arrhythmias in children
TRANSCRIPT
• 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
• 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
PEDIATRIC ARRYTHMIAS• An arrythmia is defined as an abnormality in heart rate
or rythm
• Classified as
Tachyarrythmias
Bradyarrythmias
Atrial
Junctional
Ventricular
Heart blocks
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
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
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
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.
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
• Pacemaker shifts from sinus node to another atrial site
• Normal variant
• Irregular rhythm
4.WANDERING ATRIAL PACEMAKER
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
• 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
• 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
• ECG similar to sinus tachycardia
• Differentiating features : HR>230bpm,unvarying HR,abnormal P wave axis if seen
• 3 major types- re-entrant tachycardia with an accessory pathway- Re-entrant tachycardia without an accessory pathway- Ectopic/automatic tachycardias
AVRTAVNRT ATRIAL ECTOPICSJUNCTIONAL ECTOPICSATRIAL FLUTTERATRIAL FIBRILLATION
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
• 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
- 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
MANAGEMENT OF SVT
• Non pharmacological measures like
-placing an ice bag over the face
-Valsalva maneuver
-Straining
-Breath holding
• 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)
• 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
• 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
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
ATRIAL ECTOPIC TACHYCARDIA
• Uncommon in children
• Variable HR,usually >200bpm
• Due to a single focus of automaticity
• On starting pharmacologic therapy,thetachycardia gradually slows down only to speed up again
• ECG shows ectopic p waves with an abnormal axis
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
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
• 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
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
• 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
• Temporary slowing of HR by vagalmaneuvres/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
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,pulmonaryembolism,pericarditis,cardiomyopathy
• 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)
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,notherapy needed.
• Advise patients to avoid caffeine and other stimulants
• Early, wide QRS complexes
• T waves in opposite direction of QRS
• Bigeminy, sinus beat followed by PVC,thisrepeating as a pattern also frequently seen
2. VENTRICULAR TACHYCARDIA
• Defined as atleast 3 PVC s at >120 bpm
• Paroxysmal/incessant
• Associated with myocarditis,anomalousLCA,MVP,primary cardiac tumors,cardiomyopathy / Post-op
• Prompt treatment to prevent degeneration into VF
• 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
3. VENTRICULAR FIBRILLATION
• Seen in children with long QT syndrome or Brugada syndrome
• Associated with cardiomyopathies,structuralheart diseases causing ventricular dysfunction
• Sudden death occurs unless an effective ventricular beat is reestablished rapidly
• Treatment: immediate DC defibrillation, CPR
• If ineffective,give IV amiodarone,lidocaine and repeat defibrillation
• Treat the cause once sinus rhythm is established
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
• Precipitated by exercise
• LQT1 events are stress induced
• LQT3 occur during sleep
• LQT2 have an intermediate pattern
• LQT3 has highest probability of sudden death
• 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
• Treatment - Beta blockers which blunt the HR s response to exercise
• If drug induced profound bradycardia –pacemaker
• If drug resistant,LQT3- implantable cardiac defibrillator
Bradyarrhythmias - Symptoms
• General: altered consciousness,fatigue,dizziness,syncope
• Hemodynamic instability: hypotension, poor end-organ perfusion, respiratory distress/failure, sudden collapse
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)
Bradyarrhythmias - Types
• Sinus bradycardia– Physiological (ie: sleep, athletes)
– pathologic al(ie: abnormal electrolytes, infection, drugs, hypoglycemia, hypothyroidism, ↑ICP)
• 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
• SICK SINUS SYNDROME
- Due to abnormalities in either the SA node / atrial conduction pathways / both
- Post surgery for CHD (fontan,mustard,senningprocedures) 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
• AV BLOCKSType EKG Findings Causes & Clinical Significance
1st
degreeProlonged 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 prolongationof 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
CONGENITAL COMPLETE AV BLOCK
• Autoimmune injury to the fetal conduction system by maternally derived anti-SSA/Ro,anti-SSB/Laantibodies
• Maternal SLE or sjogren syndrome
• NKX2-5 gene mutation has congenital complete avblock with asd
• High fetal loss rate
• May lead to hydrops fetalis
• Present with tiredness,frequentnaps,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
VAUGHAN WILLIAMS CLASSIFICATION
Class 1a – sodium fast channel blockers,prolongrepolarization
(quinidine,procainamide,disopyramide)
Class1b – sodium fast channel blockers,shortenrepolarization
(lidocaine,mexiletine,phenytoin)
Class 1c – sodium channel blockers
(flecainide,propafenone)
Class 2 – beta blockers
(propranolol,atenolol)
Class 3 – potassium channel openers,prolongrepolarization
(amiodarone)
Class 4 – miscellaneous
(verapamil,adenosine,digoxin)