Evaluation and Management of Heart Murmurs in Children



FREE PREVIEW Log in or buy this issue to read the full article. AAFP members and paid subscribers get free access to all articles. Subscribe now.


FREE PREVIEW Subscribe or buy this issue. AAFP members and paid subscribers get free access to all articles.

Am Fam Physician. 2011 Oct 1;84(7):793-800.

Heart murmurs are common in healthy infants, children, and adolescents. Although most are not pathologic, a murmur may be the sole manifestation of serious heart disease. Historical elements that suggest pathology include family history of sudden cardiac death or congenital heart disease, in utero exposure to certain medications or alcohol, maternal diabetes mellitus, history of rheumatic fever or Kawasaki disease, and certain genetic disorders. Physical examination should focus on vital signs; age-appropriate exercise capacity; respiratory or gastrointestinal manifestations of congestive heart failure; and a thorough cardiovascular examination, including features of the murmur, assessment of peripheral perfusion, and auscultation over the heart valves. Red flags that increase the likelihood of a pathologic murmur include a holosystolic or diastolic murmur, grade 3 or higher murmur, harsh quality, an abnormal S2, maximal murmur intensity at the upper left sternal border, a systolic click, or increased intensity when the patient stands. Electrocardiography and chest radiography rarely assist in the diagnosis. Referral to a pediatric cardiologist is recommended for patients with any other abnormal physical examination findings, a history of conditions that increase the likelihood of structural heart disease, symptoms suggesting underlying cardiac disease, or when a specific innocent murmur cannot be identified by the family physician. Echocardiography provides a definitive diagnosis and is recommended for evaluation of any potentially pathologic murmur, and for evaluation of neonatal heart murmurs because these are more likely to be manifestations of structural heart disease.

Heart murmurs are common in asymptomatic, otherwise healthy children. These murmurs are often innocent and result from the normal patterns of blood flow through the heart and vessels.1 However, a heart murmur may be the sole finding in children with structural heart disease; therefore, a thorough evaluation is necessary.

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendation Evidence rating References

Structural heart disease is more likely when the murmur is holosystolic, diastolic, grade 3 or higher, or associated with a systolic click; when it increases in intensity with standing; or when it has a harsh quality.

C

6, 10, 25

Chest radiography and electrocardiography rarely assist in the diagnosis of heart murmurs in children.

B

5, 6, 2933

Family physicians should order echocardiography or consider referral to a pediatric cardiologist for newborns with a heart murmur, even if the child is asymptomatic, because of the higher prevalence of structural heart lesions in this population.

B

28, 43


A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.org/afpsort.xml.

SORT: KEY RECOMMENDATIONS FOR PRACTICE

View Table

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendation Evidence rating References

Structural heart disease is more likely when the murmur is holosystolic, diastolic, grade 3 or higher, or associated with a systolic click; when it increases in intensity with standing; or when it has a harsh quality.

C

6, 10, 25

Chest radiography and electrocardiography rarely assist in the diagnosis of heart murmurs in children.

B

5, 6, 2933

Family physicians should order echocardiography or consider referral to a pediatric cardiologist for newborns with a heart murmur, even if the child is asymptomatic, because of the higher prevalence of structural heart lesions in this population.

B

28, 43


A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.org/afpsort.xml.

Incidence and Prevalence

Congenital heart disease (CHD) may occur in the presence or absence of a heart murmur. The incidence of CHD varies between four and 50 per 1,000 live births.2 One review found an incidence of 75 cases per 1,000 live births; of these, six cases per 1,000 were moderate or severe.3

History

Certain historical features suggest possible structural heart disease (Table 1).1,2,411  Cardiovascular signs and symptoms can be non-specific (e.g., poor feeding, failure to thrive) or specific (e.g., chest pain, palpitations), and can help identify children who are likely to have structural heart disease (Table 2).4,7,10

Table 1.

Historical Findings Suggesting Structural Heart Disease in Children with Heart Murmurs

Historical finding Significance

Family history

CHD

More common in children with a first-degree relative who has CHD (three- to 10-fold increased risk7); high penetrance with ventricular septal defect and mitral valve prolapse

Sudden cardiac death or hypertrophic cardiomyopathy

Increased risk of hypertrophic cardiomyopathy (autosomal dominant pattern)

Sudden infant death syndrome

Can be secondary to undiagnosed CHD lesions8

Personal history

Conditions that may coexist with CHD:

Certain genetic disorders (e.g., DiGeorge syndrome, velo-cardio-facial syndrome) are associated with cardiac malformations

Aneuploidy (e.g., trisomy 21, Turner syndrome)

Trisomy 21 is associated with an increased risk of atrioventricular septal defects, atrial septal defects, ventricular septal defects, patent ductus arteriosus, and tetralogy of Fallot

Connective tissue disorder (e.g., Marfan syndrome)

Turner syndrome is associated with increased risk of coarctation of the aorta, aortic valve stenosis, and left ventricular hypertrophy

Inborn error of metabolism

Marfan syndrome is associated with mitral valve prolapse, aortic root dilation, and aortic insufficiency

Major congenital defects of other organ systems

Syndrome with dysmorphic features

Frequent respiratory infections

Respiratory symptoms may be attributable to heart disease (i.e., congestive heart failure); enlarged vessels may lead to atelectasis or difficulty clearing respiratory secretions, thereby promoting infection

Kawasaki disease

Leading cause of acquired cardiac disease in children; can cause coronary artery aneurysm and stenosis9

Rheumatic fever

Associated with development of rheumatic heart disease

Prenatal or perinatal history

In utero exposure to alcohol or other toxins

Fetal alcohol syndrome is associated with an increased risk of atrial and ventricular septal defects, and tetralogy of Fallot10

In utero exposure to selective serotonin reuptake inhibitors or other potentially teratogenic medications

Selective serotonin reuptake inhibitor exposure is associated with a small but statistically significant increased risk of mild heart lesions, including ventricular septal defects and bicuspid aortic valve (although not all studies found an increased risk11)

Lithium exposure is associated with Ebstein anomaly of the tricuspid valve

Valproate (Depacon) exposure is associated with coarctation of the aorta and hypoplastic left heart syndrome

Intrauterine infection

Maternal infections may increase risk of structural heart lesions (e.g., maternal rubella infection is associated with patent ductus arteriosus and peripheral pulmonary stenosis)

Maternal diabetes mellitus

Increased risk of CHD, including transient hypertrophic cardiomyopathy, tetralogy of Fallot, truncus arteriosus, and double-outlet right ventricle

Preterm delivery

CHD is associated with other conditions (e.g., genetic disorders, in utero exposure to toxins) that can result in preterm birth; 50 percent of newborns weighing less than 3 lb, 5 oz (1,500 g) at birth have CHD (most commonly patent ductus arteriosus)7


CHD = congenital heart disease.

