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- 1. Arrhythmias Clinical Diagnosis andManagement
- 2. Normal ECGs inPediatrics • The normal ECG changes through development of the cardiac conduction system and evolving hemodynamics. • Essential to understand normal before interpretation of abnormal rhythm.
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- 4. Arrhythmia Analysis May suspectarrhythmia with: • Irregular heart rate • Inappropriate rate for age • Unexplained heart failure • Known association of systemic or cardiac disease • Symptoms: syncope, palpitations, chest pain • Family history of arrhythmia or sudden death
- 5. Stable or Unstable? Fastor Slow? Fast or Slow? Wide or Narrow? Pulse or No Pulse? Pacing Atropine Adrenaline Isoproterenol Pacing Atropine Adrenaline Isoproterenol Consider CPR Shock Unsynchronized 2-4 j/kg Shock Synchronized 0.5-2 j/kg SVT/VT VT/VFSVT VT Aberrated SVT Regular or Irregular? Vagal Maneuvers Adenosine (therapeutic or diagnostic) Lidocaine Synchronized cardioversion Rate Control Consider CV. ECG!
- 6. Unstable Tachycardias • Cardioversionwill generally be indicated. • Document rhythm and treatment with ECG. Limb leads (I, II and II) and rhythm strips may be aqeduate. • If patient has a pulse: synchronized cardioversion 0.5-2 j/kg. • No pulse (VT/VF): unsynchronized cardioversion 2-4 j/kg.
- 7. Unstable Bradycardias • Documentrhythm and determine nature of bradycardia • Pacing: external or esophageal • Atropine • Adrenaline • Isoproterenol
- 8. Sinus Node Dysfunction •Rarely congenital. • Seen in association with atrial surgeries: Mustard/Senning, Fontan, ASD repair. • Therapy for symptomatic patients: pacing.
- 9. First Degree AVBlock • Stable prolonged PR interval. • Can be seen as normal variant. • Possible causes: Increased vagal tone Medications Non-sinus atrial rhythm Conduction system disease or trauma
- 10. Type I (Wenckebach):Progressive lengthening of PR interval until non-conducted beat, with subsequent resetting of short PR. Causes grouped beats. Can be a normal variant, especially in sleep.
- 11. Second Degree AVB-TypeII Abrupt failure of AV conduction without prior PR prolongation. May progress to complete heart block.
- 12. Complete Heart Block Noatrial beats conduct to the ventricle.
- 13. Congenital Complete Heart Block •Diagnosis in fetus : 85% born alive if normal fetal echo 85% fetal death if structural heart disease • Diagnosis in infants : 85% survive beyond adolescence. • Associated with maternal SLE, often asymptomatic.
- 14. Third Degree AVBlock – Acquired • Acquired CHB associated with: Intracardiac surgeries Muscular dystrophies Myotonic dystrophy Cardiomyopathy Kearns-Sayre Syndrome Infections: Acute rheumatic fever, Diptheria, Yersinia, RMSF, Lyme disease, bacterial endocarditis, viral myocarditis.
- 15. Third Degree AVBlock - Management • Initial: CPR, atropine, adrenergic agents, temporary pacing (transcutaneous or transvenous) may be indicated if patient symptomatic. • Permanent pacing indicated for symptomatic CHB that is not expected to recover. • Many infectious causes of CHB will recover with appropriate antimicrobial therapy.
- 16. Extrasystoles • Atrial • Junctional •Ventricular
- 17. Normal QRS tachycardias •More accurate term than narrow • Re-entrant or Automatic? Include: • Reciprocating • Primary Atrial • Automatic Junctional
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- 19. Reciprocating • Orthodromic ReciprocatingTachycardia • AV Nodal Reentry Tachycardia Typical Atypical • Permanent Junctional Reciprocating Tachycardia
- 20. Re-entrant Circuit Unidirectional block Slow retrogradeconductionRapid conduction
- 21. Termination of re-entrantSVT • Vagal maneuvers (ice bag to face in infants, Valsalva maneuvers in older children.) • Adenosine • If SVT reinitiates or does not respond, consider procainamide, esmolol or verapamil (only beyond infancy).
