Atrial Tachycardia (AT)

Definition

Classification

Mechanisms

1. Enhanced/abnormal automaticity - Spontaneous phase-4 depolarization in ectopic atrial myocytes outside the sinus node
2. Triggered activity - Oscillations of membrane potential (early or delayed after-depolarizations), often drug/ischemia-related
3. Reentry (micro or macro) - Micro-reentry in focal AT; macro-reentry around surgical scars or ablation lines in reentrant AT

Anatomic Origins

• Pulmonary venous ostia (especially left superior pulmonary vein)
• Crista terminalis (right atrium)
• Atrial appendages (RA and LA) - associated with incessant tachycardia
• Tricuspid and mitral annuli
• Coronary sinus
• Atrial septa
• Aortomitral continuity
• Regions of surgical scar tissue

ECG Features

• Regular rhythm at 100-200 bpm
• Discrete abnormal P waves (morphology differs from sinus P) with isoelectric intervals between them
• P wave axis and morphology reflect site of origin (e.g., negative P in inferior leads suggests inferior RA or septal origin)
• AV conduction ratio may be 1:1, 2:1, or higher depending on rate
• May show "warm-up" (gradual rate acceleration at onset) and "cool-down" at termination
• Long RP or short RP pattern depending on rate and AV conduction

• Irregular rhythm (often mistaken for AF)
• ≥3 distinct P wave morphologies
• Varying PR intervals and P-P intervals
• Distinguished from "wandering pacemaker" only by rate (MAT ≥100 bpm)

Clinical Presentation

• Palpitations
• Dizziness / presyncope (syncope unusual unless very rapid or structural heart disease present)
• Chest pain and dyspnea
• Fatigue

• AT is common in children and young adults with structural heart disease, often triggered by a premature atrial complex (PAC)
• In patients on digoxin, AT with 2:1 AV block is a hallmark sign of digoxin toxicity - Rosen's Emergency Medicine, p. 1052
• AT with rapid rates during sleep may be 40 bpm slower than waking rates

Tachycardia-Mediated Cardiomyopathy (TMC)

• Incidence ~10% in large focal AT series
• Occurs exclusively with incessant or very frequent paroxysmal tachycardia
• Affected patients: younger, more often male, slower mean tachycardia rate (~117 bpm)
• After successful ablation, LV function normalizes in virtually all patients
• Key locations causing incessant AT: RA/LA appendages and pulmonary venous ostia

Spontaneous Remission

• AT disappeared in 55% of patients under age 25 vs. only 14% of patients aged ≥26 after cessation of medical therapy - Braunwald's Heart Disease, p. 492

Management

Step 1 - Identify and Treat Precipitants

• Hypoxia/hypoxemia, electrolyte abnormalities (especially hypomagnesemia - give 2 g IV Mg over 5 min), drug toxicity (digoxin) - Rosen's Emergency Medicine, p. 1053

Step 2 - Acute Rate Control / Termination

• Vagal maneuvers and adenosine: unlikely to terminate AT (unlike AVNRT/AVRT), but useful to unmask atrial activity by transiently blocking AV conduction
• Beta-blockers: IV metoprolol for rate control
• Calcium channel blockers: IV diltiazem or verapamil for rate control
• DC cardioversion: can restore sinus rhythm acutely, but AT often recurs (especially MAT)

Step 3 - Chronic/Long-term Management

• Goldman-Cecil Medicine, p. 3271

Catheter Ablation

• Increasingly offered as first-line therapy, especially for symptomatic or drug-refractory AT - Goldman-Cecil Medicine, p. 3271
• Uses activation mapping (earliest local activation precedes P wave onset by 15-40 ms) to localize the focus
• Success rate >90% with 3D electroanatomic mapping systems - Fuster & Hurst, p. 1141
• Phrenic nerve injury is a risk when ablating near the right superior pulmonary vein or right atrial appendage - must pace at high current to test for diaphragmatic contraction before ablation
• Multifocal AT is an important exception - very difficult to ablate; best managed by treating the underlying pulmonary/cardiac disorder

