Try to interpret the above Intracardiac tracing. Most will notice the very short VA time prior to VODP, which already argues strongly against AVRT. Just before termination, there is full RV capture at 300ms, with the atria continuing independently at 335ms. This VA dissociation would be highly unusual in AVRT, as AVRT requires both atrial and ventricular participation to sustain the circuit. The tachycardia would not persist this long under these conditions if AVRT were the mechanism. It would either terminate immediately or the atria would be accelerated to the pacing cycle length prior to termination. If the tachycardia terminates without atrial acceleration, think AVNRT. If the atria never depolarise to the pacing cycle length, atrial tachycardia is not possible. So the most likely diagnosis in above tracing is AVNRT Systematic Evaluation of EP Maneuvers to Diagnose AVNRT During Electrophysiology Study (EPS) --- Introduction Atrioventricular Nodal Reentrant Tachycardia (A...
Adenosine: Mechanism of Action and Its Role in Atrial Flutter – Including Conversion to Atrial Fibrillation with AV Block --- Introduction Adenosine is a naturally occurring purine nucleoside widely used in cardiology for the diagnosis and termination of supraventricular tachycardias (SVTs). While it is highly effective in AV node–dependent tachycardias such as AVNRT and AVRT, its role in atrial flutter is primarily diagnostic rather than therapeutic. Understanding its electrophysiologic effects is crucial, especially because adenosine can occasionally convert atrial flutter into atrial fibrillation with transient AV block — a phenomenon that can alarm clinicians if not anticipated. --- Cellular and Electrophysiologic Mechanism of Adenosine Adenosine acts via specific G-protein–coupled receptors: A1 receptors (cardiac effects – most important clinically) A2A receptors (coronary vasodilation) A2B and A3 (less relevant in arrhythmia management) 1. Action on the AV Node In the heart...