Influence of negative airway pressure on upper airway dynamic and impact on night-time apnea worsening

2012 ◽  
Vol 181 (1) ◽  
pp. 88-94 ◽  
Author(s):  
Simon Gakwaya ◽  
Germain Ethier ◽  
Frédéric Sériès
1994 ◽  
Vol 77 (2) ◽  
pp. 840-844 ◽  
Author(s):  
F. Series ◽  
I. Marc

To quantify the contribution of lung volume dependence of upper airway (UA) on continuous negative airway pressure (CNAP)-induced increase in upper airway resistance, we compared the changes in supralaryngeal resistance during an isolated decrease in lung volume and during CNAP in eight normal awake subjects. Inspiratory supralaryngeal resistance was measured at isoflow during four trials, during two CNAP trials where the pressure in a nasal mask was progressively decreased in 3- to 5-cmH2O steps and during two continuous positive extrathoracic pressure (CPEP) trials where the pressure around the chest (in an iron lung) was increased in similar steps. The CNAP and CPEP trials were done in random order. During the CPEP trial, the neck was covered by a rigid collar to prevent compression by the cervical seal of the iron lung. In each subject, resistance progressively increased during the experiments. The increase was linearily correlated with the pressure increase in the iron lung and with the square of the mask pressure during CNAP. There was a highly significant correlation between the rate of rise in resistance between CNAP and CPEP: the steeper the increase in resistance with decreasing lung volume, the steeper the increase in resistance with decreasing airway pressure. Lung volume dependence in UA resistance can account for 61% of the CNAP-induced increase in resistance. We conclude that in normal awake subjects the changes in supralaryngeal resistance induced by CNAP can partly be explained by the lung volume dependence of this resistance.


2006 ◽  
Vol 104 (6) ◽  
pp. 1155-1164 ◽  
Author(s):  
J Russell Norton ◽  
Denham S. Ward ◽  
Suzanne Karan ◽  
William A. Voter ◽  
Linda Palmer ◽  
...  

Background Upper airway obstruction (UAO) during sedation can often cause clinically significant adverse events. Direct comparison of different drugs' propensities for UAO may improve selection of appropriate sedating agents. The authors used the application of negative airway pressure to determine the pressure that causes UAO in healthy subjects sedated with midazolam or propofol infusions. Methods Twenty subjects (12 male and 8 female) completed the study. After achieving equivalent levels of sedation, the subjects' ventilation, end-tidal gases, respiratory inductance plethysmographic signals, and Bispectral Index values were monitored for 5 min. Negative airway pressure was then applied via a facemask in steps of 3 cm H(2)O from -3 to -18 cm H(2)O. UAO was assessed by cessation of inspiratory airflow and asynchrony between abdomen and chest respiratory inductance plethysmographic signals. Results Equivalent levels of sedation were achieved with both drugs with average (+/- SD) Bispectral Index levels of 75 +/- 5. Resting ventilation was mildly reduced without any changes in end-tidal pressure of carbon dioxide. There was no difference between the drugs in the negative pressure resulting in UAO. Five female subjects and one male subject with midazolam and four female subjects and one male subject with propofol did not show any UAO even at -18 cm H(2)O. Compared with males, female subjects required more negative pressures to cause UAO with midazolam (P = 0.02) but not with propofol (P = 0.1). Conclusions At the mild to moderate level of sedation studied, midazolam and propofol sedation resulted in the same propensity for UAO. In this homogeneous group of healthy subjects, there was a considerable range of negative pressures required to cause UAO. The specific factors responsible for the maintenance of the upper airway during sedation remain to be elucidated.


1993 ◽  
Vol 75 (3) ◽  
pp. 1222-1225 ◽  
Author(s):  
F. Series ◽  
I. Marc

Continuous negative airway pressure (CNAP) causes a decrease in lung volume, which is known to increase upper airway resistance by itself. We studied how this lung volume change could modify upper airway collapsibility with five normal awake subjects. In a first trial, pressure in a nasal mask (Pm) was progressively decreased in 3- to 5-cmH2O steps (CNAP). In a second trial, changes in lung volumes resulting from CNAP were prevented by applying simultaneously an equivalent level of negative extrathoracic pressure into a poncho-type respirator [isovolumetric CNAP (CNAPisovol)]. For each trial, we examined the relationship between the maximal inspiratory airflow of each flow-limited inspiratory cycle and the corresponding Pm by least-squares linear regression analysis and determined the critical pressure. We also determined the Pm threshold corresponding to the first Pm value below which flow limitation occurred. Flow limitation was observed in each subject with CNAP but in only two subjects with CNAPisovol. In these two subjects, the Pm threshold values were -20 and -9 cmH2O with CNAP and -39 and -16 cmH2O with CNAPisovol, respectively. Critical pressures for the same two subjects were -161 and -96 cmH2O with CNAP and -202 and -197 cmH2O with CNAPisovol, respectively. We conclude that CNAP-induced decreases in lung volume increase upper airway collapsibility.


