Practice Essentials

Atrial tachycardia is a supraventricular tachycardia (SVT) that does not require the
atrioventricular (AV) junction, accessory pathways, or ventricular tissue for its initiation and
maintenance. It occurs in persons with normal hearts and in those with structurally abnormal
hearts, including individuals with congenital heart disease (particularly after surgery for
repair or correction of congenital or valvular heart disease).
In patients with structurally normal hearts, atrial tachycardia is associated with a low
mortality rate. Patients with underlying structural heart disease, congenital heart disease, or
lung disease are less likely to be able to tolerate this rhythm disturbance.

Essential updates: Distinguishing between left- and right-sided atrial

tachycardia
Patterns derived from combining pulmonary artery, right atrial, and coronary sinus potentials
can be used to distinguish between left- and right-sided atrial tachycardia, according to a
study by Hirai et al. Using sequences obtained using electrode and ablation catheters, the
investigators were able to predict the presence of left-sided atrial tachycardia with 90%
accuracy, as well as a sensitivity and specificity of 78% and 100%, respectively.[1]

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 phenomenon: Tachycardia gradually speeds up soon after onset (may be

clinically inapparent)

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 Clinical Presentation for more detail.

Diagnosis
Workup for atrial tachycardia can employ the following diagnostic tools:

12-lead electrocardiography: To help identify, locate, and differentiate atrial

tachycardia

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: In patients with tachycardia-induced cardiomyopathy or complex

congenital heart disease

Computed tomography (CT) scanning: To exclude pulmonary embolism, assess the

anatomy of pulmonary veins, and provide images prior to ablative procedure

Echocardiography: To rule out structural heart disease and assess left atrial size,
pulmonary arterial pressure, left ventricular function, and pericardial pathology

See Workup for more detail.

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

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 in whom rate-control drugs are ineffective or contraindicated

Radiofrequency catheter ablation: For symptomatic, medically refractory patients[2, 3]

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: When administered to correct hypokalemia, most patients convert

to normal sinus rhythm (NSR)

Beta blockers

Antiarrhythmics

In very rare cases, when MAT is persistent and refractory, AV junctional radiofrequency
ablation and permanent pacemaker implantation should be considered. Such treatment can

provide symptomatic and hemodynamic improvement and prevent the development of

tachycardia-mediated cardiomyopathy.[4]
See Treatment and Medication for more detail.

Image Library

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.

Background
Atrial tachycardia is defined as a supraventricular tachycardia (SVT) that does not require the
atrioventricular (AV) junction, accessory pathways, or ventricular tissue for its initiation and
maintenance. Atrial tachycardia can be observed in persons with normal hearts and in those
with structurally abnormal hearts, including those with congenital heart disease and
particularly after surgery for repair or correction of congenital or valvular heart disease.
In adults, tachycardia is usually defined as a heart rate more than 100 beats per minute (bpm).
In children, the definition of tachycardia varies because the normal heart rate is age
dependent, as follows:[5, 6]

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.)

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.
The conducted ventricular rhythm is also usually regular. It may become irregular, however,
especially at higher atrial rates, because of variable conduction through the AV node, thus
producing conduction patterns such as 2:1, 4:1, a combination of those, or Wenckebach AV
block.
The P wave morphology on the ECG may give clues to the site of origin and mechanism of
the atrial tachycardia. In the case of a focal tachycardia, the P wave morphology and axis
depend on the location in the atrium from which the tachycardia originates. In the case of
macroreentrant circuits, the P wave morphology and axis depend on activation patterns (see
Workup).
Multifocal atrial tachycardia (MAT) is an arrhythmia with an irregular atrial rate greater than
100 bpm. Atrial activity is well organized, with at least 3 morphologically distinct P waves,
irregular P-P intervals, and an isoelectric baseline between the P waves.[7] Multifocal atrial
tachycardia has previously been described by names such as chaotic atrial rhythm or
tachycardia, chaotic atrial mechanism, and repetitive paroxysmal MAT. Go to Multifocal
Atrial Tachycardia for more complete information on this topic.

