Arrhythmia in Pediatric

1. Arrhythmia in Pediatric الدكتورمازن هاشم خالدطبيب اختصاص أطفالبورد عربي في طب الأطفالدبلوم عالي في طب وصحة الطفلمتدرب على فحص ومعالجة قلب الأطفال

2. 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.

3. 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

4. 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

5. 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

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

7. 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

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

9. 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.

10. 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.

11. 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.

12. Fig (7): Junctional escape rhythm Pacemakers of all beats are atrial

13. 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.

14. 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.

15. 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.

16. Fig (8): SVT

17. Fig (9): SVT + wide QRS

18. Fig (10): SVT Junctional No visible P wave

19. 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.

20. 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.

21. 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

22. 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

23. 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.

24. 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

25. 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.

26. 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

27. 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.

28. 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.

29. Fig (15): VT

30. 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.

31. Fig (16): VF Atrioventricular block

32. 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 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

33. 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

34. Fig (17): 2ed degree H.B. wenchebach

35. 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)

36. Fig (18): 3ed degree H.B.

37. 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.

38. 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

39. 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.