129. Supraventricular arrhythmias (AV-nodal reentry tachycardia, accessory pathways - WPW and LGL syndrome) - etiology, pathogenesis, clinical manifestations.

Supraventricular arrhythmias (AV- nodal reentry tachycardia, AV- nodal tachycardia in additional conduction pathways - WPW- and LGL-syndrome) – etiology, pathogenesis, and clinical manifestations.

1. 1 AV nodal reentrant tachycardia (AVNRT)

Etiology

• Usually structural dual conduction pathways within AV node (fast and slow pathways).
• Often occurs in structurally normal hearts.
• Triggered by premature atrial or ventricular extrasystoles.
• Precipitating factors: stress, caffeine, alcohol, hyperadrenergic states.

Pathogenesis

1. 1 AV node has two functionally distinct pathways:

• Fast pathway: rapid conduction, longer refractory period.
• Slow pathway: slow conduction, shorter refractory period.

2. A premature atrial beat finds the fast pathway refractory → impulse travels down slow pathway.
3. By the time impulse reaches lower common pathway, fast pathway is no longer refractory → impulse conducts retrogradely back up → reentry circuit established.
4. Leads to regular, rapid atrioventricular activation (usually 150–250 bpm).

Clinical manifestations

• Sudden onset palpitations ("pounding" heart), often abrupt termination.
• Dizziness, lightheadedness.
• Dyspnea, anxiety.
• Polyuria (due to atrial natriuretic peptide release from atrial stretch).
• Rarely, syncope if rate very high.

1. 2 AV reentrant tachycardia via accessory pathways (e.g., WPW, LGL)