Approach to Supraventricular Arrhythmias¶
Chapter 253 | Part 6: Disorders of the Cardiovascular System
KEY CLINICAL POINTS¶
- Supraventricular arrhythmias (SVAs) include tachycardias originating above the ventricles, such as atrial tachycardias, AV nodal reentry tachycardia (AVNRT), and accessory pathway-mediated tachycardias.
- Narrow-complex SVTs (QRS <120 ms) are typically AV nodal-dependent, while wide-complex tachycardias may indicate preexcitation (e.g., Wolff-Parkinson-White syndrome) or ventricular tachycardia.
- Diagnosis requires 12-lead ECG with long rhythm strip to differentiate between regular/irregular rhythms, AV block patterns, and preexcitation.
- Adenosine (6-12 mg) is first-line for AV nodal-dependent SVTs, while vagal maneuvers (e.g., carotid sinus massage) may terminate AVNRT.
- Asymptomatic SVAs often require no treatment, but symptomatic cases may need cardioversion, ablation, or rate control with AV nodal blockers.
1. DEFINITION & OVERVIEW¶
Supraventricular arrhythmias (SVAs) are abnormal rhythms originating above the ventricles, including atrial tachycardias, AV nodal reentry tachycardia (AVNRT), and accessory pathway-mediated tachycardias. They are broadly classified as narrow-complex (QRS <120 ms) or wide-complex tachycardias. SVTs are defined as heart rates >100 beats/min, with narrow-complex tachycardias typically involving AV nodal reentry or preexcitation.
Table 253-1: Mechanisms of Supraventricular Arrhythmias¶
| Category | Subcategory | Defining Features |
|---|---|---|
| Physiologic Sinus Tachycardia | Normal sinus mechanism | Precipitated by exertion, stress, or concurrent illness |
| Pathologic SVT | Atrial Tachycardias | Regular atrial tachycardia with defined P waves; may be sustained, paroxysmal, or incessant |
| Pathologic SVT | Atrial Flutter/Macroreentrant Tachycardia | Organized atrial activity on ECG (sawtooth flutter waves >200 bpm) |
| Pathologic SVT | Atrial Fibrillation | Chaotic atrial activity with variable ventricular rate; most common sustained arrhythmia in older adults |
| Pathologic SVT | Multifocal Atrial Tachycardia | Multiple discrete P waves in pulmonary disease exacerbations |
| Category | Subcategory | Defining Features |
|---|---|---|
| Pathologic SVT | AVNRT | Paroxysmal regular tachycardia with P waves at end of QRS or absent; most common in young adults |
| Pathologic SVT | Accessory Pathway Tachycardias | Wide QRS tachycardia with preexcitation (WPW) or antidromic AVRT |
1.1 Mechanisms of Supraventricular Arrhythmias¶
SVAs arise from three main mechanisms: (1) atrial tachycardias (focal or macroreentrant), (2) AV nodal reentry tachycardia (AVNRT), and (3) accessory pathway-mediated tachycardias (orthodromic AV reciprocating tachycardia [AVRT] or antidromic tachycardia). Pathologic SVTs are distinguished from physiologic sinus tachycardia by their persistence despite AV block and lack of clear precipitating factors.
2. EPIDEMIOLOGY¶
SVTs are common in adults, with AVNRT being the most prevalent form. Paroxysmal SVTs are most common in patients without structural heart disease. Atrial fibrillation is more prevalent in older adults, while accessory pathway-mediated tachycardias (e.g., AVRT) are more common in younger individuals. Preexcitation syndromes (e.g., WPW) may present with sudden cardiac arrest in patients with underlying heart disease.
2.1 Risk Factors¶
Risk factors include young age for AVNRT, structural heart disease for atrial fibrillation, and genetic predisposition for accessory pathways. Hypertension, electrolyte imbalances, and stimulant use may precipitate episodes.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
SVAs arise from abnormal electrical circuits in the atria or AV node. Atrial tachycardias result from focal automaticity or reentry, while AVNRT involves a macroreentrant circuit through the AV node. Accessory pathways (e.g., WPW) allow anterograde conduction to the ventricles, creating a reentrant circuit during AVRT. Preexcitation shortens the refractory period, enabling antidromic tachycardia with wide QRS complexes.