Classification methods
A number of methods are used to classify atrial tachycardia. Classification in terms of origin
can be based on endocardial activation mapping data, pathophysiologic mechanisms, and
anatomy.
On the basis of endocardial activation, atrial tachycardia may be divided into the following 2
groups (see Presentation):

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 is an important tool to help identify, locate, and differentiate atrial
tachycardia. Laboratory studies may be indicated to exclude systemic disorders that may be
causing the tachycardia. Electrophysiologic study may be required. (See Workup.)
The primary treatment during a bout of atrial tachycardia is considered to be rate control
using AV nodal blocking agents, such as beta blockers or calcium channel blockers (see
Treatment and Medication). Cardioversion should be considered for any patient in whom the
rhythm is not tolerated well hemodynamically and in whom rate control drugs are ineffective
or contraindicated.
Radiofrequency catheter ablation for atrial tachycardia has become a highly successful and
effective treatment option for symptomatic patients whose condition is refractory to medical
therapy or who do not desire long-term antiarrhythmic therapy. It can cure macroreentrant
and focal forms of atrial tachycardia. (See Treatment.)[8, 9]
Anatomy

Atrial tachycardia can have a right or left atrial origin. Some atrial tachycardias actually
originate outside the usual anatomic boundaries of the atria, in areas such as the superior vena
cava, pulmonary veins, and vein of Marshall, where fingers of atrial myocardium extend into
these locations. Rare locations, such as the noncoronary aortic cusp[2] and hepatic veins, have
been described, as well. (See the video below.)
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 agerelated 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[1] :

Extensive myocardial fibrosis

Myocyte hypertrophy

Endocardial fibrosis

Mononuclear cell infiltration

Mesenchymal cell proliferation

Islets of fatty tissue

Thinning

Blebs

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

Enhanced automaticity
Automatic atrial tachycardia arises due to enhanced tissue automaticity and is observed in
patients with structurally normal hearts and in those with organic heart disease. The
tachycardia typically exhibits a warm-up phenomenon, during which the atrial rate gradually
accelerates after its initiation and slows prior to its termination.
Automatic atrial tachycardia is rarely initiated or terminated by a single atrial stimulation or
rapid atrial pacing, but it may be transiently suppressed by overdrive pacing. It almost always
requires isoproterenol infusion to facilitate induction and is predictably terminated by
propranolol.[10] Carotid sinus massage and adenosine do not terminate the tachycardia even if
they produce a transient AV nodal block. Electrical cardioversion is ineffective (being
equivalent to attempting electrical cardioversion in a sinus tachycardia).

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

If single, this is recognized as an atrial ectopic beat (an extra or premature beat). If it recurs
and spontaneous depolarization continues, a sustained tachycardia may result.
Most commonly, atrial tachycardia due to triggered activity occurs in patients with digitalis
intoxication[3] or conditions associated with excess catecholamines. Characteristically, the
arrhythmia can be initiated, accelerated, and terminated by rapid atrial pacing. It may be
sensitive to physiologic maneuvers and drugs such as adenosine, verapamil, and beta
blockers, all of which can terminate the tachycardia.
Occasionally, this atrial tachycardia may arise from multiple sites in the atria, producing a
multifocal or multiform atrial tachycardia. This may be recognized by varying P wave
morphology and irregularity in the atrial rhythm.

Pulmonary vein tachycardias

Pulmonary vein tachycardias originate from the os of the pulmonary vein or even deeper
localized atrial fibers. These strands of atrial tissue are generally believed to gain electrical
independence, since they are partially isolated from the atrial myocardium. These
tachycardias are typically very rapid (heart rate of 200-220 bpm or more)
Although pulmonary vein tachycardias frequently trigger episodes of atrial fibrillation, the
associated atrial tachycardias may be the clinically dominant or exclusive manifestation. The
latter typically involves only a single pulmonary vein as opposed to the multiple pulmonary
vein involvement seen in atrial fibrillation.

Reentrant tachycardia
Intra-atrial reentry tachycardias may have either a macroreentrant or a microreentrant circuit.
Macroreentry is the usual mechanism in atrial flutter and in scar- and incision-related
(postsurgical) atrial tachycardia.
The more common and recognized form of atrial tachycardia, seen as a result of the advent of
pulmonary vein isolation and linear ablation procedures, is left atrial tachycardia. In this
situation, gaps in the ablation lines allow for slow conduction, providing the requisite
anatomic substrate for reentry. These tachycardias may be self-limiting but if they persist,
mapping and a repeat ablative procedure should be considered.
Microreentry can arise in a small focal area, such as in sinus node reentrant tachycardia.
Typically, episodes of reentrant atrial tachycardia arise suddenly, terminate suddenly, and are
paroxysmal. Carotid sinus massage and adenosine are ineffective in terminating
macroreentrant tachycardias, even if they produce a transient AV nodal block. During
electrophysiologic study, it can be induced and terminated by programmed extrastimulation.
As is typical of other reentry tachycardias, electrical cardioversion terminates this type of
atrial tachycardia.

