Ryan Parnham, MSN, APN, CNP

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Pediatric Cardiology
Originally Developed by:
Ryan Parnham, MSN, APN, CNP
OSF Critical Care Service
Revised Spring 2012
by Teresa D. Valerio, DNP, APN, FNP-BC
Today’s Topics
Cardiac Physical Examination
 Congenital Heart Disease
 Acquired Heart Disease
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Purpose
Enhance knowledge and confidence with
pediatric cardiology
 Emphasize the importance of
recognizing significant pediatric
cardiovascular abnormalities as a primary
care provider
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Readings from Textbooks
Burns, C.E. et al. (2009). Pediatric Primary Care.
– Chapter 30, pgs. 727-766.
 Chiocca, E.M. (2011). Advanced Pediatric

Assessment.
– Chapter 18, pgs. 366-390.
 Hay, W.H. et al. (2011). Current Diagnosis &
Treatment: Pediatrics.
– Chapter 19, pgs. 536-541, 547-566, 571- 582,
593-594.
Other helpful resources
Westrol, M.S. & Raffi, K. (2012). Pediatric ECG
Cases: Benign Variants or Life-Threatening
Abnormalities? (PDF emailed)
 Wierwille, L. (2011). Pediatric heart murmurs:
Evaluation and management in primary care.
The nurse practitioner, 36(3), 22-29. (PDF
emailed)
 Rheumatic fever clinical guidelines at

http://www.indianpediatrics.net/pdf/acute_rheu
matic_fever.pdf
Elements of the cardiac
physical examination
History
Pregnancy/Birth History: prenatal care,
complicated prenatal course, maternal risk
factors (diabetes assoc. with hypertrophic
cardiomyopathy), prematurity, method of
delivery, prolonged hospital stay, birth weight,
APGARs
 Family History: CHD, sudden death, SIDS,
cardiomyopathy (high incidence of inheritance,
>20%), dysrhythmias, syndromes/genetic
abnormalities
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Past Medical History
General Health
 Concerns from parents
 Growth curve and weight gain (pay
attention to stature of parents)
 Chronic respiratory difficulties- asthma,
frequent URIs/pneumonia
 Other medical issues/surgeries
 Down Syndrome, Marfan Syndrome, etc.
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Important Questions
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Persistent tachypnea?
Cyanosis?
Failure to thrive?
Tiring and/or diaphoresis with feeding/minimal activity?
Palpitations?
Chest Pain with exertion?
Syncope/Near-syncope? Syncope with exertion?
Palpitations with syncope?
Lethargy/Fatigue?
Inability to keep up with peers?
Worsening activity tolerance?
Vital Signs
Respiratory Rate- should be counted for a
full minute in infants because of variability
 Heart rate- resting if possible
 Blood pressure- bilateral upper and lower
extremities (at least once in their life,
unless more often if clinically indicated)use correct size cuff!
 Pulse ox- check/recheck multiple
extremities if abnormal reading
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Overall Appearance
Anxious, distressed, diaphoretic, pale,
tachypneic, retractions, cyanotic, difficult
to console, dysmorphic, clubbing
 A baby, child and adolescent can have a
significant cardiac lesion and appear
perfectly healthy with apparently normal
vitals signs
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Cardiovascular Assessment
Is chest symmetrical? Evidence of pectus
excavatum, pectus carinatum.
 Precordial activity quiet or hyperactive?
 PMI displaced? (usually mid-clavicular line)
 Palpable thrill over chest? Thrill at
suprasternal notch?
 JVD?
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Auscultation
Listen at all landmarks (aortic, pulmonic,
2nd pulmonic, tricuspid, mitral) with bell
and diaphragm
 Listen to heart sounds
 S1: closure of what valves?
 S2: closure of what valves?
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S1
Closure of the atrioventricular valves
(mitral and tricuspid)
 Normally heard as one sound, although
occasionally splitting may be heard
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S2
Closure of the semilunar valves (pulmonary and
aortic)
 Under normal circumstances, S2 is “split” during
or near the end of inspiration (the right ventricle
is filled more than the left with inspiration,
causing a short delay in closure of the PV)
 A fixed or widely split S2 could be pathologic, as
can a single S2 that does not split.
 www.med.ucla.edu/wilkes/inex.htm
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Murmurs
What is a heart murmur?
Murmurs
Murmurs are audible sound waves caused by
turbulent blood flow- a murmur is not a
hole, or a defective valve, etc.
