eMedicine Specialties > Cardiology > Arrhythmias

Atrial Tachycardia

Adam S Budzikowski, MD, PhD, Assistant Professor of Medicine, Division of Cardiovascular Medicine, Electrophysiology Section, State University of New York-Downstate, University Hospital of Brooklyn
Dariusz Michałkiewicz, MD, Head, Electrophysiology Department, Military Medical Institute, Poland

Updated: Aug 10, 2009

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.

Differential Diagnoses

Atrial Fibrillation
Atrial Flutter
Atrioventricular Nodal Reentry Tachycardia (AVNRT)
Atrioventricular Reentrant Tachycardia
Paroxysmal Supraventricular Tachycardia

Other Problems to Be Considered

The differential diagnosis of atrial tachycardia is the differential diagnosis of SVT and includes the following:
Sinus tachycardia
Atrial tachycardia
Atrial flutter
Atrial fibrillation
AV junction–dependent reentrant tachycardias (AV nodal reentrant tachycardia and AV reentrant tachycardia using an accessory pathway)

Differentiating among these diagnoses requires ECG analysis of the tachycardia for P wave activity. The ECG of an SVT typically has narrow QRS complexes (unless aberrant conduction with typical left or right bundle branch block occurs).

Assessment of the P waves and their relationship to the QRS complex (R waves) may reveal 2 different observations, as follows:

• In short RP (long PR interval) SVT, the differential diagnosis includes typical AV nodal reentrant tachycardia and AV reentrant tachycardia using accessory pathways and atrial tachycardia with long I°AV block or atrial tachycardia originating from the os of the coronary sinus or junctional tachycardia. To determine the diagnosis requires additional maneuvers such as vagal stimulation (eg, carotid sinus massage, Valsalva) or adenosine.
• In long RP interval (short PR interval) SVT, the differential diagnosis includes atypical (fast-slow) AV nodal reentrant tachycardia and permanent junctional reciprocating tachycardia (PJRT) due to a slowly conducting retrograde accessory pathway, sinus tachycardia, sinus node reentry, atrial tachycardia, or atrioventricular reentrant tachycardia. Diagnosis requires assessment of the patient condition, vagal maneuvers, adenosine, and cardioversion, namely procedures that may not only be diagnostic but also therapeutic.

For multifocal atrial tachycardia, the differential diagnosis includes atrial fibrillation because both can manifest with an irregular pulse.

Iatrogenic atrial tachycardias: These tachycardias are now more often seen and typically result from extensive 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 are 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 atrial fibrillation ablation procedure in the past. This is true for both catheter ablation as well as surgical epicardial ablation. Similarly, patients with prior surgical procedures involving the left atrium may have surgical incision lines and hence potential for macroentrant circuits.

Workup

Laboratory Studies

• Systemic causes of sinus tachycardia (eg, hyperthyroidism, anemia, dehydration, infection, hypoxemia, metabolic disturbance) should be excluded at the beginning of the workup for atrial tachycardia.
• A serum digoxin level should be obtained in those who are suspected to have digitalis intoxication but also in any patient who presents with an SVT, particularly if the presentation is unusual and if the patient is taking digitalis. A classic form of digoxin toxicity is atrial tachycardia with AV block.

Imaging Studies

• Chest radiography is indicated for those who present with tachycardia-induced cardiomyopathy and those with complex congenital heart disease.
• 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.
• Chest CT may be necessary at times to assess the anatomy of pulmonary veins and provide DICOM images for anatomy reconstruction prior to ablative procedure.

Other Tests

• An electrocardiogram (ECG) is an important tool to help identify, locate, and differentiate 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.
  • The diagnostic criteria for MAT include an irregular ventricular rate of more than 100 bpm, a discrete P wave with 3 or more different types of morphology without a dominant pacemaker, an irregular PP interval, and an isoelectric baseline between P waves.
• Occasionally, if enhanced automaticity or triggered activity is considered the underlying mechanism, exercise testing is used to facilitate the induction of atrial tachycardia.

