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Clinical Investigations: SLEEP AND BREATHING |

Predicting Sleep-Disordered Breathing in Patients With Cystic Fibrosis* FREE TO VIEW

Maree A. Milross, BAppSc (Pty); Amanda J. Piper, PhD; Mark Norman, BSc; Grant N. Willson, BAppSc (Pty); Ronald R. Grunstein, MD; Colin E. Sullivan, MD; Peter T. P. Bye, MD, FCCP
Author and Funding Information

*From the Royal Prince Alfred Hospital (Ms. Milross; Drs. Piper, Grunstein, and Bye; Mr. Norman, and Mr. Willson), Camperdown,Sydney; and Faculty of Medicine (Dr. Sullivan), University of Sydney, Sydney, Australia.

Correspondence to: Peter T. P. Bye, MD, FCCP, Department of Respiratory Medicine, Royal Prince Alfred Hospital, Missenden Rd, Camperdown NSW 2050, Australia; e-mail: peterb@mail.med.usyd.edu.au



Chest. 2001;120(4):1239-1245. doi:10.1378/chest.120.4.1239
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Published online

Study objectives: To examine predictors of sleep-disordered breathing in patients with cystic fibrosis (CF) and moderate-to-severe lung disease using a comprehensive evaluation of both sleep and daytime function.

Design: Cross-sectional analysis of sleep studies, lung function, respiratory muscle strength, and evening and morning arterial blood gas measurements in patients with stable CF. A questionnaire addressing sleep quality was administered. Forward stepwise regression analysis was used to identify the parameters that best predict sleep-related desaturation, hypercapnia, and respiratory disturbance.

Setting: Sleep investigation unit and lung function laboratory.

Patients: Thirty-two patients with CF and FEV1 < 65% predicted, in stable clinical condition. Patients were aged 27 ± 8 years (mean ± 1 SD) with FEV1 of 36 ± 10% predicted, evening Pao2 of 68 ± 8 mm Hg, and Paco2 of 43 ± 5 mm Hg.

Results: Evening Pao2 (p < 0.0001) and morning Paco2 (p < 0.01) were predictive of the average minimum oxyhemoglobin saturation per 30-s epoch of sleep (r2 = 0.74; p < 0.0001). Evening Pao2 (p < 0.001) was predictive of the rise in transcutaneous carbon dioxide (Tcco2) seen from non-rapid eye movement (NREM) to rapid eye movement (REM) sleep (r2 = 0.37; p < 0.001). In addition, there was some relationship between expiratory respiratory muscle strength and the REM respiratory disturbance index (r2 = 0.22; p < 0.01).

Conclusion: Evening Pao2 was found to contribute significantly to the ability to predict both sleep-related desaturation and the rise in Tcco2 from NREM sleep to REM sleep in this subgroup of patients with CF.

Figures in this Article

Sleep hypoxemia was first described in patients with cystic fibrosis (CF)> 20 years ago. Muller and colleagues1and Tepper and colleagues2showed that the desaturation occurred predominantly in rapid eye movement (REM) sleep and that hypoventilation was a contributing factor. Hypoxia is thought to be the main etiologic factor in the development of cor pulmonale in patients with CF.3Right ventricular hypertrophy is due to chronic pulmonary hypertension resulting primarily from hypoxic pulmonary vasoconstriction. Pulmonary artery systolic pressure has been shown4 to correlate highly with awake, sleep, and postexercise oxyhemoglobin saturation (Spo2) by pulse oximetry; moreover, a higher mortality is seen in patients with pulmonary hypertension. Therefore, it is important to reliably predict sleep-related hypoxia, as this could influence the timing of the initiation of treatment aimed at preventing sleep-related desaturation and reducing or minimizing the load on the cardiovascular system.

Awake resting Spo2 < 94% and an FEV1 < 65% predicted have been suggested56 as the variables with the most significant correlation with sleep-related desaturation in patients with CF. There is limited information on the predictive value of daytime Paco2 in sleep-disordered breathing, and no studies have assessed predictors of sleep-related changes in carbon dioxide levels or indexes of nocturnal respiratory disturbance in patients with CF. The aim of this study was to compare sleep variables of oxygenation, changes in carbon dioxide, and respiratory disturbance to daytime measurements of lung function, respiratory muscle strength, arterial blood gas (ABG) measurements, and subjective sleep quality in patients with CF. Furthermore, we aimed to examine for the ability of daytime variables to have significant predictive value for sleep-disordered breathing.

