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L04: Pediatric Cardiology Objectives
February 17, 2010
Pediatric Cardiology
1. Describe a heart murmur with respect to location and radiation, relationship to the cardiac cycle, intensity, quality, and
variation with position. Describe a Still murmur.
Murmurs: A heart murmur is the most common cardiovascular finding leading to a cardiology referral. Innocent or functional
heart murmurs are common, and 40-45% of children have an innocent murmur at some time during childhood.
a. Characteristics: All murmurs should be described based on the following characteristics:
i. (1) Location and radiation: Where the murmur is best heard and where the sound extends.
ii. (2) Relationship to cardiac cycle and duration: Systolic ejection (immediately following S1 with a
crescendo/decrescendo change in intensity), pansystolic (occurring throughoutmost of systole and of constant
intensity), diastolic, and continuous. The timing of the murmur provides valuable clues as to underlying
pathology
iii. (3) Intensity: Grade I describes a soft murmur heard with difficulty; grade II, soft but easily heard; grade III,
loud but without a thrill; grade IV, loud and associated with a precordial thrill; grade V, loud, with thrill, and
audible with the edge of the stethoscope; grade VI, very loud and audible with the stethoscope off the chest.
iv. (4) Quality: Harsh, musical, or rough; high, medium, or low in pitch.
v. (5) Variation with position: Audible when the patient is supine, sitting, standing, or squatting.
Still murmur- This is the most common innocent murmur of early childhood. It is typically heard between 2 and 7 years of age. It
is loudest midway between the apex and the lower left sternal border. Still murmur is a musical or vibratory, short, high-
pitched, grade I-III early systolic murmur. It is loudest when the patient is supine. It diminishes or disappears with inspiration or
when the patient is sitting. The Still murmur is louder in patients with fever, anemia, or sinus tachycardia from any reason.
INNOCENT MURMURS: the 6 MC innocent murmurs of childhood are:
i. Newborn Murmur
o Heard in the first few days of life, this murmur is at the lower left sternal border, without significant radiation. It
has a soft, short, vibratory grade I–II/VI quality that often subsides when mild pressure is applied to the abdomen.
It usually disappears by age 2–3 weeks.
ii. Peripheral Arterial Pulmonary Stenosis
o This murmur, often heard in newborns, is caused by the normal branching of the pulmonary artery. It is heard with
equal intensity at the upper left sternal border, at the back, and in both axillae. It is a soft, short, high-pitched,
grade I–II/VI systolic ejection murmur and usually disappears by age 2. This murmur must be differentiated from
true peripheral pulmonary stenosis (Williams syndrome, Alagille syndrome, or rubella syndrome), coarctation of
the thoracic aorta, and valvular pulmonary stenosis.
iii. Still Murmur
o This is the most common innocent murmur of early childhood. It is typically heard between 2 and 7 years of age. It
is loudest midway between the apex and the lower left sternal border. Still murmur is a musical or vibratory, short,
high-pitched, grade I–III early systolic murmur. It is loudest when the patient is supine. It diminishes or disappears
with inspiration or when the patient is sitting. The Still murmur is louder in patients with fever, anemia, or sinus
tachycardia from any reason.
iv. Pulmonary Ejection Murmur
o This is the most common innocent murmur in older children and adults. It is heard from age 3 years onward. It is
usually a soft systolic ejection murmur, grade I–II in intensity at the upper left sternal border. The murmur is louder
when the patient is supine or when cardiac output is increased. The pulmonary ejection murmur must be
differentiated from murmurs of pulmonary stenosis, coarctation of the aorta, atrial septal defect (ASD), and
peripheral pulmonary artery stenosis.
v. Venous Hum
o A venous hum is usually heard after age 2 years. It is located in the infraclavicular area on the right. It is a
continuous musical hum of grade I–III intensity and may be accentuated in diastole and with inspiration. It is best
heard in the sitting position. Turning the child's neck, placing the child supine, and compressing the jugular vein
obliterates the venous hum. Venous hum is caused by turbulence at the confluence of the subclavian and jugular
veins.
WHEN FUNCTIONAL MURMURS ARE FOUND IN A CHILD, THE PHYSICIAN SHOULD ASSURE THE PARENTS THAT THESE ARE
NORMAL HEART SOUNDS OF THE DEVELOPING CHILD AND THAT THEY DO NOT REPRESENT HEART DISEASE.
