• Users Online: 278
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 10  |  Issue : 1  |  Page : 32-39

Sleep patterns in table chronic obstructive pulmonary disease patients at a tertiary care center: a hospital-based observational study


1 Department of Pulmonary Medicine, Moti Lal Nehru Medical College, Prayagraj, Uttar Pradesh, India
2 Department of Tuberculosis and Respiratory Diseases, Ganesh Shankar Vidyarthi Memorial Medical College, Kanpur, Uttar Pradesh, India
3 Department of Respiratory Medicine, King George’s Medical University, Lucknow, Uttar Pradesh, India
4 Department of Medicine, Ganesh Shankar Vidyarthi Memorial Medical College, Kanpur, Uttar Pradesh, India
5 Department of Medicine, King George’s Medical University, Lucknow, Uttar Pradesh, India

Date of Submission17-Apr-2021
Date of Acceptance28-Jun-2021
Date of Web Publication19-Apr-2022

Correspondence Address:
Dr. Ajay Kumar Verma
Department of Respiratory Medicine, King George’s Medical University, Lucknow, Uttar Pradesh, 226003
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jacp.jacp_19_21

Rights and Permissions
  Abstract 


Introduction: Sleep has significant adverse consequences for breathing and gas exchange in patients with chronic obstructive pulmonary disease (COPD). This study aimed to assess sleep patterns in patients with stable COPD. Patients and methods: Patients with stable COPD were recruited from a tertiary care hospital. Data collected included demographic profile, clinical characteristics of COPD, neck circumference, Epworth sleepiness scale (ESS) score, and sleep variables using polysomnography. Results: Of recruited 40 patients, 12 fulfilled the inclusion criteria. The mean age of the patients was 57.42 ± 10.98 years and 11 were males. Eight patients (66.7%) had moderately severe COPD, three mild, and one severe COPD. Eleven patients had a normal ESS score. None had excessive day-time sleepiness. High numbers of arousal and sleep-stage change characterized major sleep fragmentation were reported in these individuals. Apnea–hypopnea index was normal, that is, 3.2 ± 1.9 (mean ± standard deviation [SD]). The total sleep time with hemoglobin saturation under 90% (T90) was 48.17 ± 5.79 minutes (mean ± SD). Hemoglobin saturation fell more in rapid eye movement (REM) sleep (87.1% ± 5.5%) than non-REM sleep (88.6% ± 4.8%). Sleep-onset latencies were 19.21 ± 4.68 (mean ± SD) minutes and REM latency was 126 ± 9.39 (mean ± SD) minutes. The mean %wake stage, mean% Stage 1 sleep, and mean% Stage 2 sleep were prolonged in most patients, whereas REM sleep was decreased in all patients. Conclusion: Sleep is characterized by major sleep fragmentation even in patients with stable COPD. Extent and duration of desaturation during sleep are significant. Wake stage, Stage 1, and Stage 2 sleep are prolonged in most patients. REM sleep is decreased in all patients.

Keywords: Chronic obstructive pulmonary disease, hemoglobin desaturation, polysomnography, sleep patterns


How to cite this article:
Singh A, Chaudhri S, Pandey AK, Verma AK, Kumar N, Kant S, Chaudhary SC. Sleep patterns in table chronic obstructive pulmonary disease patients at a tertiary care center: a hospital-based observational study. J Assoc Chest Physicians 2022;10:32-9

How to cite this URL:
Singh A, Chaudhri S, Pandey AK, Verma AK, Kumar N, Kant S, Chaudhary SC. Sleep patterns in table chronic obstructive pulmonary disease patients at a tertiary care center: a hospital-based observational study. J Assoc Chest Physicians [serial online] 2022 [cited 2022 May 28];10:32-9. Available from: https://www.jacpjournal.org/text.asp?2022/10/1/32/339686




  Introduction Top


Chronic obstructive pulmonary disease (COPD) is a crucial respiratory problem across the globe. One significant reason for morbidity in COPD populace is anomaly in gas exchange and resultant hypoxemia. Sleep has significant adverse consequences for breathing and gas exchange in patients with COPD.[1],[2] Typical sleep is a profoundly organized, complex neurologic procedure that includes a wide range of focuses inside the mind that influences the functioning of most significant organ frameworks including the respiratory framework and our physical and psychological wellness from multiple points of view.[3] During sleep, typically, there are five periods of rest: Stages 1, 2, 3, 4, and rapid eye movement (REM).

