Etiology
Most patients do not have organic heart disease. It is common in young individuals, and many have a long history of recurrent episodes.
Clinical manifestations
The tachycardia is paroxysmal, with sudden onset and termination. It can last from few minutes to several hours, or even days. Symptoms include sudden palpitations, chest tightness, anxiety, dizziness, and fatigue, as well as syncope, angina, heart failure, and shock. The severity of symptoms depends on the ventricular rate during the episode, duration, and whether there is underlying heart disease. If the ventricular rate is excessively fast, reducing cardiac output and cerebral blood flow, or if the tachycardia stops suddenly and the sinoatrial node fails to resume its rhythm, syncope may occur. During an episode, the first heart sound at the apex is constant in intensity, and the rhythm is absolutely regular.
ECG features
The ECG shows:
- A heart rate typically between 150 - 200 beats per minute, occasionally exceeding 250 bpm, especially in children
- Normal QRS morphology and duration, though abnormalities may appear with aberrant conduction or bundle branch block
- Retrograde P waves (inverted in leads II, III, aVF), often buried within or at the end of the QRS complex, maintaining a fixed relationship with the QRS
- Sudden onset, usually triggered by an atrial premature beat with a significantly prolonged PR interval, leading to tachycardia
Figure 1 Atrioventricular nodal reentrant tachycardia
Continuous, rapid, regular QRS complexes with normal morphology and duration at a rate of 154 bpm, with retrograde P waves visible at the end of the QRS complexes
Electrophysiological study
Electrophysiological study is crucial for diagnosing atrioventricular nodal reentrant tachycardia (AVNRT). In most patients, evidence of dual (common) or multiple pathways in the AV node can be found, indicated by the characteristic jump phenomenon (a sudden prolongation of the atrium-His interval by more than 50 ms as atrial pacing frequency increases, suggesting a switch from the fast to the slow pathway), followed by echo beats or tachycardia.
AVNRT is categorized into three types based on the atrium-His (AH) and His-atrium (HA) intervals and the earliest site of retrograde atrial activation:
- Slow-fast AVNRT, also known as typical AVNRT, is the most common, accounting for about 90%. It involves antegrade conduction through the slow pathway and retrograde conduction through the fast pathway, with the A wave (atrial wave) leading near the His bundle. The AH interval is significantly greater than the HA interval, and the AH interval is ≥ 200 ms.
- Fast-slow AVNRT accounts for about 5% of AVNRT, with antegrade conduction through the fast pathway and retrograde conduction through the slow pathway. The A wave near the coronary sinus ostium, with the AH interval usually less than the HA interval, typically < 200 ms, averaging 90 ms.
- Slow-slow AVNRT also accounts for about 5% of AVNRT, with antegrade and retrograde conduction through slow pathways. The A wave near the coronary sinus ostium, with the AH interval usually > HA interval, and the AH interval is ≥ 200 ms.
The fast-slow AVNRT and slow-slow AVNRT are often known as atypical AVNRT.
Treatment
During an acute episode, treatment should be based on the underlying cardiac condition, history of episodes, and tolerance to tachycardia. Some episodes may terminate spontaneously.
If patients have normal cardiac function and blood pressure, vagal maneuvers can be attempted. Patients are in supine position with lower extremities raised, the Valsalva maneuver (deep inhalation followed by breath holding and forceful exhalation) can be performed, and inducing gagging or immersing the face in ice water can be used to terminate the tachycardia. Carotid sinus massage (5 - 10 seconds per session, avoidance of bilateral massage, contraindications in older adults and those with glaucoma) can also be used. If these fail, medication or electrical cardioversion should be considered. Transesophageal rapid atrial pacing can also terminate tachycardia, but is less used due to poor patient tolerance.
Medication is the most common method to terminate tachycardia. Adenosine is the first choice due to its rapid onset. Side effects include chest tightness, dyspnea, facial flushing, sinus bradycardia, and atrioventricular block, but these resolve quickly due to adenosine's short half-life less than 6 seconds. If adenosine is ineffective, intravenous verapamil, amiodarone, diltiazem, or β-blockers can be used. Verapamil and diltiazem are contraindicated in heart failure or hypotension; β-blockers are contraindicated in decompensated heart failure.
If hemodynamic instability occurs, or if medications fail to convert or control the tachycardia, electrical cardioversion is indicated.
Catheter ablation is a safe and effective first-line treatment for AVNRT.
In patients who cannot undergo catheter ablation and experience frequent, symptomatic episodes, long-acting β-blockers or calcium channel blockers may be used for prevention. If episodes are infrequent, well tolerated, short, and self-terminating, prophylactic medication is not necessary.