Changes in upper airway resistance with lung inflation and positive airway pressure

1990 ◽  
Vol 68 (3) ◽  
pp. 1075-1079 ◽  
Author(s):  
F. Series ◽  
Y. Cormier ◽  
J. Couture ◽  
M. Desmeules
Keyword(s):  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Upper Airway ◽  
Normal Subjects ◽  
Base Line ◽  
Upper Airways ◽  
Airway Patency ◽  
Lung Inflation ◽  
Bias Flow ◽  
Expiratory Positive Airway Pressure

The influence of pulmonary inflation and positive airway pressure on nasal and pharyngeal resistance were studied in 10 normal subjects lying in an iron lung. Upper airway pressures were measured with two low-bias flow catheters while the subjects breathed by the nose through a Fleish no. 3 pneumotachograph into a spirometer. Resistances were calculated at isoflow rates in four different conditions: exclusive pulmonary inflation, achieved by applying a negative extra-thoracic pressure (NEP); expiratory positive airway pressure (EPAP), which was created by immersion of the expiratory line; continuous positive airway pressure (CPAP), realized by loading the bell of the spirometer; and CPAP without pulmonary inflation by simultaneously applying the same positive extrathoracic pressure (CPAP + PEP). Resistance measurements were obtained at 5- and 10-cmH2O pressure levels. Pharyngeal resistance (Rph) significantly decreased during each measurement; the decreases in nasal resistance were only significant with CPAP and CPAP + PEP; the deepest fall in Rph occurred with CPAP. It reached 70.8 +/- 5.5 and 54.8 +/- 6.5% (SE) of base-line values at 5 and 10 cmH2O, respectively. The changes in lung volume recorded with CPAP + PEP ranged from -180 to 120 ml at 5 cmH2O and from -240 to 120 ml at 10 cmH2O. Resistances tended to increase with CPAP + PEP compared with CPAP values, but these changes were not significant (Rph = 75.9 +/- 6.1 and 59.9 +/- 6.6% at 5 and 10 cmH2O of CPAP + PEP). We conclude that 1) the upper airway patency increases during pulmonary inflation, 2) the main effect of CPAP is related to pneumatic splinting, and 3) pulmonary inflation contributes little to the decrease in upper airways resistance observed with CPAP.

Influence of passive changes of lung volume on upper airways

1990 ◽  
Vol 68 (5) ◽  
pp. 2159-2164 ◽  
Author(s):  
F. Series ◽  
Y. Cormier ◽  
M. Desmeules
Keyword(s):  
Lung Volume ◽  
Airway Resistance ◽  
Upper Airway ◽  
Normal Subjects ◽  
Base Line ◽  
Nasal Resistance ◽  
Inspiratory Flow Rate ◽  
Upper Airways ◽  
Lung Volumes ◽  
Bias Flow

The total upper airway resistances are modified during active changes in lung volume. We studied nine normal subjects to assess the influence of passive thoracopulmonary inflation and deflation on nasal and pharyngeal resistances. With the subjects lying in an iron lung, lung volumes were changed by application of an extrathoracic pressure (Pet) from 0 to 20 (+Pet) or -20 cmH2O (-Pet) in 5-cmH2O steps. Upper airway pressures were measured with two low-bias flow catheters, one at the tip of the epiglottis and the other in the posterior nasopharynx. Breath-by-breath resistance measurements were made at an inspiratory flow rate of 300 ml/s at each Pet step. Total upper airway, nasal, and pharyngeal resistances increased with +Pet [i.e., nasal resistance = 139.6 +/- 14.4% (SE) of base-line and pharyngeal resistances = 189.7 +/- 21.1% at 10 cmH2O of +Pet]. During -Pet there were no significant changes in nasal resistance, whereas pharyngeal resistance decreased significantly (pharyngeal resistance = 73.4 +/- 7.4% at -10 cmH2O). We conclude that upper airway resistance, particularly the pharyngeal resistance, is influenced by passive changes in lung volumes, especially pulmonary deflation.

