NEUROMECHANICAL REGULATION OF RESPIRATORY MOTOR OUTPUT IN VENTILATOR-DEPENDENT C-1-C-3 QUADRIPLEGICS

To evaluate the role of phrenic and sternocleidomastoid afferents as alternate sources of inhibitory feedback. during mechanical ventilation, we studied five C-2-C-3 quadriplegics with sensory denervation of the rib cage and diaphragm, six C-1-C-2 quadriplegics with additional loss of sensory feedback from the neck muscles, and seven normal subjects. We compared the return of inspiratory muscle activity [the recruitment-threshold (PCO2RT)] during mechanical ventilation between subject groups after stepwise increases in end-tidal PCO2 (PET(CO2)) either by increasing the inspired fraction of CO2 (FICO2), decreasing tidal volume (VT; 50 ml/min), or decreasing frequency (f; 1 breath/2 min). Normal subjects were mechanically hyperventilated via a nasal mask until inspiratory activity was undetectable. Efferent input to the sternocleidomastoid was intact at both levels of spinal cord injury, but phasic activity was not evident at the quadriplegics' baseline resting ventilation. The PCO2RT was defined as the level of PET(CO2) at which phasic activity of the diaphragm in normal subjects and of the sternocleidomastoid in C-1-C-2 and C-2-C-3 quadriplegics recurred. The mean PCO2RT (in response to raising PET(CO2) via increased FICO2 while maintaining a high VT and f) was not significantly different (P = 0.6) between normal subjects (43 +/- 3 Torr) and C-2-C-3 quadriplegics (38 +/- 5 Torr). Both subject groups demonstrated a frequency- and volume-related inhibition, as evidenced by a substantially lower PCO2RT when PET(CO2) was raised by reducing either VT or f In contrast to the C-2-C-3 quadriplegics, the C-1-C-2 quadriplegics responded with a similar PCO2RT among the three different mechanical ventilation trials, independent-of whether PET(CO2) was raised with high VT and f, with reduced VT, or with reduced f. We conclude that feedback from at least some part of the chest wall is required to produce a volume- and frequency-dependent inhibition of inspiratory muscle activity observed during mechanical ventilation.