Mechanism of normal splitting of the second heart sound.

Abstract

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 ± 2.7 msec (1 SD) or 27 + 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-0. Increase in the Q-O interval accounted for only 7.7 ± 5.0 msec or 28 ± 12% of the total IA. The major single component of IA was the increase in O-P2 which averaged 11.9 ± 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.

Ventricular systolic time intervals by simultaneous echocardiographic recording of the semilunar valves during the first days of life: A study of normal newborn infants

“…Inspiratory prolongation of the Q-Pc interval appears predominantly related to increased duration of the protodiastolic interval (defined as the interval from end of "true" right ventricular systole t o pulmonic valve closure) .20,21 "True" right ventricular systole (Q-onset protodiastole) apparently contributes little to increased inspiratory duration of Q-Pc.~' Pulmonary vascular impedance (resistance and compliance) and inertia of ejected right ventricular volume are the variables which primarily affect the protodiastolic interval, while "true" right ventricular systole is influenced primarily by inspiratory augmentation of venous return. 20 The method described in this report does not differentiate "true" right ventricular systole from the protodiastolic interval. Nevertheless, the relative lack of respiratory prolongation of Q-Pc and inspiratory widening of the Ac-Pc interval during the first 3 days of life may be explained in terms of the normal hemodynamic adjustments occurring shortly after It is possible that inspiratory augmentation of venous return and ventricular filling, and the duration of "true" right ventricular systole is limited by the relatively noncompliant newborn right ventricle and by potential transient right-left shunting at the level of the patent foramen ovale."…”

An investigation of the second heart sound in the normal horse

“…Based upon the limited number of horses studied, the findings suggest that S2 should be categorised as a single sound or a sound with narrow splitting in the normal horse. No variation from the single S2 occurred due to respiration, as in man (Castle and Jones 1961;Castle, Hedden and Davis 1969;Adolph and Fowler 1970;Luisada 1971;Curtis, Matthews and Shaver 1975) or heart rate, as in the dog (Muir and Hamlin 1973;Hamlin et a1 1974).…”

Differences in the Duration of Total Ejection between Right and Left Ventricles in Chronic Pulmonary Hypertension

“…Chronic PH is a well known cause of closely split second heart sound due to delay in pulmonic valve closure 1,2 ; however this well established auscultatory principle is involuntarily neglected due to noisy, overbooked clinics and extremely busy schedules. However, its unmistakable sensitivity to identify patients with a high RV afterload due to increased resistance in the pulmonary vasculature should not be forgotten or its great clinical value ignored.…”

“…1,2 The hemodynamic alterations that lengthen RV ejection time as a result of chronic pulmonary hypertension (cPH) are most likely responsible for significantly reducing peak RV free wall longitudinal strain generation as well as delaying the development of time-to-peak strain of the RV free wall with respect to the interventricular septum thus causing dyssynchrony. 1,2 The hemodynamic alterations that lengthen RV ejection time as a result of chronic pulmonary hypertension (cPH) are most likely responsible for significantly reducing peak RV free wall longitudinal strain generation as well as delaying the development of time-to-peak strain of the RV free wall with respect to the interventricular septum thus causing dyssynchrony.…”

“…It is well-established that gradual elevation in pulmonary artery systolic pressure (PASP) delays closure of the pulmonic valve resulting in a narrowly split or single second heart sound, as long as right ventricular (RV) function is preserved. 1,2 The hemodynamic alterations that lengthen RV ejection time as a result of chronic pulmonary hypertension (cPH) are most likely responsible for significantly reducing peak RV free wall longitudinal strain generation as well as delaying the development of time-to-peak strain of the RV free wall with respect to the interventricular septum thus causing dyssynchrony. 3,4 Since our laboratory has recently published data showing how cPH lengthens time of onset of the RV outflow tract (RVOT) spectral Doppler signal while shortening both time to peak RVOT flow and overall total duration of ejection of the RVOT spectral Doppler signal 5 ; we used these observations and devised a study to determine if pulsed Doppler can detect temporal differences in ejection between RV and left ventricle (LV), as a result of cPH.…”