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Original Research: Sleep Disorders |

Impact of Acute Changes in CPAP Flow Route in Sleep Apnea Treatment FREE TO VIEW

Rafaela G.S. Andrade, PhD; Fernanda Madeiro, MD; Vivien S. Piccin, PhD; Henrique T. Moriya, PhD; Fabiola Schorr, MD, PhD; Priscila S. Sardinha, MD; Marcelo G. Gregório, MD, PhD; Pedro R. Genta, MD, PhD; Geraldo Lorenzi-Filho, MD, PhD
Author and Funding Information

FUNDING/SUPPORT: This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) and Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq).

aSleep Laboratory, Pulmonary Division, Heart Institute, University of São Paulo, São Paulo, Brazil

bBiomedical Engineering Laboratory of Escola Politécnica, University of São Paulo, São Paulo, Brazil

CORRESPONDENCE TO: Geraldo Lorenzi-Filho, MD, PhD, Sleep Laboratory, Pulmonary Division, Heart Institute, Av. Enéas Carvalho de Aguiar 44, São Paulo, Brazil


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;150(6):1194-1201. doi:10.1016/j.chest.2016.04.017
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Published online

Background  CPAP is the gold standard treatment for OSA and was conceived to be applied through a nasal interface. This study was designed to determine the acute effects of changing the nasal CPAP route to oronasal and oral in upper airway patency during sleep in patients with OSA. We hypothesized that the oronasal route may compromise CPAP’s effectiveness in treating OSA.

Methods  Eighteen patients (mean ± SD age, 44 ± 9 years; BMI, 33.8 ± 4.7 kg/m2; apnea-hypopnea index, 49.0 ± 39.1 events/hour) slept with a customized oronasal mask with nasal and oral sealed compartments connected to a multidirectional valve. Sleep was monitored by using full polysomnography and induced by low doses of midazolam. Nasal CPAP was titrated up to holding pressure. Flow route was acutely changed to the oronasal (n = 18) and oral route (n = 16) during sleep. Retroglossal area was continuously observed by using nasoendoscopy.

Results  Nasal CPAP (14.8 ± 4.1 cm H2O) was able to stabilize breathing in all patients. In contrast, CPAP delivered by the oronasal and oral routes promoted obstructive events in 12 (66.7%) and 14 (87.5%) patients, respectively. Compared with stable breathing during the nasal route, there was a significant and progressive reduction in the distance between the epiglottis and tongue base and the retroglossal area when CPAP was delivered by the oronasal and oral routes.

Conclusions  CPAP delivered through the oronasal route may compromise CPAP’s effectiveness in treating OSA.

Figures in this Article

OSA is characterized by recurrent episodes of partial or complete upper airway obstruction during sleep, leading to hypopneas and apneas, respectively. OSA is common in the general population, and may have various consequences, including excessive daytime somnolence, poor quality of life, and cardiovascular complications., CPAP is the gold standard treatment for patients with moderate to severe OSA. CPAP acts as a pneumatic splint to avoid upper airway obstruction and was conceived to be used with a nasal interface to treat OSA. The pressure delivered through the nose seals the soft palate against the tongue. CPAP is able to alleviate symptoms and improve cardiovascular outcomes.

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In clinical practice, the oronasal mask is apparently well tolerated. A significant proportion of patients with OSA are currently using oronasal masks because they were considered to be intolerant of an exclusively nasal route for delivery of CPAP. However, there is mounting evidence that oronasal masks may compromise CPAP’s efficacy to treat OSA. One recent systematic review of all observational and randomized trials comparing nasal and oronasal masks found that the oronasal mask is less effective at treating OSA and has lower CPAP adherence than the nasal mask. We have documented one patient with severe OSA who was successfully treated with nasal CPAP at 7 cm H2O. In contrast, when an oronasal mask was used, CPAP was not effective despite CPAP titration up to 16 cm H2O. Direct observation of the upper airway using nasoendoscopy during induced sleep showed that the oronasal mask was associated with a backward displacement of the tongue that caused upper airway obstruction. This observation prompted the present study, which was designed to evaluate the acute effects of changing the CPAP route to oronasal and oral routes in flow pattern and oropharyngeal patency in patients with OSA during sleep.