We studied adult patients with CF with moderate-to-severe lung disease while in a stable clinical condition, which was defined according to the criteria of Fuchs et al.7 Patients were invited to participate in the study if their FEV1 was < 65% predicted and/or their awake resting Spo2 was < 94%. Diagnostic sleep studies were performed with the patients going to bed at a time of their preference, usually between 10 pm and 11 pm, and they were awakened at 6 am.

This study was conducted at Royal Prince Alfred Hospital in Sydney, Australia, and approved by the ethics committee of our institution (protocol No. X97–0204). Written, informed consent was obtained from all patients.

Anthropometric and Lung Function Measurements

Anthropometric and lung function data were obtained on the day of the diagnostic sleep study. Measurements of spirometry were performed using a mass flow sensor (Sensormedics Vmax 20; Sensormedics Corporation; Yorba Linda, CA), which was calibrated before each study and compared with normal predicted values of Quanjer et al.8Lung volumes were determined by body plethysmography (Gould 2800; Gould Electronics; Dayton, OH). Results were compared with normal predicted values of Goldman and Becklake.9 Inspiratory muscle pressure at residual volume (Pimax) and expiratory muscle pressure at total lung capacity (Pemax) were recorded using a hand-held pressure gauge, and the results were compared with normal predicted values of Wilson et al.10 A gas chromatograph (1085 D Series PF/Dx; Medical Graphics Corporation; St. Paul, MN) was used to measure carbon monoxide transferred per liter of lung volume (Kco). The normal predicted value for Kco was 6.9 mL CO/mm Hg/min (standard temperature and pressure, dry), a value based on mean laboratory values for normal nonsmoking healthy adults obtained in our laboratory.

ABG Tensions

Initial awake ABG tensions were obtained with the patient seated and breathing room air, usually in the late afternoon prior to the sleep study. Morning ABG measurements were taken immediately on awakening, so that any delay from sleep to wakefulness was minimized.

Sleep Study Recordings

During polysomnography, continuous recordings were made on a computerized system (Sleepwatch; Compumedics; Melbourne, Australia). Sleep stage was determined from two channels of EEG (C3/A2, O2/A1), two channels of electro-oculogram (right outer canthus/A1, left outer canthus/A2), and from the submental electromyogram (EMG). Respiratory variables were monitored using abdominal and thoracic impedance bands for chest wall movement and diaphragm EMG electrodes to reflect respiratory effort. Nasal airflow was measured using nasal prongs attached to a flow sensor (AutoSet; ResMed; Sydney, Australia). Spo2 was measured with a finger probe (model 3700e; Ohmeda; Boulder, CO). The resting awake value of Spo2 was noted, and Spo2 recording continued overnight. Transcutaneous carbon dioxide (Tcco2) was also measured continuously overnight (TCM3; Radiometer; Copenhagen, Denmark). Tcco2 and Spo2 were recorded simultaneously on both the Sleepwatch system as well as a personal computer.

Sleep stages were scored in 30-s epochs according to the standard criteria of Rechtschaffen and Kales.11 An EEG arousal was defined as an abrupt increase in EEG frequency for ≥ 3 s that in REM sleep was accompanied by an increase in submental EMG amplitude. Sleep efficiency was defined as the total sleep time (TST) as a percentage of the time available for sleep. Apnea was defined as cessation of airflow for ≥ 10 s, or a cessation of airflow for < 10 s with an oxygen desaturation of ≥ 3% or an arousal. Hypopnea was defined as a reduction in amplitude of airflow, or thoracoabdominal wall movement of> 50% for ≥ 10 s, or a reduction in airflow or thoracoabdominal wall movement of > 50% for < 10 s if it was accompanied by an oxygen desaturation of ≥ 3% or an arousal. The number of apneas and hypopneas per hour of non-rapid eye movement (NREM), REM, and TST were calculated and reported as the respiratory disturbance index (RDI).

