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Diagnosis of Heart conditions

Heart conditions Diagnosis: Book Excerpts

• Ask the following questions - CARDIAC MURMURS
• Ask the following questions - CARDIAC ARRHYTHMIA
• Differential Diagnosis - Gallops & Extra Heart Sounds
• Differential Diagnosis - Irregular Heart Rhythms
• Differential Diagnosis - Murmurs - Diastolic
• Differential Diagnosis - Murmurs - Systolic
• Differential Diagnosis - Abnormal Heart Sounds
• Differential Diagnosis - Heart Failure
• Approach to the Diagnosis - MURMURS
• Approach to the Diagnosis - CARDIAC ARRHYTHMIAS
• History and physical examination - Murmurs
• History and physical examination - Pulse rhythm abnormality
• Diagnosis - Cardiac arrhythmias
• Diagnosis - Cardiac tamponade
• Diagnosis - Rheumatic fever and rheumatic heart disease
• History and physical examination - Murmurs
• History and physical examination - Pulse rhythm abnormality
• History - Heart Murmur, Diastolic
• History - Heart Murmur, Systolic
• History - Congestive Heart Failure
• Differential Overview - Cardiomegaly/Congestive Heart Failure
• Differential Overview - Discrete Heart Sounds
• Differential Overview - Diastolic Murmur
• Differential Overview - Systolic Murmur
• Differential Overview - Continuous Murmur
• Diagnosis - Cardiac tamponade
• Diagnosis - Heart failure
• Diagnosis - Rheumatic fever and rheumatic heart disease
• History - Murmurs
• History - Pulse rhythm abnormality
• History - Murmurs
• History - Pulse rhythm abnormality
• Clinical Features and Diagnosis - Heart Murmurs (Asymptomatic)
• Clinical Features and Diagnosis - Cardiac Failure
• History and physical examination - Murmurs
• History and physical examination - Pulse rhythm abnormality
• Approach to the Diagnosis - MURMURS
• Approach to the Diagnosis - CARDIAC ARRHYTHMIAS
• Learning Problems - DIAGNOSIS - Learning Problems

Diagnosis of Heart conditions: medical news summaries:

The following medical news items are relevant to diagnosis and misdiagnosis issues for Heart conditions:

• ADHD medication highlighted heart disorder
• Greater awareness needed of cardiac conditions that can cause sudden death
• Heart transplant has a good prognosis despite difficult journey
• Lupus treatment has improved over the years
• Symptoms of old age may be similar to many other treatable conditions
• Thyroid disorder underdiagnosed and misdiagnosed
• More news »

Diagnostic Tests for Heart conditions: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Heart conditions.

CARDIAC MURMURS: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Could the murmur be extracardiac in origin? Extracardiac murmurs include the pericardial friction rub and cardiorespiratory murmurs.
2. Is the murmur continuous? A continuous murmur is most often due to a patent ductus arteriosus or combined valvular stenosis and insufficiency. However, arteriovenous aneurysms and ruptured aneurysm of the sinus of Valsalva must also be considered.
3. Is the murmur systolic or diastolic? Diastolic murmurs include aortic regurgitation and mitral stenosis and are always organic. Many systolic murmurs are functional in nature.
4. Is there associated cardiomegaly? An enlarged heart associated with the murmur makes it more likely that it is pathologic. One would consider mitral regurgitation, aortic regurgitation, and aortic stenosis and various forms of congenital heart disease.
5. Is there hepatomegaly? Hepatomegaly associated with the murmur would make one think of congestive heart failure or tricuspid regurgitation and tricuspid stenosis.
6. Is there associated fever? Cardiac murmurs occurring with fever suggest acute rheumatic fever and subacute bacterial endocarditis.
7. Is there dyspnea? Dyspnea associated with a cardiac murmur suggests congestive heart failure.
8. Is there chest pain? If there is chest pain associated with a cardiac murmur, one must consider pericarditis and myocardial infarction.
9. Is there an enlarged thyroid or intention tremor? These findings suggest hyperthyroidism.
10. Is there cyanosis or clubbing? These findings suggest congenital heart disease.

DIAGNOSTIC WORKUP

If the murmur is believed to be organic, the most cost-effective approach would be to consult a cardiologist at the outset. If the astute clinician wishes to pursue the diagnostic workup on his own, it is suggested that a CBC, sedimentation rate, chemistry panel, VDRL test, and thyroid profile should be done for the initial blood work. In addition, a chest x-ray including obliques, congestive heart failure, phonocardiograms, and EKG should be performed. These findings may provide a diagnosis. If there is fever, a streptozyme test, antistreptolysin-O (ASO) titer, and serial blood culture should be performed. If congestive heart failure is suspected, venous pressure and circulation time should be determined. Pulmonary function studies are also helpful. Echocardiography will be extremely helpful in diagnosing the various forms of valvular disease and will also help in identifying a pericardial effusion, congestive heart failure, or the various cardiomyopathies. Cardiac catheterization and angiography and angiocardiography will identify the various congenital heart lesions and valvular disease. These studies, however, are most important when surgery is being considered.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

CARDIAC ARRHYTHMIA: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Is it acute or chronic? An acute cardiac arrhythmia should make one consider a myocardial infarction first.
2. Is the heart rate slow, normal, or fast? A rapid cardiac arrhythmia may be associated with hyperthyroidism, congestive heart failure, or drug toxicity. A slow cardiac arrhythmia is more likely to be associated with heart block and syncope. A myocardial infarction may produce either the rapid or slow cardiac arrhythmia.
3. Is the rhythm regular or irregular? A tachycardia with a regular rhythm is more likely to be a supraventricular tachycardia or ventricular tachycardia. A tachycardia with an irregular rhythm is more likely to be atrial fibrillation, but atrial flutter can also cause a rapid irregular rhythm. Irregular premature contractions and ventricular premature contractions may be associated with rapid, slow, or normal cardiac rates. A slow, fairly regular heart rate is associated with complete heart block.
4. Is there chest pain associated with the cardiac arrhythmia? Chest pain should make one think of myocardial infarction, pericarditis, or coronary insufficiency.
5. Is there fever? If there is fever, one should consider rheumatic fever, subacute bacterial endocarditis, and thyroid storm.
6. Is there a heart murmur associated with the arrhythmia? A heart murmur associated with arrhythmia should make one think of rheumatic fever or subacute bacterial endocarditis, myocardiopathy, or acute congestive heart failure.
7. Are there signs of congestive heart failure? Hepatomegaly, jugular vein distention, and pitting edema of the extremities would make one think that congestive heart failure was the cause of the arrhythmia.
8. Is there a thyroid enlargement? An enlarged thyroid gland would certainly make one think of thyrotoxicosis.
9. Is there hypertension? Hypertension is another important cause of cardiac arrhythmias that should not be forgotten.

DIAGNOSTIC WORKUP

All patients should have an EKG, chest x-ray, and a CBC to rule out anemia. A thyroid profile should be done to look for both hyperthyroidism and hypothyroidism. In acute arrhythmias, serial EKGs and tests for cardiac enzymes need to be done to exclude an acute myocardial infarction. Venous pressure and circulation time should be determined to rule out congestive heart failure; pulmonary function tests may be helpful, as they may rule out both congestive heart failure and emphysema. Echocardiograms should be done to rule out valvular disease and cardiomyopathy. If there are paroxysmal arrhythmias, Holter monitoring needs to be done. An exercise tolerance test may allow the recording of an arrhythmia that is only induced on exercise. Signal-averaged EKG and electrophysiologic testing should also be considered. Patients on digitalis, quinidine, or other cardiac drugs should have blood levels of these drugs measured to determine if their levels are toxic. If there is a fever, blood culture should be done to rule out bacterial endocarditis. Referral to a cardiologist can be made at any point in the diagnostic workup.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Gallops & Extra Heart Sounds: Differential Diagnosis
(In a Page: Signs and Symptoms)

• S₃ gallop
  –Low-frequency diastolic sound following S₂, best heard with bell
  –May be heard normally in healthy young adults
  –The presence of an S₃ in a patient over 40 suggests ventricular enlargement, often secondary to chronic mitral regurgitation, decreased left ventricular ejection fraction, elevated left atrial pressure, acute pulmonary edema, or high-output states (e.g., thyrotoxicosis, pregnancy)
  –Right ventricular infarct
  –Hypertrophic cardiomyopathy
• S₄ gallop
  –Low-frequency diastolic sound preceding S₁, best heard with bell
  –May be normally heard in healthy older adults
  –Occurs with hypertensive heart disease, aortic stenosis, hypertrophic cardiomyopathy, pulmonary hypertension, coronary artery disease

• Midsystolic click
  –Most commonly due to mitral valve prolapse

Summation gallop
–Fusion of S₃ and S₄ with tachycardia
–Results in a loud diastolic filling sound

• Pericardial knock
  –Early diastolic sound
  –Common in constrictive pericarditis (with
  or without pericardial calcification)

• Opening snap
  –High-frequency, early diastolic sound
  –Most commonly due to mitral stenosis,
  tricuspid stenosis, ventricular septal defect, thyrotoxicosis

• Early systolic ejection sound (ejection click)
  –Associated with a bicuspid aortic valve, mitral or tricuspid prolapse, aortic stenosis, prosthetic valves

Tumor “plop” secondary to atrial mycoma

Workup and Diagnosis

• History and physical examination
• ECG is indicated in all patients
  –Atrial fibrillation is often seen in mitral stenosis
  –Left atrial enlargement is seen in mitral stenosis or mitral regurgitation
  –Left ventricular hypertrophy is seen in patients with hypertensive heart disease, hypertrophic cardiomyopathy, or bicuspid aortic valve
  • Chest X-ray may reveal valvular calcification, pulmonary edema, or left ventricular enlargement
  • Echocardiogram is used to assess chamber size, wall thickness, ventricular function, valvular abnormalities, and left ventricular outflow obstruction
  • Consider cardiology consult

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Source: In a Page: Signs and Symptoms, 2004

Irregular Heart Rhythms: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Atrial fibrillation
  –One of the most common causes of irregular rhythm
  –Narrow QRS complex without organized atrial contraction (no P waves)
  –Etiologies include infection, thyrotoxicosis, alcohol, cocaine, amphetamines, myocarditis, pericarditis, hypertensive crisis, ischemia, MI, CHF, hypoxia, PE, hypertension, valvular heart disease
• Atrial flutter with variable block
  –Narrow QRS complex
  –ECG: “Sawtooth” flutter waves
  –Atrial rate is typically 250–350 bpm
  –Ventricular rate is usually 1/2 or 1/3 of atrial rate (2:1 or 3:1 block)
  –Irregular when variable block is present
  –Result of a macro-reentrant circuit in atrium

• Premature atrial contractions
• Paroxysmal atrial tachycardia
• Multifocal atrial tachycardia
  –Multiple areas of atrial impulses (more than three P wave morphologies) followed by a narrow QRS complex
  –HR ≥ 100 bpm
  –Most often seen in patients with lung disease
• Wandering atrial pacemaker
  –Multiple areas of atrial impulses (more than three P wave morphologies) followed by a narrow QRS complex
  –HR ≤ 100 bpm
  –Often occurs in athletes and the very young (increased vagal tone)

• Premature ventricular contractions
• Sinus arrhythmia

Workup and Diagnosis

• History and physical examination
  –Associated symptoms may include lightheadedness,
  palpitations, dyspnea, chest pain, or syncope
  –Assess for hemodynamic instability

ECG with rhythm strip is the key tool for establishing diagnosis

Initial laboratory evaluation may include CBC, electrolytes, BUN/creatinine, calcium, pulse oximetry, chest X-ray, and possibly an ABG

Consider cardiac enzymes, TSH, and toxicology screen

Echocardiogram may be necessary to evaluate for underlying disease or the presence of thrombi
–Transesophageal echocardiography is more sensitive than transthoracic echocardiography for detection of intracardiac thrombus (most commonly seen in left atrial appendage)

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Source: In a Page: Signs and Symptoms, 2004

Murmurs - Diastolic: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Aortic insufficiency
  –Decrescendo murmur heard best at the right second intercostal space
• Austin Flint murmur
  –Late diastolic rumble of severe aortic regurgitation
  –A result of aortic regurgitation so severe that it causes diastolic mitral regurgitation
• Mitral stenosis
  –Opening snap with mid-diastolic rumble, especially in the left lateral decubitus position
• Pulmonary insufficiency
  –Accentuated P2 and decrescendo murmur at the left second/third intercostal spaces
• Tricuspid stenosis
  –Mid-diastolic rumble at the left sternal border
  –Increases with inspiration
• Cervical venous hum (disappears upon pressure to the jugular vein)
• Hepatic venous hum (disappears with epigastric pressure)
• Mammary souffle (in pregnancy; disappears on compressing breast)
• PDA (continuous machinery sound)
• Coronary or pulmonary arteriovenous fistula
• Coarctation of the aorta
• ASD with left-to-right shunt
• Atrial myxoma (“tumor plop”)
• Pericardial knock (constrictive pericarditis)
• Bronchial collaterals (congenital heart disease)
• Anomalous pulmonary venous drainage with left-to-right shunt
• Pulmonary artery branch stenosis
• Carey-Coombs murmur (mid-diastolic murmur that occurs in acute rheumatic fever)

Workup and Diagnosis

• Complete history and physical examination, including cardiac maneuvers
• ECG
• Echocardiogram
• Consider chest X-ray
• Laboratory studies may include CBC, electrolytes, glucose, BUN/creatinine, TSH, liver function tests, pulse oximetry, and/or arterial blood gas
• Consider cardiology consult

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Source: In a Page: Signs and Symptoms, 2004

