A 28-year-old woman presents to the emergency department with palpitations and chest discomfort lasting 2 hours. She reports a sudden onset of rapid regular heartbeat while sitting at her desk. On examination, BP is 118/76 mmHg, HR 180/min, regular. Physical examination reveals cannon a waves in the JVP. A 12-lead ECG shows a narrow complex tachycardia with a rate of 180/min; P waves are not clearly visible. Carotid massage is attempted but produces no change in heart rate. An intravenous bolus of adenosine 6 mg is given, resulting in immediate termination of the arrhythmia and restoration of normal sinus rhythm. What is the most likely diagnosis?

Explanation

## Clinical Presentation Analysis **Key Point:** The sudden onset, regular narrow-complex tachycardia at 180/min with P waves buried in the QRS (not visible), cannon a waves in the JVP, and immediate termination with adenosine are classic features of **Atrioventricular Nodal Reentrant Tachycardia (AVNRT)** — the most common paroxysmal SVT in adults. ## Why AVNRT Is the Correct Diagnosis ### 1. Cannon A Waves — The Critical Discriminator In **typical (slow-fast) AVNRT**, the reentrant circuit uses dual AV nodal pathways: antegrade conduction down the slow pathway and retrograde conduction up the fast pathway. This results in **near-simultaneous atrial and ventricular activation**, causing the atria to contract against closed tricuspid and mitral valves → **prominent cannon a waves** in the JVP. This is a hallmark finding of AVNRT and is seen in the vast majority of cases. In **AVRT** (orthodromic), retrograde atrial activation occurs *after* ventricular activation (RP interval > 70 ms), so atrial contraction is slightly delayed relative to ventricular systole — cannon waves are less prominent and less consistent. ### 2. P Waves Not Visible In typical AVNRT, retrograde P waves are buried within or at the very end of the QRS complex (pseudo-R' in V1 or pseudo-S in inferior leads), making them invisible on standard ECG. This matches the stem. ### 3. Adenosine Response Adenosine blocks the AV node, interrupting the reentrant circuit in AVNRT → **immediate termination** and restoration of sinus rhythm. This is the expected and definitive response. ### 4. Demographics and Onset AVNRT is the most common SVT in young women (female predominance), with sudden onset at rest — consistent with this 28-year-old woman. ## Distinguishing Features: AVNRT vs AVRT | Feature | **AVNRT** | AVRT (Accessory Pathway) | |---------|-----------|--------------------------| | **Cannon a waves** | **Prominent (hallmark)** | Less prominent / inconsistent | | **Retrograde P wave** | Buried in QRS (invisible) | After QRS (short RP) | | **Accessory pathway** | Absent | Present (delta wave at baseline) | | **Adenosine** | Terminates | Terminates | | **Demographics** | Young women, common | Young patients, WPW | | **Rate** | 140–250/min | 140–250/min | ## Why Not the Other Options? - **B (AVRT via accessory pathway):** Cannon a waves are NOT a hallmark of AVRT; they are more characteristic of AVNRT. No delta wave or pre-excitation is mentioned at baseline. - **C (Atrial flutter 1:1):** Atrial flutter typically has a rate of 250–350/min with sawtooth P waves; 1:1 conduction is rare and usually requires an accessory pathway or sympathomimetic state. - **D (Sinus tachycardia with atrial ectopy):** Sinus tachycardia is gradual in onset, rate rarely exceeds 150–160/min at rest, and does not terminate abruptly with adenosine. **High-Yield:** AVNRT accounts for ~60% of all paroxysmal SVTs. The triad of **sudden onset narrow-complex tachycardia + cannon a waves + adenosine termination** is pathognomonic for AVNRT. [cite: Harrison's Principles of Internal Medicine, 21e, Ch. 297; Braunwald's Heart Disease, 12e] **Clinical Pearl:** The presence of **cannon a waves** in a narrow-complex tachycardia strongly favors AVNRT over AVRT. This is because AVNRT causes simultaneous atrial and ventricular contraction (atria contract against closed AV valves), whereas in AVRT the atrial activation is slightly delayed after ventricular activation.