title: Reservoir and conduit function of right atrium: impact on right ventricular filling and cardiac output.
abstract: The purpose of this study was to investigate the relationship between right atrial (RA) reservoir and conduit function and to determine how hemodynamic changes influence this relationship and its impact on cardiac output. In 11 open-chest sheep, RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively. Conduit function was separated into early (before A wave) and late (after A wave) components. The effects of inotropic stimulation, partial pulmonary artery occlusion, and pericardiotomy were tested. At baseline with the pericardium intact, reservoir function accounted for 0.56 (SD 0.13) of RA inflow, early conduit for 0.29 (SD 0.07), and late conduit (during RA contraction) for 0.16 (SD 0.11). Inotropic stimulation decreased conduit function and increased reservoir function, but these effects did not reach statistical significance. With partial pulmonary artery occlusion, early conduit function fell to 0.20 (SD 0.11) (P < 0.04), and the conduit-to-reservoir ratio decreased by 41% (P < 0.03). Similarly, after pericardiotomy, early conduit function fell to 0.14 (SD 0.09) (P < 0.004), reservoir function increased to 0.72 (SD 0.08) (P < 0.04), and, consequently, the early conduit-to-reservoir ratio decreased by 63% (P < 0.006). Cardiac output was inversely related to the conduit-to-reservoir ratio (r = 0.39, P < 0.001). This study demonstrated that the right atrium adjusts its ability to act more as a reservoir than a conduit in a dynamic manner. The RA conduit-to-reservoir ratio was directly related to the right ventricular pressure-RA pressure gradient at the time of maximum RA volume, with increased ventricular pressures favoring conduit function, but it was inversely related to cardiac output, with an increase in the reservoir contribution favoring improved cardiac output.
authors.affiliation: Division of Cardiothoracic Surgery, Washington University School of Medicine, St. Louis, Missouri 63110-1013, USA.
authors.forename: Sydney L
authors.initials: SL
authors.lastname: Gaynor
authors.forename: Hersh S
authors.initials: HS
authors.lastname: Maniar
authors.forename: Sunil M
authors.initials: SM
authors.lastname: Prasad
authors.forename: Paul
authors.initials: P
authors.lastname: Steendijk
authors.forename: Marc R
authors.initials: MR
authors.lastname: Moon
mesh_terms: D000208:Acute Disease; D000818:Animals; D016280:Atrial Function, Right / Q000502:physiology*; D006328:Cardiac Catheterization; D002302:Cardiac Output / Q000502:physiology*; D006976:Hypertension, Pulmonary / Q000503:physiopathology*; D011651:Pulmonary Artery / Q000503:physiopathology; D012044:Regression Analysis; D012756:Sheep; D014111:Tourniquets; D016278:Ventricular Function, Right / Q000502:physiology*; D017725:Ventricular Pressure / Q000502:physiology