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(Chest. 2005;128:3221-3228.)
© 2005 American College of Chest Physicians

Effects of Lung Volume Reduction Surgery on Sleep Quality and Nocturnal Gas Exchange in Patients With Severe Emphysema*

Samuel L. Krachman, DO, FCCP; Wissam Chatila, MD, FCCP; Ubaldo J. Martin, MD, FCCP; Thomas Nugent, MD; Joseph Crocetti, DO; John Gaughan, PhD; Gerard J. Criner, MD, FCCP; for the National Emphysema Treatment Trial Research Group

* From the Divisions of Pulmonary and Critical Care Medicine (Dr. Krachman, Chatila, Martin, Nugnet, Crocetti, and Criner) and Biostatistics (Dr. Gaughan), Temple University School of Medicine, Philadelphia, PA.

Correspondence to: Samuel L. Krachman, DO, FCCP, Temple University School of Medicine, 767 Parkinson Pavilion, Broad and Tioga Sts, Philadelphia, PA 19140; e-mail: krachms{at}TUHS.temple.edu


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: We hypothesized that associated with improvements in respiratory mechanics, lung volume reduction surgery (LVRS) would result in an improvement in both sleep quality and nocturnal oxygenation in patients with severe emphysema.

Design: Prospective randomized controlled trial.

Setting: University hospital.

Patients: Sixteen patients (10 men, 63 ± 6 years [± SD]) with severe airflow limitation (FEV1, 28 ± 10% predicted) and hyperinflation (total lung capacity, 123 ± 14% predicted) who were part of the National Emphysema Treatment Trial.

Interventions and measurements: Patients completed 6 to 10 weeks of outpatient pulmonary rehabilitation. Spirometry, measurement of lung volumes, arterial blood gas analysis, and polysomnography were performed prior to randomization and again 6 months after therapy. Ten patients underwent LVRS and optimal medical therapy, while 6 patients received optimal medical therapy only.

Results: Total sleep time and sleep efficiency improved following LVRS (from 184 ± 111 to 272 ± 126 min [p = 0.007], and from 45 ± 26 to 61 ± 26% [p = 0.01], respectively), while there was no change with medical therapy alone (236 ± 75 to 211 ± 125 min [p = 0.8], and from 60 ± 18 to 52 ± 17% [p = 0.5], respectively). The mean and lowest oxygen saturation during the night improved with LVRS (from 90 ± 7 to 93 ± 4% [p = 0.05], and from 83 ± 10 to 86 ± 10% [p = 0.03], respectively), while no change was noted in the medical therapy group (from 91 ± 5 to 91 ± 5 [p = 1.0], and from 84 ± 5 to 82 ± 6% [p = 0.3], respectively). There was a correlation between the change in FEV1 and change in the lowest oxygen saturation during the night (r = 0.6, p = 0.02). In addition, there was an inverse correlation between the change in the lowest oxygen saturation during the night and the change in residual volume (– r = 0.5, p = 0.04) and functional residual capacity (– r = 0.6, p = 0.03).

Conclusion: In patients with severe emphysema, LVRS, but not continued optimal medical therapy, results in improved sleep quality and nocturnal oxygenation. Improvements in nocturnal oxygenation correlate with improved airflow and a decrease in hyperinflation and air trapping.

Key Words: COPD • emphysema • hypoxemia • oximetry


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
In patients with severe emphysema, sleep is often disturbed, with poor sleep quality noted both subjectively and objectively.123 Emphysema patients often report difficulty initiating and maintaining sleep, resulting in increased daytime sleepiness.3 Objectively, patients have increased sleep latencies, shortened total sleep times (TSTs), and an increased number of nocturnal arousals.123 Sleep architecture is also disrupted with an increase in light sleep and a decrease in stages 3/4 and rapid eye movement (REM) sleep.

