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Nurse Practitioner:
doi: 10.1097/01.NPR.0000426409.62476.fa
Feature: SLEEP DISORDERS: CE Connection

Poor sleep, hazardous breathing: An overview of obstructive sleep apnea

Carlucci, Melissa MS, ACNP; Smith, Maureen MS, ANP, GNP; Corbridge, Susan J. PhD, ACNP, FAANP

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Author Information

Melissa Carlucci is a Clinical Instructor in the Department of Biobehavioral Health Science at the University of Illinois at Chicago College of Nursing in Chicago, Ill. Maureen Smith is a Nurse Practitioner at the Rush University Medical Center Sleep Disorders Service and Research Center in Chicago, Ill. Susan J. Corbridge is a Clinical Assistant Professor and Director of the ACNP Program at the University of Illinois at Chicago College of Nursing in Chicago, Ill.

The authors and planners have disclosed that they have no fi nancial relationships related to this article.

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Abstract

Abstract: Obstructive sleep apnea is a chronic disorder resulting from upper airway collapse during sleep. It is linked to a variety of health and safety risks but can often be effectively treated. This article provides an overview of the disorder, including an evidence-based approach to diagnosis and management.

Obstructive sleep apnea (OSA) is a common, chronic disorder that may require long-term, multidisciplinary care involving a nurse practitioner (NP). OSA is characterized by repetitive episodes of upper airway obstruction during sleep that are usually accompanied by oxygen desaturation and terminated by brief arousals that result in fragmented sleep.1 Individuals with OSA are usually unaware of this sleep disruption; however, frequent arousals result in excessive daytime sleepiness. OSA is associated with substantial morbidity and increased mortality.2 It occurs in 4% of men and 2% of women, but the prevalence is likely higher due to underrecognition and underdiagnosis, making OSA a significant public health concern.2,3 It is estimated that as many as 26% of adults are at high risk for OSA.4

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OSA is more common in men than women. It is also more common in postmenopausal women compared to premenopausal women.5 Other factors associated with increased risk include obesity, older age, increased neck circumference, craniofacial abnormalities, upper airway soft-tissue abnormalities, hypothyroidism, and acromegaly.3,5 Current smokers are nearly three times more likely to have OSA than nonsmokers.4 In addition, although not completely understood, familial and twin studies have provided evidence for the possible link between OSA and genetic factors.6

The signs, symptoms, and consequences of OSA result from recurrent collapse of the upper airway during sleep. Repeated arousals and/or hypoxemia contribute to excessive daytime sleepiness, poor neurocognitive function (such as decreased concentration and memory), decreased work productivity, decreased quality of life, and poor social functioning.3,7 In addition, OSA is associated with an increased risk of motor vehicle accidents.4 Furthermore, patients with OSA have significant local and systemic inflammation, which may predispose them to worsening apnea as well as the development of comorbidities.8 One major health burden in OSA patients is the association with an increased prevalence of cardiovascular diseases, such as hypertension, coronary artery disease, heart failure, and stroke.9 OSA is also associated with insulin resistance and increased prevalence of metabolic syndrome.10

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Pathophysiology

During normal sleep, brief periods of cessation of breathing or a marked decrease in tidal volume is common in adults. Although many factors contribute to the pathophysiology of OSA, the primary problem is recurrent collapse of the upper airway during sleep, resulting in significantly reduced airflow (hypopnea) or complete cessation of airflow (apnea) despite breathing efforts (see Upper airway structures).1 Many factors, including abnormalities of the airway structure, abnormal airway function (such as reduced activity of the dilator muscles of the pharynx), and instability in respiratory control (termed “loop gain”) contribute to the problem of OSA in various combinations.1

The human airway consists of numerous muscles and soft tissue but lacks rigid or bony support. It also contains a collapsible portion that extends from the hard palate to the vocal cords. Although this is essential for phonation and swallowing during wakefulness, the lack of rigidity also allows for collapse during sleep.1 Airway size also plays a role. Individuals with OSA have smaller upper airways than those without OSA1; from an anatomic perspective, smaller tubes are more likely to collapse than larger ones. Furthermore, unstable control of respiration—leading to recurring episodes of apnea—is also more common in patients with OSA.1

Obstructive events and disrupted breathing lead to hypercapnia and acidosis. This stimulates arousal centers in the central nervous system causing increased respiratory and pharyngeal muscle activity.1 These changes, along with increased breathing effort, ultimately overcome the obstruction, and ventilation resumes (that is, the patient wakes up to take a breath). The individual then returns to sleep, the muscles surrounding the pharynx relax, and the cycle repeats itself.11 These repetitive, obstructive events and disrupted breathing result in fragmented sleep. In severe cases, apnea and hypopnea can occur more than 100 times per hour, and each event typically lasts 20 to 40 seconds.1

