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Atrial Tachycardia Treatment & Management

  • Author: Adam S Budzikowski, MD, PhD, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
Updated: Dec 30, 2015

Approach Considerations

The primary treatment during an episode of atrial tachycardia is considered to be rate control using atrioventricular (AV) nodal blocking agents (eg, beta-blockers or calcium channel blockers). The American College of Cardiology (ACC)/American Heart Association (AHA)/European Society of Cardiology (ESC) 2003 guideline for the management of patients with supraventricular arrhythmias, the most current version available as of January 2013, is in agreement.[12]

Great caution is required, however. Numerous reports describe cardiovascular collapse and even death in patients who were given a calcium blocker on the assumption that their supraventricular tachycardia (SVT) was AV nodal dependent. If in fact the arrhythmia is a reentrant atrial tachycardia, beta-blockers and calcium channel blockers, especially verapamil, are exceedingly unlikely to terminate it. Instead, these drugs will cause peripheral vasodilation (in the case of calcium channel blockers) and myocardial depression. In patients who are hypotensive and in those with structural heart disease, the result may be hemodynamic deterioration 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 agent adenosine or the 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.

Atrial tachycardia often self-terminates and may be nonsustained if the cause is addressed. Beta-blockers may, to some extent, help decrease the frequency of episodes and reduce symptoms by decreasing AV nodal conduction to the ventricles. The rhythm itself is generally not life-threatening. Hospital admission is not generally required unless significant comorbidities exist, the tachycardia is incessant, or it is poorly tolerated.

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. In patients with documented systolic dysfunction and symptoms of heart failure, elimination of the tachycardia by ablation can afford reversal of systolic dysfunction and resolution of heart failure symptoms.



For any patient who does not tolerate the rhythm well hemodynamically and in whom rate control drugs are ineffective or contraindicated, cardioversion should be considered. The 2003 ACC/AHA/ESC guideline is in agreement.[12]

Cardioversion may pose an increased risk of thromboembolic complications, however, if the patient has a persistent tachycardia that is associated with absence of organized atrial mechanical contraction, such as in atrial fibrillation or atrial flutter. In this case, transesophageal echocardiography is recommended before attempting to cardiovert.

Some atrial tachycardias cannot be cardioverted; they are incessant and recur immediately or soon after cardioversion. Automatic atrial tachycardias and multifocal atrial tachycardia (MAT) do not respond to electrical cardioversion. However, electrical cardioversion may be attempted in unifocal atrial tachycardia because, unlike MAT, which can be identified on an electrocardiogram (ECG), automatic atrial tachycardia usually cannot be distinguished from other forms of atrial tachycardia on ECG unless long recordings are available.


Pharmacologic Treatment

Atrial tachycardia from triggered activity (most frequently found in the setting of digitalis toxicity) is sensitive to verapamil, beta-blockers, and adenosine. Verapamil alone or in combination with a beta-blocker may be effective for controlling the tachycardia.

Beta-blockers may be used to suppress atrial tachycardia due to enhanced automaticity. However, overall success rates are low.

For refractory recurrent atrial tachycardias causing symptoms (particularly recurrence after electrical cardioversion), antiarrhythmic drugs have been tried. These drugs prolong the atrial refractory period and slow conduction velocity, thereby disrupting the reentrant circuit. They also suppress the atrial premature depolarizations that commonly initiate the tachycardia.

Class Ia and Ic antiarrhythmics

For patients without cardiac failure, the ACC/AHA/ESC guideline states that intravenous (IV) class Ia and Ic agents may be used. For patients with poor ventricular function, IV amiodarone is preferable.[12]

The adverse effects of class Ia drugs are significant, and these drugs are effective only approximately 50% of the time. Therefore, the use of class Ia drugs is limited. In particular, quinidine has been replaced with more effective and safer antiarrhythmic agents and nonpharmacologic therapies.

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. Class Ic agents (particularly flecainide) should be administered with AV node–blocking drugs such as beta-blockers or calcium channel blockers.

Class III antiarrhythmics

Class III antiarrhythmic drugs such as amiodarone, sotalol, dronedarone, 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. Amiodarone and dofetilide should be used in patients with left ventricular dysfunction because they are not associated with increased mortality, as may be the case with class Ic antiarrhythmics, as well as with some class II agents (eg, sotalol, dronedarone).


