Mechanism of pulmonary venous pressure and flow waves

Abstract

The pulmonary venous systolic flow wave has been attributed both to left heart phenomena, such as left atrial relaxation and descent of the mitral annulus, 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 wave propagation and reflection. A mathematical model of the pulmonary vein was developed; the pulmonary vein was modeled as a lossless transmission line and the pulmonary bed by a three-element lumped parameter model accounting for viscous losses, compliance, and inertia. We assumed that all pulsations originate in the left atrium (LA), the pressure in the pulmonary bed being 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 during 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 pulmonary bed of tau approximately 150ms, a compliance of the pulmonary bed of C approximately 0.4 ml/mmHg, and an inertance of the pulmonary bed of 1.1 mmHgs2/ml. The pulse wave velocity of the pulmonary vein was estimated to be c approximately 1m/s. Waves, however, travel both towards the left atrium and towards the pulmonary bed. Waves traveling towards the left atrium are attributed to the reflections caused by the mismatch of impedance of line (pulmonary vein) and load (pulmonary bed). Wave intensity analysis was used to identify a period in systole of net wave propagation towards the left atrium for both measurements and model. The linear separation technique was used to split the pressure into one component traveling from the left atrium to the pulmonary bed and a reflected component propagating from the pulmonary bed to the left atrium. The peak of the reflected pressure wave corresponded well with the positive peak in wave intensity in systole. We conclude that the gross features of the pressure and flow waves in the pulmonary 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 waves traveling back to the LA. Although the gross features of the measured pressure were captured well by the model predicted pressure, there was still some discrepancy between the two. Thus, other factors initiating or influencing waves traveling towards the LA cannot be excluded.

One-Dimensional Haemodynamic Modeling and Wave Dynamics in the Entire Adult Circulation

“…Systolic flow deceleration was related to deceleration of the descending atrioventricular plane towards the end of systole (BEW add ), while late diastolic flow deceleration (known as the A--wave) was caused by atrial contraction via the BCW ac . Model--derived pulmonary venous wave dynamics were similar to the systemic side and were consistent with the two available human studies, 115,116 with all waves predicted by our model being visible in the figures of these papers. However, our model data did not predict a secondary systolic flow peak (known as S2) that is sometimes seen in vivo.…”

Noncontrast SSFP pulmonary vein magnetic resonance angiography: Impact of off‐resonance and flow

“…The maximum blood velocity was 30-35 cm/s through the cardiac cycle with minimal negative flow (-8-0 cm/s) during late diastole (after atrial contraction). Flow velocity pattern of all PVs were similar and consisted of 3 waveforms of high velocity S wave (peak velocity: 30±3 cm/s for LIPV, 36±12 cm/s for LSPV, 35±4 cm/s for RIPV, and 31±8 cm/s for RSPV) in ventricular systole, high velocity D wave (23±11 cm/s for LIPV, 24±10 cm/s for LSPV, 27±11 cm/s for RIPV, and 24±10 cm/s for RSPV) in early diastole, and low negative/reversal velocity wave (6.8±1.6 cm/s for LIPV, 8.0±1.9 cm/s for LSPV, 8.3±1.8 cm/s for RIPV, and 6.4±1.6 cm/s for RSPV) in late diastole due to atrial contraction (22). Of the six 3D SSFP PV images acquired, additional signal voids were observed in PVs and LA in four subjects when PV MRA was acquired during late diastole compared to mid diastole (Figure 6).…”

Dynamics of the Pulmonary Venous Flow in the Fetus and Its Association With Vascular Diameter

“…Other factors involved have been evaluated, such as left atrium relaxation and compliance and left ventricular function. [21][22][23][24][25][26][27] Pulmonary vein relaxation, mediated by C-type natriuretic peptide, is uniform and thus does not allow segmental variations. 28 The effects of vessel tapering in the pulmonary circulation have been studied by nonlinear models, 6,10 and the role of the vessel cross-sectional area in the flow wave dynamics has also been assessed.…”