What causes Supraventricular Tachycardia (SVT) to occur?

What Causes Supraventricular Tachycardia (SVT) to Occur

SVT occurs through three primary electrophysiological mechanisms: re-entry circuits (the most common), abnormal automaticity, and triggered activity, with re-entry accounting for the majority of clinically significant SVTs including AVNRT, AVRT, and atrial flutter. 1, 2

Primary Electrophysiological Mechanisms

Re-entry Circuits (Most Common Mechanism)

Re-entry is the dominant mechanism underlying most SVTs, involving repetitive electrical impulse conduction around a fixed obstacle in a defined circuit 1, 2. This mechanism requires:

• Unidirectional conduction block in one limb of the circuit, which occurs when a premature impulse encounters the refractory period of the pathway or when heart rate accelerates 1
• Slow conduction through at least one portion of the circuit, necessary for both initiation and maintenance of the tachycardia 1
• In orthodromic AVRT, slowed conduction through the AV node allows recovery and retrograde activation over the accessory pathway 1

Re-entry is the mechanism in AVRT, AVNRT, and atrial flutter 1, 2. A fixed obstacle is not always required—functionally determined re-entry can occur through relatively refractory tissue without a fully excitable gap 1.

Abnormal Automaticity

Tissues exhibiting abnormal automaticity demonstrate enhanced diastolic phase 4 depolarization, leading to increased firing rates compared to normal pacemaker cells 1, 2. These ectopic foci can reside in:

• The atria 1, 2
• The AV junction 1, 2
• Vessels communicating directly with the atria (vena cava or pulmonary veins) 1

When the ectopic focus firing rate exceeds the sinus node, it overdrives the sinus node and becomes the predominant pacemaker 1. The rapid firing may be incessant (>50% of the day) or episodic 1.

Triggered Activity

Triggered activity results from disturbances in repolarization where afterdepolarizations reach threshold and trigger early action potentials during repolarization 1, 2. This mechanism is associated with recovery or repolarization abnormalities 1.

Specific SVT Types and Their Etiologies

AVNRT (Atrioventricular Nodal Reentrant Tachycardia)

• Caused by a re-entry circuit within the AV node involving dual pathways (fast and slow) 2
• Most common cause of paroxysmal SVT with sudden onset and termination 1

AVRT (Atrioventricular Reciprocating Tachycardia)

Accessory pathways directly connect the atrium and ventricle, bypassing normal AV node conduction 1. Key features:

• Manifest pathways conduct anterogradely, showing pre-excitation with delta waves on ECG, occurring in 0.1-0.3% of the population 1
• Concealed pathways conduct only retrogradely without 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
• Antidromic AVRT accounts for 5% of episodes, conducting anterogradely via the accessory pathway causing pre-excited QRS 1

Special accessory pathway variants:

• PJRT (Permanent Junctional Reciprocating Tachycardia) involves a concealed posteroseptal pathway with retrograde decremental conduction, causing incessant tachycardia that may lead to tachycardia-mediated cardiomyopathy 1, 3
• Atriofascicular fibers (Mahaim fibers) connect the right atrium to distal right bundle branch with decremental anterograde conduction 1

Atrial Tachycardia

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

Atrial Flutter

A macro-reentrant circuit typically around the tricuspid annulus, often associated with structural heart disease or precipitating events 3, 2.

Predisposing Factors and Triggers

Structural Heart Disease

• Heart failure, hypertension, valvular disease, and hypertrophic cardiomyopathy 3, 2
• Valvular aortic stenosis or hypertrophic cardiomyopathy may be associated with syncope during SVT 1

Congenital Heart Disease

Carries a 10-20% incidence of SVT in adults 3. Specific associations include:

• Ebstein anomaly (most prominent association with accessory pathways and Mahaim fibers) 3, 4
• Tetralogy of Fallot 3
• Transposition of great arteries 3
• Atrial septal defects 3

Acute Precipitating Events

• Major surgery, pneumonia, acute myocardial infarction 3, 2
• Infection or volume loss requiring evaluation for stressors 1, 3
• Hyperthyroidism, electrolyte abnormalities 3, 2

Medications and Substances

• Stimulants, antiarrhythmics, caffeine 3, 2
• Digitalis toxicity (most important reversible cause of nonparoxysmal junctional tachycardia) 3
• Beta-agonist drugs (albuterol, salmeterol) 1
• Illicit stimulants (amphetamines, cocaine) 1

Critical Clinical Pitfalls

Never miss digitalis toxicity as the cause of persistent junctional tachycardia—this is the most important reversible cause 3.

Always evaluate for pre-excitation on baseline ECG because patients with accessory pathways who develop atrial fibrillation face risk of extremely rapid ventricular conduction, ventricular fibrillation, and sudden cardiac death 1, 3.

Do not delay echocardiography because persistent SVT (lasting weeks to months with fast ventricular response) may both cause and be caused by tachycardia-mediated cardiomyopathy 1, 3.

In patients with congenital heart disease, SVT carries significantly higher risks of complications including heart failure, stroke, and sudden cardiac death, requiring management in specialized centers 3, 2, 4.