Physiologic correlates of sleep quality in severe emphysema.

BACKGROUND: Sleep quality is poor in severe emphysema. We hypothesized that in addition to nocturnal oxygen desaturation, the severity of airflow obstruction and degree of thoracic hyperinflation are responsible. METHODS: Twenty-five patients (14 males, 64 ± 6 [ ± SD] yrs, BMI 24.7 ± 4.2 kg/m(2)) with severe emphysema (FEV(1) = 28 ± 8% predicted, TLC = 125 ± 14% predicted) were studied. Measurements included spirometry, lung volumes, arterial blood gas, length of the diaphragm's zone of apposition (LZAP) and a polysomnogram. RESULTS: Total sleep time (TST) was 227 ± 93 minutes with a sleep efficiency (SE) of 56 ± 21%. The mean SaO(2), lowest SaO(2), and% TST with a SaO(2) < 90% were 90 ± 5%, 83 ± 8% and 29 ± 40%, respectively. TST correlated with FEV(1)% (r = 0.5, p = 0.02), FVC% (r = 0.4, p = 0.03) and LZAP (r = 0.5, p = 0.01). SE correlated with FEV(1)% (r = 0.5, p = 0.02) and LZAP (r = 0.5, p = 0.01), but not with FVC% (r = 0.4, p = 0.07). Additionally, TST and SE correlated negatively with residual volume% (r = -0.4, p = 0.046, and r = -0.4, p = 0.03, respectively). There was no correlation between TST and SE and measures of nocturnal oxygenation. Multiple linear regression was used to predict TST, with 50% (r(2) = 0.49) explained by a combination of LZAP (27%), mean SaO(2) (23%), and the lowest SaO(2) (< 1%). To predict SE, 44% (r(2) = 0.43) was explained by a combination of LZAP (29%), mean SaO(2) (14%), and the lowest SaO(2) (1%). CONCLUSION: Although parameters of respiratory function and mechanics correlate with sleep quality, both nocturnal oxygenation and measurements of respiratory function/mechanics predict sleep quality in severe emphysema.

Effect of Triple Therapy with Budesonide-Formoterol-Tiotropium Versus Placebo-Tiotropium on Sleep Quality in Patients with Chronic Obstructive Pulmonary Disease.

BACKGROUND: Factors responsible for poor sleep quality in patients with chronic obstructive pulmonary disease (COPD) includes the effects of medications. This study evaluates the effect of the inhaled triple therapy of budesonide-formoterol-tiotropium versus placebo-tiotropium on sleep quality in COPD patients. METHODS: Twenty-three patients (11 [48%] males; age 55 [51-60, 48--5] years; body mass index [BMI] 25 [22-30, 18-40] kg/m2; forced expiratory volume in 1 second [FEV1]1.10 [0.80 -1.90, 0.60-2.80] L, 42 [31-62, 24-75] % predicted) were studied. Ten patients were randomized to budesonide-formoterol-tiotropium and 13 patients to placebo-tiotropium. At baseline and after 28 days, patients completed spirometry, polysomnography, an Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), COPD-specific St George's Respiratory Questionnaire (SGRQ-C) and short form 36 (SF 36). RESULTS: After 28 days, there was a significant 29% increase in the bedtime FEV1 in the budesonide-formoterol-tiotropium group (from 0.75 [0.55-1.30, 0.50-2.40] L to 1.00 [0.75-1.55, 0.50-3.00] L, p=0.031), with no change in the placebo-tiotropium group (from 1.20 [0.80-1.50, 0.60-1.90] L to 1.15 [0.75-1.55, 0.50-1.80] L, p=0.91). No significant change was found post treatment in sleep efficiency or total sleep time in both the budesonide-formoterol-tiotropium group (from 78 [72-92, 62-98]% to 88 [77-92, 40-98]%, p=0.70 and 290 [268-358, 252-382] min to 342 [303-358, 157-372] min, p=0.77, respectively) and the placebo-tiotropium group (from 82 [75-88, 46-93]% to 84 [77-87, 62-94]%, p=0.96 and 320 [292-350, 180-378] min to 339 [303-349, 241-366] min, p=0.79, respectively). While there was no significant change in the arousal index in the budesonide-formoterol-tiotropium group (9 [5-16, 0-48] arousals/hour to 14 [9-17, 2-36] arousals/hour, p=0.43), a significant increase was seen in the placebo-tiotropium group (11 [4-13, 3--2] arousals/hour to 17 [11-21, 2-33] arousals/hour, p=0.027). Similarly, there was no change in the ESS in the budesonide-formoterol-tiotropium group (6 [3-8, 0-11] to 6 [5-8, 0-1]), p=0.44), but a marginally significant increase in the placebo-tiotropium group (8 [5-12, 2-18] to 10 [7-13, 5-18], p=0.07), with a significant difference in the ESS 28 days post treatment between the 2 groups (6 [5-8, 0-11] versus 10 [7-13, 5-18], p=0.043). There was no significant change in nocturnal oxygenation, sleep architecture, PSQI, SGRQ-C, or SF 36 in both groups. CONCLUSION: In patients with COPD, inhaled triple therapy with budesonide-formoterol-tiotropium as compared to placebo-tiotropium improves pulmonary function while preserving sleep quality and architecture.

