1. The heart's electrical conduction system coordinates the contraction of the heart muscles. Abnormalities in this system can cause arrhythmias or irregular heart rhythms. 2. Pediatric arrhythmias are classified as tachyarrhythmias (fast rhythms) or bradyarrhythmias (slow rhythms) and can originate from the atria, junction, or ventricles. 3. Common tachyarrhythmias include supraventricular tachycardia, which has several subtypes like AV nodal re-entrant tachycardia. Bradyarrhythmias include sinus bradycardia and various types of heart block.

1. ARRYTHMIAS IN
CHILDREN
-Dr
.Apoorva.E
PG,DCMS

2. ELECTRICAL ANATOMY OF
THE HEART

3. • The heart is a functional syncytium
• Network of myocytes connected to each other
by intercalated discs which have gap junctions
• Through which electrical impulses propagate
allowing rapid,synchronous depolarization of the
myocardium

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

5. CONDUCTION PATHWAY

8. PEDIATRIC ARRYTHMIAS
• Classified as
• An arrythmia is defined as an abnormality in heart rate
or rythm
Tachyarrythmias
Bradyarrythmias
Atrial
Junctional
Ventricular
Heart blocks

9. Tachyarrhythmias - Symptoms
• General: palpitations,lightheadedness,
syncope,fatigue,SOB,chest pain
– Infants: poor feeding, tachypnoea, irritability,
sleepiness, pallor, vomiting
• Hemodynamic instability: respiratory
distress/failure,hypotension,poor end-organ
perfusion,LOC,sudden collapse

10. Tachyarrhythmias - Causes
• Primary: Underlying conduction abnormalities
• Secondary: Reversible Hs & Ts
– Toxins
– Tamponade
– Tension pneumothorax
– Thrombosis (coronary, pulmonary)
– Trauma
– Hypovolemia
– Hypoxia
– H+ ions (acidosis)
– Hypoglycemia
– Hypothermia
– Hypo/Hyperkalemia

11. Tachyarrhythmias - Originating in the
atria
1. SINUS ARRYTHMIA
• Normal physiologic variation in impulses
discharged from SA node in relation to
respiration
• HR slows during expiration,increases during
inspiration
• Drugs like digoxin exaggerate it
• Abolished by exercise

12. Varied PP interval.No significant change in
P wave morphology/PR interval

13. 2. SINUS TACHYCARDIA
• The sinus node sends out impulses faster than
usual >>HR
• In response to body’s need for >>CO :
exercise,anxiety, fever, hypovolemia or
circulatory shock, anemia, CHF, administration of
catecholamines, thyrotoxicosis & myocardial
disease.

14. P waves are present and normal , narrow
QRS, beat to beat variability

15. 3. PREMATURE ATRIAL CONTRACTIONS
• Benign in the absence of underlying heart disease
• Common in newborn period
• Depending on prematurity of the beat,PAC’s may result in
a normal/prolonged/absent QRS complex
Conducted to
ventricle with
aberrant or
widened QRS
complex
Not
conducted
to ventricle,
apparent
pause

16. Early p wave, sometimes with different morphology
than a sinus p wave

17. • Pacemaker shifts from sinus node to another
atrial site
• Normal variant
• Irregular rhythm
4.WANDERING ATRIAL PACEMAKER

18. 5.SUPRA VENTRICULAR TACHYCARDIA
• Originating above the ventricles
• Most common abnormal tachycardia seen
in pediatric practice
• Most common arrhythmia requiring
treatment in pediatric population
• Most frequent age presentation: 1st 3
months of life, 2nd peaks @ 8-10 yrs and in
adolescents

19. • Paroxysmal,sudden onset & offset
• Occuring at rest
• In infants,precipitated by infection and
in children by bronchodilators,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

20. • Older children present with palpitations
• Younger children – Basal HR higher for that age,HR
>> greatly with crying
• P waves difficult to define, but 1:1 with normal QRS

21. • ECG similar to sinus tachycardia
• Differentiating features :
HR>230bpm,unvarying HR,abnormal P wave
axis if seen

22. • 3 major types
- re-entrant tachycardia with an accessory pathway
- Re-entrant tachycardia without an accessory pathway
- Ectopic/automatic tachycardias
AVRT
AVNRT
ATRIAL ECTOPICS
JUNCTIONAL ECTOPICS
ATRIAL FLUTTER
ATRIAL FIBRILLATION

23. 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

24. • 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

26. - 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

27. • Typical features of WPW are apparent when
tachycardia subsides
• Wide QRS complexes,delta waves,short PR interval
• Risk of sudden death

28. MANAGEMENT OF SVT
• Non pharmacological measures like
-placing an ice bag over the face
-Valsalva maneuver
-Straining
-Breath holding