The absolute minimum sleep Spo2 was documented for the entire night but also for REM and NREM sleep. The percentage of TST, REM, and NREM sleep time with Spo2 ≤ 90% was calculated. The minimum average Spo2 (Spo2min·av) was calculated as the mean of the minimum value for Spo2 in each 30-s epoch of sleep. Spo2min·av was calculated for TST, NREM sleep time, and REM sleep time.

Respiratory events leading to desaturation and increases in carbon dioxide occur predominantly in REM sleep in the CF population. These changes in carbon dioxide can be represented by the change in Tcco2 from NREM to REM sleep, or the maximum Tcco2 measured during the night compared with a baseline Tcco2 reading. The change in Tcco2 from NREM to REM sleep in our study was calculated for each REM period. Due to the drift often seen in the Tcco2 trace, a line of best fit was drawn between four points on the Tcco2 trace: one at the start and end of each REM period, taking into account the approximately 3-min time delay for the device, and a point 5 min prior to and following each REM period as long as the Tcco2 reading was stable. A perpendicular line was then drawn to the peak Tcco2 reading for that REM period being measured (Fig 1 ). A weighted average was then obtained for theΔ Tcco2 for each subject. Tcco2 awake was the baseline value recorded at least 7 min after probe placement while the patient was breathing spontaneously.

Questionnaire Data

The Pittsburgh sleep quality index (PSQI) was completed on the day of the diagnostic sleep study. Administration of the questionnaire occurred during face-to-face interviews, with nondirectional guidance. The PSQI is a self-rated questionnaire that assesses sleep quality and disturbances over a 1-month time interval and has been validated for clinical populations.12

Data Analysis and Statistics

Linear correlation analyses were performed between awake and sleep measurements, but due to the large number of correlations being performed, we chose to analyze data by fitting the variables into a forward stepwise regression model to determine the most important predictor variables. Daytime variables used as potential predictor variables included lung function variables (FEV1 percent predicted, FVC percent predicted, total lung capacity [TLC] percent predicted, residual volume [RV] percent predicted, RV/TLC percent predicted, functional residual capacity percent predicted, Kco percent predicted); respiratory muscle strength measurements (Pimax percent predicted and Pemax percent predicted); anthropometric values (age, sex, and body mass index [BMI]); evening and morning ABG measurements (pH, Pao2, Paco2); and the PSQI score. In order to reduce the possibility of a type-1 error, only three sleep variables were chosen as outcome variables: Spo2min · av,Δ Tcco2 from NREM to REM sleep, and REM RDI.

As awake resting Spo2 and evening Pao2 are both measurements of the level of arterial blood oxygenation, it is logical that they are correlated highly with one another. Therefore, when fitting them into a model of forward stepwise regression, once one is selected the other does not provide any additional information. Hence, in our forward stepwise regression calculations, evening Pao2 was included as a potential predictor variable and awake resting Spo2 was not. Data are reported as mean ± 1 SD. Results were considered statistically significant at the p < 0.05 level.

Anthropometric and Lung Function Data

The mean age of the 32 subjects (17 male and 15 female) was 27 ± 8 years. Anthropometric and daytime lung function are presented in Table 1 . All subjects had moderate-to-severe lung disease with FEV1 ranging from 18 to 59% of predicted values. Subjects had evening Pao2 values ranging between 42 mm Hg and 84 mm Hg, and nine subjects were hypercapnic during wakefulness (Paco2> 45 mm Hg). Mean respiratory muscle strength was in the normal range. Subjects were hyperinflated with an RV/TLC of 223 ± 34% of predicted.

