Common Types of Supraventricular Tachycardia Diagnosis and Management PDF

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University of Michigan Health System

2023

Munima Nasir, Ashley Sturts, Adam Sturts

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supraventricular tachycardia diagnosis management cardiology

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This article discusses common types of supraventricular tachycardia (SVT). It provides information on the diagnosis, management, and causes of paroxysmal SVT. It also covers different types of SVT, including atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, and atrial tachycardia, focusing on their characteristics and potential triggers.

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Common Types of Supraventricular Tachycardia:​Diagnosis and Management Munima Nasir, MD, Milton S. Hershey Medical Center, Hershey, Pennsylvania Ashley Sturts, DO, Pennsylvania State University, Penn State Health, State College, Pennsylvania Adam Sturts, DO, Milton S. Hershey Medical Center, Hershey...

Common Types of Supraventricular Tachycardia:​Diagnosis and Management Munima Nasir, MD, Milton S. Hershey Medical Center, Hershey, Pennsylvania Ashley Sturts, DO, Pennsylvania State University, Penn State Health, State College, Pennsylvania Adam Sturts, DO, Milton S. Hershey Medical Center, Hershey, Pennsylvania Supraventricular tachycardia (SVT) is an abnormal rapid cardiac rhythm that involves atrial or atrioventricular node tissue from the His bundle or above. Paroxysmal SVT, a subset of supraventricular dysrhythmias, has three common types:​atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, and atrial tachycardia. Presenting symptoms may include altered consciousness, chest pressure or discomfort, dyspnea, fatigue, lightheadedness, or palpitations. Diagnostic evaluation may be performed in the outpatient setting and includes a comprehensive history and physical examination, electrocardiography, and laboratory workup. Extended cardiac monitoring with a Holter monitor or event recorder may be needed to confirm the diagnosis. Acute management of paroxysmal SVT is similar across the various types and is best completed in the emergency department or hospital setting. In patients who are hemodynamically unstable, synchronized cardioversion is first-line management. In those who are hemodynamically stable, vagal maneuvers are first-line management, followed by stepwise medication management if ineffective. Beta blockers and/or calcium channel blockers may be used acutely or for long-term suppressive therapy. When evaluating patients for paroxysmal SVTs, clinicians should have a low threshold for referral to a cardiologist for electrophysiologic study and appropriate intervention such as ablation. Clinicians should use a patient-centered approach when formulating a long-term management plan for atrioventricular nodal reentrant tachycardia. Catheter ablation has a high success rate and is recommended as the first-line method for long-term management of recurrent, symptomatic paroxysmal SVT, including Wolff-Parkinson-White syndrome. (Am Fam Physician. 2023;​107(6):​631-641. Copyright © 2023 American Academy of Family Physicians.) Supraventricular tachycardia (SVT) refers to tachy- cardia (i.e., atrial or ventricular rate higher than 100 beats per minute at rest) that involves tissue from the His bundle or above.1 Classically, the term paroxysmal SVT includes most tachycardias, except ventricular tachycardia and atrial fibrillation, with paroxysmal SVT comprising a subset that is characterized by a regular tachycardia having abrupt onset and termination. The prevalence of paroxysmal SVT is 2.29 per 1,000 people in the general population.1,2 Although paroxysmal SVT is a common reason for patients of all ages to visit a physician or emergency department, middle-aged women are most often affected, accounting for an estimated 62% of all cases.2,3 Paroxysmal SVT is classified based on the location of the reentrant circuit. The most common types are atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, and atrial tachycardia, which are illustrated in CME This clinical content conforms to AAFP criteria for CME. See CME Quiz on page 575. Author disclosure:​ No relevant financial relationships. Patient information:​A handout on this topic is available with the online version of this article. Figure 1.4 A high index of suspicion is needed in the primary care setting because paroxysmal SVT commonly occurs without underlying cardiac disease. Causes of Paroxysmal SVT Paroxysmal SVT is usually not associated with structural heart disease, especially in young people. Cardiac comorbidities such as coronary artery disease, congestive heart failure, cardiomyopathy, and valvular heart disease are more common in patients with paroxysmal SVT who are older than 50 years.2 Uncommon cardiac causes include congenital/ structural heart disease;​myocardial scarring from diseases such as sarcoidosis and tuberculosis;​prior atrial surgeries;​primary electrical disorders such as long QT syndrome;​and presence of accessory pathways, including familial