Sleep-associated problems and insomnia in COPD were increased in comparison with the general population.[1] Due to interrupted sleep, COPD severity, exacerbations, and mortality were increased.[2] Furthermore, poor sleeping decreases the quality of life in patients with COPD.[4],[5] There are very few studies on stable COPD and sleep variables. This study was performed to not only assess the sleep patterns but also to correlate gasometric, spirometric, and polysomnographic variables in patients with stable COPD.


  Materials and methods Top


Study design and population

The present study was conducted in the department of tuberculosis and respiratory diseases in a tertiary care center. Patients diagnosed to have COPD according to the Global Initiative for Chronic Obstructive Lung Disease criteria[6] and who were free from acute exacerbations for at least 4 weeks (stable condition) before enrollment in the study were included. Patients with diabetes mellitus, cardiovascular diseases, pregnant women, and obese patients (body mass index >30 kg/m2) were excluded from the study.

A total of 40 individuals attending the outpatient department were recruited for the study. Informed written consent was obtained from all the participants prior to enrolling in this study. Of these 40 recruited individuals, 6 were diagnosed with asthma and 16 were excluded due to obesity, diabetes, hypertension, and/or cardiovascular diseases. A total of 18 patients were diagnosed with COPD without any other disease. Four patients were excluded due to acute exacerbation. The remaining 14 patients were subjected to complete clinical examination and investigations such as a complete hemogram, fasting and postprandial blood sugar, thyroid-stimulating hormone, free T3 and T4 levels, electrocardiography (ECG), echocardiogram, and a chest X-ray. Two patients were unable to sleep for whole night during polysomnography (PSG) and were excluded from the analysis. Thus, there remained 12 patients on whom analysis was performed.

Demographic data such as age, gender, neck circumference, body mass index, alcohol consumption, smoking history, severity of COPD, and Epworth sleepiness scale (ESS) score were collected from these patients.

Polysomnography test

The patients were suggested to maintain a sleep diary for 7 days to know about their sleep habits and regularity. They were questioned as per the ESS score to determine if they had excessive day-time sleepiness. The patients were called into the hospital one night prior to the test day and were allowed to sleep in laboratory to help familiarize them with the surroundings and minimize the first night effect.[7] On the next night, PSG was performed. The sleep timings were according to the sleep rhythm of individual patients as noted in their sleep diary. Prior to PSG, an “arterial blood gas” analysis was carried out in every patient, using ROCHE Blood Gas Analyzer (Roche Diagnostics International AG, Rotkreuz, Switzerland). PSG test was performed by PSG instrument (Embla N7000, Medcare Flaga, Sidumui 24,108 Reykjavik, Iceland) for the whole night. During recording electroencephalogram, electromyogram, electro-oculogram, ECG, nasal airflow sensor, chest/abdomen belts, pulse oximetry, and snore microphone channels were used. Overnight sleep parameters were collected and stored in the computer. Electrodes were applied on the basis of the “10 to 20 system” of the International Federation of Societies for Electroencephalography and Clinical Neurophysiology.[8],[9],[10],[11] The total sleep time (TST) and the relative proportion of the night spent in each of the sleep stages were calculated.[9],[12] Sleep-onset latencies (SOLs), REM sleep (REM latency), and slow-wave sleep (SWS) were also reported.