Anticoagulation

• Embolic events and stroke are rare with AT (unlike AF/flutter); anticoagulation is generally not indicated - Braunwald's Heart Disease

Special Case: Multifocal AT (MAT)

• Associated with advanced pulmonary disease in up to 60% (primarily COPD); also primary cardiac pathology
• Relatively unresponsive to antiarrhythmic drugs
• Cardioversion can restore sinus rhythm but MAT recurs quickly
• Treatment cornerstone: manage the underlying pulmonary disease
• If acute symptom control is essential: IV diltiazem, verapamil, or metoprolol
• Prognosis determined primarily by the underlying pulmonary disease - Goldman-Cecil Medicine, p. 3281

Key Distinctions from Other SVTs

ECG Waves in Atrial Tachycardia

The Core Principle

1. The P Wave - The Defining Feature

Morphology

• The P wave is discrete and visible, with a shape different from the sinus P wave because the impulse spreads centrifugally from an ectopic atrial focus, not from the sinus node - Braunwald's Heart Disease, p. 492
• However, if the focus arises near the superior crista terminalis (high right atrium), the P wave may look almost identical to a sinus P wave - a key diagnostic trap

P Wave Axis and Localization

2. The P-to-QRS Relationship (RP/PR Interval)

Long RP Tachycardia (most common in AT)

• P wave comes well before the next QRS
• There is a clear isoelectric segment between the P wave and QRS
• The RP interval is longer than the PR interval
• Seen in slower ATs (e.g., 125-160 bpm)

Short RP Tachycardia (at rapid rates)

• At faster rates (e.g., 200-230 bpm), AV nodal conduction slows
• The P wave falls within or just after the preceding T wave
• The RP interval appears short, mimicking AVNRT
• Key differentiator: In AT, the RP-to-PR ratio can vary (called "unlinking") - this variability is virtually diagnostic of AT and does not occur in AVNRT/AVRT

The "Unlinking" Sign

• In AVNRT and AVRT, the VA (ventricle-to-atrium) time is fixed because the atria and ventricles are part of the same reentrant circuit
• In AT, the atria and ventricles are electrically independent - the tachycardia lives in the atrium and merely conducts through the AV node
• So the R-P interval can vary in AT even as the tachycardia rate stays constant - this is the key distinguishing feature

3. AV Conduction Ratio (P:QRS ratio)

• Digoxin toxicity classically produces AT with 2:1 AV block - a hallmark pairing on the ECG - Rosen's Emergency Medicine, p. 1052

4. The Isoelectric Interval

• In focal AT, there is a clear flat baseline between P waves (unlike atrial flutter where the baseline is never flat due to the sawtooth pattern)
• At very rapid rates, this isoelectric interval disappears and the tracing can resemble flutter
• The presence of an isoelectric interval strongly favours focal AT over macroreentrant AT or atrial flutter

5. Warm-Up and Cool-Down

• Warm-up: The rate gradually accelerates over 3-5 beats at the onset of the tachycardia (due to enhanced automaticity)
• Cool-down: The rate gradually slows over 3-5 beats at termination
• This is in contrast to AVNRT/AVRT which start and stop abruptly (on/off switch)
• Sudden onset is still possible in AT, particularly triggered activity forms

6. QRS Complex

• Usually narrow and normal - because ventricular conduction is unaffected
• Can become wide (aberrant) if there is rate-related bundle branch block or pre-existing BBB - this creates a wide-complex tachycardia that can mimic VT
• The QRS morphology itself gives no clue to the atrial origin

7. Multifocal AT (MAT) - A Special Pattern

• Irregularly irregular rhythm - the hallmark feature (often confused with AF)
• Three or more distinct P wave morphologies in the same lead
• Varying PR intervals and P-P intervals between beats
• Rate >100 bpm (below 100 it is "wandering atrial pacemaker")
• Key differentiator from AF: in MAT, discrete P waves are visible with isoelectric intervals between them; in AF, the baseline is chaotic with no true P waves

Summary Table: AT vs Other SVTs on ECG