Treatment of Digitalis Intoxication

Atrial tachycardia due to digitalis intoxication often manifests as AV conduction block, ventricular arrhythmias, or both. Recognizing this at an early stage is crucial because it may be a harbinger of more lethal ventricular tachyarrhythmias. Treatment often includes hospitalization, 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 ventricular tachyarrhythmias.

Go to Digitalis Toxicity for more complete information on this topic.


Treatment of Multifocal Atrial Tachycardia

In patients with multifocal atrial tachycardia (MAT), treatment and/or reversal of the precipitating cause may be the only therapy that is required; however, the arrhythmia may recur if the underlying condition worsens. Close and careful management is required because of the underlying complex cardiopulmonary medical conditions. Electrolyte and magnesium levels should be corrected as appropriate.

Treatment of underlying diseases may sometimes have arrhythmia-promoting effects; for example, theophylline and beta-agonist drugs used in patients with chronic obstructive pulmonary disease (COPD) produce an increased catecholamine state. These therapies should be used judiciously.

Prevention of MAT is best accomplished through prevention of respiratory failure. In addition, patients require careful monitoring of all electrolyte disorders—namely, hypokalemia and hypomagnesemia—and of drug therapy (in particular, digoxin therapy).

Emergency department care

Emergency department care for MAT involves simultaneous assessment and treatment. Rapidly assess and stabilize the airway, breathing, and circulation (ABCs) while providing simultaneous treatment. An upright sitting position usually is most appropriate. Establish cardiac monitoring, blood pressure monitoring, and pulse oximetry. Obtain IV access with a large-bore catheter and infuse isotonic sodium chloride solution at a to-keep-open (TKO) rate.

Administer oxygen to maintain the saturation at greater than 90%. However, avoid excessive oxygen in patients with known significant COPD; this will prevent the theoretical problem of removing the hypoxic drive for ventilation. The need for tracheal intubation is dictated by the standard clinical indications.

Assess for and treat the underlying cardiopulmonary process, theophylline toxicity, or metabolic abnormality. Bronchodilators and oxygen should be administered for treatment of decompensated COPD; activated charcoal and/or charcoal hemoperfusion is the therapy for theophylline toxicity.

Antiarrhythmics are usually not indicated for treatment of MAT, and specific antiarrhythmic therapy historically has not demonstrated great efficacy in this setting. Nevertheless, several small reports describe effectiveness with the use of magnesium sulfate (with concomitant correction of hypokalemia), verapamil, and some beta-blockers.

Calcium channel blockers are typically used as the first line of treatment. However, some authors consider magnesium sulfate to be the drug of choice.

Most patients with MAT require hospital admission to further manage their underlying cardiopulmonary diseases. These patients frequently are admitted to a monitored bed; however, the clinical scenario and the hemodynamic stability of the patient dictate disposition. For patients with theophylline toxicity, consider transfer to a hospital with hemoperfusion capabilities.

Very rarely, in patients with persistent and refractory MAT, AV junctional radiofrequency ablation and permanent pacemaker implantation should be considered. This approach can provide symptomatic and hemodynamic improvement and prevent the development of tachycardia-mediated cardiomyopathy.[13]

Magnesium sulfate

When magnesium sulfate is administered to correct hypokalemia, most patients convert to normal sinus rhythm. In a small number of patients with normal potassium levels, high-dose magnesium causes a significant decrease in the patient's heart rate and conversion to normal sinus rhythm. The dosage is 2 g IV over 1 minute, followed by 2 g/h infusion over 5 hours.[14, 15, 16, 17, 18]


Metoprolol has been used to lower the ventricular rate. Treatment with beta-blockers converts more patients to a normal sinus rhythm than does treatment with verapamil. Oral and IV dosage forms have been used. The oral dosage is 25 mg every 6 hours until the desired effects are obtained. IV bolus dosing has been administered in dosages as high as 15 mg over 10 minutes.[14, 19, 20, 21, 22]

Although no controlled studies have evaluated the use of short-acting beta-blockers in the treatment of MAT, esmolol can also be used to control the ventricular rate as an IV infusion. It has a very short half-life and can be terminated quickly in the event of an adverse reaction. The use of beta-blockers is limited by transient hypotension and by bronchospastic adverse effects (since lung disease is commonly associated with MAT).

