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Focal Atrial Tachycardia (Paroxysmal Atrial Tachycardia)

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Notes on Paroxysmal Atrial Tachycardia (PAT)/Focal Atrial Tachycardia (Focal AT.)

Focal atrial tachycardia is caused by enhanced automaticity or re-entrant circuits giving rise to a flutter like atrial and consequently ventricular tachycardia.

Dr. Mobeen discusses:

  • Properties of the focal atrial tachycardia (Focal AT.)
  • Different terms used in this class of disorders e.g. focal atrial tachycardia, paroxysmal atrial tachycardia, atypical atrial flutter, etc.
  • Causes of Focal AT.
  • Pathophysiology of Focal AT.
  • Clinical presentation.
  • EKG representation.
  • Medical and surgical treatment.


Abnormal Impulse Terms1

  • Automaticity

    • Normal Enhanced Automaticity:
      • Change in the heart rate driven by the pacemaker cells.
      • Sinus Tachycardia
      • Sinus Bradycardia
      • Sick sinus syndrome (alternating sinus tachycardia and sinus bradycardia.)
    • Abnormal Enhanced Automaticity:
      • An increased pacemaker like activity of cardiac myocytes and Purkinje cells.
  • Drivers

    • Non-nodal cardiac tissue that incorrectly starts to generate new impulses without the need to be triggered by another impulse (become automatic.) These ectopic foci are called drivers instead of pacemakers.
  • Reentry

    • Entrapment of an impulse, that originated somewhere else, in a reentrant circuit.
    • As the impulse cycles in this reentrant circuit, it sends new impulses to the neighboring cells.
  • Triggered activity

    • An impulse giving rise to further impulses due to the abnormal state of myocardial cells.
    • Note: these cells in the abnormal state cannot produce a new impulse on their own, they need an impulse acting as a trigger.
    • Drugs that prolong action potential duration (APD), e.g. class III antiarrhythmic, can cause triggered activity.
    • This triggered activity is called afterdepolarization (AD). It is of two types.
      • Early Atrial Depolarization (AED). Caused by slow activation and prolonged action potential.
      • Delayed afterdepolarization (DAD). Caused by the Ca++ overload.



Paroxysmal Atrial Tachycardia (PAT) Characteristics

A type of Supraventricular Tachycardia

  • Regular rhythm.
  • Rate from 100 to 200 beats per minute (bpm).
  • Usually, lasts for seconds or minutes. It can terminate and restart spontaneously. (It can become paroxysmal sustained tachycardia.)
  • Incessant atrial tachycardia (incessant AT) is a term used when a patient has atrial tachycardia during the 90% of the monitoring time.
  • The arrhythmia occurs due to the following abnormal impulses:
    • Enhanced automaticity of an ectopic atrial focus.
    • A reentrant circuit within atria.
    • Enhanced automaticity type may have a warm up and cool down period.
    • Reentrant form starts and stops abruptly as an atrial premature beat/contraction (PAC.) This is also called atypical atrial flutter.
  • Normal healthy individuals of all ages can experience PAT.
  • Digitalis toxicity can also cause PAT.


Causes of PAT/Focal AT

  • Atrial stretch in patients with heart diseases. (Hypertension and cardiomyopathies.)
  • Acute:
    • Myocardial infarction.
    • Pulmonary decompensation.
    • Infections.
    • Excessive alcohol ingestion.
    • Hypokalemia.
    • Hypoxia.
    • Stimulants.
    • Cocaine.
    • Theophylline.
  • More commonly it occurs in healthy individuals and is benign.
  • AT incidence is higher in patients that have undergone catheter ablation for atrial fibrillation.
  • Digitalis toxicity causes AT as well due to increased central sympathetic outflow.


Site of Abnormal Focus

  • The right atrium is involved in 63% of the cases and 37% involve the left atrium.
  • Right atrium:
    • 35% tricuspid annulus.
    • 34% crista terminalis.
    • 17% coronary sinus ostium.
    • 9% perinodal tissue.
    • 4% RA appendage/auricle.
  • Left atrium:
    • 67% pulmonary veins.
    • 17% mitral annulus.
    • 6% coronary sinus body.
    • 6% left intraatrial septum.
    • 4% LA appendage/auricle.


Clinical Presentation

  • Palpitations during the episodes/runs.
  • Rapid fluttering sensation in the chest or neck usually is associated with focal AT/PAT.
  • Patients can, rarely, present with syncope. This usually occurs when the ventricular rate is 200 beats per minute or above.
  • Symptoms of other cardiac comorbidities e.g. heart failure, angina may become exacerbated. (Dyspnea, chest pain, etc.)


PAT’s Diagnostic Criteria

  • Heart rate greater 100 beats per minute.
  • Driver/focus other than the SA node. (P wave morphology is different.)
  • Sudden in onset and offset.
  • An isoelectric interval between p waves.


