Atrial Tachycardia

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Practice Essentials

Atrial tachycardia is a supraventricular tachycardia (SVT) that does not require the atrioventricular (AV) junction, accessory pathways, or ventricular tissue for its initiation and maintenance. It occurs in persons with normal hearts and in those with structurally abnormal hearts, including individuals with congenital heart disease (particularly after surgery for repair or correction of congenital or valvular heart disease).

In patients with structurally normal hearts, atrial tachycardia is associated with a low mortality rate. Patients with underlying structural heart disease, congenital heart disease, or lung disease are less likely to be able to tolerate this rhythm disturbance.

Signs and symptoms

Manifestations of atrial tachycardia include the following:

In patients with MAT, the history may disclose an underlying illness that is causing the tachycardia. Such illnesses include pulmonary, cardiac, metabolic, and endocrinopathic disorders. Chronic obstructive pulmonary disease (COPD) is the most common underlying disease process (60%) in MAT.

Reentrant atrial tachycardia is not uncommon in patients with a history of a surgically repaired atrial septal defect. The scar tissue in the atrium may give rise to the formation of a reentrant circuit.

On physical examination, the primary abnormal finding is a rapid pulse rate. The rate is usually regular, but it may be irregular in rapid atrial tachycardias with variable AV conduction and in MAT. Blood pressure may be low in patients presenting with fatigue, lightheadedness, or presyncope.

See Clinical Presentation for more detail.

Diagnosis

Workup for atrial tachycardia can employ the following diagnostic tools:

The following laboratory studies may be indicated to exclude systemic causes of sinus tachycardia:

The following imaging studies can be useful in the evaluation of patients with atrial tachycardia:

See Workup for more detail.

Management

The primary treatment during a bout of atrial tachycardia is considered to be rate control using AV nodal blocking agents (eg, beta-blockers, calcium channel blockers). Antiarrhythmic drugs can prevent recurrences and may be required; a calcium channel blocker or beta-blocker also may be required in combination therapy. Specific antiarrhythmic therapies include the following:

Nonpharmacologic therapies for atrial tachycardia include the following:

Multifocal atrial tachycardia

Treatment of MAT involves treatment and/or reversal of the precipitating cause. Therapy also may include the following:

In very rare cases, when MAT is persistent and refractory, AV junctional radiofrequency ablation and permanent pacemaker implantation should be considered. Such treatment can provide symptomatic and hemodynamic improvement and prevent the development of tachycardia-mediated cardiomyopathy.[3]

See Treatment and Medication for more detail.

Image Library


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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 l....

Background

Atrial tachycardia is defined as a supraventricular tachycardia (SVT) that does not require the atrioventricular (AV) junction, accessory pathways, or ventricular tissue for its initiation and maintenance. 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.

In adults, tachycardia is usually defined as a heart rate more than 100 beats per minute (bpm). In children, the definition of tachycardia varies because the normal heart rate is age dependent, as follows:[4, 5]

As in most SVTs, the electrocardiogram (ECG) typically shows a narrow QRS complex tachycardia (unless bundle branch block aberration occurs). Heart rates are highly variable, with a range of 100-250 bpm. The atrial rhythm is usually regular. (See the image below.)


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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 l....

The conducted ventricular rhythm is also usually regular. It may become irregular, however, especially at higher atrial rates, because of variable conduction through the AV node, thus producing conduction patterns such as 2:1, 4:1, a combination of those, or Wenckebach AV block.

The P wave morphology 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 (see Workup).

Multifocal atrial tachycardia (MAT) is an arrhythmia with an irregular atrial rate greater than 100 bpm. Atrial activity is well organized, with at least 3 morphologically distinct P waves, irregular P-P intervals, and an isoelectric baseline between the P waves.[6] Multifocal atrial tachycardia has previously been described by names such as chaotic atrial rhythm or tachycardia, chaotic atrial mechanism, and repetitive paroxysmal MAT. Go to Multifocal Atrial Tachycardia for more complete information on this topic.

Classification methods

A number of methods are used to classify atrial tachycardia. Classification in terms of origin can be based on endocardial activation mapping data, pathophysiologic mechanisms, and anatomy.

On the basis of endocardial activation, atrial tachycardia may be divided into the following 2 groups (see Presentation):

Diagnosis and treatment

A 12-lead ECG with rhythm strip is an important tool to help identify, locate, and differentiate atrial tachycardia. Laboratory studies may be indicated to exclude systemic disorders that may be causing the tachycardia. Electrophysiologic study may be required. (See Workup.)

The primary treatment during a bout of atrial tachycardia is considered to be rate control using AV nodal blocking agents, such as beta-blockers or calcium channel blockers (see Treatment and Medication). Cardioversion should be considered for any patient in whom the rhythm is not tolerated well hemodynamically and/or in whom rate control drugs are ineffective or contraindicated.

Radiofrequency catheter ablation for atrial tachycardia has become a highly successful and effective treatment option for symptomatic patients whose condition is refractory to medical therapy or who do not desire long-term antiarrhythmic therapy. It can cure macroreentrant and focal forms of atrial tachycardia. (See Treatment.)[7, 8]

Anatomy

Atrial tachycardia can have a right or left atrial origin. Some atrial tachycardias actually originate outside the usual anatomic boundaries of the atria, in areas such as the superior vena cava, pulmonary veins, and vein of Marshall, where fingers of atrial myocardium extend into these locations. Rare locations, such as the noncoronary aortic cusp[1] and hepatic veins, have been described, as well. (See the video below.)


