Download General Pediatric Board Review Pediatric Cardiology

Daniela Rafii, M.D.
Associate Director, Pediatric Cardiology
Maimonides Infants and Children’s
Hospital of Brooklyn


Over 50% of children have an innocent heart
murmur  no intervention, require reassurance
Most common innocent heart murmurs:

Still’s murmur AKA function heart:
 Musical/twangy/vibratory systolic ejection murmur
 Louder while supine
 Usually located over the LLSB

Venous hum:
 Continuous murmur
 Softer/resolve while supine or w/ pressure to jugular vein
or w/ turning the head
 Usually RUSB or LUSB

AS 
Harsh crescendo-decrescendo
SEM
 RUSB
 Radiates to the neck


PS 
Harsh crescendo-decrescendo
SEM
 LUSB
 Radiates to the back



PDA  continuous
machinery murmur
Diastolic murmurs are
never innocent
an
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es
C.
Re
B.
Reassure the parents
about the benign
prognosis
Request a cardiology
consult
Order a chest X ray
Request a transthoracic
echocardiogram
Request an EKG
Re
as
su
re
A.

Acyanotic (pink) CHD 

ASD (left to right shunt)

VSD (left to right shunt)

PDA (left to right shunt)

AS

PS

Coarc

Acyanotic CHD

3 types

Primum

Secundum (most common)

Sinus Venosus

Asymptomatic in childhood

SEM loudest at LUSB  relative PS murmur w/
fixed widely split S2

EKG w/ right ventricular conduction delay

Dx  echo

Treatment  surgical vs percutaneous closure

Natural history in the 3rd-4th decade of life:

Arrhythmias

Pulmonary HTN

Paradoxical emboli



Acyanotic CHD
Most common CHD
4 main types of VSD
Perimembranous
 Muscular
 Inlet
 Outlet


Small VSDs  no sx


only loud harsh 3/6 holosystolic murmur loudest at
LLSB
Large VSDs  congestive heart failure (CHF)


CHF x typically start at 6-8 weeks old from a VSD
Babies present with:











Some degree of resp distress: tachypnea, retractions, abd
breathing, etc
Irritability
Hepatomegaly
Cardiomegaly
NO peripheral edema
NO cyanosis
Poor po intake, easy fatiguing w/ feeds, prolonged feeding
times
Poor weight gain: weight drops off before height
Excessive sweating
Sinus tachycardia
Loud harsh holosystolic murmur loudest at the LLSB

Cardiomegaly

Inc lung markings

Pulm edema


EKG:

Normal

Sinus tachy

LVH
Echo: diagnostic


If CHF treat with:

Digoxin 5mcg/kg/dose bid

Lasix 1mg/kg/dose bid

Enalapril  afterload reduction

Increase caloric intake  24kcal/oz formula
Surgical closure of large VSDs ~ 6 mo old 
sooner if FTT despite medical trt CHF

Small VSDs:


80% close within the 1st year of life
Large VSDs:


CHF  40% of babies will die w/o treatment in 1st
year of life
Unrepaired large VSDs past 1yo  develop
Eisenmenger’s syndrome in teen years
 Progressive pulmonary HTN w/ progressive cyanosis
 Right to left shunt
 Mean survival mid-20’s

AKA:

AV Canal

endocardial
cushion defect

AV septal defect

~50% of children w/ T21 have CHD

~40% of those with T21 and CHD have AVC

EKG: often has left superior axis

Echo: diagnostic

Treatment:

Medically manage CHF (same as w/ large VSD)

Surgical repair 4-6 months old

All babies are born with a PDA

Usually closes within 1st 2 wks of life in full term
babies

Persists longer in preterm babies

Small PDAs  no symptoms

Large PDAs  CHF sx similar to large VSDs

In preemies  resp distress can be seen in the 1st
few days of life

Classic murmur  continuous machinery
murmur secondary to continuous shunt in
systole and diastole loudest under L clavicle

Murmur is not heard in newborns secondary to
elevated pulm vascular resistance (PVR)

Murmur develops only after PVR srops


If significant sx in preterm babies 

Indomethacin

May try CHF rx

Surgical PDA ligation
If CHF sx in term babies 

Medically treat CHF

If babies can reach 10kg  percutaneous PDA closure

If cannot gain weight  surgical PDA ligation
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20% 20% 20% 20% 20%
rc
ta
C.
At
r io
B.
Coarctation of the aorta
Atrioventricular canal
defect
Patent ductus
arteriosus
Large ventricular septal
defect
Secundum atrial septal
defect
Co
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20% 20% 20% 20% 20%
Ad
m
B.
Administer furosemide
intravenously
Administer indomethacin
intravenously
Perform an echocardiogram
Defer interventions since
spontaneous closure is likely
Obtain a surgical consult for
PDA ligation
Ad
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20% 20% 20% 20% 20%
Ba
B.
Barium swallow
Cervical spine
radiography
Echocardiogram
Head ultrasound
Radiography of the
abdomen
Ce
rv
i
A.