We recruited patients of both sexes, aged between 18 and 70 years, recently referred to the Sleep Laboratory, Heart Institute, University of São Paulo Medical School, with suspicion of OSA. Patients with BMI > 40 kg/m2, severe nasal obstruction, maxillofacial deformities, previous upper airway surgery, diabetes, and significant heart or pulmonary disease were excluded; also excluded were patients with no OSA. All subjects underwent a detailed clinical history and physical examination.

The local ethics committee approved the protocol (SDC: 3830/12/086). Informed consent was obtained from each participant before entering the study.

Polysomnography

All participants underwent a standard overnight polysomnography (PSG) study (Embla N7000, Natus Medical Incorporated). This assessment included EEG, electrooculography, electromyography, pulse oximetry, a thermistor, and nasal pressure for airflow monitoring, as well as measurement of rib cage and abdominal movements during breathing, as previously described by the American Academy of Sleep Medicine. Apnea was defined as complete cessation of airflow for at least 10 s. Hypopnea was defined as a reduction of at least 30% of the nasal pressure signal for at least 10 s, associated with oxygen desaturation of at least 3% or arousal. The apnea-hypopnea index (AHI) was calculated as the total number of respiratory events (apnea plus hypopnea) per hour of sleep. OSA was defined by an AHI > 5 events/hour.

Study Setup

All patients were studied in the sleep laboratory during the morning, immediately after they underwent the diagnostic PSG. Patients were monitored with the same PSG setup except for the nasal cannula and thermistor. Patients slept wearing a customized oronasal mask (7900 series; Hans Rudolph, Inc) that had two independent and sealed compartments (nasal and oral). The mask was sealed to the skin by using spirit gum (Graftobian). Two pneumotachographs (3700A; Hans Rudolph) connected to differential pressure transducers (MP45-14-871; Validyne) were attached to the nasal and oral compartments of the mask. The other end of the two pneumotachographs was attached to a CPAP device (Philips Respironics) through a multidirectional valve (Hans Rudolph). The stopcock valve was hung to a pole to provide comfort to the patient, allowing the investigator to change CPAP route without touching the patient.

The two flow signals (nasal and oral) were recorded by using a data acquisition system at a sampling frequency of 200 Hz (LabVIEW, National Instruments) and saved to a dedicated computer system as well as to the PSG system. Mask air leaks and communication between the nasal and oral compartments were meticulously excluded by regular testing. The mask had a sealed port for the insertion of an ultra-slim endoscope (2.8-mm diameter; BF-XP160 F, Olympus). Endoscopic images were acquired at a sampling frequency of 30 frames per second, using an analog-to-digital converter (510; Pinnacle Systems) and recorded. All endoscopies were performed by the same investigator who was blinded to the patient’s AHI (Fig 1).

Figure 1
Figure Jump LinkFigure 1 Schematic representation of the study setup. The patient slept with PSG monitoring using CPAP connected to a customized oronasal mask that had two independent and sealed compartments. The flow signal and PSG recordings were sent to a dedicated computer. Retroglossal area was directly evaluated by using nasoendoscopy. PSG = polysomnography.Grahic Jump Location
Study Protocol

Sleep was induced by IV infusion of low doses of midazolam, which was slowly titrated and stopped at sleep initiation. The infusion was restarted if the patient awoke for > 2 min, as previously described. The endoscope was positioned at 10 mm from the epiglottis with the aid of a guidewire that was passed through the endoscope’s working channel. CPAP was initially delivered through the nasal route and titrated to abolish flow limitation (holding pressure). After at least 2 min of stable sleep (stage 2) at holding nasal CPAP, 2-min trials on the oral and oronasal routes were started. The objective was to obtain 3 trials on the oral and oronasal routes for each patient. At the end of the protocol, CPAP was titrated to the holding pressure on oronasal and oral routes.

