A computer simulation of physiological factors contributing to hyperventilation and breathlessness in cardiac patients.

A computer model of human respiration is of value for teaching the basic principles of respiratory physiology to students. An extension of this educational use is in the theoretical exploration of the relative importance of individual factors which may be contributing to disordered function in common clinical problems. For example, when a cardiac patient becomes breathless with increase in ventilation during exercise there are alterations in many physiological variables. The influence of their individual contributions on the total ventilation and thence possibly on breathlessness is often difficult to estimate. We present a theoretical analysis using MACPUF, a digital computer simulation of circulation and gas exchange which can be used to extimate the quantitative contribution of relevant physiological variables by altering them singly and in combination. Alterations in dead space, physiological shunt and pulmonary compliance individually produce only small increases in ventilation. Increased neurogenic drive (e.g. from lung reflexes triggered by pulmonary congestion) is a potentially important but very variable factor. A more important influence on ventilation appears when cardiac output is reduced and anaerobic metabolism simulated, causing changes in blood gas tensions and acidaemia which then change ventilation. Any increase in ventilation becomes more significant as a cause of breathlessness when ventilatory capacity is reduced, which in cardiac patients it not infrequently is.