Atrial Tachycardia Workup

Updated: Nov 16, 2019
  • Author: Bharat K Kantharia, MD, FRCP, FAHA, FACC, FESC, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
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Approach Considerations

All patients who present acutely with possible atrial tachycardia should be placed on pulse oximetry and a cardiac monitor. A 12-lead electrocardiogram (ECG) and rhythm strip is an important tool to help identify, locate, and differentiate atrial tachycardia. A nodified ECG with the Lewis lead in which the right- and left-arm electrodes are applied at the two sides of the sternum at the second and fourth intercostal spaces may be used to magnify P waves. Esophageal recording of atrial activation may be necessary to discern P waves, especially in the pediatric age group.

The following laboratory studies may be indicated to exclude systemic disorders that could be causing the tachycardia:

  • Electrolyte levels: Particularly potassium, bicarbonate, calcium, and magnesium

  • Blood glucose level

  • Complete blood cell (CBC) count

  • Toxicology screen (including the use of herbal medications or energy supplements)

  • Arterial blood gas measurement

  • Thyroid function tests

  • 24-Hour urine collection for catecholamines and catecholamine metabolites

Echocardiography can be valuable. Invasive electrophysiologic study 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.

The advent of three-dimensional (3-D) high-density and rapid electroanatomic mapping to characterize atrial tachycardias appears to have the potential to result in favorable outcomes following ablation.


Exclusion of Systemic Disorders

At the beginning of the workup for atrial tachycardia, appropriate laboratory studies should be performed to exclude systemic causes of sinus tachycardia (eg, fever, 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 red blood cell (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. For example, a serum digoxin level should be obtained in patients who are suspected of having digitalis intoxication; digitalis intoxication is classically associated with atrial tachycardia with atrioventricular block. Other symptoms of digoxin toxicity may also provide clues to the diagnosis.

Chest radiography is indicated to evaluate for a pulmonary etiology (eg, chronic obstructive pulmonary disease) and to delineate cardiac size and structures and cardiac findings in patients who present with tachycardia-induced cardiomyopathy and in those with complex congenital heart disease.

Computed tomography (CT) scanning of the chest may be necessary at times to assess the anatomy of cardiac structures, including the pulmonary veins especially, to provide digital imaging and communications in medicine (DICOM) images for anatomy reconstruction prior to an ablative procedure, and to exclude pulmonary embolism.



Ideally, a full 12-lead electrocardiogram (ECG) and rhythm strip and with a clear baseline is obtained to allow the most accurate evaluation of P wave morphology. ECG features to consider in the diagnosis of atrial tachycardia include P wave morphology and axis (see the image below), 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).

Atrial tachycardia. Note that the atrial activitie Atrial tachycardia. Note that the atrial activities originate from the right atrium and persist despite the atrioventricular block. These features essentially exclude atrioventricular nodal reentry tachycardia and atrioventricular tachycardia via an accessory pathway. Note also that the change in the P-wave axis at the onset of tachycardia makes sinus tachycardia unlikely.

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 atrioventricular (AV) nodal conduction delay, however, 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. However, 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 electrocardiogram (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 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 of 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 MAT 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. (See the image below.)

Atrial tachycardia. This electrocardiogram shows m Atrial tachycardia. This electrocardiogram shows multifocal atrial tachycardia (MAT).

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.



Echocardiography is an important diagnostic modality. It is used to assess structural heart disease and to evaluate the following:

  • Left atrial size

  • Pulmonary arterial pressure

  • Left ventricular systolic and diastolic function

  • Pericardial pathology



An electrophysiology study may be required to establish the diagnosis of atrial tachycardia, usually by excluding other tachycardia mechanisms (e, atrioventricular [AV] reentrant tachycardia [AVNRT]). In order to exclude AVNRT and an accessory AV pathway-related AVRT, certain maneuvers are performed mainly to dissociate atrial activation from the ventricular activation and to observe any linking phenomenon. This is usually achieved by introducing a premature ventricular stimulation during the tachycardia. If the premature ventricular beat during His-bundle refractoriness terminates the tachycardia without inscribing atrial activation, both atypical AVNRT and atrial tachycardia can be excluded.

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. It does not, however, prove that the pathway is involved in the tachycardia; rather, the pathway may simply be a bystander. If the premature ventricular beat advances not only subsequent atrial activation but also the entire circuit of the tachycardia, this usually implies AV reentry with pathway participation rather than atrial tachycardia.

When burst ventricular pacing accelerates the atrial rate and ventriculoatrial-AV (VAAV) response is seen after termination of ventricular pacing, this very strongly suggests atrial tachycardia. If ventricular burst or programmed extrastimulation pacing creates transient AV conduction block without altering the atrial activation, atrial tachycardia is again strongly suggested; this also excludes AV reentry as a mechanism. If ventricular pacing terminates the tachycardia without preexciting the atrium or without retrograde (VA) conduction, atrial tachycardia is generally excluded.

Typically, VA time is variable with atrial tachycardia. In addition, the changes in AA cycle length drive the change in VV cycle length.

Carotid sinus massage and adenosine have been used for diagnosing atrial tachycardia. These maneuvers reproducibly terminate AV nodal–dependent tachycardias but, due to automaticity, generally do not terminate atrial tachycardia. 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).

Inappropriate sinus tachycardia

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

Reentrant sinoatrial tachycardia

By using endocardial mapping, reentrant sinoatrial 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 reentrant sinoatrial tachycardia, isoproterenol infusion does not change the earliest activation site, although it may increase the rate.

Focal tachycardia

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 permits 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. (See the image below.)

Atrial tachycardia. An anterior-posterior mapping Atrial tachycardia. An anterior-posterior mapping projection is shown. This is an example of activation mapping using contact technique and the EnSite system. The atrial anatomy is partially reconstructed. Early activation points are marked with white/red color. The activation waveform spreads from the inferior/lateral aspect of the atrium through the entire chamber. White points indicate successful ablation sites that terminated the tachycardia. CS = shadow of the catheter inserted in the coronary sinus; TV = tricuspid valve.

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.

Distinguishing macroreentries from focal atrial tachycardias is the key for the ablation strategy. Macroreentry circuits usually involve the cavotricuspid isthmus in the right atrium, and are perimitral or roof-dependent in the left atrium. Detailed activation and entrainment mapping are necessary for successful ablation of these arrhythmias.


Event Monitoring or Home Telemetry

Event monitoring or home telemetry may provide useful information, especially in patients with paroxysmal symptoms. These procedures can be helpful for the following aspects of diagnosis:

  • Analyzing the onset and termination of atrial tachycardia

  • Identifying the AV conduction block during the atrial tachycardia

  • Correlating the symptoms with episodes of atrial tachycardia