Evaluations

Respiratory events (hypopneas and apneas) were reported according to the American Academy of Sleep Medicine criterion. The patient’s respiratory pattern on the oronasal and oral routes were classified according to the predominant respiratory behavior during the three trials as unstable breathing if respiratory events were observed. All trials that had an absence of respiratory events were classified as stable breathing. Because during the oronasal route testing patients had the possibility of breathing through the nose or mouth, we hypothesized that the occurrence of obstructive events would be preceded by predominant oral breathing. To test this hypothesis, we analyzed all trials independently and determined the percentage of nasal/oral breathing according to the following formula: (nasal tidal volume/[nasal + oral tidal volume]) × 100 of all breaths in the first 30 s at the onset of the oronasal flow route or up to the initiation of a respiratory event.

The video recordings of the upper airway images were analyzed by an investigator who was not aware of the flow route. The minimal cross-sectional area during each trial was analyzed. The analysis consisted of five measurements: (1) area between the tongue base and posterior pharyngeal wall (retroglossal); (2) area between the epiglottis and posterior pharyngeal wall (epiglottis); (3) the distance between the epiglottis and posterior pharyngeal wall; (4) the distance between the tongue base and epiglottis; and (5) the distance between the lateral pharyngeal walls. Airway area was determined by delimiting the airway lumen by using commercial software (Image-Pro Plus 4.5.0.29; Media Cybernetics). The number of pixels obtained from the delimited image was then converted to square millimeters and millimeters using the number of pixels per square millimeters or millimeters obtained from the recording of a graph paper at the same distance (as previously described)., Because each patient underwent three trials with each route, the mean value of all trials was calculated to describe distances and the minimum area of each route.

Statistical Analysis

Data are expressed as mean ± SD or median (25th-75th percentile) when appropriate. Friedman and Wilcoxon tests were used to test for differences in the retroglossal and epiglottic areas and the distance between the epiglottis and posterior pharyngeal wall, the tongue base and epiglottis, and the lateral pharyngeal walls. Repeated measure analysis of variance was used to test for differences on nasal, oronasal, and oral holding pressure. The statistical package used was R statistical software (R Foundation for Statistical Computing, 2013). Statistical significance was set at < 0.05.

A total of 25 subjects were recruited for the study. One patient was excluded because of a severe nasal obstruction, one patient had no OSA, and five patients were excluded because of technical problems with flow or video signals. The study sample (N = 18) consisted of middle-aged male and female subjects with a wide range of OSA severity (Table 1). The mean study duration was 27.9 ± 7.7 min. Sleep was induced with a mean total midazolam dose of 3.1 ± 2.2 mg.

Table Graphic Jump Location
Table 1 Baseline Characteristics and Overnight Polysomnographic Parameters
a Indicates the progressive propensity to sleep during daily activities (0 to 24).

AHI = apnea-hypopnea index; ESS = Epworth Sleepiness Scale; SaO2 = oxygen saturation.

Data are presented as mean ± SD.

Eighteen and 16 patients had at least three valid CPAP trials using the oronasal and oral routes, respectively. Two patients had insufficient data with the oral route because of instability of sleep. All patients exhibited stable breathing during nasal CPAP at a mean holding pressure of 14.8 ± 4.1 cm H2O. Of the 18 patients, six patients had stable breathing during CPAP delivered by the oronasal route. In contrast, the majority of the patients (n = 12) reported obstructive events (predominantly hypopneas in six patients and apneas in six patients) during CPAP delivered through the oronasal route. Only two of 16 patients had stable breathing during CPAP delivered by the oral route. The remaining 14 patients exhibited obstructive events (predominantly hypopneas in four patients and apneas in 10 patients). The flowchart of the patients initially evaluated and included and the predominant flow pattern of each patient, as well as the pattern of each trial, are summarized in Figure 2.

Figure 2
Figure Jump LinkFigure 2 Flowchart showing (from top to bottom) patients recruited and studied and the predominant flow pattern. The flow pattern of all trials is shown in the bottom box.Grahic Jump Location

Figure 3 illustrates the independent analysis of all trials on oronasal CPAP expressed as the median (25th-75th percentiles) of the percentage of nasal breathing at the onset of oronasal CPAP (30 s). All trials with < 50% of nasal breathing resulted in obstructive events. In contrast, stable breathing occurred only when predominant (> 50%) nasal breathing was observed. However, respiratory events were also observed in trials that were preceded by predominant or even 100% of nasal breathing.

