Cardiovascular Disorders in Pediatrics

Congenital heart disease occurs in about 1% of children. Heart murmurs are much more

The recommendations in blood pressure management are from the National

common, and may be heard in virtually every child if examined carefully.

High Blood Pressure Education Project provides tables that will give you
normal data for blood pressure that varies by age, by height of the patient.

I. Clinical Evaluation of Cardiovascular Disorders

Blood pressure should be measured in all children greater than three years of
age. Blood pressure should be measured from the patient's right arm after they

A. History
1. For neonates, a history of feeding problems, cyanosis, tachypnea, irritability or

have been sitting in a quiet room for three to five minutes. Blood pressure

grunting respirations may indicate serious cardiac pathology. A history of

should be measured twice and the results averaged, and the blood pressure

feeding less than 2 ounces at each feeding in a term infant may indicate

should be measured with an appropriate size cuff. The simplest way to

pathology. A family history of congenital heart disease may be helpful, but the

remember that is to try and get the largest cuff you can get on the child's arm.

incidence of congenital heart disease in families where the mother has

They recommend that in a pediatric practice you have six cuffs. Three small

congenital heart disease is only 5-10%.

cuffs, one adult cuff, a large adult cuff and then a thigh cuff.

2. For older children, it is unusual for a pathologic murmur to present for the first
time outside of infancy. Two notable exceptions are hypertrophic

For definition of the diastolic blood pressure, the fifth Korotkoff sound is used.

cardiomyopathy and murmurs associated with dilated cardiomyopathy.

The fifth sound is when the sound totally disappears. There are patients in

Symptoms which indicate serious pathology include exercise-induced chest

whom the fifth Korotkoff sound never occurs. In other words, the sound never

pain, exercise induced syncope, or cyanosis. Easy fatigability is non specific,

disappears, but then if it goes all the way down to zero, they don't have diastolic

and not helpful in differentiating pathologic from non-pathologic murmurs.

hypertension, which makes sense.

B. Physical Examination
1. Congenital heart disease is more common in infants with congenital anomalies.

Hypertension is defined as a child that has an average systolic or diastolic

a. Trisomy 21. The incidence of heart disease is about 50% in these children.

blood pressure greater than the 95th percentile on three separate occasions,

Anomalies include ventricular septal defects, atrioventricular canal defects,

not all done in the same day. So don't rush into the diagnosis of hypertension.

and patent ductus arteriosus.

Most children that have modest elevations in blood pressure are overweight

b. Trisomy 18. The incidence of heart disease is almost 100%in these

children. Ventricular septal defect is the most common anomaly.

and possibly have a family history of high blood pressure. Those people might
get just a very basic routine screening evaluation which might include a

c. Trisomy 13. The incidence of heart disease is about 80%, usually VSD.

urinalysis (looking for casts, hematuria, proteinuria), a BUN creatinine, looking

d. Turner syndrome (coarctation, hypertension), Marfan syndrome (aortic

for elevation of creatinine consistent with renal disease, and also a good

aneurysms), and Noonan syndrome (pulmonic stenosis, coarctation) are

cardiac physical exam, feeling femoral pulses. Those people would be treated

other congenital anomalies.

with weight reduction, dietary restrictions, and emphasis on physical activity.

2. Growth parameters may suggest failure to thrive that is caused by

cardiovascular disease. Infants with cardiovascular disease usually have a

Patients should not be restricted from physical activity because of mild

elevations in blood pressure.

normal head circumference, and height may be normal, but the weight is usually
People that have significantly elevated blood pressure, and these are the

lower than anticipated.

