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13 Obstructive Sleep Apnea (OSA) andGastroenterology
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S.Lee and collaborators were the rst to demonstrate that OSA was associated with colorectal cancer [18], and they attempted to eliminate the potential confound­ing effects of obesity by controlling BMI.They performed a retrospective study diagnosing OSA in patients who underwent overnight polysomnography (PSG) and compared the prevalence of colorectal neoplasia between patients with or without OSA according to the PSG results. For each patient with OSA, they matched one or two controls by age, BMI, sex, and smoking and did a screening colonoscopy for the rst time. This study found an OR for detecting colorectal neoplasia in patients with OSA of 3.03 times greater than controls.
Another study by Yang-Chen and collaborators in Taiwan identied more than 4000 patients with a new diagnosis of OSA, and they were compared with more than 16,000 controls from a National database. They found that patients with OSA were associated with a signicantly higher risk of colorectal cancer (HR 1.80; 95% CI,
1.28–2.52). This association was related to more frequent visits to the doctor [19].
Tumorigenesis has three stages: initiation, promotion, and progression [20, 21]. The rst stage is initiated by DNA mutations that activate oncogenes and inactivate tumor suppressor genes. Tumor promotion involves the reproduction of the mutated cells. Inammatory cytokines such as interleukins 1 and 6 and tumor necrosis factor α contribute to the growth of the tumor. However, the role of OSA in colorectal tumorigenesis remains obscure.
Abrams and colleagues suggest that hypoxia during OSA could be associated with the regression of tumors [22]. Hypoxia induces reactive oxygen species, which activates the NF-κB signal pathway that regulates various genes associated with colorectal tumor development and growth [23].
Therefore, further studies are needed to establish the mechanisms between OSA and colorectal cancer. At the same time, physicians should be aware of the associa­tion between OSA and the development of colorectal neoplasia and explain the need for colonoscopy to patients with OSA.The latter are eligible for colorectal cancer screening (Fig.13.2).
Fig. 13.2 Rectal adenocarcinoma as seen in colonoscopy
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C. A. Cortez-Hernández and J. C. Cessa-Zanatta
13.3 Obstructive Sleep Apnea (OSA) andGERD
GERD is a frequent disorder; one in ve adults will have this disease in the United States. It is an entity essential to recognize because it can cause Barrett’s esophagus and esophageal adenocarcinoma. Worldwide studies demonstrate obesity as a risk factor for GERD and esophageal adenocarcinoma [24].
Epidemiological studies demonstrated that obese people have a higher GERD prevalence compared to nonobese patients. Over more than 10,545 patients partici­pating in the Nurses’ Health Study were asked to ll a supplemental GERD ques­tionnaire, which showed that weekly symptoms had a linear increase in the adjusted OR for reux symptoms for each BMI group [25]. Similar results were obtained in a cross-sectional study with more than 80,000 patients [26].
Also the higher prevalence of erosive esophagitis in obese patients was demon­strated in a study by El-Serag etal. in which an endoscopy was made to 196 patients with weekly heartburn or regurgitation symptoms. They found esophageal erosions in 39% of overweight patients and in 41% of obese patients. This study concluded that obese participant (BMI>30) had twice the chance of having esophageal ero­sions or reux symptoms compared to nonobese participants (BMI < 25) [27]. Another study by Jacobson etal. showed that raising BMI by more than 3.5kg/m2 was associated with more frequent reux symptoms, compared to no increase at all [25].
OSA is believed to be related to GERD, but evidence at the moment hasn’t been conclusive. A meta-analysis performed [28] to identify the association between obstructive sleep apnea hypopnea syndrome and gastroesophageal reux disease, analyzing a total of 2699 patients, found a signicant relationship between obstruc­tive sleep apnea syndrome and gastroesophageal reux disease, with a pooled OR of 1.75 (95% CI 1.18–2.59, p<0.05).
Hormonal disorders observed in OSA may be relevant to the development of GERD.A study performed by Pardak and collaborators [29] aimed to assess the correlations between ghrelin, obestatin, leptin, and GERD intensity in patients with OSA through a survey. This was performed relating symptoms of GERD, gastros­copy, and esophageal pH monitoring. They concluded that in patients with OSA, GERD was twice as common compared to the group without OSA.Among subjects with severe sleep apnea (apnea hypopnea index (AHI)> 30; n = 31; 53%), we observed lower ghrelin levels, especially in the second half of the night and in the morning (p5.00 = 0.0207; p7.00 = 0.0344); the presence of OSA did not affect obestatin and leptin levels.
