Cardiovascular Disorders in Pediatrics

Cardiovascular Disorders in Pediatrics
Congenital heart disease occurs in about 1% of children. Heart murmurs are much more
common, and may be heard in virtually every child if examined carefully.
I. Clinical Evaluation of Cardiovascular Disorders
A. History
1. For neonates, a history of feeding problems, cyanosis, tachypnea, irritability or
grunting respirations may indicate serious cardiac pathology. A history of
feeding less than 2 ounces at each feeding in a term infant may indicate
pathology. A family history of congenital heart disease may be helpful, but the
incidence of congenital heart disease in families where the mother has
congenital heart disease is only 5-10%.
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
cardiomyopathy and murmurs associated with dilated cardiomyopathy.
Symptoms which indicate serious pathology include exercise-induced chest
pain, exercise induced syncope, or cyanosis. Easy fatigability is non specific,
and not helpful in differentiating pathologic from non-pathologic murmurs.
B. Physical Examination
1. Congenital heart disease is more common in infants with congenital anomalies.
a. Trisomy 21. The incidence of heart disease is about 50% in these children.
Anomalies include ventricular septal defects, atrioventricular canal defects,
and patent ductus arteriosus.
b. Trisomy 18. The incidence of heart disease is almost 100%in these
children. Ventricular septal defect is the most common anomaly.
c. Trisomy 13. The incidence of heart disease is about 80%, usually VSD.
d. Turner syndrome (coarctation, hypertension), Marfan syndrome (aortic
aneurysms), and Noonan syndrome (pulmonic stenosis, coarctation) are
other congenital anomalies.
2. Growth parameters may suggest failure to thrive that is caused by
cardiovascular disease. Infants with cardiovascular disease usually have a
normal head circumference, and height may be normal, but the weight is usually
lower than anticipated.
3. Blood pressure determination. All children 3 years of age and older should
have their blood pressure measured on a yearly basis. The blood pressure cuff
should be appropriate for the patient’s size. The width of the cuff should be at
least 2/3 the length of the upper arm, and the bladder should be long enough
to almost encircle the upper arm. Blood pressure levels vary depending on the
age of the child, and hypertension is defined as a blood pressure consistently
greater than the 95th percentile for age.
a. Presenting symptoms of severe hypertension in infants include congestive
heart failure (caused by coarctation), respiratory distress, and failure to
thrive.
b. Symptoms of severe hypertension in older children may include headache,
nausea, vomiting, mental status changes, and epistaxis.
4. Cardiovascular Examination
a. Inspection
(1) Conditions that cause cardiac enlargement (ventricular septal defect,
The recommendations in blood pressure management are from the National
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.
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
have been sitting in a quiet room for three to five minutes. Blood pressure
should be measured twice and the results averaged, and the blood pressure
should be measured with an appropriate size cuff. The simplest way to
remember that is to try and get the largest cuff you can get on the child's arm.
They recommend that in a pediatric practice you have six cuffs. Three small
cuffs, one adult cuff, a large adult cuff and then a thigh cuff.
For definition of the diastolic blood pressure, the fifth Korotkoff sound is used.
The fifth sound is when the sound totally disappears. There are patients in
whom the fifth Korotkoff sound never occurs. In other words, the sound never
disappears, but then if it goes all the way down to zero, they don't have diastolic
hypertension, which makes sense.
Hypertension is defined as a child that has an average systolic or diastolic
blood pressure greater than the 95th percentile on three separate occasions,
not all done in the same day. So don't rush into the diagnosis of hypertension.
Most children that have modest elevations in blood pressure are overweight
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
urinalysis (looking for casts, hematuria, proteinuria), a BUN creatinine, looking
for elevation of creatinine consistent with renal disease, and also a good
cardiac physical exam, feeling femoral pulses. Those people would be treated
with weight reduction, dietary restrictions, and emphasis on physical activity.
Patients should not be restricted from physical activity because of mild
elevations in blood pressure.
People that have significantly elevated blood pressure, and these are the
people in the 99th and above percentile, frequently have underlying disease
that is causing their hypertension. It is not idiopathic or familial hypertension.