Classification of atrial tachycardia

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

originates from the pulmonary veins, it may trigger atrial fibrillation and often forms a
continuum of arrhythmias.
Reentrant (usually macroreentrant) atrial tachycardias most commonly occur in persons with
structural heart disease or complex congenital heart disease, particularly after surgery
involving incisions or scarring in the atria. Electrophysiologically, these atrial tachycardias
are similar to atrial flutters, typical or atypical. Often, the distinction is semantic, typically
based on arbitrary cutoffs of atrial rate.
Some tachycardias cannot be easily classified. Reentrant sinoatrial tachycardia (or sinus node
reentry) is a subset of focal atrial tachycardia due to reentry arising within the sinus node
situated at the superior aspect of the crista terminalis. The P wave morphology and atrial
activation sequence are identical or very similar to those of sinus tachycardia.

Etiology
Atrial tachycardia can occur in individuals with structurally normal hearts or in patients with
organic heart disease. When it arises in patients with congenital heart disease who have
undergone corrective or palliative cardiac surgery, such as a Fontan procedure, an atrial
tachycardia can have potentially life-threatening consequences.
The atrial tachycardia that manifests in association with exercise, acute illness with excessive
catecholamine release, alcohol ingestion, altered fluid states, hypoxia, metabolic disturbance,
or drug use (eg, caffeine, albuterol, theophylline, cocaine) is associated with automaticity or
triggered activity. Digitalis intoxication is an important cause of atrial tachycardia, with
triggered activity being the underlying mechanism.
Reentrant atrial tachycardia tends to occur in patients with structural heart disease, including
ischemic, congenital, postoperative, and valvular disorders. Iatrogenic atrial tachycardias
have become more common and typically result from ablative procedures in the left atrium.
Several typical origination sites for these tachycardias have been identified, including the
mitral isthmus (between the left lower pulmonary vein and mitral annulus), the roof of the left
atrium, and, for reentry, around the pulmonary veins.
The most common reason for postablation tachycardias is gaps in the ablation lines, allowing
for slow conduction and initiation reentry circuits or circuits excluded by the set of ablation
lines. Typically, these patients have undergone an atrial fibrillation ablation procedure. This is
true for catheter ablation and surgical epicardial ablation. Similarly, patients with prior
surgical procedures involving the left atrium may have surgical incision lines and, hence, the
potential for macroreentrant circuits.
MAT is often related to underlying illnesses, frequently occurring in patients experiencing an
exacerbation of chronic obstructive pulmonary disease (COPD),[4] 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.

Epidemiology
Atrial tachycardia is relatively rare, constituting 5-15% of all SVTs. Atrial tachycardia has no
known racial or ethnic predilection and no known predilection for either sex. There may be
some association with pregnancy.
Atrial tachycardia may occur at any age, although it is more common in children and adults
with congenital heart disease. MAT is a relatively infrequent arrhythmia, with a prevalence
rate of 0.05-0.32% in patients who are hospitalized. It is predominantly observed in males
and in older patientsin particular, elderly patients with multiple medical problems. The
average age of patients from 9 studies was 72 years.

Prognosis
In patients with structurally normal hearts, atrial tachycardia is associated with a low
mortality rate. However, tachycardia-induced cardiomyopathies have developed in patients
with persistent or frequent atrial tachycardia. Patients with underlying structural heart
disease, congenital heart disease, or lung disease are less likely to be able to tolerate atrial
tachycardia. Other morbidity is associated with lifestyle changes and associated symptoms.

Multifocal atrial tachycardia

MAT itself is seldom life threatening. The condition is transient and resolves when the
underlying condition improves. The prognosis depends on the prognosis of any comorbid
disease.
Many patients with MAT have significant comorbidities, especially COPD and respiratory
failure, that often require treatment in an intensive care unit. Consequently, a high mortality
rate (up to 45%) is associated with this arrhythmia, although the mortality is not a direct
consequence of the rhythm abnormality.
Potential complications of MAT include development of tachycardia-induced
cardiomyopathy if the arrhythmia is persistent. Other complications include the following:

Atrial thrombi with embolization and subsequent stroke

Myocardial infarction from incongruous myocardial supply and demand

Pulmonary emboli

Patient Education
For patient education information, see the Heart Health Center, as well as Supraventricular
Tachycardia and Palpitations.
In the case of MAT related to medication, education regarding correct medication usage and
the monitoring of such medications should be considered. In the case of a pulmonary source,
education about prevention and recognition of developing pulmonary conditions may be
helpful.