Information from references 1, 2, and 4 through 11.

Table 1.   Historical Findings Suggesting Structural Heart Disease in Children with Heart Murmurs

View Table

Table 1.

Historical Findings Suggesting Structural Heart Disease in Children with Heart Murmurs

Historical finding Significance

Family history

CHD

More common in children with a first-degree relative who has CHD (three- to 10-fold increased risk7); high penetrance with ventricular septal defect and mitral valve prolapse

Sudden cardiac death or hypertrophic cardiomyopathy

Increased risk of hypertrophic cardiomyopathy (autosomal dominant pattern)

Sudden infant death syndrome

Can be secondary to undiagnosed CHD lesions8

Personal history

Conditions that may coexist with CHD:

Certain genetic disorders (e.g., DiGeorge syndrome, velo-cardio-facial syndrome) are associated with cardiac malformations

Aneuploidy (e.g., trisomy 21, Turner syndrome)

Trisomy 21 is associated with an increased risk of atrioventricular septal defects, atrial septal defects, ventricular septal defects, patent ductus arteriosus, and tetralogy of Fallot

Connective tissue disorder (e.g., Marfan syndrome)

Turner syndrome is associated with increased risk of coarctation of the aorta, aortic valve stenosis, and left ventricular hypertrophy

Inborn error of metabolism

Marfan syndrome is associated with mitral valve prolapse, aortic root dilation, and aortic insufficiency

Major congenital defects of other organ systems

Syndrome with dysmorphic features

Frequent respiratory infections

Respiratory symptoms may be attributable to heart disease (i.e., congestive heart failure); enlarged vessels may lead to atelectasis or difficulty clearing respiratory secretions, thereby promoting infection

Kawasaki disease

Leading cause of acquired cardiac disease in children; can cause coronary artery aneurysm and stenosis9

Rheumatic fever

Associated with development of rheumatic heart disease

Prenatal or perinatal history

In utero exposure to alcohol or other toxins

Fetal alcohol syndrome is associated with an increased risk of atrial and ventricular septal defects, and tetralogy of Fallot10

In utero exposure to selective serotonin reuptake inhibitors or other potentially teratogenic medications

Selective serotonin reuptake inhibitor exposure is associated with a small but statistically significant increased risk of mild heart lesions, including ventricular septal defects and bicuspid aortic valve (although not all studies found an increased risk11)

Lithium exposure is associated with Ebstein anomaly of the tricuspid valve

Valproate (Depacon) exposure is associated with coarctation of the aorta and hypoplastic left heart syndrome

Intrauterine infection

Maternal infections may increase risk of structural heart lesions (e.g., maternal rubella infection is associated with patent ductus arteriosus and peripheral pulmonary stenosis)

Maternal diabetes mellitus

Increased risk of CHD, including transient hypertrophic cardiomyopathy, tetralogy of Fallot, truncus arteriosus, and double-outlet right ventricle

Preterm delivery

CHD is associated with other conditions (e.g., genetic disorders, in utero exposure to toxins) that can result in preterm birth; 50 percent of newborns weighing less than 3 lb, 5 oz (1,500 g) at birth have CHD (most commonly patent ductus arteriosus)7


CHD = congenital heart disease.

Information from references 1, 2, and 4 through 11.

Table 2.

Symptoms Suggesting Cardiac Disease

Symptom or sign Significance

Cardiovascular

Chest pain

May be related to aortic stenosis or hypertrophic cardiomyopathy

Cyanosis

Structural heart lesion with restricted pulmonary blood flow

Dizziness

Multiple potential causes, including hypoxia and CHF

Near-syncope or syncope

May be related to aortic stenosis or hypertrophic cardiomyopathy

Palpitations

May be related to arrhythmias secondary to structural heart lesions

Constitutional

Developmental delay

Congenital heart lesions are more common in children with certain genetic disorders and syndromes

Diaphoresis

May indicate CHF or poor cardiac fitness

Easily fatigued

May indicate CHF, hypoxia, or poor cardiac fitness

Poor exercise tolerance or capacity for play

May indicate CHF, hypoxia, or poor cardiac fitness

Poor growth or failure to thrive

May indicate CHF, poor cardiac fitness, or a genetic disorder or syndrome; poor weight gain most commonly reflects decreased cardiac output or left-to-right shunts with pulmonary hypertension

Respiratory

Asthma-like symptoms

Cardiac asthma resulting from pulmonary congestion

Chronic cough

Atelectasis or difficulty clearing secretions because of pulmonary vascular congestion

Dyspnea on exertion

May indicate CHF, hypoxia, or poor cardiac fitness


CHF = congestive heart failure.

Information from references 4, 7, and 10.

Table 2.   Symptoms Suggesting Cardiac Disease

View Table

Table 2.

Symptoms Suggesting Cardiac Disease

Symptom or sign Significance

Cardiovascular

Chest pain

May be related to aortic stenosis or hypertrophic cardiomyopathy

Cyanosis

Structural heart lesion with restricted pulmonary blood flow

Dizziness

Multiple potential causes, including hypoxia and CHF

Near-syncope or syncope

May be related to aortic stenosis or hypertrophic cardiomyopathy

Palpitations

May be related to arrhythmias secondary to structural heart lesions

Constitutional

Developmental delay

Congenital heart lesions are more common in children with certain genetic disorders and syndromes

Diaphoresis

May indicate CHF or poor cardiac fitness

Easily fatigued

May indicate CHF, hypoxia, or poor cardiac fitness

Poor exercise tolerance or capacity for play

May indicate CHF, hypoxia, or poor cardiac fitness

Poor growth or failure to thrive

May indicate CHF, poor cardiac fitness, or a genetic disorder or syndrome; poor weight gain most commonly reflects decreased cardiac output or left-to-right shunts with pulmonary hypertension

Respiratory

Asthma-like symptoms

Cardiac asthma resulting from pulmonary congestion

Chronic cough

Atelectasis or difficulty clearing secretions because of pulmonary vascular congestion

Dyspnea on exertion

May indicate CHF, hypoxia, or poor cardiac fitness


CHF = congestive heart failure.

Information from references 4, 7, and 10.