The two organ systems that are most commonly implicated are the renal
system and the cardiovascular system. Remember to listen for bruits over the
abdomen because renal artery stenosis is a fairly common cause of significant
hypertension in children, and remember to feel the femoral pulses.
Now, I am going to briefly go over the cardiovascular exam, specifically the
acyanotic category for an atrioseptal defect (ASD). In order to diagnose an
ASD it is not what is outside your ears that is most important. It is what is
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
fewer ASDs.

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atrioseptal defect, and a large patent ductus arteriosus) often cause the
left side of the chest to protrude further than the right.
(2) In patients with pectus chest deformities, functional murmurs are often
heard.
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
enlargement.
(3) Palpation of femoral pulses is critical in diagnosing coarctation of the
aorta.
c. Auscultation
(1) Each sound should be listened to separately.
(2) The first heart sound (S1) is caused by closure of the mitral and
tricuspid valves, and it should be a single sound heard at the lower left
sternal boarder.
(a) The first heart sound may become inaudible at the lower left
sternal border when it is obscured by some pathologic sound. The
most common pathologic sound obscuring S1 is caused by
turbulent flow through a ventricular septal defect (VSD). VSD
murmurs are termed "holosystolic". Other sounds that could
obscure S1 are caused by AV valve regurgitation or by a PDA.
(b) First heart sounds that are "split" or double may be caused by
"clicks", or by some a slight timing difference between the closure
of the mitral and the tricuspid valves.
(c) Aortic valve clicks are heard best at the apex and do not vary with
respiration.
(d) Pulmonary valve clicks are best heard at the upper left sternal
border and do vary with respiration.
(e) Mitral valve prolapse clicks are a not pathological, and should be
ignored unless mitral valve regurgitation is present.
(3) The second heart sound (S2) is caused by the closure of the aortic
and pulmonic valves. The second heart sound should "split" with
respiration.
(a) A "fixed split" second heart sound may indicate the presence of
an ASD, especially if associated with increased precordial activity.
A fixed split S2 may also be seen in patients with complete right
bundle branch block.
(b) A loud single S2 indicates either pulmonary hypertension or the
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.
The first heart sound at the lower left sternal border, closure of the mitral and
tricuspid valve. It should be a single sound that you hear with your stethoscope.
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
split and move with respiration. You can't get a two-year-old to take a deep
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
atrial septal defect, the second heart sound is widely split and fixed. The right
ventricle is always filling. It doesn’t matter whether the patient took a deep
breath or not because blood is going from the left atrium through the atrial
septum into the right atrium. So you hear a widely split and fixed second heart
sound. It doesn't vary with respiration.
The systolic murmur heard in someone with an ASD can be very soft and not
easily audible. Many patients with large atrial septal defects have no systolic
murmur. Don't make the diagnosis of an ASD based solely on the presence or
absence of a systolic murmur. The cause of a systolic murmur in someone
with an ASD is flow across the pulmonary valve. It is just a flow murmur, so it
may sound like other innocent, benign flow murmurs. The fourth and final part
of the examination is the presence of a diastolic sound or a diastolic rumble
across the tricuspid valve. The blood that courses from the left atrium through
the ASD into the right atrium and across the tricuspid valve in diastole makes
noise. The classic exam is increased precordial activity, normal first heart
sound, a widely split second heart sound, a systolic ejection murmur at the
upper left sternal border and a diastolic rumble across the tricuspid valve.
To examine the precordial activity, put your hand on the chest. You'll feel this
dilated right ventricle beneath your hand and that should be the first tipoff that
this patient has an ASD and not a functional or innocent murmur. The second
is the wideness of that second heart sound. But if you don't put your
stethoscope at the upper left sternal border and really pay attention to what the
second heart sound is doing, you'll miss it. The last is the diastolic rumble
across the tricuspid valve. It is heard best with the bell of the stethoscope
placed over the tricuspid valve. Push down with the bell of the stethoscope and
make it function like a diaphragm, so then you'll just hear the systolic and high-
frequency sounds. When you let up on the bell of the stethoscope it will begin
to act like a bell and you will start to hear low frequency sounds.

