A 58-year-old man with a history of hypertension and recent myocardial infarction presents to the emergency department with palpitations and dizziness. His heart rate is 160 bpm with a regular rhythm. ECG shows a narrow complex tachycardia with a rate of 160 bpm. Blood pressure is 110/70 mmHg. Intravenous adenosine 6 mg is administered, which terminates the arrhythmia within seconds. Which of the following best describes the mechanism of action of adenosine in terminating this arrhythmia?

Explanation

## Mechanism of Adenosine in SVT Termination **Key Point:** Adenosine is a purine nucleoside that acts as a Class IV antiarrhythmic (calcium channel blocker equivalent) through adenosine A1 receptor activation. ### Adenosine's Mechanism of Action 1. **A1 Receptor Activation** → Opens G-protein-coupled potassium channels (K~ATP~) 2. **Hyperpolarization** → Membrane potential becomes more negative 3. **AV Node Effects** → Dramatically increases refractoriness and slows conduction 4. **Result** → Blocks reentrant circuits that depend on AV nodal conduction **High-Yield:** Adenosine is the drug of choice for acute termination of supraventricular tachycardia (SVT), particularly atrioventricular reentrant tachycardia (AVRT) and atrioventricular nodal reentrant tachycardia (AVNRT). ### Why Adenosine Works in This Case The narrow complex tachycardia at 160 bpm with abrupt termination by adenosine is pathognomonic for AVNRT or AVRT. Adenosine's potent AV nodal blocking effect breaks the reentrant circuit by preventing anterograde or retrograde conduction through the AV node. **Clinical Pearl:** Adenosine has an ultra-short half-life (~10 seconds) due to rapid cellular uptake and deamination, making it safe even if it causes transient asystole. Patients often experience a brief sensation of chest discomfort or dyspnea. ### Adenosine vs Other Antiarrhythmics | Class | Drug | Mechanism | AV Node Effect | SVT Efficacy | |-------|------|-----------|----------------|---------------| | IV (Adenosine) | Adenosine | A1 receptor → ↑ K+ efflux | ↑↑ Refractoriness, ↓↓ Conduction | 90–95% | | IV (CCB) | Verapamil | L-type Ca²⁺ channel block | ↑ Refractoriness, ↓ Conduction | 80–90% | | II (Beta-blocker) | Metoprolol | β1 antagonism | Modest ↑ Refractoriness | 50–70% | | Ia (Quinidine) | Quinidine | Na⁺ channel block | Minimal direct AV effect | Not first-line | **Mnemonic for Class IV Drugs: "VADE"** — Verapamil, Adenosine, Diltiazem, Esmolol (note: esmolol is technically β-blocker but grouped functionally). [cite:Harrison 21e Ch 297]