preexcitation syndrome.2 Reentrant tachycardias can also be triggered by hyperthyroidism, electrolyte disturbances, excessive intake of caffeine or alcohol, and use of certain medications or recreational drugs. Possible triggers are listed in Table 1. Types of Paroxysmal SVT ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA The most common type of paroxysmal SVT is atrioventricular nodal reentrant tachycardia, accounting for about two-thirds American Academy of American Family Physicians. ForPhysician the private, 631 nonFamily commercial use of one individual user of the website. All other rights reserved. Contact [email protected] for copyright questions and/or permission requests. Downloaded from the 107, American Family Copyright June 2023 ◆ Volume Number 6 Physician website at www.aafp.org/afp. www.aafp.org/afp  © 2023 Downloaded for Anonymous User (n/a) at Maccabi Healthcare Services from ClinicalKey.com by Elsevier on July 16, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved. SUPRAVENTRICULAR TACHYCARDIA of all cases.5 This type can present at any age but is more common in young adults and in women.5,6 Atrioventricular nodal reentrant tachycardia is caused by a reentry circuit formed by the atrioventricular node and perinodal atrial tissue.7 It typically involves dual electrical pathways, one slow and one fast. An episode of typical atrioventricular nodal reentrant tachycardia may be triggered by a critically timed premature atrial contraction that leads to retrograde conduction up the FIGURE 1A Lead II Sinoatrial node R PR interval T P Q S Atrioventricular node Right and left bundle branches ©David Klemm In normal sinus rhythm, impulses from the sinoatrial node travel through the conduction system and are delayed by the atrioventricular node, creating the standard PR interval. Illustration by Dave Klemm Adapted with permission from Colucci RA, Silver MJ, Shubrook J. Common types of supraventricular tachycardia:​diagnosis and management. Am Fam Physician. 2010;​82(8):​944. FIGURE 1B Lead II Lead V1 Pseudo–R wave (if visible) Retrograde impulse: Fast pathway Pseudo–S wave (if visible) Slow pathway Atrioventricular nodal reentry ©David Klemm Atrioventricular nodal reentrant tachycardia is the most common type of paroxysmal supraventricular tachycardia. In this type, the standard conduction through the atrioventricular node pairs with a fast retrograde conduction through the atrioventricular node. Most often, P waves are not seen, but occasionally a retrograde P wave may be visible early after the QRS complex as a pseudo–S wave in lead II or a pseudo–R wave in lead V1 . Illustration by Dave Klemm Adapted with permission from Colucci RA, Silver MJ, Shubrook J. Common types of supraventricular tachycardia:​diagnosis and management. Am Fam Physician. 2010;​82(8):​944. 632 American Family Physician www.aafp.org/afp Volume 107, Number 6 Downloaded for Anonymous User (n/a) at Maccabi Healthcare Services from ClinicalKey.com by Elsevier on July 16, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved. ◆ June 2023 SUPRAVENTRICULAR TACHYCARDIA fast pathway from the atrioventricular node to the atria. The retrograde impulse depolarizes the atria forming a repetitive, self-propagating circuit with a rapid and regular ventricular response. Because retrograde atrial activation and anterograde ventricular activation occur almost simultaneously, P waves are usually hidden on electrocardiography (ECG). However, if there is relatively delayed retrograde conduction, P waves may be seen as part of the terminal QRS complex (retrograde P waves) forming a pseudo–R deflection in lead V1 and a pseudo–S wave in the inferior leads. FIGURE 1C Accessory pathway Lead II P wave (if visible) Lead V1 P wave (if visible) ©David Klemm In atrioventricular reentrant tachycardia, there is an accessory pathway that distributes ventricular signals back to the atria. If visible, P waves in atrioventricular reentrant tachycardia are most often after the QRS complex. Illustration by Dave Klemm Adapted with permission from Colucci RA, Silver MJ, Shubrook J. Common types of supraventricular tachycardia:​diagnosis and management. Am Fam Physician. 2010;​82(8):​944. FIGURE 1D Abnormal origin Lead II Lead V1 ©David Klemm In atrial tachycardia, a focus within the atria provides a rapid signal that overwhelms the signal from the sinoatrial node. Atrial tachycardia typically produces normal PR intervals because the delay from the atrioventricular node is not affected. The morphology and axis of the P wave depend on the location of the atrial focus. Illustration by Dave Klemm Adapted with permission from Colucci RA, Silver MJ, Shubrook J. Common types of supraventricular tachycardia:​diagnosis and management. Am Fam Physician. 