EP Staff Education Clinical Staff Ilyas Colombowala, MD, FACC, FHRS →
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Condition

Atrial Tachycardia (focal & multifocal)

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.

ECG features

  • ▸Focal AT: regular narrow-complex tachycardia with discrete P waves distinct from sinus morphology
  • ▸Long RP (RP > PR) when 1:1 conducted; isoelectric baseline between Ps differentiates from flutter
  • ▸Warm-up and cool-down at onset and termination in automatic AT
  • ▸Variable AV conduction often present, especially with adenosine or AV nodal blockade
  • ▸MAT: at least three distinct P-wave morphologies, varying PP and PR intervals, irregular rhythm
  • ▸P-wave morphology localizes the focus: negative in aVL → left-sided; positive in V1 → left atrial; superior origin → upright inferior Ps

Differential

  • ▸Atypical atrial flutter — continuous undulating baseline, no isoelectric segment
  • ▸Sinus tachycardia or inappropriate sinus tachycardia — P morphology matches sinus
  • ▸AVNRT and AVRT — usually short RP, distinct response to adenosine
  • ▸Atrial fibrillation — irregularly irregular, no discrete Ps (MAT is the classic mimic)
  • ▸Wandering atrial pacemaker — rate <100, otherwise overlaps with MAT

Focal AT

A discrete site fires repetitively at a rate higher than sinus. Three mechanisms operate, often indistinguishable on the surface ECG.

  • Automaticity: enhanced spontaneous depolarization. Warm-up at onset, cool-down at termination, sensitive to catecholamines. Often comes and goes — frustrating to capture in the lab.
  • Triggered activity: from delayed afterdepolarizations. Adenosine-sensitive in many cases. Can mimic the others.
  • Micro-reentry: small reentrant circuit, can be entrained. More likely after atrial surgery, ablation, or scar.

Common sites

  • Right atrium: crista terminalis (most common), tricuspid annulus, CS os, right atrial appendage, perinodal area
  • Left atrium: pulmonary vein ostia (especially post-AF ablation), mitral annulus, left atrial appendage, septum, LA roof
  • The septum and perinodal region are tricky — ablation risk to the AV node is real

ECG localization

  • Lead V1: positive P → left atrial; negative or biphasic → right atrial
  • Lead aVL: negative P → left atrial; positive → right atrial
  • Inferior leads: positive → superior focus (crista, RUPV); negative → inferior focus (CS os, low crista)
  • Lead I: negative → left lateral; positive → right or septal

P morphology is best assessed during AV block (adenosine, beta-blocker bolus) or in patient’s own tachycardia at slow conduction.

Multifocal atrial tachycardia (MAT)

Not a reentrant arrhythmia and not an ablation target. MAT reflects atrial sickness from a systemic insult.

  • Setting: severe COPD exacerbation, hypoxia, theophylline or beta-agonist toxicity, sepsis, hypomagnesemia, post-cardiac surgery, decompensated heart failure
  • ECG criteria: ≥3 P-wave morphologies in the same lead, irregular PP and PR intervals, isoelectric baseline (unlike AF)
  • Treatment:
    • Fix the underlying illness — oxygenation, magnesium repletion, treat infection, dial back bronchodilators
    • Magnesium IV often helps even with normal serum levels
    • Metoprolol IV if tolerated (caution in bronchospastic disease) or diltiazem
    • Amiodarone occasionally; cardioversion is futile (rhythm is automaticity-based)
    • No role for ablation

Distinguishing AT from atypical flutter

This trips people up regularly.

  • AT: discrete P waves with an isoelectric baseline between them
  • Atypical flutter: continuous undulating atrial activity, no flat baseline
  • AT cycle length is usually 250–500 ms; flutter typically 200–300 ms but overlaps
  • Atypical flutter is often post-ablation or post-surgical; AT can occur in normal hearts
  • On the table, both behave differently — flutter is a macro-reentrant circuit you can entrain around an anatomic obstacle; focal AT entrains from one site only or doesn’t entrain at all

EP study and ablation

  • Activation mapping: identify the earliest activation site relative to the P wave onset. Look for “pre-P” activation — typically 20–40 ms before P onset at the source.
  • 3D mapping system (CARTO or EnSite) is standard. High-density mapping pays off in low-amplitude or intermittent ATs.
  • Pace mapping at the suspected focus reproduces the P-wave morphology in focal AT.
  • Entrainment is useful for micro-reentry but not for true focal mechanisms.
  • Ablation: focal lesion at the earliest site. Endpoint is non-inducibility on full isoproterenol challenge.

Practical pitfalls

  • Catecholamines required to induce — have isoproterenol ready
  • Burst pacing and PES can initiate or terminate
  • Septal and para-Hisian sites: cryo, or RF with constant monitoring of PR/AH
  • Always think about the PVs in anyone with prior AF ablation — a “focal AT” off the LSPV is really a reconnected PV

Watch

Short videos to help illustrate this topic. Embedded from the original channels — content belongs to them.

Video pending Add a youtube video ID to display: P-wave morphology and focal AT localization
P-wave morphology and focal AT localization · EP educational channel · Maps common foci to expected P-wave vectors.

Last reviewed by Dr. Colombowala on May 22, 2026.

Not medical advice. This page is educational. Your situation may differ — discuss it with Dr. Colombowala or your treating physician before making decisions.