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L04: Pediatric Cardiology Objectives
February 17, 2010
2. Compare and contrast the etiologies of newborn cyanotic vs. acyanotic heart disease.
Cyanosis (decreased sat. of O2) - This is caused usually by right (deoxygenated blood) to left shunts (tetralogy of Fallot),
decreased pulmonary blood flow (right heart valve atresia, or pulmonary valve stenosis) or arterial-ventricle discordance
(aka transposition of great arteries). These more commonly will have RV hypertrophy or strain. Can present with clubbing
if cyanosis is severe.
Acyanotic defects: Are more commonly found to cause strain on the left side of the heart, but as long as the shunts
continue going from left to right, oxygenation of the blood is not affected. These defects more commonly will have LV
hypertrophy or strain if at all.
Systolic Ejection Pansystolic Diastolic Continuous
Semilunar valve stenosis VSD Semilunar valve regurgitation Runoff lesions
(aortic stenosis Atrioventricular valve (aortic insufficiency/pulmonic (PDA/ arteriovenous
pulmonic stenosis regurgitation insufficiency/truncal malformation
truncal stenosis) (mitral/tricuspid) insufficiency) /aortopulmonary collaterals)
ASD Atrioventricular valve
stenosis (mitral/tricuspid)
Coarctation
3. Identify the typical signs and symptoms and formulate the work-up (if any) and treatment plan of the following congenital
heart conditions: SEE CHART DOC!
4. Describe the underlying pathophysiology, typical presenting signs and symptoms and formulate the work-up (if any),
treatment plan and follow-up of the following acquired heart conditions:
a. Rheumatic fever
Essentials of diagnosis
o Uncommon in the United States (approximately 2 cases/100,000 population); more common (100
cases/100,000 population) in developing countries.
o Peak incidence ages 5-15 years.
o Diagnosis based on Jones criteria and confirmation of streptococcal infection.
o May involve mitral and other valves acutely, rarely leading to heart
o a sequela to b-hemolytic streptococcal infection of the pharynx.
SSx
o Jones Criteria – either 2 major or 1 maj+2minor critera PLUS evidence of a recent streptococcal infection
Major: carditis, polyarthritis, chorea, subcutaneous nodules, erythema nodules
Minor: previous ARF, arhtralgia, Fever, prolonged PR interval, elevated acute phase reactance
o Signs of rheumatic fever usually commence 2-3 weeks after infection but may appear as early as 1 week or as
late as 5 weeks.
o peak incidence is between ages 5 and 15 years;
o rheumatic fever is rare before age 4 years
o mitral valve is attacked in 75-80% of cases, the aortic valve in 30% (but rarely as the sole valve), and the
tricuspid and pulmonary valves in under 5% of cases.
o Carditis pericarditis, cardiomegaly, CHF, mitral or aortic regurg murmurs
o Erythema marginatum & subcutaneous nodules: small, firm, and nontender and are attached to fascia or
tendon sheaths over bony prominences
o Sydenham chorea: involuntary movements of face, tongue, UE
o Polyarthritis of large joints (tx w salicylates or NSAIDs)
o Minor criteria: fever, polyarthralgias, reversible prolongation of the PR interval, and an elevated ESR or CRP.
Labs
o High or increasing titers of antistreptococcal antibodies
Treatment
o Bed rest until temperature & ESR rate normal
o Salicylates to reduce fever & relieve joint pain/ swelling
o PCN IM (or erythromycin) to eradicate strep infection
o Corticosteroids (prednisone) for joint s/s
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L04: Pediatric Cardiology Objectives
February 17, 2010
b. Kawasaki disease- leading cause of acquired heart disease in the US
Essentials of diagnosis
o Fever, bilateral conjunctivitis, oral mucosal changes, rash, cervical lymphadenopathy, peripheral extremity
changes
o Elevated ESR & CRP
o More common in pts under the age of 5 years and in males, Asian children
SSx
o fever
o 4 of following for at least 5 days
bilateral nonexudative conjunctivitis,
mucous membrane changes of at least one type (injected pharynx, erythema, swelling and fissuring of the
lips, strawberry tongue),
peripheral extremity changes of at least one type (edema, desquamation, erythema of the palms and
soles, induration of the hands and feet, Beau lines [transverse grooves of the nails]),
a polymorphous rash,
cervical lymphadenopathy greater than 1.5 cm
o myocarditis is common in acute phase
o mitral regurg
o arteritis of extremity vessels
o peripheral gangrene
o SIADH
Labs
o MRI or transthoracic echo
o Leukocytosis
o Elevated CRP & ESR
Treatment
o IVIG, 2 g/kg over 10 hours, with repeat dosing appearing to reduce cardiac complications
o plasmapheresis who are unresponsive to immune globulin is controversial.
