Background
Atrial tachycardia is a rhythm disturbance that arises in the atria. Atrial tachycardia can be observed in persons with normal hearts and in those with structurally abnormal hearts, including those with congenital heart disease and particularly after surgery for repair or correction of congenital or valvular heart disease.
Atrial tachycardia is defined as a supraventricular tachycardia (SVT) that does not require the atrioventricular (AV) junction, accessory pathways, or ventricular tissue for initiation and maintenance of the tachycardia. In common with most of the SVTs, the ECG typically shows a narrow QRS complex tachycardia (unless bundle branch block aberration occurs). Heart rates during atrial tachycardia are highly variable, with a range of 100-250 beats per minute (bpm). The atrial rhythm is usually regular. The conducted ventricular rhythm is also usually regular but may become irregular, often at higher atrial rates because of variable conduction through the AV node, thus producing conduction patterns such as 2:1, 4:1, a combination of those, or Wenckebach AV block.
The P wave morphology as observed on the ECG may give clues to the site of origin and mechanism of the atrial tachycardia. In the case of a focal tachycardia, the P wave morphology and axis depend on the location in the atrium from which the tachycardia originates. In the case of macroreentrant circuits, the P wave morphology and axis depend on activation patterns (see Workup).
Multifocal atrial tachycardia (MAT) is an arrhythmia with an irregular atrial rate greater than 100 bpm. Atrial activity is well organized, with at least 3 morphologically distinct P waves, irregular P-P intervals, and an isoelectric baseline between the P waves. Shine et al first proposed this definition in 1968.[1] Multifocal atrial tachycardia has previously been described by names such as chaotic atrial rhythm or tachycardia, chaotic atrial mechanism, and repetitive paroxysmal MAT. Go to Multifocal Atrial Tachycardia for more complete information on this topic.
A number of methods are used to classify atrial tachycardia, including origin as based on endocardial activation mapping data, pathophysiologic mechanisms, and anatomy.
Based on endocardial activation, atrial tachycardia may be divided into 2 groups. The first is focal atrial tachycardia, which arises from a localized area in the atria such as the crista terminalis, pulmonary veins, ostium of the coronary sinus, or intra-atrial septum. The second group is the reentrant atrial tachycardias. These reentrant (usually macroreentrant) atrial tachycardias most commonly occur in persons with structural heart disease, complex heart disease, and particularly after surgery involving incisions or scarring in the atria (see Clinical Presentation).
Atrial tachycardia may be classified according to the following pathophysiologic mechanisms: enhanced automaticity, triggered activity, or reentry (see Pathophysiology). Anatomical classification of atrial tachycardia is based on the location of the arrhythmogenic focus (see Anatomy).
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 study may be required (see Workup).
The primary treatment during a bout of atrial tachycardia is considered to be rate control using AV nodal blocking agents, such as beta-blockers or calcium channel blockers (see Medication). Cardioversion should be considered for any patient in whom the rhythm is not tolerated well hemodynamically and in whom rate control drugs are ineffective or contraindicated. Radiofrequency catheter ablation for atrial tachycardia has become a highly successful and effective treatment option for symptomatic, medically refractory patients or those who do not desire long-term antiarrhythmic therapy. (see Treatment and Management.)
See the images below depicting atrial tachycardia.
Propagation map of right atrial tachycardia originating from the right atrial appendage obtained with non-contact mapping using Ensite mapping system.
This 12-lead electrocardiogram demonstrates an atrial tachycardia at a rate of approximately 150 beats per minute. Note the negative P waves in leads III and aVF (upright arrows) are different from the sinus beats (downward arrows). The RP interval exceeds the PR interval during the tachycardia. Note also that the tachycardia persists despite the atrioventricular block. 
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. 