2010;​82(8):​944. June 2023 ◆ Volume 107, Number 6 www.aafp.org/afp American Family Physician 633 Downloaded for Anonymous User (n/a) at Maccabi Healthcare Services from ClinicalKey.com by Elsevier on July 16, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved. SUPRAVENTRICULAR TACHYCARDIA orthodromic type, the impulse is conducted in the anterograde direction through the natural conduction system, depolarizing the ventricles. After Triggers for Supraventricular Tachycardia conduction through the ventricles, the impulse Alcohol Drugs (continued) Electrolyte travels in the retrograde direction through the abnormalities Anemia Corticosteroids accessory pathway to the atria, where depolarizaExercise tion occurs and a repetitive, self-propagating cirCaffeine Decongestants Fever (infection, cuit with a rapid and regular ventricular response Drugs Inotropes sepsis) is formed. ECG typically shows a ventricular rate Antipsychotics Loop diuretics Hyperthyroidism ranging from 150 to 250 beats per minute, a narBronchodilators Stimulants Hypovolemia row QRS complex, inverted P waves, and an RP Cannabinoids Vasodilators interval that is usually less than one-half of the Catecholamines tachycardia RR interval. In the antidromic form of atrioventricular reentrant tachycardia, premature atrial beats are blocked by the atriovenATRIOVENTRICULAR REENTRANT TACHYCARDIA tricular node but have anterograde conduction through the Atrioventricular reentrant tachycardia is the second most accessory pathway causing ventricular depolarization. After common type of paroxysmal SVT overall (approximately conduction through the ventricles, the impulse travels in 30% of all cases) and the most common type in children.8 the retrograde direction through the His bundle and atrioThis type is a reentrant circuit tachycardia mediated by an ventricular node to the atria, completing the reentrant loop. accessory pathway. The atrioventricular accessory pathway ECG shows a ventricular rate ranging from 150 to 200 beats consists of shared proximal (atrial) and distal (ventricular) per minute, a wide QRS complex, inverted P waves, an RP tissues that form a reentrant circuit with the normal atrio- interval that is usually more than one-half of the tachycardia ventricular conduction system when triggered by a prema- RR interval, and a short PR interval. ture atrial or ventricular beat. The accessory pathway may conduct an electrical impulse in the anterograde or retro- ATRIAL TACHYCARDIA grade direction. Pathologic anterograde conduction through Atrial tachycardia is the least common type of paroxysmal the accessory pathway that reaches the ventricle before the SVT, accounting for about 10% of cases.2 It is often found impulse through the atrioventricular node causes ventricu- in otherwise healthy young adults. Focal atrial tachycardia lar preexcitation. A delta wave (slurring of the QRS complex) originates from a single site outside the sinus node within is present on ECG in most cases of anterograde accessory the atria and may be caused by a focal area of increased tracts (Figure 2 3). The combination of a delta wave, short PR interval, proFIGURE 2 longed QRS complex, and arrhythmias involving anterograde conduction via the accessory pathway is called Wolff-Parkinson-White syndrome. The most common arrhythmias in patients with this syndrome are anterograde reciprocating tachycardia (approximately 80% of cases) and atrial fibrillation (20% to 30% of cases).9 The most serious manifestation of Wolff-Parkinson-White syndrome is sudden cardiac death secondary to atrial fibrillation with preexcitation that conducts rapidly to the ventricle over the accessory pathway resulting in ventricular fibrillation. Of Preexcitation with a shortened PR interval and a note, concealed accessory pathways conduct only in the retslurred upstroke of the QRS complex (delta wave). The rograde direction and therefore do not produce delta waves. presence of delta waves and antidromic tachycardia Atrioventricular reentrant tachycardia can occur without indicates Wolff-Parkinson-White syndrome, a form of the Wolff-Parkinson-White syndrome pattern when the atrioventricular reentrant tachycardia. accessory pathway is retrograde and/or does not create Adapted with permission from Helton MR. Diagnosis and managea delta wave. ment of common types of supraventricular tachycardia. Am Fam Physician. 2015;​92(9):​794. Atrioventricular reentrant tachycardia may have an orthodromic or antidromic pattern of conduction. In the TABLE 1 634 American Family Physician www.aafp.org/afp Volume 107, Number 6 Downloaded for Anonymous User (n/a) at Maccabi Healthcare Services from ClinicalKey.com by Elsevier on July 16, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved. ◆ June 2023 SUPRAVENTRICULAR TACHYCARDIA automaticity or microreentrant circuits within the atrial tissue. Focal atrial tachycardia typically presents as a regular atrial rhythm (rate greater than 100 beats per minute) TABLE 2 Possible Symptoms of Supraventricular Tachycardia Altered consciousness* Fatigue Angina* Lightheadedness Chest pressure, tightness, or discomfort* Nausea Diaphoresis* Polyuria† Dizziness Syncope or presyncope* Palpitations Dyspnea *—Raises concern for clinical instability. †—May be due to atrial natriuretic peptide activity induced by atrial stretch. with a 1:​1 ratio of atrioventricular conduction, meaning there is one atrial beat for every one ventricular beat. Atrial tachycardia due to increased automaticity often involves a warm up phenomenon in which the atrial rate abruptly increases over