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. In addition to individuals with heart diseases, including congenital heart disease, atrial tachycardia may also occur in persons with structurally normal hearts. See the image below.
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Atrial tachycardia. This 12-lead electrocardiogram demonstrates an atrial tachycardia at a rate of approximately 150 beats per minute. Note that the n....
In clinical practice, three major types of atrial tachycardia are seen: focal atrial tachycardia, multifocal atrial tachycardia (MAT), and re-entrant atrial tachycardia. These arrhythmias have unique arrhythmic substrates and characteristics.
Focal atrial tachycardia arises from a localized atrial site and is characterized by regular, organized atrial activity with discrete P waves and, typically, an isoelectric segment between P waves. At times, irregularity is seen, especially at onset (“warm-up”) and termination (“warm-down”). Atrial mapping reveals a focal point of origin.
MAT is an irregular supraventricular tachycardia characterized by three distinct P-wave morphologies and/or patterns of atrial activation at different rates. The rhythm is always irregular.
Re-entrant atrial tachycardia is usually seen after cardiac surgery or catheter ablation with linear lesions that result in islets of scars. Re-entrant atrial tachycardias are usually incessant and may lead to cardiomyopathy.
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:
Rapid pulse rate: In most atrial tachycardias, the rapid pulse is regular; it may be irregular in rapid atrial tachycardias with variable AV conduction and in multifocal atrial tachycardia (MAT)
Episodic or paroxysmal occurrence
Sudden onset of palpitations
Continuous, sustained, or repetitive tachycardia: If atrial tachycardia is due to enhanced automaticity
"Warm-up" and "cool-off" phenomenon: Tachycardia gradually speeds up soon after onset (may be clinically inapparent); gradually slows down before termination
Dyspnea, dizziness, lightheadedness, fatigue, or chest pressure: In tachycardic episodes accompanied by palpitations
Syncope: With rapid rate and severe hypotension
Heart-failure symptoms and reduced effort tolerance: Early manifestations of tachycardia-induced cardiomyopathy in patients with frequent or incessant tachycardia
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 Presentation for more detail.
Workup
Workup for atrial tachycardia can employ the following diagnostic tools:
12-lead electrocardiography (ECG) with rhythm strip: To help identify, locate, and differentiate atrial tachycardia
Modified ECG with the Lewis lead: The right- and left-arm electrodes are applied at the two sides of the sternum at the second and fourth intercostal spaces, respectively; this may be used to magnify P waves.
Esophageal recording of atrial activation: May be necessary to discern P waves, especially in the pediatric age group
Holter monitoring: To analyze the onset and termination of atrial tachycardia, identify the AV conduction block during the episode, and correlate the symptoms to atrial tachycardia
Endocardial mapping: To localize atrial tachycardia
The following laboratory studies may be indicated to exclude systemic causes of sinus tachycardia:
Serum chemistry: To exclude electrolyte disorders
Blood hemoglobin level and red blood cell (RBC) counts: To seek evidence of anemia
Arterial blood gas level: To define pulmonary status
Serum digoxin assay: When digitalis intoxication is suspected
The following imaging studies can be useful in the evaluation of patients with atrial tachycardia:
Chest radiography: To assess pulmonary etiology (eg, COPD) and delineate cardiac size and structures (eg, in patients with tachycardia-induced cardiomyopathy or complex congenital heart disease)
Computed tomography (CT) scanning: To assess the anatomy of cardiac structures, including the pulmonary veins especially, to provide images prior to ablative procedure, and to exclude pulmonary embolism
Echocardiography: To assess structural heart disease, left atrial size, pulmonary arterial pressure, left ventricular function, and pericardial pathology
See Workup for more detail.
Treatment
The primary treatment during an episode of atrial tachycardia is considered to be ventricular 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:
Atrial tachycardia from triggered activity: Verapamil, beta-blockers, and adenosine
Atrial tachycardia from enhanced automaticity: Beta-blockers, but overall success rates are low
Refractory recurrent atrial tachycardia: Class Ic antiarrhythmic drugs
Maintenance of sinus rhythm: Class III antiarrhythmic drugs
Nonpharmacologic therapies for atrial tachycardia include the following:
Cardioversion: For patients in whom the rhythm is not well-tolerated hemodynamically and/or in whom rate-control drugs are ineffective or contraindicated
Catheter ablation: For symptomatic, medically refractory patients[1, 2]
Surgical ablation: For patients with complex congenital heart disease
Multifocal atrial tachycardia
Treatment of MAT involves treatment and/or reversal of the precipitating cause. Therapy also may include the following:
Calcium channel blockers: Used as the first line of treatment
Magnesium sulfate
Beta-blockers
Antiarrhythmics
In very rare cases, when MAT is persistent and refractory, AV junctional ablation and permanent pacemaker implantation may be considered. Such treatment can provide symptomatic and hemodynamic improvement and prevent the development of tachycardia-mediated cardiomyopathy, although patients may become pacemaker dependent.[3] In general, short and asymptomatic runs of atrial tachycardia detected as an incidental finding on ambulatory ECG do not require treatment.
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 of 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] :
Age 1-2 days: 123-159 bpm
Age 3-6 days: 129-166 bpm
Age 1-3 weeks: 107-182 bpm
Age 1-2 months: 121-179 bpm
Age 3-5 months: 106-186 bpm
Age 6-11 months: 109-169 bpm
Age 1-2 years: 89-151 bpm
Age 3-4 years: 73-137 bpm
Age 5-7 years: 65-133 bpm
Age 8-11 years: 62-130 bpm
Age 12-15 years: 60-119 bpm
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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Atrial tachycardia. This 12-lead electrocardiogram demonstrates an atrial tachycardia at a rate of approximately 150 beats per minute. Note that the n....
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 three 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 two groups (see Presentation):
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.
Reentrant atrial tachycardias: Usually macroreentrant; reentrant atrial tachycardias most commonly occur in persons with either structural or complex heart disease, particularly after surgery involving atrial incisions or scarring
Other methods of classification are as follows:
Pathophysiologic mechanisms: Atrial tachycardia can be classified as the result of enhanced automaticity, triggered activity, or reentry (see Pathophysiology)
Anatomy: Classification of atrial tachycardia can be based on the location of the arrhythmogenic focus (see Anatomy)
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. Invasive electrophysiologic study (EPS) may be required. (See Workup.) The morphology of the P wave may provide valuable clues to the origin of the tachycardia, and this is the reason why a 12-lead ECG is of special value.
The primary treatment during an episode 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.