29. •If the child is hemodynamically stable,rapid iv
push of adenosine
(risk of AF)
•In older children,CCB like verapamil can be
given iv (C/I in <1year)

30. • If the child is not stable,synchronized DC
cardioversion (1 J/kg)
• If the tachycardia is resistant, iv
procainamide,quinidine,flecainide,sotalol,
amiodarone can be tried
• If SVT still persists,catheter ablation with success
rate of 80-95%
Radiofrequency
Cryo
Surgical

31. • Maintenance therapy
- When sinus rhythm is restored,
for long term maintenance,
DOC is beta blockers in both WPW and
Non WPW syndromes
- Digoxin can be given in infants with no
accessory pathway

32. 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

33. ATRIAL ECTOPIC TACHYCARDIA
• Uncommon in children
• Variable HR,usually >200bpm
• Due to a single focus of automaticity
• On starting pharmacologic therapy,the
tachycardia gradually slows down only to
speed up again
• ECG shows ectopic p waves with an abnormal
axis

34. MULTIFOCAL ATRIAL TACHYCARDIA
• More common in infants than in older
children
• Characterized by 3 or more ectopic P
waves and varying PR intervals
• Spontaneous resolution occurs usually by
3 years of age

35. Chaotic ECG pattern with multiple ectopic P
waves with abnormal axes

36. JUNCTIONAL ECTOPIC TACHYCARDIA
• Due to an abnormal focus of automaticity
• The focus being a conducting tissue very close
to the AV node (junctional)
• Discharge of impulses from junctional tissue
exceeds SA nodal discharge leading to
AV dissociation

37. • Occurs in early post op period or may be
congenital
• IV amiodarone is the DOC for post-op JET
• Congenital JET requires catheter ablation
• Maintenance therapy with
amiodarone/sotalol

38. ATRIAL FLUTTER
• Also called intra-atrial re-entrant tachycardia
• HR > 400-600 bpm in neonates
>250-300 bpm in children
• Due to re-entrant pathway located in the right
atrium circling the tricuspid valve annulus
• AV dissociation occurs and ventricles respond
to 2nd - 4th atrial beat

39. • Occurs in neonates with normal hearts and in
children with CHD (with large stretched atria)
and post-op
Rapid and regular saw-toothed flutter
waves

40. • Temporary slowing of HR by vagal
maneuvres/adenosine/CCB
• Synchronized DC cardioversion is the TOC
• Patients with chronic atrial fluttter are at
>> risk for thromboembolism and stroke
-require anticoagulants
• Maintenance therapy with type 1 and type
3 agents

41. ATRIAL FIBRILLATION
• Uncommon in infants and children
• HR > 400-700 bpm
• Irregularly irregular rhythm on ECG and pulse
• Post op,in CHD with enlarged
atria,thyrotoxicosis,pulmonary
embolism,pericarditis,cardiomyopathy

42. • If stable,CCB iv procainamide/amiodarone
• If unstable,DC cardioversion
Absence of clear P waves and an irregularly irregular
ventricular response
(No two R-R intervals are the same)

43. Tachyarrythmias-Originating in the
ventricles
1.PREMATURE VENTRICULAR CONTRACTIONS –
• Uncommon in children
• Unifocal/multifocal
• Abolished on exercise
• If unifocal/disappearing with exercise/ associated
with normal heart,then considered benign,no
therapy needed.
• Advise patients to avoid caffeine and other
stimulants

44. • Early, wide QRS complexes
• T waves in opposite direction of QRS
• Bigeminy, sinus beat followed by PVC,this
repeating as a pattern also frequently seen

45. 2. VENTRICULAR TACHYCARDIA
• Defined as atleast 3 PVC s at >120 bpm
• Paroxysmal/incessant
• Associated with myocarditis,anomalous
LCA,MVP,primary cardiac
tumors,cardiomyopathy / Post-op
• Prompt treatment to prevent degeneration
into VF

46. • If stable,treat with IV
amiodarone/lidocaine/procainamide and
correct the cause
• If unstable,DC cardioversion
Wide QRS (>0.08 sec),
P waves may be unidentifiable or not related to
QRS

47. 3. VENTRICULAR FIBRILLATION
• Seen in children with long QT syndrome or
Brugada syndrome
• Associated with cardiomyopathies,structural
heart diseases causing ventricular dysfunction
• Sudden death occurs unless an effective
ventricular beat is reestablished rapidly

48. • Treatment: immediate DC defibrillation, CPR
• If ineffective,give IV amiodarone,lidocaine and
repeat defibrillation
• Treat the cause once sinus rhythm is
established

