Transcript Arrhythmia in Pediatric

‫الدكتور‬
‫مازن هاشم خالد‬
‫طبيب اختصاص أطفال‬
‫بورد عربي في طب األطفال‬
‫دبلوم عالي في طب وصحة الطفل‬
‫متدرب على فحص ومعالجة قلب األطفال‬
Arrhythmia in Pediatric
The term arrhythmia literally means Absent rhythm, it
is occurs when the sinus rhythm is interfered with by
ectopic beats or rhythms, Rhythms that are too fast or
too slow qualify as arrhythmia & lastly abnormal in
conductive system are categorized as arrhythmia
The major risks of any arrhythmia are those of sever
tachycardia or bradycardia leading to decreased cardiac
output, or the risk of degeneration into amore sever
arrhythmia for example ventricular fibrillation.
Normal sinus rhythm records an impuls that starts in the
(SAN) from SAN, the impuls progress to the ventricles
through the normal conductive pathway, The normal
conductive pathway starts in the SAN to atria and AVN,
then it proceeds to the bundle of his and its branches then
finally to purkinjie fibers.
The normal heart rate varies with age: The younger the
child the faster the heart rate therefor, the definition of
bradycardia is defined as aheart rate slower than the lower
limit of normal for the patient age.
Tachycardia is defined as aheart rate beyond the upper
limit of normal for the patient’s age
Fig (1): Normal sinus rhythm
I. Rhythms originating in the sinus Node
Sinus arrhythmia: Represents a normally physiologic variation in impuls
discharges from the sinus Node related to respiration
Fig (2): Sinus arrhythmia
Sinus Tachycardia:Causes of it anxiety, fever, hypovolemia or circulatory
shock, anemia, CHF, administration of catecholamines,
thyrotoxicosis & myocardial disease.
Fig (3): Sinus tachycardia
Sinus Bradycardia:Causes of it may occur in normal individuals and trained
athletes, hypothyroidism, hypothermia hypoxia,
hyperkalermia, administration of drugs such as Badrenergic blockers.
Fig (4): Sinus bradycardia
Sinus Pause: Sinus node pace maker momentarily dropped beat
relaitvely for short time, causes of it hypoxia, increased
vagal tone & diagitalis toxicity
Fig (5):
II Ectopic beats pacemakers of some beats are
ectopic
Escape ectopic beat sinus rhythm is interrupted by asinus
paused followed by one ectopic beat are may atrial
Junchoial or ventricular
Premature ectopic beat
Sinus rhythm is interrupted by apremature ectopic beat
which is followed by apanse
Premature atrial & Junctional beat, pans is usually less
than compensatory (premature cycle + pause <2 sinus
cycls) due to resetting of the SAN by premature impulse,
its axis; as that of sinus beats.
Fig (6): Premature atrial contraction
Premature ventricular beat pause is usually full
compensatory (premature cycle + pause = 2 sinus cycle) &
its axis may be different from that of sinus beats.
III. Junctional Rhythms: Pacemakers of all beats are junctional P- wave may
Absent
Retrograde
Inverted in II & up right in aVR
Just before or Just after QRS
Escape Junctional rhythm regular H.R 40-60 no Need treatment
Accelated Junctional rhythm is arrhythmia in which the
Junctional rate exceed, that of the sinus node so that
atrioventricular dissociation results. This arrhythmia is most
often recognized in the early post operative period specialy (TOF
& vommon AV caval) and may extremely difficult to controle so
that reduction of the infusion rate of catechoament and control of
fever.
Fig (7): Junctional escape rhythm
Pacemakers of all beats are atrial
Supraventricular tachycardia:
Re – entery within the A-V node is the most common
mechanism of paroxysmal atrial tachycardia, the
tachycardia is initiated by premature atrial beat that is
conducted through abypass tract within the AV Node. The
ventricular response induce an echo beat, which return to
the atrium via retrograde tract within the AV Node. This
echo beat is in turn transmitted back to the ventricle and
so on.
Attacks may last only afew seconds or may persist for
hours. The cardiac is usually exceed 180 /mint.
Infant with SVT often present with congestive heart
failure as the tachycardia goes unrecognized for long time
SVT in neonates Differentition from sinus tachycardia
may be difficult: if the rate is greater than 230 beat .mit
and there is an abnormal p wave axis.
The normal P wave is positive in (lead I and aVF) SVT is
more likely.
Differentiation from ventricular tachycardia is critical but
absence of P wave and presence of wide QRS complexes
help to diagnosis VT.
SVT may be associated with abypass, tract in one of the
pre-excitation syndromes.
SVT may be noted in the anatomically normal heart or
may be assoicated with aby pass tract in one of the preexcitation syndrome (like WPW syndrom). Heart Disease,
more commonly with Ebstien anormaly of the tricuspid
valve and corrected transposition of the great vessels.