Murmurs - Systolic: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Innocent systolic murmur
  –Heard at left sternal border
  –Increased when supine
  –May be caused by increased flow states (e.g., anemia, hypovolemia, fever)
• Still's murmur
• Mitral valve prolapse
  –Midsystolic click with late systolic murmur that shifts with maneuvers
• Aortic stenosis
  –Right side at second intercostal space
  –Radiates to carotid arteries
• Aortic sclerosis
  –Right side at second intercostal space
  –Midsystole
• Hyperthyroidism
• Cervical venous hum
  –Disappears with jugular vein pressure
• Hepatic venous hum
  –Disappears with epigastric pressure
• Mammary souffle
  –Occurs in pregnancy
  –Disappears upon compression of breast
• Bicuspid aortic valve
  –Right side at second intercostal space
  –Little radiation
  –Possible early diastolic aortic murmur
  –Opening sound of aortic valve heard in early systole (systolic ejection click)
• Mitral insufficiency
  –Holosystolic murmur heard best in the left lateral decubitus position
  –S₁ is usually diminished in intensity
• Tricuspid insufficiency
  –Holosystolic murmur at second/third intercostal spaces
• Endocarditis
  –Abrupt onset of new murmur
• Peripheral pulmonary artery stenosis
• Atrial or ventricular septal defect
• Ventricular septal defect
• Patent ductus arteriosus (continuous machinery sound, second left intercostal space)
• Coarctation of the aorta
• Left ventricular outflow tract obstruction
• Pulmonary artery stenosis
• Prosthetic valve noises
• Pericardial friction rubs
• Papillary muscle dysfunction
• Pulmonic outflow obstruction
• Coronary/pulmonary arteriovenous fistula

Workup and Diagnosis

• History and physical examination
  –Family history of sudden cardiac death
  –Past medical history of heart disease, murmurs, or rheumatic fever
  –Evaluation for jugular venous distention, carotid upstroke, and/or bruits
  –Heart, lung, and abdominal examinations
  –Peripheral pulses and evaluation for peripheral edema
• ECG
• Chest X-ray
• Echocardiogram
• Laboratory studies may include CBC, electrolytes, BUN/creatinine, glucose, and TSH
• Consider cardiac enzymes
• Consider blood cultures
• Consider cardiology referral

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Source: In a Page: Signs and Symptoms, 2004

Abnormal Heart Sounds: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Abnormal S2 –Most important auscultatory finding; normally, S2 is single on inspiration and narrowly split on expiration, indicating normal pulmonary arterial pressures; difficult to learn, especially in babies with fast heart rates or a screaming child
  –Single and/or loud S2: Increased pulmonary artery pressure (large L to R shunt, pulmonary hypertension), also seen in patients with only single outlet from heart (i.e., pulmonary atresia)
  –Wide fixed-split S2: ASD, right bundle branch block, post-cardiac surgery

• Systolic murmur
  –Up to 50% of children at some point in life
  –Mid-systolic/ejection type: S1 and S2 separate from the murmur (lub-shhh-dub), due to flow across semilunar valve, harsh indicates semilunar valve stenosis, whereas low-pitched, vibratory, musical indicates innocent murmur
  –Holosystolic/regurgitant murmur: Begins with S1 (which is not clearly heard); always pathologic (mitral valve regurgitation, VSD, subaortic stenosis)

• Diastolic sounds
  –Always abnormal
  –Early and medium/high pitch murmur indicates semilunar valve insufficiency, low frequency rumbling indicates mitral/tricuspid stenosis
  –S3/S4/opening snap: Soft S3 can be normal in healthy children; any sound clearly heard is probably an abnormality of the mitral/tricuspid valve (opening snap) or ventricular filling (S3/S4)

• Continuous murmur
  –Murmur in systole that continues into diastole (may not fill entire diastole)
  –Venous hum: Low pitched, continuous murmur at both upper sternal borders; disappears when supine; innocent
  –Patent ductus arteriosus: Harsh, machinery-like murmur at left upper sternal border (LUSB)

• Systolic ejection click
  –High-pitched sound
  –Early: Bicuspid aortic valve, loudest at apex/LLSB, often confused with split S1
  –Mid/late: Mitral valve prolapse

Workup and Diagnosis

• Majority of murmurs heard after the first year of life are systolic and innocent

• Major innocent murmurs of childhood: All must have a normal S2 and no symptoms
  –Still (vibratory) murmur: Vibratory, musical, twangy midsystolic murmur loudest at the LLSB, louder when supine, heard in toddlers
  –Venous hum: Continuous low rumbling sound at upper sternal borders, disappears when supine
  –Peripheral pulmonary stenosis (PPS): Midsystolic murmur at LUSB, radiates to back and both axillae, normal up to 1 year of age (refer for evaluation if present afterwards)
  –Innocent pulmonary flow murmur: Midsystolic murmur, LUSB, loudest when supine, adolescent age range

• Physical exam: Assess growth pattern, heart rate, organomegaly, and femoral pulses
• Four-limb blood pressures very helpful in evaluating possible aortic coarctation (higher BP in arms, lower in legs)
• Chest X-ray: Rarely useful in the routine evaluation of murmurs in children (unless pathology likely)
• 12-lead electrocardiogram useful for assessment of atrial or ventricular enlargement/hypertrophy
• Pulse-oximetry is very useful in the newborn to rule out mildly cyanotic lesions
• Echocardiography

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Source: In A Page: Pediatric Signs and Symptoms, 2007

Heart Failure: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Increased afterload

• Most common in the neonate due to left-sided obstructive lesions, which present acutely
• Aortic coarctation is most common
  –Increased pulse/BP in right arm
  –Decreased pulse/BP in lower extremities
• Critical aortic stenosis
  –Poor pulses, loud murmur
• Hypoplastic left heart syndrome, aortic arch interruption

Left-to-right shunt lesions
• Normal cardiac muscle funtion but overcirculation of lungs due to a congenital connection between the right and left side of the heart and low PVR
• Usually presents at 1–2 months of age
  –PVR drops and systemic resistance becomes higher than PV
  –Blood shunts from left to right (systemic circulation to pulmonary circulation)
  –Pulmonary overcirculation and poor systemic output (poor peripheral perfusion, low urine output)
• Ventricular septal defect (most common)
• Atrioventricular septal defect (AV canal, endocardial cushion defect), associated with Down syndrome
• Patent ductus arteriosus
• Atrial septal defect (usually asymptomatic)

Intrinsic myocardial disease
• More common cause of heart failure in older children and adolescents
• Myocarditis
  –Acute inflammation and dysfunction of cardiac muscle, usually postviral
  –1/3 remain stable, 1/3 return to normal cardiac function, and 1/3 deteriorate
• Cardiomyopathy
  –Dilated most common, but also hypertrophic and restrictive
  –Multiple genetic and metabolic causes, often positive family history, some represent old, “burned-out” myocarditis
• Myocardial infarction (rare)
  –Kawasaki disease
  –Congenital coronary abnormalities (anomalous left coronary artery)

Workup and Diagnosis

• Neonate
  –Consider left-sided obstructive lesions in any neonate with poor or differential pulses/perfusion
  –Often have respiratory distress, hepatomegaly, and metabolic acidosis
  –Critically ill requiring supplemental O2 and ventilatory support; transfer to tertiary care ICU

• Infants/children
  –History: Activity tolerance, poor feeding, diaphoresis, respiratory symptoms (wheezing or frequent infections due to pulmonary overcirculation), weight gain (poor due to increased metabolic demands or excess due to activity intolerance and edema), dyspnea on exertion for older patients
  –Physical exam: Vital signs (tachypnea, tachycardia), perfusion/pulses, edema (especially of face/eyes for infants), increased work of breathing/retractions, hepatomegaly, increased jugular venous distension

• Chest X-ray often reveals nonspecific cardiomegaly and pulmonary venous congestion
• ECG: Evaluate for ventricular hypertrophy (left-to-right shunt lesions, hypertrophic cardiomyopathy); low QRS voltage (myocarditis, dilated cardiomyopathy)
• Echocardiography and/or cardiac catheterization to further define anatomy and function
• Serum electrolytes, BUN/creatinine, and LFTs (including total protein and albumin) to further define current metabolic state before therapy

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Source: In A Page: Pediatric Signs and Symptoms, 2007

MURMURS: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

A chest x-ray with anterior oblique films during a barium swallow along with an ECG, sedimentation rate, a blood serology thyroid profile, and CBC are basic in the workup of a murmur. If there is a fever or if there is recent onset of the murmur, blood cultures, an ASO titer and C-reactive protein (CRP) should be done. An ANA test, echocardiogram, and phonocardiogram are frequently done. Referral to a cardiologist is wise if the cause is obscure or if one is unable to spend the time for a careful workup. Angiocardiography and cardiac catheterization are the only sure ways to determine the location of the valvular disease, and, in many cases, the exact cause.

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Source: Differential Diagnosis in Primary Care, 2007

CARDIAC ARRHYTHMIAS: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The diagnosis depends a lot on the type of arrhythmia. Atrial premature contractions are usually benign and an extensive workup is unnecessary unless other physical signs indicate the need for it. Infrequent ventricular premature contractions (VPCs) in otherwise healthy individuals probably can be handled the same way. When VPCs are frequent or multifocal, an exercise tolerance test, echocardiogram, and perhaps coronary angiography are indicated. Runs of ventricular tachycardia require an extensive workup, including coronary angiography, but usually there will be other signs to indicate the need for this.

Atrial tachycardia and fibrillation require a workup of hyperthyroidism and pulmonary disease, systemic hypertension, and congestive heart failure. Atrial obstruction and dilatation should be excluded by echocardiography.

Any arrhythmia warrants an ECG and possibly repeated ECGs. The Holter monitor should be used if there is doubt about the type of arrhythmia.

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Source: Differential Diagnosis in Primary Care, 2007

Murmurs: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 406.) Use the bell of your stethoscope for low-pitched murmurs and the diaphragm for high-pitched murmurs.

Next, obtain a patient history. Ask if the murmur is a new discovery or if it has been known since birth or childhood. Find out if the patient has experienced associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. Explore the patient’s medical history, noting especially an incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.

Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient’s liver tender or palpable? Does he have peripheral edema?

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Pulse rhythm abnormality: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

If the patient’s condition permits, ask if he’s experiencing pain. If so, find out about its onset and location. Does the pain radiate? Ask about a history of heart disease and treatment for arrhythmias. Obtain a drug history and check the patient’s compliance. Also, ask about caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and the use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.

Next, check the patient’s apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S₁ (lub) and S₂ (dub) may indicate a conduction defect. A faint or absent S₁ and an easily audible S₂ may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats — possibly indicating premature atrial contractions — or other variations in heart rate or rhythm. Take the patient’s apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Report your findings to the physician.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Cardiac arrhythmias: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnosis is made by tests that reveal the arrhythmia, such as 12-lead electrocardiography. Ambulatory cardiac monitoring (Holter monitoring), echocardiography, electrophysiology studies, and coronary angiography may also confirm or rule out suspected causes of arrhythmias and help determine treatment.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Cardiac tamponade: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

❑ Chest X-ray shows slightly widened mediastinum and cardiomegaly.

❑ Electrocardiography (ECG) is rarely diagnostic of tamponade but is useful in ruling out other cardiac disorders. It may reveal changes produced by acute pericarditis.

❑ Pulmonary artery catheterization detects increased right atrial pressure, right ventricular diastolic pressure, and central venous pressure (CVP).

❑ Echocardiography, computed tomography scan, or magnetic resonance imaging shows pericardial effusion with signs of right ventricular and atrial compression.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Rheumatic fever and rheumatic heart disease: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnosis depends on recognition of one or more of the classic symptoms (carditis, rheumatic fever without carditis, polyarthritis, chorea, erythema marginatum, or subcutaneous nodules) and a detailed patient history. Laboratory data support the diagnosis:

❑ White blood cell count and erythrocyte sedimentation rate may be elevated (during the acute phase); blood studies show slight anemia due to suppressed erythropoiesis during inflammation.

❑ C-reactive protein is positive (especially during acute phase).

❑ Cardiac enzyme levels may be increased in severe carditis.

❑ Antistreptolysin-O titer is elevated in 95% of patients within 2 months of onset.

❑ Electrocardiogram changes aren’t diagnostic; but PR interval is prolonged in 20% of patients.

❑ Chest X-rays show normal heart size (except with myocarditis, heart failure, or pericardial effusion).

❑ Echocardiography helps evaluate valvular damage, chamber size, and ventricular function.

❑ Cardiac catheterization evaluates valvular damage and left ventricular function in severe cardiac dysfunction.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Murmurs: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 517.) Use the bell of your stethoscope for low-pitched murmurs; the diaphragm for high-pitched murmurs.

Next, obtain a patient history. Ask if the murmur is a new discovery, or if it has been known since birth or childhood. Find out if the patient has experienced any associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. (See Differential diagnosis: Murmurs, pages 518 and 519.) Explore the patient’s medical history, noting especially any incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.

Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient’s liver tender or palpable? Does he have peripheral edema?

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Pulse rhythm abnormality: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If the patient’s condition permits, ask if he’s experiencing pain. If so, find out about onset and location. Does the pain radiate? Ask about a history of heart disease and treatments for arrhythmias. Obtain a drug history and check compliance. Also, ask about any caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.

Next, check the patient’s apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S₁ (lub) and S₂ (dub) may indicate a conduction defect. A faint or absent S₁ and an easily audible S₂ may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats—possibly indicating premature atrial contractions—or other variations in heart rate or rhythm. Take the patient’s apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Report your findings to the physician.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Heart Murmur, Diastolic: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

 A. Symptoms. Many patients with diastolic murmurs will not present with specific complaints; rather, the murmurs will be found in the course of a routine medical examination. With symptomatic lesions, the patient may experience dyspnea, chest pain, or palpitations. Pulmonary regurgitation (PR) is usually asymptomatic except in its most severe forms. More specific symptoms include chest or neck pounding in aortic regurgitation (AR); hemoptysis, embolism, or hoarseness (left recurrent laryngeal nerve compression from the left atrium) in mitral stenosis (MS); failure to thrive or frequent respiratory infections with congenital MS; edema in tricuspid stenosis (TS); and fever, anemia, weight loss, embolism, digital clubbing, arthralgias, syncope, rash, and Raynaud’s phenomenon with an atrial myxoma (1).