Procedures

• Electrophysiology studies 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 an innocent 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.
  • If overdrive 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 chance 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.
• 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 slow and terminate sinoatrial reentrant tachycardia. 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, eg, 12 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).
• Endocardial mapping is most commonly used for localizing atrial tachycardia during electrophysiology study. Using this technique, focal tachycardias can be easily distinguished from focal tachycardias. This also allows for mapping scar tissue and allows identifying 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.
• 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 may be more useful for diagnosing patients with paroxysmal symptoms.

Treatment

Medical Care

• Electrophysiology studies help identify the subset of patients with atrial tachycardia due to triggered activity. This form of tachycardia is sensitive to verapamil, beta-blockers, and adenosine. In this case, verapamil alone or in combination with a beta-blocker may be effective for controlling the tachycardia. Triggered activity–related atrial tachycardia is most frequently found in the setting of digitalis toxicity. The treatment is withdrawal of digitalis and careful observation in hospital without the use of the above-mentioned drugs. Rarely, reversal agents are necessary (eg, Digibind).
• Beta-blockers may be used to suppress atrial tachycardia due to enhanced automaticity, but overall success rates are low.
• For refractory recurrent (particularly recurrence after electrical cardioversion) atrial tachycardias causing symptoms, antiarrhythmic drugs such as quinidine or procainamide have been tried. These drugs prolong the atrial refractoriness and slow the conduction velocity, thereby disrupting the reentrant circuit. They also suppress the atrial premature depolarizations that commonly initiate the tachycardia. The adverse effects of class IA drugs are significant. Therefore, the use of class IA drugs is limited. These drugs are effective only approximately 50% of the time. Class IC drugs (ie, flecainide, propafenone) may slow the conduction and stop the tachycardia. These drugs can be proarrhythmic when used in patients with structural heart disease or even in those without disease. These drugs (particularly flecainide) should be administered with AV node–blocking drugs such as beta-blockers or calcium channel blockers.
• Class III antiarrhythmic drugs such as amiodarone, sotalol and dofetilide are not always effective in terminating the atrial tachycardia, but they may be highly effective for maintaining sinus rhythm after conversion to a normal sinus rhythm. Ibutilide and dofetilide can terminate some atrial tachycardias.
• Atrial tachycardia due to digitalis intoxication often manifests with AV conduction block and/or ventricular arrhythmias. Recognizing this at an early stage is crucial because it may be a harbinger of more lethal ventricular tachyarrhythmias. Treatment often includes prompt discontinuation of digoxin and correction of electrolyte disturbances. The administration of antidigoxin antibodies is usually indicated in patients with conduction block, severe bradycardia, ventricular arrhythmias, and congestive heart failure. Electrical cardioversion is contraindicated because it may provoke a ventricular tachyarrhythmia.
• Ablation can cure macroreentrant and focal forms of atrial tachycardia.
  • Radiofrequency catheter ablation^4,5 for atrial tachycardia has become a highly successful and effective treatment option for symptomatic, medically refractory patients. However, the success rates are not as high as those for AV nodal reentrant tachycardia or AV reentrant tachycardia using an accessory pathway, but they still high, ranging from 77-100% depending on the published series.
  • After activation mapping, the origin of the tachycardia can be localized. Focal application of radiofrequency energy via an ablation catheter to the origin of the tachycardia results in termination of the tachycardia.
  • Focal atrial tachycardia originating from the pulmonary veins has been associated with atrial fibrillation. Radiofrequency ablation abolishing the focal triggering activity within the orifices of the pulmonary vein can be curative in patients with atrial fibrillation of this mechanism.
  • Of note, complex ablation procedures primarily for atrial fibrillation that isolate pulmonary veins or make circumferential left atrial ablations lines have been associated with new reentrant atrial tachycardias or left-sided atypical atrial flutter. These tachycardias usually require a further ablation procedure.
  • Reentrant atrial tachycardias in the setting of repaired congenital heart disease may use anatomic obstacles created by the surgical incisions, and knowledge of the specific anatomic approach can guide subsequent mapping and ablation.

