arrhythmias

Disorders of cardiacDisorders of cardiac
rhythm and conductionrhythm and conduction
in childrenin children
Ass. Prof.,Ass. Prof.,
MD,PhDMD,PhD
Rakovska L.Rakovska L.

Topics for DiscussionTopics for Discussion
Definition, classification, etiology, clinical
manifestation, diagnostics, treatment and
prognosis of following arrhythmias in children:
Sinus arrhythmiasSinus arrhythmias
Extrasystole (premature beats)Extrasystole (premature beats)
TachiarrytmiasTachiarrytmias
Heart blockHeart block
Sick sinus node syndromSick sinus node syndrom
Preexcitation of ventricles syndrome (WPW)Preexcitation of ventricles syndrome (WPW)
Syndrome of long QT intervalSyndrome of long QT interval

ArrhythmiasArrhythmias
((ссardiac dysrhythmias) orardiac dysrhythmias) or
abnormal heart rhythmsabnormal heart rhythms
 disorders of frequency, regularity ofdisorders of frequency, regularity of
rhythm, source of heart impulsesrhythm, source of heart impulses
activation and it also means theactivation and it also means the
dysfunction in connection or sequencedysfunction in connection or sequence
between atrial and ventricularbetween atrial and ventricular
activationactivation..

 Less common than in adults.Less common than in adults.
 Many pediatric dysrhythmias areMany pediatric dysrhythmias are
normal variants that do not requirenormal variants that do not require
treatment or even further evaluationtreatment or even further evaluation
 Pediatric dysrhythmias can be just asPediatric dysrhythmias can be just as
life threatening.life threatening.
Pediatric DysrhythmiasPediatric Dysrhythmias

Etiological factors of arrhythmiasEtiological factors of arrhythmias
 Cardial factorsCardial factors
CongenitalCongenital
 AcquiredAcquired
 Extracardial factorsExtracardial factors

Etiological factors of arrhythmiasEtiological factors of arrhythmias
Cardial factorsCardial factors Extracardial factorsExtracardial factors
Congenital:Congenital:
1.1. CHDCHD (VSD, ASD,(VSD, ASD,
Ebstein anomaly, PDA,Ebstein anomaly, PDA,
tetralogy Fallow etc.)tetralogy Fallow etc.)
2.2. CarditisCarditis
3.3. CardiomyopathyCardiomyopathy
4.4. Anomalies of heartAnomalies of heart
conduction systemconduction system
(AV block, WPW syndrome(AV block, WPW syndrome
etcetc.).)
5.5. Mitral valve prolapseMitral valve prolapse
1.1. InfectionsInfections
2.2. Psychogenic factorsPsychogenic factors (stress)(stress)
3.3. Diseases and injuries ofDiseases and injuries of
nervous systemnervous system
4.4. Electrolyte disturbancesElectrolyte disturbances
(↓↑K+, ↓↑Ca2+, ↓Mg2+)(↓↑K+, ↓↑Ca2+, ↓Mg2+)
5.5. IntoxicationsIntoxications ((UremiaUremia))
6.6. DrugsDrugs (antiarrhythmic agents,(antiarrhythmic agents,
digoxin, sympathomimeticdigoxin, sympathomimetic
agents)agents)

Etiological factors of arrhythmias in childrenEtiological factors of arrhythmias in children
Cardial factorsCardial factors Extracardial factorsExtracardial factors
Acquired:Acquired:
1.1. Rheumatic feverRheumatic fever
2.2. Nonrheumatic carditisNonrheumatic carditis
3.3. Systemic diseases ofSystemic diseases of
connective tissueconnective tissue (SLE,(SLE,
systemic sclerosis,systemic sclerosis,
dermatomyositis)dermatomyositis)
Other:Other:
1.1. Idiopathic cardiomyopathyIdiopathic cardiomyopathy
2.2. AneurysmAneurysm
3.3. Heart tumorsHeart tumors
7.7. DyshormonalDyshormonal
conditionsconditions
((ThyrotoxicosisThyrotoxicosis,,
ppheochromocytomaheochromocytoma))
8.8. Traumas of chestTraumas of chest
and abdomenand abdomen

 Sinus rhythmSinus rhythm originates in the sinus node and hasoriginates in the sinus node and has
a normal axis P wave (upright in leads I and AVF)a normal axis P wave (upright in leads I and AVF)
preceding each QRS complex.preceding each QRS complex.
Sinus (or sinoatrial) node (1) isSinus (or sinoatrial) node (1) is
localized on the upper wall of thelocalized on the upper wall of the
right atriumright atrium
From it Kis-Flack (2) bundle outcomesFrom it Kis-Flack (2) bundle outcomes
which connects both atria and thewhich connects both atria and the
second node.second node.
A-V node (3) or is localized in the lowA-V node (3) or is localized in the low
wall of the right atrium, nearwall of the right atrium, near
septumseptum
From it the His bundle outcomes intoFrom it the His bundle outcomes into
ventricular septum (4) and then isventricular septum (4) and then is
divided into two partes – right (A)divided into two partes – right (A)
and left (and left (ББ).).
This bundle connects the bothThis bundle connects the both
ventricles.ventricles.

Working classification of cardiacWorking classification of cardiac
rhythm disorders in childrenrhythm disorders in children
((Belocon N.A., Kuberger M.B., 1987Belocon N.A., Kuberger M.B., 1987):):
 I. Disorders of impulseI. Disorders of impulse formationformation
A. Nomotopic rhythm forming disordersA. Nomotopic rhythm forming disorders
B. Heterotopic (ectopic) disorders of rhythmB. Heterotopic (ectopic) disorders of rhythm
 II. Disorders of conduction
 III. Combined arrhythmia

Working classification of cardiac rhythmWorking classification of cardiac rhythm
disorders in childrendisorders in children
 I. Disorders of impulse formationI. Disorders of impulse formation
AA.. Nomotopic rhythm forming disorders:Nomotopic rhythm forming disorders:
1) Sinus arrhythmia1) Sinus arrhythmia
2) Sinus bradycardia2) Sinus bradycardia
3) Sinus tachycardia3) Sinus tachycardia
4) Migration of pacemaker.4) Migration of pacemaker.

B.B. Heterotopic (ectopic) disorders of rhythm:Heterotopic (ectopic) disorders of rhythm:
1. Extrasystole:1. Extrasystole:
a) atrium, atrioventricular, ventricular;a) atrium, atrioventricular, ventricular;
b) single, group, allorythmic, interpolar, parasystolic;b) single, group, allorythmic, interpolar, parasystolic;
c) early and late.c) early and late.
2. Paroxysmal tachycardia:
а) supraventricular (atrial, atrioventricular);
б) ventricular.
3. Nonparoxysmal tachycardia:
а) atrial with atrioventricular block and without it;
б) atrioventricular;
в) ventricular.
4. Atrial flutter and fibrillation.
5.Ventricular flutterer and fibrillation.

II. Disorders of conduction.
1.Sinoauriculal block.
2.Intracardial block.
3. A-V block (I, II, III degree).
4. Intraventricular block:
а) onesided, bothsided;
б) incomplete, complete;
в) permanent, transitory, intermittent.

III. Combined arrhythmia.III. Combined arrhythmia.
1. Sick sinus syndrome1. Sick sinus syndrome
2. Atrioventricular dissociation.2. Atrioventricular dissociation.
3. Premature of ventricle excitement3. Premature of ventricle excitement
syndrome (preexitation syndrome).syndrome (preexitation syndrome).
4. Long QT syndrome.4. Long QT syndrome.

