What is the initial approach to managing a patient with suspected Supraventricular Tachycardia (SVT)?

EKG Mimics of SVT

The most critical EKG mimics of SVT that can lead to dangerous mismanagement are ventricular tachycardia (VT), pre-excited atrial fibrillation, and sinus tachycardia with aberrant conduction—each requiring fundamentally different treatment approaches that can be life-threatening if confused.

Wide QRS Complex Tachycardias: The Most Dangerous Mimics

Ventricular Tachycardia vs SVT with Aberrancy

When faced with a wide QRS tachycardia (>120 ms), you must assume VT until proven otherwise, as giving AV nodal blockers to VT can cause hemodynamic collapse 1.

Specific EKG Criteria Favoring VT:

• QRS width >140 ms with RBBB pattern or >160 ms with LBBB pattern strongly suggests VT 1
• RS interval >100 ms in any precordial lead is highly suggestive of VT 1
• Negative concordance (all QS complexes in precordial leads) is diagnostic of VT 1
• Positive concordance does not exclude antidromic AVRT over a left posterior accessory pathway 1
• Ventricular fusion beats indicate ventricular origin 1
• QR complexes indicate myocardial scar and are present in ~40% of post-MI VTs 1

Critical Clinical Context:

A history of previous myocardial infarction with first occurrence of wide QRS tachycardia after the infarct strongly indicates VT 1. The morphological criteria become less specific in patients taking class Ia or Ic antiarrhythmics, those with hyperkalemia, or severe heart failure 1.

Pre-Excited Atrial Fibrillation: The Lethal Mimic

Pre-excited AF appears as an irregular wide-complex tachycardia and is the most dangerous SVT mimic because standard SVT treatments can precipitate ventricular fibrillation 2.

Key Distinguishing Features:

• Irregular rhythm with varying QRS morphology and width 2
• QRS generally wider (more pre-excited) compared to sinus rhythm 1
• Extremely rapid ventricular rates (often >200 bpm) possible 2

Management Imperatives:

• Never give AV nodal blocking agents (adenosine, diltiazem, verapamil, beta-blockers) as these may accelerate ventricular rate and cause ventricular fibrillation 1, 2
• Immediate synchronized cardioversion for hemodynamically unstable patients 2
• For stable patients, use ibutilide or IV procainamide 2

Narrow QRS Complex Mimics

Sinus Tachycardia

Regular narrow-complex tachycardia with visible P waves before each QRS in normal axis distinguishes sinus tachycardia from SVT 1. Look for a physiologic cause (fever, hypovolemia, pain, anxiety, hyperthyroidism) rather than treating as primary arrhythmia 3.

Atrial Flutter with Regular Conduction

Atrial flutter typically shows characteristic "sawtooth" flutter waves, best seen in leads II, III, aVF, and V1 1. Adenosine can be diagnostically useful here—it will transiently slow AV conduction to unmask flutter waves without terminating the arrhythmia 1, 2.

Multifocal Atrial Tachycardia (MAT)

Irregular narrow-complex tachycardia with ≥3 distinct P wave morphologies suggests MAT, most commonly seen in patients with underlying pulmonary disease 2. This will not respond to adenosine or vagal maneuvers 2.

Critical Diagnostic Approach

Essential First Steps:

• Record a 12-lead EKG during tachycardia before any intervention 1, 2
• Compare with baseline EKG in sinus rhythm when available 1
• Assess hemodynamic stability immediately (hypotension, altered mental status, shock, chest pain, acute heart failure) 1, 2

The Adenosine Diagnostic Test:

Adenosine can help differentiate mechanisms but use with extreme caution 1:

• Terminates AVNRT/AVRT (90-95% success rate) 2
• Unmasks atrial flutter or atrial tachycardia by transiently blocking AV node 1, 2
• May precipitate AF in some patients 2
• Contraindicated if pre-excited AF suspected—can cause VF in patients with coronary disease and rapid AF 1, 4
• Contraindicated in severe asthma due to bronchoconstriction risk 4

Common Pitfalls to Avoid

Never assume all SVTs are regular—irregular rhythm fundamentally changes your differential to include AF, MAT, or atrial flutter with variable block 2.

Never give verapamil or diltiazem if you cannot definitively exclude VT or pre-excited AF, as this may cause hemodynamic collapse or ventricular fibrillation 1, 2.

Do not rely solely on QRS width—SVT with pre-existing bundle branch block or antidromic AVRT can have QRS >140 ms 1.

When in doubt about wide-complex tachycardia, treat as VT—this is the safer assumption 1.

Assess perfusion and mental status systematically—failure to recognize hemodynamic instability leads to dangerous delays in cardioversion 5.