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Propagation map of right atrial tachycardia originating from the right atrial appendage obtained with non-contact mapping using EnSite mapping system.

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.

Abnormalities that have been reported at the sites of atrial tachycardia origin include the following[9] :

Pathophysiology

Several pathophysiologic mechanisms have been ascribed to atrial tachycardia. These mechanisms can be differentiated on the basis of the pattern of onset and termination and the response to drugs and atrial pacing.

Enhanced automaticity

Automatic atrial tachycardia arises due to enhanced tissue automaticity and is observed in patients with structurally normal hearts 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.

Automatic atrial tachycardia is rarely initiated or terminated by a single atrial stimulation or rapid atrial pacing, but it may be transiently suppressed by overdrive pacing. It almost always requires isoproterenol infusion to facilitate induction and is predictably terminated by propranolol.[10] Carotid sinus massage and adenosine do not terminate the tachycardia even if they produce a transient AV nodal block. Electrical cardioversion is ineffective (being equivalent to attempting electrical cardioversion in a sinus tachycardia).

Triggered activity

Triggered activity is due to delayed after-depolarizations, which are low-amplitude oscillations occurring at the end of the action potential. These oscillations are triggered by the preceding action potential and are the result of calcium ion influxes into the myocardium. If these oscillations are of sufficient amplitude to reach the threshold potential, depolarization occurs again and a spontaneous action potential is generated.

If single, this is recognized as an atrial ectopic beat (an extra or premature beat). If it recurs and spontaneous depolarization continues, a sustained tachycardia may result.

Most commonly, atrial tachycardia due to triggered activity occurs in patients with digitalis intoxication[2] 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 maneuvers and drugs such as adenosine, verapamil, and beta-blockers, all of which can terminate the tachycardia.

Occasionally, this atrial tachycardia may arise from multiple sites in the atria, producing a multifocal or multiform atrial tachycardia. This may be recognized by varying P wave morphology and irregularity in the atrial rhythm.

Pulmonary vein tachycardias

Pulmonary vein tachycardias originate from the os of the pulmonary vein or even deeper localized atrial fibers. These strands of atrial tissue are generally believed to gain electrical independence, since they are partially isolated from the atrial myocardium. These tachycardias are typically very rapid (heart rate of 200-220 bpm or more)

Although pulmonary vein tachycardias frequently trigger episodes of atrial fibrillation, the associated atrial tachycardias may be the clinically dominant or exclusive manifestation. The latter typically involves only a single pulmonary vein as opposed to the multiple pulmonary vein involvement seen in atrial fibrillation.

Reentrant tachycardia

Intra-atrial reentry tachycardias may have either a macroreentrant or a microreentrant circuit. Macroreentry is the usual mechanism in atrial flutter and in scar- and incision-related (postsurgical) atrial tachycardia.

The more common and recognized form of atrial tachycardia, seen as a result of the advent of pulmonary vein isolation and linear ablation procedures, is left atrial tachycardia. In this situation, gaps in the ablation lines allow for slow conduction, providing the requisite anatomic substrate for reentry. These tachycardias may be self-limiting but if they persist, mapping and a repeat ablative procedure should be considered.

Microreentry can arise in a small focal area, such as in sinus node reentrant tachycardia. Typically, episodes of reentrant atrial tachycardia arise suddenly, terminate suddenly, and are paroxysmal. Carotid sinus massage and adenosine are ineffective in terminating macroreentrant tachycardias, even if they produce a transient AV nodal block. During electrophysiologic study, it can be induced and terminated by programmed extrastimulation. As is typical of other reentry tachycardias, electrical cardioversion terminates this type of atrial tachycardia.

Classification of atrial tachycardia

Based on endocardial activation, atrial tachycardia may be divided into 2 groups: focal and reentrant. Focal atrial tachycardia arises from a localized area in the atria such as the crista terminalis, pulmonary veins, ostium of the coronary sinus, or intra-atrial septum. If it originates from the pulmonary veins, it may trigger atrial fibrillation and often forms a continuum of arrhythmias.

Reentrant (usually macroreentrant) atrial tachycardias most commonly occur in persons with structural heart disease or complex congenital heart disease, particularly after surgery involving incisions or scarring in the atria. Electrophysiologically, these atrial tachycardias are similar to atrial flutters, typical or atypical. Often, the distinction is semantic, typically based on arbitrary cutoffs of atrial rate.

Some tachycardias cannot be easily classified. Reentrant sinoatrial tachycardia (or sinus node reentry) is a subset of focal atrial tachycardia due to reentry arising within the sinus node situated at the superior aspect of the crista terminalis. The P wave morphology and atrial activation sequence are identical or very similar to those of sinus tachycardia.

Etiology

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, an atrial tachycardia can have potentially life-threatening consequences.

