Atrial Tachycardia Workup

All patients who present acutely are placed on pulse oximetry and a cardiac monitor. A 12-lead electrocardiogram (ECG) is an important tool to help identify, locate, and differentiate atrial tachycardia. Laboratory studies may be indicated to exclude systemic disorders that may be causing the tachycardia. Electrophysiologic studies may be required. Occasionally, if enhanced automaticity or triggered activity is considered the underlying mechanism, exercise testing is used to facilitate the induction of atrial tachycardia.

ECG features of atrial tachycardia include P wave morphology and axis, PR interval, and PP interval variations. Typically, an isoelectric line is seen between consecutive P waves, while no line is seen with macroreentrant arrhythmias (eg, atrial flutter). Ideally, a full 12-lead ECG with a clear baseline is obtained to allow the most accurate evaluation of P wave morphology.

The P wave morphology in leads aVL and V₁ are most helpful for distinguishing the location of the arrhythmic focus (ie, right versus left atrium). A positive or biphasic P wave in lead aVL predicts a right atrial focus with 88% sensitivity and 79% specificity. A positive P wave in lead V₁ predicts a left atrial focus with 93% sensitivity and 88% specificity.

In most cases, the PR interval is shorter than the RP interval. In the presence of preexisting AV nodal conduction delay, the PR interval may be longer than the RP interval; thus, the P wave appears to follow the QRS complex or to fall within the QRS and mimics AV nodal reentrant tachycardia on 12-lead ECG tracings. Because the AV node is not a part of the reentrant circuit, AV nodal conduction block may cause 2-4:1 AV conduction without a termination of the atrial tachycardia, although 2:1 AV conduction is also occasionally reported in persons with AV nodal reentrant tachycardia.

Atrial tachycardia with AV conduction block is the hallmark ECG presentation in patients with digitalis intoxication.

Multifocal atrial tachycardia

The diagnosis of multifocal atrial tachycardia (MAT) is confirmed with an ECG that meets the following criteria:

• Irregular ventricular rate greater than 100 bpm
• Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead
• Irregular PP, PR, and RR intervals with an isoelectric baseline between the P waves

Some authors have suggested that patients who have rhythms with a rate less than 100 bpm but who satisfy all other criteria (including the clinical profile commonly observed with MAT) be considered to have multifocal atrial rhythm or, when the rate is less than 60 bpm, multifocal atrial bradycardia. However, a controversy arises about whether this condition should be referred to as a MAT variant or a wandering atrial pacemaker. Patients with a wandering atrial pacemaker usually do not have serious underlying illnesses.

The requirement that 3 different P waves should exist has been applied since early descriptions of the arrhythmia were recorded, but whether this should be interpreted as 2 ectopic P waves and 1 sinus P wave or 3 ectopic P waves has been a matter of controversy. The consensus favors a minimum of 3 different waveforms in addition to sinus P waves.

Baseline noise on the ECG can mimic atrial fibrillation and obscure differences in P wave morphology. Conversely, coarse atrial fibrillation on short recordings may appear to show discrete P waves prior to each QRS complex. Longer ECG recordings are therefore useful.

Note the image below.

At the beginning of the workup for atrial tachycardia, appropriate laboratory studies should be performed to exclude systemic causes of sinus tachycardia (eg, hyperthyroidism, anemia, dehydration, infection, hypoxemia, metabolic disturbance). Laboratory testing consists principally of a serum chemistry panel, blood hemoglobin level, and arterial blood gases, as follows:

• Serum chemistry - To exclude electrolyte disorders
• Blood hemoglobin level and RBC counts - To seek evidence of anemia
• Arterial blood gas level - To define pulmonary status

Additional tests include a magnesium level and a theophylline level (if the patient is on, or has access to, this medication). Obtain other laboratory tests as clinically indicated.

A serum digoxin level should be obtained in patients who are suspected of having digitalis intoxication. Other symptoms of digoxin toxicity may also provide clues to the diagnosis.

Chest radiography is indicated to evaluate for pulmonary and cardiac findings in patients who present with tachycardia-induced cardiomyopathy and in those with complex congenital heart disease.

Chest CT may be necessary at times to exclude pulmonary embolism as well as to assess the anatomy of pulmonary veins and provide digital imaging and communications in medicine (DICOM) images for anatomy reconstruction prior to ablative procedure.

