which finding is inferred from a grade 4 intensity of heart murmurs?
Am Fam Physician. 2011 Oct one;84(vii):793-800.
Article Sections
- Abstract
- Incidence and Prevalence
- History
- Physical Examination
- Office of Diagnostic Testing
- Indications for Referral
- Neonatal Heart Murmurs
- References
Heart murmurs are common in healthy infants, children, and adolescents. Although most are not pathologic, a murmur may be the sole manifestation of serious centre affliction. Historical elements that suggest pathology include family unit history of sudden cardiac decease or congenital heart disease, in utero exposure to sure 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-advisable 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 Southwardii, maximal murmur intensity at the upper left sternal edge, a systolic click, or increased intensity when the patient stands. Electrocardiography and chest radiography rarely help 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 illness, symptoms suggesting underlying cardiac disease, or when a specific innocent murmur cannot exist identified past the family dr.. Echocardiography provides a definitive diagnosis and is recommended for evaluation of any potentially pathologic murmur, and for evaluation of neonatal eye murmurs because these are more probable to be manifestations of structural heart disease.
Heart murmurs are common in asymptomatic, otherwise healthy children. These murmurs are often innocent and issue from the normal patterns of blood flow through the middle and vessels.one Nevertheless, a heart murmur may be the sole finding in children with structural heart illness; therefore, a thorough evaluation is necessary.
SORT: Fundamental RECOMMENDATIONS FOR Practice
| Clinical recommendation | Bear witness rating | References |
|---|---|---|
| Structural heart disease is more probable 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 information technology has a harsh quality. | C | 6, 10, 25 |
| Chest radiography and electrocardiography rarely assist in the diagnosis of center murmurs in children. | B | 5, 6, 29–33 |
| Family physicians should order echocardiography or consider referral to a pediatric cardiologist for newborns with a heart murmur, even if the kid is asymptomatic, because of the college prevalence of structural heart lesions in this population. | B | 28, 43 |
Incidence and Prevalence
- Abstruse
- Incidence and Prevalence
- History
- Physical Examination
- Function of Diagnostic Testing
- Indications for Referral
- Neonatal Heart Murmurs
- References
Congenital centre disease (CHD) may occur in the presence or absence of a heart murmur. The incidence of CHD varies betwixt four and 50 per 1,000 alive births.two One review found an incidence of 75 cases per 1,000 live births; of these, six cases per 1,000 were moderate or severe.iii
History
- Abstract
- Incidence and Prevalence
- History
- Concrete Examination
- Role of Diagnostic Testing
- Indications for Referral
- Neonatal Middle Murmurs
- References
Sure historical features advise possible structural heart affliction (Table 1).1,2,iv–11 Cardiovascular signs and symptoms can be non-specific (e.g., poor feeding, failure to thrive) or specific (due east.g., chest pain, palpitations), and can help identify children who are likely to take structural heart affliction (Table two).4,7,10
Table i.