Oxygen therapy in advanced COPD: in whom does it work?

Supplemental oxygen therapy is commonly used in patients with advanced chronic obstructive pulmonary disease (COPD) and severe hypoxemia at rest. Use of oxygen in these patients is justified by studies showing a mortality benefit. However, the use of oxygen in other patients with advanced COPD has not clearly been established. Long-term studies assessing not only mortality but also other outcomes that are important to patients and physicians such as dyspnea, health status, and exercise capacity are lacking. This article reviews the available studies of the use of supplemental oxygen in patients with less severe hypoxemia at rest during the day, hypoxemia occurring only at night, and hypoxemia occurring only with exercise. With the knowledge that studies in patients with advanced COPD and less severe hypoxemia are limited, recommendations are provided on oxygen use in these groups of patients.

Treatment of sleep disordered breathing in congestive heart failure.

In patients with congestive heart failure, sleep disordered breathing occurs commonly and is associated with an increased mortality. In addition to central sleep apnea (Cheyne-Stokes respiration), obstructive sleep apnea is more prevalent in patients with congestive heart failure than in the general population. As a result, a number of treatments have been investigated, with varying results. While many therapies may improve the severity of sleep disordered breathing, only positive pressure ventilation has been shown to improve cardiac function. Newer forms of positive pressure ventilation, such as adaptive servo-ventilation, appear to be even more effective at correcting central sleep apnea. Whether any of these treatments have an effect on transplant-free survival is presently unknown and awaits further study.

Use of positional therapy when incorporated into a diagnosis-treatment algorithm for obstructive sleep apnea.

PURPOSE: Positional obstructive sleep apnea (OSA) is prevalent. We hypothesized that by incorporating positional therapy into a diagnosis-treatment algorithm for OSA it would frequently be prescribed as an appropriate first-line therapy. METHODS: Fifty-nine members (45 males, 49±9 yrs, BMI 35.2±5.6 kg/m2) of the Law Enforcement Health Benefits (LEHB), Inc. of Philadelphia with clinically suspected OSA were evaluated. Patients completed an Epworth Sleepiness Scale (ESS) questionnaire and a home sleep test (HST). Patients diagnosed with positional OSA (non-supine apnea-hypopnea index [AHI] < 5 events/hr) were offered positional therapy. A cost comparison to continuous positive airway pressure (CPAP) therapy was performed. RESULTS: Fifty-four (92%) of the patients (43 males, 49±9 yrs, BMI 35.2±5.3 kg/m2) had OSA on their HST (AHI 24.2±20.1 events/hr). Sixteen (30%) patients had positional OSA. Compared to non-positional patients, patients with positional OSA were less heavy (32.4±5.1 vs. 36.4±5.1 kg/m2, respectively [p=0.009]), less sleepy (ESS 8±5 vs. 12±5, respectively [p=0.009]), and had less severe OSA (AHI 10.4±4.3 vs. 30.0±21.3 events/hr, respectively [p<0.001]). Thirteen of the 16 patients with positional OSA agreed to positional therapy and 31 non-positional OSA patients agreed to CPAP therapy. Based on initial costs, incorporating positional therapy ($189.95/device compared to CPAP therapy at $962.49/device) into the treatment algorithm resulted in a 24% cost savings compared to if all the patients were initiated on CPAP therapy. CONCLUSION: With the high prevalence of positional OSA, using a diagnosis-treatment algorithm that incorporates positional therapy allows it to be more frequently considered as a cost effective first-line therapy for OSA.

Sleep disruption as a predictor of quality of life among patients in the subpopulations and intermediate outcome measures in COPD study (SPIROMICS).