  Results Top


Sociodemographic and clinical characteristics

Sociodemographic and clinical characteristics of studied population are summarized in [Table 1]. Of the 12 patients (mean age: 57.42 ± 10.98 years), 11 were males. All patients were married. Seven patients (58.3%) were smokers. Eight patients (66.7%) had moderately severe COPD, three (25%) had mild COPD, and one (8.3%) had severe COPD. Most of them were of normal weight. Eleven patients had a normal ESS score. None of the patients showed excessive day-time sleepiness. None of the patients had increased neck circumference. The mean PaO2 value was 61.49 ± 2.68 and the mean partial pressure of CO2 (PaCO2) was 41.96 ± 3.25 mmHg.
Table 1 Socio-demographic and clinical characteristics of patients

Click here to view


Polysomnographic variables and respiratory variables at polysomnography

Polysomnographic and respiratory variables at PSG are summarized in [Table 2]. The mean total recording time from the 12 patients was 443.75 ± 19.16 minutes, and the mean TST was 354.93 ± 19.91 minutes. Only three patients (25%) had reduced TST, whereas others had normal values. The mean sleep efficiency (SE{%}) was reduced to 79.98% ± 2.45%. The mean leg movement observed was 0.17 ± 0.39, which was within normal limits. Periodic leg movement disorder (PLMD) was not observed in this sample. High numbers of arousal (107.1 ± 11.07) and sleep-stage change (SC) (89.17 ± 8.09) characterized major sleep fragmentation were reported in these individuals. The mean apnea–hypopnea index (AHI) was 3.2 ± 1.90, which belonged to the normal range, and hence, snoring observed in this group was simple snoring. All patients had a high TST with hemoglobin saturation under 90% (T90 = 48.17 ± 5.79 minutes), making them prone to adversities due to poor oxygenation. The mean hemoglobin saturation of the group was 90.58% ± 1.78%. The average hemoglobin saturation in REM and non-rapid eye movement (NREM) sleep was lower than 90%. Hemoglobin saturation fell more in REM sleep (87.1% ± 5.5%) than NREM sleep (88.6% ± 4.8%).
Table 2 Polysomnographic variables and respiratory variables at polysomnography

Click here to view


Sleep-onset latencies and rapid eye movement latencies among patients

The mean SOL was 19.21 ± 4.68 minutes in these individuals [Table 3]. Seven patients (58.3%) had normal values and five (41.7%) had prolonged values. The mean REM latency was 126 ± 9.39 minutes. Nine patients (75%) had prolonged values and five (25%) had normal values [Table 3].
Table 3 Sleep onset latencies (SOL) and rapid eye movement (REM) latencies among patients

Click here to view


Distribution of various sleep stages

The mean % wake stage for 12 patients was 16.25 ± 3.05. Only one patient (8.3%) had a normal value, whereas the rest had prolonged wake stage. The mean % Stage 1 sleep (% S1) was 14.17 ± 3.56, in which five patients (41.7%) were within normal limits. The mean % Stage 2 sleep (% S2) was 75.17 ± 3.99 minutes. All patients had prolonged % S2. The mean % Stage ¾ sleep (% S3/4) was 4.25 ± 3.65. Patients were lying within the normal range on lower side of their respective values. The mean % REM sleep was 6.42 ± 3.63. All patients had decreased REM sleep [Table 4].
Table 4 Distribution of various sleep stages

Click here to view


Correlation of sleep parameters

A significant inverse correlation (r = −0.6009 and P = 0.0388 [<0.05]) was observed between PaCO2 and forced expiratory volume in 1 second/forced vital capacity %, indicating that more severe the obstruction, the higher were the PaCO2 levels [Figure 1]a. A significant positive correlation was found between PaCO2 and T90 (duration of desaturation − hemoglobin saturation under 90%) (r = 0.7667 and P = 0.0036) [Figure 1]b, indicating that higher levels of PaCO2 correlated directly with T90 as a fraction of TST. Similarly, a significant inverse correlation was observed between PaO2 and T90 (r = −0.6250 and P = 0.0298) [Figure 1]c.
Figure 1 Correlation of sleep parameters. A significant inverse correlation (r = ‒0.6009, and P = 0.0388 [<0.05]) was observed between PaCO2 and FEV1/FVC % depicted in panel (a). Panel (b) represents the significant positive correlation of PaCO2 and T90 (r = 0.7667, and P = 0.0036). A significant inverse correlation was seen found between PaO2 and T90 (r = ‒0.6250, and P = 0.0298], in panel (c). Panel (d) represents significant inverse correlation between % S3/S4 sleep and BM (r = ‒0.8669, P = 0.0003). Panel (e) represents a significant inverse correlation of % S3/S4 sleep and AHI (r = ‒0.8925, P = <0.0001). Panel (f) depicts a significant positive correlation between REM HR and AHI (r = 0.8366, P = 0.0007). Panel (g) depicts a significant inverse correlation of % S3/S4 sleep and % S1 (r = ‒0.8151, P = 0.0012 [<0.05]). Panel (h) represents a significant positive correlation between REM latency, and sleep-stage change (r = 0.9489, P < 0.0001). Panel (i) represents nonsignificant correlation of % REM sleep and AHI (r = ‒0.384, P = 0.2179), indicates that higher numbers of AHI may be associated with decreased percentage of REM sleep.