Three of 16 subjects with an awake resting Spo2 ≥ 94% had an Spo2min·av < 90%, while 12 of 16 subjects with a resting Spo2 < 94% had an Spo2min·av ≤ 90%. Thirty of 32 patients had an absolute minimum sleep Spo2 of ≤ 90% (Table 2 ). Subjects had a mean awake Tcco2 of 47 ± 7 mm Hg, ranging from 37 to 70 mm Hg. The maximum sleep Tcco2 was 55 ± 10 mm Hg, ranging from 41 to 82 mm Hg. The rise in Tcco2 from NREM to REM sleep was 2.1 ± 1.6 mm Hg, ranging from an increase of zero to 5.6 mm Hg (Table 2). The mean values for REM, NREM, and TST RDI are shown in Table 3 . Subjects had a mean NREM RDI of 0.7 ± 1.3 events per hour, REM RDI of 12.2 ± 11.4 events per hour, and TST RDI of 3.2 ± 3.4 events per hour.

Relationship Between Baseline Data and Oxygenation During Sleep

The minimum sleep Spo2 and the Spo2min · av correlated highly with one another (r = 0.93; p < 0.0001). The same was true for the Spo2min · av and the percentage of sleep time with Spo2≤ 90% (r = 0.79; p < 0.0001). Therefore, Spo2min · av was chosen as the parameter to represent sleep-related oxygenation for the calculations of the relationship with lung function parameters, respiratory muscle strength, BMI, awake resting Spo2 percentage, evening and morning ABG measurements, and the PSQI.

Awake Spo2 (r = 0.77; p < 0.0001), evening Pao2 (r = 0.78; p < 0.0001), morning Pao2 (r = 0.70; p < 0.0001), evening Paco2 (r = −0.59; p < 0.01), morning Paco2 (r = − 0.66; p < 0.0001), and morning pH (r = 0.50; p < 0.01) were significantly correlated with Spo2av percentage. The only lung function parameter to show a significant correlation with the Spo2av was FEV1 percent predicted (r = 0.45; p < 0.01). Pimax was also significantly correlated to Spo2av (r = 0.44; p < 0.05). The PSQI did not correlate significantly with Spo2av.

Forward stepwise regression revealed the combination of evening Pao2 (p < 0.0001) and morning Paco2 (p < 0.01) to most strongly predict sleep-related oxygenation as represented by Spo2av (r2 = 0.74; p < 0.0001; Fig 2 , A and B). The remaining variables did not add significantly to the ability of the evening Pao2 and morning Paco2 to account for the variability in TST Spo2av. With simple regression, the evening Pao2 accounted for 61% (r2 = 0.61; p < 0.0001) of the variability in Spo2av, while in combination with the morning Paco2, using forward stepwise regression, 74% of the variability in Spo2av could be explained. The equation to calculate the predicted Spo2av percentage would be as follows:

Relationship Between Baseline Data and Carbon Dioxide Levels During Sleep

The maximum Tcco2 measured and the mean change in Tcco2 from NREM to REM (ΔTcco2) sleep are correlated with one another (r = 0.51; p < 0.01), and since the size of the ΔTcco2 reflects the severity of the REM-related hypoventilation, we examined the relationship of theΔ Tcco2 with daytime measurements of lung function, respiratory muscle strength, awake resting Spo2, evening and morning ABG measurements, and the PSQI.

Awake Spo2 (r = − 0.66; p < 0.0001), evening Pao2 (r = − 0.61; p < 0.01), morning Pao2 (r=− 0.53; p < 0.01), evening Paco2 (r = 0.45; p < 0.05), and morning Paco2 (r = 0.50; p < 0.01) were significantly correlated withΔ Tcco2. Lung function parameters that showed a significant correlation withΔ Tcco2 were FEV1 percent predicted (r = − 0.47; p < 0.01), RV percent predicted (r = 0.43; p < 0.05), and RV/TLC percent predicted (r = 0.39; p < 0.05). Pemax percent predicted was also significantly correlated withΔ Tcco2 (r = − 0.47; p < 0.05). PSQI did not correlate significantly withΔ Tcco2.

Evening Pao2 (p < 0.001) was the only variable identified in a forward stepwise regression model as being predictive of the change in carbon dioxide from NREM to REM sleep as represented by ΔTcco2 (r2 = 0.37; p < 0.001; Fig 3 ). Other measured variables did not add significantly to the ability of evening Pao2 to account for the variability seen inΔ Tcco2. The equation to calculate the predicted change in Tcco2 from NREM to REM sleep is as follows:

Relationship Between Patient Characteristics and RDIs During Sleep

The RDI was significantly greater during REM sleep than during NREM sleep (p < 0.0001), with a mean NREM RDI of 0.7 ± 1.3 events per hour and a REM RDI of 12.2 ± 11.4 events per hour (Table 3). As this patient group shows their greatest respiratory disturbance during REM sleep, the REM RDI was chosen as the variable for the calculations of the relationship with lung function parameters, respiratory muscle strength, awake resting Spo2, evening and morning ABG measurements, and the PSQI.

