Practice EssentialsAtrial 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 tachycardiaPatterns 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 symptomsManifestations 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.DiagnosisWorkup 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 tachycardiaThe 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 suspectedThe 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.ManagementThe 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 drugsNonpharmacologic 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 diseaseMultifocal atrial tachycardiaTreatment 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 AntiarrhythmicsIn 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 LibraryThis 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. BackgroundAtrial 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 bpmAs 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 methodsA 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 treatmentA 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] AnatomyAtrial 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 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[1] : Extensive myocardial fibrosis Myocyte hypertrophy Endocardial fibrosis Mononuclear cell infiltration Mesenchymal cell proliferation Islets of fatty tissue Thinning Blebs PathophysiologySeveral 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 automaticityAutomatic 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 activityTriggered 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 tachycardiasPulmonary 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 tachycardiaIntra-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 tachycardiaBased 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. EtiologyAtrial 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 PneumoniaUnusual forms of atrial tachycardias can be seen in patients with an infiltrative process involving the pericardium and, by extension, the atrial wall. EpidemiologyAtrial 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. PrognosisIn 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 tachycardiaMAT 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 emboliPatient EducationFor 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. HistoryFocal 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 diseaseUnderlying disorders in multifocal atrial tachycardiaIn 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 ExaminationThe 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 ConsiderationsThe 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 tachycardiaTo 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 tachycardiaDiagnosis 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 DifferentialsAtrial FibrillationAtrial FlutterAtrioventricular Nodal Reentry TachycardiaChronic AnemiaParoxysmal Supraventricular TachycardiaSympathomimetic ToxicityThyroid Hormone ToxicityTorsade de PointesVentricular TachycardiaWolff-Parkinson-White SyndromeApproach ConsiderationsThe 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. CardioversionFor 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 TreatmentAtrial 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 antiarrhythmicsFor 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 antiarrhythmicsClass 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 IntoxicationAtrial 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 TachycardiaIn 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 careEmergency 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 sulfateWhen 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 blockersMetoprolol 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 blockersDiltiazem[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. AntiarrhythmicsOral 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 cardioversionNeither 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 AblationRadiofrequency 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 fibrillationFocal 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 tachycardiaOf 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 diseaseFor 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. ConsultationsConsultation 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 SummaryThe 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 SympathomimeticClass SummaryBeta 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 informationAcebutolol (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 SelectiveClass SummaryBeta 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 informationAtenolol (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 informationEsmolol (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 informationMetoprolol (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, NonselectiveClass SummaryBeta 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 informationPropranolol (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, IIIClass SummaryMany class III antidysrhythmic agents have been shown to be effective in maintaining sinus rhythm after conversion from atrial tachycardia. View full drug informationAmiodarone (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 informationSotalol (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 informationDofetilide (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 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. View full drug informationIbutilide (Corvert)Ibutilide can terminate some atria tachycardias. Ibutilide works by increasing the action potential duration and, thereby, changing atrial cycle-length variability. Antidysrhythmics, IaClass SummaryThese 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 informationProcainamide (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 Wolff-Parkinson-White syndrome. Antidysrhythmics, IcClass SummaryThese 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 informationFlecainide (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 informationPropafenone (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 BlockersClass SummaryVia 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 informationDiltiazem (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 informationVerapamil (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, VClass SummaryDigoxin 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 informationDigoxin (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 informationMagnesium sulfateMagnesium 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 informationAdenosine (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.