What are the causes of supraventricular tachycardia (SVT)?

Causes of Supraventricular Tachycardia

Supraventricular tachycardia is primarily caused by three fundamental mechanisms: re-entry circuits (most common), abnormal automaticity, and triggered activity, with re-entry accounting for the majority of SVT cases including AVNRT, AVRT, and atrial flutter. 1, 2, 3

Primary Mechanisms

Re-entry (Most Common)

• Re-entry involves repetitive electrical impulse conduction around a fixed obstacle in a defined circuit, requiring unidirectional conduction block in one limb and slow conduction for both initiation and maintenance. 1, 2, 3
• This mechanism underlies AVNRT (atrioventricular nodal reentrant tachycardia), AVRT (atrioventricular reciprocating tachycardia), and atrial flutter. 1, 2
• Initiation occurs when a premature impulse encounters the refractory period of one pathway, forcing conduction down an alternative route. 1

Abnormal Automaticity

• Enhanced diastolic phase 4 depolarization in atrial, AV junctional, or atrial vessel tissues leads to increased firing rates compared to normal pacemaker cells. 2, 3
• This mechanism causes certain atrial tachycardias and nonparoxysmal junctional tachycardia. 2

Triggered Activity

• Disturbances in repolarization where afterdepolarizations reach threshold and trigger early action potentials during repolarization. 2, 3
• This mechanism can contribute to certain forms of atrial tachycardia. 2

Specific SVT Types and Their Causes

AVNRT (Atrioventricular Nodal Reentrant Tachycardia)

• Caused by a re-entry circuit within the AV node involving dual pathways (fast and slow conducting pathways). 3
• Most common form of paroxysmal SVT in patients without structural heart disease. 1

AVRT (Atrioventricular Reciprocating Tachycardia)

• Caused by accessory pathways (bypass tracts) that directly connect atrium and ventricle, bypassing the normal AV node conduction system. 1, 3
• Manifest accessory pathways (Wolff-Parkinson-White syndrome) occur in 0.1% to 0.3% of the population and conduct anterogradely, showing pre-excitation with delta waves on ECG. 1
• Concealed pathways conduct only retrogradely and do not cause pre-excitation on standard ECG. 1
• Orthodromic AVRT accounts for 90-95% of AVRT episodes, using the AV node anterogradely and the accessory pathway retrogradely. 1

Permanent Junctional Reciprocating Tachycardia (PJRT)

• Rare syndrome involving a slowly conducting, concealed, usually posteroseptal accessory pathway with decremental conduction properties. 1, 2
• Characterized by incessant SVT with deeply inverted P waves in leads II, III, and aVF, and long RP interval (RP > PR). 1, 2
• The incessant nature frequently leads to tachycardia-induced cardiomyopathy. 1

Atrial Tachycardia

• Can be caused by enhanced automaticity, triggered activity, or micro-reentry within atrial tissue. 2, 3
• Multifocal atrial tachycardia (MAT) is most commonly encountered in patients with chronic pulmonary disease. 1, 2

Atrial Flutter

• Macro-reentrant circuit typically around the tricuspid annulus. 2, 3
• Often associated with structural heart disease or acute precipitating events. 2

Nonparoxysmal Junctional Tachycardia

• Narrow complex tachycardia with rates of 70-120 bpm showing "warm-up" and "cool-down" patterns. 2
• Specific causes include digitalis toxicity (most important reversible cause), postcardiac surgery, hypokalemia, myocardial ischemia, chronic obstructive lung disease with hypoxia, and inflammatory myocarditis. 2

Predisposing Factors and Associated Conditions

Structural Heart Disease

• Heart failure, hypertension, valvular disease (especially aortic stenosis), and hypertrophic cardiomyopathy predispose to SVT. 1, 2, 3
• Structural abnormalities may lead to syncope during SVT episodes. 1

Congenital Heart Disease

• Ebstein anomaly, Tetralogy of Fallot, transposition of great arteries, and atrial septal defects carry a 10-20% incidence of SVT in adults with congenital heart disease. 2, 3
• Risk results from surgical scarring, ongoing hemodynamic abnormalities, residual lesions, or decreased ventricular function. 1

Acute Precipitating Events

• Major surgery, pneumonia, acute myocardial infarction, infection, and volume loss can trigger SVT. 1, 2, 3
• Fever can trigger cardiac events in patients with Brugada syndrome. 1

Metabolic and Endocrine Disorders

• Hyperthyroidism and electrolyte abnormalities (particularly hypokalemia) can precipitate SVT. 2, 3

Medications and Substances

• Digitalis toxicity is the most important reversible cause of nonparoxysmal junctional tachycardia. 2
• Stimulants, antiarrhythmics, and caffeine can trigger SVT. 2, 3

Critical High-Risk Scenarios

Wolff-Parkinson-White Syndrome with Atrial Fibrillation

• Rapid anterograde accessory pathway conduction during atrial fibrillation can result in ventricular fibrillation and sudden cardiac death, with a 10-year risk documented in patients with manifest accessory pathways. 1
• This represents the most dangerous complication of accessory pathway-mediated SVT. 1

Tachycardia-Mediated Cardiomyopathy

• Persistent SVT for weeks to months with fast ventricular response leads to tachycardia-mediated cardiomyopathy. 1, 2
• This complication usually resolves after successful treatment of the underlying arrhythmia. 1

Important Clinical Pitfalls

• Never miss digitalis toxicity as a cause of junctional tachycardia—this is the most important reversible etiology requiring immediate drug withdrawal and consideration of digitalis-binding agents. 2
• Always evaluate for pre-excitation on baseline ECG, as patients with accessory pathways who develop atrial fibrillation require immediate electrophysiological evaluation due to sudden death risk. 2, 3
• Do not attribute SVT symptoms solely to anxiety or panic—54% of SVT patients have had their symptoms incorrectly dismissed as psychiatric. 4
• Most SVT occurs in structurally normal hearts in younger individuals, but always seek associated heart disease with echocardiography, particularly in persistent cases. 1, 2