Atrial Tachycardia Treatment & Management

The primary treatment during a bout of atrial tachycardia is considered to be rate control using 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 May 2011, is in agreement.^[5] However, great caution is required. Numerous reports describe cardiovascular collapse and even deaths following the assumption that a supraventricular tachycardia (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 exceedingly rarely terminate reentrant atrial tachycardias, but they cause peripheral vasodilation (in the case of calcium channel blockers) and myocardial depression. Thus, in hypotensive patients and in those with structural heart disease, the administration of a calcium channel blocker, which may fail to terminate the SVT, may cause 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 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.

The rhythm 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 in whom the rhythm is not tolerated 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.^[5] However, if the rhythm has persisted for longer than 48 hours, cardioversion may be associated with 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, transesophageal echocardiography may be recommended as in atrial fibrillation before attempting to cardiovert.

Some atrial tachycardias cannot be cardioverted; that is, they are incessant and recur immediately or soon after cardioversion. Automatic atrial tachycardias and multifocal atrial tachycardias do not respond to electrical cardioversion. However, electrical cardioversion may be attempted in unifocal atrial tachycardia because, unlike multifocal atrial tachycardia, 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 as well in combination therapy. For patients without cardiac failure, the ACC/AHA/ESC 2003 guideline states that intravenous class Ia and Ic agents may be used. For patients with poor ventricular function, intravenous amiodarone is preferable.^[5]

Treatment of atrial tachycardia from 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 (see below).

Treatment of atrial tachycardia from enhanced automaticity

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

Treatment of refractory recurrent atrial tachycardia

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.

Treatment for maintenance of sinus rhythm

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. Amiodarone and dofetilide should be used in patients with left ventricular dysfunction since they are not associated with increased mortality, as may be the case with class Ic antiarrhythmics. 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 hospitalization and 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^{[6, 7]} 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 are 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. The ACC/AHA/ESC 2003 guideline cites the high success rate (86%) and low recurrence rate (8%) shown by pooled data from 514 patients who had catheter ablation for focal AT.^[5]

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 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.

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

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.

Consultation with a cardiologist or electrophysiologist is recommended for all patients with atrial tachycardia and when structural heart disease is diagnosed or considered. Consultation with a cardiologist or electrophysiologist is imperative before initiating therapy with any antiarrhythmic agents because the results of a comprehensive cardiac workup might be needed to guide treatment.

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.

Treatment of multifocal atrial tachycardia (MAT) involves treatment and/or reversal of the precipitating cause. This may be all 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. Go to Multifocal Atrial Tachycardia for more complete information on this topic.

Most patients 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.

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

Prehospital care of MAT includes the following:

• Assess for pulmonary causes that may be causing the arrhythmia
• Stabilize the acute situation as necessary
• Provide oxygen, cardiac monitoring, and pulse oximetry
• Establish IV access without delaying transport
• Collect medications that the patient may be taking or may have access to

Emergency department care for MAT includes the following:

• Rapidly assess and stabilize the ABCs while providing simultaneous treatment. An upright sitting position usually is most appropriate.
• Obtain IV access with a large-bore catheter with isotonic sodium chloride solution at a to-keep-open (TKO) rate.
• Administer oxygen to maintain the saturation greater than 90%, but avoid excessive oxygen in patients with known significant COPD; this will avoid the theoretical problem of removing the hypoxic drive for ventilation, which can result in increased carbon dioxide retention.
• The need for tracheal intubation is dictated by the standard clinical indications
• Establish cardiac monitor, blood pressure monitor, and pulse oximetry
• Assess for and treat the underlying cardiopulmonary process, theophylline toxicity, or metabolic abnormality; bronchodilators and oxygen should be administered for treatment of decompensated chronic obstructive pulmonary disease (COPD); activated charcoal and/or charcoal hemoperfusion is the therapy for theophylline toxicity
• Avoid sedatives

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 used as the first line of treatment. Some authors consider magnesium sulfate to be the drug of choice.

Magnesium sulfate

When magnesium sulfate is administered to correct hypokalemia, most patients convert to normal sinus rhythm (NSR). In a small number of patients, high-dose magnesium causes a significant decrease in the patient's heart rate and conversion to normal sinus rhythm. The dosage is 2 g intravenously over 1 minute, followed by 2 g/h infusion over 5 hours.^{[8, 9, 10, 11, 12]}

Beta-blockers

Metoprolol has been used to lower the ventricular rate. More patients convert to a normal sinus rhythm when treated with beta-blockers in contrast to those receiving verapamil. Both oral and intravenous dosage forms have been used. The oral dosage is 25 mg every 6 hours until the desired effects are obtained. Intravenous bolus dosing has been administered to as much as 15 mg over 10 minutes.^{[8, 13, 14, 15, 16]}

Although no controlled studies have evaluated the use of short-acting beta-blockers in treatment of MAT, esmolol can also be used to control the ventricular rate as an intravenous 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 bronchospastic adverse effects since lung disease is commonly associated with MAT.

Calcium channel blockers

Diltiazem^[17] and verapamil^{[18, 19, 8, 20, 13, 21]} decrease the atrial activity and slow atrioventricular (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 intravenous calcium gluconate (10 mL of 10% calcium gluconate). Diltiazem may be used as a 20-45 mg intravenous 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 intravenous amiodarone^{[22, 23, 24]} (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm. The success rate was 40% at 3 days with oral dosing and 75% on day 1 with intravenous dosing; however, this has been evaluated in a very small number of patients. Recent data support the use of amiodarone prophylactically postoperatively in patients with COPD. Case reports have also supported the use of ibutilide^[25] and flecainide^[26] for cardioversion.

Surgical care

Very rarely in patients with persistent and refractory MAT, AV junctional radiofrequency ablation and permanent pacemaker implantation should be considered, both for symptomatic and hemodynamic improvement, and to prevent the development of tachycardia-mediated cardiomyopathy.^[27]

Complications

Potential complications include development of tachycardia-induced cardiomyopathy if the arrhythmia is persistent. Other complications include those due to drug therapy used to treat the arrhythmia, as follows:

• Atrial thrombi with embolization and subsequent stroke
• Myocardial infarction from incongruous myocardial supply and demand
• Pulmonary emboli

Deterrence and prevention

The best means of prevention of MAT is prevention of respiratory failure plus careful monitoring of all electrolyte disorders—namely, hypokalemia, hypomagnesemia, and drug therapy (mainly digoxin toxicity).

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. Digoxin promotes afterdepolarizations, which may promote the arrhythmia. Ventricular arrhythmias, AV block, and death have been reported when excessive digoxin has been administered to patients who were incorrectly diagnosed to have atrial fibrillation. DC cardioversion is not effective in conversion to normal sinus rhythm and can precipitate more dangerous arrhythmias.

Consultations

A cardiologist may be of assistance with ECG interpretation and may be available for consultation if antiarrhythmic therapy is being considered.