Session P7A.3

Computer Model for Determination of the Physiologic Correlates of the Impedance Cardiovasculogram Associated with Acute Heart Failure

RL Summers*

University of Mississippi
Jackson, MS, USA

Background: The cardiovasculogram (CVG) is the graphical depiction of the ensembled-averaged electronic signals generated by the technique of impedance cardiography. As an interpretable waveform, the CVG represents the mechanical functioning of the cardiac cycle with specific attributes that are consistently identified in certain disease states. Previous studies have suggested that the presence of a prominent “O” wave during the diastolic portion of the CVG may be a sensitive indicator of fluid volume overload during episodes of acute decompensated heart failure (ADHF). In this study, a computer model of a circulatory system interfaced with simulated bioimpedance technology is used to determine which physiologic elements may be associated with the typical changes seen on the CVG during ADHF.
Methods: An anatomically structured computer model of a circulatory system interfaced with simulated bioimpedance technology was constructed using graphic-based simulation software (VisSim, Inc). The model software can run simulations of the dynamics of circulatory physiology while generating the resultant predicted waveform of the impedance CVG (väsamed methodology). Simulations of the conditions of ADHF (systolic and diastolic) were achieved by altering the model parameters that control ventricular contractility and compliance (1/2 normal values). For model validation, simulated changes in the O and C waveforms were compared to CVG changes in patients with ADHF. A systems analysis of the model was performed to determine the mechanisms responsible for the observed changes in the CVG.
Results: After a reduction in the model’s cardiac contractility, the simulated CVG had a 2 fold increase in the peak of the O wave with a broadening and blunting of the C wave. The simulation study of diastolic heart failure resulted in a wide and elevated O wave with minor changes in C wave morphology. The systems analysis of the model under the simulated conditions of ADHF revealed that increases in sequestered fluid volumes in the vena cava were responsible for the characteristic changes in the O waveform. When this venous congestion of blood was prevented by amelioration of the fluid overload or by artificially fixing venous compliance in the computer model, the O wave changes were much less prominent.
Conclusion: A computer model was developed for the analysis of the impedance derived CVG during ADHF. Changes in the C and O waveforms of the simulated CVG were found to be typical of those seen in patients with ADHF. A systems analysis performed using the model indicates that fluid congestion within the vena cava may be responsible for these characteristic waveform changes. This analysis also suggests that the typical CVG pattern of ADHF has a specific physiologic etiology and that the sequential examination of certain waveform elements can potentially be used for monitoring the response to treatment in these patients.

(Abstract Control Number: 205)