What is atrial tachycardia?

What is atrial tachycardia?


Atrial tachycardia (AT) is a disorder of fast heart rhythm that begins in the upper chambers of the heart, the left and right atria (1).  AT can start from one area, or focus, in either atrium and is called focal AT.  AT can also arise from multiple different areas of the atria, and is called multifocal AT.  Regardless the mechanism (focal vs. multifocal), the extra early signals that start from the focus/foci spreads centrifugally out to affect the atria and ventricles, and thus speeds up heart rate.  The racing heart may be felt by the patient as palpitations, dizziness, chest pain or lightheadedness, or in some people may be asymptomatic (2).  Occasionally, fast AT seen in younger patients can cause them to pass out.


AT has two unique characteristics that distinguish it from other similar atrial rhythm disorders:  1) they often occur in repetitive short bursts, and 2) AT episodes exhibit “warm up” and “cool down” periods where rate varies at initiation and termination of the arrhythmia (1).  Although short bursts of AT are common, sustained AT is a more rare cause of sustained arrhythmias from the atria (supraventricular tachycardia, SVT).  Of all episodes of SVT encountered by electrophysiologists, AT is the cause only about 5-15% of the time (2-3).  The diagnosis of AT is usually straightforward and starts with a thorough medical history and physical examination.  If the patient is exhibiting AT during the exam, then an electrocardiogram (ECG) may demonstrate a fast heart rhythm consistent with AT.  Cardiologists would recognize AT on the ECG as 1:1 P-QRS coupling, with non-sinus P-wave morphology, and usually long R-P interval.  In other words, there is a specific electrical signature in the atria, that is fast and different from the normal impulse, and which increases the rate of pumping of the ventricles.  It is this increase in rate that causes the symptoms of palpitations and dizziness described above.


If a patient is not exhibiting AT during the medical exam, it may be difficult to diagnose the arrhythmia because the electrical signature cannot be evaluated.  In this case, the electrophysiologist may choose to use a monitoring system to “catch” the AT when it happens.  Holter monitors, wearable loop recorders, and implantable loop recorders are examples of electronic recording devices that are commonly used to capture the electrical signature of the arrhythmia when it naturally happens.  The recorded ECG gives the physician information that may support AT as a potential diagnosis.


Sometimes, however, the arrhythmia may be so fast, that it is difficult to tell if AT or another SVT may be the cause of the arrhythmia.  In this case, an electrophysiology (EP) study may be performed to evaluate the cause and location of the arrhythmia, and during the same procedure, catheter ablation may be used to ablate the area(s) involved (4-6).  In fact, the primary treatment for sustained AT unresponsive to medications is catheter ablation, because medications and maneuvers to neurologically modify heart rhythm (such as vagal maneuvers) are often inadequate to completely suppress the arrhythmia (3, 5-7).    Catheter ablation of focal AT is highly effective with success rates usually in the 85-90% range, and with few complications (4).  Potential complications are extremely rare but do include those standard with radiofrequency ablation:  bleeding, pain, damage to heart and vessels, bleeding/effusion around the heart, damage to surrounding structures including the esophagus, and very rarely death.  Again, the advantage of radiofrequency ablation of focal AT is the targeted approach to the focus, or origin, of the arrhythmia and the high efficacy of the catheter-based treatment; patients should weigh the benefits and risks of ablation with their EP doctor prior to making any decisions re: treatment of ATs.  Finally, it is important to remember that AT is not generally a life-threatening disorder, however it does cause significant discomfort in some, and can worsen the risk of developing heart failure if it is particularly prolonged or sustained.  Thus, treatment is primarily for prevention of symptoms that are persistent and bothersome despite medications.



1. Link MS.  Evaluation and Initial Treatment of Supraventricular Tachycardia.  N Engl J Med. 2012 Oct 11;367(15):1438-48.

2. Roberts-Thomson KC, Kistler PM, Kalman JM.  Focal Atrial Tachycardia I:  Clinical Features, Diagnosis, Mechanisms, and Anatomic Location.  Pacing Clin Electrophysiol. 2006 Jun;29(6):643-52.

3. Roberts-Thomson KC, Kistler PM, Kalman JM.  Focal Atrial Tachycardia II:  Management.  Pacing Clin Electrophysiol. 2006 Jul;29(7):769-78.

4.  Lee G, Sanders P, Kalman JM.  Catheter ablation of atrial arrhythmias: state of the art.  Lancet. 2012 Oct 27;380(9852):1509-19.

5.  Rosso R, Kistler PM.  Focal Atrial Tachycardia.  Heart. 2010 Feb;96(3):181-5.

6. Shen MJ, Choi EK, Tan AY, Lin SF, Fishbein MC, Chen LS, Chen PS.  Neural Mechanisms of Atrial Arrhythmias.  Nat Rev Cardiol. 2011 Sep 27;9(1):30-9.

7. Blomström-Lundqvist C et al.  ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias- Executive Summary.  J Am Coll Cardiol. 2003 Oct 15;42(8):1493-531. Review.



Disclaimer    © 2015 www.markmccauleymd.com.  All rights served.