3. Blood pressure determination. All children 3 years of age and older should

people in the 99th and above percentile, frequently have underlying disease

have their blood pressure measured on a yearly basis. The blood pressure cuff

that is causing their hypertension. It is not idiopathic or familial hypertension.

should be appropriate for the patients size. The width of the cuff should be at

The two organ systems that are most commonly implicated are the renal

least 2/3 the length of the upper arm, and the bladder should be long enough

system and the cardiovascular system. Remember to listen for bruits over the

to almost encircle the upper arm. Blood pressure levels vary depending on the

abdomen because renal artery stenosis is a fairly common cause of significant

age of the child, and hypertension is defined as a blood pressure consistently

hypertension in children, and remember to feel the femoral pulses.

greater than the 95th percentile for age.

a. Presenting symptoms of severe hypertension in infants include congestive

Now, I am going to briefly go over the cardiovascular exam, specifically the

heart failure (caused by coarctation), respiratory distress, and failure to

acyanotic category for an atrioseptal defect (ASD). In order to diagnose an

thrive.

ASD it is not what is outside your ears that is most important. It is what is

b. Symptoms of severe hypertension in older children may include headache,

nausea, vomiting, mental status changes, and epistaxis.
4. Cardiovascular Examination

between your ears that is most important. You need to know what you are
listening for. If you can do a good ASD exam, then you know how to use your
stethoscope. If you can rule out an ASD every time you listen to a patient, you
will refer many fewer functional murmurs for evaluation, and you will miss many

a. Inspection
(1) Conditions that cause cardiac enlargement (ventricular septal defect,

fewer ASDs.

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atrioseptal defect, and a large patent ductus arteriosus) often cause the

The first heart sound at the lower left sternal border, closure of the mitral and

left side of the chest to protrude further than the right.

tricuspid valve. It should be a single sound that you hear with your stethoscope.

(2) In patients with pectus chest deformities, functional murmurs are often

The second heart sound is heard at the upper left sternal border. It is the
closure sound of the aortic and pulmonic valves. In ordinary people, it should

heard.

split and move with respiration. You can't get a two-year-old to take a deep

b. Palpation
(1) In situations where there is a large left to right shunt (ie VSD, ASD) the
precordial activity is often increased.
(2) Displacement of the apical impulse may be associated with cardiac

breath and hold it, but what you listen for is that the second heart sound is not
the same every time. The splitting of the second heart sound is caused by the
patient taking in a breath, augmenting right ventricular filling, and increasing
the time it takes for the right ventricle to eject its contents. In a patient with an

enlargement.
(3) Palpation of femoral pulses is critical in diagnosing coarctation of the

atrial septal defect, the second heart sound is widely split and fixed. The right
ventricle is always filling. It doesnt matter whether the patient took a deep

aorta.

breath or not because blood is going from the left atrium through the atrial

c. Auscultation
(1) Each sound should be listened to separately.

septum into the right atrium. So you hear a widely split and fixed second heart

(2) The first heart sound (S1) is caused by closure of the mitral and

sound. It doesn't vary with respiration.

tricuspid valves, and it should be a single sound heard at the lower left
sternal boarder.

The systolic murmur heard in someone with an ASD can be very soft and not

(a)

The first heart sound may become inaudible at the lower left

easily audible. Many patients with large atrial septal defects have no systolic

sternal border when it is obscured by some pathologic sound. The

murmur. Don't make the diagnosis of an ASD based solely on the presence or

most common pathologic sound obscuring S1 is caused by

absence of a systolic murmur. The cause of a systolic murmur in someone

turbulent flow through a ventricular septal defect (VSD). VSD

with an ASD is flow across the pulmonary valve. It is just a flow murmur, so it

murmurs are termed "holosystolic". Other sounds that could

may sound like other innocent, benign flow murmurs. The fourth and final part

obscure S1 are caused by AV valve regurgitation or by a PDA.

of the examination is the presence of a diastolic sound or a diastolic rumble

(b) First heart sounds that are "split" or double may be caused by

across the tricuspid valve. The blood that courses from the left atrium through

"clicks", or by some a slight timing difference between the closure

the ASD into the right atrium and across the tricuspid valve in diastole makes

of the mitral and the tricuspid valves.

noise. The classic exam is increased precordial activity, normal first heart

Aortic valve clicks are heard best at the apex and do not vary with

sound, a widely split second heart sound, a systolic ejection murmur at the

respiration.

upper left sternal border and a diastolic rumble across the tricuspid valve.

