Overview
Definition:
Supraventricular tachycardia (SVT) in children refers to a rapid heart rate originating above the ventricles, typically in the atria or AV node, with a heart rate exceeding 220 beats per minute in infants and 180 beats per minute in older children
It is characterized by a narrow QRS complex on electrocardiogram (ECG) unless there is aberrant conduction
Common types include AV nodal reentrant tachycardia (AVNRT), AV reentrant tachycardia (AVRT) utilizing an accessory pathway, and atrial tachycardia
SVT is the most common symptomatic tachyarrhythmia in infants and children
Clinical significance lies in its potential to cause hemodynamic instability, heart failure, and even cardiovascular collapse if prolonged or severe, necessitating prompt recognition and management.
Epidemiology:
SVT accounts for approximately 5-10% of pediatric cardiac emergencies
The incidence is estimated to be between 1 in 200 to 1 in 25,000 live births, with variations depending on the diagnostic criteria and population studied
Neonates and infants are most commonly affected, with presentation often occurring within the first year of life
Males are more commonly affected than females in infancy
Recurrence is common, with up to 50% of infants experiencing a recurrence within the first year of diagnosis
The presence of structural heart disease is uncommon in most pediatric SVT cases, with the majority being due to accessory pathways or nodal reentrant mechanisms.
Clinical Significance:
Unrecognized or inadequately treated SVT can lead to significant morbidity in children
Rapid heart rates reduce diastolic filling time, decreasing cardiac output and leading to symptoms such as irritability, poor feeding, pallor, sweating, tachypnea, and, in severe cases, hypotension, syncope, and cardiogenic shock
In infants, this can present as "Infantile Tachycardia-Induced Cardiomyopathy." Prompt diagnosis and effective management are crucial to restore sinus rhythm, prevent complications, and improve long-term outcomes
Understanding vagal maneuvers and pharmacologic interventions like adenosine is paramount for pediatricians and residents preparing for DNB and NEET SS examinations.
Clinical Presentation
Symptoms:
In infants: Irritability
Poor feeding
Lethargy
Pallor
Vomiting
Tachypnea
Sweating
In older children: Palpitations
Chest pain
Dizziness
Lightheadedness
Syncope
Anxiety
Shortness of breath.
Signs:
Heart rate >180-220 bpm (depending on age)
Narrow QRS complex (<0.08 sec) on ECG, unless bundle branch block or pre-excitation is present
Regular rhythm
May be difficult to palpate radial pulse
Signs of poor perfusion: pallor, cool extremities, delayed capillary refill
Signs of heart failure: hepatomegaly, rales, grunting respirations, increased work of breathing
Possible cannon a waves in jugular venous pulse if atrial contraction is synchronous with ventricular contraction.
Diagnostic Criteria:
Diagnosis is primarily based on ECG findings: Heart rate >180-220 bpm (infants) or >180 bpm (older children)
Regular rhythm
Narrow QRS complex
P waves may be absent, retrograde, or conducted normally but difficult to discern
Specific patterns on ECG may suggest the type of SVT (e.g., short RP’ interval in AVNRT, long RP’ interval in AVRT)
Hemodynamic stability is a key determinant for management strategy.
Diagnostic Approach
History Taking:
Detailed history of onset and duration of episodes
Frequency of episodes
Associated symptoms during episodes (irritability, feeding difficulties, syncope)
Previous episodes or known cardiac history
Family history of arrhythmias or sudden cardiac death
Medications used
Red flags: hemodynamic instability, signs of heart failure, associated congenital heart disease, syncope, family history of sudden death.
Physical Examination:
Assess vital signs, including heart rate and blood pressure
Observe for signs of distress and poor perfusion
Auscultate heart for rate and rhythm
Palpate peripheral pulses
Assess for hepatomegaly and signs of heart failure
A rapid, regular, narrow-complex tachycardia is the hallmark finding.
Investigations:
12-lead ECG is essential for diagnosis and rhythm analysis
It should be obtained during an episode if possible
If ECG is unavailable during an episode, a continuous cardiac monitor or Holter monitor may be useful for subsequent evaluation
Echocardiography may be indicated to assess for structural heart disease, particularly if the diagnosis is uncertain or if there are signs of heart failure
Serum electrolytes and thyroid function tests are generally not useful in the acute management of SVT but may be considered in recurrent or refractory cases
Advanced imaging like cardiac MRI is rarely needed for diagnosis of typical pediatric SVT.
Differential Diagnosis:
Sinus tachycardia (usually variable rate, often related to fever, dehydration, pain, anxiety, or hyperthyroidism)
Atrial flutter (sawtooth pattern of P waves)
Atrial fibrillation (irregularly irregular rhythm)
Ventricular tachycardia (wide QRS complex, usually slower rate, often associated with structural heart disease)
Sinus node reentrant tachycardia
Wandering atrial pacemaker
Supraventricular extrasystoles
Junctional ectopic tachycardia (JET), especially in post-operative cardiac patients (often wide QRS).
Management
Initial Management:
Immediate assessment of hemodynamic stability
If unstable (hypotension, altered mental status, signs of shock, acute heart failure, prolonged episode), immediate synchronized cardioversion (1-2 J/kg, increasing to 4 J/kg if needed) is the first-line treatment, irrespective of the rhythm
If stable, attempt vagal maneuvers
If unsuccessful or if the child is unable to tolerate them, pharmacologic therapy with adenosine is the next step.
