Overview
Definition:
Supraventricular tachycardia (SVT) in infants is a rapid heart rhythm originating above the ventricles, typically characterized by a heart rate exceeding 220 beats per minute in neonates and infants, often causing significant hemodynamic instability due to the immature compensatory mechanisms in this age group
It is the most common sustained tachycardia encountered in pediatric cardiology.
Epidemiology:
SVT affects approximately 0.1-1% of the pediatric population
In infants, the most common types are atrioventricular reentrant tachycardia (AVRT) involving an accessory pathway (e.g., Wolff-Parkinson-White syndrome) and atrioventricular nodal reentrant tachycardia (AVNRT)
The peak incidence occurs in the first year of life, with a bimodal distribution in adolescence
Male infants are more commonly affected than females.
Clinical Significance:
SVT in infants can lead to rapid decompensation, characterized by signs of heart failure, poor feeding, lethargy, pallor, and even shock
Persistent or poorly managed SVT can result in myocardial dysfunction (tachycardia-induced cardiomyopathy) and, in severe cases, death
Prompt and accurate diagnosis and management are crucial for preventing adverse outcomes and ensuring optimal development.
Clinical Presentation
Symptoms:
Sudden onset of rapid heart rate
Irritability and poor feeding
Lethargy and decreased activity
Pallor or cyanosis
Tachypnea and dyspnea
Vomiting or emesis
Syncope or near-syncope (rare in young infants)
Abrupt termination of episodes.
Signs:
Heart rate > 220 bpm, often regular
Narrow QRS complex (unless pre-excited)
Diminished heart sounds
Gallop rhythm
Hepatomegaly secondary to right heart failure
Hypotension
Cool extremities
Poor peripheral perfusion
Irregular pulse during very rapid rates.
Diagnostic Criteria:
Diagnosis is primarily based on electrocardiographic (ECG) findings
A sustained heart rate > 220 bpm with a narrow QRS complex (unless there is rate-related bundle branch block or an accessory pathway causing pre-excitation) strongly suggests SVT
Key features include absence of clear P waves or presence of P waves occurring after the QRS, often in retrograde fashion, leading to a short RP interval relative to the R-R interval
ECG during sinus rhythm may reveal pre-excitation patterns if an accessory pathway is present.
Diagnostic Approach
History Taking:
Focus on the onset and duration of symptoms
Identify triggers if any (though often none are apparent)
Assess for any previous similar episodes
Detailed feeding history and signs of poor growth
Family history of arrhythmias or sudden cardiac death
Maternal history of arrhythmias during pregnancy.
Physical Examination:
Assess vital signs, paying close attention to heart rate and blood pressure
Evaluate for signs of poor perfusion (capillary refill time, skin temperature)
Assess respiratory effort and oxygen saturation
Palpate for hepatomegaly
Auscultate for heart murmurs or gallops
Assess for edema.
Investigations:
12-lead ECG is the cornerstone for diagnosis, capturing the rhythm and characteristic features of SVT
ECG interpretation should focus on heart rate, rhythm regularity, QRS duration, and the relationship between P and QRS waves
If the infant is stable, a longer rhythm strip or Holter monitoring may be considered
Echocardiography can assess cardiac structure and function and rule out congenital heart disease
Blood tests (CBC, electrolytes, glucose, calcium) are important to rule out metabolic causes of tachycardia.
Differential Diagnosis:
Sinus tachycardia (often related to fever, pain, dehydration, anxiety)
Atrial flutter
Atrial fibrillation (rare in infancy)
Ventricular tachycardia (less common in neonates and infants without structural heart disease)
Sepsis
Hyperthyroidism
Anemia
Congenital heart disease with shunting.
Management
Initial Management:
Assessment of hemodynamic stability is paramount
If unstable (hypotension, altered mental status, severe respiratory distress, cardiogenic shock), immediate synchronized cardioversion (0.5-1 J/kg, increasing to 2 J/kg if needed) is indicated
If stable, pharmacologic intervention can be attempted
Always attempt vagal maneuvers first in a stable infant.
