Supraventricular Tachycardia

Table of Contents

  1. Overview
  2. Epidemiology
  3. Classification (AVNRT / AVRT / AT)
  4. Pathophysiology
  5. Clinical Presentation
  6. Diagnosis
  7. Acute Management
  8. Long-Term Management and Ablation
  9. Prognosis
  10. Research Papers
  11. Connections
  12. Featured Videos

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1. Overview

Supraventricular tachycardia (SVT) is an umbrella term for tachyarrhythmias originating above the bundle of His, producing a heart rate typically exceeding 100 beats per minute. SVT encompasses a heterogeneous group of arrhythmias unified by their supraventricular origin and characteristic narrow-complex appearance on ECG (QRS duration <120 ms) unless aberrant conduction or pre-excitation is present.

The three most common forms are: AV nodal reentrant tachycardia (AVNRT) accounting for approximately 60% of SVT cases, AV reentrant tachycardia (AVRT) accounting for 30%, and atrial tachycardia (AT) accounting for roughly 10%. SVT episodes typically manifest as sudden-onset, regular palpitations with heart rates of 150–250 bpm, often terminating abruptly.

SVT is rarely life-threatening in the absence of structural heart disease or accessory pathways with short refractory periods, but significantly impairs quality of life. Radiofrequency catheter ablation achieves cure rates exceeding 95% for AVNRT, making it the definitive treatment for symptomatic patients.

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2. Epidemiology

SVT has an estimated prevalence of approximately 2.25 per 1,000 persons and an incidence of 35 per 100,000 person-years in the general population. It affects individuals of all ages, with AVNRT more common in women (female-to-male ratio 2:1) and middle-aged adults, while AVRT is more common in young men and those with congenital accessory pathways.

The lifetime risk of experiencing an SVT episode is approximately 0.3%. Emergency department visits for SVT in the United States exceed 50,000 annually. Most episodes are paroxysmal, lasting seconds to hours, but sustained SVT can cause hemodynamic compromise, particularly in patients with underlying structural heart disease.

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3. Classification (AVNRT / AVRT / AT)

AV Nodal Reentrant Tachycardia (AVNRT) — ~60%

AVNRT arises from a reentrant circuit confined within or near the AV node, utilizing dual pathways with differing conduction velocities and refractory periods. The "slow" pathway has slower conduction but shorter refractoriness; the "fast" pathway conducts rapidly but has longer refractoriness. A premature atrial complex that blocks in the fast pathway (refractory) conducts antegradely down the slow pathway, then retrogradely up the fast pathway — initiating the reentrant circuit. In typical (slow-fast) AVNRT, the P wave is buried within or immediately after the QRS (retrograde P, RP interval <70 ms).

AV Reentrant Tachycardia (AVRT) — ~30%

AVRT uses a bypass tract (accessory pathway — Bundle of Kent) as one limb of the reentrant circuit. In orthodromic AVRT (more common, ~95% of AVRT), antegrade conduction proceeds through the AV node and retrograde conduction via the accessory pathway, producing a narrow complex tachycardia with a retrograde P wave visible after the QRS (RP interval typically 100–140 ms). In antidromic AVRT, conduction is antegrade down the accessory pathway and retrograde through the AV node, producing a wide complex tachycardia that can be confused with ventricular tachycardia. WPW syndrome represents symptomatic pre-excitation with AVRT.

Atrial Tachycardia (AT) — ~10%

Focal AT arises from enhanced automaticity, triggered activity, or micro-reentry within the atrial myocardium outside the sinus node. Common origins include the crista terminalis, pulmonary vein ostia, coronary sinus ostium, and tricuspid/mitral annuli. P waves are present before each QRS but with a morphology differing from sinus P waves, and the RP interval is typically longer than the PR interval ("long RP tachycardia"). Multifocal AT features three or more distinct P-wave morphologies and is associated with pulmonary disease and metabolic derangements.

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4. Pathophysiology

The common electrophysiologic mechanism underlying most SVTs is reentry — a circuit in which an electrical impulse continuously propagates around a closed loop, requiring: (1) two pathways with different conduction velocities and refractory periods, (2) unidirectional block in one pathway, and (3) sufficiently slow conduction in the other pathway to allow recovery of excitability in the blocked pathway.

In AVNRT, the compact AV node with its dual-pathway physiology provides this substrate. The slow pathway (posteroinferior extension) and fast pathway (anterosuperior extension) form the circuit, with the reentrant wavefront spinning within centimeters of tissue near the AV node. Simultaneous atrial and ventricular activation produces near-simultaneous P-QRS, the hallmark of typical AVNRT.

