title: Hemodynamic consequences of ventricular interaction as assessed by model analysis.
abstract: Because of close anatomic association, the pressure and volume in one ventricle can directly influence the pressure and volume in the opposite ventricle. To examine the importance of ventricular interdependence in controlling the circulation, we developed a computer model in which ventricular interdependence could be turned on and off. Left ventricular chamber contractility, as judged by maximal elastance (Emax), was enhanced on the order of 10% as a result of ventricular interaction, whereas right ventricular Emax was affected by as much as 60% under physiological conditions. With increases in systemic vascular resistance, ventricular interaction caused a smaller stroke volume (SV) decrease than with no interaction. For canine data (SV = 21.4 ml), doubling systemic vascular resistance decreased SV by 3.7 without ventricular interdependence, 3.5 with diastolic ventricular interdependence, and 3.3 ml with diastolic and systolic ventricular interdependence. In contrast, with increases in pulmonary vascular resistance, ventricular interaction caused a greater decrease in SV than with no interaction present. Decreasing left ventricular free wall elastance or right ventricular free wall elastance decreased SV. Diastolic ventricular interdependence reduced the SV changes, whereas systolic ventricular interdependence accentuated the SV changes with alterations in right and left ventricular free-wall elastance. The results of the present simulation demonstrate the importance of ventricular interdependence in the observed responses of the right ventricle to volume overload, pressure overload, and ischemia.
authors.affiliation: Philadelphia Heart Institute, Presbyterian Medical Center, Pennsylvania 19104.
authors.forename: W P
authors.initials: WP
authors.lastname: Santamore
authors.forename: D
authors.initials: D
authors.lastname: Burkhoff
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D003198:Computer Simulation; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D009200:Myocardial Contraction / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D016276:Ventricular Function