o Single-pulse corticosteroid therapy associated with a hastened resolution of inflammatory markers in primary
disease.
o infliximab, a monoclonal antibody of tumor necrosis factor-a, in treating refractory disease.
o Warfarin is indicated for aneurysms larger than 8 mm in diameter.
c. Hypertrophic Cardiomyopathy
Essentials of diagnosis
o Autosomal dominant inherited abnormality of the myocardial proteins that results in hypertrophy of the
ventricular myocardium.
o The result may be left ventricular outflow obstruction
o Septal and Left ventricular hypertrophy can develop in infants of diabetic mothers. Most familial cases are
seen in adolescents or young adults
o May present with dyspnea, chest pain, syncope.
o Though LV outflow gradient is classic, symptoms are primarily related to diastolic dysfunction.
o Echocardiogram shows septal hypertrophy, which is usually asymmetric, and enhanced contractility. Systolic
anterior motion of the anterior mitral valve is present if there is outflow tract obstruction.
o The highest risk group for sudden death includes those with a marked LVH, with a family history for sudden
death, with ventricular ectopy, and with an abnormal BP response to exercise.
o LV is usually more involved than the RV
o the atria are frequently significantly enlarged
SSx
o most frequent s/s= dyspnea and chest pain
o syncope (typically post-exertional)
o angina, palpitations, CHF, dizziness
o arrhythmias
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L04: Pediatric Cardiology Objectives
February 17, 2010
o A fib is long term consequence of elevated LA pressures & poor prognostic sign
o Bisferiens carotid pulse, triple apical impulse and loud S4.
o In cases with outflow obstruction, a loud systolic murmur is present along the left sternal border that
increases with upright posture or Valsalva maneuver and decreases with squatting
Labs/imaging
o EKG: LVH
o ECHO (diagnostic): LVH, systolic anterior motion of MV, early closing followed by reopening of the aortic valve,
a small and hypercontractile LV, and delayed relaxation and filling of the LV during diastole
o Doppler ultrasound: turbulent flow, dynamic gradient in the LV outflow tract and, mitral regurgitation
o Cardiac MRI confirms the hypertrophy
o Cardiac catheterization confirms the diagnosis and assesses the presence of CAD
Treatment
o Goals:
ruling out secondary causes,
following for progression of disease and identifying those with obstruction,
controlling symptoms and restricting activity (with avoidance of volume depletion),
identifying those at risk for sudden cardiac death,
screening of family members.
o Avoidance of competitive sports
o Beta-blockers and calcium channel blockers in young adults & adolescents (never use CCB in infants)
o Antibiotic prophylaxis is recommended for surgery
o Left ventricular myomectomy
o Transvenous dual-chamber pacing
o Transvenous catheter ablation of the septal region
o implantable cardioverter defibrillator
5. Given a child with chest pain, discuss the diagnostic approach and describe the clinical considerations.
Chest pain is a common pediatric complaint, accounting for 6 in 1000 visits to urban emergency departments and urgent
care clinics. Although children with chest pain are commonly referred for cardiac evaluation, chest pain in children is rarely
cardiac in origin. Other more likely causes of chest pain in children include reactive airways disease, musculoskeletal pain,
esophagitis, gastritis, and functional pain.
Detailed history and physical examination should guide the pediatrician to the appropriate workup of chest pain. Rarely is
there a need for laboratory tests or evaluation by a specialist. The duration, location, intensity, frequency, and radiation of
the pain should be documented, and possible triggering events preceding the pain should be explored. For instance, chest
pain following exertion may lead to a more elaborate evaluation for a cardiac disorder. The timing of the pain in relation to
meals may suggest a gastrointestinal cause. The patient should also be asked about how pain relief is achieved. A social
history to reveal psychosocial stressors and cigarette smoke exposure may be revealing. On physical examination, attention
must be placed on the vital signs; general appearance of the child; the chest wall musculature; cardiac, pulmonary, and
abdominal examination findings; and quality of peripheral pulses. If the pain can be reproduced through direct palpation of
the chest wall, it is almost always musculoskeletal in origin.
