The Splitting of the Second Heart Sound in Normal Subjects and in Patients with Congenital Heart Disease
The characteristics of the second heart sound were analyzed in 350 phonocardiograms recorded from patients in all of whom the diagnosis was proved either at operation or by detailed catheterization studies. A2-P2 during expiration averaged 10.6 msec. in normal subjects. Q-A2 changed little during inspiration, with an average decrease of only 5.2 msec., while Q-P2 increased by an average of 32.6 msec. The average increase of A2-P2 during inspiration was therefore 37.8 msec. In patients with ASD, A2-P2 during expiration averaged 50.2 msec. and the inspiratory change in Q-P2 averaged only 4.6 msec. In 115 of 118 patients with ASD the inspiratory increase of A2-P2 ranged from 0 to 10 msec. Following successful surgical closure 29 patients with ASD developed the normal inspiratory augmentation of A2-P2; in the two patients in whom the defect was not completely closed the relatively constant A2-P2 noted preoperatively persisted.
Release of the Valsalva maneuver exaggerated the inspiratory increase of A2-P2 observed in normal subjects but did not modify this interval in patients with ASD. Analysis of the effect of release of the Valsalva maneuver on A2-P2 was helpful in separating patients with ASD from normal subjects. Evidence was presented that the relative constancy of the splitting of the second heart sound in patients with ASD is due to reciprocal changes in the magnitude of the left-to-right shunt and the systemic venous inflow into the right ventricle during respiration.
In patients with moderate or severe pulmonary stenosis, A2-P2 during expiration was longer than in normal subjects and in the same range as in patients with ASD. However, patients with PS showed a normal augmentation of A2-P2 during expiration. In patients with congenital AS, and those with PDA, left ventricular ejection tended to be prolonged with reversal of the normal sequence of semilunar valve closure or simultaneous closure of these valves during expiration.
- © 1962 American Heart Association, Inc.