 B. Past medical history. Does the patient have a history of rheumatic fever (RF)? RF is the most common cause of all diastolic murmurs (mitral → aortic → tricuspid → pulmonic) (2). Of patients with mitral stenosis, 50% will have a history of rheumatic fever (3).

1. Endocarditis. Vegetations can lead to either AR/PR or MS/TS.

2. Pulmonary hypertension with PR is classically associated with the Graham Steell murmur, heard in the left third interspace near the sternum and propagated down the sternum.

3. Connective tissue and collagen vascular diseases predispose to aortic root dilatation and AR.

4. Congenital heart malformations can be associated with multiple valvular lesions, left ventricular (LV) outflow tract abnormalities, or shunts (with resultant volume overload).

5. Atrial myxoma is a rare cause of variable AV valve obstruction.

6. Syphilis can cause aortitis and AR.

Physical examination (PE)

A. Table 7.3 lists characteristic PE findings of diastolic murmurs.

B. Fine points of the physical examination

1. Is the murmur of AR louder at the right sternal border? If so, consider aortic root dilation. Remember, whereas the duration of the chronic AR murmur is directly proportional to the severity of the regurgitation, the duration of the acute AR murmur may not predict its severity (3).

2. Is the murmur of MS shorter, or does it extend closer to S₂? The length of this murmur, not its intensity, is directly proportional to the severity of the stenosis (3). In addition, the murmur may not be audible with increased heart rates because of shortening of diastole.

 3. Does the murmur of MS vary from examination to examination? If so, and especially if it is introduced by a “plop” sound, consider atrial myxoma.

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Heart Murmur, Systolic: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

A. General issues in the history. The history can provide important clues as to whether the murmur is clinically significant. Any history of rheumatic fever, previously known valvular disease, congenital heart disease, or intravenous drug abuse would be important to ascertain.

Murmurs of early adulthood suggest congenital or rheumatic disease, whereas murmurs with onset later in life are consistent with degenerative valvular changes.

 B. Patient symptoms. Patients should be asked about shortness of breath, dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. Patients with these symptoms warrant an expedited evaluation because these symptoms suggest cardiac decompensation. Advanced aortic stenosis specifically is associated with chest pain, syncope, and heart failure, although a gradient across the valve can exist for years prior to symptom onset. Chest discomfort is often present in advanced disease, but sudden death occurs in 15% of patients with no previous symptoms (1).

 C. Association of a murmur with a specific disease. Recent myocardial infarction endocarditis could cause papillary muscle dysfunction resulting in mitral or tricuspid regurgitation. Mitral regurgitation can be seen in connective tissue disease, coronary artery disease, and congenital disease, but is commonly associated with conditions leading to left ventricular dilatation such as congestive heart failure (CHF) (Chapter 7.5). Endocarditis, myocardial infarction, trauma, prolapse, or congenital heart disease usually precede tricuspid regurgitation. Mitral valve prolapse, which is clinically characterized by palpitations, fatigue, and chest pain, is often associated with anxiety. Hypertrophic cardiomyopathy can be seen in patients with a family history and usually presents between the ages of 20 and 40 years. Presenting symptoms include dyspnea on exertion, chest pain, palpitations, or syncope. It is an important cause of sudden death in athletes. A history of anemia, thyroid disease, or fever should also be elicited from patients being evaluated for
a systolic murmur as each of these conditions can cause a murmur from increased flow.

Physical examination

A. Technique. Auscultate the heart with the bell to best detect lower frequencies and the heart sounds (S₁-S₄). The quality of the murmur is best heard with the diaphragm. Inspiration increases the audibility of right ventricular sounds.

 B. Murmur characteristics. Table 7.4 presents a summary of the characteristics of different causes of systolic murmurs (2,3). Etchell et al. (3) have prepared a comprehensive review on the usefulness of specific physical examination findings in the diagnosis of systolic murmurs.

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Congestive Heart Failure: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

A. Common presenting symptoms. Does the patient have orthopnea, paroxysmal nocturnal dyspnea, or dyspnea on exertion? How much exertion triggers dyspnea? These are relatively specific symptoms for CHF. Less specific symptoms include swelling of the legs, increasing weight, and generalized fatigue. Older patients with CHF may not have dyspnea on exertion because of a sedentary baseline status; they often present with atypical symptoms such as dry cough, daytime oliguria with nocturia, and confusion (3).

B. Past medical history. Are conditions present that can cause CHF (Table 7.2)? If so, are they well-controlled with lifestyle changes, medications, or both? Uncontrolled hypertension, myocardial ischemia, and medication noncompliance frequently trigger CHF.

 C. Psychosocial history. Is there current or previous heavy alcohol use, tobacco use, or stimulant drug use? Is the patient consuming too much dietary sodium (> 2 g/d)? Are symptoms hindering the patient’s ability to perform daily activities? Is the patient depressed? How is the family coping? Poor understanding of lifestyle factors, depression, and limited family resources can lead to noncompliance and frequent CHF exacerbations.

Physical examination

A. Focused physical examination. In general, the physical examination is more sensitive in detecting acute CHF than it is in detecting chronic CHF. Evaluate the following:

1. Vital signs. Note the blood pressure; hypertension with acute CHF suggests diastolic dysfunction (4). Obtain pulse, respiratory rate, and pulse oximetry to detect hypoxia.

2. Neck. Look for jugular venous distension, one of the more reliable physical examination indicators of CHF (4).

3. Lungs. Rales are commonly heard, but wheezing (“cardiac asthma”) can also appear.

4. Heart. Palpate the apical impulse. If laterally displaced, diffuse, and especially of sustained duration, CHF caused by reduced left ventricular (LV) systolic function is likely (4). Listen for murmurs, gallops, and rubs. An S₃ gallop is generally suggestive of CHF (4), whereas an S₄ gallop may be a nonpathologic, age-related finding in elderly patients (3).

5. Abdomen. Assess for hepatosplenomegaly and try to elicit abdominojugular reflux.

 6. Extremities. Look for leg edema (pitting in acute CHF, brawny in chronic CHF).

 B. Additional physical examination. Further examination is appropriate if the history suggests specific causes for CHF: funduscopic examination to search for hypertensive retinopathy; thyroid palpation and auscultation; palpation of peripheral pulses; and carotid palpation and auscultation for evidence of stenosis, a marker of coronary atherosclerosis.

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Cardiomegaly/Congestive Heart Failure: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Congestive heart failure

❑ Hypertensive left ventricular hypertrophy

❑ Anterior myocardial ischemia

❑ Athlete’s heart

❑ Mitral regurgitation

❑ Aortic stenosis

❑ High output

❑ Hypertrophic obstructive cardiomyopathy

❑ Pulmonary hypertension

❑ Cor pulmonale

❑ Dilated cardiomyopathy

❑ Endocarditis

❑ Pericardial effusion

❑ Left ventricular aneurysm

❑ Mitral stenosis

❑ Amyloidosis

Diagnostic Approach

The Framingham criteria for congestive heart failure are a good reference point. Major criteria include paroxysmal nocturnal dyspnea, rales, cardiomegaly, acute pulmonary edema, third heart sound, jugular pressure greater than 16 cm, and positive abdominojugular reflex. Minor criteria include edema, night cough, dyspnea on exertion, hepatomegaly, pleural effusion, and pulse rate slower than 120. Functional limitation is most often classified using the New York Heart Association (NYHA) system: Class I—symptoms of heart failure only at levels of exertion that would limit normal individuals; Class II—symptoms of heart failure with ordinary exertion; Class III—symptoms of heart failure with less than ordinary exertion; Class IV—symptoms of heart failure at rest.

History is key in CHF. Findings due to excess fluid accumulation include dyspnea, edema, hepatic congestion, and ascites. Findings due to reduced cardiac output include weakness and fatigue, more pronounced with exertion. Acute and subacute CHF produce primarily shortness of breath with exertion or at rest. Other common symptoms include orthopnea, paroxysmal nocturnal dyspnea, and right upper quadrant discomfort due to hepatic congestion in right heart failure.

Decreased cardiac output is counterbalanced by increased sympathetic activity, manifest as sinus tachycardia, diaphoresis, and peripheral vasoconstriction (cool and cyanotic extremities due to decreased perfusion and increased oxygen extraction). A prominent dicrotic notch may be felt in severe left ventricular dysfunction, as the compensitory increase in total peripheral resistence and corresponding reduced aortic compliance accentuate the aortic valve closure. Pulsus alternans (alternating strong and weak pulse beats) is uncommon but pathognomonic of advanced heart failure. Volume overload is manifest as pulmonary congestion (rales), peripheral edema, and elevated jugular venous pressure. The medulla controls the respiratory rate based on pCO ₂. The length of the Cheyne-Stokes cycle is proportional to the circulatory delay from the alveoli to the arterioles (r = 0.80).

Systolic heart failure is marked by decreased cardiac output, with manifestations such as weakness, fatigue, and decreased exercise tolerance. Mitral regurgitation, especially when acute, augments early diastolic inflow and may produce an S₃ with normal systolic function. Diastolic heart failure is associated with reduced ventricular compliance and increased filling pressures with manifestations of dyspnea and rales.

Findings suggesting left ventricular hypertrophy include a sustained forceful apical thrust, a double apical impulse, an apical impulse larger than 3 cm, and a fourth heart sound on auscultation. Left ventricular enlargement will cause the apical impulse (PMI) to be displaced downward and to the left. Right ventricular hypertrophy will cause a sustained right parasternal lift. It is seen with pulmonary hypertension, pulmonic stenosis, and volume overload with tricuspid regurgitation or atrial septal defect. Right ventricular failure is recognized by edema, jugular venous distension, and abdominojugular reflex.

Key findings on physical examination:

Rales  Increased interstitial fluid/pressure causes alveoli to pop open. Pulmonary venous capacitance increases in chronic heart failure, and rales may be absent.

Third heart sound (S₃)  Ventricular vibration occurs during rapid inflow of blood in early diastole when the long-axis expansion limit is reached, due to reduced LV compliance or increased filling pressure. S₃ is a low-pitched sound over the apex, and yield is doubled in the 45 degree left lateral decubitus position. JVD and S₃ are independent on multivariate analysis.

JVD  The IJ is a right atrial manometer. High JVD (present .45 deg) has a LR 4.1 that CVP is .10 cm. Low JVD (present ,30 deg) has a LR 3.4 that CVP is ,5 cm.

Abdominojugular reflux  Apply abdominal pressure for 10 sec. A positive AJR is a 4 cm or greater drop in JVP after release, due to decreased RV compliance or increased LVEDP.

Edema  With renin-angiotensin-aldosterone activation, pulmonary and peripheral fluid accumulates. After the extracellular fluid is in excess of about five liters, symmetric, dependent, and pitting peripheral edema develops.

Valsava response  The normal response is for BP to rise .15 mm Hg during valsalva, but to fall before 10 seconds passes. When valsalva is released, the BP rises again .15 mm over the resting threshold. In CHF, an abnormal response can consist of absent phase 4 overshoot or a square wave in phase 2.

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Source: Field Guide to Bedside Diagnosis, 2007

Discrete Heart Sounds: Differential Overview
(Field Guide to Bedside Diagnosis)

Phenomena

❑ S₄ gallop

❑ Midsystolic click

❑ S₃ gallop

❑ Loud S₂

❑ Widely split S₁

❑ Widely split S₂

❑ Ejection click

❑ Variable S₁

❑ Paradoxical splitting of S₂

❑ Loud S₁

❑ Fixed splitting of S₂

❑ Opening snap

❑ Pericardial knock

❑ Tumor plop

❑ Sail sound

Diagnostic Approach

The A₂-P₂ interval normally increases with inspiration due to decreased intrathoracic pressure and increased venous return, which leads to increased stroke volume.

In my southern medical school I was taught that the cadence of the S₃ gallop matches that of the spoken word Kentucky, and of S₄, Tennessee.

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Source: Field Guide to Bedside Diagnosis, 2007

Diastolic Murmur: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Aortic regurgitation

❑ Pulmonic regurgitation

❑ Mitral stenosis

❑ Tricuspid stenosis

❑ Atrial septal defect

❑ Left anterior descending artery stenosis

❑ Atrial myxoma

Diagnostic Approach

A diastolic murmur is always abnormal. An early diastolic murmur, caused by aortic or pulmonic regurgitation, is high-pitched and decrescendo. The duration of the murmur is an index of severity. A mid-diastolic murmur suggests mitral or tricuspid stenosis.

The murmur of mitral stenosis decreases or does not change with inspiration whereas the murmur of tricuspid stenosis increases.

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Source: Field Guide to Bedside Diagnosis, 2007

Systolic Murmur: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Systolic ejection murmur

❑ Mitral regurgitation

❑ Mitral valve prolapse

❑ Aortic stenosis

❑ Aortic valve sclerosis

❑ Hypertrophic obstructive cardiomyopathy

❑ Atrial septal defect

❑ Pulmonic stenosis

❑ Tricuspid regurgitation

❑ Ventricular septal defect

❑ Aortic coarctation

Diagnostic Approach

The intensity of the murmur is proportional to the degree of stenosis until flow decreases markedly. Intensity can be expressed semiquantitatively, from grade 1/6, heard only with concentration, to grade 4/6, a loud murmur associated with a palpable thrill, to grade 6/6 with a thrill and murmur heard with the stethoscope off the chest. The duration of the murmur is proportional to the pressure differential between the two chambers.

