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Arrhythmias Nightfloat Curriculum 2010-2011 LPCH Pediatric Residency Program By Jennifer Everhart, MD.

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Presentation on theme: "Arrhythmias Nightfloat Curriculum 2010-2011 LPCH Pediatric Residency Program By Jennifer Everhart, MD."— Presentation transcript:

1 Arrhythmias Nightfloat Curriculum 2010-2011 LPCH Pediatric Residency Program By Jennifer Everhart, MD

2 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

3 Bradyarrhythmias - Symptoms General: altered LOC, fatigue, lightheadedness, dizziness, syncope Hemodynamic instability: hypotension, poor end-organ perfusion, respiratory distress/failure, sudden collapse

4 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, β- adrenergic blockers, digoxin, central α 2 -adrenergic agonists, opioids)

5 Bradyarrhythmias - Types Sinus bradycardia –Physiologic (ie: sleep, athletes) vs. pathologic (ie: abnormal lytes, infection, drugs, hypoglycemia, hypothyroidism, ↑ICP) Sinus node block –Subsidiary pacemakers lead to atrial, junctional, & idioventricular escape rhythms ↓Junctional beat

6 Bradyarrhythmias – AV Blocks TypeEKG FindingsCauses & Clinical Significance 1 st degree Prolonged PR intervalCauses 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. 2 nd degree Mobitz type I Wenchebach 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 3 rd degree heart block. 2 nd Degree Mobitz type II 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 3 rd degree heart block; often requires pacemaker. 3 rd Degree complete 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).

7 1 st degree heart block 2 nd degree heart block, Mobitz I 2 nd degree heart block, Mobitz II 3 rd degree heart block

8 Bradyarrhythmias - Management Stable patients: –12 lead EKG, +/- labs, consult cardiology Unstable patients: –ABCs –PALS Pediatric Bradycardia Algorithm Address reversible causes (Hs & Ts)


10 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 end- organ perfusion, altered LOC, sudden collapse

11 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

12 Tachyarrhythmias - Classification Narrow complex: sinus tachycardia, supraventricular tachycardia, atrial flutter Wide complex: ventricular tachycardia, supraventricular tachycardia with aberrant intraventricular conduction

13 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)

14 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

15 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

16 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

17 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

18 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

19 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

20 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 1 st dose 6 mg; additional 0.2 mg/kg if needed (max 2 nd dose 12 mg) –Cardioversion (0.5-1 J/kg; sedate if possible)




24 Case #1 9 year old boy admitted for asthma exacerbation, noted to have heart rate of 55.

25 Case #2 3 month old girl brought to ED for poor feeding and fussiness, noted to have heart rate of 230.

26 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 5 th Edition. Lippincott Williams & Williams, 2006. Pediatric Advanced Life Support. American Heart Association, 2006. Thaler MS. The Only EKG Book You’ll Ever Need 4 th Edition. Lippincott Williams & Williams, 2003. Zaoutis LB and Chiang VW. Comprehensive Pediatric Hospital Medicine. Mosby Elsevier, 2007.

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