the first five to 10 seconds of the episode, and it may occur in repetitive, short bursts.10 In contrast, atrial tachycardia due to microreentry typically starts and stops abruptly. These characteristics may be detectable with ambulatory monitoring and can help to distinguish atrial tachycardia from sinus tachycardia, which requires a longer time to speed up and slow down. P wave morphology may differ from that in the patient’s baseline ECG or may appear normal depending on the site of origin. Leads V1 and II are most useful in assessing P wave morphology. Typically, the PR interval is normal, and the RP interval is longer than the PR interval. Evaluation HISTORY The clinical manifestations of paroxysmal SVT vary, and many patients are asymptomatic. Key considerations in the patient’s history include a family history of the conTABLE 3 dition;​the onset, duration, and frequency of symptoms;​ Differential Diagnosis of Narrow Complex Tachycardia a perception of palpitations;​ Diagnosis Rhythm Origin and triggers and relieving factors.11 A variety of Atrial fibrillation Irregularly irregular Atrial tissue symptoms have been assoAtrial flutter Regularly irregular Atrial tissue ciated with paroxysmal SVT (Table 211,12) and may proAtrioventricular nodal reentrant Regular Perinodal atrial tissue (dual atriovide the first diagnostic clue. tachycardia ventricular nodal pathways) Table 3 includes the differAtrioventricular reentrant Regular Accessory atrioventricular conential diagnosis for narrow tachycardia duction pathway complex tachycardia. In Focal atrial tachycardia Regular Atrial tissue some patients, particularly young women, paroxysmal Inappropriate sinus tachycardia Regular Atrial tissue (sinoatrial node) SVT may be misdiagnosed Intra-atrial reentrant tachycardia Regular Atrial tissue as panic or anxiety attacks leading to a delay in diagnoJunctional ectopic tachycardia Regular Atrioventricular node/His bundle sis. An underlying psychiMultifocal atrial tachycardia Irregularly irregular Atrial tissue atric history has also been associated with a delay in Nonparoxysmal junctional Regular Atrioventricular node/His bundle tachycardia appropriate diagnosis of paroxysmal SVT.4,13 Information from references 11 and 12. Postural orthostatic tachycardia syndrome Regular Atrial tissue (sinoatrial node) Sinoatrial nodal reentrant tachycardia Regular Atrial tissue (sinoatrial node) DIAGNOSTIC EVALUATION Sinus tachycardia Regular Atrial tissue (sinoatrial node) The in-office evaluation of paroxysmal SVT should include a physical June 2023 ◆ Volume 107, Number 6 www.aafp.org/afp American Family Physician 635 Downloaded for Anonymous User (n/a) at Maccabi Healthcare Services from ClinicalKey.com by Elsevier on July 16, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved. SUPRAVENTRICULAR TACHYCARDIA TABLE 4 Evaluation in Patients With Possible Paroxysmal SVT System or test Possible findings Significance Focused physical examination Cardiovascular Murmur, friction rub, third heart sound Valvular heart disease, pericarditis, heart failure Respiratory Crackles Heart failure Endocrine Enlarged or tender thyroid gland Hyperthyroidism, thyroiditis In-office testing Vital signs Hemodynamic instability, fever Induce tachycardia Orthostatic blood pressure Autonomic or dehydration issues Induce tachycardia Electrocardiography Preexcitation Wolff-Parkinson-White syndrome Wide vs. narrow QRS complex Type of paroxysmal SVT (Figure 1) vs. ventricular tachycardia Q wave Ischemia Other findings Type of paroxysmal SVT (Figure 1) Laboratory testing Complete blood count Anemia, infection All can cause tachyarrhythmia Thyroid-stimulating hormone level Hyperthyroidism Basic metabolic panel Electrolyte abnormality B-type natriuretic peptide level Congestive heart failure Cardiac enzyme levels Myocardial infarction, myocardial ischemia Additional diagnostic testing Chest radiography Cardiomegaly Congestive heart failure, cardiomyopathy Transthoracic echocardiography Structural aberrations Ambulatory electrocardiography monitoring Aberrant rhythm, frequency, duration Identify structural abnormality, baseline assessment Type of tachyarrhythmia SVT = supraventricular tachycardia. Adapted with permission from Colucci RA, Silver MJ, Shubrook J. Common types of supraventricular tachycardia. Am Fam Physician. 2010;​82(8):​946. examination and ECG (Table 4 4), ideally completed when tachycardia is occurring.11 Additional cardiac testing can be performed if tachycardia is not occurring at the time of presentation, including transthoracic echocardiography, Holter monitor testing, wireless extended cardiac monitoring, or the rare use of an implantable loop recorder. The laboratory workup should include a complete blood count to evaluate for anemia or infection, a basic metabolic panel to evaluate for electrolyte abnormality, and thyroid function testing.11 Additional workup based on the patient’s cardiac risk factors can include stress testing for cardiac ischemia or electrophysiologic studies.11 Patients found to have paroxysmal SVT should be referred to a cardiologist for confirmatory testing and treatment. 