Etiologies of Supraventricular Tachycardia (SVT)
Supraventricular tachycardia is primarily caused by three main mechanisms: re-entry phenomena, abnormal automaticity, and triggered activity, with re-entry being the most common mechanism underlying most SVT subtypes. 1
Main Mechanisms of SVT
Re-entry: The most common mechanism for SVT, involving repetitive electrical impulse conduction around a fixed obstacle in a defined circuit. Requirements include unidirectional conduction block in one limb of a circuit and slow conduction for both initiation and maintenance 1
Abnormal automaticity: Occurs when tissues exhibit enhanced diastolic phase 4 depolarization, leading to increased firing rates compared to normal pacemaker cells. These ectopic foci can be located in the atria, AV junction, or vessels communicating directly with the atria (vena cava, pulmonary veins) 1
Triggered activity: Associated with disturbances in repolarization, where afterdepolarizations can reach threshold and trigger early action potentials during repolarization 1
Common Types of SVT and Their Specific Etiologies
Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
- Caused by a re-entry circuit within the AV node involving dual pathways (fast and slow) 1, 2
- Typically presents with a "short RP" interval on ECG with P waves often buried in or appearing at the end of the QRS complex (pseudo S wave in inferior leads) 1
- Most common type of paroxysmal SVT 2
Atrioventricular Reciprocating Tachycardia (AVRT)
- Involves an accessory pathway between the atria and ventricles (bypass tract) 1, 2
- Orthodromic AVRT: anterograde conduction through AV node, retrograde conduction through accessory pathway 1
- Wolff-Parkinson-White syndrome: most recognized form with pre-excitation on ECG 2, 3
- Permanent form of junctional reciprocating tachycardia (PJRT): uncommon form with decremental retrograde conduction producing a long RP interval 1
Atrial Tachycardia (AT)
- Can be caused by enhanced automaticity, triggered activity, or micro-reentry within atrial tissue 1
- Characterized by a long RP interval with P wave morphology different from sinus rhythm 1
- Focal or multifocal (MAT) variants exist 1
Atrial Flutter
- Macro-reentrant circuit, typically around the tricuspid annulus 1
- Often associated with structural heart disease or precipitating events 1
- Only 1.7% of cases have no structural cardiac disease (lone atrial flutter) 1
- Incidence increases markedly with age (from 5 per 100,000 in those >50 years to 587 per 100,000 in those >80 years) 1
- 2.5 times more common in men than women 1
Atrial Fibrillation with Rapid Ventricular Response
- Often coexists with other forms of SVT 1
- Present in 58% of patients with atrial flutter 1
- Particularly dangerous in patients with accessory pathways 4
Predisposing Factors and Associated Conditions
- Structural heart disease: Heart failure, hypertension, valvular disease 1, 4
- Congenital heart disease: Particularly Ebstein anomaly, Tetralogy of Fallot, transposition of great arteries, and atrial septal defects 4
- Acute precipitating events: Major surgery, pneumonia, acute myocardial infarction 1
- Chronic conditions: Heart failure, hypertension, chronic lung disease 1
- Metabolic disorders: Hyperthyroidism, electrolyte abnormalities 5
- Medications/substances: Stimulants, certain antiarrhythmics, caffeine 5
- Idiopathic: Some cases occur in structurally normal hearts with no identifiable cause 1, 2
Special Considerations
- Pre-excitation syndromes (e.g., Wolff-Parkinson-White) require prompt evaluation due to risk of sudden cardiac death if atrial fibrillation develops 4
- SVT in patients with congenital heart disease carries significantly higher risks of complications including heart failure, stroke, and sudden cardiac death 4
- Prolonged SVT can lead to tachycardia-mediated cardiomyopathy, especially when persistent for weeks to months 4
Understanding the specific etiology of SVT is crucial for appropriate management, as treatment strategies differ based on the underlying mechanism and type of tachyarrhythmia 1, 2, 6.