 Most murmurs are “innocent,” or Still’s
murmurs, 32-80% of all children will have a
murmur at some point in their life, often with
fever
 Structural or physiologic cardiac problems
can also cause murmurs; 1% of children
have structural heart disease
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Grading of Murmurs
1: Heard only with intense concentration
 2: Faint, but heard immediately
 3: Easily heard, of intermediate intensity
 4: Easily heard and palpable thrill present
 5: Very loud, thrill present, and audible
with edge of stethoscope on chest wall
 6: Audible with stethoscope off chest wall
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Innocent Vibratory Murmur or Still’s
Murmur
Most common during childhood
Low to medium pitch, early systole
Usually grade 2, but can range 1-3
Maximal at LLSB w/ radiation to apex
Usually loudest supine and fades with sitting and
standing
 Vibratory, harmonic, musical
 Often louder during febrile illness or times of
increased cardiac output
 Usually disappear with time and can come and
go
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Innocent Pulmonary Flow Murmur
A relatively soft systolic murmur
appreciated at the upper left sternal
border
 Often louder while lying supine and
fades/disappears with sitting
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Venous Hum
Continuous murmur usually heard at the
infraclavicular area of the anterior chest, R>L
 Loudest while sitting (venous return from the
jugular veins and subclavian veins entering the
SVC ) and disappears supine
 Can be diminished or muted with gentle
compression of jugular vein
 Commonly associated with vibratory murmur
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Pathological Systolic Murmurs
Upper Right Sternal Border: Aortic
Stenosis, subaortic membrance, PPAS
 Upper Left Sternal Border: Pulmonary
Stenosis, PDA, PPAS
 Mid to Lower Left Sternal Border: VSD,
TR, LVOT narrowing (HCM)/Subaortic
stenosis
 Apex: MR, poss VSD
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Pathological Systolic Murmurs
Usually don’t change with position, except
HCM causing LVOT obstruction
becomes louder with standing.
 MR may be somewhat more pronounced
while lying on the left side.
 Often times “harsh”, usually quite different
from an innocent murmur, but not always
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Diastolic Murmurs
Always pathological- there are no
“normal” or “innocent” diastolic murmurs
 What are some diastolic murmurs?
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“Early” Diastolic Murmurs
Decrescendo in nature
 Commonly aortic regurgitation or
pulmonary regurgitation (insufficiency)
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Mid to Late Diastolic Murmurs
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Tricuspid stenosis or mitral stenosis
Continuous Murmurs
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Heard through systole and diastole- most
common “pathological” continuous
murmur is a Patent Ductus Arteriosus
Cardiovascular Exam (cont’d)
Resp- Lungs clear? Equal? Congested?
Diminished? Tachypneic? Retractions?
 Skin- Warm? Pink? Well-perfused?
 Abdomen- soft? Liver enlarged? Ascites?
Situs solititus or inversus?
 Pulses- Weak? Bounding? Normal?
Brachial/radial-femoral delay?
 Extremities: Capillary Refill Brisk?
Clubbing? Edema?
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Exam (con’t)
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If you want to truly perform a quality
cardiovascular examination, auscultate the
patient lying, sitting, standing and
squatting, especially with athletes,
patients with syncope with exertion, or
family history of sudden death and/or
hypertrophic cardiomyopathy!
When Do You Refer for a Murmur?
Is this a new murmur?
 What are the characteristics of the
murmur? Systolic vs. diastolic.
 Is the child febrile?
 Is the child “symptomatic”?
 What testing has been done thus farEKG, CXR, ECHO
 Family history
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When Do You Refer for a Murmur?
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If no definite “red flags,” consider having the child RTC
to re-listen in a week or two (especially if febrile!!!)
If some concern, order an EKG and CXR- relatively
inexpensive and can provide useful info
If EKG and CXR normal, but still uncertain, ok to refer or
consider ordering an echo (caution- expensive and may
“over-diagnose”)
If child in obvious distress- refer immediately/admit for
evaluation
If the patient is in competitive athletics and it is a new
murmur, consider referral.
At least order an EKG and CXR prior to referralappreciated by the cardiology group!
Congenital Heart
Disease
Congenital Heart Disease
8-10/ 1,000 liveborn infants will have a
congenital cardiac malformation (0.8-1%)
 Risk of recurrence in families with one
parent or one sibling with CHD is 1-4%
 Some defects are associated with even
higher recurrence rates in families, and
geneticists are beginning to identify
certain genes that may help explain this
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What causes CHD?
Genetic factors?
 Environmental factors?
 Genetic and environmental factors?
 Possible environmental factors: maternal
infection/illness, medication use,
substance abuse, chronic diseases such as
diabetes, lupus, etc.
