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Simulation of Eisenmenger syndrome with ventricular septal defect using equivalent electronic system

Published online by Cambridge University Press:  26 September 2011

Mehmet Korurek
Affiliation:
Department of Biomedical Engineering, Faculty of Electrical and Electronic Engineering, Istanbul Technical University, Istanbul, Turkey
Mustafa Yildiz*
Affiliation:
Department of Cardiology, Kartal Kosuyolu Yuksek Ihtisas Educational and Research Hospital, Istanbul, Turkey
Ayhan Yüksel
Affiliation:
Department of Biomedical Engineering, Faculty of Electrical and Electronic Engineering, Istanbul Technical University, Istanbul, Turkey
Alparslan Şahin
Affiliation:
Department of Cardiology, Bakırköy Dr. Sadi Konuk Educational and Research Hospital, Istanbul, Turkey
*
Correspondence to: Dr M. Yildiz, MD, PhD, Assoc. Prof., Cardiologist, Internal Medicine Specialist and Physiologist, Department of Cardiology, Kartal Kosuyolu Yuksek Ihtisas Educational and Research Hospital, Istanbul, Turkey. Tel: +90 532 371 17 01; Fax: +90 0216 459 63 21; E-mail: [email protected]

Abstract

Background: In this study, we aim to investigate the simulation of the cardiovascular system using an electronic circuit model under normal and pathological conditions, especially the Eisenmenger syndrome. Methods and Results: The Eisenmenger syndrome includes a congenital communication between the systemic and pulmonary circulation, with resultant pulmonary arterial hypertension and right-to-left reversal of flow through the defect. When pulmonary vascular resistance exceeds systemic vascular resistance, it results in hypoxaemia and cyanosis. The Westkessel model including Resistor-Inductance-Capacitance pi-segments was chosen in order to simulate both systemic and pulmonary circulation. The left and right heart are represented by trapezoidal shape stiffness for better simulation results. The Eisenmenger syndrome is simulated using a resistance (septal resistance) connected between the left ventricle and right ventricle points of the model. Matlab® is used for the model implementation. In this model, although there is a remarkable increase in the pulmonary artery pressure and right ventricle pressure, left ventricle pressure, aortic pressure, aortic flow, and pulmonary compliance decrease in the Eisenmenger syndrome. In addition, left-to-right septal flow reversed in these diseases. Conclusion: Our model is effective and available for simulating normal cardiac conditions and cardiovascular diseases, especially the Eisenmenger syndrome.

Type
Original Article
Copyright
Copyright © Cambridge University Press 2012

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