Effects of positive airway pressure on upper airway dilator muscle activity and ventilatory timing

1996 ◽  
Vol 81 (1) ◽  
pp. 470-479 ◽  
Author(s):  
P. C. Deegan ◽  
P. Nolan ◽  
M. Carey ◽  
W. T. McNicholas
Keyword(s):  
Muscle Activity ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Upper Airway ◽  
Normal Subjects ◽  
Emg Activity ◽  
Ventilatory Responses ◽  
Dilator Muscle ◽  
Before And After ◽  
Expiratory Positive Airway Pressure

To determine upper airway (UA) and ventilatory responses to nasal continuous positive airway pressure (CPAP) and expiratory positive airway pressure (EPAP), we quantitated changes in alae nasi (AN) and genioglossus (GG) electromyographic (EMG) activity, ventilatory timing, and end-expiratory lung volume (EELV) at various levels of CPAP and EPAP in six normal subjects during wakefulness and in seven during sleep. The same measurements were also made before and after UA anesthesia in six normal subjects during wakefulness. During both wakefulness and sleep, CPAP application significantly increased EELV and decreased AN and GG EMG activities. In contrast, EPAP significantly increased EMG activities of both muscles while also increasing EELV during wakefulness. The EMG responses were less marked during sleep. Anesthesia of the UA abolished the EMG responses to CPAP but not to EPAP. These results suggest that, in normal subjects, CPAP application causes a reflex reduction in UA dilator muscle activity mediated by UA sensory receptors. In contrast, EPAP increases UA dilator muscle activity, with the response mediated by conscious influences or reflexes arising outside of the UA.

Effects of continuous positive airway pressure breathing on lung volume and distensibility

1990 ◽  
Vol 68 (3) ◽  
pp. 1121-1126 ◽  
Author(s):  
C. J. Duggan ◽  
W. D. Castle ◽  
N. Berend
Keyword(s):  
Continuous Positive Airway Pressure ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Transpulmonary Pressure ◽  
Normal Subjects ◽  
Small Degree ◽  
Elastic Behavior ◽  
Base Line ◽  
Upward Shift ◽  
Alveolar Duct

In this study the effects on lung elastic behavior of 10 min of breathing at a continuous positive airway pressure (CPAP) of 10 cmH2O were examined in 10 normal subjects. To investigate whether any changes were induced by release of prostaglandins, the subjects were also pretreated with the cyclooxygenase inhibitor indomethacin. CPAP produced a significant (P less than 0.001) upward shift of the pressure-volume (PV) curve [change in total lung capacity (delta TLC) 374 +/- 67 (SE) ml, mean delta volume at a transpulmonary pressure of 15 cmH2O (delta VL15) 279 +/- 31 ml] with no change in K, an index of lung distensibility. After CPAP the PV curves returned to normal base line within 20 min. The same pattern was observed after indomethacin, but the increase in TLC was significantly less (P less than 0.01) (mean delta TLC 206 +/- 42 ml) mainly because of a slight and not statistically significant increase in base-line TLC. In five subjects further PV curves with and without CPAP were obtained greater than or equal to 7 days after indomethacin. The responses were not significantly different from those obtained before indomethacin (mean delta TLC 366 +/- 89, mean delta VL15 296 +/- 42 ml). We conclude that CPAP produces an upward shift of the PV curve without a change in lung distensibility. In addition, there may be a small degree of resting alveolar duct tone that is influenced by indomethacin.

