Arrythmias in children , Nelson , Textbook of pediatrics , Pediatrics

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
• An arrythmia is defined as an abnormality in heart rate
or rythm
• Classified as
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
– Hypovolemia – Toxins
– Hypoxia – Tamponade
– H+ ions (acidosis) – Tension pneumothorax
– Hypoglycemia – Thrombosis (coronary, pulmonary)
– Hypothermia – Trauma
– 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:
– Hypoxia – Hypotension – H+ ions (acidosis)
– Heart block – Hypothermia – Hyperkalemia
– 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 !