With each episode of obstruction, hypercapnia, hypoxemia, and the resulting increased negative intrathoracic pressure against the obstructed airway lead to increased right and left ventricular afterload, decreased left ventricular compliance, increased pulmonary artery pressures, and increased myocardial oxygen demand.11 When the patient awakens at the end of the obstructive event, sympathetic discharge occurs, leading to vasoconstriction and an increase in BP/heart rate. After a period of time, blood vessels are altered, leading to sustained hypertension.1

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History and physical exam

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Figure. Upper airway...
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A diagnosis of OSA is based on clinical features, which are assessed during a sleep-oriented history, physical exam, and objective testing with sleep studies.2,3 Both clinical assessment and objective testing are required, as either element is of limited value when considered alone.2 OSA is clinically defined by the presence of daytime sleepiness, loud snoring, witnessed apneas, or arousals due to gasping or choking along with an apnea-hypopnea index (AHI) of 5 or greater or an AHI of 15 or greater without those symptoms.3 The AHI refers to the total number of apneas and hypopneas per hour of sleep. The symptom analysis occurs during the history and physical exam, and the AHI is determined by objective testing.3 A sleep history may be obtained during a routine health maintenance visit or as part of an evaluation for patients who either have symptoms of OSA or are at high risk for OSA. Screening points for a routine health maintenance visit include a history of snoring, daytime sleepiness, and the presence of obesity, retrognathia, or hypertension. Patients with positive findings on this screen should be referred for a comprehensive sleep history and physical exam.3

A comprehensive sleep history should include the evaluation of a number of symptoms associated with OSA. Snoring is the hallmark symptom and most common symptom of OSA. It occurs in up to 95% of patients, and if absent, would make a diagnosis of OSA unlikely.2 OSA is also the most common cause of excessive daytime sleepiness. A validated, easy-to-administer questionnaire, such as the Epworth Sleepiness Scale, may be used in the clinical setting to quantify a patient's subjective report of excessive sleepiness.12 Both snoring and excessive daytime sleepiness are common in the general population, so it is important to consider these symptoms in the context of the entire sleep evaluation.2 Witnessed apneas, nocturnal choking or gasping, and sleep-maintenance insomnia (difficulty staying asleep) are also frequently reported symptoms of OSA. Other symptoms may include nocturia, morning headaches or nausea, memory impairment, concentration difficulties, personality changes, and decreased libido.2,3 Important information may also be obtained from the patient's bed partner, as this person directly observes both nocturnal and daytime symptoms.2

In addition to symptomatology, patient variables that increase the likelihood of OSA should be considered. These may include the following: male gender, postmenopausal status, older age, use of sedative medications, smoking, and alcohol use.13 The presence of comorbid conditions associated with OSA are also assessed. Patients who have been diagnosed with hypertension, coronary artery disease, heart failure, stroke, cardiac dysrhythmias, diabetes, and metabolic syndrome should be considered at-risk for OSA.3,13 Additionally, gastroesophageal reflux disease (backflow of gastric acid causes laryngeal spasms that obstruct airflow into the lungs) and gout (cell damage resulting from decreased oxygen saturation leads to excess uric acid production) may also be present in patients with OSA.13 Finally, it is important to be alert to female patients with medical comorbidities, such as fibromyalgia, irritable bowel syndrome, migraines, and depression. The symptom profile associated with these disorders is also found with OSA and may present challenges with diagnosis.13

The physical exam should include the respiratory, cardiovascular, and neurologic systems with special attention given to the presence of obesity or other conditions associated with OSA and signs of upper airway narrowing.3 Obesity is common in patients with OSA. A body mass index (BMI) of 30 or greater and a neck circumference greater than 17 in. (43.18 cm) for men and greater than 16 in. (40.6 cm) for women may be suggestive of OSA. Craniofacial and soft-tissue abnormalities that cause upper airway narrowing should also be assessed during the exam. Some examples of these abnormalities include retrognathia, macroglossia, and tonsillar hypertrophy; however, the most common physical finding is a nonspecific narrowing of the oropharyngeal airway with or without increased soft-tissue deposition.2,3 After completion of the history and physical exam, patients with symptoms who are determined to be at risk for OSA should proceed to objective testing. Education about possible diagnoses, diagnostic steps, and testing procedures should be provided to these patients prior to testing.3

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Objective testing

There are two acceptable methods of objective testing to establish a diagnosis of OSA: In-laboratory polysomnography (PSG) and home-based sleep studies.3 In-laboratory PSG is the gold standard for diagnosing OSA, but, given the resource-intensive nature of these studies, home testing may also be considered.2,3 Home-based sleep studies must be conducted as part of a comprehensive sleep evaluation. They may be indicated in patients with a high likelihood of moderate-to-severe OSA or when patient conditions, such as immobility, dictate that in-laboratory PSG is not reasonable. However, patients with major comorbid conditions, such as severe pulmonary disease, are not candidates for home testing.3 Another method of determining home versus in-laboratory testing would be to consider resource limitations and the clinical index of suspicion for OSA. If resources are limited, patients with either a low or high index of suspicion may undergo home testing, but patients with an intermediate index of suspicion or those who have atypical symptoms may be better suited for in-laboratory PSG.2 Home testing carries a known rate of false negatives, and given that these studies are unattended, there is a greater chance of technically unsatisfactory results. Therefore, an in-laboratory PSG should be performed if home testing yields technically unsatisfactory results or does not establish a diagnosis in patients with a high likelihood of OSA.3

