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Arrhythmias Nightfloat Curriculum 2010-2011 LPCH Pediatric Residency Program By Jennifer Everhart, MD Learning Objectives • Recognize common pediatric cardiac arrhythmias • Recognize early signs of clinical decompensation/hemodynamic instability • Initiate management of arrhythmias in the inpatient setting, including identifying and treating reversible causes • Review PALS algorithms for bradycardia & tachycardia Bradyarrhythmias - Symptoms • General: altered LOC, fatigue, lightheadedness, dizziness, syncope • Hemodynamic instability: hypotension, poor end-organ perfusion, respiratory distress/failure, sudden collapse Bradyarrhythmias - Causes • 1º: Abnormal pacemaker/conduction system (congenital or postsurgical injury), cardiomyopathy, myocarditis • 2º: Reversible Hs & Ts: – Hypoxia – Hypotension – H+ ions (acidosis) – Heart block – Hypothermia – Hyperkalemia – Trauma (head) – Toxins/drugs (cholinesterase inhibitors, Ca++ channel blockers, βadrenergic blockers, digoxin, central α2-adrenergic agonists, opioids) Bradyarrhythmias - Types • Sinus bradycardia – Physiologic (ie: sleep, athletes) vs. pathologic (ie: abnormal lytes, infection, drugs, hypoglycemia, hypothyroidism, ↑ICP) • Sinus node block ↓Junctional beat – Subsidiary pacemakers lead to atrial, junctional, & idioventricular escape rhythms Bradyarrhythmias – AV Blocks Type EKG Findings 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 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. 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. AV dissociation. No atrial impulses are conducted to the ventricle Congenital or caused by conduction system disease or injury (ie: surgery, MI). Most symptomatic form of heart block: fatigue, presyncope, syncope. Usually requires pacemaker (especially if acquired). Mobitz type I Wenchebach 2nd Degree Mobitz type II 3rd Degree complete Causes & Clinical Significance 1st degree heart block 2nd degree heart block, Mobitz I 2nd degree heart block, Mobitz II 3rd degree heart block Bradyarrhythmias - Management • Stable patients: – 12 lead EKG, +/- labs, consult cardiology • Unstable patients: – ABCs – PALS Pediatric Bradycardia Algorithm • Address reversible causes (Hs & Ts) Tachyarrhythmias - Symptoms • General: palpitations, lightheadedness, syncope, fatigue, SOB, chest pain – Infants: poor feeding, tachypnea, irritability, sleepiness, pallor, vomiting • Hemodynamic instability: respiratory distress/failure, hypotension, poor endorgan perfusion, altered LOC, sudden collapse Tachyarrhythmias - Causes • 1º: Underlying conduction abnormalities • 2º: Reversible Hs & Ts – Hypovolemia – Toxins – Hypoxia – Tamponade (cardiac) – H+ ions (acidosis) – Tension pneumothorax – Hypoglycemia – Thrombosis (coronary, pulmonary) – Hypothermia – Trauma – Hypo/Hyperkalemia Tachyarrhythmias - Classification • Narrow complex: sinus tachycardia, supraventricular tachycardia, atrial flutter • Wide complex: ventricular tachycardia, supraventricular tachycardia with aberrant intraventricular conduction Tachyarrhythmias - Types • Sinus tachycardia – Usually <220 bpm in infants, <180 bpm in children – P waves present and normal (upgoing in I, II, AVF), narrow QRS, beat to beat variability – Response to body’s need for increased cardiac output or oxygen delivery (ie: hypoxia, hypovolemia, fever, pain, anemia) Tachyarrhythmias - Types • Supraventricular tachycardia – >220 bpm in infants, >180 bpm in children – Abrupt onset; occurs intermittently – Usually narrow QRS, absent or abnormal P waves, no beat to beat variability – Caused by accessory pathway reentry (ie: WPW), AV nodal reentry, ectopic atrial focus Tachyarrhythmias - Types • Atrial flutter – Sawtooth pattern on EKG – Atrial rate 350-400/min; ventricular rate varies • Ventricular tachycardia – Wide QRS (>0.08 sec), P waves may be unidentifiable or not related to QRS – Caused by underlying heart disease, post-heart surgery, myocarditis, cardiomyopathy, ↑QTc, ↑K+, ↓Ca++, ↓Mg++, drug toxicity Tachyarrhythmias - Types • Torsades de Pointes – Variable polarity & amplitude of QRS, appearing to rotate around the EKG isoelectric line – A type of polymorphic VT – Caused by long QT syndromes, ↓Mg++, drug toxicities (including antiarrhythmics) – Can deteriorate to ventricular fibrillation Tachyarrhythmia vs. Artifact • Differentiating arrhythmia from artifact: – Sharp spikes from QRS complexes superimposed on “arrhythmia” – Wandering baseline – Normal QRS complexes in some leads • Causes of artifact: – Simultaneous use of other equipment, muscle contractions, movement Tachyarrhythmias - Management • ABCs • If pulse → PALS tachycardia algorithms – Poor perfusion → Pediatric Tachycardia With Pulses and Poor Perfusion algorithm – Adequate perfusion → Pediatric Tachycardia With Adequate Perfusion algorithm • If no pulse → PALS Pediatric Pulseless Arrest algorithm Tachyarrhythmias - Management • In general… – Attach monitor/defibrillator, pulse ox; establish vascular access – Obtain appropriate labs (ie: blood gas, lytes) – Identify & treat any reversible causes • Torsades de Pointe or VT due to ↓Mg++ – Magnesium sulfate Tachyarrhythmias – Management • SVT with adequate perfusion – Vagal maneuvers while preparing adenosine • SVT with poor perfusion – Immediate adenosine or cardioversion • Consider vagal maneuvers if no delay – Adenosine • Rapid bolus then flush using proximal PIV or CVL • 0.1 mg/kg; max 1st dose 6 mg; additional 0.2 mg/kg if needed (max 2nd dose 12 mg) – Cardioversion (0.5-1 J/kg; sedate if possible) Case #1 • 9 year old boy admitted for asthma exacerbation, noted to have heart rate of 55. Case #2 • 3 month old girl brought to ED for poor feeding and fussiness, noted to have heart rate of 230. References • • • • • American Heart Association. 2005 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) of Pediatric and Neonatal Patients: Pediatric Advanced Life Support. Pediatrics 2006;117;e1005-1028. Fleisher GR, et al. Textbook of Pediatric Emergency Medicine 5th Edition. Lippincott Williams & Williams, 2006. Pediatric Advanced Life Support. American Heart Association, 2006. Thaler MS. The Only EKG Book You’ll Ever Need 4th Edition. Lippincott Williams & Williams, 2003. Zaoutis LB and Chiang VW. Comprehensive Pediatric Hospital Medicine. Mosby Elsevier, 2007.