Skip to content
Download PDF

Paroxysmal SupraventricularTachycardias

Chapter 256 | Part 6: Disorders of the Cardiovascular System II · Part 6 – Cardiovascular Disorders · Chapter 256

Key Clinical Points

  1. AVNRT is the most common form of PSVT, representing approximately 60% of cases referred for catheter ablation.
  2. WPW syndrome is defined as a preexcited QRS during sinus rhythm and episodes of PSVT; concealed accessory pathways allow only retrograde conduction.
  3. Acute management of stable narrow QRS PSVT utilizes vagal maneuvers, adenosine, or AV nodal blocking agents (beta blockers, calcium channel blockers).
  4. Preexcited atrial fibrillation with R-R intervals <250 ms is associated with a higher risk of ventricular fibrillation and sudden death.
  5. Catheter ablation of the slow AV nodal pathway is curative in >95% of patients with AVNRT, with a major risk of AV block requiring permanent pacemaker implantation in <1%.
  6. Catheter ablation targeting the AT focus is effective in >80% of patients and is recommended for recurrent symptomatic atrial tachycardia or incessant AT causing tachycardia-induced cardiomyopathy.
  7. Junctional ectopic tachycardia (JET) is rare in adults but frequently encountered as an incessant tachycardia in children, often in the perioperative period of surgery for congenital heart disease.
  8. Patients with preexcitation but no arrhythmia symptoms have a risk of sudden death estimated to be 1 per 1000 patient-years in adults, but ~2 per 1000 patient-years in children.
  9. Administration of AV nodal–blocking agents (verapamil, diltiazem, beta blockers, adenosine, amiodarone) is contraindicated during preexcited AF.
  10. Tachycardia-induced cardiomyopathy can occur with incessant tachycardia; anticoagulation indications for atrial tachycardia are unclear but not considered equivalent to atrial fibrillation.

1. DEFINITION & OVERVIEW

• SVT Definition: Broad group of tachyarrhythmias based on anatomic origin; includes sinus tachycardia, atrial tachycardia (AT), atrial flutter, AVNRT, and atrial fibrillation. • AVNRT: Tachycardia involving the AV node and the perinodal atrium. • Accessory Pathways (APs): Abnormal connections allowing conduction between the atrium and ventricles across the AV ring; present from birth due to failure of complete partitioning of atrium and ventricle by the fibrous AV rings. • WPW Syndrome: Defined as a preexcited QRS during sinus rhythm and episodes of PSVT. • Classification of SVT: ◦ AVNRT ◦ Junctional tachycardia ◦ AV reciprocating tachycardia (AVRT) utilizing an accessory pathway ◦ Atrial tachycardia (AT) ◦ Atrial flutter ◦ Atrial fibrillation ◦ Preexcited tachycardias (WPW syndrome) ◦ Concealed accessory pathways

2. EPIDEMIOLOGY

• Accessory Pathways: Occur in 1 in 1500–2000 people. • Associated Conditions: ◦ Mostly structurally normal hearts. ◦ Ebstein’s anomaly of the tricuspid valve. ◦ Hypertrophic cardiomyopathy (including PRKAG2 mutations, Danon’s disease, and Fabry’s disease). • AVNRT Prevalence: Most common in 2nd to 4th decades; more frequent in women. • Sudden Death Risk (Preexcitation only): ◦ Adults: ~1 per 1000 patient-years. ◦ Children: ~2 per 1000 patient-years.

3. ETIOLOGY & PATHOPHYYSOLOGY

• AVNRT Mechanism: Reentry involving the AV node and the perinodal atrium. ◦ Slow Pathway: Right inferior extension from compact AV node to coronary sinus; used for reentry. ◦ Fast Pathway: Located at the top of the AV node; provides rapid conduction to the atrium. ◦ Clinical Presentation: P wave is often hidden or occurs just before/after QRS due to similar conduction times. • Accessory Pathways (APs): ◦ Concealed APs: Allow only retrograde conduction → no preexcitation in sinus rhythm, but SVT can occur. ◦ Fasciculoventricular connections: Produce preexcitation but do not cause arrhythmia due to short circuit length. ◦ Atriofascicular pathways (Mahiam fibers): Duplicate AV node/His-Purkinje system; produce wide-complex tachycardia with LBBB configuration. • Preexcitation Morphology: ◦ Right-sided: Preexcites RV → LBBB-like configuration in lead V; marked preexcitation. ◦ Left-sided: Preexcites LV → RBB-like configuration in lead V; negative delta wave in aVL. ◦ Diaphragmatic (paraseptal): Delta waves negative in leads III and aVF.

Table 1: Accessory Pathway Locations and ECG Morphology ◦ Right-sided: Preexcites RV → LBBB-like configuration in lead V; marked preexcitation. ◦ Left-sided: Preexcites LV → RBB-like configuration in lead V; negative delta wave in aVL. ◦ Diaphragmatic surface (paraseptal): Delta waves negative in leads III and aVF.

4. CLINICAL FEATURES

• General Symptoms: Palpitations, angina (elderly), pulmonary edema (elderly), hypotension (elderly), syncope (elderly). • Physical Signs: ◦ Cannon A wave in jugular pulse. ◦ Fluttering sensation in the neck. ◦ Post-tachycardia diuresis (due to release of natriuretic peptides from elevated venous pressures). • Junctional Ectopic Tachycardia (JET): ◦ Narrow QRS tachycardia with ventriculoatrial (VA) block; AV dissociation present. ◦ Associated with increased adrenergic tone or post-ablation period. ◦ Often does not require specific therapy. • Preexcited Tachycardia: ◦ Wide QRS complex; often indistinguishable from monomorphic VT. ◦ Diagnosis suggested by preexcitation in sinus rhythm. • Preexcited Atrial Fibrillation (AF): ◦ Wide-complex, very irregular rhythm. ◦ Risk of rapid ventricular rate if AV nodal conduction is slowed while AP conduction remains fast.

