S2 Heart Sound Topic Review

The second heart sound (S2) is produced by the closure of the aortic and pulmonic valves. The sound produced by the closure of the aortic valve is termed A2, and the sound produced by the closure of the pulmonic valve is termed P2.

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The A2 sound is normally much louder than the P2 due to higher pressures in the left side of the heart; thus, A2 radiates to all cardiac listening posts (loudest at the right upper sternal border), and P2 is usually only heard at the left upper sternal border. Therefore, the A2 sound is the main component of S2.

CLINICAL PEARL: A split S2 is best heard at the pulmonic valve listening post, as P2 is much softer than A2.

Like the S1 heart sound, the S2 sound is described regarding splitting and intensity. S2 is physiologically split in about 90% of people. The S2 heart sound can exhibit persistent (widened) splitting, fixed splitting, paradoxical (reversed) splitting or the absence of splitting. The S2 heart sound intensity decreases with worsening aortic stenosis due to immobile leaflets. In severe aortic stenosis, the A2 component may not be audible at all.

CLINICAL PEARL: In severe hypertension, a loud S2 may be prolonged and slurred — falsely mimicking a split S2.

Physiologic Split S2

Normally, A2 occurs just before P2, and the combination of these sounds make up S2. A physiologic split S2 occurs when the A2 sound precedes P2 by a great enough distance to allow both sounds to be heard separately. This happens during inspiration when increased venous return to the right side of the heart delays the closure of the pulmonic valve (major effect), and decreased return to the left side of the heart hastens the closure of the aortic valve (minor effect), thereby further separating A2 and P2. During expiration, the distance narrows, and the split S2 is no longer audible.

Paradoxical Split S2

A paradoxical split S2 heart sound occurs when the splitting is heard during expiration and disappears during inspiration — opposite of the physiologic split S2. A paradoxical split S2 occurs in any setting that delays the closure of the aortic valve including severe aortic stenosis and hypertrophic obstructive cardiomyopathy, or in the presence of a left bundle branch block.

CLINICAL PEARL: A paradoxical split S2 is heard in AS, HOCM or in the presence of a LBBB.

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Persistent (Widened) Split S2

Persistent (widened) splitting occurs when both A2 and P2 are audible during the entire respiratory cycle, and the splitting becomes greater with inspiration (due to increased venous return) and less prominent with expiration. This differs from a fixed split S2, which exhibits the same amount of splitting throughout the entire respiratory cycle and is explained below.

Any condition that causes a nonfixed delay in the closure of the pulmonic valve, or early closure of the aortic valve, will result in a wide split S2. Therefore, a persistent split S2 would occur in the setting of a right bundle branch block, pulmonary hypertension or pulmonic stenosis (delayed P2) or severe mitral regurgitation/ventricular septal defect (early A2 closure).

A RBBB causes a delay in the closure of the pulmonic valve, and thus a delay in P2, without any effect on A2. In severe MR or in the setting of a VSD, the A2 occurs early. In mitral regurgitation, this is due to a large proportion of the left ventricular stroke volume entering the left atrium, causing the left ventricular pressure to decrease faster. In a VSD, a large proportion of the stroke volume goes into the RV, similarly decreasing LV pressure quickly. The P2 is not affected in severe MR or VSD unless pulmonary hypertension is present.

CLINICAL PEARL: A persistent (widened) split S2 occurs in the setting of a RBBB or severe MR.

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Fixed Split S2

A fixed split S2 is a rare finding on cardiac exam; however, when found, it almost always indicates the presence of an atrial septal defect. A fixed split S2 occurs when there is always a delay in the closure of the pulmonic valve, and there is no further delay with inspiration; compare this to a widened split S2, as described above.

To explore why an atrial septal defect results in a fixed split S2, we must consider the altered cardiac hemodynamics present, which result in a fixed delay in PV closure. During inspiration, as usual, there is an increase in venous return to the right side of the heart, and thus increased flow through the PV — delaying its closure. The alteration in a patient with an ASD occurs during expiration. As the person expires, the pressure in the right atrium decreases because there is less venous return. The decreased pressure allows more blood to flow abnormally through the ASD, from the high pressured left atrium to the right atrium, ultimately resulting again in increased flow through the pulmonic valve — again, delaying its closure.

CLINICAL PEARL: A fixed split S2 is pathognomonic for the presence of an ASD.

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