636 American Family Physician Management SHORT-TERM OR URGENT MANAGEMENT The first step in acute management of paroxysmal SVT is to determine whether it is narrow or wide QRS complex tachycardia. Acute management of narrow complex paroxysmal SVT, particularly if symptomatic, is similar across the subtypes and best initiated immediately in an emergency department or hospital setting. Synchronized cardioversion is the first-line emergent treatment in patients who are hemodynamically unstable.11 If this is unsuccessful, use of Advanced Cardiovascular Life Support pathways should be considered. Vagal maneuvers (Table 514) are first-line management for those who are hemodynamically stable, with an estimated effectiveness rate of 19% to 54%.1,11,15,16 www.aafp.org/afp Volume 107, Number 6 Downloaded for Anonymous User (n/a) at Maccabi Healthcare Services from ClinicalKey.com by Elsevier on July 16, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved. ◆ June 2023 TABLE 5 Vagal Maneuvers Carotid sinus massage (5 to 10 seconds) Diving reflex (up to 30 seconds):​patient submerges face in cold water or bags of ice are placed on the nose and forehead Valsalva maneuvers (10 to 15 seconds):​patient bears down against a closed glottis or blows through a straw or 10-mL syringe Information from reference 14. If vagal maneuvers are unsuccessful, a stepwise approach to medication management is recommended (Figure 311 and Table 6 3,11,17,18). If vagal maneuvers fail, intravenous adenosine may be used in hemodynamically stable patients as a therapeutic agent in narrow complex tachycardia or as a diagnostic and therapeutic agent in undifferentiated wide complex tachycardia without preexcitation.1,11 Additionally, adenosine TABLE 6 Options for Medication Management of Paroxysmal SVT in Adults Medication Class Characteristics Action/uses Dosage Adverse effects Short-term Adenosine IIe Endogenous purine nucleotide, depresses nodal conduction Terminates SVT, therapeutic and diagnostic in wide complex tachycardia 6 mg IV, rapid push;​ can repeat with 12 mg if needed Vasodilation leading to facial flushing, hypotension, chest discomfort, dyspnea Amiodarone IIIa Potassium channel blocker, prolongs repolarization May be used for a wide complex tachycardia that does not respond to adenosine Loading dose:​150 mg IV over 10 minutes;​can repeat, then 1 mg per minute for 6 hours, then 0.5 mg per minute for 18 hours;​continue for a total loading dose of up to 10 g Toxicity with long-term use Diltiazem, verapamil IVa Nondihydropyridine calcium channel blocker, slows atrioventricular nodal conduction, negative inotrope Decreases heart rate, terminates SVT Diltiazem:​0.25 mg per kg IV over 2 minutes;​after 15 minutes, can repeat with 0.35 mg per kg dose Bradycardia, hypotension, conduction disturbance, cutaneous hypersensitivity reactions, use with caution in patients with heart failure Beta blocker Decreases heart rate, terminates SVT Esmolol, metoprolol IIa Verapamil:​5 to 10 mg (0.075 to 0.15 mg per kg) IV over 2 minutes;​repeat with 10 mg (0.15 mg per kg) at 30 minutes after first dose Esmolol:​loading dose of 500 mcg per kg IV over 1 minute, then 50 mcg per kg per minute Bradycardia, hypotension (esmolol) Metoprolol:​5 mg IV over 1 to 2 minutes;​repeat every 5 minutes as needed to a maximum dose of 15 mg Procainamide Ia Sodium channel blocker, prolongs action potential duration Useful for wide complex tachycardia in hemodynamically stable patients Loading dose:​10 to 17 mg per kg IV at a rate of 20 to 50 mg per minute Maintenance infusion:​1 to 4 mg IV per minute Hypotension;​avoid in patients with congestive heart failure or prolonged QT interval continues IV = intravenously;​SVT = supraventricular tachycardia. June 2023 ◆ Volume 107, Number 6 www.aafp.org/afp American Family Physician 637 Downloaded for Anonymous User (n/a) at Maccabi Healthcare Services from ClinicalKey.com by Elsevier on July 16, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved. SUPRAVENTRICULAR TACHYCARDIA TABLE 6 (continued) Options for Medication Management of Paroxysmal SVT in Adults Medication Class Short-term (continued) Ibutilide IIIa Long-term Diltiazem, verapamil IVa Characteristics Action/uses Dosage Adverse effects Potassium channel blocker, prolongs repolarization Atrial fibrillation/ flutter ≥ 60 kg:​1 mg IV over 10 minutes;​may be repeated once;​discontinue as soon as arrhythmia terminates Avoid in patients with prolonged QT interval, proarrhythmic effects Calcium channel blocker Prevents SVT Diltiazem:​240 to 360 mg orally per day Bradycardia, conduction disturbance, cutaneous hypersensitivity reactions, use with caution in patients with heart failure Verapamil:​240 to 480 mg orally per day Flecainide Ic Sodium channel blocker, slows conduction Prevents SVT 50 mg orally every 12 hours;​increase by 50 mg twice daily at 4-day intervals to a maximum of 300 mg per day Proarrhythmic effects, conduction disturbance, dizziness, visual disturbance, worsening of heart failure, use with caution among patients with structural or ischemic heart disease Metoprolol IIa Beta blocker Decreases heart rate Immediate release (metoprolol tartrate):​25 to 200 mg orally twice per