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Dr. Talaat Ali Sabeeh Al-Jarrah Pediatric Cardiologist Cardiac Arrhythmias The normal heart rate varies with age. The younger the child, the faster the HR.Therefore, definitions of bradycardia (<60 bpm) and tachycardia (>100 bpm) used for adults do not apply to infants and children. Tachycardia is HR beyond the upper limit of normal for the pt age, and bradycardia is HR slower than the lower limit of normal. I-Rhythms Originating in the Sinus Node A- Regular Sinus Rhythm is regular, and the rate is normal for age. The characteristic of sinus rhythm described previously are present .This rhythm is normal at any age B-Sinus Tachycardia HR is faster than the upper limit of normal for age. A rate greater than 140 bpm in children and greater than 170 bpm in infants may be significant. The heart rate is usually less than 200 bpm in sinus tachycardia. Causes:Anxiety, fever, hypovolemia or circulatory shock, anemia, congestive heart failure (CHF), administration of catecholamines, thyrotoxicosis, and myocardial disease Management:underlying cause. C-Sinus Bradycardia:HR is slower than the lower limit of normal for the age.A rate slower than 80 bpm in newborn infants and slower than 60 bpm in older children may significant . Causes: normal individuals and trained athletes. It may occur with vagal stimulation, increased intracranial pressure, hypothyroidism, hypothermia, hypoxia, hyperkalemia, and administration of drugs such as digitalis and β-adrenergic blockers. Significance:In some patients, marked bradycardia may not maintain normal cardiac output. Management: The underlying cause is treated. D-Sinus Arrhythmiais a phasic variation in the heart rate, increasing during inspiration and decreasing during expiration. This occurs with maintenance of characteristics of sinus rhythm Causes is a normal phenomenon and is due to phasic variation in the firing rate of cardiac autonomic nerves with the phases of respiration. Significance: it is a normal finding in children. Management:No treatment is indicated II-Rhythms Originating in the Atrium Rhythms that originate in the atrium (ectopic atrial rhythm) are characterized by : 1-P waves have an unusual contour, caused by an abnormal P axis, and/or there is an abnormal number of P waves per QRS complex. 2-QRS complexes are usually of normal configuration, but occasional bizarre QRS complexes caused by aberrancy may occur . A-Atrial Flutter Description The ectopic focus, and “circus movement” in the atrium is the mechanism of this arrhythmia. Atrial flutter is characterized by an atrial rate (F wave with “sawtooth” configuration) of about 300 (range 240 to 360) bpm, a ventricular response with varying degrees of block (e.g., 2:1, 3:1, 4:1), and normal QRS complexe. Causes: usually suggests a significant cardiac pathology, although fetuses,neonates with AFL frequently have a normal heart. Structural heart disease with dilated atria, acute infectious illness, myocarditis or pericarditis, previous surgery involving atria ( Senning procedure, Fontan operation, or ASD repair), digitalis toxicity,and thyrotoxicosis are possible causes. Significance:The ventricular rate determines eventual COP; a too-rapid ventricular rate may decrease COP. Thrombus formation may lead to embolic events. Uncontrolled flutter may precipitate heart failure. The flutter may associated with syncope, presyncope, or chest pain. Management: divided into acute conversion, chronic suppression of the arrhythmia, control of ventricular rate, prevention of recurrences, and refractory cases. 1-Acute situation: a)Adenosine does not convert the arrhythmia to sinus rhythm. b)Immediate synchronized DC cardioversion is the treatment of choice for A FL of short duration, if the infant or child is in severe CHF. c)Temporary transvenous or transesophageal pacing may be used d)In children, IV amiodarone (class III) or IV procainamide (class IA) 2-For chronic cases: For long-standing AFL or fibrillation (of 24 to 48 hours) or those with unknown duration, thrombus formation, so TTE &Anticoagulation with warfarin is started and cardioversion delayed for 2 to 3 weeks. After conversion to sinus rhythm, anticoagulation is continued for an additional 3 to 4 weeks. 3-For rate control: For control of ventricular rate, calcium channel blockers appear to be the drug of choice. Propranolol equally effective. 4-For prevention of recurrences: Class I and class III antiarrhythmic drug or Amiodarone . 