A 58-year-old man from Delhi presents to the emergency department with palpitations and syncope. ECG shows a heart rate of 280 bpm with a regular rhythm and narrow QRS complexes. An intravenous bolus of adenosine is administered, which terminates the arrhythmia. The patient's baseline ECG reveals a short PR interval and a delta wave. During the tachycardia, which phase of the cardiac action potential in the accessory pathway was responsible for the rapid conduction that bypassed the AV nodal delay?

Explanation

## Understanding Accessory Pathway Conduction in Wolff-Parkinson-White Syndrome ### Clinical Context The patient presents with **Wolff-Parkinson-White (WPW) syndrome**, characterized by: - Short PR interval (< 120 ms) - Delta wave (slurred upstroke on QRS) - Accessory pathway (Kent bundle) bypassing the AV node - Orthodromic AVNRT (narrow complex tachycardia) ### Cardiac Action Potential Phases: Atrial & Accessory Pathway Tissue | Phase | Duration | Ion Channels | Membrane Potential | Tissue Type | |-------|----------|--------------|-------------------|-------------| | **0** | ~1 ms | Fast Na^+^ influx (L-type Ca^2+^ in nodal tissue) | -90 mV → +20 mV | Atrial, accessory pathway | | **1** | Brief | K^+^ efflux, Cl^−^ influx | Slight repolarization | Atrial muscle | | **2** | ~200 ms | Ca^2+^ influx (L-type) balances K^+^ efflux | Plateau (~0 mV) | Atrial, ventricular | | **3** | ~150 ms | K^+^ efflux (delayed rectifier) | -90 mV | All tissues | | **4** | Diastole | K^+^ channels open, Na^+^/K^+^ ATPase | -85 to -90 mV | Resting | ### Why Phase 0 in the Accessory Pathway? **Key Point:** Accessory pathways (Kent bundles) are composed of **ordinary atrial muscle**, not specialized nodal tissue. They conduct via **fast sodium channels** (not slow calcium channels like the AV node). 1. **Steep Phase 0 slope** (~200–500 V/s) in accessory pathway vs. ~5–15 V/s in AV node 2. **No AV nodal delay** — no slow conduction through nodal cells 3. **Rapid depolarization** allows premature ventricular activation (delta wave) 4. During orthodromic AVNRT: conduction down accessory pathway → Phase 0 fast Na^+^ influx → rapid QRS upstroke **High-Yield:** The accessory pathway bypasses the AV node's physiologic delay (mediated by slow Ca^2+^ channels in nodal tissue). This is why WPW patients are at risk for **rapid ventricular rates** (up to 300 bpm) during atrial fibrillation — the accessory pathway has no refractory period like the AV node. **Clinical Pearl:** Adenosine blocks AV nodal conduction (via A1 receptors → ↑ K^+^ efflux, ↓ cAMP). In orthodromic AVNRT, blocking the AV node terminates the circuit, confirming the diagnosis. ### Why Not Other Phases? - **Phase 1** (early repolarization) is too brief and occurs *after* depolarization is complete - **Phase 2** (plateau) maintains the action potential but does not drive the rapid upstroke - **Phase 3** (repolarization) is when the membrane becomes *less* excitable, opposite to what drives conduction