CHAPTER
7
Focal Atrial Tachyarrhythmia
UNDERSTANDING AND MANAGING FOCAL ATRIAL TACHYCARDIA
Epidemiology and Clinical Features
Focal atrial tachyarrhythmia (FAT) is observed in 0.3-0.4% of the asymptomatic population and 0.4-0.5% of the symptomatic population. It can present as:
○Paroxysmal tachycardia
○Persistent tachycardia with palpitations, chest pain, fatigue, dyspnea, or effort intolerance
If rapid rates persist, then heart failure may result (tachycardia-induced cardiomyopathy).
○Syncope is rare, but it can occur with rapid tachycardia and 1:1 conduction.
○“Silent” atrial tachycardia is detected in asymptomatic patients on electrocardiogram (ECG), Holter, or implantable devices.
Anatomy and Pathophysiology (Mechanism)
○Basic mechanism is an impulse originating from a right (80%; crista terminalis; superior vena cava [SVC]; inferior vena cava [IVC]) or left (20%; pulmonary vein, atrial septum, mitral annulus) atrial focus.
○Sub-classified based on mechanism
Abnormal automaticity (i.e., automatic ectopic atrial tachycardia [AEAT])
Triggered activity (i.e., non-automatic focal atrial tachycardia [NAFAT])
Localized (micro) reentry
Etiology
○Pulmonary disease: Chronic obstructive pulmonary disease (COPD), pulmonary hypertension, or chronic hypoxia
○Hyper-adrenergic states: Myocardial ischemia or infarction
○Metabolic or electrolyte: Hypokalemia/hypomagnesemia
○Drugs: Digoxin, theophylline
○Cardiothoracic surgery (especially for congenital heart disease)
Classification
○ Benign atrial tachyarrhythmia
Paroxysmal, regular, narrow-complex tachyarrhythmia at 80–140 bpm
○ Incessant atrial tachyarrhythmia
Persistent/permanent, regular, narrow-complex tachyarrhythmia at 100–160 bpm
○ Focal atrial tachycardia with an AV block
Regular atrial tachyarrhythmia with variable ventricular rate
Typically this is seen with digoxin toxicity, which has parasympathetic (inhibitory) effects on sinoatrial (SA node) and atrialventricular nodes (AVN) but sympathetic (stimulatory) effects on pacemaker cells (increased automaticity).
○ Multifocal atrial tachycardia
Irregular tachyarrhythmia (100–250 bpm) because of simultaneous activation of multiple (>3) foci
• Most often enhanced automaticity is seen during an acute medical illness (typically pulmonary disease).
A wandering atrial pacemaker is similar to multifocal atrial tachycardia except for the heart rate <100.
○ Junctional tachycardia (JT)
Persistent/permanent tachyarrhythmia because of enhanced automaticity or triggered activity originating at the junction between AVN and His bundle
Classification
• Focal junctional tachycardia: A heart rate of 110–250 bpm is usually due to trauma, infiltrative hemorrhage, inflammation, or pediatrics.
• Non-paroxysmal junctional tachycardia: The heart rate of 70–120 bpm is usually a marker for significant pathology (e.g., digitalis toxicity, ischemia, myocarditis).
12-Lead ECG
○ Rate: Atrial rate of 100–250 bpm
○ Rhythm: Ventricular conduction is variable:
Regular (constant ventricular conduction): Usually 1:1, 2:1, or 4:1 AV association
• Odd conduction ratios (e.g., 3:1) are rare.
Regularly irregular (dual-level AV block; i.e., 6:2)
Irregularly irregular (variable AV conduction)
• Variable AV block may be confused with irregular ventricular rhythm for atrial fibrillation.
○ P wave: Ectopic, unifocal P′ waves differ from the sinus node P wave.
FAT: Discrete P waves separated by isoelectric baseline in all leads
MAT: Multiple (≥3) different discrete P-wave morphologies with no dominant pacemaker
Table 7.1 ECG Features to Localize the Site of Origin of an Atrial Tachycardia
| Right AtriumV1: Negative P wave (Spec 100%)aVL: Positive or biphasic (Spec 76%) | Left AtriumV1: Positive (Spec 90%)aVL: Negative P wave (usually) | |
|
High II, III, aVF – positive |
SVC • Large P wave mimicking P pulmonale Crista Terminalis • P wave resembles sinus • P is negative in aVR (Spec. 93%) |
Superior PVs • Amplitude in lead II is ≥0.1 mV (Sp. 74%) • P wave is larger in ectopy than sinus (lead II; Sp. 85%) Left-sided PVs • Notching in lead II (only during ectopy; Spec. 95%) • P-wave ratio in lead III:II ≥0.8 (Spec. 75%) • V1 positive phase ≥80 ms (Spec. 73%) Right-sided PVs • Positive P wave in aVL (Spec. 100%) • P-wave amplitude in lead I ≥50 mcV (Spec. 99%) |
|
Low II, III, aVF – negative |
Inferolateral • Positive P wave in V5–V6 Inferomedial • Negative P wave in V5–V6 Apex of Triangle of Koch or Septal • P–wave duration is shorter than sinus |
○ PR interval: Isoelectric PR interval with long RP (period of absent atrial activation)
○ QRS: Narrow complex unless it is an aberrancy or bundle branch block (BBB)
○ Onset/termination: Paroxysmal or non-paroxysmal
May exhibit a rate increase (“warm-up”) at onset or a decrease (“cool down”) at termination
○ Maneuvers: Carotid sinus massage or adenosine usually increases the degree of AV block and facilitates the identification of P waves. Adenosine may rarely terminate the tachycardia.
Other Investigations
○ Laboratory investigations
Investigations into underlying cause (see Etiology)
○ 24-hour Holter monitor
Useful for diagnosis with episodes occurring more frequent than weekly
○ Event recorder
Useful for diagnosis with symptomatic episodes occurring weekly to monthly
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
