Triggers of Paroxysmal Supraventricular Tachycardia
The most crucial clinical point is that PSVT episodes are typically initiated by premature atrial or ventricular beats that encounter differential conduction properties in the reentry circuit, rather than by specific external triggers, though secondary physiological stressors can facilitate these initiating events. 1
Primary Electrophysiological Triggers
Unidirectional conduction block is the fundamental trigger mechanism for PSVT. 1 The initiation requires:
- Premature impulses (either atrial or ventricular) that impinge on the refractory period of one pathway in the reentry circuit 1
- Acceleration of heart rate that causes functional block in one limb of the circuit due to differential refractory periods 1
- Slowed conduction through the AV node, which allows recovery of the accessory pathway for retrograde activation in orthodromic AVRT 1
The guidelines emphasize that in AV nodal reentry (the most common form), two conducting pathways (alpha and beta) with different conduction times and refractory periods exist within the AV nodal tissue, and the trigger occurs when a premature beat blocks in one pathway while conducting down the other 2
Secondary Physiological Stressors
While not direct triggers of the reentry mechanism itself, these conditions facilitate the initiating premature beats or alter autonomic tone:
Sympathetic Stimulation
- Physical exertion or exercise 1
- Emotional stress and anxiety 1, 3
- Caffeine consumption 1
- Stimulant medications (albuterol, salmeterol) or illicit drugs (amphetamines, cocaine) 1
Metabolic and Systemic Factors
Critical Clinical Distinctions
It is essential to distinguish PSVT from sinus tachycardia, as the latter has entirely different triggers. 1 Key differentiating features:
- PSVT has abrupt onset and termination (paroxysmal pattern), while sinus tachycardia accelerates and decelerates gradually 1
- Sinus tachycardia responds to physiological stressors (infection, volume loss, pain) and resolves when the underlying cause is corrected 1
- PSVT episodes terminate with vagal maneuvers, which strongly suggests reentrant tachycardia involving AV nodal tissue 1
Important Clinical History Elements
When evaluating triggers, obtain specific details about: 1
- Pattern of episodes: number, duration, frequency, and exact mode of onset 1
- Activities immediately preceding onset: exercise, emotional stress, caffeine intake, medication use 1, 3
- Termination methods: whether vagal maneuvers stop the episodes (diagnostic for AV nodal involvement) 1
- Associated symptoms: palpitations (86%), chest discomfort (47%), dyspnea (38%), polyuria (from atrial natriuretic peptide release) 1, 4
Special Populations and Risk Factors
Young adults with structural heart disease face additional trigger considerations: 5, 3
- Congenital heart disease (Ebstein anomaly, Tetralogy of Fallot, transposition of great arteries, atrial septal defects) predisposes to SVT with 10-20% prevalence 5
- Wolff-Parkinson-White syndrome patients require immediate electrophysiological evaluation, as atrial fibrillation can trigger extremely rapid ventricular rates leading to ventricular fibrillation 5, 3
- Cardiomyopathies, valvular disease, and ischemic heart disease lower the threshold for sustained SVT 5, 3
Common Pitfalls to Avoid
- Do not attribute all tachycardia to anxiety without documenting the rhythm on 12-lead ECG during symptoms 3
- Do not dismiss episodes as benign without excluding pre-excitation on baseline ECG, which indicates WPW syndrome and requires specialist referral 1, 5
- Do not confuse irregular palpitations (premature beats, atrial fibrillation, multifocal atrial tachycardia) with the regular, paroxysmal pattern of PSVT 1
- Do not overlook structural heart disease in patients over 65 years, who have five times the risk of PSVT and higher complication rates 6, 3