AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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Background

Atrial tachycardia is a rhythm disturbance that arises in the atria.

Definition

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, 3:1, and 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.

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 atrial septum. Focal atrial tachycardia that originates from the pulmonary veins may trigger atrial fibrillation. 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 the typical atrial flutters, and often, the distinction is semantic.

Sinoatrial reentrant tachycardia 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 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 are 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 arrhythmic focus. Atrial tachycardia can have either a right or a left atrial origin. Some atrial tachycardias actually originate outside the atria, in areas such as the superior vena cava or pulmonary veins. 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, extra or premature beat. If it recurs and spontaneous depolarization continues, a sustained tachycardia may result.

Most commonly, atrial tachycardia due to triggered activity occurs in patients with digitalis intoxication 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 different 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.

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. 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. On 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

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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 those patients 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.
• MAT is a unique type of atrial tachycardia in which atrial activation originates from multiple atrial foci.
• • MAT often occurs in patients experiencing an exacerbation of chronic obstructive pulmonary disease, 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 MAT, with triggered activity as the mechanism.

DIFFERENTIALS

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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 bundle branch block 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. To determine the diagnosis requires additional maneuvers such as vagal stimulation (eg, carotid sinus massage, Valsalva) or adenosine.

In long RP interval (short PR) 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, sinoatrial reentrant tachycardia, atrial tachycardia, or accelerated junctional 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 MAT, the differential diagnosis includes atrial fibrillation because both can manifest with an irregular pulse.

WORKUP

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Lab 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.

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.
  • 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 overdrive ventricular pacing resets the tachycardia (entrainment), the diagnosis of AV reentrant tachycardia using an accessory pathway or AV nodal reentrant tachycardia is more likely than the usual type of focal atrial tachycardia.
  • If ventricular burst or programmed extrastimulation pacing creates transient AV conduction block without altering the atrial activation, atrial tachycardia is strongly suggested.
  • If ventricular pacing terminates the tachycardia without pre-exciting the atrium or without retrograde conduction from ventricle to atrium, atrial tachycardia is generally excluded.
• 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 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. Termination of atrial tachycardia by a vagal maneuver such as carotid sinus massage would be very unusual (just as unusual as for atrial flutter).
• Holter monitoring may be helpful to analyze the onset and termination of atrial tachycardia, identify the AV conduction block during the atrial tachycardia, and correlate the symptoms to atrial tachycardia. Event monitoring may be more useful for diagnosing patients with paroxysmal symptoms.

TREATMENT

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Medical Care

The primary treatment during a bout of atrial tachycardia is considered to be rate control using beta-blockers or calcium channel blockers. However, great caution is required. Numerous reports describe cardiovascular collapse and even deaths following the assumption that an SVT is AV junctional dependent and that a calcium channel blocker such as verapamil will terminate this tachycardia. Remember that beta-blockers and especially verapamil frequently do not terminate reentrant atrial tachycardias, but they cause peripheral vasodilation (in the case of calcium channel blockers) and myocardial depression. Thus, in the setting of patients with symptoms of hypotension and in patients with structural heart disease, the administration of a calcium channel blocker, which may fail to terminate the SVT, may cause deterioration of the hemodynamic status and collapse.

In the setting of hemodynamic compromise due to SVT or known atrial tachycardia in which a drug may be therapeutic, the ultra-short acting adenosine or short-acting beta-blocker esmolol may be tried. In the setting of structural heart disease or previous cardiac surgery (repair or corrective surgery for congenital or valvular heart disease), particularly if there is hemodynamic instability, proceeding directly to electrical cardioversion is safest.

Determining the etiology or cause of the atrial tachycardia is important because this tachycardia can also be observed in patients with underlying structural heart disease, acute pulmonary embolus, acute noncardiac illness, or thyroid disease, or it can be due to drugs, especially sympathomimetics or bronchodilators. The rhythm often self-terminates and may be nonsustained if the cause is addressed. Beta-blockers often help decrease the frequency of episodes and may reduce symptoms by decreasing AV nodal conduction to the ventricles.

The rhythm itself is generally not life threatening, and long-term management depends on the underlying cause, the frequency and severity of the episodes, and comorbidities that may determine the type of medical therapy. Antiarrhythmic drugs of various classes have been used in refractory cases.

The rhythm can be life threatening in children with complex congenital heart disease, especially after a Fontan procedure. In this case, urgent cardioversion may be required.

For any patient in whom the rhythm is not tolerated well hemodynamically and in whom rate control drugs are ineffective or contraindicated, cardioversion should be considered. However, if the rhythm has persisted for longer than 48 hours, cardioversion may be associated with the theoretically increased risk of thromboembolic complications if the tachycardia is associated with absence of organized atrial mechanical contraction, as during atrial fibrillation and atrial flutter. In this case, anticoagulation may be recommended as in atrial fibrillation before attempting to cardiovert.

Remember that some atrial tachycardias cannot be cardioverted. Automatic atrial tachycardias and MATs do not respond to electrical cardioversion. However, electrical cardioversion may be attempted in unifocal atrial tachycardia because, unlike MAT which can be distinguished from the ECG, it is usually impossible to be certain if the atrial tachycardia is focal or not.

Antiarrhythmic drugs can prevent recurrences and may be required. A calcium channel blocker or beta-blocker also may be required.

• 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.
• 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 should be administered with AV node–blocking drugs such as beta-blockers or calcium channel blockers.
• Class III antiarrhythmic drugs such as amiodarone and sotalol 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 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.
  • 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.

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 in order to prevent subsequent incisional or scar-related atrial reentrant tachycardias.

Consultations

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

MEDICATION

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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.

Drug Category: 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.

Drug Category: Class III antiarrhythmic agents

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

Drug Category: 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.

Drug Category: 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.

Drug Category: 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.

Drug Category: 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.

FOLLOW-UP

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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

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Medical/Legal 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

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Media file 1:  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.
	View Full Size Image
Media type:  ECG

Media file 2:  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.
	View Full Size Image
Media type:  ECG

REFERENCES

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• 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].
• Braunwald E, Zipes DP, eds. Specific arrhythmias: diagnosis and treatment. In: Heart Disease: A Textbook for Cardiovascular Medicine. 6th ed. Philadelphia, Pa: WB Saunders; 2001. 835-8.
• 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].
• Goodacre S, Irons R. ABC of clinical electrocardiography: Atrial arrhythmias. BMJ. Mar 9 2002;324(7337):594-7. [Medline].
• Huang SK, Wilber DJ, eds. Atrial tachycardias. In: Radiofrequency Catheter Ablation of Cardiac Arrhythmias: Basic Concepts and Clinical Applications. 2nd ed. Elmsford, NY: Futura Publishing; 2000:. 139-63.
• Josephson M, ed. Supraventricular tachycardias. In: Clinical Cardiac Electrophysiology: Techniques and Interpretations. 3rd. ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2001:. 169-271.
• Ma G, Brady WJ, Pollack M, Chan TC. Electrocardiographic manifestations: digitalis toxicity. J Emerg Med. Feb 2001;20(2):145-52. [Medline].
• McCord J, Borzak S. Multifocal atrial tachycardia. Chest. Jan 1998;113(1):203-9. [Medline].
• Morady F. Catheter ablation of supraventricular arrhythmias: state of the art. Pacing Clin Electrophysiol. Jan 2004;27(1):125-42.
• 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].
• 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].
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Article Last Updated: Jun 1, 2006