Finally, Shepherd et al. compare reux events day and night in obese and non­obese individuals with obstructive sleep apnea (OSA) and obese individuals without OSA. They found that BMI signicantly predicted the number of acidic reux events (r2=0.16, p=0.01) during the 24 hours, but OSA didn’t show an association with GERD severity [30] (Fig.13.3).
13 Obstructive Sleep Apnea (OSA) andGastroenterology
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Fig. 13.3 Los Angeles Grade B esophagitis as seen on superior endoscopy
257
Take-Home Message
• Obstructive sleep apnea (OSA) has been associated with nonalcoholic fatty liver
disease (NAFLD) in adult and pediatric populations, liver brosis, and colorectal
cancer. The mechanisms that produce these problems are multiple.
• OSA is believed to be related to GERD, but current evidence is inconclusive.
References
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2. Parikh MP, Gupta NM, McCullough AJ.Obstructive sleep apnea and the liver. Clin Liver Dis. 2019;23:363–82.
3. Trzepizur W, etal. Association between severity of obstructive sleep apnea and blood markers of liver injury. Clin Gastroenterol Hepatol. 2016;14:1657–61.
4. Hui DS, Shang Q, Ko FW, Ng SS, Szeto CC, etal. A prospective cohort study of the long-term effects of CPAP on carotid artery intima-media thickness in obstructive sleep apnea syndrome. Respir Res. 2012;13(1):22.
5. Marin JM, Carrizo SJ, Vicente E, Agusti AG.Long-term cardiovascular outcomes in men with obstructive sleep apnoeahypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005;365(9464):1046–53.
6. Liu X, Miao Y, Wu F, etal. Effect of CPAP therapy on liver disease in patients with OSA: a review. Sleep Breath. 2018:963–72.
7. Lévy P, Bonsignore MR, Eckel J. Sleep, sleep-disordered breathing and metabolic conse­quences. Eur Respir J. 2009;34(1):243–60.
8. Buzzetti E, Pinzani M, Tsochatzis EA.The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). Metabolism. 2016;65(8):1038–48.
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9. Guilherme, A., Virbasius, J. v., etal. (2008). Adipocyte dysfunctions linking obesity to insulin resistance and type 2 diabetes. Nat Rev Mol Cell Biol 9 367–377
10. Nobili V, Cutrera R, Liccardo D, etal. Obstructive sleep apnea syndrome affects liver histol­ogy and inammatory cell activation in pediatric nonalcoholic fatty liver disease, regardless of obesity/insulin resistance. Am J Respir Crit Care Med. 2014;189(1):66–76.
11. Mesarwi OA, Shin MK, Drager LF, etal. Lysyl oxidase as a serum biomarker of liver brosis in patients with severe obesity and obstructive sleep apnea. Sleep. 2015;38(10):1583–91.
12. Mesarwi OA, Shin MK, Bevans-Fonti S, etal. Hepatocyte hypoxia inducible factor-1 mediates the development of liver brosis in a mouse model of nonalcoholic fatty liver disease. PloS One. 2016;11(12):e0168572.
13. Ferlay J, Soerjomataram I, Dikshit R, etal. Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012. Int J Cancer. 2015;136(5):E359–86.
14. Flood DM, Weiss NS, Cook LS, et al. Colorectal cancer incidence in Asian migrants to the United States and their descendants. Cancer Causes Control. 2000;11(5):403–11.
15. World Cancer Research Fund/American Institute for Cancer Research (2011) Continuous update project report: colorectal cancer 2011 report—food, nutrition, physical activity, and the prevention of colorectal cancer.
16. Johnson CM, Wei C, Ensor JE, etal. Meta-analyses of colorectal cancer risk factors. Cancer Causes Control. 2013;24(6):1207–22.
17. Weitz J, Koch M, Debus J, etal. Colorectal cancer. Lancet. 2005;365(9454):153–65.
18. Lee S, Kim BG, Kim JW, etal. Obstructive sleep apnea is associated with an increased risk of colorectal neoplasia. Gastrointest Endosc. 2017;85(3):568–573.e1.