The atrial tachycardia that manifests in association with exercise, acute illness with excessive catecholamine release, alcohol ingestion, altered fluid states, hypoxia, metabolic disturbance, or drug use (eg, caffeine, albuterol, theophylline, cocaine) is associated with automaticity or triggered activity. Digitalis intoxication is an important cause of atrial tachycardia, with triggered activity being the underlying mechanism.

Reentrant atrial tachycardia tends to occur in patients with structural heart disease, including ischemic, congenital, postoperative, and valvular disorders. Iatrogenic atrial tachycardias have become more common and typically result from ablative procedures in the left atrium. Several typical origination sites for these tachycardias have been identified, including the mitral isthmus (between the left lower pulmonary vein and mitral annulus), the roof of the left atrium, and, for reentry, around the pulmonary veins.

The most common reason for postablation tachycardias is gaps in the ablation lines, allowing for slow conduction and initiation reentry circuits or circuits excluded by the set of ablation lines. Typically, these patients have undergone an atrial fibrillation ablation procedure. This is true for catheter ablation and surgical epicardial ablation. Similarly, patients with prior surgical procedures involving the left atrium may have surgical incision lines and, hence, the potential for macroreentrant circuits.

MAT is often related to underlying illnesses, frequently occurring in patients experiencing an exacerbation of chronic obstructive pulmonary disease (COPD),[3] a pulmonary thromboembolism, an exacerbation of heart failure, or severe illness, especially under critical care with inotropic infusion. MAT is often associated with hypoxia and sympathetic stimulation. Digitalis toxicity also may be present in persons with MAT, with triggered activity as the mechanism.

Other underlying conditions that are commonly associated with MAT are the following:

Unusual forms of atrial tachycardias can be seen in patients with an infiltrative process involving the pericardium and, by extension, the atrial wall.

Epidemiology

Atrial tachycardia is relatively rare, constituting 5-15% of all SVTs. Atrial tachycardia has no known racial or ethnic predilection and no known predilection for either sex. There may be some association with pregnancy.

Atrial tachycardia may occur at any age, although it is more common in children and adults with congenital heart disease. MAT is a relatively infrequent arrhythmia, with a prevalence rate of 0.05-0.32% in patients who are hospitalized. It is predominantly observed in males and in older patients—in particular, elderly patients with multiple medical problems. The average age of patients from 9 studies was 72 years.

Prognosis

In patients with structurally normal hearts, atrial tachycardia is associated with a low mortality rate. However, tachycardia-induced cardiomyopathies have developed in patients with persistent or frequent atrial tachycardia. 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.

Multifocal atrial tachycardia

MAT itself is seldom life threatening. The condition is transient and resolves when the underlying condition improves. The prognosis depends on the prognosis of any comorbid disease.

Many patients with MAT have significant comorbidities, especially COPD and respiratory failure, that often require treatment in an intensive care unit. Consequently, a high mortality rate (up to 45%) is associated with this arrhythmia, although the mortality is not a direct consequence of the rhythm abnormality.

Potential complications of MAT include development of tachycardia-induced cardiomyopathy if the arrhythmia is persistent. Other complications include the following:

Patient Education

For patient education information, see the Heart Health Center, as well as Supraventricular Tachycardia and Palpitations.

In the case of MAT related to medication, education regarding correct medication usage and the monitoring of such medications should be considered. In the case of a pulmonary source, education about prevention and recognition of developing pulmonary conditions may be helpful.

History

Focal atrial tachycardia is usually episodic or paroxysmal. Typically, atrial tachycardia manifests as a sudden onset of palpitations. Atrial tachycardia due to enhanced automaticity may be nonsustained but repetitive or it may be continuous or sustained, as in reentrant forms of atrial tachycardia.

Atrial tachycardia may gradually speed up soon after its onset (warm-up phenomenon). However, the patient may be unaware of this. In a patient with supraventricular tachycardia (SVT), the presence of warm-up phenomenon on an electrocardiogram (eg, on Holter monitoring) suggests that the SVT is atrial tachycardia.

If the tachycardic episodes are accompanied by palpitations, patients also may report dyspnea, dizziness, lightheadedness, fatigue, or chest pressure. In patients with frequent or incessant tachycardias, a decline in effort tolerance and symptoms of heart failure may represent early manifestations of tachycardia-induced cardiomyopathy.

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. A rapid rate and severe hypotension may lead to syncope.

Reentrant atrial tachycardia is not uncommon in patients with a history of a surgically repaired atrial septal defect. The scar tissue in the atrium may give rise to the formation of a reentrant circuit.

The history should include questions regarding possible causes, such as the following:

Underlying disorders in multifocal atrial tachycardia

In patients with multifocal atrial tachycardia (MAT), the history may disclose an underlying illness that is causing the tachycardia. Such illnesses include pulmonary, cardiac, metabolic, and endocrinopathic disorders.

Chronic obstructive pulmonary disease (COPD) is the most common underlying disease process (60%). The arrhythmia is commonly precipitated by exacerbation of COPD, sometimes due to infection or exacerbation of heart failure. Increasing hypoxemia with respiratory acidosis and advanced disease also leads to increased bronchodilator usage, thereby increasing catecholamine levels, which may contribute to development of MAT.

