What is the difference between supraventricular tachycardia (SVT) and ventricular tachycardia (VTach) in terms of management and prognosis, particularly in a patient with a history of myocardial infarction?

Distinguishing SVT from Ventricular Tachycardia

When faced with a wide-complex tachycardia, particularly in a patient with prior myocardial infarction, you should presume ventricular tachycardia until proven otherwise and treat accordingly—giving calcium channel blockers or verapamil for presumed SVT when VT is actually present causes hemodynamic collapse and death. 1, 2, 3

Critical Clinical Context

A history of previous myocardial infarction has a positive predictive value >95% for VT, making this the single most important clinical factor in your differential diagnosis 1, 2, 4. Additional high-risk features include:

• History of congestive heart failure (>95% positive predictive value for VT) 4
• Recent angina pectoris (>95% positive predictive value for VT) 4
• Age >35 years (85% positive predictive value for VT, 92% sensitivity) 4
• First occurrence of wide QRS tachycardia after MI strongly indicates VT 1, 2

ECG Differentiation: Narrow vs Wide QRS Complex

Narrow QRS Complex (<120 ms)

Narrow QRS tachycardia is supraventricular in origin and includes AVNRT, AVRT, atrial tachycardia, atrial flutter, and atrial fibrillation 1. Key diagnostic features:

• 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
• Irregular ventricular rate suggests atrial fibrillation, multifocal atrial tachycardia, or atrial flutter with variable AV conduction 1

Wide QRS Complex (>120 ms)

This is VT in >80% of cases, but can also represent SVT with bundle branch block or SVT with accessory pathway conduction 1, 5. The distinction is life-threatening because stable vital signs do NOT help distinguish SVT from VT 1.

Definitive ECG Criteria for VT

Pathognomonic Features

AV dissociation with ventricular rate faster than atrial rate proves VT but is only visible in 30% of cases 1, 2. Look for:

• Fusion complexes (pathognomonic for VT)—represent merger of conducted supraventricular impulses with ventricular depolarization 1
• Irregular cannon A waves in jugular venous pulse 1
• Variability in loudness of first heart sound and systolic blood pressure 1

Highly Suggestive Features

• QRS width >0.14 seconds with RBBB pattern or >0.16 seconds with LBBB pattern favors VT 1, 2
• RS interval >100 ms in any precordial lead is highly suggestive of VT 1, 2
• Negative concordance in precordial leads (all QRS complexes negative) is diagnostic for VT 1
• QR complexes indicate myocardial scar and are present in ~40% of post-MI VT 1

Acute Management Algorithm

Hemodynamically Unstable (Syncope, Severe Hypotension, Angina, Cardiac Arrest)

Immediate synchronized DC cardioversion is the only appropriate intervention—do not delay for diagnosis or 12-lead ECG 1, 2, 3. The American College of Cardiology gives this a Class I recommendation 2, 3.

Hemodynamically Stable: Narrow QRS

• First-line: Vagal maneuvers (Valsalva, carotid massage, facial immersion in cold water) 1
• Second-line: Adenosine (terminates AVNRT and AVRT, unmasks atrial flutter/tachycardia) 1
• Alternatives: Beta-blockers or calcium channel blockers 6, 7

Hemodynamically Stable: Wide QRS of Uncertain Etiology

Treat as VT if you cannot definitively prove SVT 1, 2, 3. The management hierarchy:

• Amiodarone 150 mg IV over 10 minutes is first-line (Class IIa recommendation) 2, 3, 8
• Procainamide IV is an alternative first-line option 2
• Never give verapamil, diltiazem, or adenosine unless you have definitive proof of SVT with aberrancy 2, 3

Critical Pitfalls to Avoid

The most dangerous error is giving calcium channel blockers (verapamil/diltiazem) for wide-complex tachycardia that turns out to be VT—this precipitates hemodynamic collapse 1, 2, 3. Additional pitfalls:

• Do not use adenosine in wide-complex tachycardia of uncertain etiology—it can precipitate VF in patients with coronary disease and AF with rapid ventricular rate in pre-excited tachycardias 1, 2
• Do not rely on hemodynamic stability to rule out VT 1
• QRS width criteria are less specific in patients on class Ia/Ic antiarrhythmics, with hyperkalemia, or severe heart failure 1

Prognosis and Long-Term Management

SVT

Catheter ablation has high success rates and is first-line for recurrent, symptomatic paroxysmal SVT 6, 7. The American College of Cardiology recommends referral to cardiac electrophysiology for all patients after successful SVT termination 2.

VT in Post-MI Patients

VT in the setting of prior MI carries significantly higher mortality risk and mandates:

• ICU/CCU admission 3
• Immediate cardiology/electrophysiology consultation 3
• Consideration for ICD placement (based on ejection fraction and risk stratification)
• Electrophysiology study for ablation consideration once stabilized 3

The presence of structural heart disease fundamentally changes prognosis—VT with prior MI represents substrate for sudden cardiac death, while most SVTs are benign from a mortality standpoint despite causing significant symptoms 1, 6.