19. Chen CY, Hu JM, Shen CJ, et al. Increased incidence of colorectal cancer with obstructive sleep apnea: a nationwide population-based cohort study. Sleep Med. 2020;66:15–20.
20. Liang PS, Chen TY, Giovaaucci E.Cigarette smoking and colorectal cancer incidence and mortality: Systematic review and meta-analysis. Int J Cancer. 2009;124:2406–15.
21. Buysse DJ.Sleep health: can we dene it? Does it matter? Sleep. 2014;37:9–17.
22. Toffoli S, Michiels C.Intermittent hypoxia is a key regulator of cancer cell and endothelial cell interplay in tumours. FEBS J. 2008;275:2991–3002.
23. Almendros I, Montserrat JM, Ramírez J, etal. Intermittent hypoxia enhances cancer progres­sion in a mouse model of sleep apnoea. Eur Respir J. 2012;39:215–7.
24. El-Serag H. The association between obesity and GERD: a review of the epidemiological evidence. Dig Dis Sci. 2008;53(9):2307–12.
25. Jacobson BC, Somers SC, Fuchs CS, etal. Body-mass index and symptoms of gastroesopha­geal reux in women. N Engl J Med. 2006;354(22):2340–8.
26. Corley DA, Kubo A, Zhao W.Abdominal obesity, ethnicity and gastro-oesophageal reux symptoms. Gut. 2007;56(6):756–62.
27. El-Serag HB, Graham DY, Satia JA, etal. Obesity is an independent risk factor for GERD symptoms and erosive esophagitis. Am J Gastroenterol. 2005;100(6):1243–50.
28. Wu ZH, Yang XP, etal. The relationship between obstructive sleep apnea hypopnea syndrome and gastroesophageal reux disease: a meta-analysis. Sleep Breath. 2019;23(2):389–97.
29. Pardak P, Filip R, Woliński J, etal. Associations of obstructive sleep apnea, obestatin, leptin, and ghrelin with gastroesophageal reux. J Clin Med. 2021;10(21):5195.
30. Shepherd K, Orr W.Mechanism of gastroesophageal reux in obstructive sleep apnea: airway obstruction or obesity? J Clin Sleep Med. 2016;12(1):87–94.
C. A. Cortez-Hernández and J. C. Cessa-Zanatta
Sleep-Disordered Breathing:
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AnExpanding Spectrum
14
forthePulmonologist
QantaA.A.Ahmed
14.1 Sleep Medicine asClinical Frontier:
Personal Perspectives
It is difcult to convey to those outside of the eld of sleep medicine how even today, we are practicing at the nascent frontier of this extremely exciting eld. Those of us practicing sleep medicine today have been directly trained and educated by the godfathers and pioneers of this discipline. While this is wondrous of its own accord, it also means that transitions within our eld are dramatic and confront us rapidly. It also means that each of us as a sleep specialist has a role to play in the development and advancement of sleep medicine, most impactfully, from within our own clinical practice.
While I have come from a background of pulmonary disease and critical care medicine, I was rst introduced to sleep medicine during my fellowship in NewYork in 1996 through 1999. Shortly after fellowship, I had the privilege of exploring the eld more deeply with the Stanford School of Sleep Medicine, led by Dr. Sharon Keenan as a school distinct from Stanford University but where many Stanford University pioneers of sleep medicine would come to teach newly trained academic and clinical sleep specialists. Those classes left a deep impact on me and have dened my clinical practice since. Every day, I encounter the lack of knowledge about sleep, sleep disorders, healthy sleep, the biological need for sleep, and the
Q. A. A. Ahmed (*) Department of Clinical Medicine, NYU Grossman Long Island School of Medicine, Garden City, NY, USA
NYU Langone Sleep Medicine Associates, Garden City, NY, USA
Division of Pulmonary, Critical Care and Sleep Medicine, NYU Langone Hospital-Long Island, Garden City, NY, USA
Cardiology-Sleep Specialty Center, Garden City, Garden City, NY, USA e-mail: Qanta.Ahmed@nyulangone.org
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 P. M. Baptista et al. (eds.), Obstructive Sleep Apnea,
https://doi.org/10.1007/978-3-031-35225-6_14
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impact of sleep loss and sleep disorders on both health and illness. Everyone involved in his eld must develop an appetite for becoming an ambassador to both the public and our learned colleagues to advance awareness of what is the most important frontier impacting health, disease, and wellness and because of the rela­tionship of sleep disorders with noncommunicable disease in terms of cardiovascu­lar disease, diabetes, and obesity, also determines public health around the world.