Click here to view


A significant inverse correlation was observed between % S3/S4 sleep and body movement (BM) (r = −0.8669 and P = 0.0003) [Figure 1]d, characterizing the shallowness of sleep, more fragmentation of sleep which indicates poor quality of sleep. A significant inverse correlation was found between %S3/S4 sleep (SWS) and %Stage 1 sleep (r = −0.8151 and P = 0.0012 [<0.05]) [Figure 1]e, indicating that lower the percentage of SWS, the higher will be the %Stage 1 sleep. A significant inverse correlation was observed between %S3/S4 sleep (SWS) and AHI (r = −0.8925 and P ≤ 0.0001) [Figure 1]f, indicating that those who have higher AHI will also have lower percentage of deep sleep or SWS.

A significant positive correlation was observed between REM latency and sleep SC (r = 0.9489 and P < 0.0001) [Figure 1]g, suggesting that patients with COPD have increased REM latency thereby having increased numbers of changes in sleep stages (SC), that is, a fragmented sleep architecture. A significant positive correlation was found between REM heart rate (REM HR) and AHI (r = 0.8366 and P = 0.0007) [Figure 1]h, indicating that during REM sleep, “postapnea tachycardia” occurs which leads to more numbers of arousals, awakening, and BMs (i.e., poor quality sleep). An inverse correlation (nonsignificant) was observed between %REM sleep and AHI (r = −0.384 and P = 0.2179) [Figure 1]i, indicating that higher numbers of AHI may be associated with decreased percentage of REM sleep.


  Discussion Top


Sleep disturbances are observed in patients with COPD. Symptoms related to sleep disturbances are in the form of early awakenings, day-time fatigue, lack of energy, impaired cognitive function, anxiety, reduced coping ability, reduced exercise tolerance, and excessive day-time sleepiness.[13] Various studies in COPD have reported an increase in sleep SCs, increase in SOL, increase in REM latency, frequent arousals, awakenings, decreased TST (summed Stages 1, 2, 3, 4, and REM), and nocturnal hypoxemia, especially during REM sleep.

The drop in metabolic rate that happens during sleep affects the respiratory framework. The physiologic components controlling breathing are similar to those of the conscious state, yet their intensity is modified during sleep in patients with COPD.[14] These effects include diminished ventilatory drive, increase in upper airway resistance, increased PaCO2 in arterial blood, diminished partial pressure of oxygen in arterial blood (PaO2), impaired respiratory muscle activity, decreased intercostal muscle action, reduced tidal volume (VT), decreased minute ventilation, and reduced functional residual capacity (FRC).[15]

Sleep is related with decreased responsiveness of the respiratory focus to compound mechanical and cortical sources of information, especially during REM sleep.[7] Moreover, this responsiveness gets disintegrated while resting, especially during REM, in spite of the fact that the diaphragm is less influenced than the accessory muscles.[7] There is an abatement in minute ventilation during non-REM sleep and increases further during REM sleep. The VT decreases, and as a result, there is an increase in end-tidal PCO2.[7] During REM sleep, both VT and respiratory rate are more significant factors than in non-REM sleep, especially during phasic REM.[7]

