Variations in the Second Heart Sound - S2

Increased intensity of A2 in the right 2nd interspace

(where only A2 can usually be heard) occurs in systemic hypertension because of the increased pressure load. It also occurs when the aortic root is dilated, probably because the aortic valve is then closer to the chest wall.

Physiologic splitting

Listen for physiologic splitting of S2 in the 2nd or 3rd left interspace. The pulmonic component of S2 is usually too faint to be heard at the apex or aortic area, where S2 is a single sound derived from aortic valve closure alone. Normal splitting is accentuated by inspiration and usually disappears on expiration. In some patients, especially younger ones, S2 may not become single on expiration. It may merge when the patient sits up.

Increased intensity of P2

When P2 is equal to or louder than A2, suspect pulmonary hypertension. Other causes include a dilated pulmonary artery and an atrial septal defect. When a split S2 is heard widely, even at the apex and the right base, P2 is accentuated.

Decreased or Absent A2 in the Right 2nd interspace

is noted in calcific aortic stenosis because of valve immobility. If A2 is inaudible, no splitting is heard.

Decreased or absent P2

is usually from the increased anteroposterior diameter of the chest associated with aging. It can also result from pulmonic stenosis. If P2 is inaudible, no splitting is heard.

Wide splitting of S2

refers to an increase in the usual splitting that persists throughout the respiratory cycle. Wide splitting can be caused by delayed closure of the pulmonic valve (as in pulmonic stenosis or right bundle branch block). Right bundle branch block also causes splitting of S1 into its mitral and tricuspid components. Wide splitting can also be caused by early closure of the aortic valve, as in mitral regurgitation.

Paradoxical or reversed splitting

refers to splitting that appears on expiration and disappears on inspiration. Closure of the aortic valve is abnormally delayed so that A2 follows P2 in expiration. Normal inspiratory delay of P2 makes the split disappear. The most common cause of paradoxical splitting is left bundle branch block.

Fixed splitting

refers to wide splitting that does not vary with respiration. It occurs in atrial septal defect and right ventricular failure.