day Bradycardia, sinus pause, atrioventricular block, bronchospasm, fatigue, hypoglycemia, sexual dysfunction Extended release (metoprolol succinate):​50 to 400 mg orally per day Propafenone (Rythmol) Ic Sodium channel blocker, slows conduction Prevents SVT Immediate release:​150 mg orally every 8 hours;​can be increased every 3 to 4 days to 225 to 300 mg every 8 hours Extended release:​225 mg orally every 12 hours;​can be increased every 5 days to a maximum of 425 mg every 12 hours Dizziness, nausea, unusual taste, proarrhythmic effects, hypotension;​do not use in patients with ischemic or structural heart disease, wide QRS complex, or atrioventricular blocks IV = intravenously;​SVT = supraventricular tachycardia. Information from references 3, 11, 17, and 18. should not be used in patients having preexcitation (a shortened PR interval with or without a delta wave), and the clinician should proceed to next steps in management,19 as outlined in Figure 3.11 All wide complex tachycardias warrant caution and should be treated as ventricular tachycardia until proven otherwise;​medication management for paroxysmal SVT is potentially harmful if used in ventricular tachycardia.11,20 Brugada criteria (Table 7 3) can be used to distinguish 638 American Family Physician between paroxysmal SVT with aberrant conduction and ventricular tachycardia.1 If a wide QRS complex tachycardia is identified in hemodynamically stable hospitalized patients, intravenous procainamide can be used as a first-line treatment. It has been shown to be more effective at terminating tachycardia within 40 minutes of use compared with intravenous amiodarone and has fewer adverse cardiac effects.11 Alternatives for short-term management of antidromic atrioventricular reentrant tachycardia include www.aafp.org/afp Volume 107, Number 6 Downloaded for Anonymous User (n/a) at Maccabi Healthcare Services from ClinicalKey.com by Elsevier on July 16, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved. ◆ June 2023 SUPRAVENTRICULAR TACHYCARDIA FIGURE 3 TABLE 7 Brugada Criteria for Assessing Wide Complex Tachycardia Hemodynamic stability? No Yes Vagal maneuvers Synchronized cardioversion IV adenosine (skip if preexcitation is present) QRS complex tachycardia Narrow Wide (except antidromic atrioventricular reentrant tachycardia) Nondihydropyridine calcium channel blocker Beta blocker (esmolol, metoprolol) Findings on electrocardiography Criterion present? 1. R  S complex absent from all precordial leads Yes:​VT present 2. R  S complex present and R to S interval > 100 milliseconds in one precordial lead Yes:​VT present 3. Atrioventricular dissociation present Yes:​VT present 4. Morphologic criteria for VT present in precordial leads V1 to V2 and V6 Yes:​VT present No:​proceed to 2 No:​proceed to 3 No:​proceed to 4 No:​ supraventricular tachycardia with aberrant conduction is diagnosed by exclusion VT = ventricular tachycardia. IV procainamide IV amiodarone Note: If an intervention is unsuccessful, proceed to next step. If at any point patient becomes unstable or medication pathway fails, transition to immediate synchronized cardioversion. See Table 5 for vagal maneuvers and Table 6 for medication dosing and further details. IV = intravenous. Short-term management of paroxysmal supraventricular tachycardia. Adapted with permission from Brugada J, Katritsis DG, Arbelo E, et al.;​ESC Scientific Document Group. 2019 ESC guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC) [published correction appears in Eur Heart J. 2020;​41(44):​4258]. Eur Heart J. 2020;​41(5):​672. Adapted with permission from Helton MR. Diagnosis and management of common types of supraventricular tachycardia. Am Fam Physician. 2015;​92(9):​798. TABLE 8 Indications for Cardiology Referral High-risk occupation or activity (e.g., pilot, truck driver, heavy equipment operator, scuba diver, sky diver, rock climber) Known structural heart disease Preexcitation or delta wave Symptoms not controlled with current medication management Syncopal episodes intravenous ibutilide, oral flecainide, or oral propafenone (Rythmol).11 Ultimately, if intravenous medications fail, stable paroxysmal SVT should be treated the same as if it were unstable, using synchronized cardioversion. LONG-TERM MANAGEMENT When evaluating a patient with known or suspected paroxysmal SVT in the outpatient setting, there should be a low threshold for referral to a cardiologist for electrophysiologic study and appropriate intervention such as ablation (Table 83). Ablation is a safe, potentially curative procedure recommended in contemporary guidelines for recurrent, symptomatic paroxysmal SVT.1,11 Not all patients should June 2023 ◆ Volume 107, Number 6 Uncertainty about diagnosis Uncertainty about management, including consideration for ablation Wide QRS complex Adapted with permission from Helton MR. Diagnosis and management of common types of supraventricular tachycardia. Am Fam Physician. 