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iii) Outflow tract murmurs are often heard in the adolescent and
adult.
(b) Pathologic Systolic Murmurs
i) Ejection-aortic stenosis, pulmonic stenosis, atrial septal
defect.
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) Serial Exams. Functional murmurs are often louder if the child is
examined during a high output state, such as when febrile or
when anxious.
(b) Functional murmurs change with position. They are often heard
best when the patient is supine. Standing may result in complete
resolution of the murmur.
II. Cyanotic Congenital Heart Disease
A. Transposition of the Great Vessels
1. Because these patients are often quite cyanotic, they commonly present in the
delivery room, or in the nursery when the patent ductus arteriosus begins to
close. Occasionally, very dark skinned infants with transposition may go
unrecognized.
2. Physical Exam. Increased precordial activity, cyanosis, a single second heart
sound, and a systolic "flow" murmur may be apparent.
3. Immediate treatment may include prostaglandin E1 to maintain ductal patency.
The initial dose is usually 0.05 micrograms/kg/min. Apnea is a common and
dangerous side effect.
4. Surgery usually is performed early in life, and it usually consists of an arterial
switch operation.
B. Tetralogy of Fallot. Four primary features consist of ventricular septal defect, right
ventricular outflow tract obstruction, right ventricular hypertrophy, and an
"overriding" aorta. Only the VSD and the right ventricular outflow tract obstruction
are responsible for the physiology.
1. Presentation depends on the amount of pulmonary blood flow. Patients with little
pulmonary blood flow are very cyanotic, and may need prostaglandin E1 to
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
"pink-tetralogy".
2. Tetralogy spells should be recognized as a dangerous event that require
surgical intervention (if possible). A tetralogy spell often occurs early in the
morning (upon awakening), is accompanied by intense cyanosis, and usually
occurs when the child is quiet and tachypneic.
3. Treatment of Tetralogy Spells
a. Knee chest position
b. Oxygen
c. Sedation (morphine)
d. Volume expansion
4. Intervention consists of repair in the neonatal period or palliation, followed by
repair at an older age. Survival should exceed 95%.
5. Because of abnormalities of the pulmonary arteries, some patients may be not
As an example of cyanotic heart disease I am using Tetralogy of Fallot.
Cyanosis is caused by the presence of blue blood coming out into the aorta.
So patients with ASDs and VSDs should be acyanotic. They have left to right
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.
The physiology of Tetralogy of Fallot is based solely on the presence of the
VSD and obstruction between the right ventricle and the pulmonary artery. So
as long as blood finds it easier to get from the right ventricle into the aorta, the
patient will be blue. Exactly when patients get intervened upon, that have
Tetralogy of Fallot, depends upon the severity of their pulmonary stenosis.
Their physical examination, besides the cyanosis, which again is dependent
upon their amount of pulmonary stenosis, will be that of a child with pulmonary
stenosis. You hear only the most distal obstruction. You won't hear the VSD
murmur because there is such a large hole between the left and right ventricles
that the pressure in the two ventricles is identical, so you won't hear a classic
VSD murmur. All that you will hear is a pulmonary stenosis murmur.
Pulmonary stenosis murmurs are unique in that they are associated with clicks.
Clicks sound like split first heart sounds. As the mitral and tricuspid valves
close, the pulmonary valve opens and it clicks as it opens, so the split first
heart sound is the simultaneous closure of the mitral and tricuspid valves
followed shortly thereafter by the clicking open of the pulmonary valve.
Pulmonary ejection clicks vary with respiration. So a click that varies with
respiration, murmur of the pulmonary valves, is a pulmonary ejection click. In
patients with Tetralogy of Fallot, these clicks can be so loud that you can even
palpate and feel the clicks and they will disappear when the patient takes in a
breath. The systolic murmur is caused by the blood rushing across the right
ventricular outflow tract.