Anterior-posterior projection is shown. An example of activation mapping using contact technique and 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 thought the entire chamber. White points indicate successful ablation sites that terminated the tachycardia. TV – Tricuspid valveCS – Shadow of the catheter inserted in the coronary sinus 
Intracardiac tracings showing atrial tachycardia breaking with application of radiofrequency energy. The local electrograms in the successful site preceded the surface P wave by 51 ms, consistent with successful site. Note that postablation electrograms on the ablation catheter is inscribed well past the onset of sinus rhythm P wave. The first 3 tracings show surface electrocardiograms as labeled.CS – Respective pair of electrodes of the coronary sinus catheterCS 7,8 – Located at the os of the coronary sinusCS 1,2 – Distal pair of electrodes Abl – Ablation catheter (D-distal pair of electrodes) 
An example of rapid atrial tachycardia mimicking atrial flutter. Single radiofrequency application terminates the tachycardia. The first 3 tracings show surface electrocardiograms, as labeled. HRA – High right atrial catheterRVA – Catheter located in right ventricular apexHBED and HBEP – Respectively, distal and proximal pair of electrodes in the catheter located at His bundleAblD and AblP – Respectively, distal and proximal pair of electrodes of the mapping catheterMAP – Unipolar electrograms from the tip of the mapping catheter Go to Pediatric Supraventricular Tachycardia, Atrial Ectopic Tachycardia for more complete information on this topic.
Anatomy
Atrial tachycardia can have either a right or a left atrial origin. Some atrial tachycardias actually originate outside the usual anatomic boundaries of the atria, in areas such as the superior vena cava, pulmonary veins, and vein of Marshall, where fingers of atrial myocardium extend into these locations. Rare locations such as the noncoronary aortic cusp[2] and hepatic veins have been described as well.
A number of aspects of the atrial anatomy can contribute to the substrate for arrhythmia. The orifices of the vena cava, pulmonary veins, coronary sinus, atrial septum, and mitral and tricuspid annuli are potential anatomic boundaries for reentrant circuits. Anisotropic conduction in the atria due to complex fiber orientation may create the zone of slow conduction. Certain atrial tissues, such as the crista terminalis and pulmonary veins, are common sites for automaticity or triggered activity. Additionally, disease processes or age-related degeneration of the atria may give rise to the arrhythmogenic substrate.
Pathophysiology
Several pathophysiologic mechanisms have been ascribed to atrial tachycardia. These mechanisms can be differentiated based on the pattern of onset and termination and response to drugs and atrial pacing.
Enhanced automaticity
Automatic atrial tachycardia is observed both in patients with normal heart structure and in those with organic heart disease. The tachycardia typically exhibits a warm-up phenomenon, during which the atrial rate gradually accelerates after its initiation and slows prior to its termination. It is rarely initiated or terminated by a single atrial stimulation or rapid atrial pacing, but it may be transiently suppressed by overdrive pacing. Carotid sinus massage and adenosine do not terminate the tachycardia even if they produce a transient AV nodal block. Electrical cardioversion is ineffective (being equivalent to attempting electrical cardioversion in a sinus tachycardia).
Triggered activity
Triggered activity is due to delayed after-depolarizations, which are low-amplitude oscillations occurring at the end of the action potential. These oscillations are triggered by the preceding action potential and are the result of calcium ion influxes into the myocardium. If these oscillations are of sufficient amplitude to reach the threshold potential, depolarization occurs again and a spontaneous action potential is generated. If single, this is recognized as an atrial ectopic beat (an extra or premature beat). If it recurs and spontaneous depolarization continues, a sustained tachycardia may result. These tachycardias can also be induced with rapid atrial pacing.
Most commonly, atrial tachycardia due to triggered activity occurs in patients with digitalis intoxication[3] or conditions associated with excess catecholamines. Characteristically, the arrhythmia can be initiated, accelerated, and terminated by rapid atrial pacing. It may be sensitive to physiologic and pharmacologic maneuvers such as adenosine, verapamil, and beta-blockers, which all can terminate the tachycardia. Occasionally, this atrial tachycardia may arise from multiple sites in the atria, producing a multifocal or multiform atrial tachycardia. This may be recognized by varying P wave morphology and irregularity in the atrial rhythm.
