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.

1 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823581/

https://www.uptodate.com/contents/enhanced-cardiac-automaticity

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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PAT and PSVT

• 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.

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