Pemax percent predicted was the only variable to show any correlation with REM RDI (r = − 0.47; p < 0.01). Similarly, in a forward stepwise regression, Pemax percent predicted was found to be the only variable with predictive power for REM RDI (r2 = 0.22; p < 0.01). The equation to calculate the predicted REM RDI is as follows:

Using rigorous statistical analysis of a type that has not usually been employed in many previous studies6,1314 of sleep-disordered breathing in patients with CF, we found that evening Pao2 and morning Paco2 were the variables that were the most predictive of sleep-related oxygenation in patients with moderate-to-severe lung disease. These variables accounted for 74% of the variability seen in the Spo2av percentage. Assessment of individual correlations between the awake and asleep measurements made in this study showed that other variables of lung function and gas exchange were significantly correlated with measures of sleep-related oxygenation, although they did not add significantly to the predictive ability of the evening Pao2 and morning Paco2 in the forward stepwise regression model.

Previously, Versteegh and colleagues5 showed that an awake resting Spo2 of 93.8% was the most discriminatory for predicting sleep-related Spo2, defined as one hourly mean Spo2 of ≤ 90%, with a positive predictive value of 50%, and that the addition of other variables, including exercise parameters and lung function, did not add significantly to the discriminatory power.,5 ABG tensions, measures of carbon dioxide levels during sleep, or polysomnography allowing for sleep staging and respiratory event scoring were not measured in that study. Our data have demonstrated the additional value of measuring morning Paco2 along with evening Pao2 for predicting sleep-related Spo2, and provides the clinician with a predictive equation that describes a continuum rather than a probability (50%) at a single point (93.8%). In addition, the current study is to our knowledge the first to examine the ability to predict changes in carbon dioxide and indexes of respiratory disturbance during sleep in this patient group.

An interesting observation from our work was that 3 of 16 patients, despite an awake resting Spo2 of≥ 94%, had an Spo2av of < 90%. Sleep-related hypoxemia would have been missed if sleep studies were not performed in these patients. Frangolias and colleagues15 recently reported sleep studies in a group of patients with CF, with a wide spectrum of lung disease. This study was designed to assess for the ability to predict nocturnal Spo2 using daytime pulse oximetry, exercise testing, and spirometry. There was no assessment of respiratory disturbance, sleep-related carbon dioxide changes, measurements of ABG tensions, nor full polysomnography. All patients with an awake resting Spo2 of< 93% desaturated nocturnally, but there was a heterogenous response with regard to nocturnal desaturation with values of awake resting Spo2 of > 93%.,15 Nocturnal desaturation was found to be uncommon in patients with milder lung disease (FEV1 > 65% predicted); however, when using FEV1 and awake resting Spo2 alone, they were only able to correctly predict 26% of all patients with clinically significant nocturnal desaturation, which they defined as Spo2 < 90% for > 5% of the night.,15 Further studies in patients with CF and mild lung disease, using full polysomnography and a comprehensive battery of tests including complete pulmonary function testing and ABG tension measurements, may allow us to better determine if nonsleep study measurements can predict when patients with CF first present with sleep-disordered breathing.

Previous studies have used various methods of describing desaturation during sleep. However, a definitive measure of sleep Spo2 has yet to be determined. Variables described have included the greatest percentage fall in Spo2,3,16 the percentage of time spent with Spo2 > 90% and< 90%,,6 minimum sleep Spo2,,13 mean sleep Spo2,,14 lowest hourly mean,5 and mean minimum Spo2.,17 In this study, we reported the relationship between the minimum sleep Spo2, Spo2av, and percentages of time with Spo2 ≤ 90%. In order to reduce the possibility of type-1 error, only one measure of oxygenation during sleep could be chosen as an outcome variable in this study. As the absolute minimum sleep Spo2 may not appropriately reflect the subject’s oxygenation for the entire night, we reasoned that the Spo2av more accurately quantifies sleep oxygenation due to the high sampling rate, and it was therefore chosen as the variable to reflect oxygenation during sleep in this study.

