The S₂ should be considered as an essential component of every pediatric cardiac exam, and should not be overlooked. The timing and characterization of S₂ can in some cases be the only exam finding suggesting a cardiac problem, particularly in the newborn that still has a patent ductus arteriosus. It is important that the examiner perform a deliberate, stepwise evaluation each time auscultation is performed. The S₂ is created by closure of the aortic and pulmonic valves at the end of systole, and is typically described as having an aortic (A₂) and pulmonic (P₂) component. The important characterizing aspects of S₂ are the intensity of its components, their timing and relationship to each other. Characterization of the S₂ sound can be diagnostic of congenital heart abnormalities such as atrial septal defects, more serious congenital heart disease such as pulmonary atresia, and hypoplastic left heart syndrome, and can also reveal evidence for pulmonary hypertension.

In the normal heart, the S₂ timing varies with respiration. At end expiration, the A₂ valve closes at the same time as or slightly before the pulmonary valve closes. The negative intrathoracic pressure that is created during inspiration draws slightly more blood into the right ventricle from the systemic veins; this small increase in right ventricular volume takes slightly longer to exit the right ventricle during the systolic contraction. This longer emptying time creates a relative delay of the P₂ closure component compared to A₂. As a result, the listener will hear an increased splitting of S₂ during inspiration, compared to a more narrowly split or single S₂ during expiration. The variation in S₂ splitting will be obvious in many cases, whereas it is described as a muffling of the crisp S₂ heard during expiration in others.

Another important feature of the S₂ that should be evaluated is its intensity or loudness. Normally the P₂ intensity will be significantly diminished when compared to the A₂ component. This relates to the fact that in the normal individual the pulmonary pressure is significantly lower than aortic pressure–typically about 25% of the systemic pressure. The P₂ component of the S₂ is, therefore, softer compared to the A₂ component because the pressure closing the pulmonary valve is lower than the pressure closing the
aortic valve. The intensity of the S₂ can, therefore, give great insight into the status of the pulmonary pressure.