Simulation of mechanical resistive loading on an optimal respiratory control model with added dead space and CO2 breathing

Abstract

• Simulation of how resistive loading affects the respiratory control is presented. • Behavior of optimal chemical–mechanical respiratory control model is simulated. • Respiratory signals under dead space loadings and CO 2 inhalation are optimized. • Comparisons of the respiratory control behavior were performed under various loading effects. To investigate how respiratory resistive loading affects the behavior of optimal chemical–mechanical respiratory control, respiratory signals and breathing pattern were optimized under various dead space loadings (0, 0.4, and 0.8 L) and CO 2 inhalation concentrations (0%, 3%, and 5%). The optimal respiratory control model, which has been studied earlier, was characterized to include a description of the neuromuscular drive P ( t ) as the control output and accurately derive the waveshapes of instantaneous airflow V ˙ ( t ) , lung volume V ( t ) profiles, and breathing pattern, including total and alveolar ventilation, breathing frequency, tidal volume, inspiratory and expiratory duration, duty cycle, and arterial CO 2 pressure. Simulations were performed under various respiratory resistive loads: no load (NL), inspiratory resistive load (IRL), expiratory resistive load (ERL), and continuous resistive load (CRL). The simulation results provide an extended view of breathing pattern and the respiratory signals of neural muscular driving pressure, airflow, and lung volume for rest and various specific cases with external dead space loading and/or CO 2 inhalation. The results showed that an IRL generally resulted in a higher amplitude of P ( t ) and V ( t ), with more convex upward pressure waveshapes, a prolonged inspiratory duration, and a higher duty cycle ( T I / T ≈ 0.55–0.56 at Rest, ≈ 0.54∼0.68 in Case 1, and ≈0.61∼0.69 in Case 3 during resistive loading) for the waveforms. In comparison to the resting state, an abrupt fall occurred at the beginning of the expiratory phases of P ( t ) and the peak flows ( V ˙ peak ≈ −5, −5.5, and −7 L/min in Cases 1, 2, and 3, correspondingly) in the expiratory phase were significantly boosted with ERL during CO 2 inhalation (Case 1_3%, 5%), and EDS loadings (Case 2_EDS = 0.4, 0.8), or a combination of both (Case 3_5% and EDS = 0.4). CRL in all cases exhibited greater rises in amplitude for pressure and lung volume in comparison to IRL and ERL; nevertheless, it also appeared not to have a substantial influence on the waveshapes of airflow, except in the case of a higher concentration of CO 2 inhalation.