In addition to poor sleep quality, patients with severe emphysema often have significant nocturnal oxygen desaturation (NOD), particularly during REM sleep.134567 These episodes of NOD may occur despite the presence of an awake PaO2 > 60 mm Hg, and have been associated with the development of pulmonary hypertension.8 In addition, the severity of NOD has been associated with the degree of disturbed sleep3 and with reduced survival.9 Hypoventilation has been suggested to be the mechanism by which these patients acquire NOD, secondary to a decrease in minute ventilation and tidal volume.101112

Lung volume reduction surgery (LVRS) has been shown to be an effective treatment in selected patients with severe emphysema, producing improvements in respiratory mechanics, gas exchange, exercise tolerance, quality of life, and mortality.131415161718192021222324252627 Improvements in these parameters were related to increased lung tissue elastic recoil15212223 and improved diaphragmatic function.161718202425 We hypothesized that associated with improvements in respiratory mechanics, LVRS would result in an improvement in both sleep quality and NOD in patients with severe emphysema.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patient Selection
Twenty-five patients evaluated for LVRS as part of the National Emphysema Treatment Trial (NETT) at Temple University Hospital were evaluated for this single center ancillary study. All patients had successfully completed 6 to 10 weeks of outpatient pulmonary rehabilitation before being randomized to optimal medical therapy alone or optimal medical therapy and LVRS. The pulmonary rehabilitation program consisted of a minimum of 16 education sessions and 16 exercise sessions. The protocol and NETT were explained to the patients in detail (Fig 1 ). Patients were excluded from the sleep ancillary study for the following reasons: (1) they did not wish to undergo a sleep study, (2) they withdrew from the NETT study, or (3) the refused to have their final sleep study after randomization. The NETT and sleep ancillary study were both approved by the Institutional Review Board for Human Research (Temple University School of Medicine, Philadelphia, PA).



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  		Figure 1. Outline of protocol for testing after 6 to 10 weeks of pulmonary rehabilitation and following randomization to the LVRS or medical therapy groups. PFT = pulmonary function test; ABG = arterial blood gas.

 
Pulmonary Function Tests and Arterial Blood Gases
Pulmonary function tests were performed at the end of the 6 to 10 weeks of outpatient pulmonary rehabilitation, as well as 6 months following LVRS or continued medical therapy. Pulmonary function testing was performed with a plethysmograph (System 6200 Autobox DL; SensorMedics; Yorba Linda, CA). FVC, FEV1, and FEV1/FVC were measured. Thoracic gas volumes were measured in a body plethysmograph. All data are reported after bronchodilation in absolute numbers and as a percentage of normal predicted values.2829 Arterial blood gases were drawn prior to randomization from the radial artery while breathing room air.

Sleep Studies
Polysomnography was performed on room air and consisted of rib cage and abdominal motion (Respitrace; Ambulatory Monitoring; White Plains, NY), oral and nasal thermistors, ECG, electro-oculogram, digastric electromyogram, EEG, and finger pulse oximetry (model N-100; Nellcor Puritan Bennett; Pleasanton, CA). All variables were continuously recorded and stored in a computerized system (Alice 3; Healthdyne Information Enterprises; Marietta, GA). Sleep was staged using the standard criteria of Rechtschaffen and Kales.30 Arousals were defined as the appearance of {alpha} activity for 3 to 15 s.31 TST and sleep efficiency (defined as TST divided by the time in bed) was determined. Obstructive apneas were defined by a lack of airflow for > 10 s,32 associated with rib cage and abdominal paradox, terminated with an arousal and decrease in oxygen saturation ≥ 4%. Obstructive hypopneas were defined by a 30% decrease in airflow for > 10 s, associated with rib cage and abdominal paradox, terminated by an arousal and a similar decrease in oxygen saturation.33 Central apneas were defined as a lack of airflow for > 10 s associated with a lack of respiratory effort, terminated with an arousal and decrease in oxygen saturation ≥ 4%. The apnea-hypopnea index was expressed as the number of apneas and hypopneas per hour of sleep. Sleep was staged and the respiratory component scored by a single registered polysomnographic technologist who was blinded as to the patient’s clinical history. The same author (S.K.) reviewed each study.

Pulmonary Rehabilitation
All patients participated in a total of 6 to 10 weeks of outpatient pulmonary rehabilitation. Included in the program were a minimum of 16 education sessions and 16 exercise sessions that were supervised by an exercise physiologist. An individualized program was derived based on symptom-limited maximums obtained at baseline. Exercises included lifting arm and leg weights, arm cycling, and use of a motor-driven treadmill. Increases in the intensity of the programs were based on an individual’s performance.