(c)

(d) Pulmonary valve clicks are best heard at the upper left sternal

(e)

border and do vary with respiration.

To examine the precordial activity, put your hand on the chest. You'll feel this

Mitral valve prolapse clicks are a not pathological, and should be

dilated right ventricle beneath your hand and that should be the first tipoff that

ignored unless mitral valve regurgitation is present.

this patient has an ASD and not a functional or innocent murmur. The second

(3) The second heart sound (S2) is caused by the closure of the aortic

is the wideness of that second heart sound. But if you don't put your

and pulmonic valves. The second heart sound should "split" with

stethoscope at the upper left sternal border and really pay attention to what the

respiration.

second heart sound is doing, you'll miss it. The last is the diastolic rumble

(a)

A "fixed split" second heart sound may indicate the presence of

across the tricuspid valve. It is heard best with the bell of the stethoscope

an ASD, especially if associated with increased precordial activity.

placed over the tricuspid valve. Push down with the bell of the stethoscope and

A fixed split S2 may also be seen in patients with complete right

make it function like a diaphragm, so then you'll just hear the systolic and high-

bundle branch block.

frequency sounds. When you let up on the bell of the stethoscope it will begin

(b) A loud single S2 indicates either pulmonary hypertension or the

to act like a bell and you will start to hear low frequency sounds.

absence of a closure sound from one semilunar valve. This may

be seen in severe forms of congenital heart disease, such as
truncus arteriosus, tricuspid atresia, tetralogy of Fallot,
transposition of the great vessels, pulmonary atresia, and
hypoplastic left heart syndrome.
(4) Systolic Murmurs
(a)

Innocent Systolic Murmurs

i)

Peripheral pulmonary flow murmur is heard in most babies

outside of the newborn period.

ii) Still's murmur is often heard for the first time in a 3 to 5 year
old.

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iii) Outflow tract murmurs are often heard in the adolescent and
adult.
(b) Pathologic Systolic Murmurs
i)

Cyanosis is caused by the presence of blue blood coming out into the aorta.

defect.

So patients with ASDs and VSDs should be acyanotic. They have left to right

ii) S1 coincident- VSD, PDA, AV valve regurgitation.

(5) Diastolic murmurs are always pathologic, except venous "hums".
(a)

Aortic valve insufficiency

(b) Pulmonic valve insufficiency

(6) Differentiation of Functional Murmurs from Pathologic Murmurs
(a)

As an example of cyanotic heart disease I am using Tetralogy of Fallot.

Ejection-aortic stenosis, pulmonic stenosis, atrial septal

Serial Exams. Functional murmurs are often louder if the child is

shunts. They have too much red blood going into their lungs but they don't
have blue blood going out into their aorta unless they have some additional
problem like pulmonary vascular disease. The four features of Tetralogy of
Fallot are ventricular septal defect, which sits beneath the aortic valve, the aorta
sitting on top of the VSD, a so-called overriding aorta, right ventricular outflow
tract obstruction and right ventricular hypertrophy.

examined during a high output state, such as when febrile or

when anxious.

The physiology of Tetralogy of Fallot is based solely on the presence of the

(b) Functional murmurs change with position. They are often heard

VSD and obstruction between the right ventricle and the pulmonary artery. So

best when the patient is supine. Standing may result in complete

as long as blood finds it easier to get from the right ventricle into the aorta, the

resolution of the murmur.

patient will be blue. Exactly when patients get intervened upon, that have

II. Cyanotic Congenital Heart Disease

A. Transposition of the Great Vessels

Tetralogy of Fallot, depends upon the severity of their pulmonary stenosis.

Their physical examination, besides the cyanosis, which again is dependent

1. Because these patients are often quite cyanotic, they commonly present in the

upon their amount of pulmonary stenosis, will be that of a child with pulmonary

delivery room, or in the nursery when the patent ductus arteriosus begins to

stenosis. You hear only the most distal obstruction. You won't hear the VSD

close. Occasionally, very dark skinned infants with transposition may go

murmur because there is such a large hole between the left and right ventricles

unrecognized.

that the pressure in the two ventricles is identical, so you won't hear a classic

2. Physical Exam. Increased precordial activity, cyanosis, a single second heart

VSD murmur. All that you will hear is a pulmonary stenosis murmur.

sound, and a systolic "flow" murmur may be apparent.

