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13 Obstructive Sleep Apnea (OSA) andGastroenterology
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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 identied 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 signicantly 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. Inammatory 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) andGERD
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 reux 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 etal. 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 reux symptoms compared to nonobese participants (BMI < 25) [27].
Another study by Jacobson etal. showed that raising BMI by more than 3.5kg/m2
was associated with more frequent reux 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 reux disease,
analyzing a total of 2699 patients, found a signicant relationship between obstructive sleep apnea syndrome and gastroesophageal reux 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 reux events day and night in obese and nonobese individuals with obstructive sleep apnea (OSA) and obese individuals without
OSA. They found that BMI signicantly predicted the number of acidic reux
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) andGastroenterology
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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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fatty liver disease. Am J Respir Crit Care Med. 2019;199(7):830–41.
2. Parikh MP, Gupta NM, McCullough AJ.Obstructive sleep apnea and the liver. Clin Liver Dis.
2019;23:363–82.
3. Trzepizur W, etal. 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, etal. 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, etal. 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., etal. (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, etal. Obstructive sleep apnea syndrome affects liver histology and inammatory cell activation in pediatric nonalcoholic fatty liver disease, regardless of
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11. Mesarwi OA, Shin MK, Drager LF, etal. 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, etal. 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, etal. Cancer incidence and mortality worldwide: sources,
methods and major patterns in GLOBOCAN 2012. Int J Cancer. 2015;136(5):E359–86.
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United States and their descendants. Cancer Causes Control. 2000;11(5):403–11.
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update project report: colorectal cancer 2011 report—food, nutrition, physical activity, and the
prevention of colorectal cancer.
16. Johnson CM, Wei C, Ensor JE, etal. Meta-analyses of colorectal cancer risk factors. Cancer
Causes Control. 2013;24(6):1207–22.
17. Weitz J, Koch M, Debus J, etal. Colorectal cancer. Lancet. 2005;365(9454):153–65.
18. Lee S, Kim BG, Kim JW, etal. 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 dene 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, etal. 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, etal. Body-mass index and symptoms of gastroesophageal reux in women. N Engl J Med. 2006;354(22):2340–8.
26. Corley DA, Kubo A, Zhao W.Abdominal obesity, ethnicity and gastro-oesophageal reux
symptoms. Gut. 2007;56(6):756–62.
27. El-Serag HB, Graham DY, Satia JA, etal. 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, etal. The relationship between obstructive sleep apnea hypopnea syndrome
and gastroesophageal reux disease: a meta-analysis. Sleep Breath. 2019;23(2):389–97.
29. Pardak P, Filip R, Woliński J, etal. Associations of obstructive sleep apnea, obestatin, leptin,
and ghrelin with gastroesophageal reux. J Clin Med. 2021;10(21):5195.
30. Shepherd K, Orr W.Mechanism of gastroesophageal reux in obstructive sleep apnea: airway
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C. A. Cortez-Hernández and J. C. Cessa-Zanatta

Sleep-Disordered Breathing:
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AnExpanding Spectrum
14
forthePulmonologist
QantaA.A.Ahmed
14.1 Sleep Medicine asClinical Frontier:
Personal Perspectives
It is difcult 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 NewYork
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
dened 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 ofce must respond to.
Q. A. A. Ahmed
14.2 Timeline oftheDiscipline
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 conned 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 identied 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] identied 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 10years of that
I had graduated medical school and 15years 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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261
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 claried 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 insufcient 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, insufcient sleep
hygiene, insufcient 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
specic 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
denitive 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 aBiological Necessity, Not
anExpendable 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 identied as a physiologic stressor and while it is
difcult 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” identies 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 conrming 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 andChronic Respiratory Disease
Sleep-disordered breathing (SDB) is a spectrum of breathing abnormalities conned to the sleeping state but with signicant physiologic impact and profound
waking impact. Recognition of obstructive sleep apnea syndrome—periodic airway
collapse during sleep resulting in apnea—cessation of airow—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 inuence 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 benet
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 efciency. 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 airow 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 hyperination 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 ofSleep-Related Breathing
Disorders inCOPD
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
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