The most common cause of chest pain (30% of children) is inflammation of musculoskeletal structures of the chest wall.
Costochondritis is caused by inflammation of the costochondral joints and is usually unilateral.
In most cases sophisticated testing is not required. However, if a cardiac origin is suspected, a pediatric cardiologist should
be consulted. Evaluation in these instances may include an ECG, chest radiograph, echocardiogram, Holter monitor, or
serum troponin levels.
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L04: Pediatric Cardiology Objectives
February 17, 2010
6. Summarize the non-cardiac and diagnostic examinations used to evaluate congenital heart disease. (FROM LAST YEARS)
PE
Arterial Pulse: Rate, rhythm, quality, and amplitude.
Arterial blood pressure
Ext: cyanosis, clubbing, and edema
Abdomen: Hepatomegaly-right sided HF in infants and children. Spleenomegaly- long standing CHF and endocarditis.
Ascites- CHF
ECG- This evolves with time, RV dominance is seen in neonates which switches to LV dominance in older infants.
Rates are highly variable and decrease as the child ages (70-200 bpm). Sinus rhythm.
Axis: All infants have RV dominance but if the dominance does not shift there could be a congenital defect.
PR interval increases with age and as rate decreases.
QRS complex: look for hypertrophy, hypoplasia, infarct, and bundle branch blocks.
Right Axis Deviation Left Axis Deviation
Tetralogy of Fallot Atrioventricular septal defect
Dextro transposition of the great arteries Pulmonary atresia with intact ventricular septum
Total anomalous pulmonary venous return Tricuspid atresia
Atrial septal defect
Chest X-ray (the most common X-ray ordered by PA here in TX)
Note cardiac position and size: levocardia (heart predominantly in left chest), dextrocardia (heart predominantly in right
chest), or mesocardia (midline heart). If all other organs are switch with the heart (dextrocardia), heart is usually normal
and pt has situs inversus totalis, where if all other organs are normal situs solitus, there are usually severe cardiac defects.
Pulmonary vasculature should be assessed.
Lesion-specific findings
D transposition of great arteries- Egg on a string
Tetralogy of Fallot- Boot-shaped heart
Coarctation- Figure 3 sign and rib notching
Increased Pulmonary Blood Flow Decreased Pulmonary Blood Flow
Total anomalous pulmonary venous return Pulmonic stenosis
TA/large ventricular septal defect Tricuspid atresia/restrictive ventricular septal defect
Complete transposition of the great arteries Tetralogy of Fallot
Truncus arteroisus Pulmonary atresia with intact ventricular septum
Hypoplastic left heart syndrome
Echo: This is usually the diagnostic test for all cardiac anomalies.
Can evaluate anatomy, chamber size, vessel size, and valves.
Echo with Doppler assesses cardiac output, magnitude of regurgitant and stenotic lesions, diastolic LV relaxation, and
pulmonary artery pressure.
Stress echo to see wall movement when heart is under stress.
Nuclear imaging- profusion of the heart is visualized which is important when coronary anomalies are present and in Kawasaki disease.
MRI- Valuable follow-up tool for congenital heart disease.
Dynamic evaluation of vessels follow and ventricular function (good at evaluating ejection fractions).
This can usually reconstruct a 3D image of the heart.
Cardiopulmonary stress testing:
Used in children with congenital heart disease to assess if pt needs to have physical restrictions or possibly need for
transplant.
Monitors ECG, blood pressure, O2 sat., ventilation, maximal oxygen consumption, and peak work load attained while on a
treadmill or bike.
ABG:
Partial pressure of O2 or O2 sat while on 100% O2 distinguishes between cardiac or pulmonary disease in an infant.
O2 sat slightly increases over time when it is cardiac, but it drastically increases when there is pulmonary disease.
Cardiac Cath:
Usually only needed if further evaluation (more accurate pressures, O2 sat., and blood flow) is needed to determine
therapeutic decisions or it is possible the palliative or therapeutic choice.
