Arrhythmias in children

ARRYTHMIAS IN CHILDREN

-Dr.Apoorva.E

PG,DCMS

ELECTRICAL ANATOMY OF THE HEART

• 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

CONDUCTION PATHWAY

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

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

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.

P waves are present and normal , narrow

QRS, beat to beat variability

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

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

• 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

Chaotic ECG pattern with multiple ectopic P waves with abnormal axes

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

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

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)

THAT’S ALL FOLKS !