Study Objectives: Sleep quality is poor among patients with chronic obstructive pulmonary disease (COPD), and studies show that sleep disturbance is associated with low overall quality of life in this population. We evaluated the impact of patient-reported sleep quality and sleep apnea risk on disease-specific and overall quality of life within patients with COPD enrolled in the SPIROMICS study, after accounting for demographics and COPD disease severity. Methods: Baseline data from 1341 participants [892 mild/moderate COPD (FEV1 ≥ 50% predicted); 449 severe COPD (FEV1 < 50%)] were used to perform three nested (blocks) regression models to predict quality of life (Short Form-12 mental and physical components and St. George's Respiratory Questionnaire). Dependent measures used for the nested regressions included the following: Block1: demographics and smoking history; Block 2: disease severity (forced expiratory volume 1 s; 6 min walk test); Block 3: risk for obstructive sleep apnea (OSA; Berlin questionnaire); and Block 4: sleep quality (Pittsburgh Sleep Quality Index [PSQI]). Results: Over half of participants with COPD reported poor sleep quality (Mean PSQI 6.4 ± 3.9; 50% with high risk score on the Berlin questionnaire). In all three nested regression models, sleep quality (Block 4) was a significant predictor of poor quality of life, over and above variables included in blocks 1-3. Conclusions: Poor sleep quality represents a potentially modifiable risk factor for poor quality of life in patients with COPD, over and above demographics and smoking history, disease severity, and risk for OSA. Improving sleep quality may be an important target for clinical interventions. Clinical Trial: SPIROMICS. Clinical Trial URL: http://www2.cscc.unc.edu/spiromics/. Clinical Trial Registration: ClinicalTrials.gov NCT01969344.

Effect of Emphysema Severity on the Apnea-Hypopnea Index in Smokers with Obstructive Sleep Apnea.

RATIONALE: The presence of obstructive sleep apnea (OSA) in patients with chronic obstructive pulmonary disease (COPD) is referred to as the OSA-COPD overlap syndrome. While lung inflation has been shown to be an important factor in determining upper airway stability, its role in determining OSA severity in smokers, including those with emphysema, has not been evaluated. OBJECTIVES: To evaluate the importance of lung inflation on OSA severity (apnea-hypopnea index [AHI]) in smokers with suspected OSA. METHODS: Fifty-one smokers (18 males; mean [±SD] age, 59 ± 9 yr; body mass index [BMI], 32 ± 9 kg/m(2)) who were part of the Genetic Epidemiology of COPD (COPDGene) project were studied. Patients underwent a full-night polysomnography for suspected OSA. Other testing included spirometry and volumetric chest computed tomography (CT) for quantitative measurement of CT-derived percent emphysema and CT-derived percent gas trapping. MEASUREMENTS AND MAIN RESULTS: For the group overall, there was evidence of obstructive airway disease by spirometry (FEV1, 1.4 ± 0.5 L, 58 ± 14% predicted) and emphysema by quantitative CT (CT-derived percent emphysema, 11 ± 13%; CT-derived percent gas trapping, 31.6 ± 24.1%). Twenty-nine (57%) of the patients had OSA (AHI, 18 ± 12 events/h). Patients with OSA had a higher BMI but were younger than those without OSA (BMI, 35 ± 9 kg/m(2) vs. 29 ± 7 kg/m(2), respectively [P = 0.007]; age, 56 ± 8 yr vs. 62 ± 9 yr, respectively [P = 0.01]). There was an inverse correlation between the AHI and the CT-derived percent emphysema and CT-derived percent gas trapping, both for the entire group (r = -0.41 [P < 0.01] and r = -0.44 [P < 0.01], respectively) and when just those patients with OSA were evaluated (r = -0.43 [P = 0.04] and r = -0.49 [P = 0.03], respectively). Multiple linear regression revealed that, in addition to CT-derived percent emphysema and CT-derived percent gas trapping, sex and BMI were important in determining the AHI in these patients. CONCLUSIONS: In smokers with OSA, increased gas trapping and emphysema as assessed by CT are associated with a decreased AHI. Along with sex and BMI, these measurements may be important in determining the severity of OSA in patients with COPD and may offer a protective mechanism in patients with more advanced disease.

Effects of lung volume reduction surgery on sleep quality and nocturnal gas exchange in patients with severe emphysema.

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 (FEV(1), 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 FEV(1) 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.

Self-reported sleep quality and acute exacerbations of chronic obstructive pulmonary disease.

