TY - JOUR
T1 - A comprehensive model for right-left heart interaction under the influence of pericardium and baroreflex
AU - Beshara, Mäzen
AU - Lucariello, Richard J.
AU - Chiaramida, Salvatore A.
PY - 1997/12/1
Y1 - 1997/12/1
N2 - A phenomenological model of the cardiopulmonary circulation is developed with a focus on the interaction between the right heart and the left heart. The model predicts the hemodynamic consequences of changing circulatory parameters in terms of a broad spectrum of pressure and flow waveforms. Hemodynamics are characterized by use of an electrical analog incorporating mechanisms for transseptal pressure coupling, pericardial volume coupling, intrathoracic pressure, and baroreflex control of heart rate. Computer simulations are accomplished by numerically integrating 28 differential equations that contain nonlinear and time-varying coefficients. Validity of the model is supported by its accurate fit to clinical pressure and Doppler echocardiographic recordings. The model characterizes the hemodynamic waveforms for mitral stenosis, mitral regurgitation, left heart failure, right heart failure, cardiac tamponade, pulsus paradoxus, and the Valsalva maneuver. The wave shapes of pulmonary capillary wedge pressure under the above conditions are also accurately represented. Sensitivity analysis reveals that simulated hemodynamics are insensitive to most individual model parameters with the exception of afterload resistance, preload capacitances, intrathoracic pressure, contractility, and pericardial fluid volume. Baseline hemodynamics are minimally affected by transseptal coupling (up to 2%) and significantly affected by pericardial coupling (up to 20%). The model should be useful for quantitative studies of cardiopulmonary dynamics related to the right-left heart interaction under normal and disease conditions. mathematical model; hemodynamics; cardiopulmonary circulation; septum; intrathoracic pressure; pulmonary wedge pressure; heart failure; mitral stenosis; mitral regurgitation; cardiac tamponade; pulsus paradoxus; Valsalva maneuver
AB - A phenomenological model of the cardiopulmonary circulation is developed with a focus on the interaction between the right heart and the left heart. The model predicts the hemodynamic consequences of changing circulatory parameters in terms of a broad spectrum of pressure and flow waveforms. Hemodynamics are characterized by use of an electrical analog incorporating mechanisms for transseptal pressure coupling, pericardial volume coupling, intrathoracic pressure, and baroreflex control of heart rate. Computer simulations are accomplished by numerically integrating 28 differential equations that contain nonlinear and time-varying coefficients. Validity of the model is supported by its accurate fit to clinical pressure and Doppler echocardiographic recordings. The model characterizes the hemodynamic waveforms for mitral stenosis, mitral regurgitation, left heart failure, right heart failure, cardiac tamponade, pulsus paradoxus, and the Valsalva maneuver. The wave shapes of pulmonary capillary wedge pressure under the above conditions are also accurately represented. Sensitivity analysis reveals that simulated hemodynamics are insensitive to most individual model parameters with the exception of afterload resistance, preload capacitances, intrathoracic pressure, contractility, and pericardial fluid volume. Baseline hemodynamics are minimally affected by transseptal coupling (up to 2%) and significantly affected by pericardial coupling (up to 20%). The model should be useful for quantitative studies of cardiopulmonary dynamics related to the right-left heart interaction under normal and disease conditions. mathematical model; hemodynamics; cardiopulmonary circulation; septum; intrathoracic pressure; pulmonary wedge pressure; heart failure; mitral stenosis; mitral regurgitation; cardiac tamponade; pulsus paradoxus; Valsalva maneuver
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M3 - Article
C2 - 9087629
AN - SCOPUS:0030944148
SN - 0002-9513
VL - 272
SP - H1499-H1515
JO - American Journal of Physiology
JF - American Journal of Physiology
IS - 3 PART 2
ER -