Understanding Focal Atrial Tachycardia

• Focal Atrial Tachycardia (AT) is caused by abnormal automaticity, triggered

automaticity, or a small reentry circuit in diseased atrial tissue.
• Focal ATs can originate from various regions of the atria, including atrial
tissue extending into a pulmonary vein, the coronary sinus, or vena cava.
• Focal AT accounts for approximately 10% of paroxysmal supraventricular
tachycardia (PSVT) in patients referred for catheter ablation.
• Nonsustained focal AT is commonly observed on ambulatory
electrocardiogram (ECG) recordings, and the prevalence increases with age.
• Sympathetic stimulation is a promoting factor for focal AT, and it can be a
sign of underlying illness.
• AT can occur in the absence of structural heart disease or may be
associated with any condition that causes atrial fibrosis, including prior
catheter ablation.
• Nonsustained, frequent atrial ectopy or short bursts of AT may be
symptomatic and require therapy similar to that required for focal AT.
• Focal AT can occur with atrioventricular (AV) block, which may be caused
by digitalis toxicity.

Understanding Atrial Tachycardia (AT)

• AT has variable symptoms similar to other supraventricular tachycardias
(SVTs).
• 1:1 AV conduction or AV block in Wenckebach/fixed pattern typically
presents with AT.
• AT is not dependent on AV nodal conduction and will not terminate with AV
block.
• Warm-up/cool-down phases in atrial activation rate favor AT over AV
nodal-dependent SVT.
• P-waves in AT are often discrete with an intervening isoelectric segment.
• P-wave morphology in AT usually differs from sinus P-waves.
• Focal AT often originates in areas of complex atrial anatomy and the
location can be estimated by the P-wave morphology.
Clinical features and management of focal atrial tachycardia
• AT from atrial septum has a narrower P-wave duration than sinus rhythm.
• AT from left atrium exhibits a monophasic, positive P wave in lead V1 and
negative P waves in I and aVL, indicating an activation wavefront away from
the left atrial free wall.
• AT originating from superior atrial locations is positive in inferior limb
leads II, III, and aVF, whereas AT from inferior locations like ostium of the
coronary sinus will inscribe negative P waves.
• Maneuvers increasing AV block like carotid sinus massage or Valsalva
maneuver help expose P waves.
• Pharmacological therapy response varies depending on mechanism. Acute
management of sudden-onset, sustained AT remains the same as other
PSVTs.
• Catheter ablation is the preferred management for recurrent or incessant
ATS.
• Administration of adenosine or vagal maneuvers may transiently increase
AV block in AT due to reentry.
• Beta blockers and calcium channel blockers may improve tolerance of
arrhythmias by slowing ventricular rate.
• Potential precipitating factors and underlying heart disease should be
sought and excluded.
Management of Focal Atrial Tachycardia
• Beta blockers, calcium channel blockers and antiarrhythmic drugs are
effective treatments for Focal Atrial Tachycardia (AT).
• Catheter ablation targeting the AT focus is recommended when drugs fail
for recurrent symptomatic AT.
• Long-term use of drugs for recurrent episodes of AT can lead to potential
toxicities and adverse effects.
• AT is often a precursor to atrial fibrillation or atrial flutter, but the
associated risk for stroke and indications for long-term anticoagulation are
unclear.
• The chapter acknowledges the contributions of Gregory F. Michaud and
William G. Stevenson.
• The 2019 ESC Guidelines for the management of patients with
supraventricular tachycardia and Josephson's Clinical Cardiac
Electrophysiology: Techniques and Interpretations are recommended
resources for managing Focal Atrial Tachycardia.