Calcium channel blockers

Diltiazem[23] and verapamil[14, 19, 24, 25, 26, 27] decrease atrial activity and slow AV nodal conduction, thereby decreasing ventricular rate, but they do not return all patients to normal sinus rhythm. Transient hypotension is the most common adverse effect, which may often be avoided by pretreating the patient with 1 g of IV calcium gluconate (10 mL of 10% calcium gluconate).

Diltiazem may be given in a 20-45 mg IV bolus and then as a 10-25 mg/h continuous infusion. Verapamil may worsen hypoxemia by negating the hypoxic pulmonary vasoconstriction in underventilated alveoli; this is usually not clinically significant.


Oral and IV amiodarone (300 mg orally 3 times a day or 450-1500 mg IV over 2-24 h) have been reported to convert MAT to normal sinus rhythm.[28, 29] Investigators found the success rate to be 40% at 3 days with oral dosing and 75% on day 1 with IV dosing; however, the drug was evaluated in a very small number of patients.

Prophylactic use of amiodarone has proved to be successful in preventing MAT after coronary artery surgery in patients with COPD.[30] Case reports have also supported the use of ibutilide[31] and flecainide[32] for cardioversion.

Digoxin and cardioversion

Neither digoxin nor direct current (DC) cardioversion is indicated for the treatment of MAT. Digoxin has not been found to be effective in controlling the ventricular rate or restoring normal sinus rhythm; in fact, it may promote the arrhythmia by promoting afterdepolarizations. Ventricular arrhythmias, AV block, and death have been reported in patients incorrectly diagnosed with atrial fibrillation and given excessive digoxin.

DC cardioversion is not effective in conversion to normal sinus rhythm and can precipitate more dangerous arrhythmias.


Radiofrequency Catheter Ablation

Radiofrequency catheter ablation can cure macroreentrant and focal forms of atrial tachycardia and has become a widely used treatment option for symptomatic, medically refractory cases.[7, 8] The success rates are not as high as those for AV nodal reentrant tachycardia or AV reentrant tachycardia using an accessory pathway but they are still high, ranging from 77-100% in various published series.

After activation mapping, the origin of the tachycardia can be localized. Focal application of radiofrequency energy to the site via an ablation catheter results in termination of the tachycardia. The ACC/AHA/ESC guideline cites an 86% success rate and an 8% recurrence rate in pooled data from 514 patients who had catheter ablation for focal atrial tachycardia. (See the image below.)[12]

Intracardiac tracings showing atrial tachycardia b Intracardiac tracings showing atrial tachycardia breaking with application of radiofrequency energy. Before ablation, the local electrograms from the treatment site preceded the surface P wave by 51 ms, consistent with this site being the source of the tachycardia. Note that postablation electrograms on the ablation catheter are inscribed well past the onset of the sinus rhythm P wave. The first 3 tracings show surface electrocardiograms as labeled.CS – Respective pair of electrodes of the coronary sinus catheterCS 7,8 – Located at the os of the coronary sinusCS 1,2 – Distal pair of electrodes Abl – Ablation catheter (D-distal pair of electrodes)

Atrial fibrillation

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 some patients with atrial fibrillation from this mechanism.

Reentrant atrial tachycardia

Of note, complex ablation procedures primarily for atrial fibrillation that isolate pulmonary veins or make circumferential left atrial ablation 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 patients with repaired congenital heart disease may involve pathways resulting from anatomic obstacles created by the surgical incisions. Knowledge of the specific anatomic approach used in the repair can guide subsequent mapping and ablation.

Go to Catheter Ablation for more complete information on this topic.

Congenital heart disease

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

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



Consultation with a cardiac electrophysiologist or cardiologist is recommended for all patients with atrial tachycardia and for patients in whom structural heart disease has been diagnosed or is being considered. In addition, because the results of a comprehensive cardiac workup may be needed to guide treatment, it is imperative to consult with a cardiologist or electrophysiologist before therapy with any antiarrhythmic agents is initiated. A cardiologist may also be of assistance with ECG interpretation.