It is therefore with this perspective that I bring you not my vantage from the pulmonology standpoint concerning obstructive sleep apnea syndrome but also the expanding spectrum of disorders we encounter and the increased amount of exper­tise beyond the traditional range of breathing abnormalities during sleep that a true sleep specialist in the pulmonary ofce must respond to.
Q. A. A. Ahmed
14.2 Timeline oftheDiscipline
Until 1972, when Stanford University declared the study of clinical sleep medicine a new eld and opened the rst sleep clinic in the world, our understanding of ill­ness and health had been conned to the waking patient over centuries of medical study and practice. Sleep medicine had been the purview of esoteric researchers working in isolated research labs. Onlookers were not clear as to how this eld of exploration would ever lend value to the lives of patients. A mere 20 years after REM sleep was rst identied in 1953 (and named) by then medical student William Dement [1] who would go on to become the founding father of modern sleep medi­cine, clinical sleep medicine opened enquiry of both clinical physiology and pathol­ogy of the sleeping patient, creating new frontiers in the understanding of disease. In 1973, in Italy, Dr. Elio Lugaressi [2] identied heavy snorers disease reporting the rst series of what would become the world’s rst cohort of obstructive sleep apnea patients demonstrating excessive daytime sleepiness obesity and snoring. Less than a decade later, in Australia, Dr. Colin Sullivan [3] would patent the rst prototype for continuous positive airway pressure manufacturing each facemask manually and connecting it to device that was essentially a reversed vacuum cleaner treating over 300 patients in this manner beginning in 1981. Within 10years of that I had graduated medical school and 15years later, I was treating sleep-disordered patients. A decade into my practice as a sleep specialist I referred a patient to receive one of the rst upper airway nerve stimulators for treatment of obstructive sleep apnea syndrome. And less than 5 years later, during this global pandemic, my patients are now being regularly implanted with intelligent nerve stimulators to treat central sleep apnea with transvenous phrenic nerve stimulation. This kind of prox­imity to the origin of my eld makes it extremely exciting to meet patients every day, diagnose, and then treat them—so many of them have been reporting symp­toms to an array of clinicians before the clinical constellation can be recognized by a seasoned, interested sleep specialist. I therefore underline that anybody that is in his eld can exercise an astonishing impact on the surrounding community not only of the patients entrusted to our care but also on our clinical colleagues and the very practice of our clinical discipline.
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While collective focus has been primarily on the physiology, circadian biology and mechanisms of both normal sleep and primary sleep disorders themselves, insights into the impact of systemic disease on sleep and vice versa are only begin­ning to come into view. Those discoveries have been discussed in chapters else­where. This chapter will focus not only on the presentation of obstructive sleep apnea syndrome to the pulmonologist in the setting of lung disease, but the related and unrelated diagnoses that may incidentally appear in our clinical practice. Very important is the recognition of the spectrum of sleep breathing disorders beyond obstructive sleep apnea syndrome and the critically important need to distinguish obstructive sleep apnea from central sleep apnea which today is being claried as novel and cutting-edge technology becomes accessible.
Sleep disorders specialists within pulmonary medicine will encounter diverse patient populations in both adult and pediatric practice. It is very important that we treat both the adult patient that may initially present to us while we additionally perform a comprehensive family history to identify children and younger relatives who may at the moment not be seeking attention. Treating entire families of patients is not uncommon in my practice and I believe a hallmark of good practice while our eld of professionals remains so small.
Sleep disorders are present in a number of systemic conditions that will be dis­cussed in other chapters but will almost always be at play within the pulmonary patient population. It is insufcient for the sleep specialist to know and recognize only the sleep disorder. It is imperative the seasoned sleep specialist understand the impact and interaction of the sleep disorder on the systemic disease. Equally, it is important for the sleep specialist to understand the impact of the systemic disorder on sleep architecture and sleep itself. This is seen very commonly for instance in the coexistence of obstructive sleep apnea with chronic lung disease.