Historical Findings Suggesting Structural Middle Disease in Children with Heart Murmurs
| Historical finding | Significance | |
|---|---|---|
| Family unit history | ||
| CHD | More common in children with a first-caste relative who has CHD (3- to 10-fold increased risk7); loftier penetrance with ventricular septal defect and mitral valve prolapse | |
| Sudden cardiac decease or hypertrophic cardiomyopathy | Increased risk of hypertrophic cardiomyopathy (autosomal ascendant pattern) | |
| Sudden baby death syndrome | Tin can exist secondary to undiagnosed CHD lesions8 | |
| Personal history | ||
| Atmospheric condition that may coexist with CHD: | Certain genetic disorders (e.chiliad., DiGeorge syndrome, velo-cardio-facial syndrome) are associated with cardiac malformations | |
| Aneuploidy (e.grand., trisomy 21, Turner syndrome) | ||
| Trisomy 21 is associated with an increased hazard of atrioventricular septal defects, atrial septal defects, ventricular septal defects, patent ductus arteriosus, and tetralogy of Fallot | ||
| Connective tissue disorder (eastward.g., Marfan syndrome) | ||
| Turner syndrome is associated with increased chance of coarctation of the aorta, aortic valve stenosis, and left ventricular hypertrophy | ||
| Inborn fault 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 middle disease (i.east., congestive heart failure); enlarged vessels may pb to atelectasis or difficulty clearing respiratory secretions, thereby promoting infection | |
| Kawasaki illness | Leading crusade of acquired cardiac disease in children; can cause coronary artery aneurysm and stenosis9 | |
| Rheumatic fever | Associated with development of rheumatic center disease | |
| Prenatal or perinatal history | ||
| In utero exposure to alcohol or other toxins | Fetal alcohol syndrome is associated with an increased adventure 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 minor just statistically significant increased gamble 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 bibelot of the tricuspid valve | ||
| Valproate (Depacon) exposure is associated with coarctation of the aorta and hypoplastic left heart syndrome | ||
| Intrauterine infection | Maternal infections may increment run a risk of structural heart lesions (e.g., maternal rubella infection is associated with patent ductus arteriosus and peripheral pulmonary stenosis) | |
| Maternal diabetes mellitus | Increased take chances of CHD, including transient hypertrophic cardiomyopathy, tetralogy of Fallot, truncus arteriosus, and double-outlet correct ventricle | |
| Preterm delivery | CHD is associated with other atmospheric condition (due east.m., genetic disorders, in utero exposure to toxins) that tin result in preterm birth; 50 percent of newborns weighing less than 3 lb, v oz (1,500 yard) at birth have CHD (nigh commonly patent ductus arteriosus)7 | |
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 filibuster | 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 fettle |
| Poor practice tolerance or capacity for play | May indicate CHF, hypoxia, or poor cardiac fettle |
| Poor growth or failure to thrive | May indicate CHF, poor cardiac fettle, or a genetic disorder or syndrome; poor weight gain most normally reflects decreased cardiac output or left-to-right shunts with pulmonary hypertension |
| Respiratory | |
| Asthma-similar symptoms | Cardiac asthma resulting from pulmonary congestion |
| Chronic cough | Atelectasis or difficulty clearing secretions considering of pulmonary vascular congestion |
| Dyspnea on exertion | May indicate CHF, hypoxia, or poor cardiac fitness |
In infants, feeding difficulties may exist the first sign of congestive heart failure, which is nowadays in approximately i-3rd of infants and children with CHD.4 The most mutual symptoms in a series of children presenting to the emergency department with astute center failure included dyspnea (74 pct), nausea and vomiting (60 pct), fatigue (56 per centum), and cough (twoscore pct).12
Practise tolerance should be assessed in an age-advisable way. Parents of infants should exist asked about their kid's power to play and the duration and vigor of feeding; parents of older children should compare their kid's power to participate in team sports with that of peers.iv Chest hurting is rarely a presenting symptom of cardiac disease in children.xiii,14 In a pediatric cardiology clinic, breast pain or syncope prompted consultation in approximately 10 percent of children; merely eleven pct of those with chest pain and v percentage of those with syncope had cardiac disease.14 A loftier degree of suspicion is necessary to detect underlying cardiac disease in children who written report exertional syncope or chest pain, or who have a family history of hypertrophic cardiomyopathy.1,thirteen,14
Physical Test
- Abstract
- Incidence and Prevalence
- History
- Physical Examination
- Role of Diagnostic Testing
- Indications for Referral
- Neonatal Heart Murmurs
- References
The patient's vital signs should be compared with historic period-established norms (available at http://www.cc.nih.gov/ccc/pedweb/pedsstaff/historic period.html), and a focused test of the respiratory, cardiovascular, and gastrointestinal systems should be performed5 (Table 32 ,5–7,ten,15,xvi). Congenital anomalies of other organ systems may be associated with CHD in up to 25 percent of patients.half dozen The child's appearance, activity level, color, and respiratory effort should be assessed, and the cervix should be examined for prominent vessels, abnormal pulsations, and bruits.1 Jugular venous amplification is rare in children.four The breast wall should be inspected for abnormalities of the sternum, which tin be associated with CHD,15 and for aberrant cardiac impulses or thrills.1 The lungs should be auscultated for abnormal breath sounds such as crackles, which may bespeak pulmonary congestion, or wheezing, which may bespeak cardiac asthma. Abdominal exam should focus on the liver location (seeking intestinal situs) and evaluation for liver enlargement or ascites, which may indicate congestive middle failure.v
Tabular array 3.