In infants, feeding difficulties may be the first sign of congestive heart failure, which is present in approximately one-third of infants and children with CHD.4 The most common symptoms in a series of children presenting to the emergency department with acute heart failure included dyspnea (74 percent), nausea and vomiting (60 percent), fatigue (56 percent), and cough (40 percent).12

Exercise tolerance should be assessed in an age-appropriate fashion. Parents of infants should be asked about their child's ability to play and the duration and vigor of feeding; parents of older children should compare their child's ability to participate in team sports with that of peers.4 Chest pain is rarely a presenting symptom of cardiac disease in children.13,14 In a pediatric cardiology clinic, chest pain or syncope prompted consultation in approximately 10 percent of children; only 11 percent of those with chest pain and 5 percent of those with syncope had cardiac disease.14 A high degree of suspicion is necessary to detect underlying cardiac disease in children who report exertional syncope or chest pain, or who have a family history of hypertrophic cardiomyopathy.1,13,14

Physical Examination

The patient's vital signs should be compared with age-established norms (available at http://www.cc.nih.gov/ccc/pedweb/pedsstaff/age.html), and a focused examination of the respiratory, cardiovascular, and gastrointestinal systems should be performed5  (Table 32,57,10,15,16). Congenital anomalies of other organ systems may be associated with CHD in up to 25 percent of patients.6 The child's appearance, activity level, color, and respiratory effort should be assessed, and the neck should be examined for prominent vessels, abnormal pulsations, and bruits.1 Jugular venous distension is rare in children.4 The chest wall should be inspected for abnormalities of the sternum, which can be associated with CHD,15 and for abnormal cardiac impulses or thrills.1 The lungs should be auscultated for abnormal breath sounds such as crackles, which may indicate pulmonary congestion, or wheezing, which may indicate cardiac asthma. Abdominal examination should focus on the liver location (seeking abdominal situs) and evaluation for liver enlargement or ascites, which may signal congestive heart failure.5

Table 3.

Physical Examination of Children with Heart Murmurs

Finding Significance

Abnormal growth (height and weight plotted on growth chart)

Feeding difficulties may be a sign of cardiac disease in newborns and infants (decreased exercise capacity)

Certain genetic disorders may increase risk of delayed growth and CHD

Abnormal vital signs (compared with age-adjusted norms)

Arrhythmia, tachycardia, hypoxia, and tachypnea may indicate underlying structural heart disease

Blood pressure discrepancy between upper and lower limbs may indicate coarctation of the aorta (pressure gradient of > 20 mm Hg with low blood pressure in the lower extremities)

Adventitial breath sounds (e.g., wheezing, rales, ronchi, pleural rub)

Wheezing may be associated with cardiac asthma; rales may be associated with pulmonary congestion secondary to congestive heart failure

Chest contour signaling maldevelopment of the sternum15

Defective segmentation of the sternum may occur in children with CHD

Dysmorphic features

Certain genetic or congenital conditions increase risk of CHD

Cardiovascular findings

Abnormal S2

Classic finding of wide split fixed S2 with atrial septal defects; abnormal S2 may be present in other types of CHD

Capillary refill

Normal peripheral perfusion is less than 2 to 3 seconds; delay may indicate poor perfusion secondary to diminished cardiac output

Displaced point of maximal impulse; precordial impulses (heaves, lifts, thrills)

Possible structural abnormality or ventricular enlargement

Edema

Congestive heart failure

Left-sided precordial bulge

Cardiac enlargement

S3 or S4

Can indicate structural heart disease; S3 can be a normal finding but usually disappears when patient is upright

Substernal heave

Right ventricular hypertension

Systolic ejection click

Semilunar valvular stenosis

Weak or absent femoral pulses

Coarctation of the aorta

Gastrointestinal findings

Ascites

Congestive heart failure

Hepatomegaly

Congestive heart failure

Location of liver signals abdominal situs

High rate of CHD with abdominal situs


CHD = congenital heart disease.

Information from references 2, 5 through 7, 10, 15, and 16.

Table 3.   Physical Examination of Children with Heart Murmurs

View Table

Table 3.

Physical Examination of Children with Heart Murmurs

Finding Significance

Abnormal growth (height and weight plotted on growth chart)

Feeding difficulties may be a sign of cardiac disease in newborns and infants (decreased exercise capacity)

Certain genetic disorders may increase risk of delayed growth and CHD

Abnormal vital signs (compared with age-adjusted norms)

Arrhythmia, tachycardia, hypoxia, and tachypnea may indicate underlying structural heart disease

Blood pressure discrepancy between upper and lower limbs may indicate coarctation of the aorta (pressure gradient of > 20 mm Hg with low blood pressure in the lower extremities)

Adventitial breath sounds (e.g., wheezing, rales, ronchi, pleural rub)

Wheezing may be associated with cardiac asthma; rales may be associated with pulmonary congestion secondary to congestive heart failure

Chest contour signaling maldevelopment of the sternum15

Defective segmentation of the sternum may occur in children with CHD

Dysmorphic features

Certain genetic or congenital conditions increase risk of CHD

Cardiovascular findings

Abnormal S2

Classic finding of wide split fixed S2 with atrial septal defects; abnormal S2 may be present in other types of CHD

Capillary refill

Normal peripheral perfusion is less than 2 to 3 seconds; delay may indicate poor perfusion secondary to diminished cardiac output

Displaced point of maximal impulse; precordial impulses (heaves, lifts, thrills)

Possible structural abnormality or ventricular enlargement

Edema

Congestive heart failure

Left-sided precordial bulge

Cardiac enlargement

S3 or S4

Can indicate structural heart disease; S3 can be a normal finding but usually disappears when patient is upright

Substernal heave

Right ventricular hypertension

Systolic ejection click

Semilunar valvular stenosis

Weak or absent femoral pulses

Coarctation of the aorta

Gastrointestinal findings

Ascites

Congestive heart failure

Hepatomegaly

Congestive heart failure

Location of liver signals abdominal situs

High rate of CHD with abdominal situs


CHD = congenital heart disease.

Information from references 2, 5 through 7, 10, 15, and 16.

The peripheral pulses should be examined for rate, rhythm, volume, and character, and capillary refill time should be less than three seconds.4 The heart should be auscultated over the tricuspid, pulmonary, mitral, and aortic areas with the bell and diaphragm of the stethoscope while the patient is supine, sitting, and standing17 (Figure 118).Innocent murmurs are produced by the normal flow of blood through the heart. Changing the flow by changing the patient's position (for example, decreasing flow to the heart with the Valsalva maneuver) will change the intensity of the murmur. Young children should be prompted to push out their abdomen against the examiner's hand.1 The physician should listen for normal S1 and S2; a wide fixed split S2 is characteristic of an atrial septal defect.19 Gallops can be a normal finding in adolescents.1

Figure 1.