- 22. Adenosine • Slow orblock conduction at the AV node. • Slow or block conduction at sinus node. • Very short acting. • Do not refrigerate. • Rapid IV bolus 0.1 mg/kg with rapid flush to follow, both needles in hub of IV or with three- way stopcock, via proximal IV. • Look for cough, flushing, change in ECG to indicate proper administration.
- 23. Adenosine effects • Noneor transient slowing: Sinus tachycardia or EAT Inadequate dose or failed administration. • Flutter waves/atrial fibrillation revealed. • Sudden termination: Re-entrant rhythm involving AV node. -Can resume almost immediately.
- 24. Adenosine effect onre-entrant SVT
- 25. Further Management Patient/parent education:arrhythmia recognition and vagal maneuvers. Medication: beta blockers, verapamil in older patients, digoxin less effective. Digoxin and verapamil are contraindicated in preexcited patients.
- 26. Primary Atrial Tachycardias •Atrial Flutter and Intraatrial Re-entry • Atrial Fibrillation • Automatic Ectopic Atrial Tachycardia • Chaotic Atrial Rhythm
- 27. Atrial Flutter onadenosine
- 28. Management of A-fib/flutter •Termination: Rule out atrial thrombus Ca++ Channel blockade for rate control Synchronized cardioversion Ibutilide/Pacing • Chronic therapy: Consider anticoagulation Anti-arrhythmics Anti-tachycardia pacing Radiofrequency ablation (a-flutter)
- 29. Ectopic Atrial Tachycardia •Automatic foci within the atrium. • Chronic, often incessant (risk of tachycardiomyopathy). • Can be difficult to distinguish from sinus tachycardia due to mild elevation in rate and subtle alterations in P wave morphology. Management: anti-arrhythmics, ablation.
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- 31. Junctional Ectopic Tachycardia AutomaticMechanism Congenital or Post-operative
- 32. Wide QRS Tachycardias •Supraventricular tachycardias with aberrant conduction to the ventricle. • Ventricular tachycardias. Must assume all wide QRS tachycardias are ventricular in origin until proven otherwise!
- 33. Sustained Wide QRSTachycardia
- 34. Stable Wide QRSTachycardia Regular Irregular May try Adenosine first Consider Lidocaine and Procainamide Do not use Adenosine: May be pre-excited Afib Always have cardioversion available before administration of any medication. Sedation/amnestic essential when cardioverting. 12 lead ECG
- 35. Aberrantly Conducted SVT •Tachycardias with fixed or functional bundle branch block. • Must have 1:1 AV relationship • Preexcited tachycardias: Antedromic reciprocating tachycardias Antedromic tachycardia via Mahaim Bystander accessory pathways
- 36. Preexcitation • Wolff-Parkinson-White Syndrome •Mahaim fibers Nodo-fascicular connections Nodo-ventricular connections
- 37. WPW syndrome • Ebsteinsanomaly • Corrected TGA • Mitral valve prolapse • Hypertrophic cardiomyopathy • Cardiac rhabdomyoma ISOLATED IN >90% OF PATIENTS
- 38. WPW syndrome incorrected TGA
- 39. Ventricular Tachycardias • Nonsustained •Sustained monomorphic reentry • Catecholamine-induced • Torsades de Pointes • Fascicular reentry • Incessant VT • Rapid polymorphic, ventricular flutter or ventricular fibrillation
- 40. Chronic Management ofVT • Required for sustained VT, symptomatic patients. • Will vary depending of type of VT. • Consider pediatric cardiology consultation. • Therapies include medication, surgical interventions, ablation, and implantable cardioverter defibrillators.
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- 43. After the arrhythmicevent • Consider referral to pediatric cardiology • Consider esophageal or intracardiac EP study • Medications • RFCA
- 44. Stable or Unstable? Fastor Slow? Fast or Slow? Wide or Narrow? Pulse or No Pulse? Pacing Atropine Adrenaline Isoproterenol Pacing Atropine Adrenaline Isoproterenol Consider CPR Shock Unsynchronized 2-4 j/kg Shock Synchronized 0.5-2 j/kg SVT/VT VT/VFSVT VT Aberrated SVT Regular or Irregular? Vagal Manuvers Adenosine (therapeutic or diagnostic) Lidocaine Synchronized cardioversion Rate Control Consider CV. ECG!