In the present study, we have evaluated the sleep parameters in patients with stable COPD. Poor sleep quality was found in patients with stable COPD. Oxygen saturation fell during sleep in more than half of the patients (58.3%), especially in REM sleep. The most likely cause was interference of gas exchange due to hypoventilation. Littner et al.[16] concluded similarly that patients with COPD are predisposed to develop severe nonapneic oxygen desaturation during REM sleep. Another study also reported arterial oxygen desaturation in patients with COPD, especially in the REM sleep.[17]

With regard to day-time somnolence, the Epworth sleepiness mean score was termed as nonhypersomnolent. None of the patients showed excessive day-time sleepiness; similarly Orr et al.[18] demonstrated that patients with COPD exhibited a normal mean multiple sleep latency test, regardless of short TST and many arousals from sleep. Contrary to our result, Cormick et al.[19] reported that patients with chronic obstructive lung disease had more day-time sleepiness than healthy controls. It was observed that the number of arousals as well as sleep SC was elevated. Large numbers of overnight arousals lead to sleep fragmentation, in accordance with our observation. McNicholas[7] has shown poor sleep quality, as judged by marked increase in sleep SCs, frequent arousals and awakening, and decreased TST with higher number of arousals in patients with COPD.

Our data were in line with Svorc et al.[20] that all patients had low percentage of SE. It was believed that the lowered value was due to the chronic respiratory failure, frequent arousals, and fragmented sleep. Likewise, dos Santos and Viegas[21] reported that patients with COPD have poor sleep quality in the form of low SE, high number of awakenings, and rapid shift of sleep stages.

Leg movements, in our sample, were within the normal range, but Saletu et al.[22] have shown that PLMD was found in many sleep disorders and can cause greater number of arousals. In the present study, higher BMs indicate that such patients had poor sleep quality by increased numbers of sleep stage shift and decreased percentage of SWS.

The SOL of seven patients (58.3%) had normal values and five (41.7%) had prolonged values. Regarding REM latency, nine patients (75%) had prolonged values. Similar observations were noted by Zanchet et al.[23] that patients with COPD had fragmented sleep, characterized by increasing the time of wakefulness during the entire period of sleep and high rate of awakenings.

Considering the distribution of sleep stages, none of the studied patients preserved normal pattern. Percentage (%) wake, % Stage 1, % Stage 2, and % Stage ¾ were elevated in the majority of the patients. One patient (8%) did not present REM sleep. A significant inverse correlation was observed (r = −0.8151; P = 0.0012) between % SWS and % Stage 1 sleep, indicating reduction in SWS with increase in Stage 1 sleep in these patients. Accordingly, Donald[24] had observed that with increasing age, there is downfall in percentage of SWS and REM sleep. These findings are exaggerated in patients with COPD, according to Standards for the Diagnosis and Management of Patients with COPD ATS Guidelines (2004). Polysomnographic studies have shown sleep fragmentation with frequent arousals and reduced SWS and REM sleep.[25]

We found that the mean AHI was 3.28 ± 1.90 and one patient (8.3%) exhibited higher than 5 index, characterizing obstructive sleep apnea (OSA). Guilleminault et al.[26] observed that patients with COPD had raised AHI suggesting the association of COPD and OSA. Chaouat et al.[27] reported that 11% of 265 patients with COPD had showed mixed syndrome.

The mean hemoglobin saturation of the sample was 90.58% ± 1.78%. It is well known that ventilation is reduced during sleep. Other contributing factors observed in patients with COPD were the changes of ventilation/perfusion and lowering of FRC.[20] The same status was observed by Flenley[28] who concluded that hypoxemic episodes in patients with COPD during REM sleep appear to be due to a combination of reduced ventilation, increase in the maldistribution of ventilation to perfusion, and a reduction in FRC. Patients in this study presented with a high TST with hemoglobin saturation under 90% (T90 = 48.17% ± 5.79%), which makes them more susceptible to the complications of poor oxygenation. McNicholas and Fitzgerald[29] concluded that patients admitted to hospital with an acute exacerbation of chronic bronchitis and emphysema should be carefully monitored at night, especially if they have hypercapnia. According to the American Thoracic Society (ATS) Guidelines (2004), patients with COPD desaturated during sleep and it is due to the disease itself, not due to sleep apnea, and the desaturation may be greater during extensive exercise.[11]