An early systolic murmur, decrescendo at the apex, occurs in acute, severe mitral regurgitation (MR) with papillary muscle rupture, endocarditis, ruptured chordae tendineae, or blunt chest trauma. A midsystolic murmur is typical of aortic stenosis (AS). It can also be found with hypertrophic obstructive cardiomyopathy (HOC) and with hyperdynamic states. A late systolic murmur is usually heard with mitral valve prolapse (MVP) in association with a midsystolic click. A holosystolic murmur can be produced by severe MR or tricuspid regurgitation (TR), or by a ventricular septal defect (VSD), when the pressure differential between chambers persists throughout systole. Holosystolic murmurs are almost never innocent.

Handgrip decreases AS and HOC murmurs but increases MR, aortic regurgitation (AR), VSD, and mitral stenosis (MS). Transient arterial occlusion by a blood pressure cuff 20 mm above systolic increases left-sided murmurs. Valsalva decreases most murmurs (decreased right and left ventricular filling), except HOC and MVP, which increase.

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Source: Field Guide to Bedside Diagnosis, 2007

Continuous Murmur: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Aortic stenosis/aortic insufficiency

❑ Pericardial friction rub

❑ Pulmonary arteriovenous fistula

❑ Venous hum

❑ Mammary souffle

❑ Aortic coarctation

❑ Mediastinal air dissection

❑ Patent ductus arteriosis

❑ Ruptured sinus of Valsalva

❑ Coronary artery fistula

Diagnostic Approach

Continuous murmurs begin in systole and extend into diastole without interruption. The murmur results from blood flow from a higher pressure chamber or vessel to a lower pressure system, with the gradient maintained during both systole and diastole, for example with aortopulmonary and arteriovenous connections.

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Source: Field Guide to Bedside Diagnosis, 2007

Cardiac tamponade: Diagnosis
(Handbook of Diseases)

❑ Doppler ultrasound shows exaggerated pulmonic (and tricuspid) flow during inspiration, with reciprocal changes in aortic (and mitral) flow.

❑ Chest X-ray shows slightly widened mediastinum and cardiomegaly.

❑ Electrocardiography (ECG) may reveal changes produced by acute pericarditis. This test rarely reveals tamponade but is useful to rule out other cardiac disorders.

❑ Pulmonary artery catheterization indicates increased right atrial pressure, right ventricular diastolic pressure, and central venous pressure (CVP).

❑ Echocardiography records pericardial effusion with signs of right ventricular and atrial compression.

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Source: Handbook of Diseases, 2003

Heart failure: Diagnosis
(Handbook of Diseases)

The following tests are used to diagnose heart failure:

❑ Electrocardiography reflects heart strain, enlargement, and ischemia. It may also reveal atrial enlargement, tachycardia, and extrasystole.

❑ Chest X-ray shows increased pulmonary vascular markings, interstitial edema, pleural effusion, and cardiomegaly.

❑ Pulmonary artery monitoring typically demonstrates elevated pulmonary artery and pulmonary artery wedge pressures, elevated left ventricular end-diastolic pressure in left-sided heart failure, and elevated right atrial pressure or central venous pressure in right-sided heart failure.

❑ Echocardiography demonstrates left ventricular dysfunction with a reduced ejection fraction.

❑ Brain natriuretic peptide (BNP) assay detects abnormal hormone levels produced by failing ventricles.

❑ Cardiopulmonary exercise testing determines oxygen consumption and severity of heart failure.

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Source: Handbook of Diseases, 2003

Rheumatic fever and rheumatic heart disease: Diagnosis
(Handbook of Diseases)

Recognition of one or more classic signs or symptoms (carditis, polyarthritis, chorea, erythema marginatum, or subcutaneous nodules) and a detailed patient history allow diagnosis. The following laboratory data support the diagnosis:

❑ White blood cell count and erythrocyte sedimentation rate may be elevated (during the acute phase); blood studies show slight anemia from suppressed erythropoiesis during inflammation.

❑ C-reactive protein is positive (especially during the acute phase).

❑ Cardiac enzyme levels may be increased in those with severe carditis.

❑ Antistreptolysin O titer is elevated in 95% of patients within 2 months of onset. (Rising antiDNase B test results can also detect recurrent streptococcal infection.)

❑ Electrocardiography changes aren’t diagnostic, but the PR interval is prolonged in 20% of patients.

❑ Chest X-rays show normal heart size (except with myocarditis, heart failure, or pericardial effusion).

❑ Echocardiography helps evaluate valvular damage, chamber size, and ventricular function.

❑ Cardiac catheterization evaluates valvular damage and left ventricular function in those with severe cardiac dysfunction.

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Source: Handbook of Diseases, 2003

Murmurs: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Obtain a patient history. Ask if the murmur is a new discovery, or if it has been known since birth or childhood. Find out if the patient has experienced any associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. Explore the patient’s medical history, noting especially any incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.

Physical examination

If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs.) Use the bell of your stethoscope for low-pitched murmurs; the diaphragm for high-pitched murmurs.

Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient’s liver tender or palpable? Does he have peripheral edema?

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Pulse rhythm abnormality: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

If the patient’s condition permits, ask if he’s experiencing pain. If so, ask about its onset and location. Does the pain radiate? Ask about a history of heart disease and treatments for arrhythmias. Obtain a drug history and check compliance. Also, ask about caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and the use of a sympathomimetic (such as epinephrine), quinidine, caffeine, cocaine, methamphetamine, or alcohol may cause arrhythmias.

Physical examination

Check the patient’s apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S₁ (lub) and S₂ (dub) may indicate a conduction defect. A faint or absent S₁ and an easily audible S₂ may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats — possibly indicating premature atrial contractions — or other variations in heart rate or rhythm. Take the patient’s apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Report your findings to the physician.

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Murmurs: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs.) Use the bell of your stethoscope for low-pitched murmurs; the diaphragm for high-pitched murmurs.

Next, obtain a patient history. Ask if the murmur is a new discovery or if it has been known since birth or childhood. Find out if the patient has experienced any associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. Explore the patient’s medical history, noting especially any incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Pulse rhythm abnormality: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

If the patient’s condition permits, ask if he’s experiencing pain. If so, find out about onset and location. Does the pain radiate? Ask about a history of heart disease and treatments for arrhythmias. Obtain a drug history and check compliance. Also, ask about any caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Heart Murmurs (Asymptomatic): Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Normal Murmurs

Systolic Ejection Murmurs

Normal systolicejection murmurs are grade III or less.

They begin after S1 following the isovolumiccontraction period and end before S2.

They vary from cycle to cycle withrespiration or change in position.

Intensity increases with fever, anxiety,or exercise.

Although heard with maximum intensityat specific locations on the chest wall, they are louder in supineposition.

Vibratory Systolic Murmur

Commonlyheard in childhood and less often in infancy.

Usually grade II/VI but canrange from grade I to III.

Heard with maximum intensity at lowerleft sternal border or between this area and apex.

Has distinctive vibratory quality.

Pulmonary Systolic Murmur

Frequentlyheard in childhood and adolescence.

Maximum intensity is in second intercostalspace at upper left sternal border.

Usual intensity is grade II/VIwith range from grade I to III.

Higher in pitch than vibratory systolicejection murmur.

Also heard in straight back syndrome,which is characterized by absence of normal thoracic kyphosis andnarrow anterior-posterior diameter of chest. RV and pulmonary arterylie against sternum, and murmur is easily heard. Straight back syndromealso may be associated with mitral valve prolapse.

Physiologic Peripheral Pulmonary Systolic Murmur

May be heardin neonates, especially in preterm infants.

Intensity is usually grade I–II/VI.

Heard equally well in right and leftanterior chest, axillae, and back.

Usually disappears by 3–6mos of age.

Supraclavicular or Brachiocephalic Murmur

May be heardin childhood or adolescence.

Usually grade II or III/VI.

Maximum intensity is always above medialaspect of clavicles in supraclavicular fossa but may be heard belowclavicles.

Usually louder on right side.

Shoulder maneuvers are useful in distinguishingit from other murmurs. When physician is listening for murmur, childshould sit with shoulders relaxed and arms in front of chest. Murmurdiminishes or disappears when shoulders are hyperextended with elbowsbrought behind back.

Continuous Murmurs

Venous Hum

Commonlyheard in sitting position.

Grade II–IV/VI continuousmurmur with maximal intensity in supraclavicular fossa, just lateralto sternocleidomastoid muscle with transmission below clavicles.

Usually more prominent on right side.

Diminishes or disappears with compressionof ipsilateral jugular vein, head/neck turning or positioning,or with lying down.

Pathologic Murmurs

Can be systolic,diastolic, or continuous.

Intensity is usually grade III or more,but can be grade I or II if lesion is mild.

Duration is usually longer than thatof normal murmur.

Heard with maximum intensity at specificlocations on chest wall.

Systolic Murmurs

Maximal Intensity at Upper Right Sternal Border

Valvar Aortic Stenosis

Most commontype of LV outflow tract obstruction.

Produces grade II–IV/VIharsh systolic ejection murmur that is heard with maximum intensityat upper right sternal border.

Aortic ejection click also can be heardalong left sternal border and at apex.

Prominent apical impulse is palpable.

Chest radiography shows normal to mildlyenlarged heart, normal pulmonary vascular markings, and mild dilatationof ascending aorta.

ECG is normal or shows LV hypertrophy.

2-D echocardiography shows abnormalvalve. Doppler methods demonstrate abnormal flow pattern.

Maximal Intensity at Upper Left Sternal Border

Valvar Pulmonic Stenosis

Associatedwith prominent RV impulse over lower sternum, normal S2, and systolic ejectionclick (louder on expiration) along left sternal border.

Grade II–IV/VI harshsystolic ejection murmur transmits to neck and back.

In infants, click may be absent withmild stenosis.

Chest radiograph shows normal heartsize, normal pulmonary vascular markings, and dilated main pulmonaryartery segment.

ECG is normal or shows RV hypertrophy.

2-D echocardiography shows abnormalvalve. Doppler methods demonstrate abnormal flow pattern.

Atrial Septal Defects

Includeostium secundum, ostium primum, and sinus venosus defects.

Physical exam is similar with all defects.

Prominent RV impulse, grade II–III/VIsystolic ejection murmur with maximum intensity at upper left sternalborder, usually wide fixed splitting of S2, and grade II–III/VImid-diastolic rumbling murmur with maximum intensity at lower leftsternal border.

In infants, splitting of S2 may benormal or wide and not fixed.

Systolic murmur signifies increasedblood flow across pulmonic valve, and diastolic murmur reflectsincreased flow across tricuspid valve.

Chest radiography shows mild cardiomegaly,increase in pulmonary vascular markings, and enlarged pulmonaryartery segment.

ECG shows RV hypertrophy. In ostiumprimum defect, frontal plane QRS axis often shows left axis deviation,which signifies conduction system displacement. P wave on ECG ismore horizontal with sinus venosus defect.

2-D echocardiography visualizes defectsand can distinguish between them.

Mild-to-Moderate Coarctation of Aorta

BP in rightarm is significantly higher than that in legs with coarctation ofaorta.

Femoral pulses are diminished comparedwith brachial or radial pulses.

Prominent apical impulse.

Grade II–III/VI harshsystolic ejection murmur is commonly heard at upper left sternalborder and left back.

Grade II–III/VI high-pitchedcontinuous murmur may be heard over left side of spine along scapularedge.

Presence of aortic ejection click andsystolic ejection murmur at upper right sternal border usually signifiesbicuspid aortic valve, which is commonly associated with coarctationof aorta.

Chest radiograph shows normal or mildlyenlarged heart and normal pulmonary vasculature. Ascending aortamay be dilated. In older infants and children, indentation of descendingaorta just distal to aortic arch produces "3" sign.Erosion of bone by large intercostal arteries can produce notchingof lower margins of posterior ends of ribs 3–9.

In early infancy, ECG usually showsRV hypertrophy, whereas in children it may be normal or show mildLV hypertrophy.

2-D echocardiography can often demonstratecoarctation. In older children, if coarctation is not well demonstratedby echocardiography, it may be visualized by MRI.

Small Patent Ductus Arteriosus

Common interm infants and very common in preterm infants, especially in thosewith birth weight <1,500 g.

Murmur is usually grade II–III/VIand is systolic or continuous. Systolic ejection sounds are occasionallyheard along left sternal border.

Chest radiography shows normal sizeor mildly enlarged heart with increased pulmonary vascular markings.

ECG is either normal or shows mildLV hypertrophy.

Maximal Intensity at Lower Left Sternal Border

Normal vibratory ejection murmur must bedistinguished from 2 pathologic systolic murmurs that are heardwith maximum intensity at lower left sternal border: murmurs ofventricular septal defect and tricuspid incompetence.

Ventricular Septal Defect

Murmur ofsmall VSD may be heard as early as 1–3 days of age as pulmonaryvascular resistance decreases and left-to-right shunt develops.

Palpation reveals normal-sized or mildlyenlarged heart.

Intensity and splitting of S2 are normal.

Murmur is grade II–IV/VIand is heard throughout systole. It is harsh in quality with maximalintensity at lower left sternal border.

If defect begins to close with time,duration of murmur is less.

No diastolic murmur is heard at apexunless pulmonary:systemic flow ratio is ≥2:1.

Chest radiograph shows normal or mildlyenlarged heart, and increased pulmonary vascular markings.

ECG is normal or shows mild LV hypertrophy.

2-D echocardiography may not visualizesmall defects.

Tricuspid Incompetence

Murmur ishigh pitched, usually grade II–III/VI, and heardthroughout systole with maximal intensity at lower left sternalborder.

May be heard in asymptomatic lesions(isolated mild congenital tricuspid incompetence, atrioventricularcanal defects, Ebstein anomaly) or in symptomatic ones (atrioventricularcanal defects, Ebstein anomaly, pulmonary atresia with intact septum,endocarditis, perinatal asphyxia).