Although Versteegh and colleagues5found that sleep-related desaturation occurred only in subjects with an FEV1 < 65% predicted in their study, spirometry did not add significantly to the discriminatory power of resting Spo2 to predict sleep-related desaturation. Our study did not include subjects with an FEV1 > 65% of predicted, and thus the range in spirometry was limited. Our results in patients with moderate and severe lung disease showed no additional predictive information to be gained by lung function parameters when performed in conjunction with ABG tension measurement. Similarly, in a study of overnight pulse oximetry in patients with CF, FEV1 was shown to be poorly correlated with Spo2 during sleep, defined as percentage of TST with Spo2 < 90%.6 Other studies that have examined for relationships between lung function and overnight oximetry have reported significant correlations with measures of severity of lung disease, including measures of lung hyperinflation3,13 and airflow obstruction.3,6,14 No significant correlations were shown between respiratory muscle strength or nutritional status in a previous study13 of sleep-related desaturation in patients with CF. Despite the individual correlations seen between measurements of lung function and sleep-related desaturation in the above-mentioned studies as well as this present study, we conclude that for patients with moderate-to-severe lung disease, lung function measurements when performed in conjunction with ABG measurements do not add to our ability to predict desaturation during sleep.

A novel feature of this study was the assessment of the ability to predict changes in carbon dioxide levels during sleep and indexes of nocturnal respiratory disturbance. In the forward stepwise regression model, the evening Pao2 was predictive of the Tcco2 from NREM to REM sleep, but it accounted for a lesser degree of the variability than the variables that were found to be predictive of Spo2av.

Pemax percent predicted was found to correlate significantly with and be predictive of REM RDI, although it accounted for only 22% of the variability in the REM RDI. Pemax may reflect the strength of cough. Cough has been described as contributing significantly to sleep disruption in patients with CF,16 although the contribution of cough to sleep disruption in this study was not quantified.

In this study, we have shown that evening Pao2 and morning Paco2, rather than measurements of lung function, were predictive of nocturnal oxygenation as represented by TST Spo2av in patients with CF and moderate-to-severe lung disease. Evening Pao2 was found to contribute significantly to the ability to predict both nocturnal desaturation and the rise in Tcco2 from NREM to REM sleep.

Abbreviations: ABG = arterial blood gas; BMI = body mass index; CF = cystic fibrosis; EMG = electromyogram; Kco = carbon monoxide transferred per liter of lung volume; NREM = non-rapid eye movement; Pemax = expiratory muscle pressure at total lung capacity; Pimax = inspiratory muscle pressure at residual volume; PSQI = Pittsburgh sleep quality index; RDI = respiratory disturbance index; REM = rapid eye movement; RV = residual volume; Spo2 = oxyhemoglobin saturation; Spo2min·av = minimum average oxyhemoglobin saturation; Tcco2 = transcutaneous carbon dioxide; TLC = total lung capacity; TST = total sleep time

This research was performed at Royal Prince Alfred Hospital, Camperdown, Sydney, Australia.

These studies were supported by the National Health and Medical Research Council of Australia.

Figure Jump LinkFigure 1. Typical example of Spo2 and rises in Tcco2 in REM sleep demonstrating the method of summarizing the ΔTcco2. Reprinted with permission from Milross et al.18Grahic Jump Location
Table Graphic Jump Location
Table 1. Anthropometric Data, ABG Tensions, and Lung Function Values
Table Graphic Jump Location
Table 2. Gas Exchange Variables During Sleep (n = 32)
* 

See Figure 1.