Patients with MAT frequently have structural heart disease, mainly coronary artery disease and valvular heart disease, often in conjunction with COPD. Heart failure is often present when the diagnosis of MAT is first made. Metabolic disorders may also lead to MAT. In various series, 24% of patients with MAT were found to have diabetes mellitus, 14% had hypokalemia, and 14% had azotemia.

Twenty-eight percent of patients with MAT are recovering from major surgery, while others have postoperative infections, sepsis, pulmonary embolism, and heart failure. The link between pulmonary embolism and MAT is weak (ie, 6-14% of such patients have been said to have MAT), but the methods of diagnosing pulmonary embolism in these cases have not been well documented.

Physical Examination

The primary abnormality noted on physical examination is a rapid pulse rate. In most atrial tachycardias, the rate is regular. However, in rapid atrial tachycardias with variable atrioventricular (AV) conduction and in MAT, the pulse may be irregular.

Blood pressure may be low in patients presenting with fatigue, lightheadedness, or presyncope. The cardiovascular examination should be aimed at excluding underlying structural heart diseases such as valvular abnormalities and heart failure.

Depending upon comorbid conditions or general health status, the patient may be hemodynamically unstable. However, determining whether this is due to the underlying condition or to the arrhythmia may be difficult.

Approach Considerations

All patients who present acutely with possible atrial tachycardia should be placed on pulse oximetry and a cardiac monitor. A 12-lead electrocardiogram (ECG) and rhythm strip is an important tool to help identify, locate, and differentiate atrial tachycardia.

The following laboratory studies may be indicated to exclude systemic disorders that could be causing the tachycardia:

Echocardiography can be valuable. Electrophysiologic studies may be required. Occasionally, if enhanced automaticity or triggered activity is considered the underlying mechanism, exercise testing is used to facilitate the induction of atrial tachycardia.

Exclusion of Systemic Disorders

At the beginning of the workup for atrial tachycardia, appropriate laboratory studies should be performed to exclude systemic causes of sinus tachycardia (eg, fever, hyperthyroidism, anemia, dehydration, infection, hypoxemia, metabolic disturbance). Laboratory testing consists principally of a serum chemistry panel, blood hemoglobin level, and arterial blood gases, as follows:

Additional tests include a magnesium level and a theophylline level (if the patient is on, or has access to, this medication). Obtain other laboratory tests as clinically indicated. For example, a serum digoxin level should be obtained in patients who are suspected of having digitalis intoxication. Other symptoms of digoxin toxicity may also provide clues to the diagnosis.

Chest radiography is indicated to evaluate for pulmonary and cardiac findings in patients who present with tachycardia-induced cardiomyopathy and in those with complex congenital heart disease. Computed tomography (CT) scanning of the chest may be necessary at times to exclude pulmonary embolism as well as to assess the anatomy of pulmonary veins and provide digital imaging and communications in medicine (DICOM) images for anatomy reconstruction prior to an ablative procedure.

Electrocardiography

Ideally, a full 12-lead ECG and rhythm strip and with a clear baseline is obtained to allow the most accurate evaluation of P wave morphology. ECG features to consider in the diagnosis of atrial tachycardia include P wave morphology and axis (see the image below), PR interval, and PP interval variations. Typically, an isoelectric line is seen between consecutive P waves, while no line is seen with macroreentrant arrhythmias (eg, atrial flutter).


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Note that the atrial activities originate from the right atrium and persist despite the atrioventricular block. These features essentially exclude atr....

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 atrioventricular (AV) nodal conduction delay, however, 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. However, 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.

Multifocal atrial tachycardia

The diagnosis of multifocal atrial tachycardia (MAT) is confirmed with an ECG that meets the following criteria:

Some authors have suggested that patients who have rhythms with a rate of less than 100 bpm but who satisfy all other criteria (including the clinical profile commonly observed with MAT) be considered to have multifocal atrial rhythm or, when the rate is less than 60 bpm, multifocal atrial bradycardia. However, a controversy arises about whether this condition should be referred to as a MAT variant or a wandering atrial pacemaker. Patients with a wandering atrial pacemaker usually do not have serious underlying illnesses.

The requirement that 3 different P waves should exist has been applied since early descriptions of MAT were recorded, but whether this should be interpreted as 2 ectopic P waves and 1 sinus P wave or 3 ectopic P waves has been a matter of controversy. The consensus favors a minimum of 3 different waveforms in addition to sinus P waves. (See the image below.)


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Electrocardiogram showing multifocal atrial tachycardia (MAT).

Baseline noise on the ECG can mimic atrial fibrillation and obscure differences in P wave morphology. Conversely, coarse atrial fibrillation on short recordings may appear to show discrete P waves prior to each QRS complex. Longer ECG recordings are therefore useful.

Echocardiography

Echocardiography is an important diagnostic modality. It is used to rule out structural heart disease and to assess the following:

Electrophysiology

An electrophysiology study 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. It does not, however, prove that the pathway is involved in the tachycardia; rather, the pathway may simply be a bystander. If the premature ventricular beat advances not only subsequent atrial activation but also the entire circuit of the tachycardia, this usually implies AV reentry with pathway participation rather than atrial tachycardia.