Procedures that can be done
Coil embolization of a PDA,
Balloon angioplasty with or without stent placement for aortic coarctation or branch pulmonary artery stenosis,
Balloon atrial septostomy,
Valvuloplasty of stenotic aortic or pulmonic valves, and
Placement of ASD and VSD devices.
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L04: Pediatric Cardiology Objectives
February 17, 2010
Rheumatic fever
A. Pathophys: Immune response triggered by colonization of the pharynx with group A strep
B. S&S
Two major + 1 minor, or 1 minor + supporting evidence of strep infection
Major – carditits, polyarthritis, Sydenham chorea, erythema marginatum, subq nodules
Minor – Previous rheumatic fever or rheumatic heart disease, polyarthralgia, fever, elevated ESR, CRP, leukocytosis, prolonged
PR interval
C. Tx
Eradicate strep infection – LA benzathine PCN IV is DOC (PCN V or erythromycin PO)
ASA to relief arthritis and fever
Corticosteroids with severe carditis and HF
HF treatment based on sx and severity
No school when there is clear rheumatic activity
D. F/U
Essential to reinforce the necessity for prophylaxis with reg LA benzathine PCN IM
Prevention is critical – greater risk of recurrence if future strep infection not tx
Monitor residual valvular damage
Kawasaki disease
A. Pathophys
Cause unknwn
Leading cause of acquired heart disease in children in US
B. S&S
Fever for at least 5 days + at least 4 of the following:
o Bilat, painless, non-exudative conjunctivitis
o Lip or oral cavity changes (strawberry tongue, cracking, inflame oral mucosa)
o Cervical lymphadenopathy, usually unilat
o Polymorphous exanthema
o Extremity changes (redness, edema of hand & feet, subseq desquamation)
C. Workup: Echocardiogram to detect coronary artery abn
D. Tx
Immediate - IVIG and high dose ASA
Cont low dose ASA thru subacute phase (6-8 wks)
E. F/U
Depends on degree of coronary involvement
No or min coronary disease = Echo at 2wks & 6-8wks after dx is sufficient
Repeat echo or stress testing for those with increased risk
Hypertrophic Cardiomyopathy
A. Pathophys
Familial – leading cause of sudden cardiac death in young persons
Most commonly caused by a mutation in 1 of severel genes that encode proteins of the cardiac sarcomere
B. S&S
May be asx despite significant hypertrophy
Others have angina, syncope, palpitations, exercise intolerance
Cardiac exam may be normal but eventually will develop a left precordial bulge, LV heave or S4 gallop, and possibly a murmur
that may be provoked with exercise
C. Workup
Echocardiogram – dx usually made – assymetrical septal hypertrophy
EKG – May be normal. Typically demonstrates deep Q waves in inferolat leads (II,III,aVF,V5,V6), possibly ST segment changes,
LVH/LAH often
Other: Stress test, nuclear stress test
Cardiac Cath –
D. Tx
Restrict from competitive athletics & isometric exercise
β-blockers, verapamil, or disopyramide for LV outflow tract obstruction
Sugical myectomy with resection of part of septum – good results
Internal defib placement in pts with severe hypertrophy, arrhythmias, ↑ risk of sudden death
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L04: Pediatric Cardiology Objectives
February 17, 2010
Aortic stenosis: This can be valvular (most common), sub or supravalvular.
Essentials of Diagnosis
Systolic ejection murmur at the URSB
Thrill in the carotid arteries
Systolic click at the apex
Dilation of the ascending aorta on chest radiograph.
S/S
Most no cardiovascular symptoms
rd th
Most severe cases- do well until 3 to 5 decade of life- fatigue and exercise intolerance.
LV thrust at apex
Pulses diminished with slow upstroke
Systolic thrill at right base, suprasternal notch, and both carotid arteries.
Aortic ejection click
III-V/VI rough, medium-to-high pitch ejection systolic murmur that radiates to suprasternal notch and
carotids. Grade of murmur does correlate with severity of stenosis.
Definitive treatment
Surgery for symptomatic pts., high resting gradients (60-80 mm Hg difference between the LV and the
aorta) despite balloon angioplasty, or coexisting aortic insufficiency.
All pt need close follow-up. Exercise testing should be done yearly to determine if exercise restriction is
necessary.
Short term and long-term prognosis
All LV outflow tract obstruction is progressive.