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]
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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Atrial tachycardia. This propagation map of a right atrial tachycardia originating from the right atrial appendage was obtained with non-contact mapping using the 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] :
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
Atrial tachycardia caused by triggered activity is due to delayed after-depolarizations, which are low-amplitude oscillations occurring at the end of the action potential.[11] These delayed after-depolarization–related 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 two 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.
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.[12]
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:
Valvular heart disease
Diabetes mellitus
Hypokalemia
Hypomagnesemia
Azotemia
Postoperative state
Sepsis
Methylxanthine toxicity
Myocardial infarction
Pneumonia
Unusual forms of atrial tachycardias can be seen in patients with an infiltrative process involving the pericardium and, by extension, the atrial wall.
A very unusual form of recipient-to-donor atrial tachycardia may be seen in patients who have undergone bi-atrial orthotropic cardiac transplantation.[13] In this situation, atrial arrhythmia originates in the recipient remnant of the heart or from reentry around the incision suture lines and break through to the donor heart. Because of cardiac denervation, the recipient patients usually do not develop symptoms of palpitations but rather develop tachycardia-induced cardiomyopathy in the donor heart. These atrial tachycardias are extremely difficult to treat with drugs, but they can be cured by catheter ablation. Sometimes, atrial fibrillation and atrial flutter in the recipient heart indicate rejection; hence, close vigilance is necessary.
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.
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.
A study by Chung et al indicated that in patients with acute ischemic stroke and nonsustained atrial tachycardia, an enlarged left atrium is a risk factor for stroke recurrence. The study involved 252 patients, who were followed up for a mean period of 35 months.[14]
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:
Atrial thrombi with embolization and subsequent stroke
Myocardial infarction from incongruous myocardial supply and demand
For patient education information, see the Heart Health Center, as well as Supraventricular Tachycardia and Palpitations.
In the case of multifocal atrial tachycardia (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.
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) and gradually slows down before termination ("cool-off" 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:
Medical history, especially history of tachycardia or other cardiac problems
Family history of sudden death, deafness (Jervell-Lange Nielsen syndrome), or cardiac disease
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.
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.
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. A nodified ECG with the Lewis lead in which the right- and left-arm electrodes are applied at the two sides of the sternum at the second and fourth intercostal spaces may be used to magnify P waves. Esophageal recording of atrial activation may be necessary to discern P waves, especially in the pediatric age group.
The following laboratory studies may be indicated to exclude systemic disorders that could be causing the tachycardia:
Electrolyte levels: Particularly potassium, bicarbonate, calcium, and magnesium
Blood glucose level
Complete blood cell (CBC) count
Toxicology screen (including the use of herbal medications or energy supplements)
Arterial blood gas measurement
Thyroid function tests
24-Hour urine collection for catecholamines and catecholamine metabolites
Echocardiography can be valuable. Invasive electrophysiologic study 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.
The advent of three-dimensional (3-D) high-density and rapid electroanatomic mapping to characterize atrial tachycardias appears to have the potential to result in favorable outcomes following ablation.
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:
Serum chemistry: To exclude electrolyte disorders
Blood hemoglobin level and red blood cell (RBC) counts: To seek evidence of anemia
Arterial blood gas level: To define pulmonary status
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; digitalis intoxication is classically associated with atrial tachycardia with atrioventricular block. Other symptoms of digoxin toxicity may also provide clues to the diagnosis.
Chest radiography is indicated to evaluate for a pulmonary etiology (eg, chronic obstructive pulmonary disease) and to delineate cardiac size and structures 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 assess the anatomy of cardiac structures, including the pulmonary veins especially, to provide digital imaging and communications in medicine (DICOM) images for anatomy reconstruction prior to an ablative procedure, and to exclude pulmonary embolism.
Ideally, a full 12-lead electrocardiogram (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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Atrial tachycardia. Note that the atrial activities originate from the right atrium and persist despite the atrioventricular block. These features ess....
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 electrocardiogram (ECG) that meets the following criteria:
Irregular ventricular rate greater than 100 bpm
Organized and discrete P waves with at least 3 different morphologies in the same lead
Irregular PP, PR, and RR intervals with an isoelectric baseline between the P waves
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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Atrial tachycardia. This electrocardiogram shows 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.
An electrophysiology study may be required to establish the diagnosis of atrial tachycardia, usually by excluding other tachycardia mechanisms (e, atrioventricular [AV] reentrant tachycardia [AVNRT]). In order to exclude AVNRT and an accessory AV pathway-related AVRT, certain maneuvers are performed mainly to dissociate atrial activation from the ventricular activation and to observe any linking phenomenon. This is usually achieved by introducing a premature ventricular stimulation during the tachycardia. If the premature ventricular beat during His-bundle refractoriness terminates the tachycardia without inscribing atrial activation, both atypical AVNRT and atrial tachycardia can be excluded.
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 two entities on the basis of 12-lead electrocardiograph (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.)
View Image
Atrial tachycardia. An anterior-posterior mapping projection is shown. This is an example of activation mapping using contact technique and the EnSite....
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.
Distinguishing macroreentries from focal atrial tachycardias is the key for the ablation strategy. Macroreentry circuits usually involve the cavotricuspid isthmus in the right atrium, and are perimitral or roof-dependent in the left atrium. Detailed activation and entrainment mapping are necessary for successful ablation of these arrhythmias.
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:
Analyzing the onset and termination of atrial tachycardia
Identifying the AV conduction block during the atrial tachycardia
Correlating the symptoms with episodes of atrial tachycardia
The primary treatment during an episode of atrial tachycardia is considered to be rate control using atrioventricular (AV) nodal blocking agents (eg, beta-blockers or calcium channel blockers).
Great caution is required, however. Numerous reports describe cardiovascular collapse and even death in patients who were given a calcium blocker on the assumption that their supraventricular tachycardia (SVT) was AV nodal dependent. If in fact the arrhythmia is a reentrant atrial tachycardia, beta-blockers and calcium channel blockers, especially verapamil, are exceedingly unlikely to terminate it. Instead, these drugs will cause peripheral vasodilation (in the case of calcium channel blockers) and myocardial depression. In patients who are hypotensive and in those with structural heart disease, the result may be hemodynamic deterioration and collapse.
In the setting of hemodynamic compromise due to SVT or known atrial tachycardia in which a drug may be therapeutic, the ultra ̶ short-acting agent adenosine or the short-acting beta-blocker esmolol may be tried. In the setting of structural heart disease or previous cardiac surgery (repair or corrective surgery for congenital or valvular heart disease), particularly if there is hemodynamic instability, proceeding directly to electrical cardioversion is safest.
