Auscultation and Interpretation of a Loud Second Heart Sound (S2)

Optimal Auscultation Technique

Position the stethoscope at the second left intercostal space (pulmonic area) and the second right intercostal space (aortic area) and listen during expiration, when left‑sided sounds are amplified, to determine whether the loud component is A2 (suggesting systemic hypertension) or P2 (suggesting pulmonary hypertension)【1】.
Have the patient sit upright or lie supine with the back supported and relax for at least 5 minutes before auscultation【1】.
Ensure a quiet examination room; neither examiner nor patient should speak during the assessment【1】.
Remove all clothing covering the chest wall to improve sound transmission【1】.
Use either the diaphragm or the bell of the stethoscope; the diaphragm is preferred for higher‑pitched sounds such as S2【1】.
Listen at the aortic area (second right intercostal space) to best hear A2, which becomes loud in systemic hypertension【2】【3】.
Left‑sided heart sounds (including A2) are loudest during expiration because increased venous return augments left‑ventricular stroke volume【2】【3】.
Right‑sided sounds (including P2) increase with inspiration【2】【3】.

A loud A2, best heard at the second right intercostal space, indicates systemic hypertension or a hyperdynamic circulation【2】【3】.
A loud P2, best heard at the second left intercostal space, suggests pulmonary hypertension when its intensity equals or exceeds that of A2【2】【3】.

Fixed splitting (splitting that persists throughout the respiratory cycle) is a classic finding in atrial septal defect, with a constant split interval during both inspiration and expiration【3】.
A soft or absent A2 is highly specific for severe aortic stenosis and mandates immediate transthoracic echocardiography【3】.

Always correlate auscultatory findings with additional examination signs such as carotid pulse character, jugular venous pressure, and pre‑cordial palpation【2】【3】.

Perform the Valsalva maneuver; most murmurs decrease, helping to assess changes in S2 splitting【2】【3】.
Use positional changes (standing or squatting) to modify venous return and observe corresponding alterations in S2 characteristics【2】【3】.
Apply hand‑grip exercise, which increases afterload and can accentuate certain auscultatory findings【2】【3】.

Reverse splitting occurs when P2 closes before A2, causing S2 to split during expiration and become single during inspiration, while fixed splitting maintains a constant split interval throughout the respiratory cycle without respiratory variation, as noted by the American College of Cardiology and Circulation 4, 5
Severe aortic stenosis with soft or absent A2 is associated with reverse splitting, according to the American College of Cardiology 4, 6
Fixed splitting is characterized by a constant interval during both inspiration and expiration, with no respiratory variation in the splitting interval, as described by the American College of Cardiology and Circulation 4, 5
Atrial septal defect (ASD) is a classic finding associated with fixed splitting, as reported by the American College of Cardiology and Circulation 4, 5

The American College of Cardiology recommends listening carefully during normal respiration at the pulmonic area and having the patient breathe deeply to accentuate respiratory variation, to diagnose reverse or fixed splitting 4, 5
For fixed splitting, assess for right ventricular lift and look for right axis deviation and incomplete RBBB on ECG, as suggested by Circulation 5

Reverse splitting may indicate delayed left ventricular systole requiring investigation for structural heart disease or conduction abnormalities, and in severe aortic stenosis, A2 may become so soft that single S2 is heard rather than reversed splitting, as noted by the American College of Cardiology 4, 6
Fixed splitting indicates right ventricular volume overload requiring evaluation for intracardiac shunts, and warrants echocardiography to rule out ASD or other structural abnormalities, according to Circulation 5, 6