Second Heart Sound

The second heart sound (S2), described as a dupp, results from the sudden closing of the aortic and pulmonic valves, which bulge backwards towards the ventricles until their elastic stretch recoils the blood back into the arteries.   This recoil produces vibrations that reverberate back and forth between the heart walls, arteries, and valves.  When the vibrations contact the chest wall, they create what can be heard as the second heart sound.  Since the sound is created by the aortic and pulmonic valves, it has aortic (A2) and pulmonic (P2) components.  The components of S2 vary with the respiratory cycle: they are normally fused as one sound during expiration, but become audibly separated during inspiration.

Abnormalities of S2 include alterations in its pattern, and changes in the pattern of splitting.

The intensity of S2 is determined by the velocity of the blood returning towards the valves from the aorta and the pulmonary artery after the completion of ventricular contraction, and by the swiftness with which the closing valves arrest that flow.  In systemic or pulmonary arterial hypertension, the diastolic pressure in the respective great vessel is higher than normal, increasing the velocity of the surging blood, and accentuating the S2 sound.  Conversely, in severe aortic or pulmonic valve stenosis (narrowing), the valve commissures are almost fixed in position, such that the contribution of the narrowed valve to the S2 sound is diminished.

There are a number of different effects on the splitting of the second heart sound:

Widened Splitting

Fixed Splitting

Paradoxical Splitting

There is a brief period of silence immediately following the second heart sound.

The second heart sound can be best heard over the second intercostal space, where the aorta is closest to the surface.

 

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