Atrial tachycardia often self-terminates and may be nonsustained if the cause is addressed. Beta-blockers may, to some extent, help decrease the frequency of episodes and reduce symptoms by decreasing AV nodal conduction to the ventricles. The rhythm itself is generally not life-threatening. Hospital admission is not generally required unless significant comorbidities exist, the tachycardia is incessant, or it is poorly tolerated.
The rhythm can be life-threatening in children with complex congenital heart disease, especially after a Fontan procedure. In this case, urgent cardioversion may be required. In patients with documented systolic dysfunction and symptoms of heart failure, elimination of the tachycardia by ablation can afford reversal of systolic dysfunction and resolution of heart failure symptoms.
For any patient who does not tolerate the rhythm well hemodynamically and in whom rate control drugs are ineffective or contraindicated, cardioversion should be considered.
Cardioversion may pose an increased risk of thromboembolic complications, however, if the patient has a persistent tachycardia that is associated with absence of organized atrial mechanical contraction, such as in atrial fibrillation or atrial flutter. In this case, transesophageal echocardiography is recommended before attempting to cardiovert.
Some atrial tachycardias cannot be cardioverted; they are incessant and recur immediately or soon after cardioversion. Automatic atrial tachycardias and multifocal atrial tachycardia (MAT) do not respond to electrical cardioversion. However, electrical cardioversion may be attempted in unifocal atrial tachycardia because, unlike MAT, which can be identified on an electrocardiogram (ECG), automatic atrial tachycardia usually cannot be distinguished from other forms of atrial tachycardia on ECG unless long recordings are available.
Atrial tachycardia from triggered activity (most frequently found in the setting of digitalis toxicity) is sensitive to verapamil, beta-blockers, and adenosine. Verapamil alone or in combination with a beta-blocker may be effective for controlling the tachycardia.
Beta-blockers may be used to suppress atrial tachycardia due to enhanced automaticity. However, overall success rates are low.
For refractory recurrent atrial tachycardias causing symptoms (particularly recurrence after electrical cardioversion), antiarrhythmic drugs have been tried. These drugs prolong the atrial refractory period and slow conduction velocity, thereby disrupting the reentrant circuit. They also suppress the atrial premature depolarizations that commonly initiate the tachycardia.
Class Ia and Ic antiarrhythmics
The adverse effects of class Ia drugs are significant, and these drugs are effective only approximately 50% of the time. Therefore, the use of class Ia drugs is limited. In particular, quinidine has been replaced with more effective and safer antiarrhythmic agents and nonpharmacologic therapies.
Class Ic drugs (ie, flecainide, propafenone) may slow the conduction and stop the tachycardia. These drugs can be proarrhythmic when used in patients with structural heart disease or even in those without disease. Class Ic agents (particularly flecainide) should be administered with AV node–blocking drugs such as beta-blockers or calcium channel blockers.
Class III antiarrhythmics
Class III antiarrhythmic drugs such as amiodarone, sotalol, dronedarone, and dofetilide have variable efficacy in terminating atrial tachycardia. However, these agents may be highly effective for maintaining sinus rhythm after conversion to a normal sinus rhythm. Because of the severe and potentially life-threatening adverse effect of torsade de pointes polymorphic ventricular tachycardia related to QT interval prolongation, initiation of sotalol and dofetilide therapy is performed in strict in-hospital settings with continuous telemetry monitoring and electrocardiograms to assess QT interval. Perhaps amiodarone and dofetilide are only safe drugs in patients with left ventricular dysfunction, unlike class Ic antiarrhythmics and other agents (eg, sotalol, dronedarone) that are contraindicated due to increased mortality.
Atrial tachycardia due to digitalis intoxication often manifests as AV conduction block, ventricular arrhythmias, or both. Recognizing this at an early stage is crucial because it may be a harbinger of more lethal ventricular tachyarrhythmias. Treatment often includes hospitalization, prompt discontinuation of digoxin, and correction of electrolyte disturbances.
The administration of antidigoxin antibodies is usually indicated in patients with conduction block, severe bradycardia, ventricular arrhythmias, and congestive heart failure. Electrical cardioversion is contraindicated because it may provoke ventricular tachyarrhythmias.
Go to Digitalis Toxicity for more complete information on this topic.
In patients with multifocal atrial tachycardia (MAT), treatment and/or reversal of the precipitating cause may be the only therapy that is required; however, the arrhythmia may recur if the underlying condition worsens. Close and careful management is required because of the underlying complex cardiopulmonary medical conditions. Electrolyte and magnesium levels should be corrected as appropriate.
Treatment of underlying diseases may sometimes have arrhythmia-promoting effects; for example, theophylline and beta-agonist drugs used in patients with chronic obstructive pulmonary disease (COPD) produce an increased catecholamine state. These therapies should be used judiciously.
Prevention of MAT is best accomplished through prevention of respiratory failure. In addition, patients require careful monitoring of all electrolyte disorders—namely, hypokalemia and hypomagnesemia—and of drug therapy (in particular, digoxin therapy).
Emergency department care
Emergency department care for MAT involves simultaneous assessment and treatment. Rapidly assess and stabilize the airway, breathing, and circulation (ABCs) while providing simultaneous treatment. An upright sitting position usually is most appropriate. Establish cardiac monitoring, blood pressure monitoring, and pulse oximetry. Obtain IV access with a large-bore catheter and infuse isotonic sodium chloride solution at a to-keep-open (TKO) rate.
Administer oxygen to maintain the saturation at greater than 90%. However, avoid excessive oxygen in patients with known significant COPD; this will prevent the theoretical problem of removing the hypoxic drive for ventilation. The need for tracheal intubation is dictated by the standard clinical indications.
Assess for and treat the underlying cardiopulmonary process, theophylline toxicity, or metabolic abnormality. Bronchodilators and oxygen should be administered for treatment of decompensated COPD; activated charcoal and/or charcoal hemoperfusion is the therapy for theophylline toxicity.
Antiarrhythmics are usually not indicated for treatment of MAT, and specific antiarrhythmic therapy historically has not demonstrated great efficacy in this setting. Nevertheless, several small reports describe effectiveness with the use of magnesium sulfate (with concomitant correction of hypokalemia), verapamil, and some beta-blockers.
Calcium channel blockers are typically used as the first line of treatment. However, some authors consider magnesium sulfate to be the drug of choice.
Most patients with MAT require hospital admission to further manage their underlying cardiopulmonary diseases. These patients frequently are admitted to a monitored bed; however, the clinical scenario and the hemodynamic stability of the patient dictate disposition. For patients with theophylline toxicity, consider transfer to a hospital with hemoperfusion capabilities.
