This presentation is a simplified version of the various types of cardiac arrythmias seen in pediatric age groups. We have discussed supraventricular tachycarsias and prolonged QT syndrome in details here. Hope everyone finds it useful.

1. PEDIATRIC ARRYTHMIAS
By: Dr. Sonali Paradhi Mhatre

2. ELECTRICAL CONDUCTION COMPONENTS
 Sinoatrial (SA) node
 Interatrial tract
(Bachmann’s bundle)
 Internodal tracts
 Atrioventricular (AV) node
 Bundle of His
 Right and left bundle
branches
 Purkinje fibers

3. ECG

4. Basic Definitions:
Tachycardia : HR beyond upper limit of normal for patients age.
Bradycardia: HR below lower limit of normal for patient’s age.
Sinus Rhythm: Rhythm which originated in Sinus node. It has 2
important characteristics:
1. P wave precedes each QRS complex with a regular PR
interval.
2. P axis falls between 0 and +90 degree
(Upright P wave in lead 2 and inverted P wave in aVR)

6. Age related ECG Parameters

7. Tachyarrythmias - Causes
 PRIMARY: Underlying conduction
abnormalities .
 SECONDARY: Reversible Hs & Ts
 Hypovolemia, Hypoxia, H+ ions(Acidosis)
 Hypothermia, Hypoglycemia
 Hypo/Hyperkalemia
 Toxins, Tamponade
 Tension pneumothorax
 Thrombosis (coronary, pulmonary)
 Trauma

8. Tachyarrythmias - Clinical
 Palpitations
 Lightheadedness or Syncope
 Fatigue, chest pain
 Infants: poor feeding, tachypnoea, irritability, sleepiness, pallor,
vomiting
 Hemodynamic instability: respiratory distress/failure,
 Hypotension
 Poor end-organ perfusion
 Altered sensorium
 Sudden collapse

9. Title
• Text

10. Sinus Tachycardia
• The Sinus node sends out impulses faster than usual.
• Can be a response to body’s need for increased oxygen:
Exercise,anxiety, fever, hypovolemia or circulatory shock,
anemia, CHF, administration of catecholamines, thyrotoxicosis
& myocardial disease.
• P waves are present and normal , narrow QRS, beat to beat
variability present.

11. Supraventricular Tachycardia
 Includes all forms of paroxysomal or incessant tachycardias
originating above the level of ventricles.
 This includes : Sinus Tacycardia , Reentry tachycardia, Atrial
flutter , Ectopic atrial or junctional tachycardia.
 Most common abnormal tachycardia seen in pediatric practice
and requiring treatment.
 Most frequent age presentation: 1st 3 months of life, 2nd
peaks @ 8-10 yrs and in adolescence.

12. Supraventricular Tachycardia
 Further subdivided in 3 categories:
1. Re-entrant tachycardias using an accessory pathway. (Eg. AVRT)
2. Re-entrant tachycardia without an accessory pathway.
3. Ectopic or Automatic Tachycardias.
 Atrioventricular reciprocating Tachycardia (AVRT) is the most
common mechanism of SVT in infants.
 Atrioventricular node reentry tachycardia (AVNRT) is rare in infancy
but commoner in childhood and adolescence.
 Atrial and junctional ectopic tachycardias are more commonly
associated with abnormal hearts like cardiomyopathy or in
immediate post operative period following cardiac surgery.

13. Clinical presentation in SVT
 Paroxysmal, Sudden onset and cessation.
 Occurring at rest or exercise.
 In infants, commonly precipitated by infection and in children by
bronchodilators or decongestants
 Rates of SVT vary with age (>180 bpm)
 Short paroxysms usually are not dangerous
 Prolonged attack lasting for 6-24hrs or HR > 300 bpm lead to heart
failure.
 Older children present with palpitations.
 Younger children – Basal HR higher for that age as the HR
increases greatly with crying.

14. Supraventricular Tachycardia
P waves difficult to define, but 1:1 with normal QRS
ECG similar to sinus tachycardia. The differentiation is necessary
as sinus tachycardia requires treatment of underlying cause
rather than antiarrythmia agent.

15. Difference between SVT and Sinus
tachycardia

16. ATRIOVENTRICULAR RECIPROCATING
TACHYCARDIA (AVRT)
• Most common mechanism of SVT in infants.
• Re-entrant tachycardia with an accessory pathway.
• Flow of impulses may be bidirectional or retrograde only.
• Eg. Wolff-Parkinson-White syndrome.