Surgical Care

For patients with complex congenital heart disease, surgical ablation may occasionally be useful. However, this is generally supplanted by radiofrequency ablation approaches.

At surgery, particularly for congenital heart disease and particularly if complex, such as the Fontan procedure, incisions should be situated or extended to lines of natural conduction block to prevent subsequent incisional- or scar-related atrial reentrant tachycardias.

Consultations

Consultation with a cardiologist or electrophysiologist is recommended for all patients with atrial tachycardia and when structural heart disease is diagnosed or considered.

Medication

Consultation with a cardiologist or electrophysiologist is strongly recommended before initiating therapy with any antiarrhythmic agents because the results of a comprehensive cardiac workup might be needed to guide treatment. See Medical Care for further discussion.

Beta-adrenergic blocking agents

Effective for reducing frequency and severity of episodes via control of ventricular response during tachycardia and by reduction of frequency in a subgroup of patients for whom tachycardia is sensitive to catecholamine.

Atenolol (Tenormin)

Selectively blocks beta-1 receptors, with little or no effect on beta-2 receptors.

Dosing

Adult

50 mg PO qd; increase to 100 mg/d prn

Pediatric

1-2 mg/kg/dose PO qd

Interactions

Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity

Contraindications

Documented hypersensitivity; CHF; pulmonary edema; cardiogenic shock; AV conduction abnormalities; heart block (without a pacemaker)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and may cause thyroid storm; monitor patients closely and withdraw drug slowly; during IV, carefully monitor BP, heart rate, and ECG

Acebutolol (Sectral)

Selective, hydrophilic beta-blocking drug with mild intrinsic sympathomimetic activity.

Dosing

Adult

400 mg PO qd initially given as 200 mg bid; titrate to 600-1200 mg/d in divided doses based on clinical response

Pediatric

Not established

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, or contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, or catecholamine-depleting agents

Contraindications

Documented hypersensitivity; cardiogenic shock; bradycardia or heart block; sinus node dysfunction; AV conduction abnormalities

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Beta-adrenergic blockade may decrease signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and may cause thyroid storm; withdraw drug slowly and monitor patient closely; caution in hypokalemia, peripheral vascular disease, hypomagnesemia, and CHF

Esmolol (Brevibloc)

Excellent drug for use in patients at risk for experiencing complications from beta-blockade. Selectively blocks beta-1 receptors with little or no effect on beta-2 receptors.

Dosing

Adult

Loading dose: 250-500 mcg/kg/min IV for 1 min followed by a 4-min maintenance infusion of 50 mcg/kg/min
If adequate therapeutic effect not observed within 5 min, repeat loading dose and follow with maintenance infusion using increments of 50 mcg/kg/min (for 4 min); sequence may be repeated up to 4 times prn
As the desired heart rate is approached, omit loading infusion and reduce incremental dose of maintenance infusion from 50 mcg/kg/min to 25 mcg/kg/min or lower; interval between titration steps may be increased from 5-10 min prn

Pediatric

Not established; suggested dose is 100-500 mcg/kg IV administered over 1 min

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, or contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, or catecholamine-depleting agents

Contraindications

Documented hypersensitivity; uncompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn; withdraw drug slowly and monitor patient closely

Class III antiarrhythmic agents

Amiodarone and sotalol have been shown to be effective in maintaining sinus rhythm after converting from atrial tachycardia.

Amiodarone (Cordarone)

May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Prior to administration, control ventricular rate and CHF (if present) with digoxin or calcium channel blockers.