3. Immediate treatment may include prostaglandin E1 to maintain ductal patency.

Pulmonary stenosis murmurs are unique in that they are associated with clicks.

The initial dose is usually 0.05 micrograms/kg/min. Apnea is a common and

Clicks sound like split first heart sounds. As the mitral and tricuspid valves

dangerous side effect.

close, the pulmonary valve opens and it clicks as it opens, so the split first

4. Surgery usually is performed early in life, and it usually consists of an arterial

heart sound is the simultaneous closure of the mitral and tricuspid valves
followed shortly thereafter by the clicking open of the pulmonary valve.

switch operation.
B. Tetralogy of Fallot. Four primary features consist of ventricular septal defect, right

Pulmonary ejection clicks vary with respiration. So a click that varies with

ventricular outflow tract obstruction, right ventricular hypertrophy, and an

respiration, murmur of the pulmonary valves, is a pulmonary ejection click. In

"overriding" aorta. Only the VSD and the right ventricular outflow tract obstruction

patients with Tetralogy of Fallot, these clicks can be so loud that you can even

are responsible for the physiology.

palpate and feel the clicks and they will disappear when the patient takes in a

1. Presentation depends on the amount of pulmonary blood flow. Patients with little

breath. The systolic murmur is caused by the blood rushing across the right

pulmonary blood flow are very cyanotic, and may need prostaglandin E1 to

ventricular outflow tract.

maintain ductal patency. Patients with less right ventricular outflow tract
obstruction may present with signs of a large left to right shunt, the so-called

Early problems depend upon on the amount of decreased blood flow that the

"pink-tetralogy".

patient has. Hypercyanotic spells, so-called "Tetrology spells". Frequently that

2. Tetralogy spells should be recognized as a dangerous event that require

the mother will call and say that the baby was found in the morning, very

surgical intervention (if possible). A tetralogy spell often occurs early in the

tachypneic and extremely cyanotic. Treatment for that should be knee chest

morning (upon awakening), is accompanied by intense cyanosis, and usually

position, calm down the infant, oxygen. If possible, give morphine once they get

occurs when the child is quiet and tachypneic.

into the Emergency Room. Long term treatment for that should be surgery.

3. Treatment of Tetralogy Spells

a. Knee chest position

Treatment for patients with Tetralogy of Fallot. Everyone that is operating on

b. Oxygen

these patients should achieve a mortality rate in the long run that is somewhere

c. Sedation (morphine)

less than 5%, probably in the 1-2% range. Long term complications of

d. Volume expansion

Tetralogy of Fallot repair include arrhythmias, right ventricular failure, and aortic

4. Intervention consists of repair in the neonatal period or palliation, followed by

repair at an older age. Survival should exceed 95%.

valve insufficiency, and probably the most common now is right ventricular
failure.

5. Because of abnormalities of the pulmonary arteries, some patients may be not

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be candidates for surgery. These patients may have long term complications

Long term survival after Tetralogy of Fallot repair should be excellent. After

related to the cyanosis and the polycythemia, including:

surgery patients have a 93% 20 year survival rate. In current years, this long

a. Headache

term survival rate should be even higher. So just as a reminder, when you do

b. Altered mental status

a cardiovascular exam, I would implore you to try to do an ASD exam anytime

c. Stroke

you are trying to critically evaluate a murmur. If you go through that whole

d. Epistaxis

scenario, precordial activity, first heart sound, second heart sound, systole and

e. Hemoptysis

diastole, I think that you will have to refer fewer functional or innocent murmurs

f.

and you won't miss many ASDs.

