paediatric emergency cardiology
DESCRIPTION
Gavin Burgess R5, PEM. Paediatric Emergency cardiology. General. Review common presentations Uncommon Paediatric ECG Congenital heart disease Rhythm disturbances Long QT HOCM Rheumatic fever Carditis – myo, endo, peri. General. Innocent murmurs Kawasaki disease. Fetal circulation. - PowerPoint PPT PresentationTRANSCRIPT
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Gavin Burgess R5, PEM
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General
Review common presentations Uncommon Paediatric ECG Congenital heart disease Rhythm disturbances Long QT HOCM Rheumatic fever Carditis – myo, endo, peri
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General
Innocent murmurs Kawasaki disease
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Fetal circulation
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“Normal”
Age Respiratory rate
Pulse rate Systolic BP
O-1mo 30-60 120-160 50-701-12mo 20-40 80-140 70-1001-5y 20-30 80-130 80-1106-12y 20-30 70-110 80-120adolescents 12-20 60-100 110-120
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“Normal”
Ball-park BP? Neonate? Older?
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“Normal”
Gestational age should equal MAP Systolic BP = 70 + (2 x age)
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“Normal” ECG
Typically have shorter PR, QRS, QT RV dominance, RAD
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RVH
Causes Tetralogy of Fallot PS Coarct ASD TAPVD Large VSD with Pulm HT
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LVH
Causes AS VSD PDA Complete AV block Cardiomyopathy
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Diagnosis?
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Superior or “north west” axis Endocardial cushion defect
2% of congenital heart disease Down syndrome account for 70% Fatal due to pulm HT Banding in infancy
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Myocardial infarction
AT III Cardiomyopathy Congenital heart disease CAD (ALCAPA) Drugs (cocaine) Homocystinuria Hyperlipidaemia and cholesterolaemia Kawasaki Leukaemia Marfans Haemoglobinopathies Tumours (myxoma) Rheumatic fever SLE
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Diagnosis?
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Diagnosis?
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Diagnosis?
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Which lesions give cyanosis? Tetralogy of Fallot Tricuspid atresia Transposition of the great arteries (IDM) Truncus arteriosus Total anomalous pulmonary venous
drainage Hypoplastic left heart Ebstein’s anomaly (lithium) Pulmonary atresia/severe stenosis
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Pulmonary markings
Decreased: Pulmonary atresia/stenosis Tetralogy Tricuspid atresia Ebstein’s anomaly
Increased: TGA TAPVD Truncus
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What’s the hyperoxia test? ABG Give 100% O2 Repeat ABG after 10 min If rises by >10%, likely pulmonary
lesion
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When does the ductus close? 10-14 days after birth, it is
physiologically closed
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Neonatal and infant presentations to ED What are the 4 presentations in and
infants neonates? 1) shock 2) cyanosis 3) cardiac failure 4) murmur
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What are the ductal-dependent lesions? Systemic
Coarct/interrupted arch Aortic stenosis HLH
Pulmonary PS/atresia Tricuspid atresia
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Shock
L ventricular outflow obstruction Coarct AS HLH
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Shock
Management: ABC’s Start prostin CXR ECG
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What’s prostin?
Prostaglandin E1 Rate 0.05-0.2 mcg/kg/min Side effects?
Apnoea Fever Flushing Hypotension
Prostin has an “all or nothing” action Should work in 15min
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Time to presentation of cyanotic lesions
Age ECG X-ray0-1 week TGA RVH Increased1st week TAPVD RVH Increased1-4weeks Tricuspid
AtresiaLVH Decreased
Severe PS RVH Decreased1-12weeks TOF RVH DecreasedAnytime in infancy
Truncus arteriosus
BVH Increased
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Cyanosis
What is a tetralogy of Fallot? RVH Overriding aorta VSD RV outflow obstruction
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What’s a “tet spell”?
Change in the balance of pulmonary and systemic flow
Hypoxic and cyanotic event Decreased system vascular
resistance or increased RV outflow obstruction
Increasing hypoxia
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How do I treat it?
O2 Chest-knee (why?) Analgesia B-blocker (why?)