Pulmonary vein tachycardias
Pulmonary vein tachycardias originate from the os of the pulmonary vein or even deeper localized atrial fibers. These strands of atrial tissue are generally believed to gain electrical independence, since they are partially isolated from the atrial myocardium. These tachycardias are typically very rapid (with heart rate >200-220 bpm), and although they frequently trigger episodes of atrial fibrillation, the associated atrial tachycardias may also be the clinically dominant or exclusive manifestation. The latter typically involves only a single pulmonary vein as opposed to multiple pulmonary vein involvement seen in atrial fibrillation.
Reentrant tachycardia
Intra-atrial reentry tachycardias may have either a macroreentrant or a microreentrant circuit.
Macroreentry is the usual mechanism in atrial flutter and in scar- and incision-related (postsurgical) atrial tachycardia. The more common and recognized form of atrial tachycardia seen with the advent of pulmonary vein isolation and linear ablation procedures is left atrial tachycardia, using gaps in the ablation lines that allow for slow conduction, providing the requisite anatomic substrate for reentry. These tachycardias may be self-limiting, but if they persist, mapping and a repeat ablative procedure should be considered.
Microreentry can arise in a small focal area such as in sinus node reentrant tachycardia. Typically, reentrant atrial tachycardia arises suddenly, terminates suddenly, and is paroxysmal. Carotid sinus massage and adenosine are ineffective in terminating the tachycardia even if they produce a transient AV nodal block. During electrophysiologic study, it can be induced and terminated by programmed extrastimulation. As is typical in other reentry tachycardias, electrical cardioversion terminates this type of atrial tachycardia.
Classification of atrial tachycardia
A number of methods are used to classify atrial tachycardia, including origin as based on endocardial activation mapping data, pathophysiologic mechanisms, and anatomy.
Based on endocardial activation, atrial tachycardia may be divided into 2 groups. The first is focal atrial tachycardia, which arises from a localized area in the atria such as the crista terminalis, pulmonary veins, ostium of the coronary sinus, or intra-atrial septum. Focal atrial tachycardia that originates from the pulmonary veins may trigger atrial fibrillation and often forms a continuum of arrhythmias. The second group is the reentrant atrial tachycardias. These reentrant (usually macroreentrant) atrial tachycardias most commonly occur in persons with structural heart disease or complex heart disease, particularly after surgery involving incisions or scarring in the atria. Electrophysiologically, these atrial tachycardias are similar to atrial flutters, typical or atypical. Often, the distinction is semantic, typically based on arbitrary cutoffs of atrial rate.
Some of the tachycardias cannot be easily classified. Sinoatrial reentrant tachycardia (or sinus node reentry) is a subset of focal atrial tachycardia due to reentry arising within the sinus node situated at the superior aspect of the crista terminalis. The P wave morphology and atrial activation sequence are identical or very similar to those of sinus tachycardia. Another tachycardia that mimics atrial tachycardia is inappropriate sinus tachycardia. Inappropriate sinus tachycardia and postural orthostatic tachycardia syndrome (POTS) strictly are not atrial tachycardias because their origin is not abnormal. They are due to sinus tachycardia related to enhanced sinus automaticity or due to abnormal autonomic function (dysautonomia).
Etiology
Atrial tachycardia can occur in individuals with structurally normal hearts or in patients with organic heart disease.
When it arises in patients with congenital heart disease who have undergone corrective or palliative cardiac surgery, such as a Fontan procedure, the occurrence of an atrial tachycardia can have potentially life-threatening consequences.
The atrial tachycardia that manifests during exercise, acute illness with excessive catecholamine release, alcohol ingestion, altered fluid states, hypoxia, or metabolic disturbance, or with drug use (eg, caffeine, albuterol, theophylline, cocaine), is associated with automaticity or triggered activity.