2015;​92(9):​795. undergo electrophysiologic study and ablation, but all patients should know that there may be a curative option. Atrioventricular Nodal Reentrant Tachycardia. Clinicians should use a patient-centered approach when formulating a long-term management plan for atrioventricular nodal www.aafp.org/afp American Family Physician 639 Downloaded for Anonymous User (n/a) at Maccabi Healthcare Services from ClinicalKey.com by Elsevier on July 16, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved. SUPRAVENTRICULAR TACHYCARDIA SORT:​KEY RECOMMENDATIONS FOR PRACTICE Evidence rating Clinical recommendation Comments Vagal maneuvers are recommended to terminate SVT in hemodynamically stable patients.1,11,15,16 B Consensus guidelines from the ACC and ESC;​ meta-analysis evaluating a modified Valsalva maneuver;​Cochrane review with insufficient evidence If vagal maneuvers fail, intravenous adenosine may be used in hemodynamically stable patients as a therapeutic agent in narrow complex tachycardia or as a diagnostic and therapeutic agent in undifferentiated wide complex tachycardia without preexcitation.1,11 C Consensus guidelines from the ACC and ESC Brugada criteria can be used to distinguish between SVT with aberrant conduction and ventricular tachycardia.1 C Consensus guidelines from the ACC Catheter ablation is generally recommended for recurrent, symptomatic SVT.1,11 C Consensus guidelines from the ACC and ESC ACC = American College of Cardiology;​ESC = European Society of Cardiology;​SVT = supraventricular tachycardia. A = consistent, good-quality patient-oriented evidence;​B = inconsistent or limited-quality patient-oriented evidence;​C = consensus, diseaseoriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to https://​w ww.aafp. org/afpsort. reentrant tachycardia. In addition to considering patient preference, treatment decisions depend on symptom severity, frequency of the arrhythmia, medication tolerance, and comorbidity. Among patients with infrequent episodes of tachycardia and tolerable symptoms, it may be reasonable to defer ablation or long-term pharmacotherapy.11 About 50% of these patients will eventually become asymptomatic.21 Patients who decline ablation and pharmacotherapy should be educated on vagal maneuvers to terminate any recurrent arrhythmias, and treatment should be reconsidered at follow-up. Catheter ablation is considered first-line management for symptomatic, recurrent atrioventricular nodal reentrant tachycardia.11 Ongoing pharmacologic therapy may not be needed after the procedure. For patients who are not candidates for catheter ablation or prefer not to undergo the procedure, long-term suppressive pharmacotherapy with nondihydropyridine calcium channel blockers or beta blockers may be considered.11 There are limited data comparing the effectiveness of these agents;​therefore, choice of agent may be determined based on patient factors such as baseline heart rate, blood pressure, and comorbidity. In patients who cannot tolerate nondihydropyridine calcium channel blockers or beta blockers and do not want to pursue catheter ablation, antiarrhythmic drugs may be considered with the assistance of a cardiologist. Atrioventricular Reentrant Tachycardia. For symptomatic, recurrent atrioventricular reentrant tachycardia, catheter 640 American Family Physician ablation should be considered for first-line management.11 Patients with this finding should be referred to a cardiologist to discuss individual risks, benefits, and contraindications pertaining to the procedure. If ablation is not desirable or feasible in patients who have antidromic atrioventricular reentrant tachycardia without ischemic or structural heart disease, propafenone or flecainide may be considered for long-term treatment.11 In patients with orthodromic atrioventricular reentrant tachycardia, no signs of preexcitation on ECG, and no history of heart failure with reduced ejection fraction, beta blockers or nondihydropyridine calcium channel blockers may be considered.11 Patients with Wolff-Parkinson-White syndrome should be referred to a cardiologist for electrophysiologic study and possible ablation. In patients with asymptomatic preexcitation (a Wolff-Parkinson-White ECG pattern), cardiology referral can help with risk stratification, particularly in those who have high-risk occupations or are competitive athletes.11 Catheter ablation may be considered in asymptomatic patients with high-risk features identified on electrophysiologic testing.11 Focal Atrial Tachycardia. Similar to patients with the other types of paroxysmal SVTs, patients with focal atrial tachycardia who have infrequent, brief arrhythmias with minimal symptoms may not require ongoing therapy. Guidelines recommend catheter ablation for recurrent focal atrial tachycardia, especially if it is incessant or causing cardiomyopathy.11 If ablation is not desired or feasible, clinicians can www.aafp.org/afp Volume 107, Number 6 Downloaded for Anonymous User (n/a) at Maccabi Healthcare Services from ClinicalKey.com by Elsevier on July 16, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved. ◆ June 2023 SUPRAVENTRICULAR TACHYCARDIA consider initial pharmacotherapy with a beta blocker;​a nondihydropyridine calcium channel blocker in patients who do not have reduced ejection fraction due to heart failure;​or propafenone or flecainide in patients who have ischemic or structural heart disease.11 6. Goyal R, Zivin A, Souza J, et al. Comparison of the ages of tachycardia onset in patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia. Am Heart J. 1996;​1 32(4):​ 765-767. This article updates previous articles on this topic by Helton3;​ Colucci, et al.4;​and Hebbar and Hueston. 