Supraventricular tachycardia (SVT)

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Introduction and Classification

Supraventricular tachycardia (SVT) is a general term encompassing essentially all forms of paroxysmal or incessant tachycardia originating above or within the His bundle, excluding ventricular tachycardia.
SVT is the most common mechanism of arrhythmia in infants and children, and is generally characterized by rapid activation of the ventricles via the normal His-Purkinje system, typically resulting in a narrow QRS complex.
SVT can be broadly classified into three major pathophysiologic subcategories: reentrant tachycardias using an accessory pathway (atrioventricular reciprocating tachycardia, AVRT), reentrant tachycardias without an accessory pathway (atrioventricular nodal reentry tachycardia, AVNRT), and ectopic or automatic tachycardias.

Pathophysiology and Subtypes

Atrioventricular Reciprocating Tachycardia (AVRT): This is the most common mechanism of SVT in infants, utilizing an accessory bypass tract. In Orthodromic Reentry Tachycardia (ORT), the electrical impulse travels antegrade down the normal AV node and retrograde up the accessory pathway. If the pathway conducts bidirectionally, it is known as Wolff-Parkinson-White (WPW) syndrome. Permanent Junctional Reciprocating Tachycardia (PJRT) is a specific form of ORT utilizing a concealed, slowly conducting accessory pathway typically located on the posterior tricuspid valve or proximal coronary sinus, leading to an incessant tachycardia.
Atrioventricular Nodal Reentry Tachycardia (AVNRT): This involves two functional pathways within the AV node itself—a slow pathway with a short refractory period and a fast pathway with a longer refractory period. It is rare in infancy but increases in prevalence during childhood and adolescence. "Slow-fast" AVNRT accounts for 80-90% of these cases.
Ectopic/Automatic Tachycardias: These include Atrial Ectopic Tachycardia (AET) and Junctional Ectopic Tachycardia (JET). They result from an abnormal focus with enhanced automaticity rather than a reentrant circuit, meaning they typically "warm up" and "cool down" rather than exhibiting abrupt onset and termination.

Clinical Manifestations

Clinical presentation varies significantly based on the patient's age and the duration of the tachycardia.
Fetal Presentation: Fetal SVT most commonly occurs between 24 and 32 weeks of gestation and can lead to hydrops fetalis (in utero heart failure) if sustained.
Infants: In neonates and infants, the heart rate frequently ranges from 240 to 300 beats per minute. Because infants cannot communicate palpitations, the tachycardia may go unrecognized for 6 to 24 hours or more until tachycardia-induced cardiomyopathy and overt congestive heart failure develop. These infants present with poor feeding, irritability, an ashen color, tachypnea, poor peripheral pulses, and hepatomegaly.
Older Children and Adolescents: Tachycardia rates generally range from 150 to 250 beats per minute. Patients typically experience an abrupt onset and termination of symptoms, which include an awareness of a rapid heart rate (palpitations), chest discomfort, dizziness, shortness of breath, and exercise intolerance. AVNRT is frequently triggered by exercise or stress and is occasionally associated with syncope.
Precipitating Factors: SVT episodes can be provoked by acute infections in infants, or by exposure to caffeine, nonprescription decongestants, and bronchodilators in older children.

Diagnostic Investigations

Auscultation

Auscultation reveals a rapid, extremely regular heart rate that does not vary significantly with respiration, distinguishing it from sinus tachycardia which fluctuates with parasympathetic and sympathetic tone.
If the patient has developed tachycardia-induced cardiomyopathy due to prolonged, unrecognized SVT, a pathologic gallop rhythm and signs of pulmonary congestion (respiratory crackles or wheezing) may be audible.

