A 35-year-old man with a known history of Wolff–Parkinson–White (WPW) syndrome presents to the emergency department with severe palpitations, chest discomfort, and presyncope. His wife reports he collapsed briefly 30 seconds ago. Vital signs: HR 220 bpm, BP 85/50 mmHg, RR 24/min, SpO₂ 92% on room air. 12-lead ECG shows a wide-complex tachycardia at 220 bpm with a left bundle branch block pattern. The QRS duration is 160 ms. Intravenous adenosine 6 mg is being prepared. What is the most appropriate immediate management?

Explanation

## Management of Unstable Wide-Complex Tachycardia in WPW Syndrome ### Clinical Context This patient has WPW syndrome presenting with hemodynamic instability: HR 220 bpm, BP 85/50 mmHg, presyncope, and a brief collapse. The 12-lead ECG shows wide-complex tachycardia (QRS 160 ms) consistent with antidromic AVRT or pre-excited atrial fibrillation. This is a **medical emergency**. ### The Overriding Principle: Hemodynamic Instability = Immediate Cardioversion **High-Yield:** Per ACLS guidelines and Harrison's Principles of Internal Medicine (21e, Ch. 233), **any hemodynamically unstable tachyarrhythmia** — regardless of mechanism — mandates **immediate synchronized DC cardioversion**. Pharmacologic therapy is reserved for stable patients. This patient has: - BP 85/50 mmHg (hypotension) - Presyncope and witnessed collapse - SpO₂ 92% (hypoxia) - HR 220 bpm These are unambiguous signs of hemodynamic compromise. **Synchronized DC cardioversion at 100–200 J is the correct immediate action.** ### Why the Other Options Are Wrong | Option | Problem | |--------|---------| | **A) Procainamide/Flecainide** | Correct drug class for *stable* antidromic AVRT/WPW, but pharmacologic therapy is inappropriate when the patient is hemodynamically unstable — cardioversion must not be delayed | | **C) Verapamil** | **Contraindicated** in WPW with pre-excited tachycardia — blocks AV node but not the accessory pathway, potentially accelerating ventricular rate and precipitating VF | | **D) Adenosine** | **Contraindicated** in antidromic AVRT/pre-excited AF — same mechanism as verapamil; can paradoxically increase accessory pathway conduction and cause VF | ### Why Adenosine and Verapamil Are Dangerous in WPW Both agents block AV nodal conduction selectively. In antidromic AVRT or AF with WPW: 1. The accessory pathway remains unblocked 2. Blocking the AV node removes the competing conduction limb 3. All impulses are funneled down the accessory pathway → **ventricular rate acceleration → VF** ### Decision Algorithm ``` Wide-complex tachycardia + WPW ↓ Is the patient hemodynamically UNSTABLE? YES → Synchronized DC cardioversion (100–200 J) ← CORRECT ANSWER NO → Antidromic AVRT/pre-excited AF? YES → IV Procainamide or Flecainide NO → Adenosine (orthodox SVT) ``` **Key Point:** The critical teaching point here is two-fold: (1) hemodynamic instability always mandates immediate cardioversion over any drug, and (2) in WPW, AV nodal blockers (adenosine, verapamil, digoxin) are contraindicated regardless of stability. **Clinical Pearl:** Even if procainamide/flecainide are the correct *drugs* for WPW-related tachycardia, they must never delay cardioversion in an unstable patient. Option B (synchronized DC cardioversion at 100 J) is the most appropriate **immediate** management. [cite: Harrison 21e Ch. 233; ACLS 2020 Guidelines — Tachycardia Algorithm]