Analog simulation of aortic and of mitral regurgitation.

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.

Analog simulation of two clinical conditions: (1) acute left ventricle failure; (2) exercise in patient with aortic stenosis.

A computer analysis of an equivalent electronic circuit is developed. Thus it is possible to simulate the human cardiovascular system, its negative feedback loops (including the control of venous tone, of myocardial contractility, and of heart rate) and negative intrathoracic pressure. If the simulated cardiovascular system is acted upon by various disturbances their consequences can be studied in detail. The consequences of two disturbances are studied by simulation: (i) acute left ventricular failure and (ii) exercise (decreased peripheral resistance) in aortic stenosis. However, prior to the simulation of the latter, a relatively complex condition, two additional procedures are implemented, i.e. simulations of (iii) increased sympathetic tone and of (iv) aortic stenosis are performed. Simulation of exercise (decreased peripheral resistance) in aortic stenosis is also compared with data observed in patients. Results show that, by using the present equivalent circuit, conditions described above can be qualitatively and to some extent quantitatively well simulated.

Simulation of pulmonary ventilation and its control by negative feedback.

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.

Simulation of some short-term control mechanisms in cardiovascular physiology.

The equivalent electronic circuit, developed to simulate cardiovascular physiology, is upgraded to incorporate negative feedback loops. In this way homeostasis of the arterial pressure is simulated in exercise, in haemorrhage, in the insufficiency of the aortic valve, and in hypervolemia. The results show that homeostasis supports the cardiovascular system by modulating Starling mechanism(s) in exercise, haemorrhage and hypervolemia. In aortic insufficiency it seems that only Starling mechanism(s) can maintain cardiac output and arterial pressure.

Simulation of cardiovascular physiology: the diastolic function(s) of the heart.

The cardiovascular system was simulated by using an equivalent electronic circuit. Four sets of simulations were performed. The basic variables investigated were cardiac output and stroke volume. They were studied as functions (i) of right ventricular capacitance and negative intrathoracic pressure; (ii) of left ventricular relaxation and of heart rate; and (iii) of left ventricle failure. It seems that a satisfactory simulation of systolic and diastolic functions of the heart is possible. Presented simulations improve our understanding of the role of the capacitance of both ventricles and of the diastolic relaxation in cardiovascular physiology.

Cardiovascular physiology: simulation of steady state and transient phenomena by using the equivalent electronic circuit.

By using commercially available software it is readily possible to design electronic circuits and to analyze them. By introducing the concept of equivalent quantities a simulation of various physiological phenomena is possible. This includes the steady state as well as various complex transient phenomena. This paper describes the use of an equivalent electronic circuit in simulating the cardiovascular system. It allows a stepwise upgrading. The first step is a one-ventricle circuit similar to the Starling heart-lung preparation. The final step is an equivalent circuit allowing simulation of various normal as well as pathological states (e.g. effects of heart rate, negative intrathoracic pressure, exercise, hemorrhage, heart failure, and hypertension). The degree of disturbance can be set by adjusting the value of single components. Following this, the optimal type of compensation (e.g. the increase in blood volume in failure of the right ventricle; systemic venoconstriction in failure of the left ventricle) of the basic disturbance can be searched for, activated and the consequences studied. The described approach has been found a useful tool in teaching physiology and pathophysiology for postgraduate medical students.