Surgical Technique
The approach to lung resection was by median sternotomy with bilateral stapling. The objective was to remove 20 to 40% of volume from each lung. Decisions in regards to amount and location of resected tissue were determined by a combination of preoperative high-resolution CT and quantitative ventilation/perfusion scans, as well as by visual inspection by the surgeon at the time of surgery. Attempts were made to remove areas of emphysema with poor perfusion and hyperinflation.

Data Analysis
Data represent the mean ± SD. Comparison of baseline data between the medical therapy and LVRS groups was done using an unpaired Student t test. Paired t tests were used to evaluate changes at 6 months in both of the groups. The Fisher Exact Test was performed to compare proportions between groups. The relationship between changes in respiratory mechanics and sleep parameters was assessed by Pearson correlation coefficients. All statistical analyses were performed using a commercially available computer software program (SigmaStat, version 2.0; Jandel Scientific; San Rafael, CA); p < 0.05 was considered significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Patient Characteristics
Twenty-five patients were evaluated, with 16 patients (10 men; 63 ± 6 years old; 71 ± 15 kg) with severe airflow limitation (FEV1, 28 ± 10% predicted) and hyperinflation (total lung capacity [TLC], 123 ± 14% predicted) completing the study. Nine patients refused to participate or were unable to complete the study: six patients who did not want to sleep without their oxygen, two patients who refused to return for their repeat study at 6 months, and one patient who died prior to completion of the study. There was no difference in regards to severity of airflow obstruction or oxygenation between those patients who participated (n = 16) and those who refused or were unable to complete the study (n = 9): FEV1, 0.8 ± 0.3 L (28 ± 10% predicted) and 0.8 ± 0.2 L (29 ± 6% predicted [p = 0.6]; and PaO2, 64 ± 9 mm Hg and 61 ± 8 mm Hg (p = 0.5), respectively. Baseline characteristics of the 16 patients who completed the study in pulmonary function, gas exchange, and sleep following the 6 to 10 weeks of outpatient pulmonary rehabilitation are shown in Table 1 . Six patients (4 men; 62 ± 7 years old) were randomized to optimal medical therapy, and 10 patients (6 men; 64 ± 6 years old) were randomized to LVRS and continued optimal medical therapy after completion of their pulmonary rehabilitation program. All parameters of respiration, sleep, and respiration during sleep were the same in the two groups at baseline (Table 1).


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  		Table 1. Baseline Characteristics of Patients by Treatment Group*

 
Effects of LVRS on Sleep Parameters
Total sleep time significantly increased with LVRS, from 184 ± 111 to 272 ± 126 min (p = 0.007), while there was no change in the medical therapy group, from 236 ± 75 to 211 ± 125 min (p = 0.8) [Fig 2 ]. Similarly, sleep efficiency increased from 45 ± 26 to 61 ± 26% (p = 0.01) with LVRS, with no change noted with medical therapy, from 60 ± 18 to 52 ± 17% (p = 0.5) [Fig 3 ]. The arousal index decreased with LVRS, from 12 ± 5 to 9 ± 4 arousals per hour (p = 0.03), with no change in the medical therapy group, from 12 ± 6 to 21 ± 26 arousals per hour (p = 0.8). Besides a decrease in stage 1 sleep from 19 ± 18 to 10 ± 7% (p = 0.01) with LVRS, there was no change in sleep architecture in either the LVRS or medical therapy groups. The mean oxygen saturation during the night increased in the LVRS group from 90 ± 7 to 93 ± 4% (p = 0.05), without a change in the medical therapy group, from 91 ± 5 to 91 ± 5% (p = 1.0). The lowest oxygen saturation during the night increased following LVRS, from 83 ± 10 to 86 ± 10% (p = 0.03), while the medical therapy group remained unchanged, from 84 ± 5 to 82 ± 6% (p = 0.3). Finally, the percentage of TST the oxygen saturation was < 90% decreased with LVRS, from 41 ± 47 to 15 ± 30% (p = 0.03), with no change in the medical therapy group, from 29 ± 44 to 34 ± 51% (p = 0.3).



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  		Figure 2. Effects of LVRS and medical therapy on TST after 6 months. The lines represent individual patient plots, and the bars represent the mean values. Compared to baseline, LVRS resulted in an improvement in TST (p = 0.007), with no change noted with continued medical therapy (p = 0.8).

