What causes supraventricular tachycardia (SVT)?

Causes of Supraventricular Tachycardia

Supraventricular tachycardia is primarily caused by three electrophysiological mechanisms: re-entry circuits (most common), abnormal automaticity, and triggered activity, with specific SVT subtypes arising from distinct anatomical locations and predisposing conditions. 1

Primary Electrophysiological Mechanisms

Re-entry Phenomena (Most Common)

• Re-entry is the dominant mechanism underlying most SVT subtypes, involving repetitive electrical impulse conduction around a fixed obstacle in a defined circuit 2, 1
• This mechanism requires two critical components: unidirectional conduction block in one limb of the circuit and sufficiently slow conduction to allow tissue recovery and perpetuate the arrhythmia 2, 1
• Re-entry accounts for the majority of paroxysmal SVT cases, including AVNRT and AVRT 3

Abnormal Automaticity

• Occurs when atrial, AV junctional, or atrial vessel tissues exhibit enhanced diastolic phase 4 depolarization, leading to increased spontaneous firing rates compared to normal pacemaker cells 2, 1
• This mechanism can originate from any location in the atria, AV junction, or vessels communicating directly with the atria 1

Triggered Activity

• Results from disturbances in repolarization where afterdepolarizations reach threshold and trigger premature action potentials during or immediately after repolarization 2, 1

Specific SVT Types and Their Anatomical Causes

Atrioventricular Nodal Reentrant Tachycardia (AVNRT)

• Caused by a re-entry circuit within the AV node itself, involving dual pathways (fast and slow conducting pathways) 1
• Most patients have structurally normal hearts 3

Atrioventricular Reciprocating Tachycardia (AVRT)

• Involves an accessory pathway (bypass tract) between the atria and ventricles, creating an abnormal electrical connection outside the normal conduction system 1
• Wolff-Parkinson-White syndrome is the classic example, where pre-excitation is visible on baseline ECG 4

Atrial Tachycardia

• Can arise from enhanced automaticity, triggered activity, or micro-reentry within atrial tissue 2, 1
• Characterized by a focal point of origin with discrete P waves and typically an isoelectric segment between P waves 5
• Multifocal atrial tachycardia (MAT) is most commonly encountered in patients with chronic pulmonary disease 2

Atrial Flutter

• Caused by a macro-reentrant circuit, typically around the tricuspid annulus through the cavotricuspid isthmus 2, 1
• Often associated with underlying structural heart disease or acute precipitating events 2

Junctional Tachycardias

• Nonparoxysmal junctional tachycardia results from enhanced automaticity, with specific causes including digitalis toxicity (most important reversible cause), postcardiac surgery, hypokalemia, myocardial ischemia, chronic obstructive lung disease with hypoxia, or inflammatory myocarditis 2
• Permanent junctional reciprocating tachycardia (PJRT) involves a slowly conducting, concealed, usually posteroseptal accessory pathway 2

Predisposing Conditions and Risk Factors

Structural Heart Disease

• Heart failure, hypertension, valvular disease, and hypertrophic cardiomyopathy are major predisposing factors 2, 1
• These conditions alter atrial architecture and create substrate for re-entrant circuits 1

Congenital Heart Disease

• Carries a 10-20% incidence of SVT in adults with congenital heart disease 2
• Particularly high-risk lesions include Ebstein anomaly, Tetralogy of Fallot, transposition of great arteries, and atrial septal defects 2, 1

Acute Precipitating Events

• Major surgery, pneumonia, acute myocardial infarction, hyperthyroidism, electrolyte abnormalities (especially hypokalemia), infection, and volume depletion can trigger SVT 2, 1
• These conditions alter autonomic tone or create transient electrophysiological disturbances 5

Medications and Substances

• Digitalis toxicity is the most important reversible cause of nonparoxysmal junctional tachycardia 2
• Stimulants (caffeine, amphetamines, cocaine), beta-agonists (albuterol, salmeterol), and certain antiarrhythmic drugs can precipitate SVT 5, 2

Metabolic and Systemic Disorders

• Hyperthyroidism, anemia, dehydration, fever, and pain increase sympathetic tone and can unmask or trigger SVT 5
• Anxiety is an important trigger, and patients with inappropriate sinus tachycardia may have associated anxiety disorders 5

Special Considerations and Critical Pitfalls

Inappropriate Sinus Tachycardia

• The cause remains unclear, with proposed mechanisms including dysautonomia, neurohormonal dysregulation, and intrinsic sinus node hyperactivity 5
• This is a diagnosis of exclusion—always rule out hyperthyroidism, anemia, dehydration, pain, exogenous substances, and anxiety before making this diagnosis 5

Pre-excitation Syndromes

• Patients with accessory pathways who develop atrial fibrillation are at risk for extremely rapid ventricular rates that can degenerate into ventricular fibrillation and sudden death 2, 4
• Always evaluate for pre-excitation on baseline ECG, as these patients require immediate electrophysiological evaluation 2

Tachycardia-Mediated Cardiomyopathy

• Persistent SVT lasting weeks to months with fast ventricular response can both cause and be caused by cardiomyopathy 2, 4
• This creates a vicious cycle where SVT causes ventricular dysfunction, which in turn predisposes to more SVT 2