5. DIFFERENTIAL DIAGNOSIS

• AVNRT vs. AT vs. Atrial Flutter • AVNRT vs. WPW vs. Concealed AP • Narrow QRS PSVT vs. Wide QRS Tachycardia • Monomorphic Ventricular Tachycardia vs. Preexcited Tachycardia • Orthodromic AV reentry vs. Atypical AV nodal reentry or AT • Permanent junctional reciprocating tachycardia (PJRT) vs. Orthodromic AV reentry

Distinguishing Features: ◦ AVNRT: P waves at end of QRS, negative in inferior limb leads. ◦ AT: Discrete P waves with isoelectric segments between. ◦ Atrial Flutter: Sawtooth waves, variable block. ◦ WPW: Preexcited QRS during sinus rhythm, delta waves. ◦ Concealed AP: No preexcitation during sinus rhythm, SVT episodes. ◦ PJRT: Long R-P interval, P waves negative in inferior limb leads. ◦ Mahiam: Wide-complex tachycardia with LBB configuration. ◦ Fasciculoventricular: Preexcitation without arrhythmia.

6. INVESTIGATIONS & DIAGNOSIS

  1. Initial Evaluation: ◦ Obtain 12-lead ECG to determine mechanism. ◦ Echocardiogram to exclude Ebstein’s, HCM, or tachycardia-induced cardiomyopathy.
  2. Preexcitation Assessment: Identify delta waves and short PR intervals.
  3. Stability Assessment: ◦ If stable → Vagal maneuvers or adenosine. ◦ If unstable → QRS-synchronous direct current cardioversion.
  4. Risk Stratification (Preexcited AF): ◦ Identify R-R intervals <250 ms as high risk for VF and sudden death.
  5. Invasive Evaluation: ◦ Electrophysiology study to assess if the pathway supports dangerously rapid heart rates during AF. ◦ Ambulatory monitoring/exercise testing to confirm low-risk pathways.

7. MANAGEMENT & TREATMENT

  1. Acute Management (Stable): ◦ Vagal maneuvers. ◦ Adenosine. ◦ AV nodal blocking agents: Beta blockers, Calcium channel blockers (verapamil, diltiazem).
  2. Acute Management (Unstable): ◦ QRS-synchronous direct current cardioversion.
  3. Chronic Management: ◦ Beta blockers or CCBs to slow ventricular rate. ◦ Catheter ablation: ◦ AVNRT → curative in >95% of patients; risk of AV block <1%. ◦ AT focus → effective in >80%; recommended for recurrent symptomatic AT or tachycardia-induced cardiomyopathy.
  4. Preexcited AF Management: ◦ Contraindication: AV nodal–blocking agents (verapamil, diltiazem, beta blockers, adenosine, amiodarone) are strictly contraindicated. ◦ Treatment: Electrical cardioversion or intravenous procainamide or ibutilide.

Management of Focal Atrial Tachycardia (Flowchart 1): * Focal atrial tachycardia → Hemodynamic instability? * Yes → Cardioversion → (If Recurrent or incessant) → Catheter ablation. * No → Adenosine → (If Ineffective) → Non-DHP CCB and/or beta blocker → (If Ineffective) → Antiarrhythmic therapy (see Table 250-2) → (If Recurrent or incessant) → Cather ablation. * Note: If Non-DHP CCB/beta blocker is ineffective, proceed directly to Cardioversion.

8. PROGNOSIS & COMPLICATIONS

• Tachycardia-induced cardiomyopathy: Can occur with incessant AT; requires cessation of tachycardia. • Preexcited AF Risk: ◦ Approximately 25% of APs allow R-to-R intervals <250 ms during AF. ◦ These are associated with higher risk of inducing ventricular fibrillation and sudden death. • Ablation Risks: ◦ Procedure mortality <1 in 1000 patients. ◦ Serious complications (<3%): AV block, cardiac tamponade, thromboembolism, coronary artery injury, or vascular access complications. ◦ Risk of AV block is higher if AP is near the AV node/His bundle (anteroseptal or mid-septal). • Sudden Death: ◦ Adult risk: 1 per 1000 patient-years. ◦ Child risk: ~2 per 1000 patient-years.

9. SPECIAL CONSIDERATIONS

• Pediatric Considerations: ◦ JET more common in children, often perioperatively for congenital heart disease. ◦ Higher risk of sudden death (~2 per 1000 patient-years). ◦ Use ambulatory monitoring/exercise testing to confirm low-risk AP. • Elderly Considerations: ◦ Rapid tachycardia may cause angina, pulmonary edema, hypotension, or syncope.

10. KEY PEARLS & CLINICAL TRAPS

• AVNRT is the most common form of PSVT (approx. 60% for ablation). • WPW = preexcited QRS + PSVT. • Preexcited AF with R-R <250 ms → high risk of sudden death. • No AV nodal blockers in preexcited AF (verapamil, diltiazem, beta blockers, adenosine, amiodarone). • Vagal maneuvers are first line for stable PSVT. • Catheter ablation is curative in >95% of patients with AVNRT. • Concealed APs show no preexcitation in sinus rhythm but can cause SVT. • Tachycardia-induced cardiomyopathy occurs with incessant tachycardia.