Above all a true sleep specialist must become deeply expert in all aspects of the eld of sleep medicine in order to inform the broader medical community, assist medical colleagues devoted in a discipline to recognize the nuances and manifesta­tions of sleep loss, sleep disorders, circadian rhythm disorders, insufcient sleep hygiene, insufcient sleep syndrome, and many other challenges as to how they impact the patients within their care. Sleep disorders often cluster within families, as do poor habits of sleep. We must care about both challenges. Every time we edu­cate even one of our colleagues, the impact on their patient population will be enor­mous and raising awareness both of the nature of sleep disorders and the impact on specic populations is an enormous public service which I urge you to always keep in mind.
I would also like to underline that here in the United States, sleep medicine is dominated by subspecialists in pulmonary disease and this is not always to the bet­terment of the eld. With most sleep centers in America being managed and directed by pulmonologists, there is a tremendous emphasis and bias toward identifying the most common sleep disorders which relate to obstructive sleep apnea syndrome at the expense of neglecting many other sleep disorders which have tremendous comorbidities associated with them. As we will see in the second part of this chapter one of the most overlooked disorders of breathing and sleep is central sleep apnea
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syndrome and we must work hard to help those patients be recognized and reach denitive treatment. Additionally, also because the eld in the United States is led by pulmonologists, this has resulted in a domination of therapy despite alternatives by positive airway pressure, sometimes at the expense of other extremely well­indicated treatments, surgeries and devices which are not offered to patients includ­ing oral appliance therapy of the mandibular advancement type, upper airway nerve stimulation and targeted oral maxillofacial surgery. It is imperative that every seri­ous sleep specialist that is deeply invested in the eld and her patients cultivate a multidisciplinary practice incorporating expertise relating to the upper airway out­side of the pulmonologists range but incorporating our head and neck otolaryngol­ogy colleagues, our dental sleep medicine colleagues, our EP cardiology colleagues who can place transvenous phrenic nerve stimulation and many other parallel disciplines.
I recognize this is not the mainstream view at the moment in the United States, but it certainly is the future of this eld. If pulmonologists fail to recognize these shifts and treatment options in an environment of an increasingly educated patient populace and policymakers, they will lose their domination of the clinical discipline and that may not be a bad thing for patient care.
Q. A. A. Ahmed
14.3 Sleep Is aBiological Necessity, Not
anExpendable Luxury
This is the rst maxim I teach every patient, every family member of every patient and every fellow training in my discipline. In the modern world, a culture of sleep loss is admired cultivated and emulated. This has disastrous effects and true meta­bolic impacts. Sleep loss must be identied as a physiologic stressor and while it is difcult to address in our contemporary culture of “sleep machismo” it is the rst lesson toward diagnosis and treatment for every person presenting with a sleep com­plaints. The United States, Japan, and Western Europe even in the twenty-rst cen­tury continue to see sleep as an expandable luxury rather than a biological necessity. Japan is the rst place where a word “karoshi” identies death through lack of sleep as occurred at a Toyota manufacturing plant and was rst categorized as an indus­trial injury in 2001 [4].
Rechtschaffen’s investigations [5] are among the rst and most emphatic con­rming that sleep is a biological necessity and that sleep deprivation, whether total or chronic partial deprivation, posed a serious risk for basic metabolic function. Bacterial invasion and gastrointestinal erosions seen in the rats prior to death mimic the ndings of many critically ill patients in intensive care units—environments notorious for sleep deprivation—who go on to die of sepsis and multiorgan failure.
Even more prevalent is the role of sleep deprivation in hyperphagia, blunted satiety signals, and resulting weight gain which is undoubtedly a major driver in the obesity pandemic we nd here in the United States. Additionally, we have seen acutely and painfully in the recent COVID-19 global pandemic that impacted the
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United States so severely as to how obesity strongly drives vulnerabilities in adap­tive and innate immunity responses to SARS Cov2 and is responsible for a compo­nent of the very high death rate we saw here in the United States [6]. Sadly, despite decades of escalating national obesity rates the role of sleep loss driving obesity and metabolic syndrome, the role of sleep-disordered breathing also driving obesity and metabolic syndrome remains severely unrecognized and still unacknowledged in our emerging post pandemic era.
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14.4 Sleep Deprivation Poses Enormous Public
Health Burden
Sleep loss is more prevalent and increasingly recognized. Some experts noting its catastrophic impact on some of the most notorious public health disasters in living memory, and its role in driving non communicable disease.