When burst ventricular pacing accelerates the atrial rate and ventriculoatrial-AV (VAAV) response is seen after termination of ventricular pacing, this very strongly suggests atrial tachycardia. If ventricular burst or programmed extrastimulation pacing creates transient AV conduction block without altering the atrial activation, atrial tachycardia is again strongly suggested; this also excludes AV reentry as a mechanism. If ventricular pacing terminates the tachycardia without preexciting the atrium or without retrograde (VA) conduction, atrial tachycardia is generally excluded.

Typically, VA time is variable with atrial tachycardia. In addition, the changes in AA cycle length drive the change in VV cycle length.

Carotid sinus massage and adenosine have been used for diagnosing atrial tachycardia. These maneuvers reproducibly terminate AV nodal–dependent tachycardias but, due to automaticity, generally do not terminate atrial tachycardia. However, adenosine can occasionally stop some atrial tachycardias (usually a high dose of adenosine is needed, such as 12-18 mg). Termination of atrial tachycardia by a vagal maneuver such as carotid sinus massage would be very unusual (just as unusual as for atrial flutter).

Inappropriate sinus tachycardia

Focal tachycardia originating from the superior aspect of the crista terminalis and inappropriate sinus tachycardia usually have similar P wave morphologies and axes. Although differentiating these 2 entities on the basis of 12-lead ECG tracings is nearly impossible, electrophysiologic study may be helpful in making the diagnosis. Focal tachycardia due to microreentry (such as reentrant sinoatrial tachycardia) can be induced and terminated by atrial extrastimulation or incremental atrial pacing, whereas inappropriate sinus tachycardia does not respond to these maneuvers.

Reentrant sinoatrial tachycardia

By using endocardial mapping, reentrant sinoatrial 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 reentrant sinoatrial tachycardia, isoproterenol infusion does not change the earliest activation site, although it may increase the rate.

Focal tachycardia

Endocardial mapping is most commonly used for localizing atrial tachycardia during electrophysiology study. Using this technique, focal tachycardias can be easily determined. This also allows for mapping scar tissue and permits identification of the critical isthmus of the tachycardia. Typically, only 60-70% of the total cycle length of the tachycardia is identified with activation mapping for focal tachycardias, while nearly 100% of the cycle length can be identified for macroreentrant circuits. (See the image below.)


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Anterior-posterior projection is shown. An example of activation mapping using contact technique and EnSite system. The atrial anatomy is partially re....

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.

Event Monitoring or Home Telemetry

Event monitoring or home telemetry may provide useful information, especially in patients with paroxysmal symptoms. These procedures can be helpful for the following aspects of diagnosis:

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.[11]

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.

Cardioversion

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.[11]

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.[11]

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.[12]

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.[13, 14, 15, 16, 17]

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.[13, 18, 19, 20, 21]

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[22] and verapamil[13, 18, 23, 24, 25, 26] 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.[27, 28] 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.[29] Case reports have also supported the use of ibutilide[30] and flecainide[31] 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.)[11]


View Image

Intracardiac tracings showing atrial tachycardia breaking with application of radiofrequency energy. Before ablation, the local electrograms from the ....

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.

Consultations

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.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent recurrences and complications. Consider using antiarrhythmic agents when the arrhythmia is causing symptoms and does not respond to correction or treatment of underlying diseases. A calcium channel blocker or beta-blocker also may be required as well, in combination therapy.

Calcium channel blockers are especially effective in atrial tachycardia with triggered activity as the underlying mechanism. Beta-blockers can reduce the frequency and severity of atrial tachycardia episodes by controlling ventricular response.

Acebutolol (Sectral)

Clinical Context:  Acebutolol is a selective, hydrophilic beta-blocking drug, as well as a class II antiarrhythmic agent with mild, intrinsic sympathomimetic activity. It has a labeled indication for the management of ventricular arrhythmias. Beta-blocker therapy should be tapered gradually rather than withdrawn abruptly, to avoid acute tachycardia, hypertension, and/or ischemia.

Class Summary

Beta-blockers are effective for reducing the frequency and severity of episodes via control of the ventricular response during tachycardia and by reduction of frequency in a subgroup of patients for whom tachycardia is sensitive to catecholamine. Beta-blockers that have intrinsic sympathomimetic activity are capable of demonstrating low-level agonist activity at a beta receptor while also acting as an antagonist.

Atenolol (Tenormin)

Clinical Context:  Atenolol selectively blocks beta-1 receptors, with little or no effect on beta-2 receptors except at high doses. It has an off-label indication for supraventricular and ventricular arrhythmias. Beta-blocker therapy should be tapered gradually to avoid the acute tachycardia, hypertension, and/or ischemia that may occur with abrupt withdrawal.

Esmolol (Brevibloc)

Clinical Context:  Because of its brief duration of action (10-30 minutes), esmolol is an excellent drug for use in patients at risk of experiencing complications from beta blockade. It selectively blocks beta-1 receptors, with little or no effect on beta-2 receptors.

Esmolol is also classified as a class II antiarrhythmic agent. It has a labeled indication for the treatment of supraventricular tachycardia (SVT). Beta-blocker therapy should be tapered gradually, to avoid the acute tachycardia, hypertension, and/or ischemia that may occur with abrupt withdrawal.