Correlations between sleep variables such as SWS percentage, REM sleep with BMs, and SCs were found statistically significant. It implies that the lower the level of SWS and REM sleep, the higher will be SC and BMs, portraying the sleep shallowness in these people. Fleetham et al.[17] had watched poor sleep quality as evidenced by diminished TST during room air breathing. Feelings of excitement were unequivocally connected with times of blood vessel oxygen desaturation. Cutler et al.[30] reported that basic changes happen in the airway route to obstruct airflow during OSA and the subsequent apnea actuates hypoxic and hypercapnic reflexes, which upgrades the thoughtful nerve movement and patterned changes in parasympathetic nerve action. Stege et al.[31] had reported that sleep quality was significantly affected in numerous patients with COPD and may be further worsened when comorbidities were present.


  Conclusion Top


Deprived sleep quality is present among patients with stable COPD and may not be related to hypoventilation. Further studies on large population are warranted.

Acknowledgment

Authors are grateful to participants for their participation in the study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Klink M, Quan SF. Prevalence of reported sleep disturbances in a general adult population and their relationship to obstructive airways diseases. Chest 1987;91:540-6.  Back to cited text no. 1
    
2.
Malhotra M, Sachdeva R, Sachdeva S. Assessment of sleep and quality of life among Chronic Obstructive Airways Disease patients. J Assoc Chest Physicians 2018;6:45-52.  Back to cited text no. 2
  [Full text]  
3.
Kant S, Kapoor N, Verma AK et al. Psychiatric manifestations in the patients of obstructive sleep apnea at tertiary care center of Northern India. Indian J Respir Care 2019;8:84-6.  Back to cited text no. 3
  [Full text]  
4.
Nunes DM, Mota RM, de Pontes Neto OL, Pereira ED, de Bruin VM, de Bruin PF. Impaired sleep reduces quality of life in chronic obstructive pulmonary disease. Lung 2009;187:159-63.  Back to cited text no. 4
    
5.
Sharafkhaneh A, Jayaraman G, Kaleekal T, Sharafkhaneh H, Hirshkowitz M. Sleep disorders and their management in patients with COPD. Ther Adv Respir Dis 2009;3:309-18.  Back to cited text no. 5
    
6.
Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management and Prevention of COPD. Updated 2008. Available at http://www.goldcopd.com. Accessed March 25, 2008.  Back to cited text no. 6
    
7.
McNicholas WT. Impact of sleep in COPD. Chest 2000;117:48S-53S.  Back to cited text no. 7
    
8.
Jasper HH. The 10--20 electrode system of the International Federation. Electroencephalogr Clin Neurophysiol 1958;10:370-5.  Back to cited text no. 8
    
9.
Foldvary N. Sleep and epilepsy. Curr Treat Options Neurol 2002;4:129-35.  Back to cited text no. 9
    
10.
Agnew HW Jr, Webb WB, Williams RL. The first night effect: An EEG study of sleep. Psychophysiology 1966;2:263-6.  Back to cited text no. 10
    
11.
Celli BR, MacNee W, ATS/ERS Task Force. Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J 2004;23:932-46.  Back to cited text no. 11
    
12.
Born J, DeKloet ER, Wenz H, Kern W, Fehm HL. Gluco- and antimineralocorticoid effects on human sleep: a role of central corticosteroid receptors. Am J Physiol 1991;260:E183-8.  Back to cited text no. 12
    
13.
Budhiraja R, Siddiqi TA, Quan SF. Sleep disorders in chronic obstructive pulmonary disease: etiology, impact, and management. J Clin Sleep Med 2015;11:259-70.  Back to cited text no. 13
    
14.
Ramar K. Sleep problems in chronic obstructive pulmonary disease. Turk Toraks Dergisi/Turkish Thoracic J 2008;9:117-23.  Back to cited text no. 14
    
15.
Milross MA, Piper AJ, Dobbin CJ, Bye PT, Grunstein RR. Sleep disordered breathing in cystic fibrosis. Sleep Med Rev 2004;8:295-308.  Back to cited text no. 15
    