22 8. Ko JK, Deal BJ, Strasburger JF, et al. Supraventricular tachycardia mechanisms and their age distribution in pediatric patients. Am J Cardiol. 1992;​69(12):​1028-1032. Data Sources:​A PubMed search was completed in Clinical Queries using the key terms supraventricular tachycardia, treatment, and management. The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Essential Evidence Plus and DynaMed were also searched. Review of literature included consensus treatment guidelines from the United States and Europe. Search Dates:​May 2022 and May 2023 The Authors MUNIMA NASIR, MD, FAAFP, is an associate professor in the Department of Family and Community Medicine at Milton S. Hershey Medical Center, Hershey, Pa. ASHLEY STURTS, DO, is a fellow physician in the Department of Family and Community Medicine at Pennsylvania State University, Penn State Health, State College. ADAM STURTS, DO, is a resident physician in the Department of Internal Medicine at Milton S. Hershey Medical Center. Address correspondence to Munima Nasir, MD, FAAFP, University Physicians Group – Middletown, 3100 Schoolhouse Rd., Middletown, PA 17057 (email:​mnasir@​pennstatehealth. psu.edu). Reprints are not available from the authors. 7. Katritsis DG. Atrioventricular nodal reentrant tachycardia. In:​Camm JA, Lüscher TF, Maurer G, eds. The ESC Textbook of Cardiovascular Medicine. 3rd ed. Oxford University;​2018. 9. Pappone C, Vicedomini G, Manguso F, et al. Wolff-Parkinson-White syndrome in the era of catheter ablation:​insights from a registry study of 2169 patients. Circulation. 2014;​1 30(10):​811-819. 10. Link MS. Clinical practice. Evaluation and initial treatment of supraventricular tachycardia. N Engl J Med. 2012;​367(15):​1438-1448. 11. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC) [published correction appears in Eur Heart J. 2020;​41(44):​4258]. Eur Heart J. 2020;​41(5):​ 655-720. 12. Fenelon G, Wijns W, Andries E, et al. Tachycardiomyopathy:​mechanisms and clinical implications. Pacing Clin Electrophysiol. 1996;​19(1):​ 95-106. 13. Lessmeier TJ, Gamperling D, Johnson-Liddon V, et al. Unrecognized paroxysmal supraventricular tachycardia. Potential for misdiagnosis as panic disorder. Arch Intern Med. 1997;​157(5):​537-543. 14. Niehues LJ, Klovenski V. Vagal maneuver. StatPearls. July 4, 2022. Accessed June 7, 2022. https://​w ww.ncbi.nlm.nih.gov/books/ NBK551575/ 15. Lan Q, Han B, Wu F, et al. Modified Valsalva maneuver for treatment of supraventricular tachycardias:​a meta-analysis. Am J Emerg Med. 2021;​ 50:​507-512. 16. Smith GD, Fry MM, Taylor D, et al. Effectiveness of the Valsalva manoeuvre for reversion of supraventricular tachycardia. Cochrane Database Syst Rev. 2015;​(2):​CD009502. 17. Alabed S, Sabouni A, Providencia R, et al. Adenosine versus intravenous calcium channel antagonists for supraventricular tachycardia. Cochrane Database Syst Rev. 2017;​(10):​CD005154. References 1. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia:​ a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2016;​1 3(4):​e136-e221. 2. Barzin AH, Paulus R, Arabindoo KK. Supraventricular tachycardia. October 19, 2020. Updated September 16, 2022. Accessed April 1, 2023. https://​w ww.essentialevidenceplus.com/content/eee/17 18. Lei M, Wu L, Terrar DA, et al. Modernized classification of cardiac antiarrhythmic drugs [published correction appears in Circulation. 2019;​ 139(13):​e635]. Circulation. 2018;​1 38(17):​1879-1896. 19. Okutucu S, Görenek B. Review of the 2019 European Society of Cardiology Guidelines for the management of patients with supraventricular tachycardia:​what is new and what has changed? Anatol J Cardiol. 2019;​ 22(6):​282-286. 3. Helton MR. Diagnosis and management of common types of supraventricular tachycardia. Am Fam Physician. 2015;​92(9):​793-800. 20. Stewart RB, Bardy GH, Greene HL. Wide complex tachycardia:​misdiag­ nosis and outcome after emergent therapy. Ann Intern Med. 1986;​ 104(6):​766-771. 4. Colucci RA, Silver MJ, Shubrook J. Common types of supraventricular tachycardia:​diagnosis and management. Am Fam Physician. 2010;​ 82(8):​942-952. 21. D’Este D, Zoppo F, Bertaglia E, et al. Long-term outcome of patients with atrioventricular node reentrant tachycardia. Int J Cardiol. 2007;​ 115(3):​350-353. 5. Orejarena LA, Vidaillet H Jr., DeStefano F, et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. 1998;​ 31(1):​150-157. 22. Hebbar AK, Hueston WJ. Management of common arrhythmias:​ part I. supraventricular arrhythmias. Am Fam Physician. 2002;​65(12):​ 2479-2486. June 2023 ◆ Volume 107, Number 6 www.aafp.org/afp American Family Physician 641 Downloaded for Anonymous User (n/a) at Maccabi Healthcare Services from ClinicalKey.com by Elsevier on July 16, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved.

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