BACKGROUND: Many patients with chronic obstructive pulmonary disease (COPD) suffer from poor sleep quality. We hypothesized that poor sleep quality in otherwise stable patients predicted exacerbations in these patients. METHODS: This is a secondary analysis of the results of a previously published randomized trial of azithromycin in 1,117 patients with moderate to severe COPD who were clinically stable on enrollment. Sleep quality was measured using the Pittsburgh Sleep Quality Index. Other quality of life indices included the Medical Outcome Study 36-item Short Form Health Survey and the St Georges Respiratory Questionnaire. Outcomes included time to first exacerbation and exacerbation rate. RESULTS: Sleep quality was "poor" (Pittsburgh Sleep Quality Index >5) in 53% of participants but was not related to age or severity of airflow obstruction. Quality of life scores were worse in "poor" sleepers than in "good" sleepers. Major classes of comorbid conditions, including psychiatric, neurologic, and musculoskeletal disease, were more prevalent in the "poor" sleepers. Unadjusted time to first exacerbation was shorter (190 versus 239 days) and exacerbation rate (1.7 versus 1.37 per year) was greater in the poor sleepers, but no differences were observed after adjusting for medications and comorbid conditions associated with poor sleep. CONCLUSION: Poor sleepers had greater exacerbation rates than did good sleepers. This appeared to be due largely to them having more, or more severe, concomitant medical conditions and taking more medications.

Effects of nasal continuous positive airway pressure on oxygen body stores in patients with Cheyne-Stokes respiration and congestive heart failure.

STUDY OBJECTIVES: The mechanism(s) by which nasal continuous positive airway pressure (CPAP) is effective in the treatment of Cheyne-Stokes respiration (CSR) in patients with congestive heart failure (CHF) remains uncertain, and may involve an increase in total oxygen body stores (dampening), changes in central and peripheral controller gain, and/or improvement in cardiac function. The purpose of this study was to evaluate the effects of nasal CPAP on total oxygen stores, as measured by the rate of fall of arterial oxyhemoglobin saturation (dSaO(2)/dt), to determine if dampening may play a role in the attenuation of CSR in patients with CHF. DESIGN: Prospective controlled trial. SETTING: University hospital. PATIENTS: Nine male patients (mean +/- SD age, 59 +/- 8 years) with CHF and a mean left ventricular ejection fraction (LVEF) of 16 +/- 4%. INTERVENTIONS AND MEASUREMENTS: All patients had known CSR, as identified on a baseline polysomnographic study. Patients then underwent repeat polysomnography while receiving nasal CPAP (9 +/- 0.3 cm H(2)O). The polysomnography consisted of recording of breathing pattern, pulse oximetry, and EEG. dSaO(2)/dt was measured as the slope of a line drawn adjacent to the falling linear portion of the arterial oxygen saturation (SaO(2)) curve associated with a central apnea. All patients underwent echocardiography and right-heart catheterization within 1 month of the study to measure LVEF and cardiac hemodynamics, respectively. RESULTS: There was a significant decrease in the apnea-hypopnea index (AHI) with nasal CPAP, from 44 +/- 27 events per hour at baseline to 15 +/- 24 events per hour with nasal CPAP (p = 0.004). When compared to baseline, dSaO(2)/dt significantly decreased with nasal CPAP from 0.42 +/- 0.15% to 0.20 +/- 0.07%/s (p < 0.001). The postapneic SaO(2), when compared to baseline, significantly increased with nasal CPAP, from 87 +/- 5% to 91 +/- 4% (p < 0.05). The preapneic SaO(2) did not significantly change, from a baseline of 96 +/- 2% to 96 +/- 3% with nasal CPAP (p = 0.8). When compared to baseline, the apnea duration and heart rate did not change with nasal CPAP. While there was a significant correlation noted between baseline postapneic SaO(2) and dSaO(2)/dt (r = 0.8, p = 0.02), no correlation was seen between baseline preapneic SaO(2) and dSaO(2)/dt (r = 0.1, p = 0.7). A significant correlation was noted between baseline dSaO(2)/dt and the AHI (r = 0.7, p = 0.02). With CPAP, there was a significant correlation noted between dSaO(2)/dt and the AHI (R = 0.7, p = 0.04), but no correlation was noted between dSaO(2)/dt and postapneic SaO(2) (R = 0.1, p = 0.8). CONCLUSION: Nasal CPAP significantly decreases dSaO(2)/dt and thus increases total body oxygen stores in patients with CSR and CHF. By increasing oxygen body stores, dampening may be one of the mechanisms responsible for the attenuation of CSR seen with nasal CPAP.