5-For refractory cases: Antitachycardia pacing or radiofrequency ablation may be indicated. B-Atrial Fibrillation less common than A Fl in children. The mechanism is circus movement, is characterized by an extremely fast atri al rate (f wave at a rate of 350 to 600 bpm and an irregularly irregular ventricular response with normal QRS complexes .Causes: usually associated with structural heart diseases with dilated atria( rheumatic heart disease, Ebstein's anomaly, tricuspid atresia, atrial septal defect, AV valve regurgitation, or previous intra-atrial surgery). Thyrotoxicosis, pulmonary emboli, and pericarditis should be suspected in a previously normal child who develops atrial fibrillation.Management: is similar to atrial flutter C-Supraventricular Tachycardia HR is extremely rapid and regular (usually 240 ± 40 bpm). The P wave is usually invisible.The QRS duration is usually normal, but occasionally, aberrancy increases the QRS duration, making differentiation from ventricular tachycardia difficult .the most common tachyarrhythmia seen in the pediatric age group.Patients with accessory pathways frequently have WPW preexcitation Causes 1)No heart disease is found in about half of patients. This idiopathic type of SVT occurs more commonly in young infants than in older children.2)WPW preexcitation is present in 10% to 20% of cases, which is evident only after conversion to sinus rhythm.3)Some CHD (e.g., Ebstein's anomaly, single ventricle, congenitally corrected TGA) are more susceptible.4)may occur following cardiac surgeries Significance: If SVT is sustained for 6 to 12 hours, signs of CHF usually happened. Older children :chest pain, palpitation, shortness of breath, lightheadedness, and fatigue. Management 1)Vagal stimulatory maneuvers (unilateral carotid sinus massage, gagging, pressure on an eyeball), effective in older children rarely effective in infants. ice-water bag on the face (for up to 10 seconds) is often effective in infants (by diving reflex). 2)Adenosine is considered the drug of choice. 3)If the infant is in severe CHF, emergency treatment is immediate cardioversion. The initial dose of 0.5 joule/kg is increased in steps up to 2 joule/kg. 4)Esmolol, other β-adrenergic blockers, verapamil, and digoxin have also been used with some success. 5)For postoperative SVT(which requires rapid conversion), IV amiodarone 6)Overdrive suppression (by transesophageal pacing or by atrial pacing) may be effective in children who have been digitalized. 7)Radiofrequency catheter ablation or surgical interruption of accessory pathways Prevention of Recurrence of SVT 1-In infants without WPW, oral propranolol for 12 months is effective. Verapamil can used causiousioly in patients with poor LV function and in young infants. 2-In infants in CHF and ECG evidence of WPW, start with digoxin (just to treat CHF),switched to propranolol when the infant's heart failure improves. III-Rhythms Originating in the Atrioventricular Node Rhythms that originate in the AV node are characterized by :1) P wave may be absent, or inverted P waves may follow the QRS complex.2) QRS complex is usually normal . A-NODAL PREMATURE BEATS. B-NODAL ESCAPE BEATS. C-NODAL OR JUNCTIONAL RHYTHM D-NODAL TACHYCARDIA (JUNCTIONAL ECTOPIC TACHYCARDIA). DescriptionIf the SA node consistently fails, the AV node may function as the main pacemaker of the heart, producing a relatively slow rate (40 to 60 bpm). characterized by no P waves or inverted P waves after QRS complexes and normal QRS complexes with a rate of 40 to 60 bpm. IV-Rhythms Originating in the Ventricle Rhythms that originate in the ventricle (ventricular arrhythmias) are characterized by the following:1)Bizarre and wide QRS complexes.2)waves pointing in directions opposite to QRS complexes.3)QRS complexes randomly related to P waves, if visible. B-Ventricular Tachycardia 1)VT is a series of three or more PVCs with HR of 120 to 200 bpm. QRS complexes are wide and bizarre, with T waves pointing in opposite directions. 2)The onset may be paroxysmal (sudden) or nonparoxysmal.. Causes 1)VT may occur in patients with structural heart diseases such as tetralogy of Fallot (TOF), aortic stenosis (AS), hypertrophic or DCM or MVP. 2)Postoperative CHDs (such as TOF, TGA, or double-outlet right ventricle). 3)Myocarditis, pulmonary hypertension, arrhythmogenic RV dysplasia , Brugada syndrome Chagas' disease (trypanosomiasis, in South America), myocardial tumors, myocardial ischemia, and infarction are other possible causes of VT. 4)Metabolic causes include hypoxia, acidosis, hyperkalemia, hypokalemia, and hypomagnesemia. 5)Mechanical irritation-intraventricular catheter. 6)Pharmacologic or chemical causes include catecholamine infusion, digitalis toxicity, cocaine, and organophosphate insecticides. Most antiarrhythmic drugs (especially classes IA, IC, and III) are also proarrhythmic. 7)VT may occur in healthy children who have a structurally& functionally normal heart. Significance: 1)VT may signify a serious myocardial dysfunction 2)sudden cardiac death. 3)the rhythm may deteriorate to ventricular fibrillation. Management 1-Synchronized DC cardioversion. 2)Rarely, if the patient is conscious, an IV bolus of lidocaine followed by an IV drip of lidocaine . 