Hyperuricemia and gout

III. Acute Management of Rhythm Disorders

A. A 12 lead ECG should be obtained during and after the tachycardia episode.

A pediatric cardiologist referral. Anybody that is symptomatic; If they are

B. Narrow QRS complex tachycardia

cyanotic, failure to thrive, or if you suspect that they have congestive heart

1. Sinus tachycardia (less than 220 beats/minute) may be caused by exogenous

substances (beta agonist) or hyperthyroidism.

failure, they should be sent when you suspect it. Also, patients that have
syndromes. All children with Trisomy 21 should be evaluated by a pediatric

2. If the rate is very rapid and the child is hemodynamically unstable, direct current

cardiologist at least once. There is no other screening test that you run in

cardioversion is recommended with 0.5 watt-seconds/kg, synchronize the

medicine that has a 50% true positive rate other than cardiology evaluation of

defibrillator.

Down's syndrome because half of them will have significant congenital heart

3. If the child is stable, vagal maneuvers such as an ice bag, abdominal pressure

disease. Asymptomatic patients with pathological murmurs, and I don't mean

or rectal stimulation may be successful. If vagal maneuvers are not successful,

the grade 5, PS murmurs, but I'm talking about somebody that you're not sure

adenosine may be given IV. The initial dose is 50 micrograms/kg given iv push.

if they have a tiny little muscular VSD or not. Or you're not sure if they have

The dose may be increased up to a dose of 300 micrograms/kg. Adenosine will

mild pulmonary stenosis. You should not send them until the children are over

only momentarily block AV conduction; therefore, if the patient has recurrent

two years of age, because many of those VSDs will close spontaneously. Many

SVT, adenosine will not help for more than a few seconds, and some other

of the children that have right ventricular outflow tract murmurs, as the

intervention should be used.

pulmonary arteries dilate, those murmurs will go away. If they didn't have that
done when they were three-months-old for this outflow tract murmur, frequently

C. Wide QRS Complex Tachycardia

1. If the patient is hemodynamically unstable, DC cardioversion is necessary.

the cardiologist is going to see an ASD and have to see them back to do

2. If the patient is stable, vagal maneuvers may help differentiate between SVT

another surgery.

with aberrant conduction and ventricular tachycardia.

D. Bradycardia. If the patient is stable hemodynamically the bradycardia may be of
long standing duration. Sinus bradycardia is common in the athletes, or it may
occur with complete heart block. Unstable bradycardia may be palliated with
isoproterenol or
transthoracic pacing. Long term therapy involves placement of a pacemaker.
IV. Rheumatic Fever
A. Diagnosis is based on a modification of the Jones criteria. The criteria are divided
into major and minor categories. Diagnosis requires two major criteria, or one major
and two minor criteria. The patients must have evidence of a preceding
streptococcal infection (should be present in all cases except some patients with
chorea). Evidence of a preceding streptococcal infection includes either a positive
culture, positive ASO titre or recent history of scarlet fever.

Jones Criteria for Rheumatic Fever

Major Criteria

Minor Criteria

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1. Carditis

1. Fever

2. Polyarthritis

2. Arthralgia (not when arthritis is used

as a major)

3. Chorea
4. Subcutaneous nodules

3. Prolonged PR interval on the ECG

5. Erythema marginatum

(not when carditis is used as a

major)
4. Increased acute phase reactants
(ESR, WBC or C-reactive protein)
5.Previous history of rheumatic fever

Inflammatory heart disease. Kawasaki's syndrome consists of fever over

101.5F for greater than five days, rash, conjunctivitis, swollen hands and feet,
oral

mucous

membrane

changes,

and

lymphadenopathy.

The

lymphadenopathy is the least specific of all the signs, and it is only seen in
between 50-70% of children with diagnosis of Kawasaki's. The rash can be
anything from a diaper dermatitis looking rash to a rash that looks like scarlet
fever. The conjunctivitis is very helpful. It usually spares the area around the
iris; beet red conjunctivitis but nonpurulent. If they have purulent conjunctivitis
you probably need to look for some other diagnosis. The hands can look like

V. Endocarditis
A.

Incidence is between 11 and 50 cases per million/year.

B.