History
Focal atrial tachycardia is usually episodic or paroxysmal. Typically, atrial tachycardia
manifests as a sudden onset of palpitations. Atrial tachycardia due to enhanced automaticity
may be nonsustained but repetitive or it may be continuous or sustained, as in reentrant forms
of atrial tachycardia.
Atrial tachycardia may gradually speed up soon after its onset (warm-up phenomenon).
However, the patient may be unaware of this. In a patient with supraventricular tachycardia
(SVT), the presence of warm-up phenomenon on an electrocardiogram (eg, on Holter
monitoring) suggests that the SVT is atrial tachycardia.
If the tachycardic episodes are accompanied by palpitations, patients also may report
dyspnea, dizziness, lightheadedness, fatigue, or chest pressure. In patients with frequent or
incessant tachycardias, a decline in effort tolerance and symptoms of heart failure may
represent early manifestations of tachycardia-induced cardiomyopathy.
Lightheadedness may result from relative hypotension, depending on the heart rate and other
factors, such as the state of hydration and particularly the presence of structural heart disease.

The faster the heart rate, the more likely a patient is to feel lightheaded. A rapid rate and
severe hypotension may lead to syncope.
Reentrant atrial tachycardia is not uncommon in patients with a history of a surgically
repaired atrial septal defect. The scar tissue in the atrium may give rise to the formation of a
reentrant circuit.
The history should include questions regarding possible causes, such as the following:

Medical history, especially history of tachycardia or other cardiac problems

Medications: Amphetamines, cocaine, caffeine, ephedrine, antihistamines,

phenothiazines, antidepressants, theophylline, appetite suppressants, albuterol,
digoxin

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.

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

Blood pressure may be low in patients presenting with fatigue, lightheadedness, or

presyncope. The cardiovascular examination should be aimed at excluding underlying
structural heart diseases such as valvular abnormalities and heart failure.
Depending upon comorbid conditions or general health status, the patient may be
hemodynamically unstable. However, determining whether this is due to the underlying
condition or to the arrhythmia may be difficult.

Diagnostic Considerations
The differential diagnosis of atrial tachycardia is the differential diagnosis of supraventricular
tachycardia (SVT) and includes the following:

Sinus tachycardia

Atrial flutter (see the image below)

Atrial fibrillation

Atrioventricular (AV) junctiondependent reentrant tachycardias (AV nodal reentrant

tachycardia and AV reentrant tachycardia using an accessory pathway)

An example of rapid atrial tachycardia mimicking

atrial flutter. A single radiofrequency application terminates the tachycardia. The first
3 tracings show surface electrocardiograms, as labeled. HRA High right atrial
catheter RVA Catheter located in right ventricular apex HBED and HBEP
Respectively, distal and proximal pair of electrodes in the catheter located at His
bundle AblD and AblP Respectively, distal and proximal pair of electrodes of the
mapping catheter MAP Unipolar electrograms from the tip of the mapping catheter
Differentiating among these diagnoses requires electrocardiographic (ECG) analysis of the
tachycardia for P wave activity. In SVT, the ECG typically has narrow QRS complexes
(unless aberrant conduction with typical left or right bundle-branch block occurs or a
bystander preexcitation is seen).
Assessment of the relationship of the P waves to the QRS complex (R waves) can help to
guide diagnosis. A short RP interval (P wave immediately following the QRS) suggests
different causes of the tachycardia than does a long RP interval (interval wave preceding
QRS).
In short RP interval SVT, the differential diagnosis includes the following:

Typical AV nodal reentrant tachycardia

AV reentrant tachycardia using accessory pathways

Atrial tachycardia with long first-degree AV block

Atrial tachycardia originating from the os of the coronary sinus or junctional

tachycardia

To determine the diagnosis requires additional maneuvers, such as vagal stimulation (eg,
carotid sinus massage, Valsalva maneuver), or adenosine.
In long RP interval SVT, the differential diagnosis includes the following:

