Atrial Tachycardia

Introduction
Background

Atrial tachycardia is a rhythm disturbance that arises in the atria. 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. (For more in-depth discussion please see diagnosis section.)

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 macro-reentrant) 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. 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.

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).

Atrial tachycardia may be classified according to the following pathophysiologic mechanisms: enhanced automaticity, triggered activity, or reentry.

Anatomical classification of atrial tachycardia is based on the location of the arrhythmicogenic focus. 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 like noncoronary aortic cusp1 and hepatic veins have been described as well. These may be focal or reentrant.
Pathophysiology

Arrhythmogenic atrial structures

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.

Pathophysiologic mechanisms

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 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 be also induced with rapid atrial pacing.

Most commonly, atrial tachycardia due to triggered activity occurs in patients with digitalis intoxication2 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 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 are 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 tachycardia may be self limiting, but if they persist, mapping and a repeat ablative procedure can 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.
Frequency
United States

Atrial tachycardia is relatively rare, constituting 5-15% of all SVTs. Because there is an association with congenital heart disease, it is more common in the pediatric population. 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.
International

No national differences in the incidence of atrial tachycardia have been reported.
Mortality/Morbidity

In patients with structurally normal hearts, this arrhythmia 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.
Race

Atrial tachycardia has no known racial or ethnic predilection.
Sex

The condition has no known predilection for either sex. There may be some association with pregnancy.
Age

Atrial tachycardia may occur at any age, although it is more common in children and adults with congenital heart disease.
Clinical
History

Patients with focal atrial tachycardia usually present with episodic or paroxysmal atrial tachycardia.
Typically, atrial tachycardia manifests as a sudden onset of palpitations.
If atrial tachycardia is due to enhanced automaticity, it may be nonsustained but repetitive or continuous or sustained, as in reentrant forms of atrial tachycardia.
Patients may present with a tachycardia that gradually speeds up soon after its onset (warm-up phenomenon). The patient may be unaware of this. This finding during ECG monitoring, as with a Holter, is suggestive that the supraventricular tachycardia is atrial tachycardia.
If accompanied by palpitations, patients also may report dyspnea, dizziness, lightheadedness, fatigue, or chest pressure. One should recognize the early manifestations of tachycardia-induced cardiomyopathy, ie, a decline in effort tolerance and symptoms of heart failure, in patients with frequent or incessant tachycardias.
Lightheadedness may result from relative hypotension, depending on the heart rate and other factors such as the state of hydration and particularly the presence of structural heart disease. The faster the heart rate, the more likely a patient is to feel lightheaded. If the patient has a rapid rate and severe hypotension, syncope may occur.

Physical
The primary abnormality noted upon physical examination is a rapid pulse rate. In most atrial tachycardias this is regular. However, in rapid atrial tachycardias with variable AV conduction and in multifocal atrial tachycardia (MAT), the pulse may be irregular.
Blood pressure may be low in patients presenting with fatigue, lightheadedness, or presyncope.
The cardiovascular examination should be aimed at excluding underlying structural heart diseases such as valvular abnormalities and evidence of heart failure.
Abnormal thyroid function should also be in the differential diagnosis.
Causes
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, 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 as the underlying mechanism.
Reentrant atrial tachycardia tends to occur in patients with structural heart disease, including ischemic, congenital, postoperative, and valvular heart diseases.
Multifocal atrial tachycardia is a unique type of atrial tachycardia in which atrial activation originates from multiple atrial foci. See eMedicine article Multifocal Atrial Tachycardia.
Multifocal atrial tachycardia often occurs in patients experiencing an exacerbation of chronic obstructive pulmonary disease (COPD)3 , a pulmonary thromboembolism, an exacerbation of congestive 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.
Unusual forms of atrial tachycardias can be seen in patients with an infiltrative process involving the pericardium and, by extension, the atrial wall.

http://emedicine.medscape.com/article/151456-overview