Very rarely, in patients with persistent and refractory MAT, atrioventricular (AV) junctional ablation and permanent pacemaker implantation may be considered. This approach can provide symptomatic and hemodynamic improvement and prevent the development of tachycardia-mediated cardiomyopathy, although patients may become pacemaker dependent.[15]
Magnesium sulfate
In a small number of patients with normal potassium levels, high-dose magnesium causes a significant decrease in the patient's heart rate and conversion to normal sinus rhythm. The intravenous (IV) dosage is 2 g over 1 minute, followed by 2 g/h infusion over 5 hours.[16, 17, 18, 19, 20]
Beta-blockers
Metoprolol has been used to lower the ventricular rate. Treatment with beta-blockers converts more patients to a normal sinus rhythm than does treatment with verapamil. Oral and IV dosage forms have been used. The oral dosage is 25 mg every 6 hours until the desired effects are obtained. IV bolus dosing has been administered in dosages as high as 15 mg over 10 minutes.[16, 21, 22, 23, 24]
Although no controlled studies have evaluated the use of short-acting beta-blockers in the treatment of MAT, esmolol can also be used to control the ventricular rate as an IV infusion. It has a very short half-life and can be terminated quickly in the event of an adverse reaction. The use of beta-blockers is limited by transient hypotension and by bronchospastic adverse effects (since lung disease is commonly associated with MAT).
Calcium channel blockers
Diltiazem[25] and verapamil[16, 21, 26, 27, 28, 29] decrease atrial activity and slow AV nodal conduction, thereby decreasing ventricular rate, but they do not return all patients to normal sinus rhythm. Transient hypotension is the most common adverse effect, which may often be avoided by pretreating the patient with 1 g of IV calcium gluconate (10 mL of 10% calcium gluconate).
Diltiazem may be given in a 20-45 mg IV bolus and then as a 10-25 mg/h continuous infusion. Verapamil may worsen hypoxemia by negating the hypoxic pulmonary vasoconstriction in underventilated alveoli; this is usually not clinically significant.
Antiarrhythmics
Oral and IV amiodarone (300 mg orally 3 times a day or 450-1500 mg IV over 2-24 h) have been reported to convert MAT to normal sinus rhythm.[30, 31] Investigators found the success rate to be 40% at 3 days with oral dosing and 75% on day 1 with IV dosing; however, the drug was evaluated in a very small number of patients.
Prophylactic use of amiodarone has proved to be successful in preventing MAT after coronary artery surgery in patients with COPD.[32] Case reports have also supported the use of ibutilide[33] and flecainide[34] for cardioversion.
Digoxin and cardioversion
Neither digoxin nor direct current (DC) cardioversion is indicated for the treatment of MAT. Digoxin has not been found to be effective in controlling the ventricular rate or restoring normal sinus rhythm; in fact, it may promote the arrhythmia by promoting afterdepolarizations. Ventricular arrhythmias, AV block, and death have been reported in patients incorrectly diagnosed with atrial fibrillation and given excessive digoxin.
DC cardioversion is not effective in conversion to normal sinus rhythm and can precipitate more dangerous arrhythmias.
Catheter ablation can cure macroreentrant and focal forms of atrial tachycardia and has become a widely used treatment option for symptomatic, medically refractory cases.[7, 8] The success rates are not as high as those for AV nodal reentrant tachycardia or AV reentrant tachycardia using an accessory pathway but they are still high, ranging from 77% to 100% in various published series. Although radiofrequency energy is typically used for most catheter-based ablation procedures, cryothermal energy is preferred for ablation of atrial tachycardia in the vicinity of the atrioventricular (AV) node-His bundle (“para-Hisian” atrial tachycardia) in all age groups, and in general for other forms of atrial tachycardias as well in the pediatric age group.
After activation mapping, the origin of the tachycardia can be localized. Focal application of radiofrequency energy to the site via an ablation catheter results in termination of the tachycardia. The American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) guideline cites consistent success rates in experienced centers above 90% to 95%, with a complication rate of less than 1% to 2% for catheter ablation of focal atrial tachycardia.[35] (See the image below.)
View Image
Atrial tachycardia. These intracardiac tracings showing atrial tachycardia breaking with the application of radiofrequency energy. Before ablation, th....
Atrial fibrillation
Focal atrial tachycardia originating from the pulmonary veins has been associated with atrial fibrillation. Catheter ablation abolishing the focal triggering activity within the orifices of the pulmonary vein can be curative in some patients with atrial fibrillation from this mechanism.
Reentrant atrial tachycardia
Of note, complex ablation procedures primarily for atrial fibrillation that isolate pulmonary veins or make circumferential left atrial ablation lines have been associated with new reentrant atrial tachycardias or left-sided atypical atrial flutter. These tachycardias usually require a further ablation procedure.
Reentrant atrial tachycardias in patients with repaired congenital heart disease may involve pathways resulting from anatomic obstacles created by the surgical incisions. Knowledge of the specific anatomic approach used in the repair can guide subsequent mapping and ablation.
Go to Catheter Ablation for more complete information on this topic.
Congenital heart disease
For patients with complex congenital heart disease, surgical ablation may occasionally be useful. However, this procedure has generally been supplanted by catheter-based ablation.
At surgery, particularly for congenital heart disease and particularly with complex operations, such as the Fontan procedure, incisions should be situated or extended to lines of natural conduction block. This will reduce the risk of subsequent incisional or scar-related reentrant atrial tachycardias.
Consultation with a cardiac electrophysiologist or cardiologist is recommended for all patients with atrial tachycardia and for patients in whom structural heart disease has been diagnosed or is being considered. In addition, because the results of a comprehensive cardiac workup may be needed to guide treatment, it is imperative to consult with a cardiologist or electrophysiologist before therapy with any antiarrhythmic agents is initiated. A cardiologist may also be of assistance with electrocardiographic (ECG) interpretation.
In August 2019, the European Society of Cardiology (ESC) in collaboration with the Association for European Paediatric and Congenital Cardiology (AEPC) released recommendations on the management of supraventricular tachycardia.[36, 37] Previous related guidelines include, but are not limited to, the 2015 American College of Cardiology, American Heart Association, and Heart Rhythm Society (ACC/AHA/HRS)[35] and 2017 European Heart Rhythm Association[38] guidelines for the management of supraventricular tachycardia include specific recommendations for both acute and ongoing management of atrial tachycardia. These guidelines are summarized in the following sections.
2019 ESC/AEPC Guidelines for the Management of Supraventricular Tachycardia
Supraventricular Tachycardia Clinical Practice Guidelines (2019)
Several changes from the previous guidelines (2003) include revised drug grades as well as medications that are no longer considered, and changes to ablation techniques and indications.[36, 37]
Table. Medications, Strategies, and Techniques Specified or Not Mentioned in the 2019 Guidelines
View Table
See Table
2019 New Recommendations
For detailed recommendations on specific types of SVTs, please consult the original guidelines as listed under the references.
