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Abstract: By using an equivalent electronic circuit either mitral or aortic regurgitation was simulated. Simulation allowed not only a measurement of various pressures within the cardiovascular system and cardiac output, but also mitral and aortic flow. In normal conditions mitral and aortic flows were monophasic, anterograde. In valve regurgitation mitral and aortic flows were, as expected, biphasic. In mitral regurgitation, during systole and diastole the valve flow was retrograde and anterograde, respectively. In aortic regurgitation, during systole and diastole the valve flow was anterograde and retrograde, respectively. The magnitude of the regurgitant valve flow was measured by time-integration and compared to the net flow, i.e. cardiac output. Valve flow was determined not only by the magnitude of valve dysfunction, but also by the resistive/capacitive characteristics of the “falsely” attached regurgitant circuit. If the regurgitant valve flow was large enough, it in turn affected the function of the left ventricle. The present investigation suggests that many features observed in patients with mitral or aortic regurgitation can be qualitatively satisfactorily simulated. In some respects even quantitative simulation is possible. However, for simulation of chronic mitral or aortic regurgitation, in the analog electronic circuit additional adjustments—in capacitance of the left ventricle and pulmonary system—would be required. [Copyright &y& Elsevier]

The equivalent electronic circuit developed to simulate pulmonary ventilation is upgraded to incorporate homeostasis, i.e. a negative feedback loop. The latter can be made either inactive or active. In the former condition, only the immediate consequence of a disturbance shows up. In the latter condition, however, full homeostatic—sometimes very complex—response can be studied.The effects of three types of disturbances are studied in both conditions (i.e. open loop, closed loop): increased CO2 production, temporary apnoea, and of bronchoconstriction (in the whole lung or only in part of the lung). The effect of increased CO2 production is increase in pulmonary ventilation and increase in pCO2. The latter strongly depends on the feedback response. Temporary apnoea results in a transient increase in pCO2. However, if the time constant of the feedback loop is large enough, this type of disturbance results in a maintained periodic, Cheyne–Stokes-type breathing.Bronchoconstriction in 100% of the lung results in a decrease in tidal volume. If homeostasis is active this decrease is compensated by an increase in the inspiratory effort. However, if bronchoconstriction occurs only in 50% of the lung, inspiratory effort is greatly changed through inter-alveolar elastic interactions, giving rise to the so-called pendelluft. [Copyright &y& Elsevier]