Download Paediatric Emergency cardiology

Gavin Burgess R5, PEM
PAEDIATRIC EMERGENCY
CARDIOLOGY
General
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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
“Normal”
Age
Respiratory rate
Pulse rate
Systolic BP
O-1mo
30-60
120-160
50-70
1-12mo
20-40
80-140
70-100
1-5y
20-30
80-130
80-110
6-12y
20-30
70-110
80-120
adolescents
12-20
60-100
110-120
“Normal”
 Ball-park BP?
 Neonate?
 Older?
“Normal”
 Gestational age should equal MAP
 Systolic BP = 70 + (2 x age)
“Normal” ECG
 Typically have shorter PR, QRS, QT
 RV dominance, RAD
RVH
 Causes
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Tetralogy of Fallot
PS
Coarct
ASD
TAPVD
Large VSD with Pulm HT
LVH
 Causes
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AS
VSD
PDA
Complete AV block
Cardiomyopathy
Diagnosis?
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
Myocardial infarction
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AT III
Cardiomyopathy
Congenital heart disease
CAD (ALCAPA)
Drugs (cocaine)
Homocystinuria
Hyperlipidaemia and cholesterolaemia
Kawasaki
Leukaemia
Marfans
Haemoglobinopathies
Tumours (myxoma)
Rheumatic fever
SLE
Diagnosis?
Diagnosis?
Diagnosis?
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
Pulmonary markings
 Decreased:
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Pulmonary atresia/stenosis
Tetralogy
Tricuspid atresia
Ebstein’s anomaly
 Increased:
 TGA
 TAPVD
 Truncus
What’s the hyperoxia test?
 ABG
 Give 100% O2
 Repeat ABG after 10 min
 If rises by >10%, likely pulmonary lesion
When does the ductus close?
 10-14 days after birth, it is physiologically
closed
Neonatal and infant
presentations to ED
 What are the 4 presentations in and infants
neonates?
 1) shock
 2) cyanosis
 3) cardiac failure
 4) murmur
What are the ductaldependent lesions?
 Systemic
 Coarct/interrupted arch
 Aortic stenosis
 HLH
 Pulmonary
 PS/atresia
 Tricuspid atresia
Shock
 L ventricular outflow obstruction
 Coarct
 AS
 HLH
Shock
 Management:
 ABC’s
 Start prostin
 CXR
 ECG
What’s prostin?
 Prostaglandin E1
 Rate 0.05-0.2 mcg/kg/min
 Side effects?
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Apnoea
Fever
Flushing
Hypotension
 Prostin has an “all or nothing” action
 Should work in 15min
Time to presentation of
cyanotic lesions
Age
ECG
X-ray
0-1 week
TGA
RVH
Increased
1st week
TAPVD
RVH
Increased
1-4weeks
Tricuspid Atresia
LVH
Decreased
Severe PS
RVH
Decreased
1-12weeks
TOF
RVH
Decreased
Anytime in
infancy
Truncus arteriosus BVH
Increased
Cyanosis
 What is a tetralogy of Fallot?
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RVH
Overriding aorta
VSD
RV outflow obstruction
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
How do I treat it?
 O2
 Chest-knee (why?)
 Analgesia
 B-blocker (why?)
Cardiac failure
 History:
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Fussy
Sweating
FTT
Short frequent meals
 Physical:
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HSM
Murmur
FTT
You will NOT see a JVP
AVM – auscultate the head
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
Common innocent murmurs
Type
Description
Age
Still’s
LLSB, 2/6, “twang”
3-6y
Pulmonary flow
ULSB, blowing, transmits Gone in 3-6mo
Venous hum
Supra clavicular, rotate
head, supine goes
3-6y
Carotid bruit
Over carotid
Any age
Arrhythmia
 SVT
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Very common
Tolerated well, occasional LOC change
Child is fussy
Newborn >220 bpm
<12y often accessory pathway
Arrhythmia
 SVT treatment
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In shock vs stable
Vagal stim
Adenosine
Amiodarone ,verapamil use extreme caution.
Frequently develop profound hypotension and die
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
Arrhythmia
 All first degree family members should be
screened with ECG
HOCM
 2% under 2 y, 7% under 10y
 Variable history
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CP
Palpitations
SOB
Syncope
Sudden death
High risk if syncope
Sudden death with strenuous exercise
HOCM
 Physical
 S4 gallop, mid systolic murmur
 Increased PVR decreases murmurs
Rheumatic fever
 Who was Jones?
 What where his criteria?
 What do you need to make a diagnosis?
 Which valve?
 Then?
Rheumatic fever
 What about Sydenham’s chorea?
 And the rash?
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
Myocarditis
 Various causes, most notably viral
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Coxsackie A,B, ECHO, flu’
Non-specific viral prodrome
Non-specifc fussiness, lethargy etc
Heart failure
IVIG may be indicated
Infective endocarditis
 Rheumatic fever, congenital heart defects,
catheters, IVD
 S. aureus, viridans are the usual suspects
 Fungi in neonates, usually in the NICU
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
Infective endocarditis
 Minor
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Fever (38C)
Predisposing condition/IVD
Vascular phenomena
Non-specific echo findings
Prophylaxis -1997
 High risk – amp and gent
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Prosthesis
Previous IE
Complex CHD
Surgical systemic-pulmonary shunts
 Medium risk - amp
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Other congenital heart malformation
Acquired valve dysfunction
HOCM
MVP
 Negligible risk – no Rx
 Isolated secundum; repaired ASD, VSD, PDA; bypass graft;
MVP (no regurge); “innocent” murmurs; KD with normal
valves; RF with no valve dysfunction; pacemakers
Prophylaxis
 High risk
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Prosthesis
Previous IE
Transplants
Complex CHD
 Dropped from the list…….
 Moderate risk
(PDA,VSD,primumASD,coarct,bicuspidAV)
 Calcified AS,RF,HOCM,MVP
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
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
Kawasaki disease
 3 phases
 Acute phase (10 days)
 High fever for 5 days
 4 of
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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
Kawasaki disease
 Acute
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ESR, CRP
WCC, plt
Lipids, LFTs
Echo coronary artery aneurysms unusual before 10d
 Subacute phase
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Desquamation
Coronary disease
Rash, fever, LN disappear
plt
Kawasaki disease
 Convalescent phase
 ESR, plt normalise
 Beau’s lines
Kawasaki disease
 Rx
 IVIG
 ASA
 Vaccinations
 Steroid of no benefit
 Reduces CAD from 25% to 5%
 Untreated mortality 1-5%