Class I (recommended or indicated)
For conversion of atrial flutter: Intravenous (IV) ibutilide, or IV or oral (PO) (in-hospital) dofetilide
For termination of atrial flutter (when an implanted pacemaker or defibrillator is present): High-rate atrial pacing
For asymptomatic patients with high-risk features (eg, shortest pre-excited RR interval during atrial fibrillation [SPERRI] ≤250 ms, accessory pathway [AP] effective refractory period [ERP] ≤250 ms, multiple APs, and an inducible AP-mediated tachycardia) as identified on electrophysiology testing (EPS) using isoprenaline: Catheter ablation
For tachycardia responsible for tachycardiomyopathy that cannot be ablated or controlled by drugs: Atrioventricular nodal ablation followed by pacing (“ablate and pace”) (biventricular or His-bundle pacing)
First trimester of pregnancy: Avoid all antiarrhythmic drugs, if possible
Class IIa (should be considered)
Symptomatic patients with inappropriate sinus tachycardia: Consider ivabradine alone or with a beta-blocker
Atrial flutter without atrial fibrillation: Consider anticoagulation (initiation threshold not yet established)
Asymptomatic preexcitation: Consider EPS for risk stratification
Asymptomatic preexcitation with left ventricular dysfunction due to electrical dyssynchrony: Consider catheter ablation
Class IIb (may be considered)
Acute focal atrial tachycardia: Consider IV ibutilide
Chronic focal atrial tachycardia: Consider ivabradine with a beta-blocker
Asymptomatic preexcitation: Consider noninvasive assessment of the AP conducting properties
Asymptomatic preexcitation with low-risk AP at invasive/noninvasive risk stratification: Consider catheter ablation
Prevention of SVT in pregnant women without Wolff-Parkinson-White syndrome: Consider beta-1 selective blockers (except atenolol) (preferred) or verapamil
Prevention of SVT in pregnant women without Wolff-Parkinson-White syndrome and without ischemic or structural heart disease: Consider flecainide or propafenone
Class III (not recommended)
IV amiodarone is not recommended for preexcited atrial fibrillation.
2017 EHRA Consensus Document on the Management of Supraventricular Arrhythmias
The European Heart Rhythm Association (EHRA) published its consensus document on the management of supraventricular arrhythmias, which has been endorsed by Heart Rhythm Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS), and Sociedad Latinoamericana de Estimulación Cardiaca y Electrofisiologia (SOLAECE).[38]
Acute Management (without established diagnosis)
In the setting of hemodynamically unstable supraventricular tachycardia (SVT), synchronized electrical cardioversion is recommended.
In the setting of hemodynamically stable SVT, vagal maneuvers, preferably in the supine position, or adenosine are recommended. Intravenous (IV) diltiazen or verapamil, or beta blockers, may be considered.
Sinus Tachycardia
Inappropriate sinus tachycardia
Therapy is primarily recommended for symptomatic control. Ivabradine is recommended in affected patients.
Beta blockers may be considered for second-line therapy, whereas non-dihydropyridine calcium channel blockers may be considered for third-line therapy.
Do not routinely consider catheter ablation for patients with inappropriate sinus tachycardia; restrict catheter ablation for the most symptomatic cases following failure of other therapies and measures.
Sinus nodal reentrant tachycardia
Catheter ablation may be used in symptomatic patients.
Oral beta blockers, diltiazem, or verapamil may be used in symptomatic patients
Focal Atrial Tachycardia
Acute therapy
Hemodynamically unstable patients: Synchronized DC cardioversion
Terminating a nonreentrant atrial tachycardia or diagnosing the tachycardia mechanism: Adenosine
Pharmacologic cardioversion or rate control: IV beta blockers, verapamil, or diltiazem; or IV amiodarone
Pharmacologic cardioversion in the absence of structural or ischemic heart disease: IV flecainide or propafenone
Pharmacologic cardioversion of microreentrant atrial tachycardia: IV ibutilide
Chronic therapy
Catheter ablation, especially for incessant atrial tachycardia
Consider beta blockers, verapamil, or diltiazem
Consider flecainide or propafenone in the absence of structural or ischemic heart disease
Hemodynamically unstable patients with (AFL/MRT): Synchronized direct current (DC) cardioversion
In case emergency cardioversion is necessary: Consider IV anticoagulation; continue anticoagulation for 4 weeks after sinus rhythm is established
Acute rate control in hemodynamically stable patients with AFL: IV beta blockers, diltiazem, or verapamil
To cardiovert AFL: IV ibutilide or dofetilide (under close monitoring due to proarrhythmic risk)
To control ventricular rate: Consider amiodarone
To cardiovert AFL/MRT: Consider atrial overdrive pacing (via esophagus or endocardial)
To cardiovert AFL in nonurgent situations but only in hospitalized patients (due to a proarrhythmic risk): Oral dofetilide
Avoid class Ic antiarrhythmic drugs in the absence of AV blocking agents: There's a risk of slowing the atrial rate and leading to the development of 1:1 atrioventricular (AV) conduction
Chronic therapy
Long-term alternative for patients with infrequent AFL recurrences or refusing ablation: One-time or repeated cardiversion associated with antiarrhythmic drugs
Patients with recurrent or poorly tolerated typical AFL: Cavotricuspid isthmus ablation
Patients with depressed left ventricular (LV) systolic function: Consider ablation to revert dysfunction due to tachycardiomyopathy and to prevent recurrences
Early post-atrial fibrillation (AF) ablation (3-6 months) appearance of atypical AFL/MRT: Initial treatment with cardioversion and antiarrhythmic drugs
Patients with recurrent atypical or multiple electrocardiographic (ECG) AFL patterns: Consider catheter ablation after the mechanism is documented
Consider postablation correction of "AF risk factors" (due to a high incidence of AF after CTI ablation for typical AFL)
Patients with AFL episodes: Consider anticoagulation
Stroke prevention
Recommended with the same indications as in AF among patients with typical flutter and associated AF episodes
Antithrombotic therapy not needed for low-risk AFL patients (ie, CHA2DS2-VASc score of 0 in males or 1 in females) (CHA2DS2-VASc: Cardiac failure, Hypertension, Age ≥75 [doubled], Diabetes, Stroke [doubled], Vascular disease, Age 65-74, Sex [female])
Patients with CHA2DS2-VASc ≥1: Oral anticoagulation with either a well-controlled vitamin K antagonist (VKA) with a time in therapeutic range >70%, or with a non-VKA oral anticoagulant (NOAC, either dabigatran, rivaroxaban, apixaban, or edoxaban)
Bleeding risk: Assess with HAS-BLED score (Hypertension, Abnormal renal/hepatic function, Stroke, Bleeding tendency/predisposition, Labile international normalized ratio [INR], Age [>65], Drugs [concomitant aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) or alcohol]); identify high-risk patients (score >3) for more frequent review and follow-up, as well as to address reversible bleeding risk factors. A high HAS-BLED score is not a reason to withhold anticoagulation
AV Nodal Reentrant Tachycardia (AVNRT)
Acute therapy
Valsalva maneuver, preferably in the supine position, is recommended.
