EFFECTS OF CHANGES IN FUNCTIONAL RESIDUAL CAPACITY WITH POSTURE ON MOUTH OCCLUSION PRESSURE AND VENTILATORY PATTERN

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Abstract
The inspiratory pressure developed in the mouth after 0.1 s of occlusion at functional residual capacity and the maximal rate of increase of this pressure within 0.2 s after occlusion were measured at rest and during CO2 stimulation in the seated and supine postures assumed by 6 healthy normal subjects. Minute ventilation and respiratory frequency per min, and the pattern of ventilation of individual breaths in terms of inspired volume, inspiratory time and the mean inspiratory flow rate were measured for the 2 postures. The resting mixed venous PCO2 [partial CO2 pressure], the respiratory exchange ratio and the functional residual capacity for the 2 postures were also measured. There was a significant decrease in functional residual capacity in the supine posture in comparison with the sitting position in all subjects (mean decrease 0.799 l, P < 0.01), but there was no systematic change in the resting values of inspiratory pressure after 0.1 s, in the maximum rate of increase of inspiratory pressure within 0.2 s, or in the variability of these measurements between the 2 postures. The regression coefficients of 0.1-s inspiratory pressure and of the maximal rate of its increase within 0.2 s on PCO2 were not significantly different between the 2 postures, nor were there any significant differences in minute [min] ventilation, respiratory frequency per min, inspired volume, inspiratory time or mean inspiratory flow rate. The chemical drive to respiration did not appear to change in that the resting mixed venous PCO2 and respiratory exchange ratio were not significantly changed between the 2 postures. The total inspiratory neuromuscular output, as represented by 0.1-s inspiratory pressure or its maximal rate of increase within 0.2 s, was not affected by changes from the sitting posture to the supine position or by changes in functional residual capacity of 1.4 l or less, and that there was no difference in the variability of resting 0.1-s inspiratory pressure or its maximal rate of increase within 0.2 between the 2 postures. It is possible that the neural output to the diaphragm decreased to offset the increased functional effciency of the diaphragm, which may have occurred with decreased functional residual capacity in the supine position, such that the total inspiratory neuromuscular output remained the same. Alternatively, it is possible that the lack of change in 0.1-s inspiratory pressure and its maximal rate of increase within 0.2 s reflected an absence of change in the neural and muscular inspiratory output between the 2 postures.