Atypical (fast-slow) AV nodal reentrant tachycardia

Permanent junctional reciprocating tachycardia (PJRT) due to a slowly conducting

retrograde accessory pathway

Atrial tachycardia

Sinus tachycardia

Sinus node reentry

Atrial flutter

AV reentrant tachycardia

Diagnosis requires assessment of the patient condition, vagal maneuvers, adenosine, and
cardioversionnamely, procedures that may not only be diagnostic but also therapeutic.
For multifocal atrial tachycardia (MAT), the differential diagnosis includes atrial fibrillation
because both can manifest with an irregular pulse. MAT with aberration or preexisting bundle
branch block may be misinterpreted as ventricular tachycardia (VT).
However, if the patient also has new signs or symptoms (eg, chest pain, unexplained dyspnea,
inappropriate hypotension) or a recent illness, perform a more extensive workup because
atrial tachycardia may not be the primary problem; acute pulmonary embolus, acute
noncardiac illness, thyroid disease, or drugs (especially sympathomimetics or
bronchodilators) can cause atrial tachycardia. In addition, with frequent or incessant
tachycardia, tachycardia-induced cardiomyopathy may develop.
Another tachycardia that mimics atrial tachycardia is inappropriate sinus tachycardia. Strictly
speaking, inappropriate sinus tachycardia and postural orthostatic tachycardia syndrome
(POTS) are not atrial tachycardias, because their origin is not abnormal. They are sinus
tachycardias related to enhanced sinus automaticity, abnormal autonomic function
(dysautonomia), or physiologic reflexes
Differentials

Atrial Fibrillation
Atrial Flutter
Atrioventricular Nodal Reentry Tachycardia
Chronic Anemia
Paroxysmal Supraventricular Tachycardia
Sympathomimetic Toxicity
Thyroid Hormone Toxicity
Torsade de Pointes
Ventricular Tachycardia
Wolff-Parkinson-White Syndrome
Approach Considerations

The primary treatment during an episode of atrial tachycardia is considered to be rate control
using atrioventricular (AV) nodal blocking agents (eg, beta blockers or calcium channel
blockers). The American College of Cardiology (ACC)/American Heart Association
(AHA)/European Society of Cardiology (ESC) 2003 guideline for the management of
patients with supraventricular arrhythmias, the most current version available as of January
2013, is in agreement.[11]
Great caution is required, however. Numerous reports describe cardiovascular collapse and
even death in patients who were given a calcium blocker on the assumption that their
supraventricular tachycardia (SVT) was AV nodal dependent. If in fact the arrhythmia is a
reentrant atrial tachycardia, beta blockers and calcium channel blockers, especially
verapamil, are exceedingly unlikely to terminate it. Instead, these drugs will cause peripheral
vasodilation (in the case of calcium channel blockers) and myocardial depression. In patients
who are hypotensive and in those with structural heart disease, the result may be
hemodynamic deterioration and collapse.
In the setting of hemodynamic compromise due to SVT or known atrial tachycardia in which
a drug may be therapeutic, the ultra short-acting agent adenosine or the short-acting beta
blocker esmolol may be tried. In the setting of structural heart disease or previous cardiac
surgery (repair or corrective surgery for congenital or valvular heart disease), particularly if
there is hemodynamic instability, proceeding directly to electrical cardioversion is safest.
Atrial tachycardia often self-terminates and may be nonsustained if the cause is addressed.
Beta blockers may, to some extent, help decrease the frequency of episodes and reduce
symptoms by decreasing AV nodal conduction to the ventricles. The rhythm itself is generally

not life-threatening. Hospital admission is not generally required unless significant

comorbidities exist, the tachycardia is incessant, or it is poorly tolerated.
The rhythm can be life-threatening in children with complex congenital heart disease,
especially after a Fontan procedure. In this case, urgent cardioversion may be required. In
patients with documented systolic dysfunction and symptoms of heart failure, elimination of
the tachycardia by ablation can afford reversal of systolic dysfunction and resolution of heart
failure symptoms.
Cardioversion

For any patient who does not tolerate the rhythm well hemodynamically and in whom rate
control drugs are ineffective or contraindicated, cardioversion should be considered. The
2003 ACC/AHA/ESC guideline is in agreement.[11]
Cardioversion may pose an increased risk of thromboembolic complications, however, if the
patient has a persistent tachycardia that is associated with absence of organized atrial
mechanical contraction, such as in atrial fibrillation or atrial flutter. In this case,
transesophageal echocardiography is recommended before attempting to cardiovert.
Some atrial tachycardias cannot be cardioverted; they are incessant and recur immediately or
soon after cardioversion. Automatic atrial tachycardias and multifocal atrial tachycardia
(MAT) do not respond to electrical cardioversion. However, electrical cardioversion may be
attempted in unifocal atrial tachycardia because, unlike MAT, which can be identified on an
electrocardiogram (ECG), automatic atrial tachycardia usually cannot be distinguished from
other forms of atrial tachycardia on ECG unless long recordings are available.
Pharmacologic Treatment