IV adenosine is recommended.
Hemodynamically unstable patients in whom adenosine fails to terminate the tachycardia: Synchronized DC cardioversion
In the absence of hypotension or suspicion of ventricular tachycardia or preexcited AF: IV verapamil or diltiazem
Consider IV beta blockers (metoprolol or esmolol); or IV amiodarone; or a single oral dose of diltiazem and propranolol
Chronic therapy
Symptomatic patients or patients with an implantable cardioverter-defibrillator: Catheter ablation for slow pathway modification
Consider diltiazem or verapamil; or beta blockers
Minimally symptomatic patients with infrequent, short-lived tachycardia episode: No therapy
Focal Junctional Tachycardia
In the setting of acute therapy, IV propranolol with or without procainamide, verapamil, or flecainide may be considered.
In the setting of chronic therapy, beta blockers and, in the absence of ischemic or structural heart disease, flecainide or propafenone may be considered. Catheter ablation may be considered, but there is a risk of AV block.
AV Reentrant Tachycardia (AVRT) Due to Manifest/Concealed Accessory Pathways
Acute therapy
First-line approach to terminate SVT: Vagal maneuvers (Valsalva and carotid sinus massage), preferably in the supine position
To convert to sinus rhythm: Adenosine, but use with caution (it may precipitate AF with a rapid ventricular rate and even ventricular fibrillation)
Hemodynamically unstable AVRT patients in whom vagal maneuvers or adenosine are ineffective or not feasible: Synchronized DC shock
Patients with antidromic AVRT: Consider IV ibutilide, procainamide, propafenone, or flecainide
Patients with orthodromic AVRT: Consider IV beta blockers, diltiazem, or verapamil
Patients with preexcited AF: Potentially harmful drugs include IV digoxin, beta blockers, diltiazem, verapamil and, possibly, amiodarone
Chronic therapy
Symptomatic patients with AVRT and/or preexcited AF: Catheter ablation of the accessory pathway
Symptomatic patients with frequent episodes of AVRT: Consider catheter ablation of the accessory pathway
Patients with AVRT and/or preexcited AF, but without structural or ischemic heart disease: Consider oral flecainide or propafenone, preferably in combination with a beta blocker
Chronic management of AVRT in the absence of preexcitation sign on resting ECG: Oral beta blockers, diltiazem, or verapamil
Oral amiodarone may be considered only among patients in whom other antiarrhythmic drugs are ineffective or contraindicated, and catheter ablation is not an option.
Asymptomatic Preexcitation
Patients with asymptomatic ventricular preexcitation: Consider electrophysiologic (EP) testing for risk stratification.
Asymptomatic patients with preexcited ECG: Consider screening programs for risk stratification.
Catheter ablation of accessory pathways may be considered in asymptomatic patients with accessory pathways with an antegrade refractory period of less than 240 ms, inducible AVRT triggering preexcited AF, and multiple accessory pathways.
Observation without treatment may be reasonable in asymptomatic Wolff-Parkinson-White patients who are considered to be at low risk following an EP study or due to intermittent preexcitation.
SVTs in Patients With Adult Congenital Heart Disease
Acute therapy
Hemodynamically stable SVT (NOTE: Use caution in those with sinus node dysfunction and impaired ventricular function with a need for chronotropic or inotropic support.)
Electrical cardioversion
Consider IV adenosine for conversion
Hemodynamically stable AVNRT/AVRT
Consider IV adenosine
Consider atrial overdrive pacing (via esophagus or endocardial)
Hemodynamically stable AFL / atrial tachycardia
Consider IV ibutilide for conversion of AFL (Caution: Proarrhythmia may occur in patients with impaired ventricular function.)
Consider IV metoprolol (caution for hypotension) for conversion and rate control
Consider atrial overdrive pacing for conversion of AFL (via esophagus or endocardial)
Chronic therapy
Recurrent symptomatic SVT
Initial evaluation of SVT: Consider hemodynamic evaluation of structural defect for potential repair
Consider catheter ablation
Recurrent atrial tachycardia or AFL: Consider oral beta blockers
Prevention: Consider amiodarone if other drugs and catheter ablation are ineffective or contraindicated
Antithrombotic therapy for atrial tachycardia or AFL: Same as for patients with AF
Avoid use of oral sotalol (increased risk for proarrhythmias and mortality)
Avoid use of flecainide in patients with ventricular dysfunction (increased risk for proarrhythmias and mortality)
Atrial-based pacing to decrease recurrence of atrial tachycardia/AFL: It is not recommended that a pacemaker be implanted
Planned surgical repair and symptomatic SVT
Consider surgical ablation of atrial tachycardia, AFL, or accessory pathways
Patients planned for surgical repair of Ebstein anomaly: Consider preoperative EP study as a routine test
Patients with SVT planned for surgical repair of Ebstein anomaly: Consider preoperative catheter ablation, or intraoperative surgical ablation of accessory pathways, AFL, or atrial tachycardia
SVT During Pregnancy
Acute therapy
Patients with SVT causing hemodynamic instability: DC cardioversion
Vagal maneuvers, preferably in the supine position, may be considered as first-line therapy
Adenosine may be considered if vagal maneuvers fail
IV metoprolol or propranolol may be considered as a second-line drug if adenosine is ineffective
IV verapamil may be considered if adenosine and beta blockers are ineffective or contraindicated
Chronic therapy
Patients with tolerable symptoms: Consider no medical therapy
Highly symptomatic patients: Consider metoprolol, propranolol, or acebutolol
Highly symptomatic patients when beta blockers are ineffective or contraindicated: Verapamil may be reasonable; sotalol and flecainide may be reasonable
Highly symptomatic, drug-refractory SVT after the first trimester: Consider catheter ablation
2015 ACC/AHA/HRS Guideline for the Management of Supraventricular Tachycardia
Acute atrial tachycardia
Recommendations for acute treatment are summarized below.[35]
Hemodynamically unstable patients
Intravenous (IV) adenosine (class IIa; level of evidence [LOE]: C-LD)
Synchronized cardioversion, if IV adenosine is ineffective or not feasible (class I; LOE: C-LD)
Hemodynamically stable patients
IV beta blockers, diltiazem, or verapamil (class I; LOE: C-LD)
IV adenosine, if the diagnosis is suspected but not established (class IIa; LOE: B-NR)
IV amiodarone or ibutilide, if beta blockers, diltiazem, verapamil, or adenosine are ineffective (class IIb; LOE: C-LD)
Ongoing atrial tachycardia
Catheter ablation is preferred treatment. (Class I; LOE: B-NR)
Other therapeutic options include the following:
Oral beta blockers, diltiazem, or verapamil (class IIa; LOE: C-LD)
Flecainide or propafenone in patients without structural heart disease or ischemic heart disease (class IIa; LOE: C-LD)
Oral sotalol or amiodarone (class IIb; LOE: C-LD)
Multifocal atrial tachycardia (MAT)
The guidelines emphasize that the first-line treatment is management of the underlying condition. Cardioversion and antiarrhythmic medications were not found to be helpful in suppression of MAT.
