Mechanisms of Fixed Splitting of the Second Heart Sound

Abstract

Forty-four patients with wide splitting of the second heart sound and 25 normal controls were studied with fast speed logarithmic phonocardiograms. In the control group, inspiratory augmentation of right heart filling increased the right ventricular stroke volume, prolonged the right ventricular stroke time and delayed pulmonic valve closure, thus altering the second sound from expiratory synchrony to inspiratory separation of its 2 components. In the group with atrial septal defects, the second sound normalized postoperatively, reflecting the ability of the right ventricle to undergo its normal inspiratory increase and expiratory decrease in stroke volume when the defect was closed. Before closure, the right ventricular stroke time neither shortened with expiration nor lengthened with inspiration because of the constant diastolic right ventricular hypervolemia. Hence, preoperatively the interval between aortic and pulmonic valve closures remained characteristically wide and fixed. That the preoperative delay in pulmonic valve closure could not have been a reflection of "incomplete right bundle-branch block" was illustrated by the postoperative normalization of the second sound without change in the QRS pattern of the electrocardiogram. Although the split of the second sound was not altered by respiration, it was altered by change in cycle length, widening after longer cycles and narrowing after shorter cycles. Wide splitting of the second heart sound was found in mitral insufficiency because of early aortic valve closure, in complete right bundle-branch block because of delayed pulmonic valve closure, and in complete left bundle-branch block because of a reversed sequence of aortic-pulmonic valve closure. When right ventricular failure coexisted with these lesions, the decompensated chamber did not convert its inspiratory augmentation of filling into increased stroke volume. The inspiratory increase in right ventricular stroke time and the inspiratory delay in pulmonic valve closure therefore could not occur so the split of the second sound remained fixed throughout the respiratory cycle.