52. LONG Q-T SYNDROMES
• Include genetic abnormalities of ventricular
repolarization
• Long QT – interval on ECG
• Associated with malignant ventricular
arrythmias leading to sudden death
• Atleast 50% are familial

54. • Precipitated by exercise
• LQT1 events are stress induced
• LQT3 occur during sleep
• LQT2 have an intermediate pattern
• LQT3 has highest probability of sudden death

55. • Diagnostic criteria
Present with syncope,seizures,palpitations
Corrected QT interval >0.47sec or a QT
interval >0.44sec
Notched T waves
Low HR for age
Familial history of LQTS/sudden death

56. • Treatment - Beta blockers which blunt the
HR s response to exercise
• If drug induced profound bradycardia –
pacemaker
• If drug resistant,LQT3- implantable cardiac
defibrillator

57. Bradyarrhythmias - Symptoms
• General: altered
consciousness,fatigue,dizziness,syncope
• Hemodynamic instability: hypotension, poor
end-organ perfusion, respiratory distress/failure,
sudden collapse

58. Bradyarrhythmias - Causes
• Primary : Abnormal pacemaker/conduction system
(congenital or postsurgical injury), cardiomyopathy,
myocarditis
• Secondary : Reversible Hs & Ts:
– Hypotension
– Hypothermia
– H+ ions (acidosis)
– Hyperkalemia
– Hypoxia
– Heart block
– Trauma (head)
– Toxins/drugs (cholinesterase inhibitors, Ca++ channel blockers, β blockers,
digoxin, α2 agonists, opioids)

59. Bradyarrhythmias - Types
• Sinus bradycardia
– Physiological (ie: sleep, athletes)
– pathologic al(ie: abnormal electrolytes, infection,
drugs, hypoglycemia, hypothyroidism, ↑ICP)

60. • SINUS ARREST
- Failure of impulse formation within SA node
• SINOATRIAL BLOCK
- Block between SA node and surrounding atrium
preventing conduction of impulses
Rare in children
Digoxin toxicity,extensive atrial surgery

61. • SICK SINUS SYNDROME
- Due to abnormalities in either the SA node /
atrial conduction pathways / both
- Post surgery for CHD (fontan,mustard,senning
procedures) or even in patients with normal
heart
- Usually asymptomatic and don’t require
treatment
- Periods of marked sinus slowing present with
dizziness and syncope pacemaker if symptoms
recur

62. • AV BLOCKS
Type EKG Findings Causes & Clinical Significance
1st
degree
Prolonged PR interval Causes include AV nodal disease,myocarditis,↑K+, drugs (ie:
Ca++ channel blockers, β-blockers, digoxin), acute rheumatic
fever. Usually asymptomatic.
2nd
degree
Mobitz type I
Wenchebach
Progressive prolongation
of PR interval until a P
wave is not
conducted.After this
dropped beat cycle starts
again with a short PR
interval
Usually due to block within AV node. Caused by drugs (ie: Ca++
channel blockers, β-blockers, digoxin).
Can cause dizziness. Typically transient and benign; Rarely
progresses to 3rd degree heart block.
2nd
Degree
Mobitz type II
Prolonged constant PR
interval, inhibition of a set
proportion of atrial
impulses
Usually caused by defect in conduction pathway or acute
coronary syndrome, leading to block below AV node & His
bundle. Symptoms include palpitations, presyncope, syncope.
Can progress to 3rd degree heart block; often requires
pacemaker.
3rd
Degree
complete
AV dissociation. No atrial
impulses are conducted to
the ventricle
Congenital or caused by conduction system disease(myocardial
tumors/abscess/myocarditis) or injury (surgery for vsd). Most
symptomatic form of heart block: fatigue, presyncope, syncope.
Usually requires pacemaker

65. 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 with asd
• High fetal loss rate

66. • May lead to hydrops fetalis
• Present with tiredness,frequent
naps,irritability,symptoms and signs of heart
failure
• Prominent peripheral pulses due to
compensatory >> in stroke volume
• Murmur +
• ECG shows P waves and QRS complexes having
no constant relationship

67. •If HR is 50bpm or less,signs of heart failure +,CHD+,
pacemaker placement required

69. VAUGHAN WILLIAMS CLASSIFICATION
Class 1a – sodium fast channel blockers,prolong
repolarization
(quinidine,procainamide,disopyramide)
Class1b – sodium fast channel blockers,shorten
repolarization
(lidocaine,mexiletine,phenytoin)
Class 1c – sodium channel blockers
(flecainide,propafenone)

70. Class 2 – beta blockers
(propranolol,atenolol)
Class 3 – potassium channel openers,prolong
repolarization
(amiodarone)
Class 4 – miscellaneous
(verapamil,adenosine,digoxin)

71. THAT’S ALL
FOLKS !