Table Graphic Jump Location
Table 3. Sleep and Respiratory Variables
Figure Jump LinkFigure 2. A: the relationship between evening Pao2 and the Spo2av percentage. B: the relationship between morning Paco2 and the TST Spo2av percentage.Grahic Jump Location
Figure Jump LinkFigure 3. The relationship between evening Pao2 and ΔTcco2.Grahic Jump Location

We thank Carmel Moriarty for assistance with patient recruitment, Wei Xuan for statistical advice and assistance, and the technical and nursing staff in our Lung Function Laboratory and Sleep Unit for assistance with patient testing and care.

Muller, NL, Francis, PW, Gurwitz, D, et al (1980) Mechanism of hemoglobin desaturation during rapid-eye-movement sleep in normal subjects and in patients with cystic fibrosis.Am Rev Respir Dis121,463-469. [PubMed]
 
Tepper, RS, Skatrud, JB, Dempsey, JA Ventilation and oxygenation changes during sleep in cystic fibrosis.Chest1983;84,388-393. [PubMed] [CrossRef]
 
Francis, PW, Muller, NL, Gurwitz, D, et al Hemoglobin desaturation: its occurrence during sleep in patients with cystic fibrosis.Am J Dis Child1980;134,734-740. [PubMed]
 
Fraser, KL, Tullis, DE, Sasson, Z, et al Pulmonary hypertension and cardiac function in adult cystic fibrosis.Chest1999;115,1321-1328. [PubMed]
 
Versteegh, FG, Bogaard, JM, Raatgever, JW, et al Relationship between airway obstruction, desaturation during exercise and nocturnal hypoxaemia in cystic fibrosis patients.Eur Respir J1990;3,68-73. [PubMed]
 
Braggion, C, Pradal, U, Mastella, G Hemoglobin desaturation during sleep and daytime in patients with cystic fibrosis and severe airway obstruction.Acta Paediatr1992;81,1002-1006. [PubMed]
 
Fuchs, HJ, Borowitz, DS, Christiansen, DH, et al Effect of aerosolized recombinant human DNase on exacerbations of respiratory symptoms and on pulmonary function in patients with cystic fibrosis.N Engl J Med1994;331,637-642. [PubMed]
 
Quanjer, PH, Tammeling, GJ, Cotes, JE, et al Lung volumes and forced ventilatory flows: report of the Working Party for Standardization of Lung Function Tests, European Community for Steel and Coal; official statement of the European Respiratory Society.Eur Respir J Suppl1993;16,5-40. [PubMed]
 
Goldman, H, Becklake, M Respiratory function tests: normal values at median altitudes and the prediction of normal results.Am Rev Tuberc1959;79,457-467. [PubMed]
 
Wilson, SH, Cooke, NT, Edwards, RH, et al Predicted normal values for maximal respiratory pressures in Caucasian adults and children.Thorax1984;39,535-538. [PubMed]
 
Rechtschaffen, A, Kales, A. A manual of standardized terminology, techniques, and scoring system for sleep stages of human subjects. 1968; US Government Printing Office. Washington, DC:.
 
Buysse, DJ, Reynolds, CFI, Monk, TH, et al The Pittsburgh sleep quality index: a new instrument for psychiatric practice and research.Psychiatr Res1989;28,193-213
 
Bradley, S, Solin, P, Wilson, J, et al Hypoxemia and hypercapnia during exercise and sleep in patients with cystic fibrosis.Chest1999;116,647-653. [PubMed]
 
Coffey, MJ, FitzGerald, MX, McNicholas, WT Comparison of oxygen desaturation during sleep and exercise in patients with cystic fibrosis.Chest1991;100,659-662. [PubMed]
 
Frangolias, DD, Wilcox, PG Predictability of oxygen desaturation during sleep in patients with cystic fibrosis.Chest2001;119,434-441. [PubMed]
 
Stokes, DC, McBride, JT, Wall, MA, et al Sleep hypoxemia in young adults with cystic fibrosis.Am J Dis Child1980;134,741-743. [PubMed]
 
Regnis, JA, Piper, AJ, Henke, KG, et al Benefits of nocturnal nasal CPAP in patients with cystic fibrosis.Chest1994;106,1717-1724. [PubMed]
 
Milross, MA, Piper, AJ, Norman, M, et al Low-flow oxygen and bilevel ventilatory support: effects on ventilation during sleep in cystic fibrosis.Am J Respir Crit Care Med2001;163,129-134. [PubMed]
 

