Tesi etd-09142020-114024 |
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Tipo di tesi
Tesi di laurea magistrale
Autore
BIASI, NICCOLO
URN
etd-09142020-114024
Titolo
Modelling whole heart electrical activity with heterogeneous action potentials
Applications in diagnostics and cardiac device design
Dipartimento
INGEGNERIA DELL'INFORMAZIONE
Corso di studi
BIONICS ENGINEERING
Relatori
relatore Tognetti, Alessandro
Parole chiave
- Brugada syndrome
- cardiac bidomain
- closed loop pacemaker simulation
- heart modelling
- myocardial ischemia simulation
Data inizio appello
09/10/2020
Consultabilità
Non consultabile
Data di rilascio
09/10/2090
Riassunto
We developed a finite element model of the electrical activity of the whole heart embedded in the torso that is proposed as an useful tool to simulate myocardial ischemia and cardiac pacing. The electrical activity of the cardiac tissue is reproduced with a bidomain model incorporated with modified FitzHugh-Nagumo equations. The finite element model is developed in Comsol Multiphysics, both in two and in three dimensions. Myocardial ischemia and bradycardia can be easily simulated by simple changes to the parameters of the model.
We simulated apical, anterior and posterior ischemias and the relative electrocardiographic signals.
The model was exported in Simulink environment to develop a closed-loop model of cardiac pacing.
We chose a demand inhibited pacemaker, which stimulates the myocardium only if the intrinsic activity of the heart is not revealed, but every type of pacemaker can be simulated.
Finally, we exploited the functionalities of the new developed ionic current model to simulate ventricular action potential in Brugada syndrome.
The model generates a controlled spontaneous activation in the sinoatrial node and it is also able to reproduce realistic electrocardiographic signals and the effects that the stimulation and the pathological conditions have on them.
We simulated apical, anterior and posterior ischemias and the relative electrocardiographic signals.
The model was exported in Simulink environment to develop a closed-loop model of cardiac pacing.
We chose a demand inhibited pacemaker, which stimulates the myocardium only if the intrinsic activity of the heart is not revealed, but every type of pacemaker can be simulated.
Finally, we exploited the functionalities of the new developed ionic current model to simulate ventricular action potential in Brugada syndrome.
The model generates a controlled spontaneous activation in the sinoatrial node and it is also able to reproduce realistic electrocardiographic signals and the effects that the stimulation and the pathological conditions have on them.
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