SVT: Supraventricular Tachycardia

Supraventricular tachycardia (SVT) is a rapid heart rhythm that originates from a short circuit in the upper heart chamber.1 Because the condition often starts and stops abruptly, it is also referred to as paroxysmal SVT (PSVT). Symptoms of SVT include palpitations, weakness, fatigue, dizziness, syncope, and chest pain, and can often be misdiagnosed as a panic attack.1 This article summarizes the epidemiologic characteristics, risk factors, prognosis, diagnosis, and treatment of SVT.

Epidemiologic Characteristics

The estimated prevalence of SVT is 168 to 332 cases per 100,000 individuals, with female patients constituting 67.5% of cases.2 Approximately one-half of patients with SVT are age 45 to 64 years.

The most common type of SVT in the general population is atrioventricular nodal reentrant tachycardia (AVNRT).3 More than 60% of patients who require invasive cardiac electrophysiological assessment have AVNRT.4 The other common types of SVT are atrioventricular reentrant tachycardia (AVRT) and atrial tachycardia (AT). Other than tachycardia, SVT is also the most common arrhythmia in infants and children.4

Types of SVT

The primary electrophysiologic types of SVT are AVNRT, AVRT, and AT. Junctional tachycardia is a rare form that is more prevalent in children.2

Atrioventricular Nodal Reentrant Tachycardia

AVNRT results from aberrancy between 2 distinct electrical pathways within the AV node. One of these pathways is fast, and the other is slow. Electricity can move through either pathway at different speeds with different refractory periods. When a premature beat occurs in the atria or ventricles, a reentry circuit can develop between the fast and slow pathways, leading to tachycardia.4

Atrioventricular Reentrant Tachycardia

AVRT differs from AVNRT due to the presence of an anatomical accessory pathway outside the AV node.3 This accessory pathway is an embryological remnant that connects the atria and ventricles and can conduct electricity in either or both directions. Approximately 90% of AVRTs are orthodromic, meaning that electricity flows from the atrium to the ventricle via the AV node and from the ventricle to the atrium via the accessory pathway, creating a circuit. The Wolff-Parkinson White (WPW) ECG pattern and its accompanying WPW syndrome is an example of orthodromic AVRT.3,5

Atrial Tachycardia

Unlike AVNRT and AVRT, AT originates in the atrium and operates independently of the AV node.3 ATs are categorized into 3 groups: focal, macroreentrant, and microreentrant.6 Atrial flutter, a common type of AT, arises from macroreentry around the tricuspid annulus.7 The circuit created by atrial flutter corresponds to the right atrium size.8 In microreentrant ATs, the circuit is defined by a diameter of 2 cm or less.6 Focal ATs arise from a specific site of early activation in the atria. Instead of moving in a circuit, as with reentry ATs, the electricity propagates away from the originating focus in a centrifugal pattern.8

Junctional Tachycardia

Junctional tachycardia is a type of nonreentrant SVT.6 This arrhythmia arises from the AV junction. Sinus tachycardia is categorized as physiologic or inappropriate. Physiologic sinus tachycardia results from an appropriate autonomic response to physiologic or pathologic causes. Physiologic causes include emotional responses and physical activity, while pathologic causes include fever, dehydration, anemia, heart failure, and hyperthyroidism, among others. Some patients also experience inappropriate sinus tachycardia (IST). This refers to sinus tachycardia that is unexplained by physiologic demands or another underlying cause.

Risk Factors for SVT

Various conditions can lead to the electrophysiologic abnormalities that cause SVT, including the following2,6,7:

Conditions that increase the risk of developing SVT include coronary artery disease, cardiomyopathy, and previous heart surgery.2,6 Additional risk factors include congenital heart disease and diabetes.

Prognosis

SVT is generally not life-threatening, and the prognosis is usually good in the absence of structural heart disease.2 Many asymptomatic patients do not need SVT treatment and have a generally benign disease course.7 Patients with more severe symptoms or comorbid heart disease may require earlier acute therapy intervention and long-term management.2 Rarely, SVT can cause sudden cardiac death.6

Presentation and Diagnosis of SVT

The clinical presentation of SVT depends on several factors, including the patient’s age, duration of SVT episodes, and severity of symptoms, as well as the presence of comorbid heart or lung disease.2,6 Many patients with SVT are asymptomatic. Those with symptoms typically report palpitations, chest pain, and syncope.

In addition to ascertaining symptoms and their characteristics, obtaining a medical history can provide clues toward an underlying SVT origin.2,6 Identifying potential triggers and any family or personal history of heart disease is essential when SVT is suspected.

