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. 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. 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 patients 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, 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. 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. 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. 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. 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.

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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 doesnt 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 highfrequency 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 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.

(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

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

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.

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. 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.

Jones Criteria for Rheumatic Fever Major Criteria Minor Criteria

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1. Carditis 2. Polyarthritis 3. Chorea 4. Subcutaneous nodules 5. Erythema marginatum

1. Fever 2. Arthralgia (not when arthritis is used as a major) 3. Prolonged PR interval on the ECG (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

V. Endocarditis A. B. Incidence is between 11 and 50 cases per million/year. Most common organisms 1. Alpha hemolytic strep 2. Staphylococcus aureus 3. Staphylococcus epidermidis 4. Enterococci 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. 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 flow. c. Endocarditis prophylaxis is given when bacteremia is anticipated, such as 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. VI. Kawasaki Syndrome A. KS is a multisystem probably infectious disease with an uncertain etiology. Recent 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: 1. Fever lasting five days or longer 2. Polymorphous exanthem 3. Redness or induration of the hands and/or feet 4. Bilateral non purulent conjunctival injection 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.

you probably need to look for some other diagnosis. The hands can look like 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 illness, their hands and feet will peel.

The etiology. In 1996 a paper was published where patients that had Kawasaki's syndrome, had oral, rectal and skin cultures performed. Twelve of 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.

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

Complications of Kawasaki's syndrome are coronary artery aneurysms. Around 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 descending coronary artery stops right there. This patient might benefit from coronary artery bypass grafting.

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

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. 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 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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