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.
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ABSTRACT: To investigate pulmonary vein (PV) off-resonance and blood flow as causes of signal void artifacts in noncontrast steady-state-free-precession (SSFP) PV magnetic resonance angiography (MRA). PV blood off-resonance was measured on 11 healthy adult subjects and 10 atrial fibrillation (AF) patients. Noncontrast PV MRA was performed using a 3D slab-selective SSFP sequence at 1.5T on seven healthy subjects with signal profile shifts of 0-125 Hz. The time-resolved blood flow velocity of the PVs was measured on five healthy subjects. The impact of flow was studied on six healthy subjects, on whom SSFP PV MRA was acquired twice with the electrocardiogram (ECG) trigger delay corresponding to low and high flow, respectively. The PV off-resonances were 97 ± 27 Hz, 65 ± 20 Hz, 74 ± 25 Hz, and 52 ± 17 Hz for right inferior, left inferior, right superior, and left superior PVs, respectively, on healthy subjects, and 74 ± 20 Hz, 38 ± 9 Hz, 51 ± 20 Hz, and 28 ± 11 Hz on AF patients (P<0.01 for all). The off-resonance caused severe signal voids in the PVs. Signal acquired during mid-diastole with high PV flow caused additional signal voids in the left atrium, which was reduced by setting the ECG trigger delay to late-diastole. PV off-resonance and flow causes signal void artifacts in noncontrast 3D slab-selective SSFP PV MRA.Journal of Magnetic Resonance Imaging 11/2010; 32(5):1255-61. · 2.57 Impact Factor
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ABSTRACT: Left ventricular (LV) filling velocities provide important insights into ventricular function and are useful clinical markers of diastolic dysfunction. Filling velocities can be measured at bedside by Doppler echocardiography and can be incorporated into everyday cardiology practice. Interpretation of filling velocities in a clinical context, however, requires insights into cardiac mechanics. The objective of this chapter is to review the essential physiology of filling and how changes in LV systolic and diastolic function can modify filling velocities as measured by Doppler echocardiography. This chapter addresses filling of the left ventricle only. Filling patterns for the right ventricle are of clinical importance for the diagnosis of restrictive cardiomyopathy and constrictive pericarditis and are addressed in Chapter 21.12/2007: pages 81-97;
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ABSTRACT: Left ventricular diastolic dysfunction is associated with slowing of LV relaxation and a decrease in LV chamber compliance. This impairment of function leads to changes in filling velocities as measured by pulsed wave Doppler echocardiography in the pulmonary veins and across the mitral valve, and in intraventricular flow propagation velocity as measured by color M-mode Doppler. This paper explores some of the physiology of LV filling in a clinical context.Heart Failure Reviews 11/2000; 5(4):291-299. · 4.45 Impact Factor