Maximal Intensity at Apex

Mitral Incompetence

Murmur ishigh pitched, usually grade II–IV/VI, and heardthroughout systole at apex with transmission to left axilla andback.

Heart is normal sized or mildly enlarged.

Chest radiograph and ECG are usuallynormal.

Causes include congenital defects ofmitral valve, atrioventricular canal defects, anomalous left coronaryartery from pulmonary artery, hypertrophic cardiomyopathy, Marfansyndrome, and Hurler syndrome.

Symptomatic causes include these lesionsas well as acute rheumatic fever, myocarditis, endocarditis, endocardialfibroelastosis, and perinatal asphyxia.

Mitral Valve Prolapse

Can occuras isolated defect or in association with ostium secundum atrialseptum defect, endocarditis, Hurler syndrome, Marfan syndrome, orEhlers-Danlos syndrome.

Usual finding is midsystolic nonejectionclick followed by late systolic murmur of mitral incompetence.

Murmur is heard best at apex, especiallyin standing position after squatting.

Chest radiograph is normal.

ECG may show inverted T waves in leadsII, III, and aVF as well as ST depression in left precordial leads.

Clinical diagnosis can be confirmedby M-mode or 2-D echocardiography.

Diastolic Murmurs

There havebeen some reports of normal diastolic murmurs occurring in infantsand children, but this is rare.

For this discussion, all diastolicmurmurs are considered pathologic. These murmurs usually indicate

Semilunarvalve incompetence (aortic or pulmonic valve)

Atrioventricular valve stenosis (mitralor tricuspid valve)

Severe mitral or tricuspid valve incompetence

Increased blood flow across the tricuspidvalve (atrial septal defect) or mitral valve (large ventricularseptal defect or patent ductus arteriosus)

Maximal Intensity at Upper Right Sternal Border

Aortic Valve Incompetence

Can occuras isolated congenital lesion or in association with valvar aorticstenosis, discrete subaortic stenosis, ventricular septal defect,acute rheumatic fever, or endocarditis.

Diastolic murmur of aortic valve incompetenceis grade I–IV/VI and is characterized by its highpitched decrescendo sound. Heard with maximum intensity at upperright sternal border but is also heard along left midsternal border.Murmur begins with aortic closure, and the more severe the incompetence,the longer the murmur and the wider the pulse pressure. Usuallyis louder when patient is sitting up and leaning forward.

Apical impulse may be prominent, dependingon degree of incompetence.

Chest radiography shows normal or mildlyenlarged heart.

ECG is normal or shows LV hypertrophy.

Maximal Intensity at Upper Left Sternal Border

Pulmonic Valve Incompetence

Producesmedium-pitched, grade I–IV/VI, diastolic decrescendomurmur, which begins with pulmonary closure and varies in durationdepending on severity of lesion.

Longer murmur signifies more severeincompetence.

Causes include congenital pulmonicvalve incompetence, idiopathic dilatation of pulmonary artery, valvarpulmonic stenosis, postsurgical repair (valvar pulmonary stenosis,tetralogy of Fallot), and endocarditis.

Maximal Intensity at Lower Left Sternal Border

Atrial Septal Defects

Diastolic flow rumble, usually grade I–III/VI,can be heard with maximal intensity at lower left sternal borderwith any type of ASD.

Tricuspid Stenosis

Rare lesionthat can occur as isolated congenital lesion or in association withsevere valvar pulmonic stenosis, hypoplasia of right ventricle withpulmonary atresia, or chronic rheumatic heart disease.

Murmur is grade I–III/VIdiastolic rumble with presystolic accentuation, which may increasein intensity with inspiration. Opening snap also may be heard.

Moderate-to-Severe Tricuspid Incompetence

Grade I–III/VIdiastolic flow rumble of tricuspid incompetence reflects increasein blood flow across tricuspid valve during diastole.

Systolic murmur of tricuspid incompetencealso is heard at lower left sternal border.

Affected children are usually symptomatic.

See section Tricuspid Incompetence.

Maximal Intensity at Apex

Mitral Stenosis

Murmur isgrade I–II/VI, diastolic, low-rumbling murmurwith presystolic accentuation and opening snap.

Heard with maximum intensity at apex.

May occur as isolated congenital defect,as part of Shone syndrome, or secondary to rheumatic fever.

Moderate-to-Severe Mitral Incompetence

Diastoliclow-pitched murmur heard with mitral incompetence reflects increasedantegrade blood flow across mitral valve.

Murmur varies in intensity and durationwith severity of incompetence and is heard with maximal intensityat apex.

Systolic murmur of mitral incompetenceis also heard at apex.

Moderate Left-to-Right Shunt Lesions

Lesions(e.g., VSD and patent ductus arteriosus) may produce moderate orlarge left-to-right shunts.

Grade I–III/VI low-pitcheddiastolic flow murmur can be heard at apex because of increased bloodflow across mitral valve in diastole.

Children with large left-to-right shuntsare in cardiac failure.

Continuous Murmurs

Maximal Intensity at Upper Left Sternal Border

Moderate Patent Ductus Arteriosus

Typicalmurmur of moderate-sized patent ductus arteriosus is continuousmachinery-like murmur, usually at least grade III/VI, withmaximum intensity at upper left sternal border, and transmissionalong left sternal border and in lung fields.

There is often increased LV impulse,wide but variable split of S2, and increased pulse pressure.

Chest radiograph shows mild cardiomegalyand increased pulmonary vascular markings.

ECG shows LV hypertrophy and occasionallyleft atrial enlargement.

2-D echocardiography with Doppler methodsis confirmatory.

Maximal Intensity at Left Midsternal Border

Aortic Pulmonary Window

There iscommunication between ascending aorta and main pulmonary artery.

Defect is usually large, which resultsin large amount of pulmonary blood flow.

Murmur is heard with maximum intensityat left midsternal border.

Primarily systolic with diastolic component.However, continuous murmur may be heard with rare small aortic pulmonarywindow.

Chest radiographic and ECG findingsare similar to those of patent ductus arteriosus.

2-D echocardiography with Doppler methodsis diagnostic.

Maximal Intensity with Variable Location

Coronary Arteriovenous Fistula

Communicationbetween coronary artery and heart, usually right atrium or pulmonaryartery.

Continuous murmur is usually heardover lower precordium, away from area where ductus is heard.

Cardiac catheterization and angiographyare usually necessary for definitive diagnosis.

Systemic Arteriovenous Fistula

This typeof connection within thorax can occur with communications betweensubclavian artery and innominate vein, between internal mammaryartery and vein, between bronchial arteries and branches of systemicazygous system, and between other chest wall vessels.

Continuous murmur is heard over areaof abnormal communication.

Cardiac catheterization and angiographyare necessary for definitive diagnosis.

Diagnostic Approach

To distinguisha normal from a pathologic murmur, physicians must rely on theirskill in physical exam of cardiovascular system; on their interpretationof chest radiograph, ECG, and 2-D echocardiogram; and on their knowledgeof the diagnostic possibilities that each murmur suggests.

In most cases, cardiovascular examat bedside can distinguish a normal from a pathologic murmur.

With a normalmurmur, no tests are needed. Physicians can reassure parents andexplain that the murmur is a normal phenomenon due to normal turbulenceof blood flow. They can also emphasize that the murmur is not indicativeof mild heart disease, nor is it of any importance whether it disappears.

With a pathologic murmur, precise diagnosismust be made because subsequent management depends on it. Diagnosisof pathologic murmurs is based on cardiovascular exam in conjunctionwith chest radiograph and ECG and sometimes 2-D echocardiogram.

Only rarely are cardiac catheterizationand angiography needed to clarify etiology of murmurs in asymptomaticchildren.

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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

Cardiac Failure: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Excessive Volume Load

Left-to-Right Shunt Lesions

Patent Ductus Arteriosus

Fetal ductusarteriosus is open communication between upper descending aortaand junction of main and left pulmonary arteries.

Usually closes within 1–2days after birth but can remain open, especially in preterm infants whoweigh <1,500 g.

Development of cardiac failure, whichusually occurs in neonatal period, depends on size of communicationand relationship between pulmonary and systemic resistances.

Usual physical findings include enlargedheart with prominent LV and RV impulses, narrowly split S2, gradeII–IV/VI continuous or long systolic murmur withmaximum intensity at upper left sternal border, S3 at apex, hepatomegaly,and wide pulse pressure. Systolic ejection sounds may occasionallybe heard along left sternal border.

Chest radiography shows marked cardiomegaly,enlarged left atrium, prominent main pulmonary segment, increasedpulmonary vascular markings, and occasionally Kerley b lines.

ECG shows RV or biventricular hypertrophy.

Ductus can often be visualized with2-D echocardiographic techniques and Doppler methods.

Clinical diagnosis can be difficultin preterm infants with respiratory distress syndrome who requiremechanical ventilation. Murmur may not be heard, and heart may notbe enlarged on chest radiograph. Cardiac failure should be suspectedif arterial blood gas status deteriorates or need for mechanical ventilationis prolonged.

Most children do not need invasivestudies before surgical ligation unless other defects are suspected.Cardiac catheterization and angiography may be necessary with atypicalmurmur or if findings suggest increase in pulmonary artery pressure.

Ventricular Septal Defect

Definedas opening of variable size in ventricular septum, and >1defect can exist.

Cardiac failure occurs between 1 and2 mos of age in infants with medium to large defects.

Clinical manifestations include tachypnea,tiring with feeding, and poor weight gain. Hepatomegaly and sometimessplenomegaly occur. Lung crackles and pedal edema are unusual ininfants.

Cardiac exam reveals cardiac enlargementwith prominent RV and LV impulses. Usually S2 is narrowly splitand pulmonic component is louder than normal. S3 or S4 gallop orboth may be heard. Grade III–V/VI harsh, holosystolicmurmur is heard with maximum intensity at lower left sternal border withtransmission to apex, axilla, and back. Grade I–II/VIapical mid-diastolic rumble signifies increased blood flow acrossmitral valve.

Chest radiography shows marked cardiomegaly,large left atrium, prominent main pulmonary artery segment, increasedpulmonary vascular markings, and occasionally Kerley b lines.

ECG usually shows biventricular hypertrophy.

2-D echocardiography shows VSD.

Atrial Septal Defect (Ostium Secundum)

AlthoughASD does not usually lead to cardiac failure during infancy andchildhood, cardiac failure may occur if large left-to-right shuntexists. Cardiac failure also may occur with combination of moderatesize ASD and VSD.

Tachypnea, tachycardia, cardiomegaly,and usually hepatomegaly occur.

Physical exam, radiographic, and ECGfindings are similar to those with ostium primum defect (see nextsection). Although frontal plane ECG axis of <–30degrees suggests AV canal defect, this pattern occurs in about 10% ofchildren with ostium secundum defects.

2-D echocardiography confirms diagnosis.

Atrioventricular Canal Defects

2 basictypes of AV canal defects are ostium primum and complete AV canaldefects.

In hearts with 2 ventricles, absenceor decrease in septal tissue immediately above and below normallevel of AV valves characterizes these defects.

Ostium Primum Defect

Clinicalpresentation is similar to that of ostium secundum defect, exceptthat mitral incompetence can occur with ostium primum defect becauseof cleft in mitral valve.

With presence of severe mitral incompetence,cardiac failure is more likely to occur.

Usual physical findings are enlargedheart, prominent RV impulse, normal or wide split of S2, grade II–III/VIsystolic ejection murmur with maximum intensity along upper leftsternal border, grade I–II/VI diastolic rumbleat lower left sternal border, and hepatomegaly. With significantmitral incompetence, murmur of mitral incompetence may be heardat apex.

Chest radiography shows cardiomegaly,prominent main pulmonary artery segment, and increased pulmonaryvascular markings.

ECG shows RV hypertrophy and QRS frontalplane axis that is more superior, especially in infants.

2-D echocardiography demonstrates defect.

Complete Atrioventricular Canal

Clinicalmanifestations are more diverse than those of other defects becauseof different hemodynamic situations that can exist. Lesion consistingof small VSD, large ostium primum defect, and normal mitral valvefunction presents like ostium primum defect. Lesion consisting oflarge VSD and normal mitral valve function presents like isolatedVSD. In either of these circumstances, if significant AV valve dysfunctionwith mitral or tricuspid incompetence exists, cardiac failure usuallyoccurs during first month of life.

Chest radiography shows marked cardiomegaly,enlarged main pulmonary artery segment, and increased pulmonaryvascular markings.

ECG shows RV or biventricular hypertrophyand frontal plane QRS axis of –40 to –150 degrees.

Defect may be seen with 2-D echocardiography.

Aortic Pulmonary Window

Due to failureof formation of base of spiral septum, which generally producescommunication between aorta and pulmonary artery just above semilunarvalves.

Cardiac failure occurs in early infancy.

Usual physical findings are markedcardiomegaly, accentuated pulmonary closure sound, long systolicmurmur of variable intensity along left sternal border in thirdand fourth intercostal spaces, hepatomegaly, and wide pulse pressure.

Radiographic and ECG findings are similarto those of large VSD or patent ductus arteriosus.

Usual method of diagnosis is 2-D echocardiography.

Total Anomalous Pulmonary Venous Connection without Obstruction

Severaltypes may occur. Most common is connection between pulmonary veinsand confluence behind left atrium. From this confluence, blood flowsvia anomalous vertical vein to left innominate vein and then toright superior vena cava and right atrium. Pulmonary veins alsomay connect at level of coronary sinus or posterior right atrium.

Clinical presentation and findingsare similar to those of large ASD, and cardiac failure may occurin infancy.

Chest radiography shows moderate cardiomegalywith increase in pulmonary vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography may show echo-freespace posterior to left atrium.

Cardiac catheterization and angiographyare frequently not needed.