Classification of arrhythmias inClassification of arrhythmias in
childrenchildren
1. Bradyarrhythmias1. Bradyarrhythmias
 Sinus node dysfunctionSinus node dysfunction
 Conduction blockConduction block
2. Tachyarrhythmias2. Tachyarrhythmias
 Narrow QRSNarrow QRS
 Wide QRSWide QRS
3. Premature Beats3. Premature Beats
 AtrialAtrial
 VentricularVentricular

EpidemiologyEpidemiology
Among children with arrhythmias, the mostAmong children with arrhythmias, the most
common dysrhythmias arecommon dysrhythmias are
sinus tachycardia (50%),sinus tachycardia (50%),
supraventricular tachycardia (13%),supraventricular tachycardia (13%),
bradycardia (6%),bradycardia (6%),
atrial fibrillation (4.6%)atrial fibrillation (4.6%)

Arrhythmia PresentationArrhythmia Presentation
 PalpitationPalpitation
 Feeling of intermission in heart work (Feeling of intermission in heart work (“skipped beat”)“skipped beat”)
 DizzinessDizziness
 Chest PainChest Pain
 DyspneaDyspnea
 FatigueFatigue
 HypotensionHypotension
 Nonspecific symptoms (‘‘fussiness’’ or ‘‘difficulty feeding.’’Nonspecific symptoms (‘‘fussiness’’ or ‘‘difficulty feeding.’’
 Syncope (Morgagni-Adams-Stokes attack)
 Sudden cardiac deathSudden cardiac death

Arrhythmia AssessmentArrhythmia Assessment
 ECGECG
 24h Holter monitor24h Holter monitor
 EchocardiogramEchocardiogram
 Stress testStress test
 Coronary angiographyCoronary angiography
 Electrophysiology studyElectrophysiology study

ECG INTERPRETATIONECG INTERPRETATION
Algorithm for reading ECGsAlgorithm for reading ECGs
EvaluateEvaluate
 Rhythm :Rhythm : Sinus or Non-sinusSinus or Non-sinus
 RateRate
 AxisAxis (QRS axis, T axis)(QRS axis, T axis)
 Waves:Waves:
 P wave (Atrial depolarization)P wave (Atrial depolarization)
 QRS complex (Ventricular depolarization)QRS complex (Ventricular depolarization)
 T wave (Ventricular repolarization)T wave (Ventricular repolarization)
 U wave (Late phase of ventricularU wave (Late phase of ventricular
repolarization)repolarization)
 Intervals (PR, QT (QT/QTc), QRS)Intervals (PR, QT (QT/QTc), QRS)
 ST segmentsST segments

 aa -- Paper speed is 25 mm/secPaper speed is 25 mm/sec
 1 large square (5 mm) = 0.2 sec, 1 small square (1 mm) = 0.04 sec, Voltage 101 large square (5 mm) = 0.2 sec, 1 small square (1 mm) = 0.04 sec, Voltage 10
mm/mvmm/mv
 b - Paper speed is 50 mm/secb - Paper speed is 50 mm/sec
 1 large square (5 mm) = 0.1 sec, 1 small square (1 mm) = 0.02 sec, Voltage 101 large square (5 mm) = 0.1 sec, 1 small square (1 mm) = 0.02 sec, Voltage 10
mm/mvmm/mv

Pulse rate in children of different agePulse rate in children of different age
(per min)(per min)
NeonateNeonate 120-140120-140 8 yr8 yr 80-8580-85
6 mo6 mo 130-135130-135 9 yr9 yr 80-8580-85
1 yr1 yr 120-125120-125 10 yr10 yr 78-8578-85
2 yr2 yr 110-115110-115 11 yr11 yr 78-8478-84
3 yr3 yr 105-110105-110 12 yr12 yr 75-8275-82
4 yr4 yr 100-105100-105 13 yr13 yr 72-8072-80
5 yr5 yr 98-10098-100 14 yr14 yr 72-7872-78
6 yr6 yr 90-9590-95 15 yr15 yr 70-7570-75
7 yr7 yr 85-9085-90

Normal values of heart rate in childrenNormal values of heart rate in children
Age Heart rate.
newborn 140 (<110 - >170)
10-30 days of life 140 (<110 - >170)
1-12 month 132 (<102 - >162)
1-2 years 124 (<94 - >154)
2-4 years 115 (<90 - >140)
4-6 years 106 (<86 - >126)
6-8 years 98 (<78 - >118)
8-10 years 88 (<60 - >108)
10 and older 80 (<60 - >100)
< - bradycardia, > - tachycardia.

Pediatric ECGPediatric ECG
Intrinsic Heart RatesIntrinsic Heart Rates
 Newborn to 3 years:Newborn to 3 years:
•• SA node 95 – 120SA node 95 – 120
•• AV node (junctional) 45 – 85AV node (junctional) 45 – 85
•• Purkinje (ventricular) 35 – 55Purkinje (ventricular) 35 – 55
 3 years to teenager3 years to teenager
•• SA node 55 – 120SA node 55 – 120
•• AV node (junctional) 35 – 65AV node (junctional) 35 – 65
•• Purkinje (ventricular) 25 45‐Purkinje (ventricular) 25 45‐
 AdultsAdults
•• SA node 60 – 100SA node 60 – 100
•• AV node (junctional) 40-60AV node (junctional) 40-60
•• Purkinje (ventricular) 20 40‐Purkinje (ventricular) 20 40‐

Pediatric ECG – QRS AxisPediatric ECG – QRS Axis
Hexaxial Reference SystemHexaxial Reference System

Pediatric ECG – Determining AxisPediatric ECG – Determining Axis
Using the Hexaxial Reference SystemUsing the Hexaxial Reference System
II aVFaVF

ECG criteria ofECG criteria of regular sinus rhythm:regular sinus rhythm:
 Rhythms originating in sinus node have a sinus P-Rhythms originating in sinus node have a sinus P-
wave morphologywave morphology
 1)1) regular sequential series P-P;regular sequential series P-P;
 2)2) permanent P-wave morphologypermanent P-wave morphology
––Up in I, II, AVF; down in AVRUp in I, II, AVF; down in AVR
 3)3) P-wave precedes every QRS-complex;P-wave precedes every QRS-complex;
 4)4) Position of AP in frontal view 0Position of AP in frontal view 000
- + 90- + 900;0;
 5)5) Normal QRS-complex.Normal QRS-complex.

SINUS RHYTHMSINUS RHYTHM
QRS AFTER EVERY P
P BEFORE EVERY QRS
ALL P WAVES
LOOK THE
SAME
P WAVE UPRIGHT IN LEADS I AND aVF

Nomotopic rhythm formingNomotopic rhythm forming
disordersdisorders
A)A) ECG of healthy childECG of healthy child
B)B)Sinus tachycardiaSinus tachycardia
C)C)Sinus bradycardiaSinus bradycardia

Sinus tachycardiaSinus tachycardia
Sinus tachycardiaSinus tachycardia is defined as acceleration of beatis defined as acceleration of beat
rate at rest by 20-40 beats per minute with therate at rest by 20-40 beats per minute with the
regular rhythm being maintained.regular rhythm being maintained.
Causes:Causes:
1.1. PhysiologicalPhysiological
 Vegetative dysfunctions (sympathetic nervous systemVegetative dysfunctions (sympathetic nervous system
ton increase, vagus nerve ton reduction)ton increase, vagus nerve ton reduction)
 Physical activityPhysical activity
 Emotional factorsEmotional factors
2.2. Organic heart lesions (Organic heart lesions (myocarditis, congential andmyocarditis, congential and
acquired valvular diseases, etc)acquired valvular diseases, etc)
3.3. Adverse factors, directly affecting the sinus nodeAdverse factors, directly affecting the sinus node
cellscells (hypoxemia, infections, toxemia, acidosis, fiver, etc.)(hypoxemia, infections, toxemia, acidosis, fiver, etc.)

ECG criteria ofECG criteria of
Sinus tachycardiaSinus tachycardia
11)) R-R interval is permanent;R-R interval is permanent;
2) QRS-complex rate in children of elder age is more then 90 –2) QRS-complex rate in children of elder age is more then 90 –
100/min, in children of younger age 10 – 15 beats more as compared100/min, in children of younger age 10 – 15 beats more as compared
with age norm;with age norm;
3) P-wave precedes every QRS-complex, the positive in I, II standard3) P-wave precedes every QRS-complex, the positive in I, II standard
leads, aVL, V3-V6 and the negative one in VR lead;leads, aVL, V3-V6 and the negative one in VR lead;
4) QRS-complex is not changed;4) QRS-complex is not changed;
5) P-R interval is permanent and corresponds to child age5) P-R interval is permanent and corresponds to child age..

Sinus bradycardiaSinus bradycardia
is due to slow discharge of impulses from the sinusis due to slow discharge of impulses from the sinus
node.node.
 A sinus rate <90A sinus rate <90-100-100 beats/min in neonates andbeats/min in neonates and
<60<60-80-80 beats/min thereafter is considered to bebeats/min thereafter is considered to be
sinus bradycardia.sinus bradycardia.
 Sinus bradycardia is common in:Sinus bradycardia is common in:
- well-trained athletes;- well-trained athletes;
- healthy individuals during sleep,- healthy individuals during sleep,
-- vagus nerve tone increasingvagus nerve tone increasing

Causes of pathological sinusCauses of pathological sinus
bradycardia:bradycardia:
 DiseasesDiseases (hypothyroidism, stomach ulcer, hepatitis)(hypothyroidism, stomach ulcer, hepatitis)
 Increased intracranial pressureIncreased intracranial pressure ((cerebralcerebral
edema, meningitis, cerebal tumors, etcedema, meningitis, cerebal tumors, etc),),
 Patophysiological conditionsPatophysiological conditions ((hypothermia,hypothermia,
profound hypoxia, hyperkalemia)profound hypoxia, hyperkalemia)
 drugsdrugs ((glycosides, b-adrenoreceptor antagonist,glycosides, b-adrenoreceptor antagonist,
etcetc))

ECG criteria ofECG criteria of Sinus bradycardiaSinus bradycardia
1)1) QRS-complex rate is less then 100/min in the
children of first months of life and less than 60/min in
the children of more elderly age;
2) R-R interval permanent;
3) P-wave precedes every QRS-complex;
4) P-wave axe is permanent, localized between 00
and
900
(under normal heart position);
5) P-R interval is permanent and corresponds to the
child age.