17. Wolff-Parkinson-White syndrome
• Characterized by the presence of a muscular bridge connecting atria
and ventricles on either the right or left side of AV ring
• Flow of impulses is bidirectional

18. Wolff-Parkinson-White syndrome
• Flow of impulses is antegrade
through the AV node and
retrograde through the
accessory pathway towards the
atrium.
• SVT in a child with WPW
showing normal QRS
complexes with P waves seen
on upstroke of T waves.
• Typical features of WPW are
apparent when tachycardia
subsides Wide QRS
complexes,delta waves,short
PR interval
• Risk of sudden death

19. Wolff-Parkinson-White syndrome
• 24 hour electrocardiographic recordings (Holter) are useful in
diagnosing and monitoring the course of therapy.
• More detailed electrophysiologic studies, performed in cardiac
catheterisation lab are often indicated in patients with refractory SVT.
• Management involves Catheter Ablation of the accessory pathway in
children and teenagers and in those who have poor arrythmia control
or intolerance to drugs.
• Ablation can be done using radiofrequency or cryoablation.
• The overall initial success rate for catheter ablation is 90-98%,
depending on location of accessory pathway.

20. AV NODAL RE-ENTRANT TACHYCARDIA
 Common form of SVT in adolescents
 Involves the use of 2 pathways within the AV node
 Precipitated by exercise
 Present with syncopal attacks
 Good control on antiarrythmic therapy
 Beta blockers remain the drug of choice for maintenance.

21. Atrial Flutter
•
• Also called intra-atrial re-entrant tachycardia
• HR > 400-600 bpm in neonates and >250-300 bpm in children
• Due to re-entrant pathway located in the right atrium circling the
tricuspid valve annulus
• Occurs in neonates with normal hearts and in children with CHD
(with large stretched atria) and post-OP.

22. Atrial Flutter
• AV dissociation occurs and ventricles respond to 2nd - 4th atrial
beat.
• Rapid and regular saw-toothed flutter waves are seen on ECG.

23. Management of Atrial Flutter
• Temporary slowing of HR by vagal maneuvres/adenosine/CCB.
• Synchronized DC cardioversion is the TOC .
• Patients with chronic atrial fluttter are at increased risk for
thromboembolic events and require anticoagulants.
• Maintenance therapy with type 1 and type 3 agents.

24. Atrial Fibrillation
• Uncommon in infants and children
• HR > 400-700 bpm with Irregularly irregular rhythm.
• Seen in Post operative cases of CHD with enlarged atria,
thyrotoxicosis, pulmonary embolism, pericarditis & cardiomyopathy.
• Management: If stable, CCB or IV Procainamide/ Amiodarone
If unstable, DC cardioversion

25. Management of SVT
1. Non- Pharmacological
methods:
 Vagal stimulation by Ice pack on
forehead.
 Older child- Valsalva maneuver,
straining, breath holding.
 Ocular pressure and carotid
massage are now Obsolete.

26. Management of SVT
2. Pharmacological methods:
A. Adenosine
 In Stable patients, IV Adenosine is the drug of choice because of its rapid onset
of action and minimal effects on cardiac contractility.
 Because of its potential to initiate atrial fibrillation, a DC conversion has to be
available bedside before administering Adenosine.
 Dose : 50mcg/kg by rapid IV push stat. Can be increased by 50-100mcg/kg (Max
18 mg)
B. Calcium channel blockers
Verapamil has been used in older children as drug of choice.
C. DC Cardioversion – Modality of choice when symptoms of severe heart failure
have already occurred.

27. Management of SVT
Maintainence care:
 Post the emergency event, a longer acting agent is selected for maintainance
therapy.
 In patients without accessory pathway, B-blockers are drug of choice. Digoxin
may also be used.
 In patients with WPW syndrome, calcium channel blockers and Digoxin are
contraindicated as they may precipitate ventricular tachycardias. B-blockers can
be used in these children.
 In resistant cases, Flecainide, propafenone, sotalol and amidarone have been
used.

28. Prognosis of SVT
 If cardiac failure occurs in infants with prolonged tachycardia, in a normal
heart, cardiac function returns to normal (days to weeks).
 Infants diagnosed within 1st 3-4 months of life have a lower incidence of
recurrence, than those diagnosed at later age.
 These patients have 80% chance of resolution by 1st year of life.
 30 % chances of recurrence persists.
 If medical therapy is started, it can be tapered off within a year and child
watched for signs of recurrence.
 Parents should be taught to measure heart rate so that SVT is caught
earlier (before heart failure).