More common in males

Almost always juxtaductal [A]

Preductal [B]  present earlier

Postductal [C]  present later

85% of children with coarc have a BAV

Frequently seen in Turners syndrome {45, XO}

10% have severe coarc

30% have bicuspid aortic valve (BAV)

Variable presentation 

Infant with cardiogenic shock

Child or adolescent with systemic hypertension

Child with a heart murmur

Severe coarc in a neonate 
Often present before 2 weeks old
 Cardiogenic shock: resp distress/failure, poor
perfusion, altered metal status
 Multisystem organ failure: NEC, renal failure,
intracranial bleed
 **Diminished lower extremity pulses


Moderate coarc in a neonate 


CHF: resp distress, poor feeding, poor growth
Mild coarc in a neonate 

No symptoms +/- murmur

Older children and adolescents do NOT
present with heart failure sx

Can have upper extremity hypertension
refractory to antihypertensive rx

Can have diminished lower extremity pulses

Can have claudication

Can just have a murmur

EKG:

Often normal

Can have LVH with strain pattern (ST elevation +/- T
wave inversion in precordial leads)

CXR: often nonspecific findings, normal or:

Cardiomegaly

Increase pulm vascular markings

Rib notching (not seen in infants, uncommon prior to 5
years old)

Echo: diagnostic

Treatment:

Infant in shock  immediate PGE + aggressively trt
shock

Surgical repair for children or for complex coarc

Percutaneous stent placement in adult sized patients

Varying degrees of left heart hypoplasia

Babies present in cardiogenic shock when PDA
closes

Immediate treatment with PGE IV infusion

Surgical treatment:



Norwood palliation  1st week of life
Bidirectional Glenn  4-6 months old
Fontan palliation  2-4 years old
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Po
ly
C.
20% 20% 20% 20% 20%
ric
a
B.
Polycythemia
Postpericardiotomy
syndrome
Protein-losing
enteropathy
Superior vena cava
syndrome
Thoracic duct injury
Po
st
pe
A.






Stenosis may be valvular,
subvalvar, or supravalvar
Mild-mod PS  no sx
Severe or critical PS 
cyanosis
Murmur  harsh SEM at
LUSB
Echo –> diagnostic
Treatment: ballooning or
surgical







Stenosis may valvular,
subvalvar, or supravalvar
More common in males
More significant lesion
compared to PS, no
cyanosis, (+) heart
failure/cardiogenic shock
Valvar AS is often
associated w/ BAV
Murmur  harsh SEM at
RUSB
Echo –> diagnostic
Treatment: ballooning or
surgical




Mild to severe usually asymmetric thickening
of the myocardium
Often autosomal dominant
Incidence 1:500
Symptoms:
Sudden death (on exertion)
 Arrhythmias
 Syncope
 Chest pain

de
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ica
B.
Critical aortic stenosis
Erythroblastosis fetalis
Patent ducts arteriosus
Severe hypovolemia
Ventricular septal
defect
Cr
it
A.
20% 20% 20% 20% 20%
A.
B.
C.
D.
E.
Dopamine infusion
Loading dose of
digoxin
25% glucose and
water solution
Furosemide
Prostaglandin E1
Do
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20% 20% 20% 20% 20%


Cyanotic (blue) CHD  Often have cyanosis with
NO resp distress
Need some sort of L to Right shunt to have cyanosis

TOF (right to left shunt)

TGA

Tricuspid atresia (right to left shunt)

Truncus arteriosus

TAPVR

Ebstein’s Anomaly (right to left shunt)

Single Ventricles

PS

VSD

Overriding aorta

Right ventricular
hypertrophy (RVH)


Most common cyanotic heart lesion
Signs/symptoms:
Cyanosis
 Loud harsh SEM at the LUSB (PS murmur)
 Squatting in older kids
 Tet spells  cyanosis often worsened or caused by
crying

 Lose PS murmur b/c less blood across pulm valve
 Increase right to left shunt across VSD
 Trt  calm kid down, knees to chest, morphine, oxygen,
general anesthesia