Differential diagnosis of sinusDifferential diagnosis of sinus
bradycardiabradycardia
 Sinoatrial and AV blockSinoatrial and AV block..
 Children with sinus bradycardia are able toChildren with sinus bradycardia are able to
increase their heart rate with exercise to aincrease their heart rate with exercise to a
much higher rate than 100 beats/min,much higher rate than 100 beats/min,
whereas patients with AV block are usuallywhereas patients with AV block are usually
unable to do so.unable to do so.

Sinus arrhythmiaSinus arrhythmia
(irregular sinus rhythm)(irregular sinus rhythm)
 common finding in healthy children and represents acommon finding in healthy children and represents a
normal variation in the HR associated with breathing.normal variation in the HR associated with breathing.
The HR slows during expiration and acceleratesThe HR slows during expiration and accelerates
during inspiration.during inspiration.
 Anxiety, febrile illnesses and by vagus nerveAnxiety, febrile illnesses and by vagus nerve
stimulation (drugs, Valsava test); it is usuallystimulation (drugs, Valsava test); it is usually
disappears by exercise, breath-holding, functional testdisappears by exercise, breath-holding, functional test
with atropine.with atropine.
 Thyrotoxicosis, anemia, hypovolemia, shock, hypoxia,Thyrotoxicosis, anemia, hypovolemia, shock, hypoxia,
congestive heart failure, myocardial disease,congestive heart failure, myocardial disease,
medications (catecholamines), hypocalcemia, andmedications (catecholamines), hypocalcemia, and

ECG criteria of sinus arrhythmiaECG criteria of sinus arrhythmia
 R-R interval is not permanent;R-R interval is not permanent;
 R-R interval changes permanently all the time ofR-R interval changes permanently all the time of
breathing (shortens during inspiration);breathing (shortens during inspiration);
 P-P interval is not permanent;P-P interval is not permanent;
 P-wave precedes every QRS-complex;P-wave precedes every QRS-complex;
 P-wave axis is between 0P-wave axis is between 000
and 90and 9000
;;
 PR interval changes less than 0,2 sec.PR interval changes less than 0,2 sec.

 Respiratory sinus arrhythmia does notRespiratory sinus arrhythmia does not
require further evaluation or treatment.require further evaluation or treatment.
 Non-respiratory sinus arrhythmiaNon-respiratory sinus arrhythmia
(unrelated with respiration) is concomitant(unrelated with respiration) is concomitant
to heart disease, intracranial pressure rise.to heart disease, intracranial pressure rise.
 Treat etiology, not the tachycardia!Treat etiology, not the tachycardia!

Wandering atrial pacemakerWandering atrial pacemaker
 Atrial pacemaker shifts from sinus node toAtrial pacemaker shifts from sinus node to
another atrial siteanother atrial site
 Normal variant, irregular rhythmNormal variant, irregular rhythm

Extrasystole (PrematureExtrasystole (Premature
complexes, Escape Beats)complexes, Escape Beats)
 denotes premature heart contraction,denotes premature heart contraction,
induced by the ectopic impulse.induced by the ectopic impulse.

ExtrasystoleExtrasystole
According to the ectopic focus localizationAccording to the ectopic focus localization::
 SinusSinus
 AtrialAtrial
 AtrioventricularAtrioventricular
 VentricularVentricular
According to the number of ectopic focuses:According to the number of ectopic focuses:
 MonotopicMonotopic
 PolytopicPolytopic
According to the frequency:According to the frequency:
 Infrequent (1-2 per min)Infrequent (1-2 per min)
 Medium frequent (8-10 per min)Medium frequent (8-10 per min)
 Frequent (more than 10 per min)Frequent (more than 10 per min)
Extrasystoles can be single or group character, may assume a definiteExtrasystoles can be single or group character, may assume a definite
rhythm:rhythm: bigeminybigeminy (alternating with normal beats),(alternating with normal beats), trigeminytrigeminy
(occurring after two normal beats), qudrigeminy (occurring after(occurring after two normal beats), qudrigeminy (occurring after
three normal beats).three normal beats).

Extrasystole (PrematureExtrasystole (Premature
complexes, Escape Beats)complexes, Escape Beats)
 Usually, isolated extrasystoles are of noUsually, isolated extrasystoles are of no
clinical or prognostic significance andclinical or prognostic significance and
observed among healthy children.observed among healthy children.
 Extrasystoles are frequent causes ofExtrasystoles are frequent causes of
organic heart disease (inflammation,organic heart disease (inflammation,
ischemia, fibrosis) or of drug toxicity,ischemia, fibrosis) or of drug toxicity,
especially from digitalis.especially from digitalis.

Premature atrial complexesPremature atrial complexes
(atrial extrasystole)(atrial extrasystole)
are caused byare caused by
impulse comingimpulse coming
from the ectopicfrom the ectopic
focus in the atria.focus in the atria.
 That relativelyThat relatively
common prenatallycommon prenatally
and in infants,and in infants,
even in theeven in the
absence of cardiacabsence of cardiac
disease.disease.

Signs of atrial extrasystole on ECGSigns of atrial extrasystole on ECG
1)1) Premature appearance of P wave and QRS complex;Premature appearance of P wave and QRS complex;
2)2) Negative P wave in standart leads;Negative P wave in standart leads;
3)3) P-R interval more frequenly is shortened but may be normalP-R interval more frequenly is shortened but may be normal
and prolonged;and prolonged;
4)4) QRS complex is of normal form (or aberrant);QRS complex is of normal form (or aberrant);
5)5) Compensatory pause incomplete (under usual QRS complexCompensatory pause incomplete (under usual QRS complex
configuration).configuration).

Premature ventricular contractionsPremature ventricular contractions
(PVCs) or ventricular extrasystole(PVCs) or ventricular extrasystole
 is a premature, wide QRS complex that hasis a premature, wide QRS complex that has
a distinct configuration and is not precededa distinct configuration and is not preceded
by a P wave.by a P wave.

EtiologyEtiology
 PVCs can occur in healthy heartsPVCs can occur in healthy hearts ((50-75% of50-75% of
otherwise normal children may have PVCs)otherwise normal children may have PVCs)
 PVC is less common than PAC in infancyPVC is less common than PAC in infancy
but more common in older children andbut more common in older children and
adolescents.adolescents.
 Can be associated with CHD, mitral valveCan be associated with CHD, mitral valve
prolapse, prolonged QT syndrome, andprolapse, prolonged QT syndrome, and
cardiomyopathies (dilated and hypertrophic).cardiomyopathies (dilated and hypertrophic).

PVCs. EtiologyPVCs. Etiology
Malignant origins includeMalignant origins include
electrolyte imbalances,electrolyte imbalances,
drug toxicities (eg, general anesthesia, digoxin,drug toxicities (eg, general anesthesia, digoxin,
catecholamines, amphetamines,catecholamines, amphetamines,
sympathomimetics, and phenothiazines),sympathomimetics, and phenothiazines),
cardiac injury, cardiac tumors, myocarditis (Lymecardiac injury, cardiac tumors, myocarditis (Lyme
and viral diseases),and viral diseases),
hypoxia, and an intraventricular catheter.hypoxia, and an intraventricular catheter.

Clinical manifestation of PVCClinical manifestation of PVC
 Usually asymptomaticUsually asymptomatic
 May be aware of a “skipped beat” over theMay be aware of a “skipped beat” over the
precordium. This sensation is due to theprecordium. This sensation is due to the
increased stroke volume of the normal beatincreased stroke volume of the normal beat
after a compensatory pause.after a compensatory pause.
 Unrecognized and untreated PVCs are, a riskUnrecognized and untreated PVCs are, a risk
of developing ventricular tachycardia inof developing ventricular tachycardia in
patients who have a serious underlying cause.patients who have a serious underlying cause.

Signs of ventricular extrasystoleSigns of ventricular extrasystole
(premature ventricular contractions(premature ventricular contractions
(PVCs) on ESG(PVCs) on ESG
1)1) Premature appearance of QRS complex;Premature appearance of QRS complex;
2)2) Widening and deformation of the QRS complex;Widening and deformation of the QRS complex;
3)3) Changing of ST-T interval;Changing of ST-T interval;
4)4) Absence of P wave before QRS complex.Absence of P wave before QRS complex.