29. Ventricular Tachycardia
• Ventricular tachycardia in pediatrics is defined as three or more
consecutive ventricular beats on ECG at >120beats/min.
• Seen to be associated with myocarditis, mitral valve prolapse, primary
cardiac tumors, cardiomyopathies.
• It is considered sustained if the rhythm lasts longer than 30 seconds,
and this indicates likely need for intervention.
• ECG diagnosis of VT is characterized by the presence of a regular
rhythm with wide QRS complex, as defined by age-appropriate criteria.

30. Ventricular Tachycardia
• For hemodyanamically stable patients: Initial drugs of choice are IV
Amidarone, Lidocaine, Procainamide.
• If hemodyanamically unstable, VT should be immediately treated
with DC Cardioversion.
• In neonates, ventricular tachycardia may be associated with
anamolous left coronary artery or a myocardial tumor.
• Unless a clearly reversible cause is identified, electrophysiologis
study is indicated in patients with VT, and according to the cause,
catheter ablation and/ or ICD implantation may be indicated.

31. Ventricular Fibrillation
• Ventricular fibrillation is a chaotic rhythm that results in death unless
an effective ventricular beat is rapidly re-established.
• VF is characterized by an ECG waveform that is chaotic and
unpredictable with variable amplitude and direction and no
identifiable P waves or QRS complexes. This rhythm stems from
uncoordinated ventricular contraction.
• Usually, CPR and DC defibrillation is required.
• If defibrillation is ineffective or VF recurs, Amidarone or Lidocaine is
given IV and defibrillation repeated.

32. Long QT syndrome
• These are genetic abnormalities of ventricular repolarization.
• Incidence – approx. 1 in 10000 births.
• They present as long QT interval on ECG and are associated with
malignant ventricular arrythmias.
• They can cause syncope or sudden death.
• 80% cases have an identifiable genetic mutation in cardiac sodium and
potassium channels.
• Asymptomatic but At-risk patients may not have prolonged QT duration
but may become apparent with exercise or catecholamine infusion.

33. Long QT syndrome

34. Long QT syndrome
• Clinical manifestations:
Syncopal attack brought on by exercise, fright or startle.
Some may present as seizures, presyncope or palpitations.
10% are in clinical arrest as first presentation.
• Diagnosis is ECG based. A corrected QT interval of >0.47 seconds is
highly indicative.
A cQT interval of >0.44sec is suggestive.
• A 24 hour Holter monitoring and exercise testing are adjuvants to
diagnosis.
• Treatment includes : B blocking agents (Propranolol and Nadolol may
be considered)
• In patients with continued syncope despite treatment, an implantable
cardiac defibrillator is indicated.

35. A
P
P
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A
C
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36. Bradyarrythmias
Sick Sinus Syndrome
• Resultant of abnormalities in SA-node, conduction pathways or both.
• Seen commonly after surgical corrections – esp fontans or senning
procedures.
• Most patients remain asymptomatic. Syncope or dizziness have
been reported.
• Pacemaker therapy is indicated in patients with exercise intolerance
or syncope events.

37. Atrio-Ventricular Blocks

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40. Congenital complete AV Block
• Autoimmune injury to the fetal conduction system by
maternally derived anti-SSA/Ro,anti-SSB/La antibodies
• Maternal SLE or sjogren syndrome
• NKX2-5 gene mutation has congenital complete AV block.
• High Fetal loss rate.
• May lead to hydrops fetalis

41. • Presents with tiredness, frequent naps, irritability, symptoms
and signs of heart failure
• Prominent peripheral pulses due to compensatory >> in
stroke volume.
• ECG shows P waves and QRS complexes having no constant
relationship.
• If HR is 50bpm or less, signs of heart failure+, CHD+
Pacemaker placement is indicated.
Congenital complete AV Block

42. Antiarrythmia
Medications

43. Title
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Abbott MB, Vlasses CH. Nelson textbook of pediatrics. Jama. 2011 Dec 7;306(21):2387-8.

44. Title
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Abbott MB, Vlasses CH. Nelson textbook of pediatrics. Jama. 2011 Dec 7;306(21):2387-8.

45. THANK
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