Vagal Maneuvers:
These aim to stimulate the vagus nerve to slow conduction through the AV node
In infants and younger children: facial immersion in ice water (Valsalva maneuver with face mask)
In older children: Valsalva maneuver (bearing down), carotid sinus massage (contraindicated in children with risk factors for carotid artery disease), or gagging
Success rates vary, with higher success in conscious older children
Perform with caution, especially carotid sinus massage.
Adenosine Pharmacology:
Adenosine is a nucleoside that acts as a negative chronotrope and dromotrope by slowing conduction through the AV node and producing transient AV block
It is the drug of choice for pharmacologic termination of most narrow-complex SVTs
Pediatric dose: Rapid IV bolus of 0.1 mg/kg (max 6 mg), followed by a second bolus of 0.2 mg/kg (max 12 mg) if the first dose is ineffective
Administer as a rapid bolus followed immediately by a 5-10 mL saline flush to minimize the short half-life and local effects
Common side effects include transient flushing, dyspnea, chest discomfort, and a brief period of asystole or bradycardia, which are usually well-tolerated
It is ineffective for SVTs originating above the AV node (e.g., atrial tachycardia).
Pharmacological Treatment Guidelines:
If vagal maneuvers fail in a stable child, administer adenosine as described
If adenosine is ineffective, consider other antiarrhythmic agents like procainamide (pediatric dose 2-5 mg/kg IV over 10-30 minutes, may repeat) or amiodarone (pediatric dose 5 mg/kg IV over 30-60 minutes)
Verapamil is generally avoided in infants due to risk of profound hypotension and myocardial depression but may be considered cautiously in older children with documented AVNRT
Long-term management may involve daily oral antiarrhythmic therapy (e.g., flecainide, sotalol, propranolol) or radiofrequency catheter ablation, especially for recurrent or difficult-to-manage SVT.
Supportive Care:
Continuous cardiac monitoring is essential during and after treatment
Observe for recurrence of SVT or development of other arrhythmias
Monitor vital signs, including blood pressure and oxygen saturation
Ensure adequate IV access
Provide reassurance and comfort to the child and family.
Complications
Early Complications:
Hypotension and shock from prolonged SVT or adverse drug reactions to adenosine (e.g., severe bradycardia, asystole)
Paradoxical conversion to atrial fibrillation or flutter
Myocardial dysfunction or heart failure due to prolonged tachycardia
Injury from cardioversion (burns, arrhythmias).
Late Complications:
Recurrent SVT episodes
Development of atrial fibrillation in patients with accessory pathways
Progressive left ventricular dysfunction (tachycardia-induced cardiomyopathy) if chronic or untreated SVT
Developmental delays or neurological deficits if significant hypoxic events occurred
Increased risk of syncope or falls in older children.
Prevention Strategies:
Early identification and treatment of SVT episodes
Maintaining sinus rhythm through optimal antiarrhythmic therapy or catheter ablation
Education of parents/guardians on recognizing SVT and when to seek medical attention
Regular follow-up with a pediatric cardiologist
Avoiding triggers if known (e.g., dehydration, excessive stimulant intake in older children).
Prognosis
Factors Affecting Prognosis:
Hemodynamic stability during episodes
Presence or absence of structural heart disease
Age at presentation (infants may have more severe initial presentation)
Effectiveness of acute treatment and long-term management
Frequency and duration of recurrent episodes.
Outcomes:
The prognosis for most children with SVT is excellent, especially those with no underlying cardiac structural abnormalities and those who respond well to treatment
The majority of episodes can be terminated with vagal maneuvers or adenosine
Recurrence rates can be high, but many children outgrow SVT or can be effectively managed with medication or ablation
Tachycardia-induced cardiomyopathy usually resolves with restoration and maintenance of sinus rhythm
Long-term outcomes are generally favorable with appropriate medical follow-up.
Follow Up:
Children with SVT should have regular follow-up with a pediatric cardiologist to monitor for recurrences, assess the effectiveness of therapy, and re-evaluate the need for long-term management
This may include serial ECGs, Holter monitoring, and echocardiography as indicated
Decision for electrophysiology study and catheter ablation is based on symptom burden, recurrence rates, and patient preference
Education regarding recognition of symptoms and when to seek emergency care is crucial for families.
Key Points
Exam Focus:
DNB/NEET SS will focus on differentiating SVT from sinus tachycardia and VT
Know the pediatric doses of adenosine (0.1 mg/kg, then 0.2 mg/kg) and the importance of rapid IV push with saline flush
Understand the indications for cardioversion versus pharmacologic therapy based on hemodynamic stability
Recognize the ECG features of SVT
Be aware of common causes of pediatric SVT (AVNRT, AVRT).
Clinical Pearls:
Always assess hemodynamic stability first before attempting interventions
Vagal maneuvers are safe and often effective, especially in older children
Adenosine is the first-line drug for stable narrow-complex SVT, but it will not terminate atrial tachycardia
If the child is refractory to adenosine, consider procainamide or amiodarone
Be cautious with verapamil in infants
Monitor for post-adenosine asystole as a benign but sometimes startling effect
Recurrence is common, so patient education is key.
Common Mistakes:
Confusing sinus tachycardia with SVT
Delaying cardioversion in an unstable child
Administering adenosine for atrial tachycardia
Inadequate saline flush with adenosine, leading to prolonged side effects
Using verapamil in infants without extreme caution
Misinterpreting wide-complex tachycardias as SVT with aberrancy without considering VT
Forgetting to reassess hemodynamic status after interventions.