Signs of atrio-ventricular (node)Signs of atrio-ventricular (node)
extrasystole on ECGextrasystole on ECG
1)1) P wave of extrasystole is not revealed or localised after QRSP wave of extrasystole is not revealed or localised after QRS
complex, inverted in II,III, aVF leads;complex, inverted in II,III, aVF leads;
2)2) QRS complex form mostly is not changed;QRS complex form mostly is not changed;
3)3) Compensatory pause is incomplete.Compensatory pause is incomplete.

 A)A) bigeminybigeminy
 B)B) trigeminytrigeminy
 C) coupletsC) couplets
 D) qudrugeminiD) qudrugemini
A)
A)
B)
D)
A)
C)C)

The occurrence of three or more consecutive PVCs
is considered ventricular tachycardia.

 If the heart is structurally normal, and theIf the heart is structurally normal, and the
PVCs are singleton, uniform in focus, andPVCs are singleton, uniform in focus, and
disappear with increased heart rate, the PVCsdisappear with increased heart rate, the PVCs
are usually benign and require no treatment.are usually benign and require no treatment.
 Any deviation from the presentation (historyAny deviation from the presentation (history
of syncope or a family history of suddenof syncope or a family history of sudden
death) requires further investigation anddeath) requires further investigation and
possiblypossibly treatment with antiarrhythmictreatment with antiarrhythmic
medications.medications.


Criteria for investigation of PVCsCriteria for investigation of PVCs
 two or more PVC in a row,two or more PVC in a row,
 multifocal origin,multifocal origin,
 increased ventricular ectopic activity withincreased ventricular ectopic activity with
exercise,exercise,
 ““R on T phenomenon” (premature ventricularR on T phenomenon” (premature ventricular
depolarization occurs on the T wave of thedepolarization occurs on the T wave of the
preceding beat),preceding beat),
 presence of underlying heart disease.presence of underlying heart disease.
That could requireThat could require suppressive therapysuppressive therapy..

TACHYARRHYTHMIASTACHYARRHYTHMIAS
SupraventricularSupraventricular VentricularVentricular
atrial atrioventricular

Supraventricular tachycardia (SVT)Supraventricular tachycardia (SVT)
 denotes the paroxysm of heart beat accelerated (HRdenotes the paroxysm of heart beat accelerated (HR
is greater than 220 BPM in newborns and infants;is greater than 220 BPM in newborns and infants;
and more than 180 BPM in older children)and more than 180 BPM in older children)
 Rapid,Rapid, regularregular, usually narrow QRS rhythm,, usually narrow QRS rhythm,
originating above the ventriclesoriginating above the ventricles

Supraventricular tachycardiaSupraventricular tachycardia
 It is theIt is the most common symptomaticmost common symptomatic
dysrhythmiadysrhythmia in infants and children.in infants and children.
 Most common arrhythmia requiring treatmentMost common arrhythmia requiring treatment inin
pediatric populationpediatric population
 Most frequent age presentation: 1Most frequent age presentation: 1stst
3 months of3 months of
life, 2life, 2ndnd
peaks at 8-10 yr and in adolescencepeaks at 8-10 yr and in adolescence
 Although most patients with SVT haveAlthough most patients with SVT have
structurally normal hearts and normal baselinestructurally normal hearts and normal baseline
ECGs, 25% children have Wolff-Parkinson-ECGs, 25% children have Wolff-Parkinson-
White syndrome or Ebstein’s anomaly as theWhite syndrome or Ebstein’s anomaly as the
cause of the dysrhythmia.cause of the dysrhythmia.

SVT. Clinical manifestations.SVT. Clinical manifestations.
 Heart rate that is ‘‘too fast to count.’’Heart rate that is ‘‘too fast to count.’’
 Infants often present with nonspecific complaintsInfants often present with nonspecific complaints
such as ‘‘fussiness,’’ lethargy, poor feeding, pallor,such as ‘‘fussiness,’’ lethargy, poor feeding, pallor,
sweating with feeds, or simply ‘‘not acting right”sweating with feeds, or simply ‘‘not acting right”
 Older children: palpitations, chest pain, dizziness, orOlder children: palpitations, chest pain, dizziness, or
shortness of breath.shortness of breath.
 History: relationship to exercise, meals, stress, colorHistory: relationship to exercise, meals, stress, color
changes, neurologic changes, or syncopechanges, neurologic changes, or syncope
 A medical history significant for cardiac problems, currentA medical history significant for cardiac problems, current
medications, allergies, or a family history of sudden death ormedications, allergies, or a family history of sudden death or
cardiac disease should be investigated.cardiac disease should be investigated.

ECG signs of SVTECG signs of SVT
1) The rhythm has a rapid,
regular rate with a narrow
QRS complex
2) HR more than 200/min for
the children of early age and
more than 150/min for
children of eldery age (range,
180-320 beats/min);
3) Abnormal P-wave shape or
axis or absent P waves;
4) Paroxysm consists of not less
than 3 contractions;
5) There are secondary changes
of ST-T interval.

Atrial tachyarrhythmiasAtrial tachyarrhythmias
 The source of impulses is localized withinThe source of impulses is localized within
atrium.atrium.
 Atrial tachyarrhythmias include fibrillation.Atrial tachyarrhythmias include fibrillation.
 Atrioventricular tachyarrhythmias includeAtrioventricular tachyarrhythmias include
atrioventricular nodular tachyarrhythmia andatrioventricular nodular tachyarrhythmia and
atrioventricular tachycardia with participationatrioventricular tachycardia with participation
of accessory pathways.of accessory pathways.

Atrial fibrillationAtrial fibrillation
 Atrial fibrillationAtrial fibrillation occur when impulses areoccur when impulses are
generated in atria is chaotic and more rapidgenerated in atria is chaotic and more rapid
(300–700 beats/min). It produces(300–700 beats/min). It produces
uncoordinated contractions of separateuncoordinated contractions of separate
muscle fibers and an irregular ventricularmuscle fibers and an irregular ventricular
response and pulse.response and pulse.

 It is much less common in children and rare in infants andIt is much less common in children and rare in infants and
occurs most frequently in older children with rheumaticoccurs most frequently in older children with rheumatic
mitral valve disease. Atrial fibrillation may be familial.mitral valve disease. Atrial fibrillation may be familial.
 Thyrotoxicosis, pulmonary emboli, and pericarditis should beThyrotoxicosis, pulmonary emboli, and pericarditis should be
suspected in a previously normal older child or adolescentsuspected in a previously normal older child or adolescent
with atrial fibrillationwith atrial fibrillation..

1)1) Fibrillation waves (f) ofFibrillation waves (f) of
various amplitude form,various amplitude form,
duration without atrial Pduration without atrial P
wave;wave;
2) Irregular ventricular2) Irregular ventricular
rhythm;rhythm;
3) QRS complexes are normal3) QRS complexes are normal
or aberrant;or aberrant;
4) Number of atrial4) Number of atrial
contraction within 400 –contraction within 400 –
700/min.700/min.

Atrial flutterAtrial flutter
(intra-atrial re-entrant tachycardia)(intra-atrial re-entrant tachycardia)
 is a regular oris a regular or
regularly irregularregularly irregular
tachycardiatachycardia
characterized bycharacterized by
atrial activity at aatrial activity at a
rate of 250–400rate of 250–400
beats/min.beats/min.
 Uncommon rhythmUncommon rhythm
in the pediatricin the pediatric
populationpopulation..

Atrial flutterAtrial flutter
 ‘‘‘‘saw-toothed’’ flutter waves,saw-toothed’’ flutter waves,
 Because the AV node cannotBecause the AV node cannot
respond this quickly, there is anrespond this quickly, there is an
AV blockAV block
1)1) Quick, regular, serratedQuick, regular, serrated
waves in two leads and more;waves in two leads and more;
2)2) Number of mentioned wavesNumber of mentioned waves
(they are named as F-waves)(they are named as F-waves)
– from 250 to 350/min;– from 250 to 350/min;
3)3) Isoelectric line between FIsoelectric line between F
waves is absent;waves is absent;
4)4) Number and regularity ofNumber and regularity of
QRS complexes depend onQRS complexes depend on
the state of atrio-ventricularthe state of atrio-ventricular
conduction;conduction;
5)5) QRS complexes are normal,QRS complexes are normal,
widened or deformed andwidened or deformed and
depend on the primarydepend on the primary
condition of intraventricularcondition of intraventricular
conduction, presence ofconduction, presence of
accessory pathways.accessory pathways.