Metoprolol (Lopressor)

Clinical Context:  Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG. Metoprolol has an off-label indication for MAT. Beta-blocker therapy should be tapered gradually, to avoid the acute tachycardia, hypertension, and/or ischemia that may occur with abrupt withdrawal.

Class Summary

Beta-blockers are effective for reducing the frequency and severity of episodes, via control of the ventricular response during tachycardia, and for reducing the frequency of episodes in a subgroup of patients whose tachycardia is sensitive to catecholamine. Beta-1 selective drugs are also known as cardioselective agents, because they act on beta-1 receptors on the myocardium.

Propranolol (Inderal)

Clinical Context:  Propranolol is a class II antiarrhythmic. It is a nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions. Do not administer an IV dose faster than 1 mg/min.

Class Summary

Beta-blockers reduce the frequency and severity of episodes via control of ventricular response during tachycardia and by reduction of frequency in a subgroup of patients in whom tachycardia is sensitive to catecholamine. Nonselective agents block beta-1 and beta-2 receptors.

Amiodarone (Cordarone, Pacerone, Nexterone)

Clinical Context:  Amiodarone has antiarrhythmic effects that overlap all 4 Vaughn-Williams antiarrhythmic classes. It may inhibit atrioventricular (AV) conduction and sinus node function. It prolongs action potential and the refractory period in myocardium and inhibits adrenergic stimulation. It blocks sodium channels with high affinity for inactive channels, blocks potassium channels, and weakly blocks calcium channels. In addition, this agent noncompetitively blocks alpha- and beta-adrenergic receptors.

Amiodarone has a labeled indication for the management of life-threatening recurrent ventricular fibrillation and hemodynamically-unstable ventricular tachycardia (VT) refractory to other antiarrhythmic agents. It is very effective in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence of these arrhythmias.

Amiodarone is the only agent proven to reduce the incidence and risk of cardiac sudden death, with or without obstruction to left ventricular outflow. With exception of disorders of prolonged repolarization (eg, long QT syndrome), amiodarone may be the drug of choice for life-threatening ventricular arrhythmias refractory to beta blockade and initial therapy with other agents.

Before administering amiodarone, control the ventricular rate and congestive heart failure (if present) with digoxin or calcium channel blockers. Most clinicians are comfortable with inpatient or outpatient loading with 400 mg orally 3 times a day for 1 week, because of low proarrhythmic effect, followed by weekly reductions with the goal of the lowest dose with the desired therapeutic benefit. During loading, patients must be monitored for bradyarrhythmias. With oral dosing, achieving efficacy may take weeks.

Sotalol (Betapace, Betapace AF, Sorine)

Clinical Context:  This class III antiarrhythmic agent blocks K+ channels, prolongs action potential duration, and lengthens the QT interval. It is a non–cardiac-selective beta-adrenergic blocker. Sotalol is effective in the maintenance of sinus rhythm, even in patients with underlying structural heart disease. Class III effects are seen only at oral doses of 160mg/day or higher.

Dofetilide (Tikosyn)

Clinical Context:  Dofetilide is a class III antiarrhythmic agent. It has been approved by the US Food and Drug Administration (FDA) for maintenance of sinus rhythm after conversion from atrial fibrillation or atrial flutter lasting longer than 1 week.

Dofetilide blocks delayed rectifier current and prolongs action potential duration; indeed, even at higher doses it has no effect on other depolarizing potassium currents. It terminates induced reentrant tachyarrhythmias (atrial fibrillation/flutter and VT) and prevents their reinduction. At clinically prescribed concentrations, it has no effect on sodium channels, which are associated with class I effects. Furthermore, no effect is noted on alpha- or beta-adrenergic receptors.

Dofetilide must be initiated with continuous electrocardiographic (ECG) monitoring and monitoring must be continued for 6 doses of the medication. The dose must be individualized according to creatinine clearance (CrCl) and the corrected QT interval (QTc; use the QT interval if the heart rate is less than 60 bpm). There is no information on the use of this drug for heart rates below 50 bpm.

Ibutilide (Corvert)

Clinical Context:  Ibutilide can terminate some atria tachycardias. Ibutilide works by increasing the action potential duration and, thereby, changing atrial cycle-length variability.

Class Summary

Many class III antidysrhythmic agents have been shown to be effective in maintaining sinus rhythm after conversion from atrial tachycardia.

Procainamide (Procanbid, Pronestyl)

Clinical Context:  Procainamide increases the refractory period of atria and ventricles. Myocardial excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity. Procainamide has a labeled indication for the treatment of life-threatening ventricular arrhythmias. It is indicated in recurrent VT not responsive to lidocaine, refractory SVT, refractory ventricular fibrillation, pulseless VT, and atrial fibrillation with rapid rate in Wolff-Parkinson-White syndrome.

Class Summary

These drugs have been tried in patients with refractory recurrent atrial tachycardia and disabling symptoms in whom beta-blockers or calcium channel blockers were unsuccessful. 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.

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

Flecainide (Tambocor)

Clinical Context:  Flecainide blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of the heart. This agent increases electrical stimulation of the threshold of the ventricle and His-Purkinje system, and by shortening phase 2 and 3 repolarization, it decreases action potential duration and effective refractory periods.