3)Treatment of reversible of VT (e.g., hypokalemia, hypoxemia) 4)IV amiodarone is used in patients with drug-refractory VT, 5)Virtually all classes of AAD including all class I and III drugs, with varying levels of success. 6)IV injection of magnesium sulfate is reportedly effective and safe treatment for torsades de pointes in adults (2 g in an IV bolus). 7)Recurrence may be prevented with administration of propranolol, atenolol, phenytoin sodium, or quinidine . 8)Patients with long QT syndrome are treated with β-blockers, which alleviate symptoms in 75% to 80%. 9)Some incessant VTs need surgical or radiofrequency ablation. 10)ICD has become the established standard treatment C-Ventricular Fibrillation is rare in the pediatric population. QRS bizarre ,of varying sizes and configurations. The rate is rapid and irregular,VF due to multiple reentrant circuits make portions of the myocardium are depolarizing constantly. Causes All the causes listed for VT can cause ventricular fibrillation Significance: It is usually a degeneration of VT and is terminal arrhythmia because it results in ineffective circulation. Immediate resuscitation must be provided. Management 1-Acute care: a)Immediate cardiac and pulmonary resuscitation (CPR), b)Defibrillation with 2 joule/kg. c)Administration of epinephrine by the IV or intraosseous (IO) d)One should identify and treat causes, including metabolic environment (hypoxia, acidosis). e)One of the following antiarrhythmic agents may be used: Amiodarone,Lidocaine ,Magnesium sulfate for torsades de pointes or hypomagnesemia 2-A child with susceptibility to ventricular fibrillation and those resuscitated from the arrhythmia should have a comprehensive pediatric electrophysiology evaluation. 3-ICDs are often indicated in patients who survived ventricular fibrillation.. V-Long QT Syndrome is a disorder of myocardial repolarization characterized by a prolonged QT interval on the ECG and ventricular arrhythmias, usually torsades de pointes, that may result in sudden death. Patients with LQTS may present with complaints of syncope, seizures, or palpitation during exercise or with emotion. The first manifestation may be cardiac arrest.The QT prolongation may be congenital or acquired. 1- Congenital LQTS is caused by mutations of cardiac ion channel genes.Romano-Ward syndrome(AD,NO DEAFNESS)& Jervell- Lange-Nielsen syndrome(AR, DEAFNESS) are identified. 2-Acquired prolongation of the QT interval can be caused by a number of drugs, electrolyte disturbances, and other underlying medical conditions . Clinical Manifestations1)The family history is positive in 60% of patients, and deafness in 5% . 2)Presenting symptoms: syncope (26%), seizure (10%), cardiac arrest (9%), presyncope, or palpitation (6%). Ppt factor occur during exercise or with emotion. Diagnosis A)The ECG shows :1) prolonged QT interval with a QTc usually greater than 0.46 second the upper limit of normal is 0.44 second. 2)Abnormal T-wave morphology (bifid, diphasic, or notched) is frequent.B)Holter monitoring :QTc interval on Holter monitor may be longer than standard ECG .C)family history. D) exercise testing,(TMT). E) electrophysiology study, F)Genetic testing identify genotypes of the LQTS. Although it is not widely available. MANAGEMENT A)Treat risk factors for sudden death:1)Bradycardia for age 2) extremely long QTc interval (>0.55 second),3)Symptoms at presentation (syncope, seizure, cardiac arrest),4)Young age at presentation (<1 month), and 5)Documented torsades de pointes or ventricular fibrillation. B)General measures:Avoid:1) medications that prolong the QT interval 2) Catecholamines and sympathomimetic drugs should be avoided because trigger torsades de pointes 3)competitive sports policy applies.4)poor compliant with their medications. C)Treatment of Congenital LQTS: aimed at1) interrupting sympathetic input to the myocardium with β-blockers. 2)cardiac pacemaker & ICD.3)Surgical approach to interrupting sympathetic input to the heart (through left cardiac sympathetic denervation surgery) is no longer frequently used.4)Targeted pharmacologic therapy(sodium channel blocker- e.g mexiletine-,or Potassium supplementation might improve repolarization abnormalities or Gene therapy). PROGNOSIS very poor in untreated patients, with annual mortality as high as 20% and 10-year mortality of 50%. β-Blockers may reduce mortality to some extent, but they do not completely protect patients from sudden death. The ICD appears promising in improving prognosis. VI-Disturbances of Atrioventricular Conduction disturbance in conduction between normal sinus impulse& eventual ventricular response. A-First-Degree Atrioventricular Block Description:PR interval is prolonged beyond the upper limits of normal for the patient's age and HR . Causes:1)healthy children and young adults, particularly in athletes.2)congenital heart diseases (such as endocardial cushion defect, atrial septal defect, Ebstein's anomaly),3) infectious disease, 4)inflammatory conditions (rheumatic fever),5) cardiac surgery,6)certain drugs (such as digitalis, calcium channel blockers). Significance:does not produce HDD. It sometimes progresses to a more AV block.Management:No treatment is indicated, except when the block is caused by digitalis toxicity B-Second Degree Atrioventricular Block Some, but not all, P waves are followed by a QRS (dropped beats. 