Ventricular tachycardiaVentricular tachycardia
EtiologyEtiology
Ventricular tachycardia may result fromVentricular tachycardia may result from
electrolyte disturbances (hyper- and hypokalemia,electrolyte disturbances (hyper- and hypokalemia,
and hypocalcemia),and hypocalcemia),
metabolic abnormalities,metabolic abnormalities,
Congenital and acquired heart disorders,Congenital and acquired heart disorders,
myocarditis, or drug toxicity.myocarditis, or drug toxicity.
Other causes include cardiomyopathies, cardiacOther causes include cardiomyopathies, cardiac
tumors, prolonged QT syndrome, and idiopathictumors, prolonged QT syndrome, and idiopathic
causes.causes.

 Nonperfusing ventricular rhythms areNonperfusing ventricular rhythms are
seen in up to 19% of pediatric cardiacseen in up to 19% of pediatric cardiac
arrests, when sudden infant deatharrests, when sudden infant death
syndrome (SIDS) cases are excludedsyndrome (SIDS) cases are excluded

Ventricular paroxysmalVentricular paroxysmal
tachycardiatachycardia
1)1) Changed and widened QRS complex (ranging from 0.06Changed and widened QRS complex (ranging from 0.06
to 0.14 sec) with secondary internal ST-T deviation;to 0.14 sec) with secondary internal ST-T deviation;
2)2) Frequency of ventricular contractions 150 – 200/min;Frequency of ventricular contractions 150 – 200/min;
3)3) Stable R-R interval;Stable R-R interval;
4)4) Usually complexes appear monomorphic with aUsually complexes appear monomorphic with a
uniform contour and absent or retrograde P wave,uniform contour and absent or retrograde P wave,
5)5) Atrio-ventricular dissociation;Atrio-ventricular dissociation;

Ventricular paroxysmal tachycardiaVentricular paroxysmal tachycardia

Ventricular flutter and fibrillationVentricular flutter and fibrillation
 is an uncommon rhythm in the pediatricis an uncommon rhythm in the pediatric
population but is certainly life threatening.population but is certainly life threatening.
 The hallmark is chaotic, irregular ventricularThe hallmark is chaotic, irregular ventricular
contractions without circulation to the body.contractions without circulation to the body.

Ventricular flutter and fibrillationVentricular flutter and fibrillation
EtiologyEtiology
 The causes include electric trauma,The causes include electric trauma,
postoperative complications from CHD repair,postoperative complications from CHD repair,
myocarditis, cardiomyopathy, medicationsmyocarditis, cardiomyopathy, medications
(digitalis, quinidine, catecholamines, and(digitalis, quinidine, catecholamines, and
anesthesia), complete block, and myocardialanesthesia), complete block, and myocardial
infarction, and any severe diseases with markedinfarction, and any severe diseases with marked
metabolic disorders.metabolic disorders.

 Ventricular flutterVentricular flutter is characterized byis characterized by
frequent rhythmic impulses in thefrequent rhythmic impulses in the
ventricular myocardium with the heart rateventricular myocardium with the heart rate
reaching 250-350 beats per minute.reaching 250-350 beats per minute.
 Ventricular fibrillationVentricular fibrillation is distinguished byis distinguished by
the chaotic, disorganized activation ofthe chaotic, disorganized activation of
separate muscle fibers in the ventricles withseparate muscle fibers in the ventricles with
heart rate reaching 600 beats per minute.heart rate reaching 600 beats per minute.

Ventricular fibrillation and flutter
Clinical criteria:
- circulatory arrest (pulse not felt, heart sounds are not
heard) ,
- loss of consciousness,
- Apparent death.

Ventricular flutter and fibrillation

ECG: under ventricular flutter there are
registered serrated waves without differention of
usual ECG elements (P, T waves, QRS complex
are absent). Impulses rate is 200 – 300/min.
Isoelectric line is absent. Under ventricular
fibrillation the waves are more frequent ( more
than 300/min), of changeable form, width and
amplitude. Diastole is absent. A-V block II – III
degree, idioventricular rhythm may precede
ventricular flutter and fibrillation.

CardiacCardiac BlocksBlocks
It is disorders of impulse conduction in theIt is disorders of impulse conduction in the
heart.heart.
-- sinoatrialsinoatrial
- intra-atrial- intra-atrial
- atrioventricularatrioventricular
- intraventricular- intraventricular

Sinoauricular (sinoatrial) block.Sinoauricular (sinoatrial) block.
Sinus arrestSinus arrest andand sinoatrial blocksinoatrial block may causemay cause
a sudden pause in the heartbeat.a sudden pause in the heartbeat.
Nature of this phenomenon is disorder of impulseNature of this phenomenon is disorder of impulse
transmission from the sinus node to atria.transmission from the sinus node to atria.
These arrhythmias are rare in childhood except asThese arrhythmias are rare in childhood except as
manifestations of digitalis intoxication or inmanifestations of digitalis intoxication or in
patients who have had extensive atrial surgery.patients who have had extensive atrial surgery.

Sinoatrial block.Sinoatrial block.
 ECG shows the loss of atrial and associated ventricularECG shows the loss of atrial and associated ventricular
complex after 2-3 normal heart beats, which results incomplex after 2-3 normal heart beats, which results in
the long pausethe long pause

Intra-atrial blockIntra-atrial block
There is disorder of impulse transmission viaThere is disorder of impulse transmission via
intra-atrial conductive ways that is why theintra-atrial conductive ways that is why the
synchronous activity of both atria disordersynchronous activity of both atria disorder
appears. On ECG changes of morphology andappears. On ECG changes of morphology and
duration of P wave are found, as well as itsduration of P wave are found, as well as its
widening to 0,11 – 0,12 sec and more.widening to 0,11 – 0,12 sec and more.

Atrio-ventricular heart blockAtrio-ventricular heart block

Are characterized by disorder of impulseAre characterized by disorder of impulse
conduction between the atria and ventriclesconduction between the atria and ventricles
at the level of AV septum.at the level of AV septum.
 AV block are induced by organic heartAV block are induced by organic heart
diseases (rheumatic fever,diseases (rheumatic fever,
cardiomyopathies), drug intoxicationscardiomyopathies), drug intoxications
(digoxin), severe infections diseases.(digoxin), severe infections diseases.

Bradyarrhythmias – AV Blocks
Type EKG Findings Causes & Clinical Significance
1st
degree
Prolonged PR interval Causes include AV nodal disease, ↑vagal tone,
myocarditis, abn electrolytes (ie: ↑K+
), MI, 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 atrial
impulse not conducted
to ventricles
Usually due to block within AV node. Caused by
↑parasympathetic tone, MI, 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
Constant prolongation
of 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
Congenital or caused by conduction system disease or
injury (ie: surgery, MI). Most symptomatic form of heart
block: fatigue, presyncope, syncope. Usually requires

AV BlockAV Block
 In 1st-degree block, the P-R interval is prolonged,In 1st-degree block, the P-R interval is prolonged,
but all the atrial impulses are conducted to thebut all the atrial impulses are conducted to the
ventricle. (ventricle. (There are no dropped beatsThere are no dropped beats))
 It is asymptomatic and when present in otherwise normalIt is asymptomatic and when present in otherwise normal
children requires no evaluation or treatment.children requires no evaluation or treatment.

AV block 2AV block 2ndnd
degreedegree
 Some impulses are notSome impulses are not
conducted to the ventricle.conducted to the ventricle.
 Mobitz Type I (Wenckebach) –Mobitz Type I (Wenckebach) –
progressive lengthening of theprogressive lengthening of the
PR interval until a droppedPR interval until a dropped
beatbeat

AV block 2AV block 2ndnd
degreedegree
 In Mobitz type II, the P-R interval does notIn Mobitz type II, the P-R interval does not
change, but an occasional atrial beat does notchange, but an occasional atrial beat does not
conduct to the ventricle. Itconduct to the ventricle. It is known as the ‘‘allis known as the ‘‘all
or none’’ phenomenaor none’’ phenomena
 This form may progress to complete heartThis form may progress to complete heart
block and may require pacemaker placement.block and may require pacemaker placement.

AV block 3AV block 3rdrd
degreedegree
(complete heart block)(complete heart block)
 3rd-degree block3rd-degree block occurs when none of theoccurs when none of the
atrial impulses is conducted to the ventricles.atrial impulses is conducted to the ventricles.

Third degree AV blockThird degree AV block
 Most common cause of abnormal bradycardia inMost common cause of abnormal bradycardia in
infants and childreninfants and children
 Complete disassociation between P waves andComplete disassociation between P waves and
QRS complexesQRS complexes

Congenital complete AV blockCongenital complete AV block
 Autoimmune injury of the fetal conductionAutoimmune injury of the fetal conduction
system by maternally derived IgG antibodies.system by maternally derived IgG antibodies.
SStrongly associatedtrongly associated with maternal SLEwith maternal SLE
 Congenital heart disease and abnormalCongenital heart disease and abnormal
embryonic development of the conductionembryonic development of the conduction
system.system.
 Myocardial tumors and myocarditis.Myocardial tumors and myocarditis.