4. CLINICAL FEATURES¶
Symptoms include palpitations, chest pain, dyspnea, and syncope. Asymptomatic cases may be detected on routine ECG. Complications include hemodynamic instability, cardiac arrest (especially in WPW with rapid rates >250 bpm), and increased risk of stroke in atrial fibrillation. Atrial flutter may present with palpitations and fatigue, while AVNRT is often associated with sudden onset of regular tachycardia.
4.1 Differential Diagnosis¶
Differentiate between narrow-complex SVTs (AVNRT, AVRT, atrial tachycardia) and wide-complex tachycardias (ventricular tachycardia, preexcited tachycardia). Consider sinus tachycardia, junctional rhythms, and atrial fibrillation with preexcitation.
5. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis requires 12-lead ECG with long rhythm strip to assess rhythm regularity, AV block, and preexcitation. Narrow-complex tachycardia suggests AV nodal or atrial origin, while wide QRS may indicate preexcitation. Ambulatory ECG monitoring is used for transient arrhythmias. Electrophysiology studies may be required for complex cases.
Table 253-2: Vagal Maneuvers¶
| Maneuver | Mechanism | Effect |
|---|---|---|
| Carotid sinus massage | Stimulates vagus nerve | Induces transient AV block |
| Valsalva maneuver | Increases intrathoracic pressure | May terminate AVNRT |
| Cold water immersion | Diver’s reflex | Induces vagal response |
| Adenosine administration | AV node blockade | Terminates AV nodal-dependent tachycardia |
5.1 Diagnostic Algorithm¶
- Obtain 12-lead ECG with long rhythm strip.
- Assess rhythm regularity and QRS morphology.
- Identify AV block patterns (e.g., 2:1 block in AVNRT).
- Look for preexcitation (delta waves) in wide-complex tachycardia.
- Use adenosine or vagal maneuvers to test for AV nodal dependency.
6. MANAGEMENT & TREATMENT¶
Acute management includes vagal maneuvers, adenosine (6-12 mg), or calcium channel blockers (e.g., verapamil). For recurrent episodes, catheter ablation is curative for AVNRT and accessory pathway-mediated tachycardias. Rate control with beta-blockers or calcium channel blockers is used for atrial fibrillation. Long-term management focuses on preventing recurrence and addressing underlying heart disease.
6.1 Treatment Algorithm¶
- Acute termination: Adenosine (6-12 mg) or vagal maneuvers.
- If adenosine fails, use calcium channel blockers (verapamil) or beta-blockers.
- For accessory pathway-mediated tachycardia, consider synchronized cardioversion.
- Long-term: Catheter ablation for recurrent SVTs.
- Rate control for atrial fibrillation with AV nodal blockers.
7. PROGNOSIS & COMPLICATIONS¶
Prognosis is generally favorable for AVNRT and focal atrial tachycardia, but complications include hemodynamic instability, syncope, and cardiac arrest in preexcited tachycardias. Atrial fibrillation carries a higher risk of stroke and heart failure. Untreated SVTs may lead to progressive heart failure or sudden cardiac death in patients with underlying disease.
8. SPECIAL CONSIDERATIONS¶
In pregnancy, AVNRT is common and typically benign, but anticoagulation is required for atrial fibrillation. In pediatrics, SVTs are often benign but may require ablation. Elderly patients with atrial fibrillation require careful anticoagulation to prevent stroke. Patients with WPW and rapid rates (>250 bpm) are at risk for hemodynamic collapse and require immediate intervention.
9. KEY POINTS & CLINICAL PEARLS¶
- Narrow-complex SVTs are AV nodal-dependent; wide-complex tachycardias may indicate preexcitation or ventricular tachycardia.
- Adenosine is first-line for AV nodal-dependent SVTs; vagal maneuvers may terminate AVNRT.
- Asymptomatic SVAs often require no treatment, but symptomatic cases need cardioversion or ablation.
- Atrial fibrillation with preexcitation carries a risk of ventricular fibrillation at rates >250 bpm.
- Catheter ablation is curative for most SVTs, especially AVNRT and accessory pathway-mediated tachycardias.