Flecainide is indicated for the treatment of paroxysmal atrial fibrillation/flutter associated with disabling symptoms and paroxysmal SVTs, including AV nodal reentrant tachycardia, AV reentrant tachycardia, and other SVTs of unspecified mechanism associated with disabling symptoms in patients without structural heart disease. It is also indicated for prevention of documented life-threatening ventricular arrhythmias (eg, sustained VT). It is not recommended in less severe ventricular arrhythmias, even if patients are symptomatic.

Propafenone (Rythmol)

Clinical Context:  Propafenone shortens upstroke velocity (phase 0) of the monophasic action potential. It reduces fast inward current carried by sodium ions in Purkinje fibers and, to a lesser extent, myocardial fibers, and it may increase the diastolic excitability threshold and prolong the effective refractory period. Propafenone reduces spontaneous automaticity and depresses triggered activity.

This agent is indicated for the treatment of documented life-threatening ventricular arrhythmias (eg, sustained VT). Propafenone appears to be effective in the treatment of SVTs, including atrial fibrillation and flutter. It is not recommended in patients with less severe ventricular arrhythmias, even if symptomatic.

Class Summary

These 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 a beta-blocker or calcium channel blocker.

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

Clinical Context:  During depolarization, diltiazem inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. Diltiazem injection has a labeled indication for the conversion of paroxysmal SVT and control of rapid ventricular rate in patients with atrial fibrillation and atrial flutter.

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

Clinical Context:  During depolarization, verapamil inhibits calcium ions from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium. It has a labeled indication for the treatment of ST.

Class Summary

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

Magnesium sulfate

Clinical Context:  Magnesium is used for replacement therapy in magnesium deficiency, especially in acute hypomagnesemia accompanied by signs of tetany similar to those observed in hypocalcemia. 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 levels cause a significant decrease in the patient's heart rate and conversion to normal sinus rhythm.

Magnesium is the drug of choice for torsade de pointes and also may be useful for treating conventional VT, especially when hypomagnesemia is confirmed. When administering treatment with magnesium sulfate, monitor for hypermagnesemia because overdose can cause cardiorespiratory collapse and paralysis.

Digoxin (Lanoxicaps, Lanoxin)

Clinical Context:  Digoxin is a cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. It acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure. It is used to control the ventricular rate when administering propafenone, flecainide, or procainamide.

To achieve a total digitalizing dose, initially administer 50% of the dose. Then administer the remaining two 25% portions at 6- to 12-hour intervals (ie, 1/2, 1/4, 1/4).

Adenosine (Adenocard, Adenoscan)

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

Adenosine is a first-line medical treatment for termination of paroxysmal SVT. It is effective in terminating AV nodal reentrant tachycardia and AV reciprocating tachycardia. More than 90% of patients convert to sinus rhythm with adenosine 12 mg.

Class Summary

Digoxin and adenosine 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 diagnosing SVTs of unknown origin, in terminating SVTs that are dependent on the AV junction, and in some focal atrial tachycardias. If adenosine successfully terminates an atrial tachycardia, the patient may respond to beta-blockers or calcium channel blockers.

Author

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

Disclosure: Boston Scientific Consulting fee Speaking and teaching; St. Jude Medical Honoraria Speaking and teaching; Zoll Honoraria Speaking and teaching

Coauthor(s)

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

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Additional Contributors

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.

