Role of Kinetic Energy in Pulmonary Valvar Pressure Gradients

Abstract

Peak systolic pulmonary valvar pressure gradients are frequently seen in large intracardiac left-to-right shunt lesions. Conventionally, this has been attributed to "relative" pulmonic stenosis. Theoretical considerations suggest that this gradient is due to differences in expression of the total fluid energy. The side pressure, the downstream pressure, the end pressure, and the flow velocity in the pulmonary artery (PA) and the right ventricle (RV) pressure were measured in 11 dogs in the control state, and after increasing the velocity of the pulmonary arterial flow either by administration of isoproterenol or atropine, or by creating an arteriovenous fistula. The RV pressure and the end PA pressure were not significantly different ( P > 0.05), and were higher ( P < 0.01) than the side and downstream PA pressure in the control state, but increased to higher levels ( P < 0.01) after increasing the velocity of flow in the pulmonary artery. The mean pulmonary valve peak systolic gradient (RV-side PA pressure difference) was 8.8 mm Hg in the control state and increased to 19.1 mm Hg after isoproterenol infusion ( P < 0.01). This change in pulmonary valvar gradient is proportional to the increase in the PA flow velocity. The side pressure measures only the potential energy, and the end pressure measures both the potential and kinetic energies. In the right ventricle, only the potential energy is recorded where the kinetic energy is practically nonexistent. The difference between the RV (or end PA) pressure and side PA pressure is proportional to velocity of flow in the pulmonary artery and is due to partial transformation of fluid energy into kinetic energy. Thus, our study helps to explain the pressure gradient across the pulmonary valve in large left-to-right shunt lesions. These studies also raise questions as to the validity of interpretations of the gradients produced in the RV outflow tract after isoproterenol or exercise.