A patient with Wolff-Parkinson-White (WPW) syndrome presents with a wide-complex tachycardia. The cardiology team avoids IV adenosine, IV verapamil, and IV diltiazem. The reason for avoiding these agents in WPW with pre-excitation is:
- A They cause paradoxical enhancement of conduction through the His-Purkinje system
- B They increase the QTc interval, predisposing to torsades de pointes in WPW
- C They decrease the effective refractory period of the accessory pathway by releasing catecholamines reflexly
- D By blocking the AV node, they may allow exclusive conduction down the accessory pathway, accelerating ventricular rate and precipitating ventricular fibrillation ✓
Explanation
In WPW with a pre-excited tachycardia, drugs that block the AV node (adenosine, verapamil, diltiazem) can eliminate the normal conduction pathway as a competing route. This forces all impulses down the accessory bundle (which has a short refractory period and no decremental conduction), leading to extremely rapid ventricular rates and degeneration to ventricular fibrillation. Procainamide or electrical cardioversion is preferred. QTc prolongation is associated with Class IA and III drugs, not adenosine or calcium channel blockers.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.