Listening areas for clicks: upper right sternal border (URSB) for aortic valve clicks; upper left sternal border (ULSB) for pulmonary valve clicks; lower left sternal border (LLSB), or the tricuspid area, for ventricular septal defects; and the apex for aortic or mitral valve clicks.

Reprinted with permission from McConnell ME, Adkins SB III, Hannon DW. Heart murmurs in pediatric patients: when do you refer? Am Fam Physician. 1999;60(2):560.

View Large


Figure 1.

Listening areas for clicks: upper right sternal border (URSB) for aortic valve clicks; upper left sternal border (ULSB) for pulmonary valve clicks; lower left sternal border (LLSB), or the tricuspid area, for ventricular septal defects; and the apex for aortic or mitral valve clicks.

Reprinted with permission from McConnell ME, Adkins SB III, Hannon DW. Heart murmurs in pediatric patients: when do you refer? Am Fam Physician. 1999;60(2):560.


Figure 1.

Listening areas for clicks: upper right sternal border (URSB) for aortic valve clicks; upper left sternal border (ULSB) for pulmonary valve clicks; lower left sternal border (LLSB), or the tricuspid area, for ventricular septal defects; and the apex for aortic or mitral valve clicks.

Reprinted with permission from McConnell ME, Adkins SB III, Hannon DW. Heart murmurs in pediatric patients: when do you refer? Am Fam Physician. 1999;60(2):560.

The heart murmur is characterized by its timing during the cardiac cycle; its location, quality, intensity, and pitch (how it sounds); and the presence or absence of clicks1  (Table 4 5,7,17  and Table 5 2023). The intensity of heart murmurs is graded from 1 to 6. Grade 1 murmurs are barely audible; grade 2 murmurs are faint but can be heard immediately; grade 3 murmurs can be heard easily and are moderately loud; grade 4 murmurs can be heard easily over a wide area but do not have a palpable thrill; grade 5 murmurs are loud and have a precordial thrill; and grade 6 murmurs are loud enough to hear with the stethoscope raised off the chest.17,24 Certain characteristics of the murmur may be considered red flags, prompting stronger consideration for structural heart disease. These include a holosystolic murmur (odds ratio [OR] of pathologic murmur = 54), grade 3 or higher (OR = 4.8), harsh quality (OR = 2.4), an abnormal S2 (OR = 4.1), maximal intensity at the upper left sternal border (OR = 4.2), a systolic click (OR = 8.3), diastolic murmur, or increased murmur intensity with standing.6,10,25 A decrease or lack of change in the murmur intensity with passive leg elevation (likelihood ratio [LR] = 8.0) or when the child moves from standing to squatting (LR = 4.5) increases the likelihood of hypertrophic cardiomyopathy.26

Table 4.

Characteristics of Innocent Heart Murmurs

Type Description Age at detection Can sound like

Aortic systolic murmur

Systolic ejection murmur best heard over the aortic valve

Older childhood into adulthood

Mammary artery soufflé*

High-pitched systolic murmur that can extend into diastole; best heard along the anterior chest wall over the breast

Rare in adolescence

Arteriovenous anastomoses or patent ductus arteriosus

Peripheral pulmonary stenosis

Grade 1 or 2, low-pitched, early- to mid-systolic ejection murmur heard over axilla or back

< 1 year

Pulmonary artery stenosis or normal breath sounds

Pulmonary flow murmur

Grade 2 or 3, crescendo-decrescendo, early- to mid-systolic murmur peaking in mid-systole; best heard at the left sternal border between the second and third intercostal spaces; characterized by a rough, dissonant quality; loudest when patient is supine and decreases when patient is upright and holding breath

All

Atrial septal defect or pulmonary valve stenosis

Still murmur

Grade 1 to 3, early systolic murmur; low to medium pitch with a vibratory or musical quality; best heard at lower left sternal border; loudest when patient is supine and decreases when patient stands

Infancy to adolescence, often 2 to 6 years

Ventricular septal defect or hypertrophic cardiomyopathy

Supraclavicular\brachiocephalic systolic murmur

Brief, low-pitched, crescendo-decrescendo murmur heard in the first two-thirds of systole; best heard above clavicles; radiates to neck; diminishes when patient hyperextends shoulders

Childhood to young adulthood

Bicuspid/stenotic aortic valve, pulmonary valve stenosis, or coarctation of the aorta

Venous hum

Grade 1 to 6 continuous murmur; accentuated in diastole; has a whining, roaring, or whirring quality; best heard over low anterior neck, lateral to the sternocleinomastoid; louder on right; resolves or changes when patient is supine

3 to 8 years

Cervical arteriovenous fistulas or patent ductus arteriosus


*—Mammary artery soufflé murmur is caused by blood flow in the arteries and veins leading to and from the breasts.

Information from references 5, 7, and 17.

Table 4.   Characteristics of Innocent Heart Murmurs

View Table

Table 4.

Characteristics of Innocent Heart Murmurs

Type Description Age at detection Can sound like

Aortic systolic murmur

Systolic ejection murmur best heard over the aortic valve

Older childhood into adulthood

Mammary artery soufflé*

High-pitched systolic murmur that can extend into diastole; best heard along the anterior chest wall over the breast

Rare in adolescence

Arteriovenous anastomoses or patent ductus arteriosus

Peripheral pulmonary stenosis

Grade 1 or 2, low-pitched, early- to mid-systolic ejection murmur heard over axilla or back

< 1 year

Pulmonary artery stenosis or normal breath sounds

Pulmonary flow murmur

Grade 2 or 3, crescendo-decrescendo, early- to mid-systolic murmur peaking in mid-systole; best heard at the left sternal border between the second and third intercostal spaces; characterized by a rough, dissonant quality; loudest when patient is supine and decreases when patient is upright and holding breath

All

Atrial septal defect or pulmonary valve stenosis

Still murmur

Grade 1 to 3, early systolic murmur; low to medium pitch with a vibratory or musical quality; best heard at lower left sternal border; loudest when patient is supine and decreases when patient stands

Infancy to adolescence, often 2 to 6 years

Ventricular septal defect or hypertrophic cardiomyopathy

Supraclavicular\brachiocephalic systolic murmur

Brief, low-pitched, crescendo-decrescendo murmur heard in the first two-thirds of systole; best heard above clavicles; radiates to neck; diminishes when patient hyperextends shoulders

Childhood to young adulthood

Bicuspid/stenotic aortic valve, pulmonary valve stenosis, or coarctation of the aorta

Venous hum

Grade 1 to 6 continuous murmur; accentuated in diastole; has a whining, roaring, or whirring quality; best heard over low anterior neck, lateral to the sternocleinomastoid; louder on right; resolves or changes when patient is supine

3 to 8 years

Cervical arteriovenous fistulas or patent ductus arteriosus


*—Mammary artery soufflé murmur is caused by blood flow in the arteries and veins leading to and from the breasts.