References

  1. Weber R, Letsas KP, Arentz T, Kalusche D. Adenosine sensitive focal atrial tachycardia originating from the non-coronary aortic cusp. Europace. Jun 2009;11(6):823-6. [View Abstract]
  2. Ma G, Brady WJ, Pollack M, Chan TC. Electrocardiographic manifestations: digitalis toxicity. J Emerg Med. Feb 2001;20(2):145-52. [View Abstract]
  3. McCord J, Borzak S. Multifocal atrial tachycardia. Chest. Jan 1998;113(1):203-9. [View Abstract]
  4. Lennox EG. Cardiology. In: Tschudy MM, Arcara KM, eds. Johns Hopkins: The Harriet Lane Handbook. 19th ed. Philadelphia, PA: Mosby Elsevier Inc; 2012.
  5. Song MK, Baek JS, Kwon BS, Kim GB, Bae EJ, Noh CI, et al. Clinical spectrum and prognostic factors of pediatric ventricular tachycardia. Circ J. Sep 2010;74(9):1951-8. [View Abstract]
  6. Shine KI, Kastor JA, Yurchak PM. Multifocal atrial tachycardia. Clinical and electrocardiographic features in 32 patients. N Engl J Med. Aug 15 1968;279(7):344-9. [View Abstract]
  7. Wu RC, Berger R, Calkins H. Catheter ablation of atrial flutter and macroreentrant atrial tachycardia. Curr Opin Cardiol. Jan 2002;17(1):58-64. [View Abstract]
  8. Knecht S, Veenhuyzen G, O'Neill MD, Wright M, Nault I, Weerasooriya R, et al. Atrial tachycardias encountered in the context of catheter ablation for atrial fibrillation part ii: mapping and ablation. Pacing Clin Electrophysiol. Apr 2009;32(4):528-38. [View Abstract]
  9. Hirai Y, Nakano Y, Yamamoto H, Ogi H, Yamamoto Y, Suenari K, et al. Pulmonary artery mapping for differential diagnosis of left-sided atrial tachycardia. Circ J. 2013;77(2):345-51. [View Abstract]
  10. Chen SA, Chiang CE, Yang CJ, et al. Sustained atrial tachycardia in adult patients. Electrophysiological characteristics, pharmacological response, possible mechanisms, and effects of radiofrequency ablation. Circulation. 1994;90(3):1262-78.
  11. [Guideline] Blomström-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 committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society. J Am Coll Cardiol. Oct 15 2003;42(8):1493-531. [View Abstract]
  12. Tucker KJ, Law J, Rodriques MJ. Treatment of refractory recurrent multifocal atrial tachycardia with atrioventricular junction ablation and permanent pacing. J Invasive Cardiol. Sep 1995;7(7):207-12. [View Abstract]
  13. Kastor JA. Multifocal atrial tachycardia. N Engl J Med. Jun 14 1990;322(24):1713-7. [View Abstract]
  14. Cohen L, Kitzes R, Shnaider H. Multifocal atrial tachycardia responsive to parenteral magnesium. Magnes Res. Dec 1988;1(3-4):239-42. [View Abstract]
  15. Iseri LT, Fairshter RD, Hardemann JL, Brodsky MA. Magnesium and potassium therapy in multifocal atrial tachycardia. Am Heart J. Oct 1985;110(4):789-94. [View Abstract]
  16. McCord JK, Borzak S, Davis T, Gheorghiade M. Usefulness of intravenous magnesium for multifocal atrial tachycardia in patients with chronic obstructive pulmonary disease. Am J Cardiol. Jan 1 1998;81(1):91-3. [View Abstract]
  17. Ho KM. Intravenous magnesium for cardiac arrhythmias: jack of all trades. Magnes Res. Mar 2008;21(1):65-8. [View Abstract]
  18. Parillo JE. Treating Multifocal Atrial Tachycardia (MAT) in a critical care unit: new data regarding verapamil and metoprlol. Update Crit Care Med. 1987;2:3-5.
  19. Arsura E, Lefkin AS, Scher DL, Solar M, Tessler S. A randomized, double-blind, placebo-controlled study of verapamil and metoprolol in treatment of multifocal atrial tachycardia. Am J Med. Oct 1988;85(4):519-24. [View Abstract]
  20. Arsura EL, Solar M, Lefkin AS, Scher DL, Tessler S. Metoprolol in the treatment of multifocal atrial tachycardia. Crit Care Med. Jun 1987;15(6):591-4. [View Abstract]
  21. Hazard PB, Burnett CR. Treatment of multifocal atrial tachycardia with metoprolol. Crit Care Med. Jan 1987;15(1):20-5. [View Abstract]
  22. Adcock JT, Heiselman DE, Hulisz DT. Continuous infusion diltiazem hydrochloride for treatment of multifocal atrial tachycardia (abstract). Clin Res. 1994;42:430A.
  23. Aronow WS, Plasencia G, Wong R. Effect of verapamil versus placebo on PAT and MAT. Current Ther Res. 1980;27:823-29.
  24. Hazard PB, Burnett CR. Verapamil in multifocal atrial tachycardia. Hemodynamic and respiratory changes. Chest. Jan 1987;91(1):68-70. [View Abstract]
  25. Levine JH, Michael JR, Guarnieri T. Treatment of multifocal atrial tachycardia with verapamil. N Engl J Med. Jan 3 1985;312(1):21-5. [View Abstract]
  26. Salerno DM, Anderson B, Sharkey PJ, Iber C. Intravenous verapamil for treatment of multifocal atrial tachycardia with and without calcium pretreatment. Ann Intern Med. Nov 1987;107(5):623-8. [View Abstract]
  27. Kouvaras G, Cokkinos DV, Halal G, Chronopoulos G, Ioannou N. The effective treatment of multifocal atrial tachycardia with amiodarone. Jpn Heart J. May 1989;30(3):301-12. [View Abstract]
  28. Hsieh MY, Lee PC, Hwang B, Meng CC. Multifocal atrial tachycardia in 2 children. J Chin Med Assoc. Sep 2006;69(9):439-43. [View Abstract]
  29. Kuralay E, Cingöz F, Kiliç S, Bolcal C, Günay C, Demirkiliç U, et al. Supraventricular tachyarrythmia prophylaxis after coronary artery surgery in chronic obstructive pulmonary disease patients (early amiodarone prophylaxis trial). Eur J Cardiothorac Surg. Feb 2004;25(2):224-30. [View Abstract]
  30. Pierce WJ, McGroary K. Multifocal atrial tachycardia and Ibutilide. Am J Geriatr Cardiol. Jul-Aug 2001;10(4):193-5. [View Abstract]
  31. Barranco F, Sanchez M, Rodriguez J, Guerrero M. Efficacy of flecainide in patients with supraventricular arrhythmias and respiratory insufficiency. Intensive Care Med. 1994;20(1):42-4. [View Abstract]

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.

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.

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

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.

Electrocardiogram showing multifocal atrial tachycardia (MAT).

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)

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).