Özet:
Heart failure is a syndrome when the heart is damaged permanently and lost its full functionality. In this case, the tissues cannot be fed sufficiently with blood and oxygen and compensatory mechanisms are triggered. These mechanisms are the sym pathetic nervous system, Renin-Angiotensin-Aldosterone, Antidiuretic Hormone and Natriuretic Peptides which help a healthy human body to reach homeostatic balance. When the balance is impaired, they work as negative feedback loops to reach equi librium. However, these mechanisms can create a vicious cycle for people who have damaged heart and vascular structures. Due to the permanent damage of heart, blood and oxygen supply to the tissues is insufficient and all these mechanisms are activated. Continuous activation of these mechanisms deteriorates the structure and performance of the heart. In this study, a simulation model of Acute Heart Failure Syndrome is constructed. It consists of many subsystems and their complex interactions which are controlled by feedback mechanisms. Excessive accumulation of water and sodium and vasoconstriction are effective in the progress of acute heart failure. Pulmonary edema and increased systolic pressure cause to decrease oxygen supply and to increase cardiac load. Consequently, positive feedback mechanisms are activated and cardiac function loss can occur within hours. Quantitative and qualitative data is obtained from the literature. Healthy individual and patient values are determined and the relationships between the model variables are defined based on investigation. The model is vali dated after many tests. In the scenario analysis section, various treatment strategies and average hourly sodium intake amounts are simulated. The aim of the study is to minimize the hospital discharge time of the patient. The objective includes pulmonary edema excretion time and time of the stabilization of the variables.