Early problems depend upon on the amount of decreased blood flow that the
patient has. Hypercyanotic spells, so-called "Tetrology spells". Frequently that
the mother will call and say that the baby was found in the morning, very
tachypneic and extremely cyanotic. Treatment for that should be knee chest
position, calm down the infant, oxygen. If possible, give morphine once they get
into the Emergency Room. Long term treatment for that should be surgery.
Treatment for patients with Tetralogy of Fallot. Everyone that is operating on
these patients should achieve a mortality rate in the long run that is somewhere
less than 5%, probably in the 1-2% range. Long term complications of
Tetralogy of Fallot repair include arrhythmias, right ventricular failure, and aortic
valve insufficiency, and probably the most common now is right ventricular
failure.

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be candidates for surgery. These patients may have long term complications
related to the cyanosis and the polycythemia, including:
a. Headache
b. Altered mental status
c. Stroke
d. Epistaxis
e. Hemoptysis
f. Hyperuricemia and gout
III. Acute Management of Rhythm Disorders
A. A 12 lead ECG should be obtained during and after the tachycardia episode.
B. Narrow QRS complex tachycardia
1. Sinus tachycardia (less than 220 beats/minute) may be caused by exogenous
substances (beta agonist) or hyperthyroidism.
2. If the rate is very rapid and the child is hemodynamically unstable, direct current
cardioversion is recommended with 0.5 watt-seconds/kg, synchronize the
defibrillator.
3. If the child is stable, vagal maneuvers such as an ice bag, abdominal pressure
or rectal stimulation may be successful. If vagal maneuvers are not successful,
adenosine may be given IV. The initial dose is 50 micrograms/kg given iv push.
The dose may be increased up to a dose of 300 micrograms/kg. Adenosine will
only momentarily block AV conduction; therefore, if the patient has recurrent
SVT, adenosine will not help for more than a few seconds, and some other
intervention should be used.
C. Wide QRS Complex Tachycardia
1. If the patient is hemodynamically unstable, DC cardioversion is necessary.
2. If the patient is stable, vagal maneuvers may help differentiate between SVT
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
Long term survival after Tetralogy of Fallot repair should be excellent. After
surgery patients have a 93% 20 year survival rate. In current years, this long
term survival rate should be even higher. So just as a reminder, when you do
a cardiovascular exam, I would implore you to try to do an ASD exam anytime
you are trying to critically evaluate a murmur. If you go through that whole
scenario, precordial activity, first heart sound, second heart sound, systole and
diastole, I think that you will have to refer fewer functional or innocent murmurs
and you won't miss many ASDs.
A pediatric cardiologist referral. Anybody that is symptomatic; If they are
cyanotic, failure to thrive, or if you suspect that they have congestive heart
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
cardiologist at least once. There is no other screening test that you run in
medicine that has a 50% true positive rate other than cardiology evaluation of
Down's syndrome because half of them will have significant congenital heart
disease. Asymptomatic patients with pathological murmurs, and I don't mean
the grade 5, PS murmurs, but I'm talking about somebody that you're not sure
if they have a tiny little muscular VSD or not. Or you're not sure if they have
mild pulmonary stenosis. You should not send them until the children are over
two years of age, because many of those VSDs will close spontaneously. Many
of the children that have right ventricular outflow tract murmurs, as the
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
the cardiologist is going to see an ASD and have to see them back to do
another surgery.

1. Carditis 1. Fever
2. Polyarthritis 2. Arthralgia (not when arthritis is used
Inflammatory heart disease. Kawasaki's syndrome consists of fever over
3. Chorea as a major)
4. Subcutaneous nodules 3. Prolonged PR interval on the ECG
101.5ºF for greater than five days, rash, conjunctivitis, swollen hands and feet,
5. Erythema marginatum (not when carditis is used as a
oral mucous membrane changes, and lymphadenopathy. The
major)
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
4. Increased acute phase reactants
anything from a diaper dermatitis looking rash to a rash that looks like scarlet
(ESR, WBC or C-reactive protein)
fever. The conjunctivitis is very helpful. It usually spares the area around the
5.Previous history of rheumatic fever
iris; beet red conjunctivitis but nonpurulent. If they have purulent conjunctivitis
V. Endocarditis you probably need to look for some other diagnosis. The hands can look like
A. Incidence is between 11 and 50 cases per million/year. they were banging them on something hard. They can get swollen and the feet
B. can be so involved that the children cannot walk. The lips, dry, cracked, red. Most common organisms
Also the tongue will have a "strawberry" appearance. Two weeks after the 1. Alpha hemolytic strep
