Journal of applied physiology
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Comparative Study
Correlation between ventilation and perfusion determines VA/Q heterogeneity in endotoxemia.
Endotoxin increases ventilation-to-perfusion ratio (VA/Q) heterogeneity in the lung, but the precise changes in alveolar ventilation (VA) and perfusion that lead to VA/Q heterogeneity are unknown. The purpose of this study was to determine how endotoxin affects the distributions of ventilation and perfusion and the impact of these changes on VA/Q heterogeneity. Seven anesthetized, mechanically ventilated juvenile pigs were given E. coli endotoxin intravenously, and regional ventilation and perfusion were measured simultaneously by using aerosolized and injected fluorescent microspheres. ⋯ In contrast, ventilation heterogeneity did not change, and redistribution of ventilation was modest. The decrease in correlation between regional ventilation and perfusion was responsible for significantly more VA/Q heterogeneity than were changes in ventilation or perfusion heterogeneity. We conclude that VA/Q heterogeneity increases during endotoxemia primarily as a result of the decrease in correlation between regional ventilation and perfusion, which is in turn determined primarily by changes in perfusion.
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A mathematical model was developed to analyze the mechanisms of expiratory asynchrony during pressure support ventilation (PSV). Solving the model revealed several results. 1) Ratio of the flow at the end of patient neural inspiration to peak inspiratory flow (VTI/V(peak)) during PSV is determined by the ratio of time constant of the respiratory system (tau) to patient neural inspiratory time (TI) and the ratio of the set pressure support (Pps) level to maximal inspiratory muscle pressure (Pmus max). 2) VTI/V(peak) is affected more by tau/TI than by Pps/Pmus max. VTI/V(peak) increases in a sigmoidal relationship to tau/TI. ⋯ Increasing the expiratory trigger sensitivity of a ventilator shifts the synchronized zone to the right, causing less delayed and more premature termination. Automation of expiratory trigger sensitivity in future mechanical ventilators may also be possible. In conclusion, our model provides a useful tool to analyze the mechanisms of expiratory asynchrony in PSV.