Figure 3
Figure Jump LinkFigure 3 Each dot represents one single trial of oronasal CPAP. The trials were grouped as stable breathing, hypopnea, or apnea according to the respiratory pattern observed during oronasal CPAP (x-axis). Each dot is expressed as the median (25th-75th percentiles) of the percentage of nasal breathing during 30 s initiated at the onset of oronasal CPAP or up to the first respiratory event (hypopnea or apnea). The dots across the top of the graph represent trials with 100% of nasal breathing (the absence of error bars indicates absence of variability on the percentage of nasal breathing). The graph shows that all trials with < 50% nasal breathing resulted in an obstructive event. In contrast, stable breathing occurred only when predominant (> 50%) nasal breathing was observed. However, respiratory events were also observed in trials that were preceded by predominant or even 100% of nasal breathing.Grahic Jump Location

Oropharyngeal dimensions were determined during each experimental trial in all patients. The effect of CPAP route on oropharyngeal dimensions is illustrated in one patient (Fig 4). Group data showed that there was a reduction in the distance between epiglottis and tongue base during the oronasal and oral routes compared with the nasal route (Fig 5A). There was a significant reduction in the retroglossal area during the oronasal and oral routes compared with the nasal route (Fig 5B). In contrast, the distances between the epiglottis and posterior pharyngeal wall, lateral pharyngeal walls, and the epiglottis area did not change significantly (data not shown).

Figure 4
Figure Jump LinkFigure 4 A-C, Upper airway images of the retroglossal airway during nasal, oronasal, and oral routes. A significant reduction of the retroglossal area was observed in the nasal (7.88 mm2), oronasal (2.41 mm2), and oral (0 mm2) routes. The white lines demarcate the retroglossal and epiglottic areas. A, Distance between epiglottis and posterior pharyngeal wall. B, Distance between epiglottis and tongue base. C, Distance between the lateral pharyngeal wall.Grahic Jump Location
Figure 5
Figure Jump LinkFigure 5 Distance between epiglottis and tongue base and the retroglossal area during CPAP delivered by the nasal, oronasal and oral routes. Each dot represents the average of the distance between (A) the epiglottis and tongue base and (B) the avarege of the retroglossal area obtained from three trials of each individual undergoing treatment with the nasal, oronasal, and oral routes. The solid bars represent the median (25th-75th percentile) of the group data. aP < .05.Grahic Jump Location

We attempted to perform CPAP titration on oranasal and oral routes in 10 patients at the end of the protocol. Two patients continued exhibiting flow limitations despite titration up to 20 cm H2O on the oronasal route. During the oral route, four patients experienced respiratory events despite titration up to 20 cm H2O, and one patient was unable to sleep during CPAP titration with the oral route. The holding pressures in the patients who had all sets of data (n = 9) were 14.1 ± 3.5, 16.1 ± 3.7, and 17.2 ± 4.0 cm H2O during the nasal, oronasal and oral routes, respectively (P = .003). A post hoc comparison found that the nasal CPAP was different from the remaining routes, whereas the oronasal and oral routes did not reach statistical difference.

Our study was designed to evaluate the acute impact of changing the CPAP route from nasal to oronasal and oral during sleep in patients treated for OSA. As expected, nasal CPAP was able to stabilize ventilation in all patients. In contrast, the majority of patients experienced obstructive events when the flow route was changed to the oronasal (66.7%) and oral (87.5%) routes. Compared with nasal CPAP, the direct observation of the upper airway evaluated by using nasoendoscopy revealed a progressive obstruction of the upper airway at the level of the retroglossal area during oronasal and oral CPAP. Airway obstruction occurred due to a posterior displacement of the tongue, as demonstrated by a significant decrease in the distance between the epiglottis and tongue base. Holding CPAP pressures during the oronasal and oral routes were difficult to obtain in some patients because of persistent obstructive events despite titration up to 20 cm H2O and were on average significantly higher than with the nasal route. Finally, during oronasal CPAP trials, stable breathing occurred only during predominant nasal breathing. Although respiratory events occurred in all trials with predominant oral breathing, respiratory events could also be found during trials with predominant nasal breathing. Our results obtained during acute flow route change are consistent with the hypothesis that the oronasal mask may compromise the effectiveness of CPAP to treat OSA.