Dosing

Adult

Loading dose: 600-1200 mg/d PO in 1-2 doses for 1-2 wk; then, decrease to 400-600 mg/d in 1-2 doses for 1-3 wk
Maintenance dose: 200 mg/d PO
Alternatively: 150 mg (10 mL) IV over first 10 min, followed by 360 mg (200 mL) over next 6 h, then 540 mg over next 18 h

Pediatric

10-15 mg/kg/d or 600-800 mg/1.73 m²/d PO for 4-14 d or until adequate control of arrhythmia is attained

Interactions

Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and further decrease myocardial contractility; cimetidine may increase levels; protease inhibitors (eg, indinavir, ritonavir, amprenavir, nelfinavir) inhibit metabolism, resulting in increased serum levels and possible prolongation of QT interval

Contraindications

Documented hypersensitivity; complete AV block; intraventricular conduction defects; coadministration with ritonavir or sparfloxacin

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in thyroid or liver disease

Sotalol (Betapace)

Class III antiarrhythmic agent, which blocks potassium channels, prolongs action potential duration, and lengthens QT interval. Non–cardiac-selective beta-adrenergic blocker.

Dosing

Adult

80 mg PO bid and increase dose gradually q2-3d to 240-320 mg/d

Pediatric

Not established

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, calcium channel blockers, quinidine, flecainide, or contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, or catecholamine-depleting agents

Contraindications

Documented hypersensitivity; sinus bradycardia; second- or third-degree AV block; baseline QT interval >450 milliseconds; bronchial asthma or chronic obstructive pulmonary disease; cardiogenic shock; congenital or acquired long QT syndromes; creatinine clearance <40 mL/min; overt cardiac failure

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Beta-adrenergic blockade may decrease signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor patient closely; caution in hypokalemia, peripheral vascular disease, hypomagnesemia, and CHF

Class IA antiarrhythmic agents

Have been tried in patients with atrial tachycardia and disabling symptoms in whom beta-blockers or calcium channel blockers were unsuccessful. These agents are proarrhythmic; use caution.

Procainamide (Procanbid, Pronestyl)

Increases refractory period of atria and ventricles. Myocardial excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.

Dosing

Adult

20-30 mg/min IV at continued infusion rates until arrhythmia is suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or a maximum dose of 17 mg/kg is administered
Once arrhythmia is suppressed, may infuse at a continuous rate of 1-4 mg/min

Pediatric

Not established; the following doses have been suggested:
15-50 mg/kg/d PO divided q3-6h; not to exceed 4 g/d
20-30 mg/kg/d IM divided q4-6h; not to exceed 4 g/d
3-6 mg/kg/dose IV infused over 5 min
Maintenance: 20-80 mcg/kg/min administered as continuous infusion; not to exceed 100 mg/dose or 2 g/d

Interactions

Can expect increased levels of procainamide metabolite NAPA in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim or quinidine; may increase effect of skeletal muscle relaxants (eg, quinidine, lidocaine) and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity

Contraindications

Complete heart block or second- or third-degree heart block, if a pacemaker is not in place; torsade de pointes; documented hypersensitivity; systemic lupus erythematosus

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for hypotension; plasma concentrations of procainamide and active metabolite NAPA may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency

Class IC antiarrhythmic agents

Have been used in patients with atrial tachycardia and disabling symptoms in whom beta-blockers or calcium channel blockers were unsuccessful. Recommended use is with beta-blocker or calcium channel blocker.

Flecainide (Tambocor)

Blocks sodium channels, producing dose-related decrease in intracardiac conduction in all parts of heart. Increases electrical stimulation of threshold of ventricle, His-Purkinje system. Shortens phase 2 and 3 repolarization, resulting in decreased action potential duration and effective refractory period.
Indicated for the treatment of paroxysmal atrial fibrillation/flutter associated with disabling symptoms and paroxysmal SVTs, including AV nodal reentrant tachycardia, AV reentrant tachycardia, and other SVTs of unspecified mechanism associated with disabling symptoms in patients without structural heart disease. Also indicated for prevention of documented life-threatening ventricular arrhythmias (eg, sustained ventricular tachycardia). Not recommended in less severe ventricular arrhythmias, even if patients are symptomatic.