Most common organisms

they were banging them on something hard. They can get swollen and the feet
can be so involved that the children cannot walk. The lips, dry, cracked, red.
Also the tongue will have a "strawberry" appearance. Two weeks after the

1. Alpha hemolytic strep

illness, their hands and feet will peel.

2. Staphylococcus aureus
3. Staphylococcus epidermidis

The etiology. In 1996 a paper was published where patients that had

4. Enterococci

Kawasaki's syndrome, had oral, rectal and skin cultures performed. Twelve of

C. Clinical Evaluation
1. Fever, heart murmur, splenomegaly (seen in <50%).
2. Less common features include petechiae, splinter hemorrhages, retinal
hemorrhages (Roth spot), systemic emboli, renal insufficiency.
3. Positive blood cultures, elevated ESR.

the 16 patients were culture positive for superantigen producing

staphylococcus. The hypothesis is that the Staph produces the superantigen,
and then it is the immunogenic reaction to that superantigen that causes
Kawasaki's.

4. Echocardiography is indicated if endocarditis is suspected clinically.

5. Antibiotic Prophylaxis Against Endocarditis
a. Prophylaxis is necessary for all children with high velocity jets in their hearts
(VSD, aortic stenosis, pulmonic stenosis, history of rheumatic fever with
valve damage, mitral or tricuspid regurgitation, patent ductus arteriosus,
surgically created shunts)
b. Prophylaxis is not necessary for atrial septal defect or mitral valve prolapse
without mitral regurgitation because there are no areas of high velocity blood

Therapy for Kawasaki's. Aspirin is also given concurrent with the gamma
globulin. The current dose of gamma globulin is 2 gm/kg given intravenously.
It is a one time dose. It is no longer the 400 mg over 5 days. Remember though
that these patients are under some bit of cardiovascular stress when they're
sick and you're giving them a large protein load when you give them the gamma
globulin. So they can get tachypneic or tachycardic while they're getting their
gamma globulin. You might have to decrease the rate a little bit and you might
have to give them diuretics, but the gamma globulin is the cure. Don't stop

flow.
c. Endocarditis prophylaxis is given when bacteremia is anticipated, such as

giving it just because they appear to be having some problems with the protein.

with dental cleanings, tonsillectomy, or cystoscopy.

d. Prophylaxis is not recommended for cardiac catheterization, orthodontic
manipulation, or tympanostomy tube placement.
e. SBE prophylaxis usually consists of one dose of amoxicillin, one given
before the dental procedure.

5% of patients develop coronary artery aneurysms. Patients that do badly and

require a lot of intensive follow up are those that have so-called giant
aneurysms. By giant I mean greater than 8 mm. One of the major problems is
that giant aneurysms develop and that is stenosis. You see the left anterior

VI. Kawasaki Syndrome

A.

Complications of Kawasaki's syndrome are coronary artery aneurysms. Around

KS is a multisystem probably infectious disease with an uncertain etiology. Recent

theories suggest the patients with KS have a high incidence of superantigen

descending coronary artery stops right there. This patient might benefit from
coronary artery bypass grafting.

producing staphylococcus aureus or group A beta-hemolytic streptococci.

B.

Diagnosis of KS is based on the presence of five of the following:

1. Fever lasting five days or longer

Follow up in patients with Kawasaki's depends on the severity of their coronary

involvement. People that have no pulmonary involvement or minimal pulmonary
involvement that returns to normal can be released and followed up after

2. Polymorphous exanthem
3. Redness or induration of the hands and/or feet
4. Bilateral non purulent conjunctival injection

approximately one year and should be treated as normal for the remainder of
their lives.

5. Erythema of the lips or tongue

6. Non-purulent swelling of the cervical lymph nodes
C. Complications include coronary artery aneurysms, seen in as many as 20% of
untreated cases.

Endocarditis. There are between 11 and 50 cases per million population per
year, which comes out to about 4,000 to 8,000 cases of endocarditis across
the United States per year. Most of those people that develop endocarditis, at

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1. Treated cases have a 2% incidence of aneurysms.

least 75% have some underlying cardiovascular etiology - either mitral valve

2. About 50% of aneurysms resolve spontaneously

insufficiency, a ventricular septal defect, an abnormal aortic valve, etc.