The reasons why oronasal CPAP may induce upper airway obstruction are not totally understood. One possibility is that the oronasal mask pushes the chin and the tongue backward, inducing upper airway obstruction. Mandibular stabilization can decrease oropharyngeal collapsibility during midazolam-induced sleep at the retropalatal and retroglossal region. Mandibular stabilization can also reduce velopharyngeal resistance and oronasal CPAP level. In our study, this variable was well controlled because we used a mask that stabilizes the chin, and the flow route was changed without patient contact. However, we were unable to control for minimal mouth opening. Mouth opening is associated with a significant reduction in retropalatal and retroglossal cross-sectional areas in awake subjects and with a more positive pharyngeal critical closing pressure during natural sleep and during midazolam sedation., The most plausible explanation for our findings is that oronasal CPAP applies positive pressure in both nasopharyngeal and oropharyngeal compartments without generating a pressure gradient, allowing gravity to displace the tongue and soft palate backward and causing airway obstruction., Supporting this hypothesis, Smith et al found that oronasal CPAP was unable to open the upper airway even with CPAP higher than the critical closing pressure obtained with a nasal mask. Similarly, Ebben et al found that in contrast to nasal CPAP, the oronasal CPAP mask was not able to open the upper airway in awake patients with OSA evaluated by using MRI. Moreover, and in accordance with other studies,, the holding pressures evaluated in nine patients during oronasal CPAP were on average 2 cm H2O higher than during nasal CPAP. Therefore, our results are compatible with the concept that the oronasal mask increases upper airway resistance and may induce obstructive events. Our results could help explain the recent observation of persistent clinical symptoms among patients with OSA treated with oronasal CPAP.

Because oronasal CPAP allows nasal, oral, or mixed oronasal breathing, we also tested the hypothesis that obstructive events would be preceded by predominantly oral breathing. Consistent with this hypothesis, all patients who exhibited predominantly oral breathing at the onset of oronasal CPAP experienced obstructive events. However, several patients had upper airway obstruction during oronasal CPAP despite predominant or even 100% nasal breathing preceding the obstructive event (Fig 3). We speculate that positive pressure was transmitted through the mouth and pushed the tongue posteriorly despite no detectable flow. However, future studies are necessary to clarify this finding.

The present study has several potential limitations. We studied patients under induced sleep by using low doses of midazolam that could, at least in theory, promote upper airway obstruction. However, we have previously shown that the pharyngeal critical closing pressure, a marker of upper airway collapsibility, is similar during natural sleep and during sleep induced by low doses of midazolam. Moreover, nasal CPAP was able to abolish OSA in all patients. Because there were several variables studied, we made available the option of maintaining the levels of CPAP obtained during the nasal route. It is possible that higher pressures would be sufficient to eliminate OSA with the oronasal route. Conversely, there were several patients who were difficult to titrate on the oronasal and oral routes, suggesting that increasing the CPAP levels does not necessarily eliminate OSA. In addition, the fixed sequence that was used (nasal–oral–oronasal) during the study may have influenced the results. However, the observation that the upper airway obstruction was more severe during oral than oronasal CPAP is consistent with the hypothesis that the oral route may compromise CPAP effectiveness (Fig 5).

In addition, we only evaluated the retroglossal area. It is possible that oronasal flow also affects the retropalatal area. We only studied patients without nasal obstruction during acute changes of CPAP route. It is conceivable that the behavior of the upper airway during sleep is different in patients with nasal obstruction who are mouth breathers and use an oronasal mask for prolonged periods. Finally, when CPAP was offered through either the nose or mouth, the other route was kept obstructed, which is slightly different from what occurs clinically. For instance, when using a nasal CPAP, the mouth may be open to atmospheric pressure. However, the mouth usually remains closed or can be forced to remain closed by using a chinstrap. Therefore, our study raises serious concerns but does not allow direct extrapolation and definitive conclusions about the clinical practice of CPAP delivered by oronasal mask to treat OSA.

