Beth talk at kottayam
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Transcript of Beth talk at kottayam
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Arrhythmias
Clinical Diagnosis and Management
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Normal ECGs in Pediatrics
• 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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Normal infant
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Arrhythmia Analysis
May suspect arrhythmia 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
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Stable or Unstable?
Fast or Slow? Fast or Slow?
Wide or Narrow? Pulse or No Pulse? PacingAtropineAdrenalineIsoproterenol
PacingAtropineAdrenalineIsoproterenol
Consider CPR
ShockUnsynchronized2-4 j/kg
ShockSynchronized0.5-2 j/kg
SVT/VT VT/VFSVT
VTAberrated SVT
Regular or Irregular?
Vagal ManeuversAdenosine(therapeutic or diagnostic)
LidocaineSynchronizedcardioversion
Rate ControlConsider CV.
ECG!
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Unstable Tachycardias
• Cardioversion will 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.
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Unstable Bradycardias
• Document rhythm and determine nature of bradycardia
• Pacing: external or esophageal• Atropine• Adrenaline• Isoproterenol
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Sinus Node Dysfunction
• Rarely congenital.• Seen in association with atrial surgeries:
Mustard/Senning, Fontan, ASD repair.
• Therapy for symptomatic patients: pacing.
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First Degree AV Block• 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
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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.
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Second Degree AVB-Type II
Abrupt failure of AV conduction without prior PR prolongation. May progress to complete heart block.
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Complete Heart Block
No atrial beats conduct to the ventricle.
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Congenital Complete Heart Block
• Diagnosis in fetus : 85% born alive if normal fetal echo85% fetal death if structural heart disease
• Diagnosis in infants :85% survive beyond adolescence.
• Associated with maternal SLE, often asymptomatic.
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Third Degree AV Block – 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.
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Third Degree AV Block - 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.
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Extrasystoles• Atrial
• Junctional
• Ventricular
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Normal QRS tachycardias
• More accurate term than narrow• Re-entrant or Automatic?
Include:• Reciprocating• Primary Atrial• Automatic Junctional
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Narrow QRS Tachycardia
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Reciprocating
• Orthodromic Reciprocating Tachycardia• AV Nodal Reentry Tachycardia
Typical
Atypical• Permanent Junctional Reciprocating
Tachycardia
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Re-entrant Circuit
Unidirectional block Slow retrograde conductionRapid conduction
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Termination of re-entrant SVT
• 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).
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Adenosine• Slow or block 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.
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Adenosine effects
• None or 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.
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Adenosine effect on re-entrant SVT
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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.
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Primary Atrial Tachycardias
• Atrial Flutter and Intraatrial Re-entry• Atrial Fibrillation• Automatic Ectopic Atrial Tachycardia• Chaotic Atrial Rhythm
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Atrial Flutter on adenosine
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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)
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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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Ectopic Atrial Tachycardia
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Junctional Ectopic TachycardiaAutomatic Mechanism
Congenital or Post-operative
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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!
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Sustained Wide QRS Tachycardia
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Stable Wide QRS Tachycardia
Regular Irregular
May try Adenosine firstConsider 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
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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
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Preexcitation
• Wolff-Parkinson-White Syndrome• Mahaim fibers
Nodo-fascicular connections
Nodo-ventricular connections
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WPW syndrome
• Ebsteins anomaly• Corrected TGA• Mitral valve prolapse• Hypertrophic cardiomyopathy• Cardiac rhabdomyoma
ISOLATED IN >90% OF PATIENTS
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WPW syndrome in corrected TGA
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Ventricular Tachycardias
• Nonsustained• Sustained monomorphic reentry• Catecholamine-induced • Torsades de Pointes• Fascicular reentry• Incessant VT• Rapid polymorphic, ventricular flutter or
ventricular fibrillation
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Chronic Management of VT
• 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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Long QT syndrome
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TORSADES DE POINTES
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After the arrhythmic event
• Consider referral to pediatric cardiology• Consider esophageal or intracardiac EP
study• Medications• RFCA
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Stable or Unstable?
Fast or Slow? Fast or Slow?
Wide or Narrow? Pulse or No Pulse? PacingAtropineAdrenalineIsoproterenol
PacingAtropineAdrenalineIsoproterenol
Consider CPR
ShockUnsynchronized2-4 j/kg
ShockSynchronized0.5-2 j/kg
SVT/VT VT/VFSVT
VTAberrated SVT
Regular or Irregular?
Vagal ManuversAdenosine(therapeutic or diagnostic)
LidocaineSynchronizedcardioversion
Rate ControlConsider CV.
ECG!