In AVRT, the reentrant circuit is larger, encompassing the atria, AV node, His-Purkinje system, ventricles, and the accessory pathway — a muscular bridge crossing the AV groove. The RP interval in orthodromic AVRT reflects the time required for retrograde conduction through the accessory pathway, typically producing an RP interval of 100–160 ms (P visible in ST segment, particularly in leads II, III, aVF).

Triggered activity from delayed afterdepolarizations (DADs) underlies some focal ATs and is potentiated by catecholamines, digitalis toxicity, and intracellular calcium overload.

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5. Clinical Presentation

SVT classically presents as paroxysmal palpitations of sudden onset and termination ("on-off switch" quality). Patients often describe "flip-flopping," "racing," or "fluttering" in the chest. Associated symptoms include:

Episodes may be triggered by caffeine, stress, exercise, alcohol, or may occur spontaneously. Duration ranges from seconds to hours. Heart rates during SVT are typically 150–220 bpm. Blood pressure may be reduced due to reduced diastolic filling time at rapid rates.

Physical examination during SVT: regular rapid pulse, hypotension possible, cannon A waves in the JVP (AVNRT), warm extremities (unlike VT which often presents with shock).

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6. Diagnosis

12-lead ECG during SVT is the cornerstone of diagnosis:

Vagal maneuvers (Valsalva, carotid sinus massage) transiently increase vagal tone, slowing AV nodal conduction. In the modified Valsalva maneuver (REVERT trial, 2015), the patient strains in semi-recumbent position then immediately lies supine with passive leg raise — this modification increased termination rate from 17% to 43% vs. standard Valsalva. Termination of tachycardia with vagal maneuvers strongly supports AVNRT or AVRT (both circuit-dependent on AV node).

Adenosine 6 mg IV rapid push (followed by 12 mg if no response): blocks AV nodal conduction transiently, terminating AVNRT/AVRT. AT may slow transiently (unmasking P waves) but not terminate. Adenosine has a half-life of <10 seconds; patients must be warned of transient chest tightness, flushing, and sense of doom.

Ambulatory monitoring: Holter (24–48h), event recorder, or implantable loop recorder for paroxysmal SVT documentation.

Electrophysiology study (EPS): Invasive catheter study mapping the reentrant circuit, confirming SVT mechanism, localizing accessory pathways, and providing definitive ablation in the same session.

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7. Acute Management

Hemodynamically unstable SVT (hypotension, altered consciousness, severe dyspnea): immediate synchronized DC cardioversion (50–100 J biphasic).

Hemodynamically stable SVT:

  1. Vagal maneuvers — modified Valsalva first; carotid sinus massage (unilateral, 5–10 seconds, avoid in carotid disease or recent stroke)
  2. Adenosine 6 mg IV rapid push via antecubital vein followed by saline flush; repeat 12 mg × 2 if no conversion; reduces to 3 mg if central line used or in heart transplant patients
  3. Verapamil 5–10 mg IV or diltiazem 0.25 mg/kg IV if adenosine fails or is contraindicated; avoid in pre-excitation/WPW (can accelerate antegrade conduction over accessory pathway)
  4. Beta-blockers IV: Metoprolol 5 mg IV, esmolol infusion
  5. DC cardioversion if pharmacologic measures fail

Avoid digoxin, verapamil, and diltiazem if WPW is suspected (pre-excitation on baseline ECG) — these block the AV node and can paradoxically accelerate conduction over the accessory pathway in AF/flutter, potentially precipitating ventricular fibrillation.

Procainamide is the preferred IV agent for SVT with suspected WPW or pre-excitation: 20–50 mg/min IV infusion up to 17 mg/kg.

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8. Long-Term Management and Ablation

Catheter ablation is first-line definitive therapy for symptomatic recurrent SVT:

Antiarrhythmic drugs for patients unwilling to undergo ablation or with infrequent/mild symptoms:

Lifestyle modifications: Reduce caffeine, alcohol; manage stress; identify personal triggers.

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9. Prognosis

SVT is generally benign in patients without structural heart disease. Spontaneous termination is common; mortality directly attributable to SVT is rare. Key prognosis points:

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Research Papers

The following PubMed topic searches return current peer-reviewed literature relevant to this condition. Each link opens a live PubMed query.

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Connections

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