Systemic Arteriovenous Fistulas

Usuallycongenital and can occur in cranium, liver, thorax, or extremity.

Clinical course is determined by amountof blood flow through fistula. If flow is large enough, increasein venous return produces increased volume load on heart.

Usual physical findings are markedcardiomegaly; normally split S2 with accentuated pulmonary component;continuous murmur over cranium, liver, or extremity; hepatomegaly;and wide pulse pressure. With intracranial fistula, neck veins aredistended and carotid pulses are bounding.

Chest radiography shows enlarged heartand increase in pulmonary vascular markings.

ECG shows RV or biventricular hypertrophy.

Head CT or MRI can help visualize anyintracranial pathology. Definitive diagnosis of intracranial orperipheral fistulas can be made by angiography.

Valvular Incompetence

Aortic Incompetence

Can be associatedwith unicuspid or bicuspid aortic valve, acute rheumatic fever,endocarditis, supracristal VSD, and Marfan syndrome.

Clinical course depends on acutenessof onset and severity of incompetence.

Mild aortic incompetence is asymptomatic,whereas acute severe aortic incompetence results in low cardiacoutput and hypotension. Chronic moderate-to-severe incompetenceproduces cardiac failure. Diastolic pressure of <50 mmHg and pulse pressure >50 mm Hg indicate significant incompetence.

When severe, LV impulse is increasedand displaced toward axilla. Pulse pressure is wide with boundingpulses. Murmur of aortic incompetence is diastolic decrescendo murmurthat begins with aortic closure. Its maximum intensity is at upperright sternal and left midsternal borders. The longer the murmur,the more severe the incompetence. Fluttering of anterior mitralvalve leaflet also can produce mid-diastolic apical murmur (AustinFlint murmur).

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG shows LV hypertrophy. Severe lesionmay produce subendocardial ischemia with ST depression and T-waveinversion.

2-D echocardiography with Doppler methodsis usually diagnostic.

Mitral Incompetence

Congenitalmitral incompetence is rare but may be due to underdevelopment ofvalve leaflets or short, thick chordae tendinae (parachute mitralvalve). Also may occur with AV canal defects and idiopathic hypertrophicsubaortic stenosis.

Acquired mitral incompetence is morecommon and can be seen with acute rheumatic fever or any cause ofLV failure, when there is dilatation of mitral valve annulus. Closedchest trauma, anomalous left coronary artery, Kawasaki disease,severe aortic stenosis, or coronary arterial disease may cause papillarymuscle infarction or rupture. Endocarditis may perforate valve orrupture chordae tendinae. Mitral valve also may undergo degenerationwith Marfan or Hurler disease. Another cause is prolapsing mitralleaflet syndrome, but severe incompetence is unusual with this lesion.

Clinical course depends on how severethe lesion is. Mild incompetence is asymptomatic, and moderate incompetencemay be tolerated for many years before cardiac failure occurs. Classicmurmur of mitral incompetence is grade III–IV/VIhigh pitched holosystolic murmur with maximum intensity at apexand transmission to left axilla and back. In severe mitral incompetence,prominent LV impulse, S3, and diastolic rumble at apex are commonfindings.

Chest radiography shows marked cardiomegalywith enlarged left atrium and pulmonary venous congestion.

ECG shows left atrial enlargement andmay show LV hypertrophy.

2-D echocardiography can assess anatomyof valve and its attachments as well as any associated abnormalities.Doppler methods can assess severity of incompetence.

Pulmonary Incompetence

Most commoncause is surgical valvotomy. Other causes include isolated congenital incompetenceof pulmonic valve, bicuspid pulmonic valve, and idiopathic dilatationof main pulmonary artery. Absence of pulmonic valve, which is usuallyassociated with VSD and infundibular pulmonic stenosis, causes severeincompetence.

Usual physical findings with moderate-to-severeincompetence include prominent RV impulse, delayed or absent pulmoniccomponent of S2, and characteristic grade II–IV/VImedium-pitched diastolic decrescendo murmur heard with maximum intensityat upper and middle left sternal border.

Chest radiography shows marked cardiomegaly.

ECG shows RV hypertrophy.

2-D echocardiography and Doppler methodsare usually diagnostic.

Tricuspid Incompetence

Congenitaland acquired cardiac lesions may produce tricuspid incompetence.Occasionally, valve leaflets do not form and cardiac failure mayoccur in utero. Isolated tricuspid incompetence may be due to dysmorphicvalve, cleft in valve, or abnormal chordae tendinae. Incompetenceof tricuspid valve also may occur with AV canal defects and Ebsteinanomaly. Acquired causes include severe perinatal asphyxia, acuterheumatic fever, and endocarditis.

Physical exam can establish diagnosisof significant tricuspid incompetence. Typical murmur is grade III/VIhigh-pitched holosystolic murmur that is louder on inspiration andheard with maximum intensity at lower left sternal border. Livermay be enlarged and show systolic pulsations. Jugular venous pulseshows prominent v wave followed by deep y descent. Mid-diastolicrumble that reflects increased blood flow across tricuspid valvealso may be heard at lower left sternal border. Other findings can includecyanosis, peripheral edema, and ascites.

Chest radiography shows cardiomegaly,which is due to large right atrium.

ECG findings depend on associated lesions,but large P waves indicate right atrial enlargement.

2-D echocardiography can assess anatomy,whereas Doppler methods can be helpful in estimating severity ofincompetence.

Excessive Pressure Load

Left Ventricular Outflow Tract Obstruction

Hypertrophic Cardiomyopathy

Genetictransmission is usually autosomal-dominant.

Some individuals have obstructive form,with massive hypertrophy of ventricular musculature, especiallyventricular septum. Abnormal systolic anterior motion of anteriormitral leaflet also produces dynamic subaortic obstruction. Besidescardiac failure, angina and syncope also may occur.

Usual physical findings include sustainedthrusting single or bifid apical pulse, variable splitting of S2depending on how severe obstruction is, grade II–III/VIsystolic ejection murmur with maximum intensity along left midsternalborder, jerky pulse with rapid upstroke, and hepatomegaly. Occasionally,murmur of mitral incompetence is heard at apex.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG shows LV or biventricular hypertrophy.

2-D echocardiography can effectivelydelineate extent of hypertrophy.

Congenital Valvar Aortic Stenosis

Due to imperfectcusp development and leaflet thickening.

Severe stenosis can cause cardiac failurein early infancy.

Usualphysical findings include ejection click and systolic ejection murmur,which may be heard with maximum intensity at upper right and middleleft sternal borders. If cardiac output is reduced, murmur may besoft or absent.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG often shows RV forces in infants <1mo of age. In infants with critical aortic stenosis, ST depressionand T-wave inversion may be seen in left precordial leads.

2-D echocardiography usually showsabnormal aortic valve and poorly contractile LV.

Other manifestations in older childrenare angina, dyspnea on exertion, and syncope.

There is usually prominent LV impulseat apex, narrowly or paradoxically split S2, grade II–IV/VIharsh systolic ejection murmur with maximum intensity at upper rightsternal border, aortic ejection click, sometimes S3 and S4 at apex,and pulse with slow upstroke and narrow pulse pressure.

Chest radiography shows enlarged heartwith prominent ascending aorta and pulmonary venous congestion.

ECG usually shows LV hypertrophy withor without ST depression and T-wave inversion.

2-D echocardiography shows abnormalaortic valve, and Doppler methods can estimate pressure differenceacross valve.

Discrete Subvalvar Aortic Stenosis

Obstructionbelow aortic valve may be due to thin membrane diaphragm or thickfibromuscular tissue. Diaphragm also may be associated with aorticinsufficiency.

Clinical findings are similar to thosewith valvar aortic stenosis, except that aortic ejection click isless common and aortic dilatation is less prominent.

2-D echocardiography usually demonstratestype and location of obstruction. Otherwise, cardiac catheterizationand angiography are diagnostic.

Supravalvar Aortic Stenosis

Definedas localized or diffuse narrowing of ascending aorta just abovelevel of coronary arteries.

Can occur as familial or sporadic isolatedlesion but is often associated with Williams syndrome, whose featuresinclude elfin facies and mental retardation. Many individuals, especiallyif they have Williams syndrome, usually have RV outflow tract obstruction,which can occur at valvar, supravalvar, and peripheral pulmonaryartery levels.

Clinical findings are similar to thoseof congenital valvar aortic stenosis, except that murmur is heardhigher on chest wall and ejection click is unusual. Suprasternalnotch thrill is common.

BP in right arm may be 20 mm Hg higherthan that in left arm because of stenosis at origin of left subclavianartery or jet effect of blood with ejection from LV into ascendingaorta.

Chest radiography shows enlarged heartwithout poststenotic dilatation of ascending aorta.

ECG shows LV hypertrophy and, if stenosisis severe, T-wave inversion in left chest leads.

2-D echocardiography demonstrates narrowing,and Doppler methods can assess pressure gradient across ascendingaorta.

Cardiac catheterization and angiographyare usually performed because of high incidence of associated abnormalities,which include patent ductus arteriosus, coarctation of aorta, pulmonarystenosis, and mitral insufficiency.

Aortic Arch Hypoplasia or Interruption

Most commonlyoccurs in aortic isthmus but may occur anywhere in aortic arch.Most extreme form is interruption of arch, which can occur proximalto left carotid artery, distal to left subclavian artery, or betweenleft subclavian and left carotid arteries.

In almost all cases, patent ductusarteriosus provides blood flow to lower part of body.

With rare exceptions, there are associateddefects (e.g., VSD, double outlet RV, AV canal defect, and tricuspidatresia with aortopulmonary transposition).

Clinical findings depend on severityof intracardiac defects, pulmonary vascular resistance, and sizeof ductus arteriosus. Almost all infants develop severe cardiacfailure during first week of life.

Differential cyanosis of extremitiesdepends on degree of ventricular shunting and is variable finding.

Femoral pulses are diminished or absent.No murmur is specific.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG may show RV or biventricular hypertrophy.

Although 2-D echocardiography may bediagnostic, cardiac catheterization and angiography are definitive.

Localized Juxtaductal Coarctation of Aorta

Definedas congenital narrowing of upper descending aorta that is usuallylocated near ductus arteriosus.

Primary coarctation of aorta occurswith or without patent ductus arteriosus but without other majorcardiac defects.

Complex coarctation is associationof other cardiac defects with coarctation [e.g., VSD, aorticvalvar stenosis, or mitral stenosis (Shone syndrome)].

Severe primary coarctation of aortausually presents with cardiac failure during first month of life.Delay in onset is possibly related to ductal closure at aortic end.With complex coarctation, cardiac failure usually appears duringfirst week of life.

Usual physical findings in child withprimary coarctation of aorta are arm BP that is ≥20 mm Hg higherthan pressure in legs, diminished or absent femoral pulses, andgrade II–III/VI systolic ejection murmur withmaximum intensity along left sternal border or over scapula in leftback. Arm BPs may be unequal if anomalous right subclavian arteryis present below coarctation or left subclavian artery is narrowedat origin of coarctation. Clinical findings with complex coarctationdepend on presence of associated lesions. Murmurs of VSD, valvaraortic stenosis, or mitral incompetence usually can be heard ifthese defects are present.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

In early infancy, ECG usually showsRV hypertrophy. In later infancy and childhood, it usually showsLV or biventricular hypertrophy, which is usual finding with complexcoarctation.

In neonates 2-D echocardiography canoften visualize coarctation, and Doppler methods can estimate itsseverity.

MRI can help define anatomy in somecases. If precise diagnosis of coarctation and associated lesionscan be accurately made, cardiac catheterization may not be necessary.

Right Ventricular Outflow Tract Obstruction

Can occurat level of pulmonary valve or above or below valve leaflets.

Valvar pulmonic stenosis is most commonform.

Congenital Valvar Pulmonic Stenosis

Neonateswith critical pulmonary valvar stenosis develop cardiac failurein immediate postnatal period.

Often infundibular hypertrophy occurswith valvar stenosis and tends to be progressive. Asymptomatic infantsand children may develop progressive severe pulmonary stenosis withonset of cardiac failure in adulthood.

Usual physical findings are prominentRV impulse; normal or diminished pulmonary component of S2; gradeII–IV/VI systolic ejection murmur with maximumintensity at upper left sternal border; and hepatomegaly. Severestenosis produces delay in peak intensity of murmur and delay in pulmonaryvalve closure. Occasionally, continuous murmur of patent ductusarteriosus or pansystolic murmur of tricuspid incompetence is heard.

Chest radiography shows cardiomegalyand decreased pulmonary vascular markings.

ECG usually shows RV hypertrophy, unlessRV is hypoplastic. T-wave inversion is sometimes seen in right precordialleads.

2-D echocardiography can visualizethickened, stenotic valve and narrowed infundibulum. Doppler methodsindicate severity of obstruction.

Left Ventricular Inflow Tract Obstruction

Pulmonary Vein Stenosis

Obstructionof normally connected pulmonary veins may be due to intrinsic narrowing(diffuse hypoplasia, localized diaphragm, narrowing on entry toleft atrium) or occasionally by external compression by posteriormediastinal mass.

Presentation is similar to that oftotal anomalous pulmonary venous connection with obstruction. Usualphysical findings are prominent RV impulse and accentuated pulmonaryclosure sound. No specific murmurs are heard.

Chest radiography shows near-normalheart size with increase in pulmonary venous vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography can sometimesview stenoses directly.

Cardiac catheterization and angiographyare definitive.

Total Anomalous Pulmonary Venous Connection with Obstruction

Pulmonaryvenous drainage below diaphragm to ductus venosus with venous return viainferior vena cava produces pulmonary venous obstruction.

Supracardiac or cardiac connectionsof pulmonary veins can cause pulmonary venous obstruction, but thisis uncommon.

Severe obstruction produces severecyanosis and respiratory distress in neonatal period.