2002 ◽  
Vol 96 (2) ◽  
pp. 342-345 ◽  
Author(s):  
Ronald S. Litman ◽  
Jennifer L. Hayes ◽  
Matthew G. Basco ◽  
Alan R. Schwartz ◽  
Peter L. Bailey ◽  
...  

Background Traditional methods of assessing ventilatory effects of sedative agents do not measure their propensity to cause upper airway obstruction (UAO). The primary objective of this study was to develop a method, using dynamic negative airway pressure (DNAP), for replicating UAO during deep sedation. Methods A state of deep sedation (defined as an Observer Assessment of Alertness and Sedation score of 3 and a bispectral index < 80) was attained in 10 healthy volunteers, aged 19-41, using midazolam. Volunteers breathed through a chamber connected to a regulated source of negative pressure that was gradually adjusted downward to produce UAO based on maximal inspiratory flow. The study consisted of three phases: A control phase while awake, a study phase during midazolam deep sedation, and a recovery phase after flumazenil administration. Results During the control phase no subject demonstrated airway obstruction at negative pressures to -30-cm H2O. All subjects exhibited complete UAO during DNAP episodes while sedated. Negative pressures required to cause complete UAO (Pcrit) ranged from -2 to -14 cm H2O. After administration of flumazenil, all subjects attained full consciousness within 5 min and did not demonstrate UAO at negative pressures to -30-cm H2O. Conclusions Dynamic Negative Airway Pressure is a useful method for provoking midazolam-induced UAO, and may potentially be used to compare the potential for different sedatives and patient factors to cause UAO. Flumazenil was completely effective in reversing the potential for midazolam to cause UAO.


1989 ◽  
Vol 66 (3) ◽  
pp. 1373-1382 ◽  
Author(s):  
R. M. Aronson ◽  
E. Onal ◽  
D. W. Carley ◽  
M. Lopata

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.


1995 ◽  
Vol 78 (6) ◽  
pp. 2180-2186 ◽  
Author(s):  
J. A. Innes ◽  
M. J. Morrell ◽  
I. Kobayashi ◽  
R. D. Hamilton ◽  
A. Guz

Inspiratory activation of the genioglossus (GG) may occur by central drive or as a reflex to negative airway pressure. To distinguish between these, we studied seven laryngectomy patients who breathe via tracheal stomas. Negative pressure stimuli (-15 and -25 cmH2O for 500 ms) were applied 1) at functional residual capacity and 2) during early inspiration via (i) the upper airway (UA) and (ii) the tracheal stoma. Intraoral surface GG electromyogram was quantified, as described previously (R. L. Horner, J. A. Innes, K. Murphy, and A. Guz, J. Physiol. Lond. 436: 15-29, 1991). Phasic GG activity was also measured from an integrated electromyogram during spontaneous and inspiratory loaded breathing. Reflex GG activation occurred with negative UA pressure both at functional residual capacity and during inspiration (P < 0.001), but pressure stimuli at the stoma caused no significant activation (P = 0.07). Phasic inspiratory activation occurred in four patients at rest and in all seven patients during inspiratory loading (P < 0.02). These patients demonstrate 1) reflex activation of the GG by negative UA pressure without airflow or respiratory effort and 2) central inspiratory GG activation that is not mediated by negative airway pressure.


1996 ◽  
Vol 80 (5) ◽  
pp. 1466-1474 ◽  
Author(s):  
F. Philip-Joet ◽  
I. Marc ◽  
F. Series

Continuous negative airway pressure (CNAP) trials can be used to measure upper airway (UA) collapsibility. This procedure can be accompanied by an increase in UA muscle activity. The purpose of this study was to evaluate the influence of CNAP-induced increase in genioglossal (GG) activity on UA collapsibility in 10 healthy sleeping men. UA collapsibility was measured on two occasions; each recording was preceded by the administration of a placebo or diazepam (0.15 mg/kg) in a randomized double-blind crossover design. In seven subjects, the decrease in mask pressure (Pmask) was associated with an increase in mean GG electromyographic (EMG) activity during the placebo trial, with a significant negative relationship between these two variables. This relationship was still observed with diazepam. In six subjects, the slope of the relationship between mean EMG and Pmask was less negative with diazepam. This was associated with an increase in critical pressure (Pcrit). With the placebo, a positive relationship was found between Pcrit and the slope of the mean EMG/Pmask relationship. We conclude that Pcrit is influenced by the GG response to the decrease in Pmask during CNAP.


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