Sleep and long-term ventilation.

The development of sleep-disordered breathing is common in patients with chronic respiratory insufficiency due to neuromuscular and restrictive disorders, as well as in those with COPD. Nocturnal hypoventilation and obstructive and central apneas result in daytime symptoms of hypersomnolence and fatigue, and contribute to abnormalities in awake gas exchange. Long-term mechanical ventilation, delivered invasively by tracheostomy or more recently by NPPV, has been shown to eliminate sleep-disordered breathing and correct abnormalities in nocturnal gas exchange, resulting in an improvement in sleep quality. Improved daytime symptoms and gas exchange, with the suggestion of a decrease in morbidity and mortality, support the use of long-term mechanical ventilation during sleep in selected patients with these disorders.

Determinants of CPAP Adherence in Hispanics with Obstructive Sleep Apnea.

Purpose. We hypothesized that socioeconomic factors and a language barrier would impact adherence with continuous positive airway pressure (CPAP) among Hispanics with obstructive sleep apnea (OSA). Methods. Patients with OSA who were prescribed CPAP for at least 1 year and completed a questionnaire evaluating demographic data, socioeconomic status, and CPAP knowledge and adherence participated in the study. Results. Seventy-nine patients (26 males; 53 ± 11 yrs; body mass index (BMI) = 45 ± 9 kg/m(2)) with apnea-hypopnea index (AHI) 33 ± 30 events/hr completed the study. Included were 25 Hispanics, 39 African Americans, and 15 Caucasians, with no difference in age, AHI, CPAP use, or BMI between the groups. While there was a difference in educational level (P = 0.006), income level (P < 0.001), and employment status (P = 0.03) between the groups, these did not influence CPAP adherence. Instead, overall improvement in quality of life and health status and perceived benefit from CPAP influenced adherence, both for the group as a whole (P = 0.03, P = 0.004, and P = 0.001, resp.), as well as in Hispanics (P = 0.02, P = 0.02, P = 0.03, resp.). Conclusion. In Hispanic patients with OSA, perceived benefit with therapy, rather than socioeconomic status or a language barrier, appears to be the most important factor in determining CPAP adherence.

Comparison of positional therapy to CPAP in patients with positional obstructive sleep apnea.

STUDY OBJECTIVES: We hypothesized that positional therapy would be equivalent to continuous positive airway pressure (CPAP) at normalizing the apnea-hypopnea index (AHI) in patients with positional obstructive sleep apnea (OSA). METHODS: Thirty-eight patients (25 men, 49 +/- 12 years of age, body mass index 31 +/- 5 kg/m2) with positional OSA (nonsupine AHI <5 events/h) identified on a baseline polysomnogram were studied. Patients were randomly assigned to a night with a positional device (PD) and a night on CPAP (10 +/- 3 cm H2O). RESULTS: Positional therapy was equivalent to CPAP at normalizing the AHI to less than 5 events per hour (92% and 97%, respectively [p = 0.16]). The AHI decreased from a median of 11 events per hour (interquartile range 9-15, range 6-26) to 2 (1-4, 0-8) and 0 events per hour (0-2, 0-7) with the PD and CPAP, respectively; the difference between treatments was significant (p < 0.001). The percentage of total sleep time in the supine position decreased from 40% (23%-67%, 7%-82%) to 0% (0%-0%, 0%-27%) with the PD (p < 0.001) but was unchanged with CPAP (51% [36%-69%, 0%-100%]). The lowest SaO2 increased with the PD and CPAP therapy, from 85% (83%-89%, 76%-93%) to 89% (86%-9%1, 78%-95%) and 89% (87%-91%, 81%-95%), respectively (p < 0.001). The total sleep time was unchanged with the PD, but decreased with CPAP, from 338 (303-374, 159-449) minutes to 334 (287-366, 194-397) and 319 (266-343, 170-386) minutes, respectively (p = 0.02). Sleep efficiency, spontaneous arousal index, and sleep architecture were unchanged with both therapies. CONCLUSION: Positional therapy is equivalent to CPAP at normalizing the AHI in patients with positional OSA, with similar effects on sleep quality and nocturnal oxygenation.

Oxygen therapy for patients with COPD: current evidence and the long-term oxygen treatment trial.