Aorta arises from the RV and the pulmonary
artery arises from the LV
Mixing of blood occurs at the PFO/ASD, PDA,
+/-VSD
Sx:
Cyanosis
 +/- murmur
 May have higher sats in the lower
extremities vs the upper extremities


Echo: diagnostic

TA  left superior axis on EKG (like AVC)

Sx occur when pulm veins are obstructed

Can occur soon after birth

Babies present with severe cyanosis
(unresponsive to O2) and resp distress

No murmur

Treatment  emergent surgery


Apical displacement of the tricuspid valve
Can present with:




Severe TR
R to L shunting  neonatal cyanosis
25% can have SVT or WPW
Neonatal treatment  decrease PVR
iNO
 Oxygen


CXR  severe cardiomegaly
fF
al
de
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lo
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of
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ic
D.
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Ao
rt
B.
Aortic stenosis
Coarctation of the aorta
Myocarditis
Tetralogy of Fallot
Ventricular septal defect
Co
a
A.
st
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is
20% 20% 20% 20% 20%
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20% 20% 20% 20% 20%
bt
a
B.
Obtain a stat EKG to evaluate for SVT
Intubate the infant and place on 100% O2
Start IV PGE infusion at 0.050.2mcg/kg/min
Start iNO at 40ppm inspired to reduce
PVR
Arrange for transfer to a facility capable
of ECMO
O
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20% 20% 20% 20% 20%
Primary pulmonary hypertension of
the newborn
Pulmonary valve atresia
Transient tachypnea of the newborn
Transposition of the great arteries
Truncus arteriosus
Pr
im
A.
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20% 20% 20%
si
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ne
m
E.
A
D.
le
C.
20% 20%
st
ic
B.
Anemia
Hypoplastic left heart
syndrome
Neonatal sepsis
Retained fetal lung liquid
syndrome
Tracheoesophageal fistula
H
yp
op
la
A.






Most common arrhythmia in childhood
Babies present with poor feeding, pallor, irritability
Older kids present w/ palp, dizziness, fatigue
EKG diagnostic  narrow complex regular tachy
>220bpm
Can be associated with WPW
If patient hemodynamically stable  vagal
maneuvers:
Ice to face
 Valsalva



If doesn’t work  adenosine
If patient hemodynamically unstable 
synchronized cardioversion

Ice to face

“Bearing down”

Blowing against and occluded straw

Gag

Cough




Atrial flutter: saw tooth p waves
Atrial fib: irregularly irregular
Adenosine is diagnostic not therapeutic
Treat both with synchronized cardioversion

1st degree HB: prolonged PR interval


2nd degree HB:



Rheumatic fever, myocarditis, KD, congenital
Type I: Wenkebach, progressive prolongation of PR interval
then dropped beat  high vagal tone, benign
Type II: dropped (nonconducted beats)  can progress to
CHB  pacemaker
3rd degree: complete HB


Postop, lyme disease, myocarditis
Congenital CHB  maternal SLE




QTc >0.45 sec
Genetic  often family hx sudden death
Arrhythmia  torsades de pointes (type of VT)
Be suspicious if:
Family hx SCD
 Hx seizure d/o
 Congenital deafness
 Syncope following loud noises, being startled



Acute treatment: magnesium
Long term treatment: beta blockers

Sudden, blunt, non-penetrating trauma to the
chest  V fib  sudden death

Typical story: healthy kid gets hit with a
baseball to the chest and drops

Treatment  stat defib

Benign causes of syncope:





Vasovagal: during blood draws, site of blood
Orthostatic hypotension: standing up quickly,
standing up for too long, especially if hot
Hyperventilation
Breath holding spells: 6-18mo, associated w crying,
+/- cyanosis
Concerning, potentially life-threatening syncope:



Associated w/ exertion (VT, LQTS, HCM, other
cardiomyopathy)
Associated w/ excitement/startle (LQTS)
Family hx sudden death
HCM
3
22
Coronary
Anomalies
AS
6
3
3
36
Ruptured Ao
5
Tunnelled LAD
5
Myocarditis
4
19
Dilated CM
ARVD

Carditis refers to inflammation of any of the 3
layers of the heart, occur in isolation or
conjunction with one another

Endocarditis  inflammation of the cardiac valves 
valvar dysfunction

Myocarditis  inflammation of the muscular walls of
the heart  myocardial dysfunction, conduction
abnormalities (heart block, arrhythmias)