Atrial tachycardia from triggered activity (most frequently found in the setting of digitalis
toxicity) is sensitive to verapamil, beta blockers, and adenosine. Verapamil alone or in
combination with a beta blocker may be effective for controlling the tachycardia.
Beta blockers may be used to suppress atrial tachycardia due to enhanced automaticity.
However, overall success rates are low.
For refractory recurrent atrial tachycardias causing symptoms (particularly recurrence after
electrical cardioversion), antiarrhythmic drugs have been tried. These drugs prolong the atrial
refractory period and slow conduction velocity, thereby disrupting the reentrant circuit. They
also suppress the atrial premature depolarizations that commonly initiate the tachycardia.
Class Ia and Ic antiarrhythmics

For patients without cardiac failure, the ACC/AHA/ESC guideline states that intravenous
(IV) class Ia and Ic agents may be used. For patients with poor ventricular function, IV
amiodarone is preferable.[11]

The adverse effects of class Ia drugs are significant, and these drugs are effective only
approximately 50% of the time. Therefore, the use of class Ia drugs is limited. In particular,
quinidine has been replaced with more effective and safer antiarrhythmic agents and
nonpharmacologic therapies.
Class Ic drugs (ie, flecainide, propafenone) may slow the conduction and stop the
tachycardia. These drugs can be proarrhythmic when used in patients with structural heart
disease or even in those without disease. Class Ic agents (particularly flecainide) should be
administered with AV nodeblocking drugs such as beta blockers or calcium channel
blockers.
Class III antiarrhythmics

Class III antiarrhythmic drugs such as amiodarone, sotalol, dronedarone, and dofetilide are
not always effective in terminating the atrial tachycardia, but they may be highly effective for
maintaining sinus rhythm after conversion to a normal sinus rhythm. Amiodarone and
dofetilide should be used in patients with left ventricular dysfunction because they are not
associated with increased mortality, as may be the case with class Ic antiarrhythmics, as well
as with some class II agents (eg, sotalol, dronedarone).
Treatment of Digitalis Intoxication

Atrial tachycardia due to digitalis intoxication often manifests as AV conduction block,

ventricular arrhythmias, or both. Recognizing this at an early stage is crucial because it may
be a harbinger of more lethal ventricular tachyarrhythmias. Treatment often includes
hospitalization, prompt discontinuation of digoxin, and correction of electrolyte disturbances.
The administration of antidigoxin antibodies is usually indicated in patients with conduction
block, severe bradycardia, ventricular arrhythmias, and congestive heart failure. Electrical
cardioversion is contraindicated because it may provoke ventricular tachyarrhythmias.
Go to Digitalis Toxicity for more complete information on this topic.
Treatment of Multifocal Atrial Tachycardia

In patients with multifocal atrial tachycardia (MAT), treatment and/or reversal of the
precipitating cause may be the only therapy that is required; however, the arrhythmia may
recur if the underlying condition worsens. Close and careful management is required because
of the underlying complex cardiopulmonary medical conditions. Electrolyte and magnesium
levels should be corrected as appropriate.
Treatment of underlying diseases may sometimes have arrhythmia-promoting effects; for
example, theophylline and beta-agonist drugs used in patients with chronic obstructive
pulmonary disease (COPD) produce an increased catecholamine state. These therapies should
be used judiciously.

Prevention of MAT is best accomplished through prevention of respiratory failure. In

addition, patients require careful monitoring of all electrolyte disordersnamely,
hypokalemia and hypomagnesemiaand of drug therapy (in particular, digoxin therapy).
Emergency department care

Emergency department care for MAT involves simultaneous assessment and treatment.
Rapidly assess and stabilize the airway, breathing, and circulation (ABCs) while providing
simultaneous treatment. An upright sitting position usually is most appropriate. Establish
cardiac monitoring, blood pressure monitoring, and pulse oximetry. Obtain IV access with a
large-bore catheter and infuse isotonic sodium chloride solution at a to-keep-open (TKO)
rate.
Administer oxygen to maintain the saturation at greater than 90%. However, avoid excessive
oxygen in patients with known significant COPD; this will prevent the theoretical problem of
removing the hypoxic drive for ventilation. The need for tracheal intubation is dictated by the
standard clinical indications.
Assess for and treat the underlying cardiopulmonary process, theophylline toxicity, or
metabolic abnormality. Bronchodilators and oxygen should be administered for treatment of
decompensated COPD; activated charcoal and/or charcoal hemoperfusion is the therapy for
theophylline toxicity.
Antiarrhythmics are usually not indicated for treatment of MAT, and specific antiarrhythmic
therapy historically has not demonstrated great efficacy in this setting. Nevertheless, several
small reports describe effectiveness with the use of magnesium sulfate (with concomitant
correction of hypokalemia), verapamil, and some beta blockers.
Calcium channel blockers are typically used as the first line of treatment. However, some
authors consider magnesium sulfate to be the drug of choice.
Most patients with MAT require hospital admission to further manage their underlying
cardiopulmonary diseases. These patients frequently are admitted to a monitored bed;
however, the clinical scenario and the hemodynamic stability of the patient dictate
disposition. For patients with theophylline toxicity, consider transfer to a hospital with
hemoperfusion capabilities.
Very rarely, in patients with persistent and refractory MAT, AV junctional radiofrequency
ablation and permanent pacemaker implantation should be considered. This approach can
provide symptomatic and hemodynamic improvement and prevent the development of
tachycardia-mediated cardiomyopathy.[12]
Magnesium sulfate

