Objectives: We sought to define the hemodynamic determinants of pulmonary venous (PV) flow velocities to assess how these are affected by respiration, heart rate and loading conditions.
Background: Pulmonary venous flow velocity (PVFV) recorded with pulsed wave Doppler technique is currently used in the noninvasive evaluation of left ventricular (LV) diastolic function and filling pressures. Although previous studies in both animals and humans have shown that PV flow is pulsatile, the hemodynamic determinants of the individual components of this flow remain controversial. Understanding the physiologic mechanisms should help to better define the clinical utility of these Doppler techniques.
Methods: PV flow velocities obtained with transesophageal pulsed wave Doppler imaging were recorded together with PV, left atrial (LA) and LV pressures in 10 sedated, spontaneously breathing normal dogs. PVFV and hemodynamic data were analyzed during apnea, inspiration and expiration, at atrial paced heart rates of 60, 80, 100 and 120 beats/min and mean LA pressures of 6, 12, 18 and 24 mm Hg.
Results: The data showed that 1) PV pressure varied depending on recording site, resembling pulmonary artery pressure closer to the pulmonary capillary bed and LA pressure closer to the venoatrial junction; 2) PVFV qualitatively followed changes in the PV-LA pressure gradient; 3) four PVFV components exist under normal conditions-three of which follow phasic changes in LA pressure and one of which (the late systolic component) is more influenced by RV stroke volume and the compliance of the pulmonary veins and left atrium; 4) normal respiration and changes in heart rate significantly alter PVFV variables--in particular, reverse flow velocity at atrial contraction; and 5) increasing LA pressure results in larger PV A wave and PV early systolic flow velocities, as well as an earlier peak in PV late systolic flow velocity and a more prominent velocity minimum before PV diastolic flow.
Conclusions: Using transesophageal pulsed wave Doppler technique, four PVFV components are identifiable and determined by PV-LA hemodynamic pressure gradients. These gradients appear to be influenced by a combination of physiologic events that include RV stroke volume, the compliance of the pulmonary vasculature and left atrium and phasic changes in LA pressure. PV flow velocity components are significantly influenced by heart rate, respiration and LA pressure. These findings have implications for the interpretation of LV diastolic function and filling pressures by current Doppler echocardiographic techniques but require further clinical investigation.