Atrial Tachycardia


  • Definition:
    • Atrial rhythm ≥ 100bpm initiated from a discrete origin
    • Ventricular rate varies depending on AV nodal conduction
    • Can be paroxysmal, sustained, or incessant
  • ECG Features
    • The key is to find the P-waves!
      • Depending on velocity of AV conduction, P-waves can be located anywhere in the cycle (commonly in the QRS or T-wave)
    • P-waves often have different morphology to sinus P-waves (compare to sinus ECG)
        • Caveat: P-wave morphology can match sinus P-waves when the focus is close to the sinus node.
        • P-wave morphology can resemble retro-conducted P-waves if the origin is low in the atrium or close to the AV node.
    • Sometimes a “Warm-Up” and “Cool-Off” phenomenon can be seen where the tachycardia accelerates and gradually slows down before terminating.
    • SVT that terminates on a P-wave is significantly less likely to be AT
      • Explanation: If a tachycardia terminates on a P-wave, the atrial focus must stop firing, and the AV node must block on the same beat.  Both of these events are statistically unlikely to happen on the same beat.

Sinus Tachycardia: Note that there is a discrete initiation with an early P-wave. Termination happens on a QRS.
Unlikely to be sinus tachycardia: Terminates on a P-wave

Response To Adenosine

  • Adenosine blocks the AV node, which stops ventricular activation, revealing AT P-waves. 
    • Compare these P-waves to the sinus ECG.
    • Usually P-waves are discrete and separated by an isoeletric period
  • Tachycardia continues after adenosine effect wears off. 
  • NOTE: Some atrial tachycardias are adenosine-sensitive, and can slow down or terminate with adenosine.

Localizing Atrial Origin (Advanced)

  • Negative P wave in lead I and aVL suggests LA origin
  • V1 is negative –> lateral RA
  • V1 is biphasic or positive –> Septal RA and LA
  • Negative in inferior leads –> Inferior origin
  • Positive in inferior leads –> Superior origin

Acute Therapy

If unstable –> Cardioversion (Class IA)

  1. Identify and treat associated conditions:
    • LA stretch (HF, CMP, HTN), MI, PE, infection, alcohol, electrolytes, cocaine/stimulants, theophyline
  2. Adenosine (IIA)
    • Rarely work.
    • Adenosine can convert DAD-triggered AT
  3. B-Blockers (IIA)
    • Can terminate or slow the rate
    • Avoid in decompensated HF
    • Metoprolol 2.5-5mg IV over 2-5min (max 15mg)
  4. CCB (IIA)
    • Avoid in Hypotension and HFrEF
    • Diltiazem 20mg IV bolus over 2min, repeat q15min
    • Verapamil: 5-10mg IV over 2min.  Additional 10mg IV can be given after 15-30min
ESC 2019 Guideline: Acute management of focal AT Focal AT Acute

4. Class IA, IC, and III drugs can prolong refractoriness or suppress automaticity

    • IV Ibutilide
    • IV flecainide or propafenone
    • IV Amiodarone (preferred if acute HF or hypotensive

5. Cardioversion may not be effective due to automaticity (especially incessant AT).  If it works, tachycardia can reinitiate. 

6. IV Amiodarone

Chronic Therapy

  • If rare and brief episodes, may not need chronic therapy
    • Anticoagulation not necessary (low risk of embolism)
  • 1st line: Catheter Ablation is Preferred (Class I)
    • Especially if insessant or TCM
    • Ablation is effective (75-100% success rate)
  • Medication (if ablation not feasible/desirable)
    • 2nd line: CCB and BB may be effective (IIA)
      • If one fails, try another
    • 2nd line: Class IC may be effective
      • Flecainide and propafenone  (if no structural/ischemic heart disease) (IIA)
      • (Decide with experts)
      • Ivabradine can be effective for focal AT (give with BB)
    • 3rd line: Amiodarone (avoid due to side-effect profile)
  • If all options fail –> AV Node Ablation with pacing
ESC 2019 Guideline: Chronic Management of AT
ESC 2019 Guideline: Focal Atrial Tachycardia