Fig (8): SVT
Fig (9): SVT + wide QRS
Fig (10): SVT Junctional No visible P wave
Management:
Vagal stimulatory maneuvers
Placing an ice bag on the face for up to 10 second is often
effective in infant
Adenosine is given by rapid intravenous bolus followed by
asaline flush starting at 50 Mg /kg and increment of 50 Mg /kg
every 1 to 2 min (maximum 250 Mg /kg)
When the tachycardia is converted to sinus rhythm either
digitalization or B- blocker are started
If adenosine is not available initial cardioversion may be
performed in infant with CHF the initial dose 0.5 Jouls /kg.
Digitalization may be used in infant without CHF and those
with mild CHF.
Intravenous administration of propranold or verpamil may
be tried but these drugs are not treatment of choice , They may
produce extreme bradycardia and hypotension in infant
younger than 1 year of age
In patient with post operative atrial tachycardia for which
arapid conversion is required intravenous administration of
amiodarone has provided excellent result
The recurrent SVT should be prevented with maintenance
dose of digoxen for 3- 6 month. In children older than 8 years
of age with wpw syndrome propranold is preferable to digoxis
Occasionally radiofrequency catheter ablation or surgical
interruption of accessory pathway should be considered if
medical management fail.
Mulitfocal atrial tachycardia
Is characterized by two or more ectopic P waves with two
or more different ectopic P-Pcycled, frequent blocked Pwaves, and varying P- R intervals of conducted beat. This
arrhythmia usually occurs in the absence of cardiac
disease and usually terminates spontaneously after weeks
or months.
Fig (11): Chaiotic atrial Rhythmia
Wandering atrial pacemaker:
Is defined as an intermittent shift in the pacemaker of the
heart from the sinus node to another part of the atrium.
This is not uncommon in childhood and usually
represents anormal variant.
Fig (12): Wandering pacemaker
Ectopic atrial tachycardia:
Ectopic atrial tachycardia is an uncommon tachycardia in
childhood
It is characterized by avariable rate (seldom greater than
200) identifiable P waves with an abnormal axis. In this
form of atrial tachycardia, there is asingle automatic focus
rather than the more usual re-entry mechanism.
This dysrhythmia is usually more difficult to control
pharmacologically than the more commen (SVT); therpy
should be directed toward slowing atrioventricular
conduction with digitalis or propranolol rather than
relying on drug that suppress atrial automaticity as
quinidine and disopyramils in some cases no treatment is
necessary.
Atrial Flutter:
Is regular or (regular) irregular tachycardia due to atrial activity at arate of
250-400/min, Because the atrioventricular node cannot transmit such rapid
impulses, there is virtually always some degree of A-V block and the
ventride respond to every 2nd – 4th atrial beat.
In older children atrial flutter usually occurs in the setting of cong. Heart
disease, In Neonate with atrial flutter frequently have normal heart
Atrial flutter usually convert immediately to sinus rhythm by DC
cardioversion, Digitalis slows the ventricular response in atrial flutter by
prolonging conduction through the AV node.
Fig (13): Atrial flutter
Recent report suggest that amiodarone may be more
effective than digoxin in treating atrial flutter.
When electric cardio version required digitalis should be
disocontinued for at 48hr. and start anticogulation with
warfarin is recommended before cardioversion to prevent
embolization.
Recent report suggest that amiodarone may be more
elective than digoxin in treating a trial flutter.
When electric cardio version required digitalis should be
discontinued for at 48 hr.
Start anticoagulation with warfarin is recommended
before cardioversion to prevent embolization.
Atrial Fibrillation
The mechansim of this arrhythmia is “circus movement” as in atrial flutter,
Atrial fibrillation is characterized by an extremely fast atrial rate (f wave at
arate of 350 to 600 beat / minute) and an irregularly irregular ventricular
response with normal QRS complexes.
Causes; dilated atrial, myocarditis, digitalis toxicity or previous intra – atrial
surgery, hyperthrodism
The significance of it is decrease cardiac output
Fig (14): Atrial fibrillation
Treatment: If atrial fibrillation has been present for more than 48hr. One should use
anticoagulation with warfarin for 3 wks to prevent systemic embolization of
atrial thrombus if the conversion can be delayed. Anticoagulation is continued
for 4 wks after the restoration of sinus rhythm. If cardioversion cannot be
delayed heparin should be started, with subsequent oral anticoagulation.
Digoxin is provided to slow the ventricular rate propranolol may be added.