We found that acute changes of flow route during sleep from nasal to oronasal and oral routes induced obstructive events in the vast majority of patients with OSA and decreased oropharyngeal dimensions. Our study raises a warning and illustrates that oronasal CPAP may compromise OSA treatment effectiveness. Our findings suggest that patients changing from a nasal to an oronasal interface should be submitted to CPAP retitration because the oronasal interface may compromise CPAP’s efficacy. Future studies are necessary to evaluate patients with OSA that are apparently well treated with CPAP by using oronasal mask.

Author contributions: Each author had full access to the data and takes responsibility for the integrity and accuracy of the analysis. All authors contributed to and approved of the final submitted manuscript. R. G. S. A. was responsible for study design, data collection, analysis, and manuscript preparation; F. M. was responsible for data collection and analysis; V. S. P., F. S., and M. G. G. were responsible for data collection; H. T. M. developed software for the data analysis and interpretation; P. S. S. was responsible for the PSG analysis; and P. R. G. and G. L.-F. were responsible for study design and manuscript preparation.

Financial/nonfinancial disclosures: None declared.

Role of sponsors: The sponsor had no role in the design of the study, the collection and analysis of the data, or the preparation of the manuscript.

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Figures

Figure Jump LinkFigure 1 Schematic representation of the study setup. The patient slept with PSG monitoring using CPAP connected to a customized oronasal mask that had two independent and sealed compartments. The flow signal and PSG recordings were sent to a dedicated computer. Retroglossal area was directly evaluated by using nasoendoscopy. PSG = polysomnography.Grahic Jump Location
Figure Jump LinkFigure 2 Flowchart showing (from top to bottom) patients recruited and studied and the predominant flow pattern. The flow pattern of all trials is shown in the bottom box.Grahic Jump Location
Figure Jump LinkFigure 3 Each dot represents one single trial of oronasal CPAP. The trials were grouped as stable breathing, hypopnea, or apnea according to the respiratory pattern observed during oronasal CPAP (x-axis). Each dot is expressed as the median (25th-75th percentiles) of the percentage of nasal breathing during 30 s initiated at the onset of oronasal CPAP or up to the first respiratory event (hypopnea or apnea). The dots across the top of the graph represent trials with 100% of nasal breathing (the absence of error bars indicates absence of variability on the percentage of nasal breathing). The graph shows that all trials with < 50% nasal breathing resulted in an obstructive event. In contrast, stable breathing occurred only when predominant (> 50%) nasal breathing was observed. However, respiratory events were also observed in trials that were preceded by predominant or even 100% of nasal breathing.Grahic Jump Location
Figure Jump LinkFigure 4 A-C, Upper airway images of the retroglossal airway during nasal, oronasal, and oral routes. A significant reduction of the retroglossal area was observed in the nasal (7.88 mm2), oronasal (2.41 mm2), and oral (0 mm2) routes. The white lines demarcate the retroglossal and epiglottic areas. A, Distance between epiglottis and posterior pharyngeal wall. B, Distance between epiglottis and tongue base. C, Distance between the lateral pharyngeal wall.Grahic Jump Location
Figure Jump LinkFigure 5 Distance between epiglottis and tongue base and the retroglossal area during CPAP delivered by the nasal, oronasal and oral routes. Each dot represents the average of the distance between (A) the epiglottis and tongue base and (B) the avarege of the retroglossal area obtained from three trials of each individual undergoing treatment with the nasal, oronasal, and oral routes. The solid bars represent the median (25th-75th percentile) of the group data. aP < .05.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 Baseline Characteristics and Overnight Polysomnographic Parameters
a Indicates the progressive propensity to sleep during daily activities (0 to 24).

AHI = apnea-hypopnea index; ESS = Epworth Sleepiness Scale; SaO2 = oxygen saturation.

Data are presented as mean ± SD.

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