Medical Management:
Vagal Maneuvers: Ice to the face (or a bowl of ice water for face immersion) for 10-20 seconds is the preferred method in infants
Other maneuvers like carotid sinus massage are generally avoided in infants due to risk of bradycardia or asystole
Adenosine: If vagal maneuvers are unsuccessful, intravenous adenosine is the first-line pharmacologic agent for stable SVT
Dose: 0.1 mg/kg per dose, maximum 6 mg per dose
If ineffective, may repeat at 0.2 mg/kg per dose, maximum 12 mg per dose
Administer as a rapid bolus (over 1-2 seconds) with a rapid saline flush
Monitor for transient asystole, bradycardia, flushing, and bronchospasm
Amiodarone or Flecainide: May be used if adenosine is ineffective or contraindicated, but with caution due to potential proarrhythmic effects and side effects, particularly in infants with structural heart disease
Digoxin: Generally not recommended for acute termination of SVT due to slow onset of action and potential for toxicity, but may be used for rate control in certain chronic tachyarrhythmias or post-acute management.
Surgical Management:
Not typically for acute management
Electrophysiology (EP) study with catheter ablation is considered for recurrent, symptomatic, or drug-refractory SVT, especially AVRT due to accessory pathways
This is usually deferred until the child is older, but can be performed in infants with severe, life-threatening SVT.
Supportive Care:
Continuous cardiac monitoring (ECG, SpO2, BP) is essential during and after treatment
Maintain airway and adequate oxygenation
Ensure adequate hydration
Manage any signs of heart failure with appropriate diuretics if necessary
Provide comfort measures for the infant.
Complications
Early Complications:
Hemodynamic instability, shock, cardiogenic shock
Myocardial dysfunction leading to heart failure
Myocardial infarction (rare)
Seizures
Transient neurological deficits
Death.
Late Complications:
Tachycardia-induced cardiomyopathy if SVT is prolonged or recurrent
Developmental delay secondary to prolonged episodes of poor perfusion
Recurrence of SVT episodes
Risk of sudden cardiac death (rare).
Prevention Strategies:
For infants with known accessory pathways or recurrent SVT, long-term oral antiarrhythmic therapy is often initiated
Beta-blockers (e.g., propranolol, metoprolol) or flecainide are common choices
Amiodarone may be used but has more significant long-term side effects
Catheter ablation offers a curative option for selected patients with recurrent or drug-refractory SVT and is becoming more common in infants and children.
Prognosis
Factors Affecting Prognosis:
The primary factors influencing prognosis are the hemodynamic stability during episodes, the response to treatment, and the underlying mechanism of SVT
Infants with stable SVT and prompt response to vagal maneuvers or adenosine generally have a good prognosis
Infants presenting with significant instability, heart failure, or those requiring multiple interventions have a poorer short-term outlook.
Outcomes:
With effective management, most infants with SVT achieve resolution of their condition or effective control with medication
Many infants, especially those with AVNRT, may outgrow their SVT
Those with accessory pathways may require ablation
Long-term outcomes are generally excellent with appropriate intervention and follow-up.
Follow Up:
Infants treated for SVT should have regular cardiology follow-up
The frequency depends on the severity of episodes, response to treatment, and underlying cause
Follow-up may involve ECG, Holter monitoring, or echocardiography
For those on antiarrhythmic medications, monitoring for drug efficacy and side effects is crucial
Patients undergoing ablation require post-procedural monitoring.
Key Points
Exam Focus:
Differentiate SVT from sinus tachycardia in infants
Recognize the ECG hallmarks of SVT (narrow complex, rate > 220 bpm)
Know the management algorithm for stable vs
unstable SVT
Identify adenosine as the first-line drug for stable SVT and its dose
Understand the role of vagal maneuvers (ice to face)
Recognize that SVT can lead to tachycardia-induced cardiomyopathy.
Clinical Pearls:
Always assess hemodynamic stability first
this dictates the management approach
Use the smallest effective dose of adenosine and administer it rapidly
Remember the potential for transient asystole after adenosine
Consider the ice-to-face maneuver as the initial step for stable infants
Be vigilant for signs of heart failure, which can develop rapidly
Differentiate between AVNRT and AVRT based on ECG findings if possible.
Common Mistakes:
Treating sinus tachycardia as SVT or vice-versa
Delaying cardioversion in unstable infants
Using incorrect adenosine dosing or administration technique
Forgetting to attempt vagal maneuvers first in stable infants
Over-reliance on digoxin for acute SVT termination
Failing to monitor for recurrence or long-term complications like cardiomyopathy.