Figures

Figure Jump LinkFigure 1. Typical example of Spo2 and rises in Tcco2 in REM sleep demonstrating the method of summarizing the ΔTcco2. Reprinted with permission from Milross et al.18Grahic Jump Location
Figure Jump LinkFigure 2. A: the relationship between evening Pao2 and the Spo2av percentage. B: the relationship between morning Paco2 and the TST Spo2av percentage.Grahic Jump Location
Figure Jump LinkFigure 3. The relationship between evening Pao2 and ΔTcco2.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Anthropometric Data, ABG Tensions, and Lung Function Values
Table Graphic Jump Location
Table 2. Gas Exchange Variables During Sleep (n = 32)
* 

See Figure 1.

Table Graphic Jump Location
Table 3. Sleep and Respiratory Variables

References

Muller, NL, Francis, PW, Gurwitz, D, et al (1980) Mechanism of hemoglobin desaturation during rapid-eye-movement sleep in normal subjects and in patients with cystic fibrosis.Am Rev Respir Dis121,463-469. [PubMed]
 
Tepper, RS, Skatrud, JB, Dempsey, JA Ventilation and oxygenation changes during sleep in cystic fibrosis.Chest1983;84,388-393. [PubMed] [CrossRef]
 
Francis, PW, Muller, NL, Gurwitz, D, et al Hemoglobin desaturation: its occurrence during sleep in patients with cystic fibrosis.Am J Dis Child1980;134,734-740. [PubMed]
 
Fraser, KL, Tullis, DE, Sasson, Z, et al Pulmonary hypertension and cardiac function in adult cystic fibrosis.Chest1999;115,1321-1328. [PubMed]
 
Versteegh, FG, Bogaard, JM, Raatgever, JW, et al Relationship between airway obstruction, desaturation during exercise and nocturnal hypoxaemia in cystic fibrosis patients.Eur Respir J1990;3,68-73. [PubMed]
 
Braggion, C, Pradal, U, Mastella, G Hemoglobin desaturation during sleep and daytime in patients with cystic fibrosis and severe airway obstruction.Acta Paediatr1992;81,1002-1006. [PubMed]
 
Fuchs, HJ, Borowitz, DS, Christiansen, DH, et al Effect of aerosolized recombinant human DNase on exacerbations of respiratory symptoms and on pulmonary function in patients with cystic fibrosis.N Engl J Med1994;331,637-642. [PubMed]
 
Quanjer, PH, Tammeling, GJ, Cotes, JE, et al Lung volumes and forced ventilatory flows: report of the Working Party for Standardization of Lung Function Tests, European Community for Steel and Coal; official statement of the European Respiratory Society.Eur Respir J Suppl1993;16,5-40. [PubMed]
 
Goldman, H, Becklake, M Respiratory function tests: normal values at median altitudes and the prediction of normal results.Am Rev Tuberc1959;79,457-467. [PubMed]
 
Wilson, SH, Cooke, NT, Edwards, RH, et al Predicted normal values for maximal respiratory pressures in Caucasian adults and children.Thorax1984;39,535-538. [PubMed]
 
Rechtschaffen, A, Kales, A. A manual of standardized terminology, techniques, and scoring system for sleep stages of human subjects. 1968; US Government Printing Office. Washington, DC:.
 
Buysse, DJ, Reynolds, CFI, Monk, TH, et al The Pittsburgh sleep quality index: a new instrument for psychiatric practice and research.Psychiatr Res1989;28,193-213
 
Bradley, S, Solin, P, Wilson, J, et al Hypoxemia and hypercapnia during exercise and sleep in patients with cystic fibrosis.Chest1999;116,647-653. [PubMed]
 
Coffey, MJ, FitzGerald, MX, McNicholas, WT Comparison of oxygen desaturation during sleep and exercise in patients with cystic fibrosis.Chest1991;100,659-662. [PubMed]
 
Frangolias, DD, Wilcox, PG Predictability of oxygen desaturation during sleep in patients with cystic fibrosis.Chest2001;119,434-441. [PubMed]
 
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  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543