16.
Littner MR, McGinty DJ, Arand DL. Determinants of oxygen desaturation in the course of ventilation during sleep in chronic obstructive pulmonary disease. Am Rev Respir Dis 1980;122:849-57.  Back to cited text no. 16
    
17.
Fleetham J, West P, Mezon B, Conway W, Roth T, Kryger M. Sleep, arousals, and oxygen desaturation in chronic obstructive pulmonary disease. The effect of oxygen therapy. Am Rev Respir Dis 1982;126:429-33.  Back to cited text no. 17
    
18.
Orr WC, Shamma-Othman Z, Levin D, Othman J, Rundell OH. Persistent hypoxemia and excessive daytime sleepiness in chronic obstructive pulmonary disease (COPD). Chest 1990;97:583-5.  Back to cited text no. 18
    
19.
Cormick W, Olson LG, Hensley MJ, Saunders NA. Nocturnal hypoxaemia and quality of sleep in patients with chronic obstructive lung disease. Thorax 1986;41:846-54.  Back to cited text no. 19
    
20.
Svorc P, Bacova I, Svorc P Jr., Novakova M, Marossy A. Chronobiological aspects of impact of apnoic episode and reoxygenation on the electrical myocardial properties and autonomic nervous system activity in Wistar rats. Cardiac Arrhythmias: Mechanisms, Pathophysiology, and Treatment. 2014;12:45. http://dx.doi.org/10.5772/57168  Back to cited text no. 20
    
21.
dos Santos CE, Viegas CA. Sleep pattern in patients with chronic obstructive pulmonary disease and correlation among gasometric, spirometric, and polysomnographic variables. J Pneumol 2003;29:69-74.  Back to cited text no. 21
    
22.
Saletu M, Anderer P, Saletu B et al. Sleep laboratory studies in periodic limb movement disorder (PLMD) patients as compared with normals and acute effects of ropinirole. Hum Psychopharmacol 2001;16:177-87.  Back to cited text no. 22
    
23.
Zanchet CR, de Assis Lima VC, do Socorro Macêdo T. Influence of pulmonary rehabilitation on the pattern of sleep of patients with chronic obstructive pulmonary disease. J Bras Pneumol 2004;30:439-44.  Back to cited text no. 23
    
24.
Donald LB. Sleep in normal aging and dementia. Sleep 1993;16:140-81.  Back to cited text no. 24
    
25.
Vardar-Yagli N, Saglam M, Savci S et al. Impact of sleep quality on functional capacity, peripheral muscle strength and quality of life in patients with chronic obstructive pulmonary disease. Expert Rev Respir Med 2015;9:233-9.  Back to cited text no. 25
    
26.
Guilleminault C, Cummiskey J, Motta J. Chronic obstructive airflow disease and sleep studies. Am Rev Respir Dis 1980;122:397-406.  Back to cited text no. 26
    
27.
Chaouat A, Weitzenblum E, Krieger J, Ifoundza T, Oswald M, Kessler R. Association of chronic obstructive pulmonary disease and sleep apnea syndrome. Am J Respir Crit Care Med 1995;151:82-6.  Back to cited text no. 27
    
28.
Flenley DC. Sleep in chronic obstructive lung disease. Clin Chest Med 1985;6:651-61.  Back to cited text no. 28
    
29.
McNicholas WT, Fitzgerald MX. Nocturnal deaths among patients with chronic bronchitis and emphysema. Br Med J (Clin Res Ed) 1984;289:878.  Back to cited text no. 29
    
30.
Cutler MJ, Hamdan AL, Hamdan MH, Ramaswamy K, Smith ML. Sleep apnea: from the nose to the heart. J Am Board Fam Pract 2002;15:128-41.  Back to cited text no. 30
    
31.
Stege G, Vos PJ, van den Elshout FJ, Richard Dekhuijzen PN, van de Ven MJ, Heijdra YF. Sleep, hypnotics and chronic obstructive pulmonary disease. Respir Med 2008;102:801-14.  Back to cited text no. 31
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Materials and me...
Results
Discussion
Conclusion
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed264    
    Printed4    
    Emailed0    
    PDF Downloaded24    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]