Dosing

Adult

50 mg PO q12h; increase q4d; not to exceed 300 mg/d
As little as 50 mg PO q12h may be effective in children and adults

Pediatric

3-6 mg/kg/d or 100-150 mg/m²/d PO divided tid to 11 mg/kg/d or 200 mg/m²/d

Interactions

May increase toxicity of digoxin; beta-adrenergic blockers, verapamil, and disopyramide may have additive inotropic effects when administered with flecainide; CYP-4502D6 inhibitors (eg, ritonavir, cimetidine, amiodarone) may increase serum levels and cardiotoxicity

Contraindications

Documented hypersensitivity; preexisting second- or third-degree AV block; right bundle-branch block associated with left hemiblock (bifascicular block) or trifascicular block (unless a pacemaker is present to sustain the cardiac rhythm if complete heart block occurs); concurrent use of ritonavir or amprenavir; recent MI

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in preexisting sinus node dysfunction, history of CHF, sick sinus syndrome, post-MI, or myocardial dysfunction; reserve use for life-threatening arrhythmias, deaths are associated with proarrhythmic effects of class IC antiarrhythmics; adjust dose in renal or hepatic impairment

Propafenone (Rythmol)

Shortens upstroke velocity (phase 0) of monophasic action potential. Reduces fast inward current carried by sodium ions in Purkinje fibers, and, to a lesser extent, myocardial fibers. May increase diastolic excitability threshold and prolong effective refractory period. Reduces spontaneous automaticity and depresses triggered activity.
Indicated for treatment of documented life-threatening ventricular arrhythmias (eg, sustained ventricular tachycardia). Appears effective in treatment of SVTs, including atrial fibrillation and flutter. Not recommended in patients with less severe ventricular arrhythmias, even if symptomatic.

Dosing

Adult

150 mg PO q8h and increase at 3- to 4-d intervals; not to exceed 300 mg q8h

Pediatric

Not established

Interactions

Rifampin may decrease plasma levels; quinidine may increase pharmacologic effects; may increase plasma levels of beta-blockers, cyclosporine, warfarin, and digoxin; CYP-4502D6 inhibitors (eg, ritonavir, cimetidine, amiodarone) may increase serum levels and cardiotoxicity

Contraindications

Documented hypersensitivity; second- or third-degree AV block; right bundle-branch block associated with left hemiblock (bifascicular block) or trifascicular block; concurrent use of ritonavir or amprenavir

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in preexisting sinus node dysfunction, history of CHF, sick sinus syndrome, post-MI, or myocardial dysfunction; reserve use for life-threatening arrhythmias, deaths are associated with proarrhythmic effects of class IC antiarrhythmics; adjust dose in renal or hepatic impairment

Calcium channel blockers

Via specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Inhibit movement of calcium ions across cell membrane, depressing both impulse formation (automaticity) and conduction velocity. Especially effective in atrial tachycardia with triggered activity as underlying mechanism.

Diltiazem (Cardizem CD, Cardizem SR, Dilacor, Tiazac)

During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Dosing

Adult

Cardizem SR: 60-120 mg PO bid
Cardizem CD: 180-240 mg PO qd
Dilacor: 180-240 mg PO qd

Pediatric

Not established

Interactions

May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output; when given with beta-blockers, may increase cardiac depression; cimetidine may increase levels

Contraindications

Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired renal or hepatic function; may increase LFT results, and hepatic injury may occur

Verapamil (Calan, Calan SR, Covera HS, Verelan)

During depolarization, inhibits calcium ion from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium.

Dosing

Adult

80-160 mg PO tid
Alternatively: 5-10 mg IV followed by a second dose 15-30 min later if patient does not satisfactorily respond to initial dose
ER dosage form may be given qd

Pediatric

Not established

Interactions

May increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; when administered concurrently with beta-blockers, may increase cardiac depression; cimetidine may increase levels; may increase theophylline levels

Contraindications

Documented hypersensitivity; severe CHF; sick sinus syndrome or second- or third-degree AV block; hypotension (<90 mm Hg systolic)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued treatment); monitor liver function periodically

Miscellaneous antiarrhythmic agents

Alter the electrophysiologic mechanisms responsible for arrhythmia.