Usual physical findings are prominentRV impulse, narrowly split S2, and hepatomegaly. These murmurs aresometimes heard: murmur of tricuspid incompetence; continuous murmuralong left sternal border, which reflects blood flow through anomalouschannel; and systolic ejection murmur along upper left sternal border,which reflects blood flow across pulmonary valve.

Chest radiography usually shows mildcardiomegaly and intense increase in pulmonary vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography shows enlargedRV, and no pulmonary veins are seen entering left atrium. If pulmonaryveins empty into coronary sinus or into large channel behind atria,these structures can be seen.

Cardiac catheterization and angiographyare definitive.

Cor Triatriatum

Failureof resorption of common pulmonary vein results in cor triatriatumwith division of left atrium into upper and lower chambers usuallyconnected by restrictive opening.

Clinical presentation is same as pulmonaryvenous obstruction. Usual physical findings are prominent RV impulseand accentuated pulmonary closure sound. No specific murmurs are heard.

Chest radiography shows mild cardiomegalyand increase in pulmonary venous vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography or MRI can bediagnostic.

Supravalvular Stenosing Ring of Left Atrium

Fibrousring located on atrial side of mitral annulus sometimes protrudesinto mitral orifice, causing inflow obstruction of LV. Occurs asisolated lesion or in association with parachute mitral valve, subaorticstenosis, and coarctation of aorta (Shone syndrome).

Clinical presentation and findingsare similar to those for cor triatriatum.

Although this lesion can be visualizedby 2-D echocardiography, cardiac catheterization and angiographyare definitive.

Tumor

Tumor withinleft atrium, usually myxoma, can produce findings similar to mitral stenosis,but if tumor is on pedicle that sometimes protrudes into mitralvalve orifice, findings may be intermittent.

2-D echocardiography and MRI revealtumor mass.

Mitral Valve Obstruction (Atresia, Stenosis, Parachute Mitral Valve)

Most severeform is mitral atresia, which is discussed later in section Hypoplastic Left Heart Complex.

Mitral stenosis is prototype lesionof LV inflow tract obstruction. Congenital mitral stenosis occursas isolated lesion or in association with other lesions (e.g., aorticstenosis, VSD, ASD, coarctation of aorta, or endocardial fibroelastosis).Cusps may be abnormal, commissures may fuse, or chordae tendinaemay join below valve ring. Parachute valve with chordae tendinaeattached to single papillary muscle also may cause obstruction toblood flow at mitral valve level.

Congenital forms of mitral stenosisare usually severe, and infants present with cardiac failure. Usualphysical findings are prominent RV impulse, loud S1, and accentuatedpulmonic component of S2. Apical mid-diastolic murmur with presystolicaccentuation may not be heard with severe cardiac failure but maybe heard once failure is controlled. Opening snap of mitral valvemay not be heard because of thickness and immobility of valve. Variousdegrees of mitral incompetence may occur, and typical apical murmurof mitral insufficiency may be heard. With severe pulmonary arteryhypertension and RV dilatation, murmur of tricuspid insufficiencyalso may be heard.

Chest radiography shows left atrialenlargement out of proportion to cardiac enlargement, large pulmonaryartery segment, and pulmonary edema in severe cases.

ECG shows hypertrophy of RV and bothatria.

2-D echocardiography shows anatomyand function of valve and presence of any other abnormalities. Dopplermethods can also estimate flow and pressure difference across valve.

Diagnosis rarely needs confirmationby cardiac catheterization and angiography.

Right Ventricular Inflow Tract Obstruction

Systemic Venous Obstruction

May be dueto obstruction of venous return in superior or inferior vena cavaby thrombus, mediastinal mass, or secondary to atrial baffle procedurefor aortopulmonary transposition.

Venous distension and edema of thatportion of body drained by obstructed vessel usually occurs.

Right Atrium Obstruction

Thrombusformation may produce obstruction and can be complication of indwelling cathetersin vena cava or right atrium.

Right atrial myxoma and extension ofWilms tumor or hepatic tumor also may produce obstruction.

Tricuspid Valve Obstruction

Tricuspidatresia is most severe form of tricuspid valve obstruction. See Chap. 12, Cyanosis.

Isolated tricuspid stenosis is rare,and if atrial septum is intact, findings are those of venous obstruction.If stenosis is severe, there is mid-diastolic rumbling murmur atlower left sternal border, and prominent S3 and S4.

ECG shows tall peaked P waves indicativeof right atrial enlargement. Right atrium is also enlarged on chestradiograph.

2-D echocardiography is diagnostic.

Ebstein Anomaly

Septal andinferior leaflets of tricuspid valve are displaced into RV withanomalous attachments to wall of RV.

Depending on specific anatomy, widespectrum of clinical presentations occurs. With severe RV dysfunctionand increased pulmonary vascular resistance, intense cyanosis andcardiac failure can occur in neonatal period. Usual physical findingsare wide splitting of S2, prominent S3 and S4, murmur of tricuspidincompetence, and hepatomegaly.

Chest radiography shows marked cardiomegalywith enlargement of right atrium (heart shape is globular) and usuallydecreased pulmonary vascular markings.

ECG commonly shows right atrial hypertrophy,prolonged PR interval, right bundle branch block, and sometimesWolff-Parkinson-White syndrome.

2-D echocardiography is diagnostic.

When specific anatomic details needto be evaluated, cardiac catheterization and angiography are necessary.

Cor Pulmonale

Definedas pulmonary hypertension complicating lung disease.

Most common causes in pediatric populationare bronchopulmonary dysplasia, cystic fibrosis, and chronic upperairway obstruction.

Patients may experience dyspnea, fatigue,exercise intolerance, chest pain, syncope, and cyanosis. Physicalfindings include RV heave, increase in intensity of S2 with narrowor fixed splitting, jugular venous distension, hepatomegaly, andperipheral edema.

Chest radiographic findings may showevidence of chronic lung disease with RV enlargement and dilatedcentral pulmonary arteries.

ECG usually shows RV hypertrophy.

Systemic Hypertension

Althoughcommon cause of cardiac failure in adults, children with hypertensiondo not usually develop failure unless onset is acute or hypertensionis extremely severe.

Most common cause of acute severe hypertensionin childhood is acute glomerulonephritis.

BP should always be measured in anyonewith cardiac failure.

See Chap.32, Hypertension.

Disturbance in Myocardial Function

Acute Rheumatic Fever and Rheumatic Heart Disease

Acute andchronic cardiac failure can result from rheumatic heart disease.Most common valve lesions are mitral and aortic incompetence.

See Chap.37, Limp.

Kawasaki Disease

Most seriouscomplications are coronary artery aneurysm, coronary thrombosis,myocarditis, mitral valve incompetence, pericardial effusion, andarrhythmias.

Indications of cardiac involvementare murmur of mitral incompetence, pericardial friction rub, chestradiographic findings of cardiomegaly and pulmonary venous congestion,ST and T-wave changes on ECG, and coronary aneurysms as shown by2-D echocardiography.

See Chap.21, Fever.

Myocarditis

Usual causeis enteroviral infection. Isolation of pathogen from myocardiumis most reliable way to determine etiology; however, this is notalways possible. Isolation from other tissues or body fluids orserologic tests can be used.

Clinical manifestations include fatigue,dyspnea, chest pain, and tachypnea. Cardiac failure with pulmonaryedema and shock also may occur.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG findings suggestive of myocarditisare generalized low-voltage QRS complexes, T-wave inversion, andarrhythmias (e.g., ventricular extrasystoles and atrial tachycardia).

2-D echocardiography shows dilatationof chambers and poor contractility.

Pericarditis

Acute pericarditisis inflammation of parietal pericardium, which can be associated withinfectious or noninfectious disorder.

Infectious causes include viruses (enterovirusesmost commonly), pyogenic bacteria (S. aureus, S. pneumoniae, N.meningitidis, and H. influenzae type b most commonly), M. tuberculosis, andfungi (Candida and Aspergillus species).

Noninfectious causes include acuterheumatic fever, juvenile rheumatoid arthritis, Kawasaki disease,and postpericardiotomy syndrome.

Can occur in asymptomatic individualwith mild pericardial effusion or as life-threatening process inwhich large effusion may compromise cardiac function (cardiac tamponade).Chest pain is most common symptom of pericarditis, but exerciseintolerance and fever also may occur. Cardiac exam reveals muffledheart sounds, tachycardia, and friction rub if effusion is smallvolume. Rub is grating to and fro sound heard best in inspirationwith patient leaning forward. Manifestations of tamponade includetachycardia, reduced BP, and pulsus paradoxus with >10mm Hg decrease in systolic BP during inspiration as result of decreasedcardiac filling.

Chest radiography shows increase insize of cardiac shadow.

ECG shows low-voltage QRS complexesand generalized ST segment elevation.

2-D echocardiography can demonstrateeffusion.

Specific etiology of infectious pericarditisis best determined by evaluation of pericardial fluid obtained bypericardiocentesis. Appropriate viral, bacterial, mycobacteria,and fungal cultures should be performed. Serologic tests may benecessary for diagnosis of viral disease.

Endocarditis

Infectionof cardiac endothelial surface signifies endocarditis.

In pediatric population, usually occursas complication of congenital or rheumatic heart disease, valvehomografts, or artificial heart valves. Most frequent pathogensin childhood are viridans streptococci and S. aureus.

Common findings include fever, malaise,anorexia, and weight loss. New or changed murmur, splenomegaly,petechiae, and embolic phenomena are often found, but Osler nodes,Roth spots, Janeway lesions, and splinter hemorrhages are uncommon.

Although clinical findings suggestdiagnosis, positive blood culture confirms specific pathogen involved.2-D echocardiography can show characteristic vegetations.

Cardiomyopathy

Chronicmyocardial diseases can be classified as dilated, hypertrophic,or restrictive cardiomyopathies.

Dilated cardiomyopathy is thought to be primaryor result from viral myocarditis.

Hypertrophic cardiomyopathy is oftengenetic and may be associated with neuromuscular disorders.

Restrictive cardiomyopathy may be associatedwith infiltrative disorders.

Chest radiography usually shows enlargedheart.

ECG often shows LV hypertrophy, STsegment flattening, and T-wave inversion.

Echocardiography shows marked ventricularenlargement and poor contractile function with dilated cardiomyopathy,massive septal hypertrophy with hypertrophic cardiomyopathy, andlarge dilated atria with reduced ventricular filling with restrictivecardiomyopathy.

Cardiac biopsy is only occasionallyuseful in making specific diagnosis.

Myocardial Infarction

Anomalous Left Coronary Artery from Pulmonary Artery

May presentwith acute myocardial infarction and cardiac failure in infancy.Murmur of mitral incompetence may be heard.

Chest radiography shows cardiomegalyand pulmonary venous congestion.

ECG shows anterior or anteroseptalmyocardial infarction with deep Q waves and T-wave inversion inleads 1, aVL, and left precordial leads.

2-D echocardiography with Doppler methodsis almost always diagnostic.

Cardiac catheterization and angiographyare definitive.

Older children are usually asymptomaticand may only present with murmur of mitral incompetence or continuousmurmur at upper left or mid-sternal border. Presence of deep Q wavesin leads 1, aVL, and V4–V6 suggests diagnosis.

Atherosclerosis

Familialhypercholesterolemia (familial hyperlipoproteinemia type II) cancause atherosclerosis and myocardial infarction in childhood.

Genetic transmission is autosomal-dominant.

Tendon and tuberous xanthomas are common.

Plasma cholesterol is high (600–1,000mg/dL), plasma triglycerides are normal, and low-densitylipoproteins are elevated.

Cardiac Tumor

Mass withinchamber can cause inflow or outflow tract obstruction. Involvementof myocardium can cause cardiac failure.

Benign tumors include rhabdomyoma,fibroma, myxoma, and teratoma, whereas malignant tumors includerhabdomyosarcoma and teratoma. Leukemia and lymphoma can involvepericardium and cause pericardial compression.

Clinical manifestations vary dependingon location and histologic type.

2-D echocardiography and MRI locateand define extent of mass lesion.

Histologic diagnosis is definitive.

Metabolic Heart Disease

Severalcommon metabolic problems that affect myocardial function are discussedin this section.

See Garson et al. (1998) for detaileddiscussion of metabolic disorders affecting heart.

Perinatal Asphyxia

Can producetransient ischemia of myocardium and cardiac failure.

Gallop rhythm and murmurs of mitralor tricuspid incompetence may be heard.

Chest radiography shows cardiomegalywith pulmonary venous congestion.

ECG shows RV hypertrophy, ST depression,and T-wave flattening. Abnormal Q waves in limb and chest leadssuggest anterior or inferior myocardial infarction.

2-D echocardiography sometimes showsdecreased myocardial contractility.

Hypocalcemia

Can causedilated cardiomyopathy in neonates and older children.

Cardiac failure usually resolves withrepletion of calcium.

Hypoglycemia

In neonateshypoglycemia may cause cardiomegaly and cardiac failure.

Risk factors include maternal diabetesmellitus, low birth weight, and septicemia.

Severe Anemia

Any severe chronic anemia with hemoglobinconcentration <5 g/dL may produce cardiac failure.

Drugs

Anthracyclineantibiotics doxorubicin and daunomycin are cancer chemotherapeutic agentsthat can damage myocardium. Development of cardiac failure is relatedto cumulative dose.

Echocardiographic ejection fractionmeasurements are useful for monitoring individuals who are takingthese drugs.

Complex Anatomic Lesions

5 lesionsin this section involve intracardiac or ductal right-to-left shunts.

Cardiac failure is most obvious manifestation,and cyanosis is not often clinically visible.

Hypoplastic Left Heart Complex

2 basic types of hypoplastic left heart complexare (a) aortic and mitral atresia with absent or slitlike LV, and(b) aortic and mitral stenosis with small LV.