Congenital complete AV blockCongenital complete AV block
Indications for the implantation of aIndications for the implantation of a
permanent cardiac pacemaker:permanent cardiac pacemaker:
episodes of exercise intolerance, dizziness,episodes of exercise intolerance, dizziness,
and syncope (Stokes-Adams attacks);and syncope (Stokes-Adams attacks);
progressive cardiac enlargement,progressive cardiac enlargement,
prolonged pauses, or awake heart rates ofprolonged pauses, or awake heart rates of
≤40 beats/min.≤40 beats/min.
Isoproterenol, atropine, or epinephrine mayIsoproterenol, atropine, or epinephrine may
be used to try to increase the heart ratebe used to try to increase the heart rate
temporarily until pacemaker placement cantemporarily until pacemaker placement can
be arranged.be arranged.

Intraventricular heart blocks.Intraventricular heart blocks.
They appear as a result of delay orThey appear as a result of delay or
interruption of impulse conduction viainterruption of impulse conduction via
branches of His bundle and Purkinje’sbranches of His bundle and Purkinje’s
fibers.fibers.
It usually caused by organic heart lesion.It usually caused by organic heart lesion.
Actually there are no clinical symptomsActually there are no clinical symptoms
of the block.of the block.

Right bundle-branch blockRight bundle-branch block
ECG signs of incomplete right bundle-branch block are:ECG signs of incomplete right bundle-branch block are:
1.1. QRS complex in V1 is in form rSr, RSR;QRS complex in V1 is in form rSr, RSR;
2.2. Duration of QRS interval is to 0,1sec.Duration of QRS interval is to 0,1sec.
ECG signs of complete right bundle-branch block are:ECG signs of complete right bundle-branch block are:
1.1. Widening of QRS complex to 0,1 sec and more;Widening of QRS complex to 0,1 sec and more;
2.2. Morphololgy of QRS complex in the right precardialMorphololgy of QRS complex in the right precardial
leads is presented in form rSR, rSr, RSR;leads is presented in form rSR, rSr, RSR;
3.3. Widening of S wave in I, V5, 6 and aVL leads;Widening of S wave in I, V5, 6 and aVL leads;
4.4. Deviation of electric axis to the right more thanDeviation of electric axis to the right more than
corresponding age;corresponding age;
5.5. Wide and split R wave in aVR lead;Wide and split R wave in aVR lead;
6.6. Absence of Q wave in I and aVL lead;Absence of Q wave in I and aVL lead;
7.7. Interval S-T and T wave are discordant to the final partInterval S-T and T wave are discordant to the final part
of QRS complex in the lead where it is the most evidentof QRS complex in the lead where it is the most evident..

Right bundle-branch blockRight bundle-branch block

LeftLeft bundle-branch blockbundle-branch block
1)1) Widening of QRS complex more 0,1sec, but in childrenWidening of QRS complex more 0,1sec, but in children
elder 14yr. – more 0,12sec.;elder 14yr. – more 0,12sec.;
2)2) rR form of QRS complex in I, aVL;V5, 6 leads;rR form of QRS complex in I, aVL;V5, 6 leads;
3)3) Absence of Q wave in the rhight precardial leads;Absence of Q wave in the rhight precardial leads;
4)4) QS-form in the right precardial leads;QS-form in the right precardial leads;
5)5) Shifting of S-T internal and T wave in the directionShifting of S-T internal and T wave in the direction
opposite to main deviation of QRS complex.opposite to main deviation of QRS complex.

Combined arrhythmiasCombined arrhythmias
Sick sinus syndromeSick sinus syndrome is the result ofis the result of
abnormalities in the sinus node or atrialabnormalities in the sinus node or atrial
conduction pathways, or both.conduction pathways, or both.
This syndrome may occur in the absence ofThis syndrome may occur in the absence of
congenital heart disease and has been reportedcongenital heart disease and has been reported
in siblings, but it is most commonly seen afterin siblings, but it is most commonly seen after
surgical correction of congenital heart defects,surgical correction of congenital heart defects,
especially the atrial switch (Mustard or Senning)especially the atrial switch (Mustard or Senning)
operation for transposition of the great arteries.operation for transposition of the great arteries.

Sick sinus syndromeSick sinus syndrome
 Clinical manifestationsClinical manifestations depend on thedepend on the
heart rate. Most patients remain asymptomaticheart rate. Most patients remain asymptomatic
without treatment, but dizziness and syncopewithout treatment, but dizziness and syncope
can occur during periods of marked sinuscan occur during periods of marked sinus
slowing with failure of junctional escape.slowing with failure of junctional escape.
 Pacemaker therapy is indicated in patients whoPacemaker therapy is indicated in patients who
experience symptoms.experience symptoms.

Sick sinus syndrome. ECGSick sinus syndrome. ECG
 Sinus bradycardia,Sinus bradycardia,
 bradycardia-tachycardia syndrome,bradycardia-tachycardia syndrome,
 sinoatrial block,sinoatrial block,
 asystole.asystole.
 Against background of bradycardia and asystole theAgainst background of bradycardia and asystole the
secondary “replacing” rhythms appear as atrial flutter orsecondary “replacing” rhythms appear as atrial flutter or
fibrillation, nonparoxysmal and paroxysmal tachycardia,fibrillation, nonparoxysmal and paroxysmal tachycardia,
extrasystole.extrasystole.

Preexcitation of ventriclesPreexcitation of ventricles
syndromesyndrome
Anatomic nature of syndrome is accessoryAnatomic nature of syndrome is accessory
conductive ways which give the possibilityconductive ways which give the possibility
for spreading of impulses from atria tofor spreading of impulses from atria to
ventricles escaping atrioventricularventricles escaping atrioventricular
communication. That is why there is nocommunication. That is why there is no
delay physiological impulses in the last anddelay physiological impulses in the last and
ventricular myocardium excites partly orventricular myocardium excites partly or
completely earlier than impulse comingcompletely earlier than impulse coming
normal pathway reachs ventricle.normal pathway reachs ventricle.

Types of preexcitation of ventriclesTypes of preexcitation of ventricles
syndromes:syndromes:
1)1) Syndrome Wolff-Parkinson-WhiteSyndrome Wolff-Parkinson-White
(WPW)(WPW);;
2)2) Lown-Ganong-Levine syndrom (LGL) -Lown-Ganong-Levine syndrom (LGL) -
Clerc-Levy-Cristesko syndrome- shortClerc-Levy-Cristesko syndrome- short
PQ syndromePQ syndrome;;
3)3) Preexcitation of Muchine typePreexcitation of Muchine type;;
4)4) Combination of several accessoryCombination of several accessory
pathwayspathways..

Accessory PathwaysAccessory Pathways
 If accessory pathway hasIf accessory pathway has
retrograde conduction, canretrograde conduction, can
cause narrow-complex SVTcause narrow-complex SVT
(orthodromic reciprocating(orthodromic reciprocating
tachycardia –ORT)tachycardia –ORT)
 If accessory pathway hasIf accessory pathway has
antegrade conduction, canantegrade conduction, can
cause wide complex SVTcause wide complex SVT
(antidromic reciprocating(antidromic reciprocating
tachycardia –ART) –very raretachycardia –ART) –very rare

Accessory Pathway -WPWAccessory Pathway -WPW
Seen on ECG as delta wave (early depolarization of
ventricular myocardium) and short PR interval

ECG criteria of WPW syndromeECG criteria of WPW syndrome
1)1) Shortening (less 0,1sec)Shortening (less 0,1sec)
of P-R interval;of P-R interval;
2)2) Widening QRS complexWidening QRS complex
more 0,1 – 0,12 sec.;more 0,1 – 0,12 sec.;
3)3) Presence of delta wavePresence of delta wave;;
4)4) Secondary changes of ST-Secondary changes of ST-
T interval;T interval;
5)5) Frequent combinationFrequent combination
with paroxysmalwith paroxysmal
tachycardia andtachycardia and
extrasystole.extrasystole.

Wolff-Parkinson-White (WPW)Wolff-Parkinson-White (WPW)
SyndromeSyndrome

 Rapid conduction throughRapid conduction through
Accessory Pathway during atrialAccessory Pathway during atrial
fibrillation can result in ventricularfibrillation can result in ventricular
fibrillation and SUDDENfibrillation and SUDDEN
CARDIAC DEATH !!!CARDIAC DEATH !!!