Digitalis intoxication is one of the important causes of atrial tachycardia, with triggered activity being the underlying mechanism.
Reentrant atrial tachycardia tends to occur in patients with structural heart disease, including ischemic, congenital, postoperative, and valvular heart diseases.
Iatrogenic atrial tachycardias are now more often seen and typically result from ablative procedures in the left atrium. Several areas of typical location for these tachycardias have been identified. These locations include the mitral isthmus (between the left lower pulmonary vein and mitral annulus), the roof of the left atrium, or reentry around the pulmonary veins.
The most common reason for these tachycardias is gaps in the ablation lines, allowing for slow conduction and initiation reentry circuits or circuits excluded by the set of ablation lines. Typically, these patients have undergone an atrial fibrillation ablation procedure in the past. This is true for both catheter ablation and surgical epicardial ablation. Similarly, patients with prior surgical procedures involving the left atrium may have surgical incision lines and, hence, the potential for macroentrant circuits.
Multifocal atrial tachycardia (MAT) is often related to underlying illnesses. MAT often occurs in patients experiencing an exacerbation of chronic obstructive pulmonary disease (COPD),[4] a pulmonary thromboembolism, an exacerbation of heart failure, or severe illness, especially under critical care with inotropic infusion. It is often associated with hypoxia and sympathetic stimulation. Digitalis toxicity also may be present in persons with multifocal atrial tachycardia, with triggered activity as the mechanism. Other underlying conditions that are commonly associated with MAT are the following:
- Valvular heart disease
- Diabetes mellitus
- Hypokalemia
- Hypomagnesemia
- Azotemia
- Postoperative state
- Sepsis
- Methylxanthine toxicity
- Myocardial infarction
- Pneumonia
Unusual forms of atrial tachycardias can be seen in patients with an infiltrative process involving the pericardium and, by extension, the atrial wall.
Epidemiology
Atrial tachycardia is relatively rare, constituting 5-15% of all supraventricular tachycardias (SVTs). Because there is an association with congenital heart disease, it is more common in the pediatric population.
Atrial tachycardia has no known racial or ethnic predilection and no known predilection for either sex. There may be some association with pregnancy. Atrial tachycardia may occur at any age, although it is more common in children and adults with congenital heart disease. Go to Pediatric Supraventricular Tachycardia, Atrial Ectopic Tachycardia for more complete information on this topic.
MAT is a relatively infrequent arrhythmia, with a prevalence rate of 0.05-0.32% in patients who are hospitalized. It is predominantly observed in males and in older patients—in particular, elderly patients with multiple medical problems. The average age of patients from 9 studies was 72 years.
Prognosis
In patients with structurally normal hearts, atrial tachycardia is associated with a low mortality rate. However, tachycardia-induced cardiomyopathies have been associated with atrial tachycardia in patients in whom the rhythm is persistent or frequently incessant. Patients with underlying structural heart disease, congenital heart disease, or lung disease are less likely to be able to tolerate atrial tachycardia. Other morbidity is associated with lifestyle changes and associated symptoms.
MAT itself is seldom life threatening. The condition is transient and resolves when the underlying condition improves. The prognosis depends on the prognosis of any comorbid disease. Patients with MAT frequently have significant comorbidities, especially COPD and respiratory failure, that often require treatment in an intensive care unit. Consequently, a high mortality rate (ie, up to 45%) is associated with this arrhythmia, although the mortality is not a direct consequence of the rhythm abnormality.
Patient Education
For patient education information, visit eMedicine's Heart Center, as well as Supraventricular Tachycardia and Palpitations.
In the case of MAT related to medication use, education regarding the correct use and how to monitor such medications should be considered. In the case of a pulmonary source, education about prevention and recognition of developing pulmonary conditions may be helpful.
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