Information from references 5, 7, and 17.

Table 5.

Prevalence and Characteristics of Pathologic Heart Murmurs

Type of structural heart lesion Prevalence among children with congenital heart disease (%) Symptoms and clinical course Characteristics

Ventricular septal defect

20 to 25

Small defects: usually asymptomatic

Small defects: loud holosystolic murmur at LLSB (may not last throughout systole if defect is very small)

Medium or large defects: CHF, symptoms of bronchial obstruction, frequent respiratory infections

Medium and large defects: increased right-to-left ventricular impulses; thrill at LLSB; split or loud single S2; holosystolic murmur at LLSB without radiation; grade 2 to 5; may also hear a grade 1 or 2 mid-diastolic rumble

Atrial septal defect

8 to 13

Usually asymptomatic and incidentally found on physical examination or echocardiography; large defects can be present in infants with CHF

Grade 2 or 3 systolic ejection murmur best heard at ULSB; wide split fixed S2; absent thrill; may have a grade 1 or 2 diastolic flow rumble at LLSB

Patent ductus arteriosus

6 to 11

May be asymptomatic; can cause easy fatigue, CHF, and respiratory symptoms

Continuous murmur (grade 1 to 5) in ULSB (crescendo in systole and decrescendo into diastole); normal S1; S2 may be “buried” in the murmur; thrill or hyperdynamic left ventricular impulse may be present

Tetralogy of Fallot

10

Onset depends on severity of pulmonary stenosis; cyanosis may appear in infancy (2 to 6 months of age) or in childhood; other symptoms include hypercyanotic spells or decreased exercise tolerance

Central cyanosis; clubbing of nail beds; grade 3 or 4 long systolic ejection murmur heard at ULSB; may have holosystolic murmur at LLSB; systolic thrill at ULSB; normal to slightly increased S1; single S2

Pulmonary stenosis

7.5 to 9

Usually asymptomatic but may have symptoms secondary to pulmonary congestion

Systolic ejection murmur (grade 2 to 5); heard best at ULSB radiating to infraclavicular regions, axillae, and back; normal or loud S1; variable S2; systolic ejection click may be heard at left sternal border and may vary with respiration

Coarctation of the aorta

5.1 to 8.1

Newborns and infants may present with CHF; older children are usually asymptomatic or may have leg pain or weakness

Systolic ejection murmur best heard over interscapular region; normal S1 and S2; decreased or delayed femoral pulse; may have increased left ventricular impulse

Aortic stenosis

5 to 6

Usually asymptomatic; symptoms may include dyspnea, easy fatigue, chest pain, or syncope; newborns and infants may present with CHF

Systolic ejection murmur (grade 2 to 5) best heard at upper right sternal border with radiation to carotid arteries; left ventricular heave; thrill at ULSB or suprasternal notch

Transposition of the great arteries

5

Variable presentation depending on type; may include cyanosis or CHF in first week of life

Cyanosis; clubbing of nail beds; single S2; murmur may be absent or grade 1 or 2 nonspecific systolic ejection murmur; may have a grade 3 or 4 holosystolic murmur at LLSB and mid-diastolic murmur at apex

Total anomalous pulmonary venous connection

2 to 3

Onset of CHF at 4 to 6 weeks of age

Grade 2 or 3 systolic ejection murmur at ULSB; grade 1 or 2 mid-diastolic flow rumble at LLSB; wide split fixed S2

Tricuspid atresia

1.4

Early-onset cyanosis or CHF within the first month of life

Cyanosis; clubbing of nail beds; normal pulses; single S2; holosystolic murmur at LLSB or midsternal border; murmur may be absent; mid-diastolic flow murmur at apex may be present

Hypoplastic left heart syndrome

Rare

May be asymptomatic at birth, with cyanosis and CHF developing with duct closure

Hyperdynamic precordium; single S2; nonspecific grade 1 or 2 systolic ejection murmur along left sternal border

Truncus arteriosus

Rare

Onset of CHF in first few weeks of life; minimal cyanosis

Increased cardiac impulses; holosystolic murmur (ventricular septal defect); mid-diastolic rumble


CHF = congestive heart failure; LLSB = lower left sternal border; ULSB = upper left sternal border.

Information from references 20 through 23.

Table 5.   Prevalence and Characteristics of Pathologic Heart Murmurs

View Table

Table 5.

Prevalence and Characteristics of Pathologic Heart Murmurs

Type of structural heart lesion Prevalence among children with congenital heart disease (%) Symptoms and clinical course Characteristics

Ventricular septal defect

20 to 25

Small defects: usually asymptomatic

Small defects: loud holosystolic murmur at LLSB (may not last throughout systole if defect is very small)

Medium or large defects: CHF, symptoms of bronchial obstruction, frequent respiratory infections

Medium and large defects: increased right-to-left ventricular impulses; thrill at LLSB; split or loud single S2; holosystolic murmur at LLSB without radiation; grade 2 to 5; may also hear a grade 1 or 2 mid-diastolic rumble

Atrial septal defect

8 to 13

Usually asymptomatic and incidentally found on physical examination or echocardiography; large defects can be present in infants with CHF

Grade 2 or 3 systolic ejection murmur best heard at ULSB; wide split fixed S2; absent thrill; may have a grade 1 or 2 diastolic flow rumble at LLSB

Patent ductus arteriosus

6 to 11

May be asymptomatic; can cause easy fatigue, CHF, and respiratory symptoms

Continuous murmur (grade 1 to 5) in ULSB (crescendo in systole and decrescendo into diastole); normal S1; S2 may be “buried” in the murmur; thrill or hyperdynamic left ventricular impulse may be present

Tetralogy of Fallot

10

Onset depends on severity of pulmonary stenosis; cyanosis may appear in infancy (2 to 6 months of age) or in childhood; other symptoms include hypercyanotic spells or decreased exercise tolerance