Digitalis in toxic doses can cause atrial tachycardia. In therapeutic doses, digitalis may be useful in some focal atrial tachycardias. It should be considered if beta-blockers are contraindicated or if beta-blockers and calcium channel blockers are unsuccessful in controlling the arrhythmia medically.

Adenosine is an ultra–short-acting drug that is useful in SVTs of unknown origin both in making the diagnosis and in terminating those that are dependent on the AV junction and some focal atrial tachycardia. If adenosine successfully terminates an atrial tachycardia, those patients may respond to beta-blockers or calcium channel blockers.

Digoxin (Lanoxicaps, Lanoxin)

Has direct inotropic effects and indirect effects on the cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Dosing

Adult

0.5 mg IV over 10-15 min, followed by 0.25 mg q6-8h; not to exceed 1.5 mg/d
Alternatively: 0.5-0.75 mg PO initially, followed by 0.125-0.375 mg q6h
Maintenance: 0.125-0.375 mg PO qd

Pediatric

Digitalization in infants and children not generally recommended; suggested doses are as follows:
Premature neonates: 15-25 mcg/kg PO/IV divided into 3 or more doses (first dose equal to half total dose); then, remaining doses q6-8h
Maintenance for premature neonates: 4-6 mcg/kg/d PO/IV divided bid
Neonates: 20-30 mcg/kg PO/IV divided into 3 or more doses (first dose equal to half total dose); then, remaining doses q6-8h
Maintenance for neonates: 5-8 mcg/kg/d PO/IV divided bid
<2 years: 30-50 mcg/kg PO/IV divided into 3 or more doses (first dose half total dose); then, remaining doses q6-8h; 7.5-12 mcg/kg/d PO/IV divided bid
2-5 years: 25-35 mcg/kg PO/IV divided into 3 or more doses (first dose equal to half total dose); then, remaining doses q6-8h
Maintenance for <2 years and 2-5 years: 6-9 mcg/kg/d PO/IV divided bid
6-10 years: 15-30 mcg/kg PO/IV divided into 3 or more doses (first dose equal to half total dose); then, remaining doses q6-8h
Maintenance for 6-10 years: 4-8 mcg/kg/d PO/IV divided bid
>10 years: 8-12 mcg/kg PO/IV divided into 3 or more doses (first dose equal to half total dose); then, remaining doses q6-8h
Maintenance for >10 years: 2-3 mcg/kg/d PO/IV qd

Interactions

IV calcium may produce arrhythmias in digitalized patients; medications that may increase levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil
Medications that may decrease serum levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Contraindications

Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypokalemia may reduce positive inotropic effect of digitalis; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis; adjust dose in renal impairment; highly toxic (overdoses can be fatal)

Adenosine (Adenocard)

Short-acting agent that alters potassium conductance into cells and results in hyperpolarization of nodal cells. This increases the threshold to trigger an action potential and results in sinus slowing and blockage of AV conduction. As a result of its short half-life, adenosine is best administered in an antecubital vein as an IV bolus followed by rapid saline infusion.

Dosing

Adult

6 mg rapid IV bolus (antecubital vein) initially, followed by saline flush; second bolus of 12 mg may be given if initial bolus is unsuccessful

Pediatric

0.05-0.1 mg/kg rapid IV push, increasing increments of 0.05 mg/kg IV bolus q2min until tachycardia resolves; not to exceed 12 mg

Interactions

Coadministration with carbamazepine may produce higher degrees of heart block; dipyridamole may potentiate effects; methylxanthines may antagonize effects

Contraindications

Documented hypersensitivity; second- or third-degree AV block or sick sinus syndrome (except in patients with functioning artificial pacemaker); atrial flutter; atrial fibrillation; ventricular tachycardia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adenosine-induced bronchoconstriction may occur in patients with asthma

Follow-up

Further Inpatient Care

Admission is not generally required unless significant comorbidities exist, the tachycardia is incessant, or it is poorly tolerated. Initial ECG and immediate telemetry evaluations in the emergency department help document the tachycardia.

