Clinical reference for EP conditions.

Disorganized atrial activation, most commonly driven by triggers from the pulmonary vein sleeves. Spectrum from paroxysmal to long-standing persistent, with progressive atrial remodeling over time.

Tachycardia originating from a discrete atrial focus (focal AT) or multiple competing atrial foci (MAT). Mechanisms span automaticity, triggered activity, and micro-reentry — each behaving differently on the table.

Macro-reentrant atrial tachycardia using a circuit other than the cavotricuspid isthmus — usually left-atrial roof, mitral isthmus, or scar-mediated. Common after AF ablation or atrial surgery. Long cases, lower success rates, high-density mapping essential.

Impaired conduction between atria and ventricles, graded by severity and localized to the AV node or the His-Purkinje system. Level of block, not just degree, drives the pacing decision.

Reentrant tachycardia within the AV nodal region using two functionally distinct inputs — a slow pathway with short refractoriness and a fast pathway with long refractoriness. The most common regular SVT in adults, especially women.

Reentrant tachycardia using an accessory pathway between atrium and ventricle as one limb and the AV node-His system as the other. Includes manifest pre-excitation (WPW) and concealed pathways without resting delta wave.

Delayed activation of one ventricle due to disease in the right or left bundle. Different patterns, different prognostic weight, different implications for ischemia interpretation and CRT candidacy.

A spectrum of sinus node and atrial pathology producing inappropriate bradycardia, pauses, chronotropic incompetence, and often coexisting atrial tachyarrhythmias. The most common indication for permanent pacing in adults.

Macro-reentrant tachycardia in the right atrium using the cavotricuspid isthmus as a critical zone of slow conduction. Highly stereotyped circuit, highly ablatable — one of the most satisfying cases on the schedule.

Wide-complex tachycardia originating below the His bundle. Mechanism, substrate, and management depend critically on whether the heart is structurally normal or scarred.