Central cyanosis; clubbing of nail beds; grade 3 or 4 long systolic ejection murmur heard at ULSB; may have holosystolic murmur at LLSB; systolic thrill at ULSB; normal to slightly increased S1; single S2

Pulmonary stenosis

7.5 to 9

Usually asymptomatic but may have symptoms secondary to pulmonary congestion

Systolic ejection murmur (grade 2 to 5); heard best at ULSB radiating to infraclavicular regions, axillae, and back; normal or loud S1; variable S2; systolic ejection click may be heard at left sternal border and may vary with respiration

Coarctation of the aorta

5.1 to 8.1

Newborns and infants may present with CHF; older children are usually asymptomatic or may have leg pain or weakness

Systolic ejection murmur best heard over interscapular region; normal S1 and S2; decreased or delayed femoral pulse; may have increased left ventricular impulse

Aortic stenosis

5 to 6

Usually asymptomatic; symptoms may include dyspnea, easy fatigue, chest pain, or syncope; newborns and infants may present with CHF

Systolic ejection murmur (grade 2 to 5) best heard at upper right sternal border with radiation to carotid arteries; left ventricular heave; thrill at ULSB or suprasternal notch

Transposition of the great arteries

5

Variable presentation depending on type; may include cyanosis or CHF in first week of life

Cyanosis; clubbing of nail beds; single S2; murmur may be absent or grade 1 or 2 nonspecific systolic ejection murmur; may have a grade 3 or 4 holosystolic murmur at LLSB and mid-diastolic murmur at apex

Total anomalous pulmonary venous connection

2 to 3

Onset of CHF at 4 to 6 weeks of age

Grade 2 or 3 systolic ejection murmur at ULSB; grade 1 or 2 mid-diastolic flow rumble at LLSB; wide split fixed S2

Tricuspid atresia

1.4

Early-onset cyanosis or CHF within the first month of life

Cyanosis; clubbing of nail beds; normal pulses; single S2; holosystolic murmur at LLSB or midsternal border; murmur may be absent; mid-diastolic flow murmur at apex may be present

Hypoplastic left heart syndrome

Rare

May be asymptomatic at birth, with cyanosis and CHF developing with duct closure

Hyperdynamic precordium; single S2; nonspecific grade 1 or 2 systolic ejection murmur along left sternal border

Truncus arteriosus

Rare

Onset of CHF in first few weeks of life; minimal cyanosis

Increased cardiac impulses; holosystolic murmur (ventricular septal defect); mid-diastolic rumble


CHF = congestive heart failure; LLSB = lower left sternal border; ULSB = upper left sternal border.

Information from references 20 through 23.

Characteristics that are more likely to be associated with an innocent murmur include a systolic (rather than diastolic) murmur; soft sound; short duration; musical or low pitch; varying intensity with phases of respiration and posture (louder in supine position); and murmurs that become louder with exercise, anxiety, or fear 17,24  (Table 6 27). The most common innocent murmur is a Still murmur, which is characteristically loudest at the lower left sternal border and has a musical or vibratory quality that is thought to represent vibrations of the left outflow tract.1,5

Table 6.

The Seven S's: Key Features of Innocent Murmurs

Sensitive (changes with child's position or with respiration)

Short duration (not holosystolic)

Single (no associated clicks or gallops)

Small (murmur limited to a small area and nonradiating)

Soft (low amplitude)

Sweet (not harsh sounding)

Systolic (occurs during and is limited to systole)


Information from reference 27.

Table 6.   The Seven S's: Key Features of Innocent Murmurs

View Table

Table 6.

The Seven S's: Key Features of Innocent Murmurs

Sensitive (changes with child's position or with respiration)

Short duration (not holosystolic)

Single (no associated clicks or gallops)

Small (murmur limited to a small area and nonradiating)

Soft (low amplitude)

Sweet (not harsh sounding)

Systolic (occurs during and is limited to systole)


Information from reference 27.

Auscultation may be less accurate in younger patients, when other signs or symptoms of cardiovascular disease are present, and when findings on radiography or electrocardiography (ECG) are abnormal.28  Online libraries of digital heart sounds are available to familiarize physicians with the characteristics of abnormal heart sounds (Table 7).

Table 7.

Online Resources for Pediatric Cardiac Auscultation

The Auscultation Assistant

Web site: http://www.wilkes.med.ucla.edu/inex.htm

Blaufuss Medical Multimedia Laboratories

Web site: http://www.blaufuss.org

Heart Sounds and Murmurs

Web site: http://www.dundee.ac.uk/medther/Cardiology/hsmur.html

Johns Hopkins University Cardiac Auscultatory Recording Database

Web site: http://www.murmurlab.com/card6/ (registrationrequired)

Texas Heart Institute

Web site: http://www.texasheart.org/education/cme/explore/events/eventdetail_5469.cfm

University of Michigan Heart Sound and Murmur Library

Web site: http://www.med.umich.edu/lrc/psb/heartsounds/index.htm

University of Washington Department of Medicine

Demonstrations: Heart Sounds and Murmurs

Web site: http://depts.washington.edu/physdx/heart/demo.html

Table 7.   Online Resources for Pediatric Cardiac Auscultation

View Table

Table 7.

Online Resources for Pediatric Cardiac Auscultation

The Auscultation Assistant

Web site: http://www.wilkes.med.ucla.edu/inex.htm

Blaufuss Medical Multimedia Laboratories

Web site: http://www.blaufuss.org

Heart Sounds and Murmurs

Web site: http://www.dundee.ac.uk/medther/Cardiology/hsmur.html

Johns Hopkins University Cardiac Auscultatory Recording Database

Web site: http://www.murmurlab.com/card6/ (registrationrequired)

Texas Heart Institute

Web site: http://www.texasheart.org/education/cme/explore/events/eventdetail_5469.cfm

University of Michigan Heart Sound and Murmur Library

Web site: http://www.med.umich.edu/lrc/psb/heartsounds/index.htm

University of Washington Department of Medicine

Demonstrations: Heart Sounds and Murmurs

Web site: http://depts.washington.edu/physdx/heart/demo.html

Role of Diagnostic Testing

Chest radiography and ECG rarely assist in the diagnosis of a heart murmur.5,6,29 Studies in newborns30 and children31 with asymptomatic murmurs have shown that chest radiography does not influence clinical management or assist with diagnosis. A prospective study of 201 newborns who were referred to pediatric cardiologists for evaluation of a heart murmur found that the addition of ECG to clinical assessment did not improve the sensitivity or specificity of detecting structural heart lesions.32 In a study of 128 infants and children who were evaluated for heart murmurs, the addition of ECG and chest radiography to cardiac auscultation was more likely to mislead than assist the physician in making the correct diagnosis.33

In a study of more than 900 children in a pediatric cardiology clinic who had innocent-sounding murmurs, an abnormal finding from the history, physical examination, or diagnostic tests (ECG, chest radiography, or pulse oximetry) was 67 percent sensitive but only 38 percent specific for the presence of a structural heart lesion in infants younger than six weeks, yielding positive and negative LRs very near 1.0 (i.e., no useful diagnostic information).28 In infants older than six weeks, sensitivity increased to 100 percent, but specificity decreased to 28 percent (positive LR = 1.6; negative LR = 0.026). Thus, this information is helpful for ruling out structural causes of an innocent-sounding murmur in infants and children older than six weeks, but it is not helpful in younger infants.