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Cardiac failure
History: Fussy Sweating FTT Short frequent meals
Physical: HSM Murmur FTT You will NOT see a JVP AVM – auscultate the head
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Murmurs
Features of an innocent murmur 80% of children will have a murmur at
some time in their lives All have normal ECG and X-rays Never diastolic
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Common innocent murmurs
Type Description AgeStill’s LLSB, 2/6, “twang” 3-6yPulmonary flow ULSB, blowing,
transmitsGone in 3-6mo
Venous hum Supra clavicular, rotate head, supine goes
3-6y
Carotid bruit Over carotid Any age
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Arrhythmia
SVT Very common Tolerated well, occasional LOC change Child is fussy Newborn >220 bpm <12y often accessory pathway
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Arrhythmia
SVT treatment In shock vs stable Vagal stim Adenosine Amiodarone ,verapamil use extreme
caution. Frequently develop profound hypotension and die
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Arrhythmia Long QT
History Deafness Single person MVC Swimming syncope Exercise syncope Family history of sudden death Seizure of unknown etiology Recurrent syncope/lightheadedness Sibling with SIDS
Physical Infant with bradycardia
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Arrhythmia
All first degree family members should be screened with ECG
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HOCM
2% under 2 y, 7% under 10y Variable history
CP Palpitations SOB Syncope Sudden death High risk if syncope Sudden death with strenuous exercise
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HOCM
Physical S4 gallop, mid systolic murmur Increased PVR decreases murmurs
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Rheumatic fever
Who was Jones? What where his criteria? What do you need to make a
diagnosis? Which valve? Then?
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Rheumatic fever
What about Sydenham’s chorea? And the rash?
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Rheumatic fever
Treatment ASA 75-100mg/kg Prednisone 1-2mg/kg Benzathine (Pen G) 600 000U (27kg), 1.2
million U (27kg) Prophylaxis Age questioned
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Myocarditis
Various causes, most notably viral Coxsackie A,B, ECHO, flu’ Non-specific viral prodrome Non-specifc fussiness, lethargy etc Heart failure IVIG may be indicated
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Infective endocarditis
Rheumatic fever, congenital heart defects, catheters, IVD
S. aureus, viridans are the usual suspects
Fungi in neonates, usually in the NICU
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Infective endocarditis
Major 2 + BC, (viridans, s. bovis, HACEK, S. aureus,
enterococci Persistently + BC (1 hr between multiple, or
12h or 3h +) + echo mass at typical sites Intracardiac abscess Prosthesis failure New regurgitant murmur
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Infective endocarditis
Minor Fever (38C) Predisposing condition/IVD Vascular phenomena Non-specific echo findings
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Prophylaxis -1997
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Prophylaxis
High risk Prosthesis Previous IE Transplants Complex CHD
Dropped from the list……. Moderate risk
(PDA,VSD,primumASD,coarct,bicuspidAV) Calcified AS,RF,HOCM,MVP
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Pericarditis
Classic chest pain worse when lying flat
Radiation to L shoulder Friction rub Most often viral causes Diffuse ST changes, “saddle”shaped CXR important Cefotaxime, ASA, prednisone,
colchicine
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Kawasaki disease
Etiology unkown, presumed infectious
More common in Asian and Pacific islanders
Peaks around 1-2years, 80% under 4y, 50% under 2y
Slight male preponderance 3mo-8y is typical range
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Kawasaki disease
3 phases Acute phase (10 days)
High fever for 5 days 4 of
rash (ANY rash, no bullae/vesicles), oedema of extremities/ peeling of extremities Non-exudative bulbar conjuctivitis Mucosal changes (cracked lips, strawberry
tongue – even on HISTORY) Cervical LN (1.5cm)
Carditis, other organs (arthritis, pyuria, gallbladder/liver, menigitis, irritable
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Kawasaki disease
Acute ESR, CRP WCC, plt Lipids, LFTs Echo coronary artery aneurysms unusual
before 10d Subacute phase
Desquamation Coronary disease Rash, fever, LN disappear plt
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Kawasaki disease
Convalescent phase ESR, plt normalise Beau’s lines
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Kawasaki disease
Rx IVIG ASA Vaccinations Steroid of no benefit Reduces CAD from 25% to 5% Untreated mortality 1-5%