Physical Examination Findings

The findings from a physical examination of patients with SVT are often unremarkable other than arrhythmic episodes.2 Younger patients without other medical problems are most likely to have unremarkable findings on examination, with or without the presence of tachycardia.6

When conducting a physical examination for possible SVT, the main focus should be on the cardiovascular system, but a complete examination includes the respiratory and endocrine systems.2 The presence of cardiac examination abnormalities can point to certain origins, including valvular heart disease, pericarditis, and heart failure.

On pulmonary examination, patients with heart failure leading to tachycardia may have crackles from fluid accumulation in their lungs.2 Patients with hyperthyroidism or thyroiditis may exhibit an enlarged or tender thyroid gland during assessment. Depending on the patient and their comorbidities, additional important abnormalities may be identified in other systems during the examination.

Diagnostic Workup

Patients with suspected SVT based on medical history and examination findings require further diagnostic workup.2 An ECG should be performed initially in hemodynamically stable patients. A Holter monitor or event recorder can help diagnose infrequent SVT that is not identified on a 12-lead ECG. Other potentially useful diagnostic tests for SVT include the following2-3,6,7:

SVT Treatment

The management of SVT differs based on patient stability, patient preference, and the underlying SVT mechanism. The treatments described in the following sections are based on the 2015 American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) guidelines for treating SVT.6

SVT of Unknown Origin

Vagal maneuvers, including the Valsalva maneuver and carotid sinus massage, are the first-line interventions for SVT of unknown origin in stable patients.6 If vagal maneuvers do not terminate the SVT, intravenous (IV) adenosine is recommended. When first-line therapy is ineffective or contraindicated, and the patient is hemodynamically stable, IV beta blockers, IV verapamil, or IV diltiazem are recommended. If after receiving medical therapy patients are still in regular SVT, synchronized cardioversion is recommended. Hemodynamically unstable patients with regular SVT should undergo synchronized cardioversion.

Sinus Tachycardia

Most often, sinus tachycardia resolves when its underlying cause, such as infection or dehydration, is treated.6 Inappropriate sinus tachycardia often does not require treatment because the prognosis is generally benign. There are no specific recommendations for the acute treatment of IST. However, once physiologic sinus tachycardia has been ruled out, ongoing IST can be treated with ivabradine or beta blockers, although the focus of treatment is on symptom reduction. For some patients with refractory symptoms, ivabradine and beta blockers in combination may be beneficial.

Focal and Multifocal Atrial Tachycardia

In the acute setting, hemodynamically stable patients with suspected focal AT should receive IV beta blockers, diltiazem, or verapamil.6 In patients who are hemodynamically stable and whose diagnosis is unclear, IV adenosine can help differentiate focal AT from AVNRT and AVRT. If neither of these options works, treatment with IV amiodarone or IV ibutilide is recommended.

For hemodynamically unstable patients, IV adenosine is recommended. Adenosine can help restore sinus rhythm.6 If treatment with adenosine is not feasible or ineffective, synchronized cardioversion should be initiated in hemodynamically unstable patients.

Long-term management of focal AT involves either catheter ablation or pharmacological management, depending on patient preference and candidacy.6 Catheter ablation is preferred for most patients; beta blockers, diltiazem, or verapamil are second-line drug therapy options.

To treat multifocal AT in the acute setting, IV metoprolol or verapamil is recommended.6 Long-term, recurrent symptomatic multifocal AT can be treated with oral verapamil or diltiazem.

Atrioventricular Nodal Reentrant Tachycardia

First-line treatment for AVNRT in the acute setting is vagal maneuvers and/or IV adenosine.6 If these interventions are ineffective and the patient is hemodynamically stable, IV beta blockers, diltiazem, or verapamil are recommended. Oral versions of these drugs are also reasonable options for AVNRT in certain patients. If these drugs are ineffective, IV amiodarone is recommended. Hemodynamically unstable patients should receive synchronized cardioversion.

Long-term care of asymptomatic patients with AVNRT can include observation without treatment.6 Symptomatic patients should be offered catheter ablation. If the patient prefers drug therapy, beta blockers, diltiazem, or verapamil should be offered.

Atrioventricular Reentrant Tachycardia

As with AVNRT, first-line acute orthodromic AVRT treatment is vagal maneuvers and/or IV adenosine.6 If these are ineffective and the patient is hemodynamically stable, IV beta blockers, diltiazem, or verapamil are recommended. These medications should be used carefully in stable patients with preexcitation on their resting ECG because of an increased risk of developing atrial fibrillation or ventricular arrhythmias.

If drug therapy is ineffective for stable patients, synchronized cardioversion is recommended.6 Hemodynamically unstable patients should also undergo synchronized cardioversion.

For long-term management, catheter ablation is the first-line treatment for AVRT, regardless of preexcitation.7 Patients with preexcitation who prefer drug therapy should be offered flecainide or propafenone unless they have structural heart disease. Beta blockers, diltiazem, or verapamil are recommended for patients without preexcitation.