In two separate populations geographically remote from a pediatric cardiologist, phonocardiography (i.e., digital heart sound recordings reviewed by a pediatric cardiologist) had high sensitivity and specificity, and good intraobserver agreement in distinguishing between innocent murmurs and murmurs that were potentially or probably pathologic and that required echocardiography.34,35

Indications for Referral

In children and adolescents, the diagnosis of an innocent heart murmur can be made if four criteria are met: absence of abnormal physical examination findings (except for the murmur); a negative review of systems (i.e., child is asymptomatic); a history that is negative for features that increase the risk of structural heart disease; and characteristic auscultatory features of a specific innocent heart murmur.2,5 These criteria are not appropriate for newborns or infants younger than one year because these patients have a higher rate of asymptomatic structural heart disease.36 When an innocent murmur cannot be definitively diagnosed, the child should be referred for echocardiography, to a pediatric cardiologist, or both.

A study in Oman found that the prevalence of abnormal findings on echocardiography was not significantly different between patients referred by pediatric cardiologists and those referred by primary care physicians.37 However, pediatric cardiologists more accurately detect structural heart lesions in newborns and children with heart murmurs,32,38 and can assist family physicians in the assessment of a suspicious murmur. For both innocent and pathologic murmurs, referral to a pediatric cardiologist for confirmation or clarification of the diagnosis is associated with decreased parental anxiety.39

Neonatal Heart Murmurs

Newborns are at higher risk of having serious structural heart disease that presents as an asymptomatic murmur.6,10 Approximately 1 percent of newborns have a heart murmur, and 31 to 86 percent of these infants have structural heart disease,4042 including asymptomatic newborns. Because of the higher likelihood of structural heart disease in asymptomatic newborns and young infants with heart murmurs, referral to a pediatric cardiologist and/or for echocardiography is recommended.28,42,43 Even potentially life-threatening heart defects may not be associated with any initial signs or symptoms other than a heart murmur.41,42

The reported sensitivity for detection of a pathologic heart murmur in newborns ranges from 80.5 to 94.9 percent among pediatric cardiologists, with specificity ranging from 25 to 92 percent.32,43 These variations are significant because the lowest specificity corresponds to positive and negative LRs of 1.1 and 0.7, which are uninformative, and the highest specificity corresponds to positive and negative LRs of 10 and 0.21, which are quite accurate. The ability of a pediatric cardiologist to accurately identify pathologic murmurs depends on multiple factors, including his or her confidence in the diagnosis. Echocardiography may not be required in newborns with a heart murmur if a pediatric cardiologist has diagnosed an innocent murmur with a high degree of confidence32; however, it is important to consider the relatively high prevalence of structural heart disease among asymptomatic newborns with a heart murmur.

The evaluation of newborns for CHD may include pulse oximetry after 24 hours of life. Clinical examination of asymptomatic newborns has a sensitivity of 46 percent for detection of CHD; this sensitivity increases to 77 percent when clinical examination is combined with pulse oximetry (with a cutoff of 94 percent).44

The Authors

JENNIFER E. FRANK, MD, FAAFP, is in private practice at Theda Care Physicians in Neenah, Wis. At the time this article was written, she was an assistant professor of family medicine at the University of Wisconsin School of Medicine and Public Health, Madison, and a faculty member at the University of Wisconsin Fox Valley Family Medicine Residency Program, Appleton.

KATHRYN M. JACOBE, MD, is a third-year resident at the University of Wisconsin Fox Valley Family Medicine Residency Program.

Address correspondence to Jennifer E. Frank, MD, FAAFP, 1380 Tullar Rd., Neenah, WI 54956 (e-mail: jennifer.frank@thedacare.org). Reprints are not available from the authors.

Author disclosure: No relevant financial affiliations to disclose.

REFERENCES

1. Biancaniello T. Innocent murmurs. Circulation. 2005;111(3):e20–e22.

2. Harris JP. Consultation with the specialist. Evaluation of heart murmurs. Pediatr Rev. 1994;15(12):490–494.

3. Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol. 2002;39(12):1890–1900.

4. Pelech AN. Evaluation of the pediatric patient with a cardiac murmur. Pediatr Clin North Am. 1999;46(2):167–188.

5. Danford DA. Effective use of the consultant, laboratory testing, and echocardiography for the pediatric patient with heart murmur. Pediatr Ann. 2000;29(8):482–488.

6. Poddar B, Basu S. Approach to a child with a heart murmur. Indian J Pediatr. 2004;71(1):63–66.

7. Martins P, Dinis A, Canha J, Ramalheiro G, Castela E. Innocent heart murmurs. Rev Port Cardiol. 2008;27(6):815–831.

8. Weber MA, Ashworth MT, Risdon RA, Brooke I, Malone M, Sebire NJ. Sudden unexpected neonatal death in the first week of life: autopsy findings from a specialist centre. J Matern Fetal Neonatal Med. 2009;22(5):398–404.

9. Gordon JB, Kahn AM, Burns JC. When children with Kawasaki disease grow up: myocardial and vascular complications in adulthood. J Am Coll Cardiol. 2009;54(21):1911–1920.

10. Frommelt MA. Differential diagnosis and approach to a heart murmur in term infants. Pediatr Clin North Am. 2004;51(4):1023–1032.

11. Merlob P, Birk E, Sirota L, et al. Are selective serotonin reuptake inhibitors cardiac teratogens? Echocardiographic screening of newborns with persistent heart murmur. Birth Defects Res A Clin Mol Teratol. 2009;85(10):837–841.

12. Macicek SM, Macias CG, Jefferies JL, Kim JJ, Price JF. Acute heart failure syndromes in the pediatric emergency department. Pediatrics. 2009;124(5):e898–e904.

