What is the diagnosis and management for a 20-year-old individual with episodic wide QRS (Quadrature Amplitude Modulation Ratio of the S wave) tachycardia, hemodynamic instability, and spontaneous reversion, with subsequent ECG (Electrocardiogram) showing transient ST depression in inferior leads and elevation in the ABR (Atrioventricular Block Ratio), then recovering to normal?

Diagnosis: Wolff-Parkinson-White (WPW) Syndrome with Antidromic AVRT

This 20-year-old with episodic wide QRS tachycardia, hemodynamic instability, spontaneous reversion, and transient ST changes that normalize represents pre-excitation syndrome (WPW) with antidromic atrioventricular reciprocating tachycardia (AVRT), not ventricular tachycardia. The key distinguishing features are the young age without structural heart disease, spontaneous termination, and complete ECG normalization afterward—all atypical for VT but classic for accessory pathway-mediated tachycardia 1.

Critical Diagnostic Features

The wide QRS tachycardia in this young patient is most likely antidromic AVRT, where conduction proceeds down the accessory pathway (creating the wide QRS) and returns via the AV node 2. The ACC/AHA guidelines emphasize that QRS width criteria are not helpful for differentiating VT from SVT with AV conduction over an accessory pathway 2.

Why This Is NOT Ventricular Tachycardia:

• Age and structural heart disease matter: While VT is the most common cause of wide QRS tachycardia in adults (85% in one series), this applies primarily to patients with atherosclerotic heart disease and prior myocardial infarction (73-75% of cases) 3, 4
• The 20-year-old age makes structural heart disease and VT far less likely 3
• Complete ECG normalization after the episode strongly suggests a functional (accessory pathway) rather than structural (scar-related VT) mechanism 1
• Spontaneous termination with hemodynamic recovery is more consistent with AVRT than sustained VT 4

The Transient ST Changes Are Key:

• The transient ST depression in inferior leads and ST elevation that then normalize represent repolarization abnormalities from the rapid rate and/or catecholamine surge during tachycardia 1
• These changes resolve because there is no underlying ischemia or infarction—this is a young heart with an electrical problem, not a structural one
• In VT associated with prior MI, you would expect persistent ECG abnormalities (Q waves, persistent ST changes) even after conversion 2

Immediate Management Approach

If Hemodynamically Unstable (As Described):

Immediate synchronized DC cardioversion is the treatment of choice for any wide QRS tachycardia with hemodynamic instability, regardless of the underlying mechanism 2. The ACC/AHA guidelines state unequivocally that "the most effective and rapid means of terminating any hemodynamically unstable narrow or wide QRS-complex tachycardia is DC cardioversion" 2.

• Start with 100-200 joules synchronized 2
• Do not delay for pharmacologic therapy when the patient is unstable 2

If Hemodynamically Stable (For Future Episodes):

If the diagnosis of wide QRS tachycardia cannot be definitively made, treat as VT to avoid potentially fatal mismanagement 2, 1. However, given the clinical context suggesting WPW:

• Avoid AV nodal blocking agents (adenosine, calcium channel blockers, beta-blockers, digoxin) in suspected pre-excitation, as these can precipitate ventricular fibrillation if atrial fibrillation develops 2
• Procainamide is the preferred agent for stable wide QRS tachycardia when pre-excitation is suspected, as it slows conduction through both the AV node and accessory pathway 4
• Amiodarone can be used but with caution, as it has complex effects on accessory pathways 5

Critical Next Steps

Obtain 12-Lead ECG in Sinus Rhythm:

The definitive diagnosis requires a 12-lead ECG during normal sinus rhythm to look for pre-excitation (short PR interval, delta wave, wide QRS) 1, 6. This is the single most important diagnostic test.

• If delta waves are present, this confirms WPW syndrome 1
• If the baseline ECG is completely normal, this suggests concealed accessory pathway or intermittent pre-excitation 1, 6

Electrophysiology Study and Ablation:

This patient requires referral to electrophysiology for definitive management 1, 6. The ACC/AHA guidelines support that patients with symptomatic pre-excitation and documented tachycardia are candidates for catheter ablation 2.

• Catheter ablation has >95% success rate for accessory pathway ablation and is curative 1
• This is particularly important in a 20-year-old to avoid lifelong antiarrhythmic therapy and risk of sudden death 1

Common Pitfalls to Avoid

Do Not Assume Hemodynamic Stability Rules Out VT:

Patients with VT can maintain hemodynamic stability for hours (mean 4.8 hours in one series with mean systolic BP 111 mmHg) 3, 4. However, in this young patient without structural heart disease, the complete normalization of the ECG afterward is the key distinguishing feature.

Do Not Give Adenosine If Pre-Excitation Is Suspected:

Adenosine should be used with extreme caution when the diagnosis is unclear, as it may produce ventricular fibrillation in patients with atrial fibrillation and pre-excitation 2. The guidelines explicitly warn that adenosine can cause "AF with a rapid ventricular rate in pre-excited tachycardias" 2.

Do Not Rely on QRS Morphology Alone:

In pre-excited tachycardias, the QRS is generally wider (more pre-excited) compared with sinus rhythm, and standard VT criteria (concordance, axis, morphology) may not apply 2. The clinical context (age, structural heart disease, post-episode ECG) is equally important 1, 3.

Document the Arrhythmia:

If the patient is not currently in tachycardia, obtain a 12-lead ECG during the next episode 1, 6. Consider event monitoring or implantable loop recorder if episodes are infrequent 6.