Complications

Frequent and incessant atrial tachycardia has been associated with tachycardia-induced cardiomyopathy. This might be reversible if atrial tachycardia is treated promptly.

Prognosis

If the patient does not have structural heart disease, the prognosis is good and the associated mortality rate is extremely low. Atrial tachycardia is a relatively difficult arrhythmia to treat in those patients with frequent episodes. If it is persistent and the ventricular rate is rapid, over time it may cause a tachycardia-induced cardiomyopathy.

Patient Education

For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education articles Supraventricular Tachycardia and Palpitations.

Miscellaneous

Medicolegal Pitfalls

The full clinical presentation must be considered. New-onset atrial tachycardias by themselves are relatively benign. However, if the patient also has new problems (eg, chest pain, unexplained dyspnea, inappropriate hypotension) or a recent illness, perform a more extensive workup because atrial tachycardia may not be the primary problem. Also, with frequent or incessant tachycardia, tachycardia-induced cardiomyopathy may develop.

Multimedia

Media file 1: Propagation map of right atrial tachycardia originating from the right atrial appendage obtained with non-contact mapping using Ensite mapping system.

Video available at http://img.medscape.com/pi/emed/ckb/cardiology/150072-1332317-151456-1657459.flv.

Media file 2: 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.

Media file 3: This intracardiac recording revealed the same rhythm as shown on the electrocardiogram in Image 1. 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.

Media file 4: 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 valve
CS – Shadow of the catheter inserted in the coronary sinus

Media file 5: 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 catheter
CS 7,8 – Located at the os of the coronary sinus
CS 1,2 – Distal pair of electrodes
Abl – Ablation catheter (D-distal pair of electrodes)

Media file 6: An example of rapid atrial tachycardia mimicking atrial flutter. Single lesion application terminates the tachycardia. The first 3 tracings show surface electrocardiograms, as labeled.
HRA – High right atrial catheter
RVA – Catheter located in right ventricular apex
HBED and HBEP – Respectively, distal and proximal pair of electrodes in the catheter located at His bundle
AblD and AblP – Respectively, distal and proximal pair of electrodes of the mapping catheter
MAP – Unipolar electrograms from the tip of the mapping catheter

References

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2. Ma G, Brady WJ, Pollack M, Chan TC. Electrocardiographic manifestations: digitalis toxicity. J Emerg Med. Feb 2001;20(2):145-52. [Medline].

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5. Knecht S, Veenhuyzen G, O'Neill MD, Wright M, Nault I, Weerasooriya R. Atrial tachycardias encountered in the context of catheter ablation for atrial fibrillation part ii: mapping and ablation. Pacing Clin Electrophysiol. Apr 2009;32(4):528-38. [Medline].

6. [Guideline] Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary. a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology. J Am Coll Cardiol. Oct 15 2003;42(8):1493-531. [Medline].

7. Braunwald E, Zipes DP, eds. Specific arrhythmias: diagnosis and treatment. In: Heart Disease: A Textbook for Cardiovascular Medicine. 6^th ed. Philadelphia, Pa: WB Saunders; 2001:835-8.

8. Chen SA, Tai CT, Chiang CE, et al. Focal atrial tachycardia: reanalysis of the clinical and electrophysiologic characteristics and prediction of successful radiofrequency ablation. J Cardiovasc Electrophysiol. Apr 1998;9(4):355-65. [Medline].

9. Goodacre S, Irons R. ABC of clinical electrocardiography: Atrial arrhythmias. BMJ. Mar 9 2002;324(7337):594-7. [Medline].

10. Huang SK, Wilber DJ, eds. Atrial tachycardias. In: Radiofrequency Catheter Ablation of Cardiac Arrhythmias: Basic Concepts and Clinical Applications. 2^nd ed. Elmsford, NY: Futura Publishing; 2000:139-63.