 In children with WPW syndrome digoxin orIn children with WPW syndrome digoxin or
calcium channel blockers may increase the rate ofcalcium channel blockers may increase the rate of
anterograde conduction of impulses through theanterograde conduction of impulses through the
bypass tract and should be avoided.bypass tract and should be avoided.
 These patients are usually managed in the long termThese patients are usually managed in the long term
with propranolol.with propranolol.
 In patients with resistant tachycardias,In patients with resistant tachycardias,
procainamide, quinidine, flecainide, propafenone,procainamide, quinidine, flecainide, propafenone,
sotalol, and amiodarone have all been used.sotalol, and amiodarone have all been used.
 It should be recognized that most antiarrhythmicIt should be recognized that most antiarrhythmic
agents could have proarrhythmic and negativeagents could have proarrhythmic and negative
inotropic effects.inotropic effects.

Syndrome of long QT intervalSyndrome of long QT interval
(Long Q-T syndromes (LQTS)(Long Q-T syndromes (LQTS)
 It is genetic abnormalities of ventricular repolarization andIt is genetic abnormalities of ventricular repolarization and
characterised with pathologic long QT interval on ECG,characterised with pathologic long QT interval on ECG,
paroxysms of loss consciousness, caused by malignantparoxysms of loss consciousness, caused by malignant
ventricular tachyarrhythmia and high risk of sudden death.ventricular tachyarrhythmia and high risk of sudden death.
 Genetic studies have identified mutations in cardiacGenetic studies have identified mutations in cardiac
potassium and sodium channels.potassium and sodium channels.
 Drugs may prolong the QT interval directly (terfenadine,Drugs may prolong the QT interval directly (terfenadine,
astemizole, cisapride, droperidol), but more often do soastemizole, cisapride, droperidol), but more often do so
when drugs such as erythromycin or ketoconazole inhibitwhen drugs such as erythromycin or ketoconazole inhibit
their metabolism.their metabolism.

Drugs that prolong the QTDrugs that prolong the QT
intervalinterval
 Antiarrhythmics (class 1A and 3)Antiarrhythmics (class 1A and 3)
 Antiemetic (droperidol)Antiemetic (droperidol)
 Antifungals (ketoconazole)Antifungals (ketoconazole)
 Antihistamines (astemizole, terfenidine)Antihistamines (astemizole, terfenidine)
 Antimicrobials (erythromycin, trimethoprim-Antimicrobials (erythromycin, trimethoprim-
sulfamethoxazole)sulfamethoxazole)
 Antipsychotics (haloperidol, risperidone)Antipsychotics (haloperidol, risperidone)
 Organophosphate insecticidesOrganophosphate insecticides
 Phenothiazines (thioridazine)Phenothiazines (thioridazine)

 TheThe clinical manifestationclinical manifestation of LQTS inof LQTS in
children is most often a syncopal episodechildren is most often a syncopal episode
brought on by exercise, fright, or a suddenbrought on by exercise, fright, or a sudden
startle; some events occur during sleep.startle; some events occur during sleep.
 Patients can initially be seen with seizures,Patients can initially be seen with seizures,
presyncope, or palpitations; about 10% arepresyncope, or palpitations; about 10% are
initially in cardiac arrest.initially in cardiac arrest.

ECG criteria of LQTSECG criteria of LQTS
 A heart rate–corrected Q-T interval of >0.47 secA heart rate–corrected Q-T interval of >0.47 sec
is highly indicative, whereas a Q-T interval ofis highly indicative, whereas a Q-T interval of
>0.44 sec is suggestive.>0.44 sec is suggestive.
 Other features include notched T waves, T waveOther features include notched T waves, T wave
alternans, a low heart rate for age, a history ofalternans, a low heart rate for age, a history of
syncope (especially with stress), and a familialsyncope (especially with stress), and a familial
history of either LQTS or unexplained suddenhistory of either LQTS or unexplained sudden
death.death.

Corrected QT interval (QTc )Corrected QT interval (QTc )
Select the longest QT intervalSelect the longest QT interval
Measure QT interval from beginning of Q wave toMeasure QT interval from beginning of Q wave to
end of T waveend of T wave
Measure R-R interval from the complex in whichMeasure R-R interval from the complex in which
QT is measured to preceding RQT is measured to preceding R
QTc interval (s)=QTc interval (s)= QT interval (s)QT interval (s)
R-R interval(s)R-R interval(s)
((Bazett formulaBazett formula))

I think the child has anI think the child has an
arrhythmia, what should I do?arrhythmia, what should I do?

Pediatric dysrhythmiasPediatric dysrhythmias
Treatment not requiredTreatment not required TreatmentTreatment isis requiredrequired
Sinus arrhythmiaSinus arrhythmia Supraventricular tachycardiaSupraventricular tachycardia
Wandering atrial pacemakerWandering atrial pacemaker
Isolated premature atrialIsolated premature atrial
contractionscontractions
Isolated prematureIsolated premature
ventricular contractionsventricular contractions
Ventricular tachycardiaVentricular tachycardia
First degree AV blockFirst degree AV block Third degree AV block withThird degree AV block with
symptomssymptoms
Reproduced from Zitelli’s Atlas of Pediatric physical diagnosis, 2007, pg 140.

Acute Management of ArrhythmiasAcute Management of Arrhythmias
 STABLE OR UNSTABLE??STABLE OR UNSTABLE??
 FAST OR SLOW??FAST OR SLOW??
 WIDE OR NARROW??WIDE OR NARROW??

I think the patient has anI think the patient has an
arrhythmia, what should I do?arrhythmia, what should I do?
Start with ABC!Start with ABC!
Check for a pulseCheck for a pulse
Give oxygen!Give oxygen!
Get the patient on a cardiac monitorGet the patient on a cardiac monitor
Insert an iv cannulaInsert an iv cannula
Assess for adverse featuresAssess for adverse features
Get a 12 lead ECGGet a 12 lead ECG

Classification of Drugs for AntiarrhythmiaClassification of Drugs for Antiarrhythmia
ClassClass ActionAction Example(s)Example(s)
II Depression of phase of depolarization (rate of upstroke of actionDepression of phase of depolarization (rate of upstroke of action
potential); sodium channel blockadepotential); sodium channel blockade
IaIa Prolongation of QRS complex and QTProlongation of QRS complex and QT
intervalinterval
Quinidine, procainamide,Quinidine, procainamide,
disopyramidedisopyramide
IbIb Significant effect on abnormal conductionSignificant effect on abnormal conduction Lidocaine, mexiletine,Lidocaine, mexiletine,
phenytoin, tocainidephenytoin, tocainide
IcIc Prolongation of QRS complex and PRProlongation of QRS complex and PR
intervalinterval
Flecainide, propafenone,Flecainide, propafenone,
moricizine?moricizine?
IIII ββ blockade; slowing of sinus rate;blockade; slowing of sinus rate;
prolongation of PR intervalprolongation of PR interval
Propranolol, atenolol,Propranolol, atenolol,
acebutololacebutolol
IIIIII Prolongation of action potential; prolongationProlongation of action potential; prolongation
of PR, QT intervals, QRS complex; sodiumof PR, QT intervals, QRS complex; sodium
and calcium channel blockadeand calcium channel blockade
Bretylium, amiodarone,Bretylium, amiodarone,
sotalolsotalol
IVIV Calcium channel blockade; reduction in sinusCalcium channel blockade; reduction in sinus
and AV node pacemaker activity andand AV node pacemaker activity and
conduction; prolongation of PR intervalconduction; prolongation of PR interval
Verapamil and otherVerapamil and other
calcium channel blockingcalcium channel blocking
agentsagents

Anti-tachycardia agentsAnti-tachycardia agents
 Modified Vaugham Williams classificationModified Vaugham Williams classification
1.1. I class: Natrium channel blockerI class: Natrium channel blocker
2.2. II class: ß-receptor blockerII class: ß-receptor blocker
3.3. III class: Potassium channel blockerIII class: Potassium channel blocker
4.4. IV class: Calcium channel blockerIV class: Calcium channel blocker
5.5. Others: Adenosine, DigitalOthers: Adenosine, Digital

Treatment of children with sinusTreatment of children with sinus
tachycardia (bradycardia)tachycardia (bradycardia)
 Usually, no therapy is necessary.Usually, no therapy is necessary.
 Treatment of the principal diseases.Treatment of the principal diseases.
 Symptomatic treatment is used in situation whenSymptomatic treatment is used in situation when
increasing of heart rate causes discomfort. It isincreasing of heart rate causes discomfort. It is
prescribed psychotherapy, sedative drugs. B-prescribed psychotherapy, sedative drugs. B-
adrenoblockers. Normalization of sleep, rationaladrenoblockers. Normalization of sleep, rational
rest are very important.rest are very important.
 In patients with sinus bradycardia it is necessaryIn patients with sinus bradycardia it is necessary
to reveal the cause of its appearance. In case ofto reveal the cause of its appearance. In case of
appearance such symptoms as flaccidity,appearance such symptoms as flaccidity,
somnolency, fatigability- M-anticholinergic drugssomnolency, fatigability- M-anticholinergic drugs
(Belloid), widening of movement regimen.(Belloid), widening of movement regimen.

