Expiratory pharyngeal narrowing during central hypocapnic hypopnea

Abstract

Rationale: Ventilatory motor output is an important determinant of upper airway patency during sleep.

Objectives: We hypothesized that central hypocapnic hypopnea would lead to increased expiratory upper airway resistance and pharyngeal narrowing during non-REM sleep.

Methods: Noninvasive positive pressure ventilation was used to induce hypocapnic hypopnea in 20 healthy subjects. Expiratory pressure was set at the lowest pressure (2 cm H(2)O), and inspiratory pressure was increased gradually during each 3-minute noninvasive positive pressure ventilation trial by increments of 2 cm H(2)O. Analysis 1 (n = 9) included measured retropalatal cross-sectional area (CSA) using nasopharyngoscope to compare CSA at five points of the respiratory cycle between control (eupneic) and hypopneic breaths. The pharyngeal pressure (P(ph)) was measured using a catheter positioned at the palatal rim. Analysis 2 (n = 11) included measured supraglottic pressure and airflow to compare inspiratory and expiratory upper airway resistance (R(UA)) at peak flow between eupneic and hypopneic breaths.

Measurements and main results: Expiratory CSA during hypopneic breaths was decreased relative to eupnea (CSA at beginning of expiration [BI]: 101.5 +/- 6.3 vs. 121.6 +/- 8.9%; P < 0.05); P(ph)-BI was lower than that generated during eupnea (1.5 +/- 0.3 vs. 3.3 +/- 0.9 cm H(2)O; P < 0.05). Body mass index was an independent predictor of retropalatal narrowing during hypopnea. Hypopnea-R(UA) increased during expiration relative to eupnea (14.0 +/- 5.7 vs. 10.6 +/- 2.5 cm H(2)O/L/s; P = 0.01), with no change in inspiratory resistance.

Conclusions: Expiratory pharyngeal narrowing occurs during central hypocapnic hypopnea. Reduced ventilatory drive leads to increased expiratory, but not inspiratory, upper airway resistance. Central hypopneas are obstructive events because they cause pharyngeal narrowing.

Figure 1.

Polygraph record of a trial from analysis 1 that illustrates breaths before and during noninvasive positive pressure ventilation (NPPV) followed by central hypopnea. Three breaths preceding NPPV (control, arrows) were compared with the breaths after termination of NPPV (hypocapnic hypopnea, arrows). Pet_CO2 = end tidal CO₂; P_ph = pharyngeal pressure; P_M = mask pressure; Sa_O2 = arterial oxygen saturation.

Figure 2.

Fiberoptic images of the retropalatal airway from representative subject for one respiratory cycle. The cross-sectional area (CSA) and pharyngeal pressure (P_ph) were measured simultaneously for control (closed circle and solid line) and central hypopnea after mechanical hyperventilation (open circles and dashed line). Note the smaller area and pressure in hypopnea compared with control. Horizontal arrows refer to the three dynamic phases of each analyzed breath. BE = beginning of expiration; BI = beginning of inspiration; EE = end expiration; EI = end inspiration; PE = peak expiration; PI = peak inspiration.

Figure 3.

(A) Retropalatal cross-sectional area (CSA) during control and hypocapnic hypopnea. Note the significant CSA change throughout the respiratory cycle within the control breaths in comparison to the hypopnea breaths. Control (closed circles) and hypocapnic hypopnea (open circles). There was a statistically significant interaction between respiratory phase and breath type (control vs. hypopnea) (⁺P = 0.002). (B) Pharyngeal pressure (P_ph) during control (closed circles) and hypocapnic hypopnea (open circles). Note the difference in P_ph within control breaths (^#P < 0.001). (C) Flow during control (closed circles) and hypocapnic hypopnea (open circles). BE = beginning expiration; BI = beginning inspiration; EE = end expiration; EI = end inspiration; PE = peak expiration; PI = peak inspiration. (D) P_ph at peak inspiratory and expiratory flow during control (black bars) and hypopnea (gray bars). P_ph at peak expiratory flow decreased significantly during hypopnea. (E) CSA at peak inspiratory and expiratory flow during control and hypopnea. CSA at peak inspiratory flow did not change between control and hypopnea. CSA at peak expiratory flow decreased significantly during hypopnea. CSA reached nadir at peak inspiration. All data are mean ± SE.

Figure 4.

Relationship of cross-sectional area (CSA) to pharyngeal pressure (P_ph) during the control (black bars) and hypocapnic hypopnea (white bars) in three dynamic phases from one respiratory cycle for three different phases: (1) beginning of inspiration to nadir CSA (BI-nadir) at peak inspiration, (2) from nadir to maximal CSA (CSA_nadir–CSA_max) at peak expiration, and (3) from maximal CSA to end expiration (as depicted previously by the horizontal arrows in Figure 2). ΔCSA/ΔP_ph were calculated as the CSA and the corresponding P_ph change between the beginning and the end of each phase transition.

Figure 5.

Inspiratory and expiratory upper airway resistance (R_UA) measured during the control (black bars) and hypocapnic hypopnea (gray bars). Expiratory R_UA increased significantly during hypopnea.

Figure 6.

Individual (open circles) and group (closed circles) mean end-expiratory supraglottic pressure (EEP) for control (C) and first hypopnea breath (H1).

Figure 7.

Schematic illustration for the collapsible segment of upper airway during hypocapnic hypopnea as a Starling Resistor. In this model, flow is determined by the gradient between the upstream segment and critical closing pressure (Pcrit). During inspiration (A), when upstream pressure (Pus) (i.e., nasal pressure) is below the Pcrit, the collapsible segment is closed, and no flow occurs. During expiration (B), when Pus in the supraglottic area is below the Pcrit, the collapsible segment is closed, and no flow occurs. During hypocapnic hypopnea, expiratory flow is limited, correlating with the gradient between the supraglottic pressure and Pcrit. Hence, this pressure gradient is important determinant of pharyngeal narrowing. Rus = upstream resistance; V_max = maximal flow. Asterisk represents the site of retropalatal pressure measurement.