Echocardiography is an important diagnostic modality to rule out the possibility of structural heart disease and to assess left atrial size, pulmonary arterial pressure, left ventricular function, and pericardial pathology.

Electrophysiology study may be required to establish the diagnosis of atrial tachycardia, usually by excluding other tachycardia mechanisms. In order to exclude an accessory AV pathway, the atrial activation must be dissociated from the ventricular activation. This is usually achieved by introducing a premature ventricular stimulation during the tachycardia.

If the premature ventricular beat advances the next atrial activation while the His bundle is refractory, this proves that an accessory AV pathway is present. This does not, however, prove that the tachycardia is an AV reentrant (accessory pathway–dependent) tachycardia. This only proves the existence of an accessory pathway; the accessory pathway could be either an integral component of the reentrant circuit or a bystander. If, with this maneuver, not only subsequent atrial activation is advanced but also the entire circuit of the tachycardia, this usually implies atrioventricular reentry with pathway participation rather that atrial tachycardia.

When burst ventricular pacing accelerates atrial rate and VAAV response is seen after termination of ventricular pacing, this very strongly predicts atrial tachycardia. If ventricular burst or programmed extrastimulation pacing creates transient AV conduction block without altering the atrial activation, atrial tachycardia is strongly suggested; that also excludes AV reentry as mechanism. If ventricular pacing terminates the tachycardia without pre-exciting the atrium or without retrograde conduction from ventricle to atrium, atrial tachycardia is generally excluded.

Typically, VA time is wobbly with atrial tachycardia, and the changes in AA cycle length drive the change in VV cycle length.

Focal tachycardia originating from the superior aspect of the crista terminalis and inappropriate sinus tachycardia usually have similar P wave morphologies and axes. Differentiating these 2 entities based on 12-lead ECG tracings is nearly impossible. Electrophysiologic study may be helpful to make the diagnosis. Focal tachycardia due to microreentry (such as sinoatrial reentrant tachycardia) can be induced and terminated by atrial extrastimulation or incremental atrial pacing, whereas inappropriate sinus tachycardia does not respond to these maneuvers.

By using endocardial mapping, sinoatrial reentrant tachycardia may be distinguished from inappropriate sinus tachycardia. The activation sequence in the region of the superior aspect of the crista terminalis can be recorded with a mapping catheter. The focus of earliest activation of inappropriate sinus tachycardia migrates superiorly or inferiorly along the crista terminalis as the rate increases or decreases, respectively, in response to an isoproterenol infusion. However, in the case of sinoatrial reentrant tachycardia, isoproterenol infusion does not change the earliest activation site, although it may increase the rate.

Endocardial mapping is most commonly used for localizing atrial tachycardia during electrophysiology study. Using this technique, focal tachycardias can be easily determined. This also allows for mapping scar tissue and allows identification of the critical isthmus of the tachycardia. Typically, only 60-70% of the total cycle length of the tachycardia is identified with activation mapping for focal tachycardias, while nearly 100% of the cycle length can be identified for macroreentrant circuits.

Focal atrial tachycardia due to microreentry may be initiated or terminated reproducibly with the same premature zone of atrial extrastimulation. Focal atrial tachycardia due to enhanced automaticity cannot easily be initiated or terminated by atrial extrastimulation but can usually be suppressed by overdrive atrial pacing. Focal atrial tachycardia due to triggered activity can be initiated, accelerated, and terminated by rapid atrial pacing.

Carotid sinus massage and adenosine have been used for diagnosing atrial tachycardia. These maneuvers reproducibly terminate AV nodal dependent tachycardias. For atrial tachycardia due to automaticity, carotid sinus massage and adenosine produce AV conduction block and generally do not affect the automatic focus; therefore, the atrial tachycardia continues. However, adenosine can occasionally stop some atrial tachycardias (usually a high dose of adenosine is needed, such as 12-18 mg). Termination of atrial tachycardia by a vagal maneuver such as carotid sinus massage would be very unusual (just as unusual as for atrial flutter).

Holter monitoring may be helpful to analyze the onset and termination of atrial tachycardia, identify the AV conduction block during the atrial tachycardia, and correlate the symptoms to atrial tachycardia. Event monitoring or home telemetry may be more useful for diagnosing patients with paroxysmal symptoms.