Focal Atrial Tachyarrhythmia

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

image

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

Pwave 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

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Feb 28, 2017 | Posted by in CARDIOLOGY | Comments Off on Focal Atrial Tachyarrhythmia

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