Pericarditis  inflammation of the pericardium 
pericardial effusion


Diagnosis  Modified Duke Criteria

2 major

1 major + 3 minor

5 minor
Treatment  IV abx, type and length of
treatment vary

Positive Bcx w/ typical IE microorganism:

Typical microorganism consistent w/ IE from 2 separate Bcx:
 Viridans-grp strep, or
 Strept bovis including nutritional variant strains, or
 HACEK group (Haemophilus spp, Actinobacillus, Cardiobacteriom
hominis, Eikenella spp, Kingella), or
 Staph aureus, or
 Community-acquired Enterococci, in the absence of a primary focus

Microorganisms consistent w/ IE from persistently (+) Bcx:
 2 positive Bcx drawn >12 hours apart, or
 All of 3 or a majority of 4 or more separate Bcx (w/ first and last sample
drawn at least 1 hour apart)
 Coxiella burnetii on at least 1 (+) Bcx or antiphase I IgG antibody titer
>1:800

Evidence of endocardial involvement w/ (+) echo:



Oscillating intracardiac mass on valve or supporting structure, or in
the path of regurgitant jet, or on implanted material, or
Abscess, or
New partial dehiscence of prosthetic valve or new valve
regurgitation





Predisposing factor: CHD, recreational IV drug
use
Fever >38°C
Evidence of embolism: arterial emboli, pulmonary
infarct, Janeway lesions, conjunctival hemorrhage,
mycotic aneurysm, intracarnial hemorrhage
Immunological problems: glomerulonephritis,
Osler’s nodes, Roth spots, rheumatoid factor
Positive Bcx (that doesn't meet a major criterion)
or serologic evidence of infection w/ organism
consistent with IE but not satisfying major
criterion



Janeway lesions: small,
erythematous, non-tender,
macular or nodular lesion on
soles/palms  septic emboli 
microbscesses
Osler’s nodes: painful, red, raised
lesions on hands/feet  immune
complex deposition
Roth spots: retinal hemorrhages
w/ white or pale centers
composed of coagulated fibrin 
immune complex mediated
vasculitis

2007 AHA guidelines:

Prosthetic valves

Previous IE

Unrepaired cyanotic heart disease

Repaired CHD <6 months after surgery

Repaired CHD >6mo if residual lesion near prosthetic
material

Cardiac transplant with valvulopathy



Myocarditis  inflammation of the muscular
walls of the heart  myocardial
dysfunction/failure, heart block, arrhythmias
Presentation in babies  irritability, poor
feeding, pallor, shock, cardiomegaly,
hepatomegaly, pulm edema
Presentation in older kids  fatigue, dyspnea,
chest pain, palpitations, pallor, hypotension,
cardiomegaly, hepatomegaly, pulm edema
Infectious vs noninfectious vs idiopathic
 Viral  most common cause in US: coxsackie,
adenovirus, parvovirus B19, enterovirus, EBV,
CMV, HSV 6
 Other infectious  Lyme dz and other
spirochetes, fungal, bacterial
 Toxic/hypersenstivity reactions 
chemotherapeutic agents, abx, amphetamines
 Systemic dz  Giant-cell myocarditis,
sarcoidosis, KD, Crohn’s, UC, SLE, thyrotoxicosis


No single clinical or imaging test to confirm dx
Dx made by:
Clinical sx
 Serologic: CKMB, troponin, BNP, CRP
 Noninvasive: EKG, echo, MRI
 Invasive: myocardial biopsy



Treatment: depends on severity of sx, mostly
supportive: ionotropic support, mechanical vent,
ECMO, trt CHF, antiarrhythmics, temporary
pacing, IVIG or steroids
Long term: fully recover (50%), chronic heart
failure, need for transplant

Viral pericarditis most common

Preceded by a viral URI

Sx: sharp chest pain, improves with leaning forward

PE: friction rub, pulses paradoxus (exaggeration of
normal finding of dec in systolic BP w/ inspiration)

EKG diagnostic: diffuse ST segment elevation

Echo: pericardial effusion

Risk  cardiac tamponade

Treatment  NSAID, pericardiocentesis if severe
20% 20% 20% 20% 20%
m
a
ia
le
de
e
m
ol
u
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no
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E.
Cy
a
D.
gh
C.
Co
u
B.
Ascites
Cough
Cyanosis
Diminished
feeding volume
Pretibial edema
As
c it
es
A.
20%
20%
20%
m
on
th
s
12
hs
6
m
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hs
m
on
t
2
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w
E.
2
D.
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C.
da
y
B.
20%
2 days
2 weeks
2 months
6 months
12 months
2
A.
20%