V. Ventricular Rhythms:
1. Ventricular tachycardia
Is defined as at least 3 premature ventricular contraction (PVCs) at greater than
120 beat / mit
Ventricular ectopic focus QRS is wide, T direction is opposite QRS & signs of AV
dissociation
Causes of it: may be associated with Myocardites arrhythmogenic right
ventricular dysplasia, coronary art. anomalous, mitral value prolapse,
cardiomyopathy, prolonged QT interval, WPW.
Management:
VT must be treated promptly with synchronized cardioversion
l Jovu /kg if patient is unconscious.
If patient is conscious, an intravenous bolus of lidocain (1mg
/kg / dose) over 1 to 2 min followed by I.V. drip of lidocain 20
to 50 Mg / kg. min)
If lidocain is unsuccessful use bretylium tosylate
Intravenous injection of magnesium sulfate
In post operative VT is resistant to other antiarrhythmic agent
intravenous administration of amiodarone
If antiarrhythmic control is inadequate invasive
electrophysiologic studies should be considered
Rarely ventricular or atrial pacing combined with
antiarrhythmic agent.
Fig (15): VT
2. Ventricular fibrillation:
Is a chaotic dysrhythmia that results in death unless an effective ventricular
beat is rapidly restored. QRS is lost & characterized by bizarre wave with
varying sizes & configuration the rate is rapid and irregular.
Causes:
Sever hypoxia , hypekalemia , digitalis toxicity myocarditis.
Management
Athumb on the chest sometimes restores sinus rhythm. Usually external
cardiac massage with artificial ventilation and DC delibrllation
Electrophysiologie study is usually indicated for patient who have
developed ventricular fibrillation unless a clearly reversible cause is
indentified.
For patient who are refractory to pharmacologie therapy an automatic
implantable cardioverter defibrillator can be inserted.
Fig (16): VF
Atrioventricular block
The PR interval is prolonged beyond the upper limits of
normal for the patient age and heart rate.
Causes:
Rheumatic fever, cardiomyopathies cong. heart delect (ASD,
Ebstein’s anomaly endocardial cushion defect) cardiac surgery
and digitalis toxicity.
No treatment is indicated.
• Second degree AV block.
I Mobitz type I (wencke Bach) progressively prolonged pRinterval from beat to beat followed by anon- conducted P then
the cyde is repeated (group beating).
The rate of prolongation is decremental; that mean PR interval
shorters gradually during each cycle due to decremental in crease
in the PR intervals
Causes:
Appears in other wise healthy children , other causes myocarditis
cardiomypathy , cong . heart delect , cardiac surgery management the
underlying causes are treated
Mobitz type II
PR – uniform some of them associated with 1st degree heart bloc
P: QRS ratis:
• Eveny few conducted Ps one P is non conducted then the cycle is
repeated
• High-grade block may be 3:1, 4:1, 5:1 of variable block.
Significance of Mobitz type II is more serious than type I block
because it may progress to complete heart block
Fig (17): 2ed degree H.B. wenchebach
Management:
The underlying causes are treated prophylactic pacemaker
therapy may be indicated
• Third degree atrioventricular block (complete heart
block)
The p waves are regular (regular PP interval) with a rate
comparable to the normal heart rate for the patients age, the
QRS complexes also are regular ( but disossation between p &
QRS)
Fig (18): 3ed degree H.B.
Causes:
Congenital type: maternal systemic lupus erythematosus,
sjogren’s syndrome or structural heart disease such as congenitally
corrected transposition of the great arteries.
Acquired type:
Lyme carditis, diphtheria, myocardial infarction,
cardiomyopathies.
Significance:
•
congestive heart failure may develop in infancy
•
syncopal attacks may occur with a heart rate below 40 to 45
beat / minute
Neonates with ventricular rate <50 beats /min may developed
heart failure after birth require cardiac pacing; atropine or
epinephrine may be used arranging for pacemaker placement.
Transthoracic epicardial pacemaker implants have been
traditionally used infants, however transvenenous placement of
pacemaker leads is gaining acceptance for older infants and young
children Dual- chambered pacing is preferable to single chamber
pacing in the ventricle.
Dual – chamber pacing ensures atrioventricular syncrony,
which may be important to maximize hemodynamics in
patient with structurally abnormal hearts
WOLFF – PARKINSON WHITH SYNDROME:It results from an anomalous conduction pathway (i.e. bundle
of kent) between the atrium and the ventricle, by passing the
normal delay of conduction in the AV node. The premature
depolarization of aventricle produces adelta wave and results
in prolongation of the QRS duration Criteria for WPW
syndrome
Short PR interval
Delta wave (initial slurring of the QRS complex)
Wide QRS duration
Fig: (19) WPW
Patient with WPW syndrome are prone to attacks of
SVT, WPW syndrome mimic other ECG abnormalities
such as ventricular hypertrophy, RBBB or myocardial
disorders but large QRS deflections are often seen in
this condition.