Aortic and Mitral Atresia

Usuallypresent within 48 hrs of birth with cardiac failure and mild cyanosis.Usual physical findings are prominent RV impulse, single loud S2,grade II/VI systolic ejection murmur along left sternalborder, hepatomegaly, and diminished peripheral pulses.

Chest radiography shows moderate cardiomegalyand pulmonary venous congestion.

ECG shows RV hypertrophy.

2-D echocardiography shows large RV,small or absent LV, mitral and aortic atresia, and hypoplastic ascendingaorta.

Aortic and Mitral Stenosis

Usuallypresent with cardiac failure in first or second week after birth.Usual physical findings are prominent RV impulse or LV impulse dependingon size of LV, single or narrow split of S2, murmur of aortic stenosis,hepatomegaly, and diminished pulses.

Chest radiography shows enlarged heartand pulmonary venous congestion.

ECG usually shows LV hypertrophy withoccasional ST depression and T-wave flattening or inversion in leftprecordial leads.

2-D echocardiography is usually diagnostic.

Transposition of Great Arteries with Large Ventricular SeptalDefect

The aortarises from RV, while pulmonary artery arises from LV. Large communicationexists at ventricular level and also may occur at ductal level.

Cardiac failure and mild cyanosis occurat 2–4 wks of age. Murmur of VSD can be heard. S2 is narrowwith accentuated pulmonary component.

Chest radiography shows cardiomegaly,increase in pulmonary vascular markings, an absent pulmonary arterysegment.

ECG shows RV or biventricular hypertrophy.

2-D echocardiography is diagnostic.

Double-Outlet Right Ventricle

Both aortaand pulmonary artery arise entirely or in large part from RV. VSDis part of this lesion and can be subaortic, subpulmonic, doublycommitted, or noncommitted. Subaortic and subpulmonic defects aremost common.

Clinical presentation of subaorticdefect is similar to that of isolated large VSD, whereas clinicalpresentation of subpulmonic defect is similar to that of transpositionof great arteries with intact ventricular septum.

2-D echocardiography is usually diagnostic.

Cardiac catheterization and angiographyare important in planning of surgery.

Truncus Arteriosus

1 greatartery with single semilunar valve arises from base of heart. Systemic,coronary, and 1 or 2 pulmonary arteries arise from this artery.Beneath valve is VSD. Usually presents during neonatal period withcardiac failure and mild cyanosis.

Usual physical findings are diffuseprominent impulse at lower left sternal border, occasional ejectionclick, grade II–IV/VI systolic ejection murmuralong left sternal border, wide pulse pressure, and hepatomegaly.Other possible findings are early diastolic murmur along left sternalborder, which signifies truncal incompetence, or continuous murmurat 1 or both upper sternal borders, which reflects stenosis of originof 1 or both pulmonary arteries. Stenosis of truncal valve may produceharsh systolic ejection murmur at upper right sternal border.

Chest radiography shows cardiomegaly,increase in pulmonary vascular markings, deficient main pulmonaryartery segment, and frequently right aortic arch.

ECG shows RV hypertrophy and frequentlybiventricular hypertrophy.

2-D echocardiography is diagnostic.

Cardiac catheterization and angiographycan define anatomy of pulmonary arteries, aortic arch, truncal valve,and hemodynamic state.

Univentricular Atrioventricular Connections

Definedas malformations in which both AV valves or common AV valve openinto same ventricle.

In absence of pulmonary stenosis oratresia, clinical presentation of this lesion is similar to thatof large VSD.

Chest radiography shows cardiomegalywith increase in pulmonary vascular markings.

ECG may show increased voltage in eitherright or left precordial leads.

2-D echocardiography and cardiac catheterizationand angiography are diagnostic.

Abnormal Cardiac Rhythms

Supraventricular Tachycardia

Most childrenhave structurally normal heart; however, some may have Wolff-Parkinson-Whitesyndrome.

Mechanisms include reentry using accessorypathway, reentry without accessory pathway, and automatic tachycardia.

In infants <1 yr of age, ventricularrate varies from 220 to 280 bpm, whereas in older children it variesfrom 180 to 240 bpm. RR interval is regular, and onset and terminationof rhythm are usually sudden. P waves may or may not be visible.They follow or precede each QRS or are unrelated (AV dissociation).

In infants left bundle branch blockpattern with aberrant conduction is common. Neonates may developcardiac failure if arrhythmia lasts only few hours. Infants whohave this abnormal rhythm for >24 hrs are at risk for developmentof cardiac failure.

ECG confirms diagnosis. Fetal echocardiographymay confirm diagnosis in utero.

Atrial Flutter

Can occurin individuals with normal heart, in those with structural defects,and after surgery for congenital heart defects.

Can cause cardiac failure, especiallyin young infant.

Atrial rate varies from 250 to 500bpm. With 1:1 conduction, ventricular rate is too fast for ventriclesto fill in diastole, and low cardiac output occurs. With some degreeof AV block such that conduction is 2:1, assuming atrial rate of300 bpm and ventricular rate of 150 bpm, cardiac failure is unlikely. RRinterval is usually regular, but it can be irregular in presenceof AV block.

Sawtooth flutter waves are diagnostic.

Complete Heart Block

Congenitalcomplete heart block can occur in infants with otherwise normalheart, in some neonates whose mothers have systemic lupus erythematosus,and in infants with ventricular inversion and transposition of greatarteries.

May occur following surgical correctionof congenital heart defects.

Cardiac failure occurs only if ventricularrate is too slow to maintain normal cardiac output. In neonates,ventricular rate of <40 bpm usually results in cardiacfailure, whereas infants with ventricular rate of >50 bpmare usually asymptomatic.

ECG shows lack of conduction of atrialimpulses to ventricles with faster atrial rate and slower ventricularrate.

Diagnostic Approach

Diagnosis of Cardiac Failure

Diagnosisof cardiac failure is clinical and is based on history and physicalexam findings.

Most cardiac disease produces LV orbiventricular failure. Pure right heart failure is uncommon.

Manifestations of cardiac failure ininfants are increased work of breathing, tiring with feedings, andpoor weight gain.

Tachycardia, sweating, gallop rhythm,and cardiac enlargement indicate impaired myocardial performance.

Tachypnea, dyspnea, wheezing, cough,crackles, and cyanosis are manifestations of pulmonary venous congestion.

Signs of systemic venous congestionare hepatomegaly, neck vein distension, peripheral edema, splenomegaly,and ascites.

Diminished peripheral pulses and hypotensionreflect decreased cardiac output.

In infancy, crackles may not be heard,neck vein distension is difficult to evaluate, and peripheral edemais uncommon.

Once diagnosis is made, next task isto determine specific cause.

Age of Onset of Cardiac Failure

Often providesclue to specific cause of cardiac failure.

Birth–1 wk: Causes of cardiacfailure include perinatal asphyxia, severe anemia, complete heartblock, supraventricular tachycardia, hypoplastic left heart syndrome,critical aortic stenosis, critical pulmonary stenosis, complex coarctationof aorta, VSD with absent pulmonary valve, aortic incompetence (aorta–LVtunnel syndrome), isolated tricuspid incompetence, and Ebstein anomaly.

1–6 wks: Common causes ofcardiac failure include patent ductus arteriosus, VSD, complete AVcanal, double-outlet RV, truncus arteriosus, transposition of greatarteries with large VSD or patent ductus arteriosus, univentricularAV connections, simple or complex coarctation of aorta, total anomalous pulmonaryvenous connection with obstruction, severe aortic stenosis, anycause of pulmonary venous obstruction, myocarditis, anomalous leftcoronary artery, and any cause of severe anemia.

Common acquired causes of cardiac failureare myocarditis, cardiomyopathy, pericarditis, acute rheumatic fever,endocarditis, postcardiac surgery for complex lesions, and arrhythmias.

Diagnostic Categories

Many cardiaclesions can be grouped together in diagnostic categories based onpresence or absence of cyanosis, physical exam findings, and chestradiographic findings (Table 7.1 ).

Other tests (e.g., ECG, 2-D echocardiographywith Doppler methods and cardiac catheterization with angiography)can be used to make definitive diagnosis.

Table 7.1. Diagnostic Classification of Common Causes of CardiacFailure

Group	Findings	Possible Causes
I	Acyanotic	Left-to-right shunt lesions
	Cardiomegaly
	Increased pulmonary vascular markings
II	Acyanotic	Left-sided obstructive lesions
	Cardiomegaly
	Pulmonary venous congestion
III	Acyanotic usually	Myocarditis
	Cardiomegaly	Cardiomyopathy
	Pulmonary venous congestion	Anomalous coronary artery
	No heart murmur frequently
IV	Mild cyanosis	Transposition with large VSD
	Cardiomegaly	Hypoplastic left heart syndrome
	Increased pulmonary vascular markings	Double-outlet RV
		Truncus arteriosus
		Univentricular AV connections
V	Marked cyanosis	Pulmonary venous obstruction
	Normal-sized heart or mild cardiomegaly
	Pulmonary venous congestion
VI	Cyanosis	Critical pulmonic stenosis
	Cardiomegaly	Ebstein anomaly
	Decreased pulmonary vascular markings

Evaluation

These testsshould generally be performed in any infant or child with cardiacfailure: chest radiography; ECG; CBC with differential; analysisof serum electrolytes, glucose, creatinine; blood urea nitrogen;pulse oximetry; and 2-D echocardiography.

Chest radiography shows presence ofcardiomegaly and whether pulmonary vascular markings are normal,increased, or decreased.

ECG indicates presence of hypertrophyof chambers and permits diagnosis of arrhythmias.

Hyponatremia is common and reflectsincrease in water retention in excess of sodium.

2-D echocardiography with Doppler methodsis often diagnostic or at very least provides useful informationin many cases of cardiac failure. Cardiac catheterization with angiographyprovides definitive diagnosis for selected heart lesions.

>>>>>>>

» READ BOOK EXCERPT ONLINE »

Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

Murmurs: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 398.) Use the bell of your stethoscope for low-pitched murmurs and the diaphragm for high-pitched murmurs.

Next, obtain a patient history. Ask if the murmur is a new discovery or if it has been known since birth or childhood. Find out if the patient has experienced associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. Explore the patient's medical history, noting especially an incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.

Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient's liver tender or palpable? Does he have peripheral edema?

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Pulse rhythm abnormality: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

If the patient's condition permits, ask if he's experiencing pain. If so, find out about its onset and location. Does the pain radiate? Ask about a history of heart disease and treatment for arrhythmias. Obtain a drug history and check the patient's compliance. Also, ask about caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and the use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.

Next, check the patient's apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S₁ (lub) and S₂ (dub) may indicate a conduction defect. A faint or absent S₁ and an easily audible S₂ may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats—possibly indicating premature atrial contractions—or other variations in heart rate or rhythm. Take the patient's apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Place the patient on a cardiac monitor and obtain an ECG to evaluate the cardiac rhythm. Report your findings to the practitioner.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

MURMURS: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

A chest x-ray with anterior oblique films during a barium swallow along with an electrocardiogram (ECG), sedimentation rate, blood serology thyroid profile, and CBC are basic in the workup of a murmur. If there is a fever or if there is recent onset of the murmur, blood cultures, an antistreptolysin-O (ASO) titer, and a C-reactive protein (CRP) test should be done. An antinuclear antibody (ANA) test, ECG, and phonocardiogram are frequently done. Referral to a cardiologist is wise if the cause is obscure or if one is unable to spend the time for a careful workup. Angiocardiography and cardiac catheterization are the only sure ways to determine the location of the valvular disease, and, in many cases, the exact cause.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

CARDIAC ARRHYTHMIAS: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The diagnosis depends a lot on the type of arrhythmia. Atrial premature contractions are usually benign, and an extensive workup is unnecessary unless other physical signs indicate the need for it. Infrequent ventricular premature contractions (VPCs) in otherwise healthy individuals probably can be handled the same way. When VPCs are frequent or multifocal, an exercise tolerance test, echocardiogram, and perhaps coronary angiography are indicated. Runs of ventricular tachycardia require an extensive workup, including coronary angiography, but usually there will be other signs to indicate the need for this. Atrial tachycardia and fibrillation require a workup of hyperthyroidism and pulmonary disease, systemic hypertension, and congestive heart failure (CHF). Atrial obstruction and dilatation should be excluded by echocardiography.

Any arrhythmia warrants an electrocardiogram (ECG) and possibly repeated ECGs. The Holter monitor should be used if there is doubt about the type of arrhythmia.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

Learning Problems: Learning Problems - DIAGNOSIS
(The 5-Minute Pediatric Consult)

• General goal is to determine whether the learning problems result from a primary medical or psychosocial condition. If no such condition is identified, then the patient may have a specific learning disability.
• The pediatrician also is in a good position to identify social and environmental factors that may be associated with learning problems, and can coordinate the appropriate medical, psychiatric, and/or psychoeducational evaluation, with consultation as indicated.
• Early identification of learning problems and appropriate intervention help to prevent the cascade of negative consequences triggered by poor academic achievement:
  • Phase 1a:
    • Identify and address medical factors that may affect learning (e.g., sensory impairments, lead intoxication, absence seizures, iatrogenic interventions).
    • Consider subtle genetic syndromes (e.g., fragile X syndrome in girls) that may cause learning problems without causing other major medical abnormalities.
  • Phase 1b:
    • Screen for psychiatric conditions and for social and environmental factors that may be associated with learning problems.
    • Psychosocial stresses may exacerbate learning difficulties or be a primary etiologic factor.
    • If indicated, refer to appropriate consultants.
  • Phase 2:
    • For patients with learning problems that are suspected to be primary (i.e., specific learning disabilities), a complete psychoeducational evaluation is indicated.
    • If ADHD present, treatment may be directed by the primary care physician or by a subspecialist.

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008

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