Using a human cardiopulmonary model to study and predict normal and diseased ventricular mechanics, septal interaction, and atrio-ventricular blood flow patterns.
We upgraded our human cardiopulmonary (CP) model with additional data that enables it to more accurately simulate normal physiology. We then tested its ability to explain human disease by changing two parameter values that decrease ventricular compliance, and found that it could predict many of the hemodynamic, gas exchange, and autonomic abnormalities found in patients with left ventricular diastolic dysfunction (LVDD). The newly incorporated information includes high-fidelity pressure tracings simultaneously recorded from the RV and LV of a normal human in a cardiac catheterization laboratory, Doppler echocardiographic inlet flow velocity patterns, measures of right and left ventricular impedance, and atrial volumes. The revised cardiovascular section details the hemodynamics of a normal subject to the extent that it can now explain the effects of septal compliance on ventricular interaction, the differences in left and right ventricular pressure development, and venous blood gas mixing in the right atrium. The model can isolate the highly interrelated features of normal and abnormal physiology, and simultaneously demonstrate their interaction in a manner that would be very difficult or impossible using an intact organism. It may therefore help physicians and scientists understand, diagnose, and improve their treatment of complicated cardiovascular and pulmonary diseases. It could also simulate the hemodynamic and respiratory effects of ventricular and pulmonary assist devices, and thus help with their development.
Luo
C
C
Department of Electrical and Computer Engineering, Rice University, 6100 Main St., Houston, TX 77005-1892, USA.
Ware
D L
DL
Zwischenberger
J B
JB
Clark
J W
JW
D001696:Biomechanical Phenomena / Q000379:methods; D001783:Blood Flow Velocity; D001794:Blood Pressure; D006325:Heart Atria / Q000503:physiopathology*; D006346:Heart Septum / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D008954:Models, Biological; D009200:Myocardial Contraction; D011652:Pulmonary Circulation; D013318:Stroke Volume; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*