One of the proposed advantages of proportional assist ventilation (PAV) has been the automatic synchrony between the end of the patient's inspiratory effort and the ventilator cycle (i.e., expiratory synchrony). However, recent clinical studies have shown a prolonged ventilator inspiratory time or even a "runaway" phenomenon with the normal use of PAV. We hypothesize that control-system delay may account for this, because in reality there is always some degree of delays between control-system's input and output in all ventilators. Computer simulation study to date has not taken into account the potential effect of control-system delay on expiratory synchrony. We therefore created a computer model in which the parameter of control-system delay time was introduced. We found that significant expiratory asynchrony may occur with this more realistic model of PAV. The ventilator flow termination may fall behind the completion of the patient inspiration by as long as 0.33 seconds under the selected simulation conditions. The inspiratory termination delay time is in proportion to the control-system delay time, the respiratory time constant, and the assist gain settings. In conclusion, this model indicates that due to the unavoidable control-system delay in the ventilators, expiratory asynchrony may be an inherent shortcoming associated with PAV.

The extent to which respiratory muscles are exerted during partially supported ventilation is difficult to differentiate, because these muscles and the ventilator work simultaneously to produce ventilation. We have developed a new method for determining the pressure developed by the respiratory muscles in partially supported ventilation. In seven patients on pressure-support ventilation (PSV), pressure, flow, and lung volume change were measured at the airway opening. Various PSV levels (0-15 cmH2O) were applied to each patient in random order. By utilizing a model of respiratory mechanics, we calculated the pressure developed by the respiratory muscles and the inspiratory work performed by the muscles from the measured parameters by use of the resistance and elastance of the respiratory system obtained during controlled ventilation. Increasing PSV from 0 to 15 cmH2O modulated the resultant breathing pattern, i.e., increasing tidal volume and decreasing respiratory rate. The respiratory muscle pressure, although less negative, had a shape that corresponded to the shape of airway occlusion pressure at each PSV level, and both pressures decreased concomitantly with increasing PSV. The respiratory muscle work progressively decreased with increasing PSV. This analysis enabled clear and continuous quantifications of the respiratory muscle force generation and inspiratory work during partially supported ventilation.

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