Physical Exam of Children with Heart Murmurs
| Finding | Significance | |
|---|---|---|
| Abnormal growth (top and weight plotted on growth chart) | Feeding difficulties may exist a sign of cardiac affliction in newborns and infants (decreased exercise capacity) | |
| Sure genetic disorders may increment 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 force per unit area discrepancy between upper and lower limbs may indicate coarctation of the aorta (pressure gradient of > 20 mm Hg with depression blood pressure level 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 | |
| Breast contour signaling maldevelopment of the sternum15 | Defective sectionalization of the sternum may occur in children with CHD | |
| Dysmorphic features | Certain genetic or congenital conditions increase risk of CHD | |
| Cardiovascular findings | ||
| Abnormal South2 | Archetype finding of wide split fixed S2 with atrial septal defects; abnormal Southward2 may be present in other types of CHD | |
| Capillary refill | Normal peripheral perfusion is less than 2 to 3 seconds; delay may betoken poor perfusion secondary to diminished cardiac output | |
| Displaced bespeak of maximal impulse; precordial impulses (heaves, lifts, thrills) | Possible structural abnormality or ventricular enlargement | |
| Edema | Congestive middle failure | |
| Left-sided precordial burl | Cardiac enlargement | |
| Sthree or Siv | Tin can indicate structural middle disease; Southiii can be a normal finding but usually disappears when patient is upright | |
| Substernal boost | Right ventricular hypertension | |
| Systolic ejection click | Semilunar valvular stenosis | |
| Weak or absent-minded femoral pulses | Coarctation of the aorta | |
| Gastrointestinal findings | ||
| Ascites | Congestive center failure | |
| Hepatomegaly | Congestive eye failure | |
| Location of liver signals intestinal situs | High rate of CHD with abdominal situs | |
The peripheral pulses should be examined for rate, rhythm, volume, and grapheme, and capillary refill time should be less than three seconds.iv The heart should exist 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 (Effigy 1 18).Innocent murmurs are produced by the normal period of blood through the middle. Irresolute the flow past 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 exist prompted to button out their abdomen against the examiner's mitt.1 The physician should listen for normal S1 and Sii; a wide fixed split Stwo is feature of an atrial septal defect.nineteen Gallops tin can exist a normal finding in adolescents.i
Figure 1.
Listening areas for clicks: upper correct 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. Middle murmurs in pediatric patients: when exercise you refer? Am Fam Md. 1999;sixty(ii):560.
The centre murmur is characterized past its timing during the cardiac bicycle; its location, quality, intensity, and pitch (how information technology sounds); and the presence or absence of clicks1 (Table iv 5,seven,17 and Table 5 twenty–23). The intensity of heart murmurs is graded from 1 to half-dozen. Course 1 murmurs are barely audible; form 2 murmurs are faint but can exist heard immediately; grade iii murmurs can be heard hands and are moderately loud; grade 4 murmurs can be heard easily over a broad area but do not have a palpable thrill; course 5 murmurs are loud and have a precordial thrill; and class 6 murmurs are loud enough to hear with the stethoscope raised off the breast.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 iii or higher (OR = four.8), harsh quality (OR = 2.four), an abnormal Sii (OR = four.1), maximal intensity at the upper left sternal edge (OR = 4.2), a systolic click (OR = 8.iii), diastolic murmur, or increased murmur intensity with standing.6,ten,25 A subtract or lack of change in the murmur intensity with passive leg elevation (likelihood ratio [LR] = viii.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 | Clarification | Historic period at detection | Can audio 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 inductive chest wall over the breast | Rare in boyhood | Arteriovenous anastomoses or patent ductus arteriosus |
| Peripheral pulmonary stenosis | Grade 1 or ii, depression-pitched, early- to mid-systolic ejection murmur heard over axilla or back | < 1 year | Pulmonary artery stenosis or normal breath sounds |
| Pulmonary menses murmur | Course two or three, crescendo-decrescendo, early- to mid-systolic murmur peaking in mid-systole; all-time heard at the left sternal edge between the 2d and third intercostal spaces; characterized past 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 |
| All the same murmur | Grade 1 to iii, early on systolic murmur; low to medium pitch with a vibratory or musical quality; best heard at lower left sternal edge; loudest when patient is supine and decreases when patient stands | Infancy to boyhood, frequently 2 to six years | Ventricular septal defect or hypertrophic cardiomyopathy |
| Supraclavicular\brachiocephalic systolic murmur | Brief, depression-pitched, crescendo-decrescendo murmur heard in the first two-thirds of systole; best heard to a higher place 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 | Course i 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 correct; resolves or changes when patient is supine | 3 to 8 years | Cervical arteriovenous fistulas or patent ductus arteriosus |
Tabular array 5.