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Review of Fetal Circulation
Congenital Cardiac
Lesions
Acyanotic and Cyanotic
Acyanotic Lesions
Atrial Septal Defect (ASD)
 Ventricular Septal Defect (VSD)
 Atrioventricular Septal Defects/AV Canal
 Patent Ductus Arteriosus (PDA)
 Aortic Stenosis
 Pulmonary Stenosis
 Coarctation of the Aorta
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Cyanotic Lesions
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d-transposition of the great arteries (d-TGA)
Tetralogy of Fallot
Hypoplastic right heart syndrome
Hypoplastic left heart syndrome
Double outlet right ventricle (DORV)
Truncus arteriosus
Total anomalous pulmonary venous return
(TAPVR)
Commonly Seen
Acyanotic Lesions
Atrial Septal Defects (ASD)
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Common defect
May be a PFO/small secundum ASD- 20-25% of
the population has this
May be larger, causing significant L to R
shunting
Can go undetected for years
Exam: wide, fixed splitting of S2, often a systolic
murmur r/t increased pulm flow
“Easily” fixed (surgery vs. transcatheter)
Ventricular Septal Defect
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Ventricular septum fails to “fill in” completely
during embryonic development
Various degrees of VSDs from tiny to large
May be asymptomatic, mildly symptomatic, or in
congestive heart failure
May not present clinically until 1-2 months of life
Often associated with other lesions
Isolated VSD’s typically have favorable surgical
outcomes
Many small and even mod sized VSD’s can close
spontaneously for up to 4 years of age
Mitral Valve Prolapse
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The most common valvular abnormality (2-6% of the
population)- more common in females than males (2:1)
Usually benign, but may also have mitral regurgitation
Can worsen with time, or improve
Exam: mid-late systolic click (often), blowing,
holosystolic murmur if significant degree of MR
Diagnosis- echocardiogram (often wrongly and overdiagnosed by exam only)
May be associated with connective tissue disorders such
as Marfan Syndrome
Coarctation of the Aorta
Narrowed area of the aorta (usually descending
or transverse arch)
 May cause hypertension
 Often systolic murmur LUSB with radiation to left
back
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 Discrepancy
between upper and
lower extremity blood pressure
and pulses
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Usually an “easy” repair
Common Cyanotic
Lesions
Tetralogy of Fallot
4 defining characteristics- Pulmonary
stenosis, RVH, VSD, and aortic override
 May be associated with a genetic
syndrome
 Surgical repair in first year of life (often
need a shunt placed soon after birth)
 If PV is replaced, usually have some
degree of dysfunction that needs to be
monitored over time
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D-transposition of the Great
Arteries
Aorta rises from the RV and Pulmonary
Artery rises from the LV- complete
separation of pulmonary and systemic
circulations
 Arterial switch procedure
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There are many advances underway
in pediatric cardiac surgery and
cardiac catheterization techniques
that are not only improving surgical
outcomes, but resulting in shorter
hospital stays and a better quality of
life.
Acquired Heart Disease
Kawasaki Disease (KD)
An acute, self-limited vasculitis
 Unknown cause, but an infectious
cause/virus is suspected
 Leading cause of acquired heart disease in
US and Japan
 Usually seen in children <5 y.o.
 First described by Dr. Kawasaki in Japan,
1961
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KD- Diagnostic Criteria
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Fever >/= 5 days
Bilateral conjuctival injection
Changes of mucous membranes- injected
pharynx, fissured lips, strawberry tongue
Changes of peripheral extremities- peripheral
edema, peripheral erythema, desquamation of
palms
Polymorphous rash
Cervical adenopathy
Diagnosis is presence of fever and 4 of 5
remaining criteria
KD- Cardiovascular concerns
Development of coronary artery aneurysms
(usually around 2 wks after onset of symptoms)
 Evaluated by echocardiogram
 Half of patients with aneurysms will remodel
vessel wall- never completely normal. Probably
at higher risk for future coronary artery diseaselong-term antiplatelet therapy generally
recommended
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Strawberry Tongue
Treatment
Standard treatment is high-dose IVIG
(immunoglobulins) in combination with
high doses of aspirin
 Screening/repeat echocardiograms
 Possible cardiac cath with intervention if
coronary artery aneurysms causing
myocardial dysfunction or for further
evaluation
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Long-term prognosis without
coronary aneurysm
No significant risk of increased mortality
 Possible increased risk of premature
atherosclerosis r/t vasculitis?
 Little long-term data, although there have
been a couple of studies suggesting
abnormal vasodilatory properties of
coronary arteries in KD patients with
seemingly “unaffected” coronaries
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Rheumatic Fever
A systemic illness thought to occur following
group A beta hemolytic streptococcal pharyngitis
(GABHS) in children, median age 10 years (can
happen in adults though)
 Although uncommon in present day, accurate
clinical diagnosis is vital for optimal long-term
prognosis.