D. Treatment of Kawasaki Syndrome

1. High dose aspirin (100 mg/kg) is continued until signs of inflammation have
subsided. This may be based on laboratory (ESR) or clinical grounds.
2. IV gamma globulin (2 grams/kg given over 8 to 12 hours).
a. Most gamma globulin contains high concentrations of antibodies that inhibit
T cell response to staphylococcal superantigens.
b. Patients with clinical failure to IV gamma globulin should be retreated.

Diagnosis is based not on fever and go straight to an echo, but repeated

positive blood cultures with the same organism, possibly associated with
systemic emboli and then go to an echo. But an echo has extremely low
sensitivity and specificity if used as a sort of front line tool to rule out
endocarditis. Prevention of endocarditis. The best we can do is so-called
antibiotic prophylaxis at times of endocarditis risk. What that means is that any
patient that you have that is at risk for developing endocarditis and what that

3. Long Term Follow-up

a. The vast majority of children with Kawasaki syndrome will have no
aneurysms and will have completed therapy within 6 to 8 weeks.
b. Children with coronary changes that resolve quickly do not require
medication and should have no exercise restrictions.
c. Children with chronic aneurysms require long term follow up, exercise
testing, and exercise restrictions.

means is that they have a high velocity jet lesion somewhere in their
cardiovascular system, those people should receive antibiotics prior to
becoming predictably bacteremic. That doesn't mean that the child just fell in
a mud puddle and scraped his knee. You couldn't predict that. So they don't
get antibiotics retrospectively for something like that. But they do get it when
they do to the dentist, if they are going to have cystoscopy, rigid bronchoscopy,
sigmoidoscopy, etc. Procedures that would cause them to become predictably
bacteremic. Even in cases with prosthetic valves, the American Heart
Association recommends that the prophylaxis be performed with amoxicillin.
No longer do you have to admit them and put them on IV antibiotics unless they
have things like antibiotic allergies or other problems.

Just to hammer home the point of the high velocity jets. Patients with VSDs,
for example, where blood is flying through from the left ventricle to the right
ventricle. Those patients should receive antibiotic prophylaxis at time of
endocarditis risk. Patients with mitral valve regurgitation. This echocardiogram
depicts the turbulence of blood as it comes across the mitral valve in systole.
Patients that have mitral valve prolapse clicks, just the click, but no mitral valve
insufficiency, the American Heart Association is very clear that those people
do not require antibiotic prophylaxis at time of endocarditis risk. Six percent of
normal females in your practice should have clicks of mitral valve prolapse
which I would hope you would diagnose as split first heart sounds. Two
percent of males should have those same clicks, but only about 0.2 or 0.4%
should have a click and murmur of mitral valve regurgitation. Those are the
people that have true mitral valve disease that would have an echocardiogram
like this and would be at risk for developing endocarditis.

Children that are not at risk for developing endocarditis are those that have low
velocity shunts within their heart. This is an echocardiogram of a child with an
atrial septal defect. You can see blood coursing through the ASD and it is
laminar, it doesnt speed up, it doesn't change colors, it doesn't make any
noise. So it doesn't denude the epithelium as blood comes across the atrial
septum, across the tricuspid valve in diastole. Patients with ASD do not require
antibiotic prophylaxis at times of endocarditis risk. Procedures that do not
cause you to become bacteremic are for example tympanostomy tubes. There
are not enough blood vessels in the tympanic membrane to cause you to
become bacteremic when you put the tympanostomy tubes in place.

In summary, when we talk about blood pressure measurement, I would

encourage you to try and get a hold of that article that was in Pediatrics in

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October of 1996. Those tables can be very useful. Don't overcall hypertension.
Somebody has got to be in the 95th percentile on average for three separate
evaluations. Remember how to do the ASD exam and try to do that on every
single patient that you evaluate before referring to a pediatric cardiologist. For
inflammatory heart disease remember the diagnostic criteria for Kawasaki's.

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