Long-term use of supplemental oxygen improves survival in patients with COPD and severe resting hypoxemia. However, the role of oxygen in symptomatic patients with COPD and more moderate hypoxemia at rest and desaturation with activity is unclear. The few long-term reports of supplemental oxygen in this group have been of small size and insufficient to demonstrate a survival benefit. Short-term trials have suggested beneficial effects other than survival in patients with COPD and moderate hypoxemia at rest. In addition, supplemental oxygen appeared to improve exercise performance in small short-term investigations of patients with COPD and moderate hypoxemia at rest and desaturation with exercise, but long-term trials evaluating patient-reported outcomes are lacking. This article reviews the evidence for long-term use of supplemental oxygen therapy and provides a rationale for the National Heart, Lung, and Blood Institute Long-term Oxygen Treatment Trial. The trial plans to enroll subjects with COPD with moderate hypoxemia at rest or desaturation with exercise and compare tailored oxygen therapy to no oxygen therapy.

Sleep abnormalities and treatment in emphysema.

Sleep abnormalities are common in severe emphysema, and include poor sleep quality, the development of nocturnal oxygen desaturation, and the presence of coexistent obstructive sleep apnea. With lower baseline oxygenation and abnormal respiratory mechanics in patients with severe emphysema, alterations in ventilatory control and respiratory muscle function that normally occur during sleep can have profound effects, and contribute to the development of sleep abnormalities. The impact on quality of life, cardiopulmonary hemodynamics, and overall survival remains uncertain. In addition, treatment for chronic obstructive pulmonary disease and its effect on sleep abnormalities have demonstrated conflicting results. More recently, as part of the National Emphysema Treatment Trial, lung volume reduction surgery has been shown to improve both sleep quality and nocturnal oxygenation in emphysema. Although indications for performing an overnight polysomnogram in patients with emphysema have been debated, recommendations have been presented. Future studies investigating disease mechanism and response to therapy in patients with sleep abnormalities and severe emphysema are warranted.

Effects of oxygen therapy on left ventricular function in patients with Cheyne-Stokes respiration and congestive heart failure.

STUDY OBJECTIVES: Whereas both oxygen therapy and nasal continuous positive airway pressure (CPAP) decrease the apnea-hypopnea index (AHI) in patients with Cheyne-Stokes respiration (CSR) and congestive heart failure (CHF), only nasal CPAP is known to affect the left ventricular ejection fraction (LVEF). We therefore evaluated the effects of 1 month of nocturnal oxygen therapy on LVEF. METHODS: Ten patients (52 +/- 12 years) with CHF (LVEF of 12% +/- 5%) and CSR (AHI 57 +/- 61 events/hour) were studied. Polysomnograms identified CSR and were repeated on oxygen initially (oxygen night 1 [2 L/min]) and after 30 nights (oxygen night 2). LVEF was measured by radionuclide ventriculography. RESULTS: Oxygen therapy decreased the AHI from a baseline of 57 +/- 61 to 9 +/- 11 and 12 +/- 17 events per hour during oxygen nights 1 and 2, respectively (p < .05), with no difference between treatment nights. The lowest oxygen saturation increased during oxygen nights 1 and 2, from a baseline of 87% +/- 7% to 94% +/- 4% and 91% +/- 7%, respectively (p < .05), with no difference between treatment nights. The LVEF did not significantly change from a baseline of 22% +/- 11% to 19% +/- 9% after 1 month of nocturnal oxygen (p = .05). Compared to baseline, there was no change in circulation time during oxygen nights 1 and 2, from 24 +/- 8 seconds to 30 +/- 15 seconds and 23 +/- 6 seconds, respectively (p = .2). Total sleep time, sleep efficiency, and sleep architecture, when compared with baseline, remained unchanged during both oxygen therapy nights. CONCLUSIONS: Although 1 month of nocturnal oxygen therapy decreases the AHI in patients with CSR and CHF, there is no improvement in left ventricular function.

Cor pulmonale and sleep-disordered breathing in patients with restrictive lung disease and neuromuscular disorders.

Cor pulmonale frequently develops in patients with restrictive lung disease and neuromuscular disorders. Sleep disordered breathing, including nocturnal hypoventilation and obstructive apnea, has been associated with the development of cor pulmonale and may affect morbidity. The mechanisms responsible for sleep disordered breathing include defects in the control of breathing, respiratory muscle dysfunction, and abnormalities in chest wall and lung compliance. Symptoms of disturbed sleep may allow patients with sleep disordered breathing to be appropriately diagnosed and treated, often with nocturnal ventilation, before the development of right-sided heart failure.