Treatment of extrasystolesTreatment of extrasystoles
 Correction of the underlying abnormality.Correction of the underlying abnormality.
 Limitation of sport activityLimitation of sport activity
 AmiodaroneAmiodarone
 Lidocaine IV bolusLidocaine IV bolus (1 mg/kg/dose),(1 mg/kg/dose), is theis the
1st line of therapy of malignant PVCs,1st line of therapy of malignant PVCs,
followed by a lidocaine drip (20–50followed by a lidocaine drip (20–50
mg/kg/min).mg/kg/min).
 Amiodarone, procainamide, and b blockersAmiodarone, procainamide, and b blockers
are reserved for conditions that are refractoryare reserved for conditions that are refractory
to lidocaineto lidocaine

Acute treatment of SVTAcute treatment of SVT
 In children who present with asymptomatic SVTIn children who present with asymptomatic SVT
Vagal maneuvers:Vagal maneuvers:
 Valsava test (maneuver): straining effort under closedValsava test (maneuver): straining effort under closed
nose during 10 sec);nose during 10 sec);
 eyeball pressure,eyeball pressure,
 carotid sinus massage during 5 – 10 sec. first on hiscarotid sinus massage during 5 – 10 sec. first on his
right and in absence of effect – on the left;right and in absence of effect – on the left;
 breath holding, drinking ice water;breath holding, drinking ice water;
 submersion into ice-cold water or by placing an ice bagsubmersion into ice-cold water or by placing an ice bag
over the face (in infants) may abort the attackover the face (in infants) may abort the attack
 inducing vomiting: pressing with spatula on the root ofinducing vomiting: pressing with spatula on the root of
tongue, cold rub-down.tongue, cold rub-down.
OxigenotherapyOxigenotherapy

Pharmacologic treatment of SVTPharmacologic treatment of SVT
 Adenosine IV 0,1-0,2 mg/kgAdenosine IV 0,1-0,2 mg/kg (Blocks AV(Blocks AV
node for short period of time)node for short period of time)
 VerapamilVerapamil (Calcium channel blockers) –if(Calcium channel blockers) –if
over 2-5 years of age 0.1-0,15 mg/kg overover 2-5 years of age 0.1-0,15 mg/kg over
5 minutes (Blocks AV node for longer5 minutes (Blocks AV node for longer
period of time)period of time)
Verapamil contraindicated in infants younger than 1 yrVerapamil contraindicated in infants younger than 1 yr
(may reduce cardiac output and produce hypotension and(may reduce cardiac output and produce hypotension and
cardiac arrest).cardiac arrest).

Pharmacologic treatment of SVTPharmacologic treatment of SVT
 ProcainamideProcainamide 5-15 mg/kg over 15-45 minutes5-15 mg/kg over 15-45 minutes
to 20 -60 mcg/kg/min (Blocks accessoryto 20 -60 mcg/kg/min (Blocks accessory
pathway; may speed or slow AV node)pathway; may speed or slow AV node)
 AmiodaroneAmiodarone 1 mg/kg over 10 minutes repeated1 mg/kg over 10 minutes repeated
to total of ~ 5 mg/kg (Blocks accessory pathwayto total of ~ 5 mg/kg (Blocks accessory pathway
and AV node)and AV node)
 Phenylephrine (Mesaton) or edrophoniumPhenylephrine (Mesaton) or edrophonium
(Tensilon), which increase vagal tone through(Tensilon), which increase vagal tone through
the baroreflexthe baroreflex

Acute treatment of SVTAcute treatment of SVT
 DC-Cardioversion (0.5–2 J/kg) is recommendedDC-Cardioversion (0.5–2 J/kg) is recommended
as the initial management if hemodynamicallyas the initial management if hemodynamically
unstable childunstable child
 Consider esophageal pacing if hemodynamicallyConsider esophageal pacing if hemodynamically
significant and frequent recurrencessignificant and frequent recurrences

Chronic treatment of SVTChronic treatment of SVT
 Can treat all with POCan treat all with PO propranolol/atenololpropranolol/atenolol
 Can treat with POCan treat with PO digoxindigoxin if not WPWif not WPW
 Can treat withCan treat with verapamilverapamil if not WPW and if >2-5if not WPW and if >2-5
years)years)
 Second line:Second line: FlecainideFlecainide
 Third line:Third line: AmiodaroneAmiodarone ororsotalolsotalol
 When pharmacologic treatments fail,When pharmacologic treatments fail,
radiofrequency catheter ablation has an 85% to 95%radiofrequency catheter ablation has an 85% to 95%
success rate of preventing recurrence of SVTsuccess rate of preventing recurrence of SVT

Acute treatment of ventricularAcute treatment of ventricular
paroxysmal tachycardiaparoxysmal tachycardia
 Ventricular tachycardia with a pulse in an unstableVentricular tachycardia with a pulse in an unstable
patientpatient warrants immediate synchronizedwarrants immediate synchronized
cardioversion at 0.5 to 1 J/kg.cardioversion at 0.5 to 1 J/kg.
 It is important to pretreat conscious patients with lightIt is important to pretreat conscious patients with light
sedation (eg, midazolam, 0.1 mg/kg).sedation (eg, midazolam, 0.1 mg/kg).
 AmiodaroneAmiodarone (5 mg/kg IV over 20–60 min; max daily dose 15(5 mg/kg IV over 20–60 min; max daily dose 15
mg/kg/d),mg/kg/d),
 ProcainamideProcainamide ((15 mg IV over 30–60 min15 mg IV over 30–60 min), or), or
 LidocaineLidocaine (1 mg/kg IV bolus, repeat every 5–10 min, with max(1 mg/kg IV bolus, repeat every 5–10 min, with max
total of 3 mg/kg)total of 3 mg/kg)
 For polymorphic ventricular tachycardiaFor polymorphic ventricular tachycardia magnesiummagnesium (20–50(20–50
mg/kg, IV).mg/kg, IV).

Tretment of VentricularTretment of Ventricular
fibrillation and flutterfibrillation and flutter
 Defibrillation 2 to 4 J/kgDefibrillation 2 to 4 J/kg
 If defibrillation is unsuccessful, epinephrineIf defibrillation is unsuccessful, epinephrine
(0.01 mg/kg, 1:10,000 solution) and repeated(0.01 mg/kg, 1:10,000 solution) and repeated
every 3 to 5 minutes as necessary.every 3 to 5 minutes as necessary.
 If it is refractory to defibrillation, antiarrhythmicIf it is refractory to defibrillation, antiarrhythmic
drugs are indicated, such as amiodarone (5drugs are indicated, such as amiodarone (5
mg/kg, IV bolus) or lidocaine (1 mg/kg, IVmg/kg, IV bolus) or lidocaine (1 mg/kg, IV
bolus, and repeated to a maximum of 3 mg/kg).bolus, and repeated to a maximum of 3 mg/kg).

Treatment of LQTSTreatment of LQTS
 ββ-blocking agents-blocking agents
 Some patients require aSome patients require a pacemakerpacemaker because ofbecause of
drug-induced profound bradycardia.drug-induced profound bradycardia.
 In patients with continued syncope despiteIn patients with continued syncope despite
treatment, an implantable cardiac defibrillator istreatment, an implantable cardiac defibrillator is
indicated for those who do not respond toindicated for those who do not respond to ββ--
blocking drugs and those who have experiencedblocking drugs and those who have experienced
cardiac arrest.cardiac arrest.

Management of bradycardiaManagement of bradycardia
 Identification of the cause and appropriateIdentification of the cause and appropriate
cardiopulmonary resuscitation (ventilation,cardiopulmonary resuscitation (ventilation,
oxygenation, and chest compressions)oxygenation, and chest compressions)
 Pharmacologic intervention:Pharmacologic intervention: epinephrineepinephrine (0.01(0.01
mg/kg IV; 0.1 mL/kg of 1:10,000 solution) ormg/kg IV; 0.1 mL/kg of 1:10,000 solution) or
atropineatropine (0.02 mg/kg, IV, minimum 0.1 mg; max(0.02 mg/kg, IV, minimum 0.1 mg; max
dose is 0.5 mg in children and 1 mg indose is 0.5 mg in children and 1 mg in
adolescents).adolescents).
 Chest compressions are indicated for neonates orChest compressions are indicated for neonates or
children with heart rates less than 60 BPM withchildren with heart rates less than 60 BPM with
hemodynamic compromisehemodynamic compromise

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