1-MOBITZ TYPE I:PR interval progressively prolonged until one QRS complex is dropped completely .Causes 1)otherwise healthy children. Other causes include 2)myocarditis, cardiomyopathy,3) myocardial infarction,4) congenital heart defect, 5)cardiac surgery, and6) digitalis toxicity.SignificanceIt usually does not progress to complete heart block. It occurs in individuals with vagal dominance. Management The underlying causes are treated 2-MOBITZ TYPE II DescriptionThe AV conduction is “all or none” .i.e it is either normal or completely blocked Causes: are the same as for Mobitz type I. SignificanceThe block is at the level of the bundle of His. It is more serious than type I block because it may progress to complete heart block, resulting in Stokes-Adams attack. Management: treat underlying causes. Prophylactic pacemaker therapy may be indicated C- Third-Degree Atrioventricular Block CHB: atrial & ventricular activities are entirely independent of each other 1)In congenital complete heart block,a) duration of the QRS complex is normal because the pacemaker for the ventricular complex is at a level higher than the bifurcation of the bundle of His. b)The ventricular rate is faster (50 to 80 bpm) than that in the acquired type, and c) the ventricular rate is somewhat variable in response to varying physiologic conditions. 2)In surgically induced or acquired complete heart block,a) the QRS duration is prolonged because the pacemaker for the ventricular complex is at a level below the bifurcation of the bundle of His ,B)The ventricular rate is in the range of 40 to 50 bpm (idioventricular rhythm) and c)the ventricular rate is relatively fixed. Causes: Congenital Type :TGA, or maternal SLE, Sjögren's syndrome, or other connective tissue disease. Acquired Type: 1)Cardiac surgery most common . Other rare causes include 2) severe myocarditis.3) Lyme carditis, 4)acute rheumatic fever,5) mumps,6) diphtheria,7) cardiomyopathies, 8)tumors in the conduction system,9) overdoses of certain drugs, and 10) myocardial infarction. These causes produce either temporary or permanent heart block. Significance:1)Congestive heart failure, may develop in infancy, particularly when there are associated congenital heart defects. 2)Patients with isolated congenital heart block who survive infancy are usually asymptomatic and achieve normal growth and development for 5 to 10 years. Chest x-ray films may show cardiomegaly. 3)Syncopal attacks (Stokes-Adams attacks) may occur with a heart rate below 40 to 45 bpm. A sudden onset of acquired heart block may result in death unless treatment maintains the heart rate in the acceptable range. Management 1)Atropine or isoproterenol is indicated in symptomatic children 2)A temporary transvenous ventricular pacemaker is indicated 3)No treatment is required for children with asymptomatic congenital complete heart block with acceptable rate, narrow QRS complex, and normal ventricular function. 4)Pacemaker therapy is indicated in patients with congenital heart block: a)If the patient is symptomatic or develops CHF. Dizziness or lightheadedness may be an early warning sign of the need for a pacemaker. b)If an infant has a ventricular rate less than 50 to 55 bpm or if the infant has a congenital heart defect with a ventricular rate less than 70 bpm. c)If the patient has a wide QRS escape rhythm, complex ventricular ectopy, or ventricular dysfunction. d)A permanent artificial ventricular pacemaker is indicated in patients with surgically induced heart block that is not expected to resolve or persists at least 7 days post surgery. VII- Cardiac Pacemakers and Implantable CardioverterDefibrillators in Children A pacemaker is a device that delivers battery-supplied electrical stimuli over leads to electrodes that are in contact with the heart. It primarily treats bradycardia. An implantable cardioverter-defibrillator (ICD) is a multiprogrammable antiarrhythmic device for treating ventricular tachycardia and ventricular fibrillation. The ICD also possesses pacemaking capability to treat bradycardia. The electrical leads are either placed directly over the epicardium or inserted transvenously into the cardiac chambers. Electronic circuitry regulates the timing and characteristics of the stimuli. The power source is usually a lithiumiodine batter.