 


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  		Figure 3. Effects of LVRS and medical therapy on sleep efficiency after 6 months. The lines represent individual patient plots, and the bars represent the mean values. When compared to baseline, sleep efficiency increased following LVRS after 6 months (p = 0.01) but not with continued medical therapy (p = 0.5).

 
Effects of LVRS on Respiratory Mechanics
Table 2 shows the effects of medical therapy and LVRS on respiratory mechanics as measured at 6 months. LVRS resulted in a 27% increase in FEV1 and a 19% increase in FVC. TLC, residual volume (RV), and functional residual capacity (FRC) decreased by 13%, 26%, and 20%, respectively. There were no significant changes in any of these parameters in the medical therapy group.


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  		Table 2. Effects of Medical Therapy and LVRS on Respiratory Mechanics*

 
Correlation Between Sleep and Respiratory Mechanic Parameters
For the group of patients as a whole, there was no significant correlation found between changes in sleep quality (as measured by TST and sleep efficiency, respectively) and changes in nocturnal oxygenation during the night, including mean oxygen saturation (r = 0.1, p = 0.8, and r = 0.1, p = 0.9), lowest oxygen saturation (r = 0.4, p = 0.3, and r = 0.1, p = 0.9), and percentage of TST the oxygen saturation was < 90% (r = 0.1, p = 0.8, and r = 0.2, p = 0.6).

There was a significant correlation noted between the change in FEV1 and change in the lowest oxygen saturation during the night (r = 0.6, p = 0.02) [Fig 4 ]. In addition, there was a significant inverse correlation noted between the change in the lowest oxygen saturation during the night and changes in RV and FRC (– r = 0.5, p = 0.04, and – r = 0.6, p = 0.03, respectively) [Fig 5 ].



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  		Figure 4. There was a significant correlation between the change in FEV1 (from baseline to 6 months) and the change in lowest SaO2 during the night (n = 16, r = 0.6, p = 0.02).

 


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  		Figure 5. There was a significant inverse correlation between the change in lowest SaO2 during the night (from baseline to 6 months) and changes in RV and FRC (n = 16, r = – 0.5, p = 0.04, and r = – 0.6, p = 0.03, respectively).

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
While LVRS has been shown to improve a number of daytime physiologic parameters in patients with severe emphysema,1314151617181920212223242526 its effects on sleep quality and nocturnal oxygenation have not been previously reported. There are three major findings in this study: (1) baseline sleep quality was poor and nocturnal oxygen desaturation was common in patients with severe emphysema; (2) LVRS with optimal medical therapy, but not optimal medical therapy alone, improved sleep quality and nocturnal oxygenation; and (3) there was a significant correlation between improvements in nocturnal oxygenation and improvements in pulmonary mechanics.

Poor sleep quality has been reported, both subjectively and objectively, in patients with severe emphysema.2345 Calverley et al2 studied 20 patients with severe emphysema (FEV1 < 1.0 L) and found an increased sleep latency and decreased duration of uninterrupted sleep when compared to normal control subjects. Fleetham et al5 reported a decreased TST and an increase in arousal index in 15 patients with severe emphysema when compared to historical control subjects. Subjective complaints of difficulty initiating and maintaining sleep with associated daytime sleepiness was reported by Cormick et al3 in 50 patients with severe emphysema. The arousal frequency on overnight polysomnography appeared to correlate with the severity of nocturnal hypoxemia, suggesting that sleep quality was worse in those who were more hypoxic during the night. Our patients demonstrated similar findings in regards to poor sleep quality, with a TST of 203 ± 100 min, sleep efficiency of 50 ± 24%, and arousal index of 12 ± 5 arousals per hour (Table 1). There were no significant differences in these baseline variables between patients receiving LVRS or medical therapy (Table 1).