Changes in lung volume and upper airway using MRI during application of nasal expiratory positive airway pressure in patients with sleep-disordered breathing

2011 ◽  
Vol 111 (5) ◽  
pp. 1400-1409 ◽  
Author(s):  
C. W. Braga ◽  
Q. Chen ◽  
O. E. Burschtin ◽  
D. M. Rapoport ◽  
I. Ayappa
Keyword(s):  
Lung Volume ◽  
Airway Pressure ◽  
Sleep Disordered Breathing ◽  
Positive Airway Pressure ◽  
Upper Airway ◽  
Mechanisms Of Action ◽  
Cross Sectional ◽  
Expiratory Positive Airway Pressure ◽  
End Tidal ◽  
Disordered Breathing

Nasal expiratory positive airway pressure (nEPAP) delivered with a disposable device (Provent, Ventus Medical) has been shown to improve sleep-disordered breathing (SDB) in some subjects. Possible mechanisms of action are 1) increased functional residual capacity (FRC), producing tracheal traction and reducing upper airway (UA) collapsibility, and 2) passive dilatation of the airway by the expiratory pressure, carrying over into inspiration. Using MRI, we estimated change in FRC and ventilation, as well as UA cross-sectional area (CSA), in awake patients breathing on and off the nEPAP device. Ten patients with SDB underwent nocturnal polysomnography and MRI with and without nEPAP. Simultaneous images of the lung and UA were obtained at 6 images/s. Image sequences were obtained during mouth and nose breathing with and without the nEPAP device. The nEPAP device produced an end-expiratory pressure of 4–17 cmH2O. End-tidal Pco2rose from 39.7 ± 5.3 to 47.1 ± 6.0 Torr ( P < 0.01). Lung volume changes were estimated from sagittal MRI of the right lung. Changes in UA CSA were calculated from transverse MRI at the level of the pharynx above the epiglottis. FRC determined by MRI was well correlated to FRC determined by N2washout ( r = 0.76, P = 0.03). nEPAP resulted in a consistent increase in FRC (46 ± 29%, P < 0.001) and decrease in ventilation (50 ± 15%, P < 0.001), with no change in respiratory frequency. UA CSA at end expiration showed a trend to increase. During wakefulness, nEPAP caused significant hyperinflation, consistent with an increase in tracheal traction and a decrease in UA collapsibility. Direct imaging effects on the UA were less consistent, but there was a trend to dilatation. Finally, we showed significant hypoventilation and rise in Pco2during use of the nEPAP device during wakefulness and sleep. Thus, at least three mechanisms of action have the potential to contribute to the therapeutic effect of nEPAP on SDB.

Upper airway and respiratory muscle responses to continuous negative airway pressure

1989 ◽  
Vol 66 (3) ◽  
pp. 1373-1382 ◽  
Author(s):  
R. M. Aronson ◽  
E. Onal ◽  
D. W. Carley ◽  
M. Lopata
Keyword(s):  
Eye Movement ◽  
Airway Pressure ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Normal Subjects ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Airway Patency ◽  
Negative Airway Pressure ◽  
Muscle Responses

To determine upper airway and respiratory muscle responses to nasal continuous negative airway pressure (CNAP), we quantitated the changes in diaphragmatic and genioglossal electromyographic activity, inspiratory duration, tidal volume, minute ventilation, and end-expiratory lung volume (EEL) during CNAP in six normal subjects during wakefulness and five during sleep. During wakefulness, CNAP resulted in immediate increases in electromyographic diaphragmatic and genioglossal muscle activity, and inspiratory duration, preserved or increased tidal volume and minute ventilation, and decreased EEL. During non-rapid-eye-movement and rapid-eye-movement sleep, CNAP was associated with no immediate muscle or timing responses, incomplete or complete upper airway occlusion, and decreased EEL. Progressive diaphragmatic and genioglossal responses were observed during non-rapid-eye-movement sleep in association with arterial O2 desaturation, but airway patency was not reestablished until further increases occurred with arousal. These results indicate that normal subjects, while awake, can fully compensate for CNAP by increasing respiratory and upper airway muscle activities but are unable to do so during sleep in the absence of arousal. This sleep-induced failure of load compensation predisposes the airways to collapse under conditions which threaten airway patency during sleep. The abrupt electromyogram responses seen during wakefulness and arousal are indicative of the importance of state effects, whereas the gradual increases seen during sleep probably reflect responses to changing blood gas composition.

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