11. Josephson M, ed. Supraventricular tachycardias. In: Clinical Cardiac Electrophysiology: Techniques and Interpretations. 3^rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2001:169-271.

12. Lee BK, Olgin JE. Ablation of Focal Atrial Tachycardia. In: Huang SKS, Wood MA. Catheter Ablation of Cardiac Arrhythmias. Philadelphia, PA: Elsevier; 2006:Chapter 10.

13. Morady F. Catheter ablation of supraventricular arrhythmias: state of the art. Pacing Clin Electrophysiol. Jan 2004;27(1):125-42. [Medline].

14. Paul T, Bertram H, Bokenkamp R, Hausdorf G. Supraventricular tachycardia in infants, children and adolescents: diagnosis, and pharmacological and interventional therapy. Paediatr Drugs. May-Jun 2000;2(3):171-81. [Medline].

15. Saoudi N, Cosio F, Waldo A, Chen SA, Iesaka Y, Lesh M. Classification of atrial flutter and regular atrial tachycardia according to electrophysiologic mechanism and anatomic bases: a statement from a joint expert group from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. J Cardiovasc Electrophysiol. Jul 2001;12(7):852-66. [Medline].

16. Saoudi N, Cosio F, Waldo A, et al. A classification of atrial flutter and regular atrial tachycardia according to electrophysiological mechanisms and anatomical bases. Eur Heart J. Jul 2001;22(14):1162-82. [Medline].

17. Shalganov TN, Dinov BB, Traykov VB, Vatasescu R, Paprika D, Balabanski TL. Bi-atrial and right atrial activation times help to differentiate focal from macroreentrant right atrial tachycardias. Acta Cardiol. Feb 2009;64(1):17-21. [Medline].

18. Sung RJ, Lauer MR, eds. Atrial tachycardias and atrial flutter. In: Fundamental Approaches to the Management of Cardiac Arrhythmias. First ed. Dordrecht, The Netherlands: Kluwer Academic; 2000:609-49.

19. Szumowski L, Glowniak A, Zakrzewska J, Derejko P, Szufladowicz E, Bodalski R. [Pseudo atypical atrial flutter or atrial tachycardia dependent on complex substrate in a patient with univentricular heart after palliative operations - mapping and ablation]. Kardiol Pol. Jan 2009;67(1):95-100. [Medline].

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Keywords

supraventricular tachycardia, SVT, palpitations, PAT, AT, focal atrial tachycardia, macroreentrant tachycardia, macro-reentrant tachycardia, cardiomyopathy, cardiomyopathies, micro-reentrant tachycardia, microreentrant tachycardia, heart palpitations, arrhythmia, tachycardia, multifocal atrial tachycardia, multiform atrial tachycardia, pulmonary vein tachycardia.

Contributor Information and Disclosures

Author

Adam S Budzikowski, MD, PhD, Assistant Professor of Medicine, Division of Cardiovascular Medicine, Electrophysiology Section, State University of New York-Downstate, University Hospital of Brooklyn
Adam S Budzikowski, MD, PhD is a member of the following medical societies: American College of Cardiology, European Society of Cardiology, and Polish Society of Cardiology
Disclosure: Nothing to disclose.

Coauthor(s)

Dariusz Michałkiewicz, MD, Head, Electrophysiology Department, Military Medical Institute, Poland
Dariusz Michałkiewicz, MD is a member of the following medical societies: Heart Rhythm Society and Polish Society of Cardiology
Disclosure: Nothing to disclose.

Medical Editor

Justin D Pearlman, MD, PhD, ME, MA, Director of Advanced Cardiovascular Imaging, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center
Justin D Pearlman, MD, PhD, ME, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Director, Clinical Cardiac Electrophysiology Fellowship Program, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center
Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Li Zhou, MD; Grzegorz Rozmus, MD; James P Daubert, MD; David Huang, MD; Andrzej M Okreglicki, MB, ChB, MMed; and Hongsheng M Guo, MD.

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