ARF results from a complex interaction btw GAS
and a susceptible host
Abnormal immune response leads to acute
inflammation of joints, brain, heart, and or skin
All organ systems recover w/o sequelae except
the heart

ARF can lead to chronic RHD

Diagnosis  modified Jones Criteria


2 major or 1 major + 2 minor
And evidence of a preceding streptococcal
infection


Major criteria:






Except w/ presence of chorea or indolent carditis
Polyarthritis
Carditis
Sydenham’s chorea
Erythema marginatum
Subcutaneous nodules—extensor surf
Minor criteria




Fever
Polyarthralgia
Elevated acute phase reactants (ESR, CRP)
Prolonged PR interval



Initial cardiac involvement is a pancarditis
Most prominent feature is valve involvement

#1 mitral (MR)

#2 mitral + aortic (MR + AI)

#3 aortic (AI)
Treatment:
Primary ppx: Treat strep infection
 High dose aspirin or NSAIDs or steroids (4-6 weeks)
 Secondary ppx: monthly IM PCN


Long term RHD: MR + AI  MR/MS + AI/AS



Arteritis of medium size arteries
AKA mucocutaneous lymph node syndrome
Diagnosis  5 days of fever + 4/5 of the
following:





B/l nonexudative conjunctivitis
Erythema of the lips or oral mucosa
Changes in the extremities: swelling, erythema
Rash
Cervical LAN, >1.5cm
Supplemental laboratory
criteria:
 Albumin </=3.0 g/dL
 Anemia for age
 Elevation of ALT
 Plt after 7d >/=450
 WBC >/= 15
 Urine 10 WBC/highpower field
Newburger, J. W. et al. Circulation 2004;110:2747-2771

Treatment for typical and atypical KD is the same






IVIG w/i 10 days of fever, may repeat if still febrile
High dose aspirin
W/o treatment  20% of children will develop
coronary artery aneurysms
W/ treatment w/ IVIG and ASA5% of pts will
develop aneurysms
Aneurysms develop usually w/i 2 weeks
Can have an associated mild myocarditis











T21: CHD incidence 50%, think AV canal defects
Turner’s: 10% coarc, 30% BAV
Pompe’s: Hypertrophic cardiomyopathy (HCM)
Alagille : Peripheral pulmonic stenosis (PPS)
Williams’s: Supravalvar aortic stenosis, PPS
Noonan: PPS and (HCM)
Marfan’s: Aortic root dilatation, MVP
DiGeorge (22q11 del): TOF, truncus arteriosus,
interrupted Ao arch, right aortic arch
Kartagener: dextrocardia, situs inversus totalis,
immotile cilia
Holt-Oram: Limb abnormalities, ASD
Ellis-van Creveld: ASD









Lithium: Ebstein’s anomaly
Ethanol: ASD,VSD (fetal alcohol syndrome)
Anticonvulsants: PS, AS, TOF
Retinoic Acid: TGA
Rubella: PDA, PPS
Coxsachie B: Neonatal myocarditis
Maternal Diabetes: HCM, TGA
Maternal Lupus: Complete heart block
PKU: VSD, ASD, complex CHD
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Corrected QT interval
of 0.52 sec
P wave axis of -30
degrees
PR interval of 0.81 sec
QRS axis of -15 degrees
QRS interval of 0.12 sec
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20% 20% 20% 20% 20%
w
B.
She was standing in line waiting to
see “The Hunger Games:
Mockingjay part 2” when she
passed out
She fainted once before when she
had a blood test
After falling to the ground she came
to quickly and remembered feeling
warm and dizzy
She was lying on the sofa watching
TV when a door slammed and she
suddenly became unresponsive
S1 and S2 were normal and no
murmurs were noted
Sh
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20% 20% 20% 20% 20%
ho
ca
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B.
Echocardiography
Electrocardiography
Exercise myocardial perfusion
scintigraphy
Genetic testing for myosin chain
mutations
Genetic testing for troponin
mutations
Ec
A.
al
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Pa
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20% 20% 20% 20% 20%
cu
t
B.
Acute rheumatic fever
Infective endocarditis
Myocarditis
Paroxysmal atrial
tachycardia
Pericarditis
A
A.
tis
Pe
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a
rd
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um
C.
20% 20% 20% 20% 20%
er
B.
Acute rheumatic
fever
Arrhythmia
Costochondritis
Myocardial ischemia
Pericarditis
Ac
ut
A.