Prevalence and Characteristics of Pathologic Heart Murmurs
| Type of structural centre lesion | Prevalence among children with congenital center illness (%) | Symptoms and clinical course | Characteristics |
|---|---|---|---|
| Ventricular septal defect | xx to 25 | Pocket-sized defects: usually asymptomatic | Pocket-sized defects: loud holosystolic murmur at LLSB (may not last throughout systole if defect is very pocket-sized) |
| Medium or large defects: CHF, symptoms of bronchial obstruction, frequent respiratory infections | |||
| Medium and large defects: increased correct-to-left ventricular impulses; thrill at LLSB; carve up or loud unmarried Stwo; holosystolic murmur at LLSB without radiations; grade ii to 5; may as well hear a form 1 or 2 mid-diastolic rumble | |||
| Atrial septal defect | 8 to xiii | Usually asymptomatic and incidentally found on concrete examination or echocardiography; large defects tin can be present in infants with CHF | Grade 2 or 3 systolic ejection murmur best heard at ULSB; wide separate stock-still Sii; absent thrill; may have a course 1 or two diastolic flow rumble at LLSB |
| Patent ductus arteriosus | 6 to 11 | May be asymptomatic; tin can cause easy fatigue, CHF, and respiratory symptoms | Continuous murmur (class one to v) in ULSB (crescendo in systole and decrescendo into diastole); normal Sone; S2 may be "buried" in the murmur; thrill or hyperdynamic left ventricular impulse may be nowadays |
| 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 do tolerance | Central cyanosis; clubbing of nail beds; grade iii or 4 long systolic ejection murmur heard at ULSB; may have holosystolic murmur at LLSB; systolic thrill at ULSB; normal to slightly increased Sane; unmarried S2 |
| Pulmonary stenosis | 7.five to 9 | Usually asymptomatic but may have symptoms secondary to pulmonary congestion | Systolic ejection murmur (grade two 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.one | Newborns and infants may present with CHF; older children are ordinarily asymptomatic or may have leg pain or weakness | Systolic ejection murmur all-time heard over interscapular region; normal Sone and S2; decreased or delayed femoral pulse; may have increased left ventricular impulse |
| Aortic stenosis | 5 to six | Usually asymptomatic; symptoms may include dyspnea, piece of cake 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 boost; thrill at ULSB or suprasternal notch |
| Transposition of the great arteries | 5 | Variable presentation depending on blazon; may include cyanosis or CHF in get-go week of life | Cyanosis; clubbing of boom beds; single S2; murmur may be absent or grade one or ii nonspecific systolic ejection murmur; may take a form 3 or 4 holosystolic murmur at LLSB and mid-diastolic murmur at apex |
| Total dissonant pulmonary venous connexion | 2 to three | Onset of CHF at 4 to 6 weeks of age | Grade 2 or iii systolic ejection murmur at ULSB; grade i or 2 mid-diastolic flow rumble at LLSB; wide divide stock-still Southward2 |
| Tricuspid atresia | 1.iv | 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 period murmur at noon may be present |
| Hypoplastic left heart syndrome | Rare | May be asymptomatic at nativity, with cyanosis and CHF developing with duct closure | Hyperdynamic precordium; single S2; nonspecific course 1 or 2 systolic ejection murmur forth 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 |
Characteristics that are more probable to be associated with an innocent murmur include a systolic (rather than diastolic) murmur; soft sound; short elapsing; musical or low pitch; varying intensity with phases of respiration and posture (louder in supine position); and murmurs that get louder with do, anxiety, or fear 17,24 (Tabular array 6 27). The most mutual innocent murmur is a However murmur, which is characteristically loudest at the lower left sternal border and has a musical or vibratory quality that is idea to represent vibrations of the left outflow tract.ane,v
Tabular array 6.
