Atrial Tachycardia Treatment & Management

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).

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. 

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.

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

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 have variable efficacy in terminating atrial tachycardia. However, these agents may be highly effective for maintaining sinus rhythm after conversion to a normal sinus rhythm. Because of the severe and potentially life-threatening adverse effect of torsade de pointes polymorphic ventricular tachycardia related to QT interval prolongation, initiation of sotalol and dofetilide therapy is performed in strict in-hospital settings with continuous telemetry monitoring and electrocardiograms to assess QT interval. Perhaps amiodarone and dofetilide are only safe drugs in patients with left ventricular dysfunction, unlike class Ic antiarrhythmics and other agents (eg, sotalol, dronedarone) that are contraindicated due to increased mortality.

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.

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, atrioventricular (AV) junctional ablation and permanent pacemaker implantation may be considered. This approach can provide symptomatic and hemodynamic improvement and prevent the development of tachycardia-mediated cardiomyopathy, although patients may become pacemaker dependent. ^[15]

Magnesium sulfate

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 intravenous (IV) dosage is 2 g over 1 minute, followed by 2 g/h infusion over 5 hours. ^{[16, 17, 18, 19, 20]}

Beta-blockers

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. ^{[16, 21, 22, 23, 24]}

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 ^[25] and verapamil ^{[16, 21, 26, 27, 28, 29]} 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.

Antiarrhythmics

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. ^{[30, 31]} 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. ^[32] Case reports have also supported the use of ibutilide ^[33] and flecainide ^[34] 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.

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% to 100% in various published series. Although radiofrequency energy is typically used for most catheter-based ablation procedures, cryothermal energy is preferred for ablation of atrial tachycardia in the vicinity of the atrioventricular (AV) node-His bundle (“para-Hisian” atrial tachycardia) in all age groups, and in general for other forms of atrial tachycardias as well in the pediatric age group.

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 American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) guideline cites consistent success rates in experienced centers above 90% to 95%, with a complication rate of less than 1% to 2% for catheter ablation of focal atrial tachycardia. ^[35] (See the image below.)

Atrial tachycardia. These intracardiac tracings showing atrial tachycardia breaking with the 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 three tracings show surface electrocardiograms as labeled. Abl = ablation catheter (D-distal pair of electrodes); CS = respective pair of electrodes of the coronary sinus catheter; CS 1,2 = distal pair of electrodes; CS 7,8 = electrodes located at the os of the coronary sinus.

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Atrial fibrillation

Focal atrial tachycardia originating from the pulmonary veins has been associated with atrial fibrillation. Catheter 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 catheter-based 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 electrocardiographic (ECG) interpretation.