a. Height and weight. Slow weight gain, or crossing growth percentiles, can be seen in left-to-right shunting lesions associated with volume overload.
b. Pulse oximetry. Cyanosis that persists despite supplemental oxygen suggests intracardiac mixing, or right-to-left shunting from a cyanotic form of congenital heart disease.
c. Heart rate. Neonates cannot increase stroke volume and thus rely on increased heart rate to maintain cardiac output.
d. BP. A wide pulse pressure can be seen in diastolic run-off lesions, such as PDA, aortic insufficiency, coronary fistula, aortopulmonary window, or arteriovenous malformation. Discrepancy between upper and lower extremity BP is seen in coarctation of the aorta and interrupted aortic arch.
2. Chest. Extreme ventricular hypertrophy can cause chest asymmetry. Single-ventricle lesions or ventricular hypertrophy causes a ventricular lift or heave.
3. Heart. Auscultation is the most important aspect of the cardiac physical exam. Listen for the first and second heart sounds (S1 and S2), and for normal splitting of S2 with inspiration. Decide if murmur is systolic, diastolic, or continuous. Listen for extra heart sounds, such as systolic clicks or a rub. A third heart sound (S3), or diastolic rumble, in an infant is most often attributable to increased flow across atrioventricular valves in left-to-right shunting lesions. A fourth heart sound (S4) is not common in pediatric patients, but may be heard in cardiomyopathies.
a. Holosystolic murmur. A murmur that is the same frequency and intensity throughout systole and may obscure S2. VSD causes a holosystolic murmur because there is shunting between the higher-pressure left ventricle and lower-pressure right ventricle throughout systole. Intensity of the murmur diminishes as right ventricular pressure increases in association with development of pulmonary hypertension, or if the defect is large enough to not be pressure restrictive. Tricuspid or mitral regurgitation also causes a holosystolic murmur.
b. Systolic ejection murmur. Sometimes referred to as a "crescendo-decrescendo" murmur, it begins after S1, increases in midsystole, and decreases before S2; both heart sounds will be audible. This type of murmur is heard in semilunar (aortic or pulmonary) stenosis but may be innocent as well. Pulmonary valve stenosis is heard at the pul-monic area (left second intercostal space), with radiation to lung fields and back. Valvular aortic stenosis is best heard at the left midsternal border, radiating toward the right base and neck. An ejection click, or high-pitched opening sound, often precedes the systolic ejection murmur in aortic or pulmonic stenosis, distinguishing it from an innocent flow murmur c. Diastolic murmur. The murmur of semilunar valve insufficiency (eg, pulmonary or aortic regurgitation) begins immediately after S2 and has a blowing, decrescendo quality. A middiastolic sound of relative tricuspid valve stenosis is heard at the left lower sternal border in atrial septal defect. Left heart volume overload (eg, from VSD or large PDA) causes a diastolic rumble of relative mitral stenosis, heard at the apex and left fifth intercostal space. d. Continuous murmur. A murmur that is systolic and continues into or throughout diastole. Lesions associated with continuous murmurs include PDA, less commonly arteriovenous malformation, aortopulmonary window, and coronary artery fistula. Also includes venous hums.
4. Pulses. Examine distal pulses, and palpate brachial and femoral pulses simultaneously. Absent or delayed femoral pulses, associated with higher arm BP, are indicative of coarctation of the aorta. Wide pulse pressure is associated with sharp upstroke, and rapid fall-off (water-hammer pulse), with aortic run-off lesions.
5. Skin. Examine for the characteristic rash of erythema marginatum, seen in rheumatic fever, as well as rare cutaneous manifestations of bacterial endocarditis (Janeway lesions, Olser nodules).
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