title: Numerical simulation of the influence of gravity and posture on cardiac performance.
abstract: A numerical model of the cardiovascular system was used to quantify the influences on cardiac function of intrathoracic pressure and intravascular and intraventricular hydrostatic pressure, which are fundamental biomechanical stimuli for orthostatic response. The model included a detailed arterial circulation with lumped parameter models of the atria, ventricles, pulmonary circulation, and venous circulation. The venous circulation was divided into cranial, central, and caudal regions with nonlinear compliance. Changes in intrathoracic pressure and the effects of hydrostatic pressure were simulated in supine, launch, sitting, and standing postures for 0, 1, and 1.8 G. Increasing intrathoracic pressure experienced with increasing gravity caused 12% and 14% decreases in cardiac output for 1 and 1.8 G supine, respectively, compared to 0 G. Similar results were obtained for launch posture, in which the effects of changing intrathoracic pressure dominated those of hydrostatic pressure. Compared to 0 G, cardiac output decreased 0.9% for 1 G launch and 15% for 1.8 G launch. In sitting and standing, the position of the heart above the hydrostatic indifference level caused the effects of changing hydrostatic pressure to dominate those of intrathoracic pressure. Compared to 0 G, cardiac output decreased 13% for 1 G sitting and 23% for 1.8 G sitting, and decreased 17% for 1 G standing and 31% for 1.8 G standing. For a posture change from supine to standing in 1 G, cardiac output decreased, consistent with the trend necessary to explain orthostatic intolerance in some astronauts during postflight stand tests. Simulated lower body negative pressure (LBNP) in 0 G reduced cardiac output and mean aortic pressure similar to I G standing, suggesting that LBNP provides at least some cardiovascular stimuli that may be useful in preventing postflight orthostatic intolerance. A unifying concept, consistent with the Frank-Starling mechanism of the heart, was that cardiac output was proportional to cardiac diastolic transmural pressure for all postures and gravitational accelerations.
authors.affiliation: Department of Mechanical Engineering, University of Louisville, KY 40292, USA.
authors.forename: Kristy
authors.initials: K
authors.lastname: Peterson
authors.forename: Edwin T
authors.initials: ET
authors.lastname: Ozawa
authors.forename: George M
authors.initials: GM
authors.lastname: Pantalos
authors.forename: M Keith
authors.initials: MK
authors.lastname: Sharp
mesh_terms: D000222:Adaptation, Physiological; D001794:Blood Pressure / Q000502:physiology; D003198:Computer Simulation; D006112:Gravitation; D006321:Heart / Q000502:physiology / Q000503:physiopathology*; D006334:Heart Function Tests / Q000379:methods*; D006439:Hemodynamics; D006801:Humans; D007024:Hypotension, Orthostatic / Q000209:etiology* / Q000503:physiopathology; D008955:Models, Cardiovascular; D011187:Posture / Q000502:physiology*; D012680:Sensitivity and Specificity; D013909:Thorax / Q000503:physiopathology; D014893:Weightlessness / Q000009:adverse effects; D018474:Weightlessness Simulation / Q000009:adverse effects*