Electrocardiogram (ECG)

The classic ECG finding in neonates and children with SVT is a narrow QRS complex tachycardia (typically <0.08 seconds in neonates and <0.12 seconds in older adolescents) with a rigidly fixed R-R interval.
AVNRT: During tachycardia, the QRS is normal, and a retrograde P wave may be visible in lead V1, often mimicking a subtle "RSr'" pattern that is absent during normal sinus rhythm.
Orthodromic AVRT: Demonstrates a normal QRS during tachycardia with a retrograde P wave featuring a negative axis in the inferior leads (II, III, aVF) and a relatively short VA interval, though typically >70 milliseconds.
Wolff-Parkinson-White (WPW) Syndrome: During normal sinus rhythm, the ECG reveals the classic preexcitation triad: a short PR interval, a wide QRS complex, and a slurred QRS upstroke known as a delta wave.
PJRT: Characterized by a prolonged RP interval (the RP interval is greater than half of the RR interval) with inverted P waves in leads II, III, and aVF.
Atrial Ectopic Tachycardia (AET): Displays a variable rate (seldom >200 beats/min) with identifiable, abnormal P wave morphology and axis compared to baseline sinus rhythm, often with variable AV conduction.

Echocardiography

Echocardiography is crucial to assess for structural congenital heart disease and to evaluate left ventricular systolic function.
It is particularly important for identifying tachycardia-induced cardiomyopathy (ventricular dysfunction and dilation) in infants presenting with incessant tachycardias like PJRT or prolonged AVRT.
Certain structural lesions have highly specific associations with SVT mechanisms; for example, Ebstein anomaly, congenitally corrected transposition of the great arteries (L-TGA), and hypertrophic cardiomyopathy are highly associated with the presence of accessory pathways and WPW syndrome.

Cardiac Catheterization and Electrophysiology

Invasive intracardiac electrophysiology studies (EPS) are utilized to evaluate the conduction characteristics of the AV node and accessory pathways, to initiate the tachyarrhythmia, and to map the precise anatomic location of the arrhythmogenic focus or bypass tract.
During an EPS for AVRT, mapping demonstrates retrograde atrial activation via the accessory pathway.
For asymptomatic patients with WPW, EPS may be used for risk stratification to determine the shortest preexcited R-R interval (SPRRI) during induced atrial fibrillation; an SPRRI ≤ 250 ms indicates a high-risk pathway capable of rapid antegrade conduction that could degenerate into ventricular fibrillation.

Management

Acute Management

Vagal Maneuvers: In stable patients, vagal stimulation is the first-line therapy. In infants, this is achieved by applying an ice bag to the entire face for 15 to 30 seconds. Older children can perform the Valsalva maneuver, bear down, or perform a headstand. Ocular pressure is strictly contraindicated.
Pharmacologic Cardioversion: If vagal maneuvers fail, intravenous Adenosine is the drug of choice due to its rapid onset and short half-life. It is administered via rapid IV push starting at 0.1 mg/kg (maximum 6 mg), which can be increased to 0.2 mg/kg (maximum 12 mg) if unsuccessful. Adenosine blocks AV nodal conduction, terminating reentrant circuits that rely on the AV node (AVRT and AVNRT).
Direct Current (DC) Cardioversion: In cases of hemodynamic instability, cardiogenic shock, or severe heart failure, synchronized DC cardioversion at 0.5 to 2 Joules/kg is the immediate treatment of choice to restore sinus rhythm.

Chronic and Preventive Therapy

Non-WPW SVT (e.g., AVNRT): Beta-adrenergic blockers are the mainstay of chronic drug therapy. Digoxin may also be effective in infants but is less reliable in older children.
WPW Syndrome: Digoxin and intravenous calcium channel blockers (like verapamil) are absolutely contraindicated as they may preferentially block the AV node and accelerate antegrade conduction down the accessory pathway, risking fatal ventricular fibrillation. These patients are safely managed with beta-blockers.
Refractory Cases: For tachycardias resistant to first-line agents, stronger antiarrhythmics such as flecainide, propafenone, sotalol, or amiodarone may be required, provided the patient has structurally normal heart function without contraindications.

Catheter Ablation

Transcatheter radiofrequency or cryoablation is the definitive, curative treatment for pediatric SVT.
Ablation is indicated for older children and adolescents, for patients with arrhythmias refractory to medical therapy, for those experiencing intolerable drug side effects, and for patients with WPW who exhibit high-risk features or have survived a sudden cardiac arrest.
Catheter ablation offers a success rate of 90% to 98% for eliminating accessory pathways and >95% success for curing AVNRT, though it carries a small but real risk of iatrogenic complete AV block requiring permanent pacemaker placement.