When magnesium sulfate is administered to correct hypokalemia, most patients convert to

normal sinus rhythm. In a small number of patients with normal potassium levels, high-dose
magnesium causes a significant decrease in the patient's heart rate and conversion to normal
sinus rhythm. The dosage is 2 g IV over 1 minute, followed by 2 g/h infusion over 5 hours.[13,
14, 15, 16, 17]

Beta blockers
Metoprolol has been used to lower the ventricular rate. Treatment with beta blockers converts
more patients to a normal sinus rhythm than does treatment with verapamil. Oral and IV
dosage forms have been used. The oral dosage is 25 mg every 6 hours until the desired effects
are obtained. IV bolus dosing has been administered in dosages as high as 15 mg over 10
minutes.[13, 18, 19, 20, 21]
Although no controlled studies have evaluated the use of short-acting beta blockers in the
treatment of MAT, esmolol can also be used to control the ventricular rate as an IV infusion.
It has a very short half-life and can be terminated quickly in the event of an adverse reaction.
The use of beta blockers is limited by transient hypotension and by bronchospastic adverse
effects (since lung disease is commonly associated with MAT).
Calcium channel blockers
Diltiazem[22] and verapamil[13, 18, 23, 24, 25, 26] decrease atrial activity and slow AV nodal
conduction, thereby decreasing ventricular rate, but they do not return all patients to normal
sinus rhythm. Transient hypotension is the most common adverse effect, which may often be
avoided by pretreating the patient with 1 g of IV calcium gluconate (10 mL of 10% calcium
gluconate).
Diltiazem may be given in a 20-45 mg IV bolus and then as a 10-25 mg/h continuous
infusion. Verapamil may worsen hypoxemia by negating the hypoxic pulmonary
vasoconstriction in underventilated alveoli; this is usually not clinically significant.
Antiarrhythmics
Oral and IV amiodarone (300 mg orally 3 times a day or 450-1500 mg IV over 2-24 h) have
been reported to convert MAT to normal sinus rhythm.[27, 28] Investigators found the success
rate to be 40% at 3 days with oral dosing and 75% on day 1 with IV dosing; however, the
drug was evaluated in a very small number of patients.
Prophylactic use of amiodarone has proved to be successful in preventing MAT after
coronary artery surgery in patients with COPD.[29] Case reports have also supported the use of
ibutilide[30] and flecainide[31] for cardioversion.
Digoxin and cardioversion

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

Radiofrequency catheter ablation can cure macroreentrant and focal forms of atrial
tachycardia and has become a widely used treatment option for symptomatic, medically
refractory cases.[8, 9] The success rates are not as high as those for AV nodal reentrant
tachycardia or AV reentrant tachycardia using an accessory pathway but they are still high,
ranging from 77-100% in various published series.
After activation mapping, the origin of the tachycardia can be localized. Focal application of
radiofrequency energy to the site via an ablation catheter results in termination of the
tachycardia. The ACC/AHA/ESC guideline cites an 86% success rate and an 8% recurrence
rate in pooled data from 514 patients who had catheter ablation for focal atrial tachycardia.
(See the image below.)[11]

Intracardiac tracings showing atrial tachycardia

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

Focal atrial tachycardia originating from the pulmonary veins has been associated with atrial
fibrillation. Radiofrequency ablation abolishing the focal triggering activity within the
orifices of the pulmonary vein can be curative in some patients with atrial fibrillation from
this mechanism.
Reentrant atrial tachycardia

Of note, complex ablation procedures primarily for atrial fibrillation that isolate pulmonary
veins or make circumferential left atrial ablation lines have been associated with new
reentrant atrial tachycardias or left-sided atypical atrial flutter. These tachycardias usually
require a further ablation procedure.
Reentrant atrial tachycardias in patients with repaired congenital heart disease may involve
pathways resulting from anatomic obstacles created by the surgical incisions. Knowledge of
the specific anatomic approach used in the repair can guide subsequent mapping and ablation.
Go to Catheter Ablation for more complete information on this topic.
Congenital heart disease

