Effect of respiratory muscle weakness on P0.1 induced by partial curarization

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Abstract
Mouth occlusion pressure 0.1 s after onset of inspiration (P0.1) reflects central respiratory drive (CRD), but its dependence on respiratory muscle strength is unknown. To clarify this relationship, progressive levels of respiratory muscle weakness were produced by infusion of d-tubocurarine in 8 supine spontaneously breathing normal subjects. Hypercapnic ventilatory response (HCVR) was measured before curarization and at mild (mean inspiratory effort 62 .+-. 3% of control), moderate (42 .+-. 3%), and severe (23 .+-. 1%) weakness. At the severe level of weakness supine functional residual capacity was not significantly changed from base line, the percent of base-line slope of .DELTA.P0.1/.DELTA.PCO2 [change in CO2 tension] (122 .+-. 27%) was significantly greater (P < 0.01) than that for change in expired minute ventilation (.DELTA..ovrhdot.VE)/.DELTA.PCO2 (39 .+-. 10%), the percent of base-line .DELTA.P0.1/.DELTA..ovrhdot.VE (381 .+-. 46%) during HCVR was significantly increased (P < 0.01), the P0.1 response was significantly increased from base line at 2 of 3 specific levels of PCO2 while the .ovrhdot.VE was unchanged or significantly decreased, and peak inspiratory resistance did not significantly change. P0.1, unlike .ovrhdot.VE, did not decrease with even severe respiratory muscle weakness. Indeed, P0.1 increased at 2 of 3 levels of PCO2 under circumstances when higher CRD is expected. One potential explanation for the results is that P0.1 may at least qualitatively reflect CRD up to the level of severe respiratory muscle weakness attained in this study.

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