actually present causes hemodynamic collapse and death. 1

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Critical Clinical Context That Proves VT

• Prior myocardial infarction has a >95% positive predictive value for VT and is the single most important clinical factor in your differential diagnosis 1
• The first occurrence of wide QRS tachycardia after MI strongly indicates VT 2, 1
• VT accounts for >80% of all wide-complex tachycardias in adults 3

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ECG Differentiation: Narrow vs Wide Complex

Narrow QRS Tachycardia (QRS <120 ms)

• All narrow-complex tachycardias are supraventricular and include AVNRT, AVRT, atrial tachycardia, atrial flutter, and atrial fibrillation 1
• Pseudo R' wave in V1 and pseudo S wave in inferior leads are pathognomonic for AVNRT 1
• P wave in ST segment separated from QRS by >70 ms suggests AVRT 1

Wide QRS Tachycardia (QRS >120 ms)

This represents either VT or SVT with aberrant conduction. Use these criteria to diagnose VT:

Pathognomonic Features for VT

• AV dissociation with ventricular rate faster than atrial rate proves VT (but only visible in 30% of cases) 2, 1
• Fusion complexes are pathognomonic for VT—these represent merger of conducted supraventricular impulses with ventricular depolarization 2, 1

Highly Suggestive Features for VT

• RS interval >100 ms from initial R to nadir of S in any precordial lead is highly specific for VT 2, 4
• Negative concordance (all QS complexes) in precordial leads is diagnostic for VT 2
• QRS width >140 ms with RBBB pattern or >160 ms with LBBB pattern favors VT 2
• QR complexes indicate myocardial scar and are present in ~40% of VTs after MI 2

Physical Examination Clues for VT

• Irregular cannon A waves in jugular venous pulse 2
• Variability in loudness of first heart sound 2
• Variability in systolic blood pressure 2

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Acute Management Algorithm

Step 1: Assess Hemodynamic Stability

For ANY hemodynamically unstable patient (syncope, cardiac arrest, severe hypotension, angina):

• Immediate synchronized DC cardioversion is the only appropriate intervention 2, 1, 4, 3
• Do not delay for diagnosis—cardiovert first, diagnose later 3

Step 2: Management of Stable Narrow-Complex Tachycardia

1. First-line: Vagal maneuvers (Valsalva, carotid massage, facial immersion in cold water) 2, 1
2. Second-line: IV adenosine if vagal maneuvers fail 2, 1
   • Adenosine is preferred over calcium channel blockers due to rapid onset and short half-life 2
   • Contraindicated in severe asthma 2
   • Higher doses needed in patients on theophylline; effects potentiated by dipyridamole 2

Step 3: Management of Stable Wide-Complex Tachycardia

If you cannot definitively prove SVT, treat as VT: 2, 1, 4

• IV procainamide and/or sotalol for stable wide-complex tachycardia of ventricular origin 4
• Amiodarone for patients with impaired left ventricular function or heart failure 4

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Critical Pitfalls to Avoid

The Most Dangerous Error

Never give calcium channel blockers (verapamil/diltiazem) for wide-complex tachycardia of uncertain etiology—this precipitates hemodynamic collapse in VT and accelerates ventricular rate in pre-excited atrial fibrillation 1, 4

Adenosine Cautions

• Do not use adenosine in wide-complex tachycardia of uncertain etiology 2, 1
• Can precipitate ventricular fibrillation in patients with coronary artery disease 2, 1
• Can cause AF with rapid ventricular rate in pre-excited tachycardias 2, 1

Diagnostic Pitfalls

• Width and morphological criteria are less specific in patients taking antiarrhythmic agents, those with hyperkalemia, or severe heart failure 2
• Atrial fibrillation with rapid ventricular response can be misdiagnosed as regular SVT when irregularity is less easily detected 2
• A baseline conduction abnormality (bundle branch block in sinus rhythm) reduces the value of QRS morphology analysis 4

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Post-Acute Management and Prognosis

VT in Setting of Prior MI

• Mandates ICU/CCU admission 1
• Immediate cardiology/electrophysiology consultation 1
• Consider ICD placement 1
• Electrophysiology study for ablation consideration 1
• Carries significantly higher mortality risk and represents substrate for sudden cardiac death 1

After Successful Termination of Wide-Complex Tachycardia

• Refer all patients with wide QRS-complex tachycardia of unknown etiology to an arrhythmia specialist 4
• For confirmed Wolff-Parkinson-White syndrome, catheter ablation or drug therapy are long-term options 4

SVT Prognosis

• Most SVTs are benign from a mortality standpoint despite causing significant symptoms 1
• Catheter ablation has high success rate and is first-line for long-term management of recurrent, symptomatic paroxysmal SVT 5