Mechanism of pulmonary venous pressure and flow waves

The pulmonary venous systolic flow wave has been attributed both to left he art phenomena, such as left atrial relaxation and descent of the mitral ann ulus, and to propagation of the pulmonary artery pressure pulse through the pulmonary bed from the right ventricle. In this study we hypothesized that all waves in the pulmonary veins originate in the left heart, and that the gross wave features observed in measurements can be explained simply by wa ve propagation and reflection. A mathematical model of the pulmonary vein w as developed; the pulmonary vein was modeled as a lossless transmission lin e and the pulmonary bed by a three-element lumped parameter model accountin g for viscous losses, compliance, and inertia. We assumed that all pulsatio ns originate in the left atrium (LA), the pressure in the pulmonary bed bei ng constant. The model was validated using pulmonary vein pressure and flow recorded 1 cm proximal to the junction of the vein with the left atrium du ring aortocoronary bypass surgery. For a pressure drop of 6 mmHg across the pulmonary bed, we found a transit time from the left atrium to the pulmona ry bed of tau approximate to 150ms, a compliance of the pulmonary bed of C approximate to 0.4 ml/mmHg, and an inertance of the pulmonary bed of 1.1 mm Hg s(2)/ml. The pulse wave velocity of the pulmonary vein was estimated to be c approximate to 1 m/s. Waves, however, travel both towards the left atr ium and towards the pulmonary bed. Waves traveling towards the left atrium are attributed to the reflections caused by the mismatch of impedance of li ne (pulmonary vein) and load (pulmonary bed). Wave intensity analysis was u sed to identify a period in systole of net wave propagation towards the lef t atrium for both measurements and model. The linear separation technique w as used to split the pressure into one component traveling from the left at rium to the pulmonary bed and a reflected component propagating from the pu lmonary bed to the left atrium. The peak of the reflected pressure wave cor responded well with the positive peak in wave intensity in systole. We conc lude that the gross features of the pressure and flow waves in the pulmonar y vein can be explained in the following manner: the waves originate in the LA and travel towards the pulmonary bed, where reflections give rise to wa ves traveling back to the LA. Although the gross features of the measured p ressure were captured well by the model predicted pressure, there was still some discrepancy between the two. Thus, other factors initiating or influe ncing waves traveling towards the LA cannot be excluded.