For acute treatment in patients with MAT, IV metoprolol or verapamil were recommended; for ongoing management of recurrent symptomatic MAT, oral verapamil (class IIa; LOE: B-NR), metoprolol, or diltiazem may be used. (All class IIa; LOE: C-LD)[35]
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Clinical Context:
Ibutilide can terminate some atria tachycardias. Ibutilide works by increasing the action potential duration and, thereby, changing atrial cycle-length variability.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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).
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.
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.
What is included in the workup of atrial tachycardia?What is atrial tachycardia?What are the signs and symptoms of atrial tachycardia?How is atrial tachycardia treated?How is multifocal atrial tachycardia treated?How is atrial tachycardia defined?How is atrial tachycardia classified?How is atrial tachycardia diagnosed and treated?Which cardiac anatomy is relevant to atrial tachycardia?Which anatomic abnormalities may be present at the site of atrial tachycardia?How are the pathophysiologic mechanisms of atrial tachycardia differentiated?What is the role of enhanced automaticity in the pathophysiology of atrial tachycardia?What is the role of triggered activity in the pathophysiology of atrial tachycardia?What is the role of pulmonary vein tachycardias in atrial tachycardia?What is the pathophysiology of intra-atrial reentry tachycardia?What is the pathophysiologic classification of atrial tachycardia?What causes atrial tachycardia?What is the prevalence of atrial tachycardia?Which age groups have the highest prevalence of atrial tachycardia?What is the prognosis of atrial tachycardia?What is the prognosis of multifocal atrial tachycardia?What is included in patient education about atrial tachycardia?Which clinical history findings are characteristic of atrial tachycardia?What is the focus of the clinical history to evaluate for atrial tachycardia?Which clinical history findings are characteristic of multifocal atrial tachycardia?Which physical findings are characteristic of atrial tachycardia?Which conditions are included in the differential diagnoses of atrial tachycardia?What is the role of ECG analysis in differentiating atrial tachycardia from other diagnoses?Which conditions are included in the differential diagnoses of atrial tachycardia with short RP interval SVT?Which conditions are included in the differential diagnoses of atrial tachycardia with long RP interval SVT?What is required to diagnose atrial tachycardia?Which conditions are included in the differential diagnoses of multifocal atrial tachycardia?How is atrial tachycardia differentiated from inappropriate sinus tachycardia?What are the differential diagnoses for Atrial Tachycardia?Which tests are initially performed in the workup of atrial tachycardia?Which lab tests are performed in the workup of atrial tachycardia?Which cardiac tests may be beneficial in the workup of atrial tachycardia?How are systemic disorders excluded in the workup of atrial tachycardia?What is the role of imaging studies in the workup of atrial tachycardia?What is the role of ECG in the workup of atrial tachycardia?What is the role of ECG in the workup of multifocal atrial tachycardia?What is the role of echocardiography in the workup of atrial tachycardia?What is the role of electrophysiology studies in the workup of atrial tachycardia?Which electrophysiology findings are used to differentiate inappropriate sinus tachycardia from atrial tachycardia?What is the role of endocardial mapping in the workup of reentrant sinoatrial tachycardia?What is the role of endocardial mapping in the workup of focal atrial tachycardia?What is the role of home telemetry in the workup of atrial tachycardia?What is the primary treatment during an episode of atrial tachycardia?What is the role of cardioversion in the treatment of atrial tachycardia?Which medications are used in the treatment of atrial tachycardia?What is the role of class Ia and Ic antiarrhythmics in the treatment of atrial tachycardia?What is the role of class III antiarrhythmics in the treatment of atrial tachycardia?How is digitalis intoxication treated in patients with atrial tachycardia?How is multifocal atrial tachycardia treated?How is multifocal atrial tachycardia treated in the emergency department (ED)?What is the role of catheter ablation in the treatment of atrial tachycardia?How is atrial fibrillation treated in atrial tachycardia?What is the role of catheter ablation in the treatment of reentrant atrial tachycardia?How is congenital heart disease treated in patients with atrial tachycardia?Which specialist consultations are beneficial to patients with atrial tachycardia?Which guidelines have been issued on the treatment of atrial tachycardia?Which medications were omitted from the 2019 revision of the ESC/AEPC atrial tachycardia guidelines?What are the new recommendations in the 2019 revision of the ESC/AEPC atrial tachycardia guidelines?What are the EHRA treatment guidelines for sinus tachycardia?What are the EHRA treatment guidelines for focal atrial tachycardia?What are the EHRA guidelines on the treatment of atrial flutter (AFL)/ macroreentrant tachycardia (MRT)?What are the EHRA guidelines on the treatment of AV nodal reentrant tachycardia (AVNRT)?What are the EHRA guidelines on the treatment of AV nodal reentrant tachycardia (AVNRT) due to concealed accessory pathways?What are the EHRA guidelines on the treatment of atrial tachycardia during pregnancy?Which organizations have endorsed the 2017 EHRA guidelines on atrial tachycardia?What are the EHRA guidelines on acute management of atrial tachycardia?What are the EHRA guidelines on the treatment of SVTs with adult congenital heart disease?What are the EHRA guidelines on the treatment of focal junctional tachycardia?What are the EHRA guidelines on the treatment of asymptomatic preexcitation?What are the ACC/AHA/HRS guidelines on the treatment of acute atrial tachycardia?What are the ACC/AHA/HRS guidelines on the treatment of ongoing atrial tachycardia?What are the ACC/AHA/HRS guidelines on the treatment of multifocal atrial tachycardia?Where are guidelines on atrial tachycardia found online?What is the role of medications in the treatment of atrial tachycardia?Which medications in the drug class Antidysrhythmics, V are used in the treatment of Atrial Tachycardia?Which medications in the drug class Calcium Channel Blockers are used in the treatment of Atrial Tachycardia?Which medications in the drug class Antidysrhythmics, Ic are used in the treatment of Atrial Tachycardia?Which medications in the drug class Antidysrhythmics, Ia are used in the treatment of Atrial Tachycardia?Which medications in the drug class Antidysrhythmics, III are used in the treatment of Atrial Tachycardia?Which medications in the drug class Beta Blockers, Nonselective are used in the treatment of Atrial Tachycardia?Which medications in the drug class Beta-Blockers, Beta-1 Selective are used in the treatment of Atrial Tachycardia?Which medications in the drug class Beta Blockers, Intrinsic Sympathomimetic are used in the treatment of Atrial Tachycardia?