For patients with complex congenital heart disease, surgical ablation may occasionally be
useful. However, this procedure has generally been supplanted by radiofrequency ablation.
At surgery, particularly for congenital heart disease and particularly with complex operations,
such as the Fontan procedure, incisions should be situated or extended to lines of natural
conduction block. This will reduce the risk of subsequent incisional or scar-related reentrant
atrial tachycardias.
Consultations

Consultation with a cardiac electrophysiologist or cardiologist is recommended for all

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

The goals of pharmacotherapy are to reduce morbidity and to prevent recurrences and
complications. Consider using antiarrhythmic agents when the arrhythmia is causing
symptoms and does not respond to correction or treatment of underlying diseases. A calcium
channel blocker or beta blocker also may be required as well, in combination therapy.
Calcium channel blockers are especially effective in atrial tachycardia with triggered activity
as the underlying mechanism. Beta blockers can reduce the frequency and severity of atrial
tachycardia episodes by controlling ventricular response.
Beta Blockers, Intrinsic Sympathomimetic
Class Summary

Beta blockers are effective for reducing the frequency and severity of episodes via control of
the ventricular response during tachycardia and by reduction of frequency in a subgroup of

patients for whom tachycardia is sensitive to catecholamine. Beta blockers that have intrinsic
sympathomimetic activity are capable of demonstrating low-level agonist activity at a beta
receptor while also acting as an antagonist.
View full drug information
Acebutolol (Sectral)

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, Beta-1 Selective
Class Summary

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

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.
View full drug information
Esmolol (Brevibloc)

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.
View full drug information
Metoprolol (Lopressor)

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, Nonselective
Class Summary

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

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.
Antidysrhythmics, III
Class Summary

Many class III antidysrhythmic agents have been shown to be effective in maintaining sinus
rhythm after conversion from atrial tachycardia.
View full drug information
Amiodarone (Cordarone, Pacerone, Nexterone)

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.
View full drug information
Sotalol (Betapace, Betapace AF, Sorine)

This class III antiarrhythmic agent blocks K+ channels, prolongs action potential duration,
and lengthens the QT interval. It is a noncardiac-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.
View full drug information
Dofetilide (Tikosyn)

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 betaadrenergic 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.
View full drug information
Ibutilide (Corvert)

Ibutilide can terminate some atria tachycardias. Ibutilide works by increasing the action
potential duration and, thereby, changing atrial cycle-length variability.
Antidysrhythmics, Ia
Class Summary

These drugs have been tried in patients with refractory recurrent atrial tachycardia and
disabling symptoms in whom beta blockers or calcium channel blockers were unsuccessful.
These drugs prolong the atrial refractoriness and slow the conduction velocity, thereby
disrupting the reentrant circuit. They also suppress the atrial premature depolarizations that
commonly initiate the tachycardia.
Class Ia drugs, which are proarrhythmic, are effective only approximately 50% of the time.
Therefore, the use of these agents is limited. In particular, quinidine has been replaced with
more effective and safer antiarrhythmic agents and nonpharmacologic therapies.
View full drug information
Procainamide (Procanbid, Pronestyl)

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 WolffParkinson-White syndrome.
Antidysrhythmics, Ic
Class Summary

These agents have been used in patients with atrial tachycardia and disabling symptoms in
whom beta blockers or calcium channel blockers were unsuccessful. Recommended use is
with a beta blocker or calcium channel blocker.
View full drug information
Flecainide (Tambocor)

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.
View full drug information
Propafenone (Rythmol)

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.
Calcium Channel Blockers
Class Summary

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

View full drug information

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

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.
View full drug information
Verapamil (Calan, Calan SR, Covera HS, Verelan)

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.
Antidysrhythmics, V
Class Summary

Digoxin and adenosine alter the electrophysiologic mechanisms responsible for arrhythmia.
Digitalis in toxic doses can cause atrial tachycardia. In therapeutic doses, digitalis may be
useful in some focal atrial tachycardias. It should be considered if beta blockers are
contraindicated or if beta blockers and calcium channel blockers are unsuccessful in
controlling the arrhythmia medically.
Adenosine is an ultrashort-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.
View full drug information
Digoxin (Lanoxicaps, Lanoxin)

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).
View full drug information
Magnesium sulfate

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.
View full drug information
Adenosine (Adenocard, Adenoscan)

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.