title: Genesis of the characteristic pulmonary venous pressure waveform as described by the reservoir-wave model.
abstract: Conventional haemodynamic analysis of pulmonary venous and left atrial (LA) pressure waveforms yields substantial forward and backward waves throughout the cardiac cycle; the reservoir wave model provides an alternative analysis with minimal waves during diastole. Pressure and flow in a single pulmonary vein (PV) and the main pulmonary artery (PA) were measured in anaesthetized dogs and the effects of hypoxia and nitric oxide, volume loading, and positive-end expiratory pressure (PEEP) were observed. The reservoir wave model was used to determine the reservoir contribution to PV pressure and flow. Subtracting reservoir pressure and flow resulted in 'excess' quantities which were treated as wave-related.Wave intensity analysis of excess pressure and flow quantified the contributions of waves originating upstream (from the PA) and downstream (from the LA and/or left ventricle (LV)).Major features of the characteristic PV waveform are caused by sequential LA and LV contraction and relaxation creating backward compression (i.e.pressure-increasing) waves followed by decompression (i.e. pressure-decreasing) waves. Mitral valve opening is linked to a backwards decompression wave (i.e. diastolic suction). During late systole and early diastole, forward waves originating in the PA are significant. These waves were attenuated less with volume loading and delayed with PEEP. The reservoir wave model shows that the forward and backward waves are negligible during LV diastasis and that the changes in pressure and flow can be accounted for by the discharge of upstream reservoirs. In sharp contrast, conventional analysis posits forward and backward waves such that much of the energy of the forward wave is opposed by the backward wave.
authors.affiliation: Libin Cardiovascular Institute of Alberta, University of Calgary, Calgary, Alberta, Canada james.bouwmeester@yale.edu.
authors.forename: J Christopher
authors.initials: JC
authors.lastname: Bouwmeester
authors.affiliation: Libin Cardiovascular Institute of Alberta, University of Calgary, Calgary, Alberta, Canada Department of Cardiac Sciences, University of Calgary, Calgary, Alberta, Canada Department of Medicine, University of Calgary, Calgary, Alberta, Canada.
authors.forename: Israel
authors.initials: I
authors.lastname: Belenkie
authors.affiliation: Department of Civil Engineering, University of Calgary, Calgary, Alberta, Canada.
authors.forename: Nigel G
authors.initials: NG
authors.lastname: Shrive
authors.affiliation: Libin Cardiovascular Institute of Alberta, University of Calgary, Calgary, Alberta, Canada Department of Cardiac Sciences, University of Calgary, Calgary, Alberta, Canada Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada.
authors.forename: John V
authors.initials: JV
authors.lastname: Tyberg
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure; D004285:Dogs; D005260:Female; D008297:Male; D008943:Mitral Valve / Q000502:physiology; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D009569:Nitric Oxide / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D011651:Pulmonary Artery / Q000378:metabolism / Q000502:physiology; D011667:Pulmonary Veins / Q000378:metabolism / Q000502:physiology*; D016276:Ventricular Function
chemical_list: D009569:Nitric Oxide; D010100:Oxygen