EKG Presentation

  • Heart rate greater 100 beats per minute.
  • Driver/focus other than the SA node. (P wave morphology is different.)
  • As the arrhythmia is focal (from a single point of origin) and sustained. EKG displays p waves that can have morphology from normal to abnormal. P wave morphology, however, will be consistent.
  • The cycle length of tachycardia is variable.
  • Warm up and cool down phases are short (a few beats.) Sinus tachycardia takes 30 seconds to minutes to warm up or cool down.
  • Intermittent AV blocks may occur. These blocks, however, do not affect the PAT’s runs.
  • The Same focal driver can erratically fire between runs, adding atrial ectopic p waves. These p waves will have the same morphology to the p waves during the PAT’s runs.


Mapping the origin of the focus

  • An elaborate algorithm that predicted the arrhythmogenic focus in 93% of the patients has been devised.
  • V1 is important:
    • Generally, a positive p wave or biphasic p wave with positive first is an indicator of the focus in the right atrium ( the majority of the cases.)
    • A negative p wave or biphasic p wave with the negative phase first is an indicator of the focus in the left atrium.
  • Careful inspection of the p waves in the other leads can help locate the origin in possibly one of the following locations:
    • Coronary sinus, crista terminalis, right atrial appendage.
    • Interatrial septum.
    • Pulmonary veins, left atrial appendage.
  • Locating the focus is important for the surgical ablation.


EKG Image

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  • Usually one cannot tell the difference between the focal atrial tachycardia (paroxysmal atrial tachycardia) and paroxysmal supraventricular tachycardia.
  • Warm up and cool down rhythms are unique to PAT if present.
  • Carotid massage does not affect PAT.
  • PSVT can slow down or terminate with carotid massage.


Treatment of PAT

Consistent with 2015 American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS)

  • Acute

    • Rate, symptoms and hemodynamic status guides the acute treatment.
    • Treat the precipitating causes:
    • Administer potassium to hypokalemic patients.
    • If digitalis toxicity is suspected then discontinue digitalis and administer anti-digitalis antibodies if the hemodynamic status or other arrhythmias are life-threatening.
    • The vagal maneuver can be performed by the patient, or administer intravenous adenosine. (Both of these are usually less effective.)
    • IV beta blockers or nondihydropyridine Ca++ channel blockers (verapamil, diltiazem) can be given to hemodynamically stable patients.
    • IV Amiodarone can be better than the beta blockers, and verapamil and diltiazem.
    • Amiodarone can control acute tachycardia, terminate arrhythmia, and cause less hypotension.
    • Cardioversion may be tried but it is usually less effective for the following reasons:
    • Underlying pathology causing the arrhythmia may continue to trigger arrhythmias.
    • Enhanced automaticity of non-nodal tissue usually does not respond to cardioversion.
    • Hemodynamically unstable patients who fail to respond to above therapies may respond to chemical cardioversion with Amiodarone.
  • Chronic suppressive or prophylactic

    • Patients with few or no symptoms and rare/brief spells of arrhythmia may not need chronic treatment.
    • Patients that do not respond to medical therapy or have been on drugs for a long time may need catheter ablation.
    • Patients that do not want catheter ablation may need amiodarone, or class Ic (flecainide, propafenone), or class III (sotalol) antiarrhythmic. Which drug to use should be consulted with a cardiologist experienced with arrhythmia management.
    • If catheter ablation also fails then cardiac pacemaker with AV nodal ablation may be considered.
  • Treatment of incessant AT

    • Aggressive management to restore normal sinus rhythm should be made.
    • Beta blockers
    • Class Ic drugs (flecainide).
    • Usually, patients with incessant AT and LV systolic dysfunction that are not responding to medical therapy will need to undergo catheter ablation.


Drbeen Corp Disclaimer

  • All information contained in and produced by the drbeen corp., is provided for educational purposes only. This information should not be used for the diagnosis or treatment of any health problem or disease.


In this video we will learn about :

1. Automaticity. 

2. Definition of paroxysmal atrial tachycardia. 

3. ECG changes during PAT.

4. Causes of PAT. 

5. Mapping of abonrmal focus.

6. Clinical presentation.

7. PAT and PSVT.

8. Treatment of PAT. 

Following answers are created by ChatGPT. Occasionally the answer may be harmful, incorrect, false, misleading, incomplete, or limited in knowledge of world. Please contact your doctor for all healthcare decisions. Also, double check the answer provided by the AI below.


Dr. Mobeen Syed

Dr. Mobeen Syed

Mobeen Syed is the CEO of DrBeen Corp, a modern online medical education marketplace. Mobeen is a medical doctor and a software engineer. He graduated from the prestigious King Edward Medical University Lahore. He has been teaching medicine since 1994. Mobeen is also a software engineer and engineering leader. In this role, Mobeen has run teams consisting of hundreds of engineers and millions of dollars of budgets. Mobeen loves music, teaching, and doing business. He lives in Cupertino CA.

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