The Seven South's: Cardinal 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 express to a small area and nonradiating) |
| Soft (low amplitude) |
| Sweet (not harsh sounding) |
| Systolic (occurs during and is limited to systole) |
Auscultation may be less authentic 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 middle sounds (Table 7).
Role of Diagnostic Testing
- Abstruse
- Incidence and Prevalence
- History
- Physical Examination
- Part of Diagnostic Testing
- Indications for Referral
- Neonatal Heart Murmurs
- References
Chest radiography and ECG rarely assist in the diagnosis of a heart murmur.5,half dozen,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 report of 201 newborns who were referred to pediatric cardiologists for evaluation of a centre murmur found that the improver of ECG to clinical cess did non amend 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 add-on of ECG and chest radiography to cardiac auscultation was more than likely to mislead than assist the physician in making the correct diagnosis.33
In a study of more than than 900 children in a pediatric cardiology dispensary who had innocent-sounding murmurs, an aberrant finding from the history, physical examination, or diagnostic tests (ECG, breast radiography, or pulse oximetry) was 67 percent sensitive but merely 38 percent specific for the presence of a structural eye 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 half dozen weeks, sensitivity increased to 100 percent, but specificity decreased to 28 percent (positive LR = 1.half-dozen; 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 half dozen weeks, but it is not helpful in younger infants.
In two split populations geographically remote from a pediatric cardiologist, phonocardiography (i.e., digital heart audio recordings reviewed by a pediatric cardiologist) had loftier sensitivity and specificity, and proficient intraobserver understanding in distinguishing between innocent murmurs and murmurs that were potentially or probably pathologic and that required echocardiography.34,35
Indications for Referral
- Abstract
- Incidence and Prevalence
- History
- Physical Examination
- Role of Diagnostic Testing
- Indications for Referral
- Neonatal Heart Murmurs
- References
In children and adolescents, the diagnosis of an innocent heart murmur tin can be fabricated if 4 criteria are met: absenteeism of abnormal physical examination findings (except for the murmur); a negative review of systems (i.due east., child is asymptomatic); a history that is negative for features that increase the adventure of structural centre disease; and characteristic auscultatory features of a specific innocent heart murmur.ii,5 These criteria are not appropriate for newborns or infants younger than one year because these patients have a college rate of asymptomatic structural center illness.36 When an innocent murmur cannot exist definitively diagnosed, the child should exist 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 past pediatric cardiologists and those referred past primary intendance physicians.37 Nevertheless, pediatric cardiologists more than accurately discover structural eye lesions in newborns and children with centre murmurs,32,38 and tin 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 Center Murmurs
- Abstruse
- Incidence and Prevalence
- History
- Physical Exam
- Function of Diagnostic Testing
- Indications for Referral
- Neonatal Center Murmurs
- References
Newborns are at higher risk of having serious structural middle disease that presents as an asymptomatic murmur.6,10 Approximately i percent of newborns have a heart murmur, and 31 to 86 percent of these infants have structural heart disease,40–42 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 Fifty-fifty potentially life-threatening heart defects may not be associated with any initial signs or symptoms other than a middle murmur.41,42
The reported sensitivity for detection of a pathologic heart murmur in newborns ranges from fourscore.5 to 94.nine percent amongst 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 i.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 authentic. The power 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 of import 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 subsequently 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 exam is combined with pulse oximetry (with a cutoff of 94 percent).44
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