Nocturnal oxygen desaturation is noted to occur in severe emphysema, even in those patients with an awake PaO2 > 60 mm Hg.1345 The most significant episodes of oxygen desaturation appear to occur during REM sleep.13456 Koo et al4 measured serial arterial blood gases during the night in 15 patients with severe emphysema; the mean decrease in PaO2 was 14 mm Hg during the night in the patients, compared to 6 mm Hg in normal control subjects. Wynne et al1 noted episodes of oxygen desaturation as great as 36% in six of seven patients with severe emphysema, most significantly during REM sleep. Others3456 have noted similar degrees of oxygen desaturation during the night in patients with severe emphysema. Fletcher et al6 reported that 27% of 135 patients with severe emphysema demonstrated predominantly REM-associated NOD, despite an awake PaO2 > 60 mm Hg. Our patients demonstrated similar decreases in oxygen saturation during the night, with a lowest arterial oxygen saturation (SaO2) of 83 ± 8% and a percentage of TST the SaO2 was < 90% of 37 ± 45%. These episodes of oxygen desaturation occurred despite an awake PaO2 of 64 ± 9 mm Hg, and many demonstrated their lowest and most prolonged episodes of oxygen desaturation during REM sleep. Again, baseline variables in regards to awake and nocturnal oxygenation were no different between those patients who received LVRS and those who continued medical therapy alone (Table 1).

LVRS has been shown to improve a number of awake physiologic parameters in severe emphysema, including respiratory mechanics, gas exchange, exercise capacity, quality of life, and survival.131415161718192021222324252627 Increases in tidal volume breathing during exercise following LVRS1316171819202425 may be related to decreases in hyperinflation and end expiratory lung volume,24 resulting in improved diaphragmatic function. A similar change in tidal volume breathing during sleep may be responsible for the improvement in nocturnal oxygenation observed in our patients following LVRS. Others have noted alterations in ventilation/perfusion heterogeneity as a mechanism by which LVRS results in an improvement in awake PaO2,34 and may play a role in our patient’s results in regards to nocturnal oxygenation.

The mechanism by which LVRS resulted in an improvement in sleep quality also remains uncertain. One may assume that the improvement in nocturnal oxygenation may be responsible. However, we have previously shown that in patients with severe emphysema, sleep quality correlates with the severity of airflow obstruction and air trapping, and not with measurements of nocturnal oxygenation.35 In addition, we previously demonstrated that the improvement in sleep quality with the use of noninvasive ventilation in patients with severe emphysema is unrelated to improvements in nocturnal oxygenation.36 Therefore, other mechanisms, including a decrease in hyperinflation and improvement in respiratory muscle function, may be responsible for the improvement in sleep quality following LVRS.

There are a number of limitations with our study that need to be addressed. First, the number of patients that were studied was small. Not all patients who were enrolled in the NETT at our institution agreed to participate in the sleep substudy. However, there was no difference in regards to severity of airflow obstruction or oxygenation between those patients who participated (n = 16) and those who refused or were unable to complete the study (n = 9). In addition, the severity of airflow obstruction and oxygenation in our patients was similar to those enrolled from all the participating centers of the NETT.27 Second, we only evaluated the changes in sleep quality and nocturnal oxygenation 6 months following LVRS or continued medical therapy. Whether similar results would still be present after 1 to 2 years is presently unknown. Finally, the mechanism by which nocturnal oxygenation and sleep quality improved following LVRS was not determined. Many of our patients did not remain calibrated during the night in regards to the inductance plethysmography that was used to monitor respiratory patterns, and thus an accurate measurement of tidal volume could not be obtained in all patients. Therefore, whether there was a correlation between improvement in nocturnal oxygenation and an increase in tidal volume breathing during sleep could not be assessed.

In conclusion, patients with severe emphysema sleep poorly and demonstrate significant nocturnal oxygen desaturation. LVRS, but not continued medical therapy, results in improved sleep quality and nocturnal oxygenation. Improvements in nocturnal oxygenation correlate with decreases in hyperinflation and air trapping, as well as improvements in airflow. Whether the beneficial effects of LVRS in regards to sleep quality and nocturnal oxygenation are sustained beyond 6 months awaits further study.


   Footnotes
 
Abbreviations: FRC = functional residual capacity; LVRS = lung volume reduction surgery; NETT = National Emphysema Treatment Trial; NOD = nocturnal oxygen desaturation; REM = rapid eye movement; RV = residual volume; SaO2 = arterial oxygen saturation; TLC = total lung capacity; TST = total sleep time

Support for the National Emphysema Treatment Trial Research Group was provided in part by National Heart, Lung, and Blood Institute contract No. 1–76116, the Centers for Medicare and Medicaid Services, and the Agency for Healthcare Research and Quality.

Received for publication December 16, 2004. Accepted for publication April 9, 2005.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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