The mechanism of splitting of the second heart sound in atrial septal defect.

Publisher Website
Google Scholar
Abstract
The mechanism underlying the width of splitting of the 2nd heart sound (S2) was investigated in 27 patients with ostium secundum atrial septal defect (ASD), all of whom had significant left to right shunting. Micromanometer catheters were used to record simultaneous high fidelity right ventricular (RV) and pulmonary arterial (PA) pressures. The patients were divided into 3 groups. There were 14 patients in group 1 (normotensive ASD) with sinus rhythm and normal PA pressure (mean < 21 mm Hg); in group II (hyperkinetic pulmonary hypertension) there were 7 patients with sinus rhythm and elevated PA pressure (mean PA > 23 mm Hg) and group III consisted of 6 patients with atrial fibrillation. For normotensive ASD, A2-P2 and hangout intervals correlated well (r = 0.91) and were essentially equal. QA2 and Q-RV intervals were also approximately equal, indicating that the electromechanical interval was essentially equal for right and left ventricles (LV). In hyperkinetic pulmonary hypertension the hangout interval was relatively narrow as compared to group I (P < 0.001) and the splitting interval varied from narrow to wide, depending upon the relative durations of Q-RV and QA2. The QA2 indices tended to be within normal limits, suggesting that the duration of Q-RV was the major determinant of the width of splitting. In atrial fibrillation, HO was fixed and narrow; A2-P2 and Q-RV intervals were directly related to preceding cycle length. An understanding of the mechanism of splitting of the 2nd heart sound in ASD must reflect the HO [hangout] interval as well as the relative durations of RV and LV electromechanical systoles.