Preoperative or postoperative children with mild to moderate obstruction appear to have normal oxygen
consumption and max voluntary working capacity.
Severe stenosis can lead to ventricular dysrhythmias.
Mitral valve prolapse
Essentials of Diagnosis
Midsystolic click best heard with the pt in the standing position or during valsalva maneuver
Late systolic “whooping” or “honking” murmur.
S/S
Usually a finding in older pediatric pts and more common in women.
Asymptomatic
Significant dysrhythmias have been reported.
Systolic click that is accentuated when LV volume is decreased.
Murmur (not pansystolic) after click means mitral insufficiency which is less common than the prolapse.
Definitive treatment
Propranolol for arrhythmias
Antibiotic prophylaxis for endocarditis is needed in pt with mitral insufficiency
Surgery for mitral insufficiency is rarely needed.
Valvular pulmonary stenosis
Essentials of Diagnosis
Classic valve is smooth with doming and fusion of commissures
Pulmonary artery is often severely dilated due to associated collagen defect
Dysplastic valve occurs in Noonan’s syndrome
Pulmonary artery size is normal
Increased resistance to RV outflow, increased RV pressure, decreased pulmonary blood flow
Pulmonary stenosis is often associated with other cardiac lesions
Without shunting, arterial saturation normal
However, severe stenosis causes peripheral cyanosis mostly due to reduced RV compliance and opening of
a patent foramen ovale
S/S
Mild: asymptomatic
Moderate: asymptomatic early, with dyspnea, syncope, and chest pain evolving in adulthood
Severe: right-sided congestive heart failure
Palpable parasternal lift
nd
Loud, harsh systolic ejection murmur and thrill in 2 LICS, radiating to left shoulder; murmur increases with
inspiration
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L04: Pediatric Cardiology Objectives
February 17, 2010
P2 delayed and soft or absent; ejection click decreases with inspiration
Definitive treatment
Treatment indications
o All symptomatic pts
o Pts with resting gradient>50 mm Hg, regardless of symptoms
o Asymptomatic pts with peak gradient >40 mm Hg
Treatment of choice
o Percutaneous balloon valvuloplasty for domed stenotic valve
o Pulmonic valve replacement for dysplastic valve
Short term and long-term prognosis
Pulmonary valvuloplasty has excellent 10-year results, especially if postoperative gradient < 30 mm Hg
Surgery has excellent long-term results but a 2–4% operative mortality rate
Pulmonary atresia (no opening) with intact ventricular septum (uncommon)
Essentials of Diagnosis
Cyanosis at birth
Chest radiograph with a concave pulmonary artery segment and the apex tilted upward.
S/S
Cyanosis worsens when ductus arteriosus closes
PDA murmur if associated.
Pansystolic murmur when significant tricuspid insufficiency develops which is common.
Definitive treatment
Stabilize pt with PGE1 to keep a PDA
Surgery should be done ASAP
Cath- pulmonary valve plate opened to stimulate RV growth.
Ultimate plans are either two-ventricular repair, Fontan procedure, or cardiac transplant depending on pt’s
anatomy.
Short term and long-term prognosis
This is guarded, meaning that it can be very bad (leading to transplant as a child)
Tricuspid atresia (no opening)- rare
Essentials of Diagnosis
Marked cyanosis present from birth
ECG with left axis deviation, right atrial enlargement, and LVH
S/S
Symptoms develop early in infancy
Cyanosis at birth, poor growth and development
Exhaustion during feedings, tachypnea, and dyspnea
May develop CHF
Digital clubbing in older children
VSD murmur usually present, II-III/VI. Heard best at LLSB.
Definitive treatment
Treat congestive symptoms.
PCE1 to open ductus arteriosus until surgical correction can occur
Surgical repair is done in stages (Fontan procedure)
Short term and long-term prognosis
Depends on getting balance of pulmonary blood flow that permits adequate oxygenation of the tissues
without producing CHF.
Long-term prognosis of children with Fontan procedure unknown
Short-term, children with low pulmonary artery pressures prior to open heart surgery have the best results
with Fontan procedure.
More notes
Two normal murmurs in neonates
Closing ductus arteriosus- may be heard in the first 24 hours of life. Where do you hear it?
Pulmonary branch stenosis- occurs in young infants secondary to small size of the branch pulmonary arteries at birth.
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