Inhibition of ventilatory motor output increases expiratory retro palatal compliance during sleep

Abstract

We hypothesized that inhibition of ventilatory motor output leads to increased pharyngeal compliance during NREM sleep, independent of lung volume.

Methods: Eighteen subjects were studied using noninvasive positive pressure ventilation (NPPV) to inhibit ventilatory motor output during stable NREM sleep. Nasopharyngoscopy was used to measure the retro palatal cross-sectional area/pressure relationship (CSA/Pph) in 8 subjects. The effect of NPPV on neck circumference (NC) and end-expiratory lung volumes (EELV) was studied in 10 additional subjects using strain gauge plethysmography and respitrace, respectively.

Results: (1) The CSA/Pph was increased during expiration under passive compared to active breathing (11.7 ± 7.1 vs. 8.5 ± 5.6mm(2)/cmH(2)O, respectively; p < 0.05) but not during inspiration. (2) NC correlated with the CSA/Pph during passive expiration (R(2) = 0.77, p < 0.05). (3) NC and EELV did not change between active and passive breaths (p = NS).

Conclusions: (1) Inhibiting the ventilatory motor output increases the pharyngeal compliance. (2) Increased passive expiratory pharyngeal compliance was not associated with changes in NC or EELV.

Figure 1

Polygraph record of a trial that illustrates breaths during noninvasive positive pressure ventilation (NPPV) followed by central apnea. Ventilatory motor output inhibition was confirmed by the absence of negative pressure deflection on pharyngeal pressure (red arrows) and by the occurrence of central apnea upon termination of NPPV. First three breaths at the beginning of mechanical ventilation (active breaths) were compared to the last three breaths preceding the termination of NPPV (passive breaths). The horizontal dotted line indicates the level of end-tidal CO₂ at baseline. Pph, pharyngeal pressure; P_ETCO2, end-tidal CO₂; Sa_O2, oxygen saturation.

Figure 2

Fiberoptic image of the retro palatal airway with anatomic landmarks identified.

Figure 3

Polygraph record of a trial that illustrates breaths during noninvasive positive pressure ventilation (NPPV) followed by central apnea. End-expiratory lung volume (EELV) and end-expiratory pharyngeal pressure (EEP) were indicated by the dotted lines. RIP: respiratory inductive plethysmograph, Psg: supraglottic pressure, P_ETCO2, end-tidal CO₂, P_ETCO2, end-tidal O₂.

Figure 4

(A) Retro palatal cross-sectional area (CSA) during eupnoea and mechanical ventilation (active and passive, respectively). Note the larger CSA for the mechanical ventilation breaths in comparison to the eupnoea breaths at P_I and B_E (*p < 0.05 eupnoea vs. active and passive). No difference was found between active vs. passive breaths (p>0.05). There was a statistically significant interaction between phase and type (p <0.001); the effect of different levels of phase depends on what level of type is present. Note that the CSA was similar during eupnoea among the different phases of each respiratory cycle (from B_I to E_E) but different during mechanical ventilation for active and passive breaths, respectively (+p<0.01). Pharyngeal pressure (Pph) was higher during mechanical ventilation at P_I and B_E phases in comparison to eupnoea (p<0.05). Pph profile was higher at B_E compared to P_I during eupnoea (++ p <0.001) and among the different phases of each respiratory cycle of active and passive breaths (++ p<0.001). (B) The top panel illustrates the CSA at peak inspiration and expiration. Note that CSA not change between active and passive breaths (p=NS). Bottom panel illustrates the Pph which were higher during active than passive breathing at peak inspiration and expiration (P<0.05). B_I: Beginning inspiration, P_I: peak inspiration, E_I/B_E: end inspiration/beginning expiration P_E: peak expiration, E_E: end expiration. All presented data are mean ± SE.

Figure 5

Representative example of retro palatal cross sectional area (CSA) and pharyngeal pressure (Pph) relationships for active and passive breaths (dotted and solid lines, respectively). Note that the passive breath displayed hysteresis relative to the triggered active breath on the same positive pressure. The total slope of passive breath is significantly higher than active breath. Partitioned slope of the passive breath is higher during expiration relative to the active breath. Phase 1 (inspiratory) was defined as the slope of the regression line between the beginning of inspiration and peak inspiration. Phase 2 (post-inspiratory) was defined as the slope of the regression line between the peak inspiration and end inspiration. Phase 3 (expiratory) was defined as the slope of CSA vs. Pph between the beginning of expiration and end of expiration. The straight lines represent the total area-pressure relationship for each individual representative breaths defined as the slope of the regression line between the beginning of inspiration and end expiration.

Figure 6

Grouped data for CSA/Pph relationship during active and passive breaths (Phase 1: inspiratory; phase 2: post-inspiratory; and phase 3: expiratory, respectively). Note that the expiratory CSA/Pph relationship for passive (gray bars) was higher than for active breaths (black bars) on the same airway pressure (p<0.05). All presented data are mean ± SE.

Figure 7

Neck circumference (NC) during eupnoea and mechanical ventilation (active and passive, respectively). Note the larger NC for the mechanical ventilation breaths in comparison to the eupnoea breaths (# p < 0.05 eupnoea vs. active). No difference was found between active vs. passive breaths (p>0.05). Supraglottic pressure (Psg) was higher during mechanical ventilation relative to eupnoea at P_I, B_E, P_E phases in comparison to eupnoea (* p<0.05). B_I: Beginning inspiration, P_I: peak inspiration, E_I/B_E: end inspiration/beginning expiration P_E: peak expiration, E_E: end expiration. All presented data are mean ± SE.

Figure 8

Relationship between neck circumference (NC) and expiratory CSA-Pph slopes during passive state.