 Was the leading cause of death in patients aged
5-20 in the US about 100 yrs ago.
 Increased risk- untreated or delayed treatment
of a strep infection
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History
Sore throat 1-5 wks prior to onset of RF
symptoms
 Fever, rash, headache, wt loss, fatigue,
diaphoresis, chest pain/pounding, migratory
joint pain, skin nodules, motor dysfunction,
previous RF (higher risk of recurrence)
 Can cause endocarditis, myocarditis, and
pericarditis. Usually affecting the mitral and
aortic valves resulting in regurgitation
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Jones Criteria
Requires presence of 2 major, or 1
major and 2 minor criteria. Previous
Group A strep is also necessary
Major Criteria
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Carditis (EKG, CXR, ECHO, Exam)- new murmur and
tachycardia. Wide pulse pressure if severe aortic
regurgitation. May also have CHF- JVD, hepatomegaly,
gallop rhythm, friction rub, peripheral edema
Polyarthritis
Chorea- brief, irregular, unpredictable, purposeless
movements that flow from one body part to another
without a rhythmic pattern
Erythema marginatum- 1 to 3 cm pink/red nonpruitic
macules or papules on trunk and limbs (not on face)
Subcutaneous nodules- infrequent, but occur on surfaces
of elbows, knees, ankles, knuckles, and other spinous
processes- firm and nontender
Subcutaneous Nodules
Erythema Marginatum
Minor Criteria
Fever- usually greater than 39 deg C,
although may be low-grade, may last 2-3
weeks
 Arthralgia- cannot be considered minor if
arthritis is present
 Prolonged PR interval in EKG
 Elevated erythrocyte sedimentation rate
(ESR) and C-Reactive Protein (CRP)
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Evidence of GAS pharyngitis – one
of the following MUST be present
Positive throat culture or rapid strep
antigen test
 Elevated or rising streptococcal antibody
titer (such as antistreptolysin O [ASO])
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Lab Studies
Throat culture
 Rapid antigen detection test
 Antistreptococcal antibodies- usually using
antistreptolysin O (ASO)
 C-RP, ESR
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Imaging
CXR- pulm cong/CHF
 Echo- MR, AR, LV dilation
 ECG- sinus tachy, 1st, 2nd or 3rd degree AV
block (myocarditis), ST segment elevation,
atrial arrhythmias
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Treatment
Antibiotics- Oral penicillin remains drug of choicealternatives: IM Pen G, E-mycin, 1st gen Cephalosporin
(do not use tetracyclines or sulfonamides)
 High dose aspirin and steroid to treat inflammation (cont
to monitor C-RP and ESR for effectiveness)
 Digoxin, diuretics, afterload reduction depending on
cardiac manifestations
 After acute phase symptoms have subsided, improved,
may undergo cardiac surgery for valve
repair/replacement- if AV and/or MV replaced with
prosthetic, will require lifetime anticoagulation (Warfarin)
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What does this mean as FNP’s
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Recognizing and treating streptococcal infections
in a timely manner
Awareness of potential systemic symptoms
related to untreated/delayed treatment of a
strep infection- these may not occur until up to
several weeks after the sore throat has resolved
Only infections of the pharynx initiate RF (in
developed countries)
Secondary prophylaxis of patients with history of
RF- daily PCN or injections q 3-4 wks
SBE prophylaxis with antibiotics prior to dental
and other procedures
Revised AHA guidelines for
Bacterial Endocarditis Prevention
Previous guidelines recommended antibiotics
prior to dental/surgical procedures for anyone
with any type of intracardiac abnormality (MVP,
bicuspid AV, etc)
 Recent findings- bactremia is transient and can
occur with routine activities (brushing teeth,
flossing, chewing)
 Only “high-risk” patients are recommended to
have antibiotic SBE prophylaxis
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“High risk” population includes:
Prosthetic heart valves
Previous endocarditis
 Unrepaired cyanotic defect
 Palliative shunt/conduit present
 Complete repair with prosthetic material for first 6
months after procedure
 Heart transplantation
 Recommended only for procedures which manipulates
the tissue or oral mucosa causing bleeding, etc. (not a
routing cleaning)
 Those not in “high risk” category are not at zero riskstill slightly elevated compared to those without
intracardiac abnormalities
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Other common complaints
Chest pain- rarely attributed to any underlying
cardiovascular disease. Coronary artery
abnormalities in children rarely present with
chest pain
 Syncope- very common in adolescents and
teenagers. Usually vasovagally mediated and r/t
hydration, eating habits, etc. “Red flags”syncope during strenuous activity, accompanied
with palpitations, family history of sudden death
or arrhythmias
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