A precordial bulge to the left of the sternum with increased precordial activity suggests cardiac enlargement; such bulges can often best be appreciated by having the child lay supine with the examiner looking up from the child’s feet.
A substernal thrust indicates the presence of right ventricular enlargement, whereas an apical heave is noted with left ventricular hypertrophy.
A hyperdynamic precordium suggests a volume load such as that found with a large left-to-right shunt, although it may be normal in a thin patient.
A silent precordium with a barely detectable apical impulse suggests pericardial effusion or severe cardiomyopathy; it may be normal in an obese patient.
The relationship of the apical impulse to the midclavicular line is also helpful in the estimation of cardiac size: the apical impulse moves laterally and inferiorly with enlargement of the left ventricle. Right-sided apical impulses signify dextrocardia, tension pneumothorax, or left-sided thoracic space-occupying lesions (e.g., diaphragmatic hernia).
Thrills are the palpable equivalent of murmurs and correlate with the area of maximal auscultatory intensity of the murmur. It is important to palpate the suprasternal notch and neck for aortic bruits, which may indicate the presence of aortic stenosis or, when faint, pulmonary stenosis. Right lower sternal border and apical systolic thrills are characteristic of ventricular septal defect and mitral insufficiency, respectively. Diastolic thrills are occasionally palpable in the presence of atrioventricular valve stenosis. The timing and localization of thrills should be carefully noted.
Auscultation is an art that improves with practice. The diaphragm of the stethoscope is placed firmly on the chest for high-pitched sounds; a lightly placed bell is optimal for low-pitched sounds. The physician should initially concentrate on the characteristics of the individual heart sounds and their variation with respirations and later concentrate on murmurs. The patient should be supine, lying quietly, and breathing normally. The 1st heart sound is best heard at the apex, whereas the 2nd heart sound should be evaluated at the upper left and right sternal borders. The 1st heart sound is caused by closure of the atrioventricular valves (mitral and tricuspid); the 2nd sound is caused by closure of the semilunar valves (aortic and pulmonary) .During inspiration, the decrease in intrathoracic pressure results in increased filling of the right side of the heart, which leads to an increased right ventricular ejection time and thus delayed closure of the pulmonary valve; consequently, splitting of the 2nd heart sound increases during inspiration and decreases during expiration.
Often, the 2nd heart sound seems to be single during expiration. The presence of a normally split 2nd sound is strong evidence against the diagnosis of atrial septal defect.
A 3rd heart sound is best heard with the bell at the apex in mid-diastole.
A 4th sound occurring in conjunction with atrial contraction may be heard just before the 1st heart sound in late diastole. The 3rd sound may be normal in an adolescent with a relatively slow heart rate, but in a patient with the clinical signs of heart failure and tachycardia, it may be heard as a gallop rhythm and may merge with a 4th heart sound, a finding known as a summation gallop. A gallop rhythm is attributed to poor compliance of the ventricle, and exaggeration of the normal 3rd sound is associated with ventricular filling.
Ejection clicks, which are heard in early systole, may be related to dilatation of the aorta or pulmonary artery or to a mildly to moderately stenotic semilunar valve. They are heard so close to the 1st heart sound that they may be mistaken for a split 1st sound.
A midsystolic click heard at the apex, often preceding a late systolic murmur, suggests mitral valve prolapse.
Murmurs should be described according to their intensity, pitch, timing (systolic or diastolic), variation in intensity, time to peak intensity, area of maximal intensity, and radiation to other areas. Auscultation for murmurs should be carried out across the upper precordium, down the left or right sternal border, and out to the apex and left axilla. Auscultation should also always be performed in the right axilla and over the back.
Systolic murmurs are classified as ejection, pansystolic, or late systolic according to the timing of the murmur in relation to the 1st and 2nd heart sounds. The intensity of systolic murmurs is graded from I to VI: I, barely audible; II, medium intensity; III, loud but no thrill; IV, loud with a thrill; V, very loud but still requiring positioning of the stethoscope at least partly on the chest; and VI, so loud that the murmur can be heard with the stethoscope off the chest.
A continuous murmur is a systolic murmur that continues or “spills” into diastole and indicates continuous flow, such as in the presence of a patent ductus arteriosus or other aortopulmonary communication. This murmur should be differentiated from a to-and-fro murmur, which indicates that the systolic component of the murmur ends at or before the 2nd sound and the diastolic murmur begins after semilunar valve closure (aortic or pulmonary stenosis combined with insufficiency). A late systolic murmur begins well beyond the 1st heart sound and continues until the end of systole. Such murmurs may be heard after a midsystolic click in patients with mitral valve prolapse and insufficiency.
Several types of diastolic murmurs (graded I–IV) can be identified. A decrescendo diastolic murmur is a blowing murmur along the left sternal border that begins with S2 and diminishes toward mid-diastole. When high-pitched, this murmur is associated with aortic valve insufficiency or pulmonary insufficiency related to pulmonary hypertension. When low-pitched, this murmur is associated with pulmonary valve insufficiency in the absence of pulmonary hypertension.
The absence of a precordial murmur does not rule out significant congenital or acquired heart disease. Congenital heart defects, some of which are ductal dependent, may not demonstrate a murmur if the ductus arteriosus closes. These lesions include pulmonary or tricuspid valve atresia and transposition of the great arteries. Murmurs may seem insignificant in patients with severe aortic stenosis, atrial septal defects, anomalous pulmonary venous return, atrioventricular septal defects, coarctation of the aorta, or anomalous insertion of a coronary artery. Careful attention to other components of the physical examination (growth failure, cyanosis, peripheral pulses, precordial impulse, heart sounds) increases the index of suspicion of congenital heart defects in these cases. In contrast, loud murmurs may be present in the absence of structural heart disease, for example, in patients with a large noncardiac arteriovenous malformation, myocarditis, severe anemia, or hypertension.
Many murmurs are not associated with significant hemodynamic abnormalities. These murmurs are referred to as functional, normal, insignificant, or innocent (the preferred term).
A venous hum is another example of a common innocent murmur heard during childhood. Such hums are produced by turbulence of blood in the jugular venous system; they have no pathologic significance and may be heard in the neck or anterior portion of the upper part of the chest.
The lack of significance of an innocent murmur should be discussed with the child’s parents. It is important to offer complete reassurance because lingering doubts about the importance of a cardiac murmur may have profound effects on child-rearing practices, most often in the form of overprotectiveness. An underlying fear that a cardiac abnormality is present may negatively affect a child’s self-image and subtly influence personality development. The physician should explain that an innocent murmur is simply a “noise” and does not indicate the presence of a significant cardiac defect. When asked, “Will it go away?” the best response is to state that because the murmur has no clinical significance, it therefore does not matter whether it “goes away.”
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