2. Staphylococcus aureus illness, their hands and feet will peel.
3. Staphylococcus epidermidis
4. Enterococci The etiology. In 1996 a paper was published where patients that had
C. Clinical Evaluation Kawasaki's syndrome, had oral, rectal and skin cultures performed. Twelve of
the 16 patients were culture positive for superantigen producing1. Fever, heart murmur, splenomegaly (seen in <50%).
2. Less common features include petechiae, splinter hemorrhages, retinal staphylococcus. The hypothesis is that the Staph produces the superantigen,
hemorrhages (Roth spot), systemic emboli, renal insufficiency. and then it is the immunogenic reaction to that superantigen that causes
3. Positive blood cultures, elevated ESR. Kawasaki's.
4. Echocardiography is indicated if endocarditis is suspected clinically.
Therapy for Kawasaki's. Aspirin is also given concurrent with the gamma 5. Antibiotic Prophylaxis Against Endocarditis
globulin. The current dose of gamma globulin is 2 gm/kg given intravenously. a. Prophylaxis is necessary for all children with high velocity jets in their hearts
(VSD, aortic stenosis, pulmonic stenosis, history of rheumatic fever with It is a one time dose. It is no longer the 400 mg over 5 days. Remember though
valve damage, mitral or tricuspid regurgitation, patent ductus arteriosus, that these patients are under some bit of cardiovascular stress when they're
surgically created shunts) 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 b. Prophylaxis is not necessary for atrial septal defect or mitral valve prolapse
gamma globulin. You might have to decrease the rate a little bit and you might without mitral regurgitation because there are no areas of high velocity blood
flow. have to give them diuretics, but the gamma globulin is the cure. Don't stop
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. Complications of Kawasaki's syndrome are coronary artery aneurysms. Around Prophylaxis is not recommended for cardiac catheterization, orthodontic
5% of patients develop coronary artery aneurysms. Patients that do badly and manipulation, or tympanostomy tube placement.
e. SBE prophylaxis usually consists of one dose of amoxicillin, one given require a lot of intensive follow up are those that have so-called giant
before the dental procedure. aneurysms. By giant I mean greater than 8 mm. One of the major problems is
VI. Kawasaki Syndrome that giant aneurysms develop and that is stenosis. You see the left anterior
A. KS is a multisystem probably infectious disease with an uncertain etiology. Recent descending coronary artery stops right there. This patient might benefit from
coronary artery bypass grafting.theories suggest the patients with KS have a high incidence of superantigen
producing staphylococcus aureus or group A beta-hemolytic streptococci.
B. Diagnosis of KS is based on the presence of five of the following: Follow up in patients with Kawasaki's depends on the severity of their coronary
1. Fever lasting five days or longer involvement. People that have no pulmonary involvement or minimal pulmonary
2. Polymorphous exanthem involvement that returns to normal can be released and followed up after
approximately one year and should be treated as normal for the remainder of 3. Redness or induration of the hands and/or feet
their lives.4. Bilateral non purulent conjunctival injection
5. Erythema of the lips or tongue
6. Non-purulent swelling of the cervical lymph nodes Endocarditis. There are between 11 and 50 cases per million population per
C. Complications include coronary artery aneurysms, seen in as many as 20% of year, which comes out to about 4,000 to 8,000 cases of endocarditis across
untreated cases. 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.
2. About 50% of aneurysms resolve spontaneously
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.
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.
least 75% have some underlying cardiovascular etiology - either mitral valve
insufficiency, a ventricular septal defect, an abnormal aortic valve, etc.
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
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 doesn’t 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.