Consequences of sleep loss can be physiologically catastrophic for both the indi­vidual and society. Notorious public health disasters have been caused by sleep deprivation. The Exxon Valdez oil spill (often wrongly attributed to the inebriation of the ship’s captain) was due to the sleep-deprived shipmate who assumed control of the doomed vessel. The shipmate had been working for over 36 h before he assumed control of the oil tanker that would lead to the world’s most devastating oil spill in history.
The Chernobyl explosion in the Ukrainian city of Pripyat killed hundreds of people directly and indirectly in the worst nuclear power plant in history due to worker error caused by sleep loss.
Three Mile Island Plant Unit 2 Reactor in Pennsylvania, shift-workers on duty failed to recognize and react to the lack of core coolant which had been obstructed by a defective valve. While the mechanical problem of a dysfunctional valve was to blame for the near meltdown, Mitler and colleagues determined it was worker fatigue and sleep loss which resulted in the human error.
Much more common than meltdowns in nuclear reactors are motor vehicle acci­dents. The busy pulmonologist will often encounter people who present to the sleep specialist either mandated by the Department of Motor Vehicles and the police or so frightened by the experience that they nally come to seek attention with a sleep specialist [7]. Every sleep patient that comes to see me in my practice will leave educated about driving and sleep. This is where a sleep specialist can have a tremen­dous public health impact and each visit documents the driving sleep education provided to the patient.
We examine the impact of sleep disorders and sleep deprivation in the commer­cial driver—and by extension all drivers—later in this chapter. The high prevalence of driving in the United States sleepy driving poses a tremendous public health burden: the National Transportation Safety Board (NTSB) estimates more than 100,000 motor vehicle accidents each year can be attributed to drowsiness at the wheel or “fatigue.”
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Q. A. A. Ahmed
14.5 Sleep andChronic Respiratory Disease
Sleep-disordered breathing (SDB) is a spectrum of breathing abnormalities con­ned to the sleeping state but with signicant physiologic impact and profound waking impact. Recognition of obstructive sleep apnea syndrome—periodic airway collapse during sleep resulting in apnea—cessation of airow—followed by recov­ery hyperpnea events causing EEG arousals and recurrent oxygen desaturation and reoxygenation—is now most widely recognized.
Both obstructive sleep apnea syndrome and chronic obstructive pulmonary dis­ease noted Chronic Obstructive Pulmonary Disease (COPD) are very highly preva­lent. Distinct clinical phenotypes of COPD inuence the likelihood of coexistent OSA.Some experts believe that increased lung volumes and lower body mass asso­ciated with the predominant emphysema phenotype might protect against obstruc­tive sleep apnea syndrome, but this does not account for craniofacial abnormalities which can predispose obstructive sleep apnea syndrome even in the lean patient. Certainly, a higher body mass which is often associated with the predominant chronic bronchitis phenotype may well strongly promote obstructive sleep apnea syndrome and complicate and already vulnerable patient during the breathing in sleep.
Always an awareness of obstructive sleep apnea syndrome in patients with COPD is necessary and requires clinical suspicion, screening questionnaires and careful clinical and anatomical evaluation to identify patients who would benet from overnight polysomnography [9].
Managing the obstructive sleep apnea COPD overlap patient differs for manag­ing COPD alone and survival of overlap patients who receive positive airway pres­sure during sleep is superior to those who would like to treatment. This makes the recognition even more important.
Patients with chronic respiratory disease report impaired sleep quality been mea­sured to have reduced sleep efciency. Reduction in dream sleep and this reduction correlate with oxygenation measured when they are awake with arterial oxygen tension but not with the degree of obstruction of airow measured on pulmonary function testing. Some argue that reduction in REM sleep percentages could be protective from the exacerbation of OSAS which occurs during REM sleep. COPD patients with lung hyperination have been associated to report poor sleep quality. Using measures of quality-of-life sleep disturbance and COPD is measured in asso­ciation with reducing quality of life suggesting that treating sleep disorders in this patient population will improve quality of life scores [10].
14.6 Pathophysiology ofSleep-Related Breathing
Disorders inCOPD
Respiratory mechanics and ventilatory control are disturbed during sleep in the COPD patient due to a number of factors. These disturbances in ventilation and gas exchange occur during sleep and are related to hypersensitive or accentuated