Contributor Information and Disclosures

Adam S Budzikowski, MD, PhD, FHRS Assistant Professor of Medicine, Division of Cardiovascular Medicine, Electrophysiology Section, State University of New York Downstate Medical Center, University Hospital of Brooklyn

Adam S Budzikowski, MD, PhD, FHRS is a member of the following medical societies: European Society of Cardiology, Heart Rhythm Society

Disclosure: Received consulting fee from Boston Scientific for speaking and teaching; Received honoraria from St. Jude Medical for speaking and teaching; Received honoraria from Zoll for speaking and teaching.


Christine S Cho, MD, MPH, MEd Assistant Professor, Departments of Pediatrics and Emergency Medicine, University of California, San Francisco, School of Medicine

Christine S Cho, MD, MPH, MEd is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.


Mirna M Farah, MD Associate Professor of Pediatrics, University of Pennsylvania School of Medicine; Attending Physician, Division of Emergency Medicine, Children's Hospital of Philadelphia

Mirna M Farah, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Dariusz Michałkiewicz, MD Head, Electrophysiology Department, Military Medical Institute, Poland

Disclosure: Nothing to disclose.

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; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

David A Peak, MD Assistant Residency Director of Harvard Affiliated Emergency Medicine Residency, Attending Physician, Massachusetts General Hospital; Consulting Staff, Department of Hyperbaric Medicine, Massachusetts Eye and Ear Infirmary

David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society

Disclosure: Pfizer Salary Employment

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.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Grace M Young, MD Associate Professor, Department of Pediatrics, University of Maryland Medical Center

Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians

Disclosure: Nothing to disclose.

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This 12-lead electrocardiogram demonstrates an atrial tachycardia at a rate of approximately 150 beats per minute. Note that 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.
Propagation map of right atrial tachycardia originating from the right atrial appendage obtained with non-contact mapping using EnSite mapping system.
Note that the atrial activities originate from the right atrium and persist despite the atrioventricular block. These features essentially exclude atrioventricular nodal reentry tachycardia and atrioventricular tachycardia via an accessory pathway. Note also that the change in the P wave axis at the onset of tachycardia makes sinus tachycardia unlikely.
Anterior-posterior projection is shown. An example of activation mapping using contact technique and EnSite system. The atrial anatomy is partially reconstructed. Early activation points are marked with white/red color. The activation waveform spreads from the inferior/lateral aspect of the atrium through the entire chamber. White points indicate successful ablation sites that terminated the tachycardia. TV – Tricuspid valveCS – Shadow of the catheter inserted in the coronary sinus
Intracardiac tracings showing atrial tachycardia breaking with application of radiofrequency energy. Before ablation, the local electrograms from the treatment site preceded the surface P wave by 51 ms, consistent with this site being the source of the tachycardia. Note that postablation electrograms on the ablation catheter are inscribed well past the onset of the sinus rhythm P wave. The first 3 tracings show surface electrocardiograms as labeled.CS – Respective pair of electrodes of the coronary sinus catheterCS 7,8 – Located at the os of the coronary sinusCS 1,2 – Distal pair of electrodes Abl – Ablation catheter (D-distal pair of electrodes)
An example of rapid atrial tachycardia mimicking atrial flutter. A single radiofrequency 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
Electrocardiogram showing multifocal atrial tachycardia (MAT).
This electrocardiogram belongs to an asymptomatic 17-year-old male who was incidentally discovered to have Wolff-Parkinson-White (WPW) pattern. It shows sinus rhythm with evident preexcitation. To locate the accessory pathway (AP), the initial 40 milliseconds of the QRS (delta wave) are evaluated. Note that the delta wave is positive in lead I and aVL, negative in III and aVF, isoelectric in V1, and positive in the rest of the precordial leads. Therefore, this is likely a posteroseptal AP.
This is a 12-lead electrocardiogram from an asymptomatic 7-year-old boy with Wolff-Parkinson-White (WPW) pattern. Delta waves are positive in leads I and aVL; negative in II, III, and aVF; isoelectric in V1; and positive in the rest of the precordial leads. This again predicts a posteroseptal location for the accessory pathway (AP).
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