13. Kane DA, Fulton DR, Saleeb S, Zhou J, Lock JE, Geggel RL. Needles in hay: chest pain as the presenting symptom in children with serious underlying cardiac pathology. Congenit Heart Dis. 2010;5(4):366–373.

14. Geggel RL. Conditions leading to pediatric cardiology consultation in a tertiary academic hospital. Pediatrics. 2004;114(4):e409–e417.

15. Andren L, Hall P. Diminished segmentation or premature ossification of the sternum in congenital heart disease. Br Heart J. 1961;23:140–142.

16. Washington R. Sports cardiology in the adolescent athlete: concerns for the pediatrician. Pediatr Ann. 2007;36(11):698–702.

17. Pelech AN. The physiology of cardiac auscultation. Pediatr Clin North Am. 2004;51(6):1515–1535.

18. McConnell ME, Adkins SB III, Hannon DW. Heart murmurs in pediatric patients: when do you refer? Am Fam Physician. 1999;60(2):558–565.

19. Christensen DD, Vincent RN, Campbell RM. Presentation of atrial septal defect in the pediatric population. Pediatr Cardiol. 2005;26(6):812–814.

20. Syamasundar Rao P. Diagnosis and management of acyanotic heart disease: part I — obstructive lesions. Indian J Pediatr. 2005;72(6):496–502.

21. Syamasundar Rao P. Diagnosis and management of acyanotic heart disease: part II — left-to-right shunt lesions. Indian J Pediatr. 2005;72(6):503–512.

22. Rao PS. Diagnosis and management of cyanotic congenital heart disease: part I. Indian J Pediatr. 2009;76(1):57–70.

23. Syamasundar Rao P. Diagnosis and management of cyanotic congenital heart disease: part II. Indian J Pediatr. 2009;76(3):297–308.

24. Uner A, Doğan M, Bay A, Cakin C, Kaya A, Sal E. The ratio of congenital heart disease and innocent murmur in children in Van city, the Eastern Turkey. Anadolu Kardiyol Derg. 2009;9(1):29–34.

25. McCrindle BW, Shaffer KM, Kan JS, Zahka KG, Rowe SA, Kidd L. Cardinal clinical signs in the differentiation of heart murmurs in children. Arch Pediatr Adolesc Med. 1996;150(2):169–174.

26. Etchells E, Bell C, Robb K. Does this patient have an abnormal systolic murmur? JAMA. 1997;277(7):564–571.

27. Bronzetti G, Corzani A. The seven “S” murmurs: an alliteration about innocent murmurs in cardiac auscultation. Clin Pediatr (Phila). 2010;49(7):713.

28. Danford DA, Martin AB, Fletcher SE, Gumbiner CH. Echocardiographic yield in children when innocent murmur seems likely but doubts linger. Pediatr Cardiol. 2002;23(4):410–414.

29. Yi MS, Kimball TR, Tsevat J, Mrus JM, Kotagal UR. Evaluation of heart murmurs in children: cost-effectiveness and practical implications. J Pediatr. 2002;141(4):504–511.

30. Oeppen RS, Fairhurst JJ, Argent JD. Diagnostic value of the chest radiograph in asymptomatic neonates with a cardiac murmur. Clin Radiol. 2002;57(8):736–740.

31. Birkebaek NH, Hansen LK, Elle B, et al. Chest roentgenogram in the evaluation of heart defects in asymptomatic infants and children with a cardiac murmur: reproducibility and accuracy. Pediatrics. 1999;103(2):E15.

32. Mackie AS, Jutras LC, Dancea AB, Rohlicek CV, Platt R, Béland MJ. Can cardiologists distinguish innocent from pathologic murmurs in neonates? J Pediatr. 2009;154(1):50–54.

33. Rajakumar K, Weisse M, Rosas A, et al. Comparative study of clinical evaluation of heart murmurs by general pediatricians and pediatric cardiologists. Clin Pediatr (Phila). 1999;38(9):511–518.

34. Mahnke CB, Mulreany MP, Inafuku J, Abbas M, Feingold B, Paolillo JA. Utility of store-and-forward pediatric telecardiology evaluation in distinguishing normal from pathologic pediatric heart sounds. Clin Pediatr (Phila). 2008;47(9):919–925.

35. Germanakis I, Dittrich S, Perakaki R, Kalmanti M. Digital phonocardiography as a screening tool for heart disease in childhood. Acta Paediatr. 2008;97(4):470–473.

36. Koo S, Yung TC, Lun KS, Chau AK, Cheung YF. Cardiovascular symptoms and signs in evaluating cardiac murmurs in children. Pediatr Int. 2008;50(2):145–149.

37. Venugopalan P, Agarwal AK, Johnston WJ, Riveria E. Spread of heart diseases seen in an open-access paediatric echocardiography clinic. Int J Cardiol. 2002;84(2–3):211–216.

38. Advani N, Menahem S, Wilkinson JL. The diagnosis of innocent murmurs in childhood. Cardiol Young. 2000;10(4):340–342.

39. Giuffre RM, Walker I, Vaillancourt S, Gupta S. Opening Pandora's box: parental anxiety and the assessment of childhood murmurs. Can J Cardiol. 2002;18(4):406–414.

40. Bansal M, Jain H. Cardiac murmur in neonates. Indian Pediatr. 2005;42(4):397–398.

41. Rein AJ, Omokhodion SI, Nir A. Significance of a cardiac murmur as the sole clinical sign in the newborn. Clin Pediatr (Phila). 2000;39(9):511–520.

42. Ainsworth S, Wyllie JP, Wren C. Prevalence and clinical significance of cardiac murmurs in neonates. Arch Dis Child Fetal Neonatal Ed. 1999;80(1):F43–F45.

43. Azhar AS, Habib HS. Accuracy of the initial evaluation of heart murmurs in neonates: do we need an echocardiogram? Pediatr Cardiol. 2006;27(2):234–237.

44. Bakr AF, Habib HS. Combining pulse oximetry and clinical examination in screening for congenital heart disease. Pediatr Cardiol. 2005;26(6):832–835.


Copyright © 2011 by the American Academy of Family Physicians.
This content is owned by the AAFP. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP. Contact afpserv@aafp.org for copyright questions and/or permission requests.

Want to use this article elsewhere? Get Permissions


Article Tools

  • Download PDF
  • Print page
  • Share this page
  • AFP CME Quiz

Information From Industry

More in AFP

More in Pubmed

Navigate this Article