Bharat K Kantharia, MD, FRCP, FAHA, FACC, FESC, FHRS, Clinical Professor of Medicine, Icahn School of Medicine at Mount Sinai; Cardiac Electrophysiologist, Mount Sinai Health System, New York-Presbyterian Healthcare System, Montefiore Medical Center, Lennox Hill Hospital
Disclosure: Nothing to disclose.
Coauthor(s)
Arti N Shah, MD, MS, FACC, FACP, CEPS-AC, CEDS, Assistant Professor of Medicine, Mount Sinai School of Medicine; Director of Electrophysiology, Elmhurst Hospital Center and Queens Hospital Center
Disclosure: Nothing to disclose.
Munish Sharma, MBBS, Resident Physician, Department of Internal Medicine, Easton Hospital
Disclosure: Nothing to disclose.
Chief Editor
Jeffrey N Rottman, MD, Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System
Disclosure: Nothing to disclose.
Additional Contributors
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: Received consulting fee from Boston Scientific for speaking and teaching; Received honoraria from St. Jude Medical for speaking and teaching; Received honoraria from Zoll for speaking and teaching.
Christine S Cho, MD, MPH, MEd, Assistant Professor, Departments of Pediatrics and Emergency Medicine, University of California, San Francisco, School of Medicine
Disclosure: Nothing to disclose.
Acknowledgements
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
Parillo JE. Treating Multifocal Atrial Tachycardia (MAT) in a critical care unit: new data regarding verapamil and metoprolol. Update Crit Care Med. 1987. 2:3-5.
Davenport L. New ESC guideline on SVT management: catheter ablation key. Medscape Medical News. Available at https://www.medscape.com/viewarticle/917569. September 2, 2019; Accessed: September 24, 2019.
Atrial tachycardia. 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.
Atrial tachycardia. 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.
Atrial tachycardia. This propagation map of a right atrial tachycardia originating from the right atrial appendage was obtained with non-contact mapping using the EnSite mapping system.
Atrial tachycardia. This image shows an example of rapid atrial tachycardia mimicking atrial flutter. A single radiofrequency application terminates the tachycardia. The first three tracings show surface electrocardiograms, as labeled. AblD and AblP = distal and proximal pair of electrodes of the mapping catheter, respectively; HBED and HBEP = distal and proximal pair of electrodes in the catheter located at His bundle, respectively; HRA = high right atrial catheter; MAP = unipolar electrograms from the tip of the mapping catheter; RVA = catheter located in right ventricular apex.
Atrial tachycardia. 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.
Atrial tachycardia. This electrocardiogram shows multifocal atrial tachycardia (MAT).
Atrial tachycardia. An anterior-posterior mapping projection is shown. This is an example of activation mapping using contact technique and the 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. CS = shadow of the catheter inserted in the coronary sinus; TV = tricuspid valve.
Atrial tachycardia. These intracardiac tracings showing atrial tachycardia breaking with the application of radiofrequency energy. Before ablation, the local electrograms from the treatment site preceded the surface P wave by 51 ms, consistent with this site being the source of the tachycardia. Note that postablation electrograms on the ablation catheter are inscribed well past the onset of the sinus rhythm P wave. The first three tracings show surface electrocardiograms as labeled. Abl = ablation catheter (D-distal pair of electrodes); CS = respective pair of electrodes of the coronary sinus catheter; CS 1,2 = distal pair of electrodes; CS 7,8 = electrodes located at the os of the coronary sinus.
Atrial tachycardia. 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.
Atrial tachycardia. This propagation map of a right atrial tachycardia originating from the right atrial appendage was obtained with non-contact mapping using the EnSite mapping system.
Atrial tachycardia. 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.
Atrial tachycardia. An anterior-posterior mapping projection is shown. This is an example of activation mapping using contact technique and the 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. CS = shadow of the catheter inserted in the coronary sinus; TV = tricuspid valve.
Atrial tachycardia. These intracardiac tracings showing atrial tachycardia breaking with the application of radiofrequency energy. Before ablation, the local electrograms from the treatment site preceded the surface P wave by 51 ms, consistent with this site being the source of the tachycardia. Note that postablation electrograms on the ablation catheter are inscribed well past the onset of the sinus rhythm P wave. The first three tracings show surface electrocardiograms as labeled. Abl = ablation catheter (D-distal pair of electrodes); CS = respective pair of electrodes of the coronary sinus catheter; CS 1,2 = distal pair of electrodes; CS 7,8 = electrodes located at the os of the coronary sinus.
Atrial tachycardia. This image shows an example of rapid atrial tachycardia mimicking atrial flutter. A single radiofrequency application terminates the tachycardia. The first three tracings show surface electrocardiograms, as labeled. AblD and AblP = distal and proximal pair of electrodes of the mapping catheter, respectively; HBED and HBEP = distal and proximal pair of electrodes in the catheter located at His bundle, respectively; HRA = high right atrial catheter; MAP = unipolar electrograms from the tip of the mapping catheter; RVA = catheter located in right ventricular apex.
Atrial tachycardia. This electrocardiogram shows multifocal atrial tachycardia (MAT).
Atrial tachycardia. 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.
Atrial tachycardia. 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).
Type of Tachycardia
Treatment (Grade)
Not Mentioned in 2019 Guidelines
Narrow QRS tachycardias
Verapamil and diltiazem; beta-blockers (now all are grade IIa)
Verapamil (IIa); catheter ablation (IIa when fluoroless ablation is available)
Sotalol, propafenone, quinidine, procainamide
Adapted from Brugada J, Katritsis DG, Arbelo E, et al, for the ESC Scientific Document Group. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J. 2019 Aug 31;ehz467. https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehz467/5556821
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