Arrhythmiaspowerpoin..

Report
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.

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