Arrhythmia in Pediatric

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Arrhythmia in Pediatric

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• 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.

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• 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 patients age

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Fig (1) Normal sinus rhythm
Fig (1) Normal sinus rhythm
Fig (1) Normal sinus rhythm
Fig (1) Normal sinus rhythm
Fig (1) Normal sinus rhythm

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• 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

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• Sinus Tachycardia-
• Causes of it anxiety, fever, hypovolemia or
  circulatory shock, anemia, CHF, administration of
  catecholamines, thyrotoxicosis myocardial
  disease.
• Fig (3) Sinus tachycardia

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• Sinus Bradycardia-
• Causes of it may occur in normal individuals and
  trained athletes, hypothyroidism, hypothermia
  hypoxia, hyperkalermia, administration of drugs
  such as B- adrenergic blockers.
•  
•  Fig (4) Sinus bradycardia

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• Sinus Pause -
• Sinus node pace maker momentarily dropped beat
  relaitvely for short time, causes of it hypoxia,
  increased vagal tone diagitalis toxicity
• Fig (5)

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• 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 lt2 sinus cycls) due to resetting of the SAN
  by premature impulse, its axis as that of sinus
  beats.

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• 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.

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• 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.

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• Fig (7) Junctional escape rhythm
• Pacemakers of all beats are atrial

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• 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.

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• 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.

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• 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 pre-excitation syndrome (like WPW
  syndrom). Heart Disease, more commonly with
  Ebstien anormaly of the tricuspid valve and
  corrected transposition of the great vessels.

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• Fig (8) SVT

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• Fig (9) SVT wide QRS

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• Fig (10) SVT Junctional No visible P wave

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• 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.

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• 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.

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• Mulitfocal atrial tachycardia
• Is characterized by two or more ectopic P waves
  with two or more different ectopic P-Pcycled,
  frequent blocked P- waves, 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

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• 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

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• 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.

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• 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

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• 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.

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• 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

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• 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.

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• 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.

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• Fig (15) VT

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• 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.

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• Fig (16) VF

Atrioventricular block
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• 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, Ebsteins 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 p-Rinterval 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

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• 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 31, 41, 51 of variable
  block.
• Significance of Mobitz type II is more serious
  than type I block because it may progress to
  complete heart block

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Fig (17) 2ed degree H.B. wenchebach
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• 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)

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• Fig (18) 3ed degree H.B.

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• Causes
• Congenital type maternal systemic lupus
  erythematosus, sjogrens 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 lt50 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.

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• 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

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• 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.