For asymptomatic patients with preexcitation AVRT, an electrophysiological study is recommended to stratify risk.6 Patients at higher risk for arrhythmic events should be offered cardiac ablation.

Atrial Flutter

The acute management of atrial flutter is divided into rate and rhythm control.6 If rhythm control is the goal for hemodynamically stable patients, synchronized cardioversion, oral dofetilide, IV ibutilide, and/or rapid atrial pacing are options. First-line options for rate control in stable patients are IV beta blockers, IV diltiazem, or IV verapamil. For unstable patients, rhythm control involves synchronized cardioversion, while rate control involves IV amiodarone.

Long-term management is also categorized as rhythm or rate control.6 Beta blockers, diltiazem, or verapamil can be used for rate control. Catheter ablation is the first-line option for rhythm control, followed by amiodarone, dofetilide, or sotalol.

Junctional Tachycardia

In the acute setting, IV beta blockers, diltiazem, procainamide, or verapamil are options for symptomatic junctional tachycardia.6 For long-term management of junctional tachycardia, beta blockers, diltiazem, or verapamil are first-line options. Flecainide or propafenone are also options in the absence of structural heart disease. If these are ineffective, catheter ablation may be offered.

Adverse Effects of SVT Treatments

Adverse Effects of Medications for SVT

Pharmacotherapy for SVT requires close follow-up to monitor adverse effects and drug interactions. The Table summarizes the safety profiles of select medications used as first-line therapy for SVT in the acute setting.6

Table. Safety Profiles of Select Medications for SVT

DrugPotential adverse effectsPrecautions (exclude or use cautiously)Drug interactions

AV = atrioventricular; CYP = cytochrome P450; PVC = premature ventricular contraction; SA = sinoatrial; WPW = Wolff-Parkinson White.

From American College of Cardiology/American Heart Association/Heart Rhythm Society guidelines.6

Adverse Effects of Catheter Ablation

Cardiac catheter ablation is generally considered safe and typically requires less recovery time than surgical ablation. Risks associated with catheter ablation include the following9:

Complications of SVT

Patients with other medical conditions are more likely to experience SVT complications.6 Those with frequent episodes of untreated SVT are at an increased risk of developing heart failure.2 Treating SVT and avoiding triggers, such as smoking, alcohol, and stress, can help prevent heart failure.10 Patients who develop heart failure will require evidence-based heart failure management. Rarely, an SVT episode can cause loss of consciousness or cardiac arrest. If this occurs, basic life support and advanced cardiac life support interventions are indicated.

SVT Guidelines

Guidelines relevant to the care of patients with SVT include the following6,7:

References

  1. Paroxysmal supraventricular tachycardia (PSVT). Johns Hopkins Medicine. Accessed February 4, 2025. https://www.hopkinsmedicine.org/health/conditions-and-diseases/paroxysmal-supraventricular-tachycardia
  2. Peng G, Zei PC. Diagnosis and management of paroxysmal supraventricular tachycardia. JAMA. 2024;331(7):601-610. doi:10.1001/jama.2024.0076
  3. Kotadia ID, Williams SE, O’Neill M. Supraventricular tachycardia: An overview of diagnosis and management. Clin Med (Lond). 2020;20(1):43-47. doi:10.7861/clinmed.cme.20.1.3
  4. Kafalı HC, Ergül Y. Common supraventricular and ventricular arrhythmias in children. Turk Arch Pediatr. 2022;57(5):476-488. doi:10.5152/TurkArchPediatr.2022.22099
  5. Wolff-Parkinson White syndrome (WPW): Atrioventricular reentry tachycardia. AF-Ablation. Accessed February 4, 2025. https://af-ablation.org/en/arrhythmological-disorders/supraventricular-tachycardia/wolff-parkinson-white-syndrome-wpw-atrio-ventricular-reentry-tachycardia/
  6. 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. Circulation. 2016;133(14):e506-574. doi:10.1161/CIR.0000000000000311
  7. 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). Eur Heart J. 2020;41(5):655-720. doi:10.1093/eurheartj/ehz467
  8. Burns E, Buttner R. Atrial flutter. Life in the Fastlane. Updated October 8, 2024. Accessed February 4, 2025. https://litfl.com/atrial-flutter-ecg-library/
  9. Benali K, Khairy P, Hammache N, et al. Procedure-related complications of catheter ablation for atrial fibrillation. J Am Coll Cardiol. 2023;81(21):2089-2099. doi:10.1016/j.jacc.2023.03.418
  10. Heart failure: Treatment. National Heart, Lung, and Blood Institute. Updated March 24, 2022. Accessed February 4, 2025. https://www.nhlbi.nih.gov/health/heart-failure/treatment

Link nội dung: https://diendanmarketing.edu.vn/svxt-a4192.html