Mechanism of normal splitting of the second heart sound.

The mode of inspiratory augmentation (1A) of the A2-P2 interval was investigated in seven normal volunteers (group 1) and six patients with pulmonary hypertension of diverse etiology (group 2) using catheter-tip micromanometers. In group 1 subjects, inspiratory widening of this interval was found to average 27.2 msec, of which 7.6 plus or minus 2.7 msec (1 sd) or 27 plus or minus 7% was due to a decrease in the Q-A2 interval. The major contribution of Q-P2 interval prolongation was divided into two components: a) Q-O was measured from the onset of the QRS to the onset of the rapid descent of the right ventricular (RV) negative dp/dt, which was felt to reflect the duration of RV electromechanical systole, b) O-P2 or Q-P2 - Q-O. Increase in the Q-O interval accounted for only 7.7 plus or minus 5.0 msec or 28 plus or minus 12% of the total IA. The major single component of IA was the increase in O-P2 which averaged 11.9 plus or minus 3.0 msec. Five of six group 2 patients demonstrated significant respiratory change in Q-P2 intervals. In contrast to group 1 subjects, however, this was accomplished primarily via increases in the duration of RV electromechanical systole. The O-P2 interval is felt to primarily reflect the impedance characteristics of the pulmonary vascular bed. It is concluded that physiologic splitting of the second heart sound in normal subjects is most probably due to an inspiratory decrease in impedance of the pulmonary bed rather than the traditional explanation of prolongation of RV systole secondary to an increase in venous return. When the normal impedance characteristics of this bed are lost, as in pulmonary hypertension, IA must occur primarily via increases in the duration of RV systole. The inspiratory delay from the conclusion of RV systole to the occurrence of P2 is attributed to the inertiance of the RV stroke mass.