For in-laboratory PSG, the following physiologic parameters are documented: electroencephalogram, electrooculogram, chin electromyogram, airflow, oxygen saturation, respiratory effort, and ECG. Additionally, body position and leg electromyogram are recommended.3 A recording of body position may help to account for variability in the AHI, as the AHI is generally higher in the supine position.2 A full-night PSG is recommended, but a split-night study may be conducted if the AHI is 40 per hour or greater in 2 hours of a diagnostic PSG and considered if the AHI is 20 to 40 per hour based on clinical judgment.3 A split-night study is divided into two parts: the first part establishes a diagnosis, and the second part is focused on continuous positive airway pressure (CPAP) titration.3 For home-based sleep studies, documented parameters should at minimum include airflow, respiratory effort, and oxygen saturation.3 In addition to OSA diagnosis, objective testing can establish OSA severity based on the AHI. The severity of OSA is defined as mild for an AHI of 5 to 15 per hour, moderate for an AHI of 15 to 30 per hour, and severe for an AHI greater than 30 per hour.2,3,13

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Treatment

Treatment options for OSA may be medical, behavioral, and/or surgical (see Flow chart for evaluation of patients suspected of having OSA). It is important to choose an appropriate therapy based on disease severity; however, patient involvement should be sought whenever possible with consideration given to adherence and tolerability.3,14 Regardless of the type of therapy, a general OSA outcomes assessment should be completed to evaluate the effectiveness of treatment. Outcome measures include the following: resolution of daytime sleepiness, improved OSA-specific quality of life, patient and partner satisfaction, adherence to therapy, avoidance of aggravating factors, adequate sleep, proper sleep hygiene, and weight loss for overweight patients.3 With the exception of mild cases that may resolve with weight reduction or the avoidance of supine sleeping in patients who show positional changes in their nocturnal breathing, the clinical treatment of OSA is considered chronic disease management.3

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CPAP

The treatment of choice for mild, moderate, and severe OSA is positive airway pressure (PAP) during sleep. PAP can be delivered in a variety of ways, but the recommended mode is CPAP.3,11,14 CPAP functions as a pneumatic splint, maintaining a constant upper airway pressure and preventing the pharyngeal instability and collapse that occur during an apneic event. This results in upper airway patency throughout the respiratory cycle.11,15 Studies have shown that CPAP can decrease daytime sleepiness, cognitive impairment, BP, and improve sleep quality. In addition, historical data indicate increased survival rates in CPAP-treated patients.11,16

CPAP is delivered through an interface with the patient, which involves a mask secured to the face and attached to a CPAP machine. CPAP machines are designed to be compact and lightweight, so they easily fit on a bedside table and are portable for travel.15 A variety of masks are available for patient choice and best comfort. A nasal mask, which may be a conventional mask that fits securely over the nose or a newer nasal pillow with nasal cannula that rest in the nares, is the preferred method. Nasal pillows are best suited for patients who are claustrophobic or have low tolerance of anything on the face at night. Other delivery systems, such as a full-face mask, can be considered to address technical or comfort issues. Full-face masks fit over both the nose and mouth and are indicated primarily for patients who are mouth breathers and need the additional oral cover-up to prevent air leakage during CPAP delivery.3,11,15

The amount of pressure delivered by the CPAP system is titrated to the optimal level during PSG. A full-night, in-laboratory PSG is preferred, but a split-night PSG is generally adequate.3 There are no absolute contraindications to CPAP, and adverse effects are generally minor. Common adverse effects may be irritation, pain, rash, or skin breakdown related to mask pressure, dry mucous membranes, nasal congestion, and rhinorrhea. These can often be alleviated by simple interventions, such as over-the-counter saline sprays, adjusting the mask and pressure level, adding humidification, or a short course of nasal corticosteroid spray.11,15 Although CPAP is the recommended mode of pressure delivery, there are other options. Bilevel, autotitrating, or pressure relief modes may be considered in CPAP-intolerant patients.3,11 Once CPAP has been initiated, patients should be followed carefully to objectively monitor nightly CPAP usage and assess for problems with therapy.3,11 The accepted standard of good adherence is CPAP use for at least 4 hours per night—on at least 70% of nights—for at least 30 days in the first 3 months after CPAP initiation.17 Most machines can produce CPAP utilization reports to compare with the patient's subjective report, which is often overestimated.11

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Oral appliances

Figure. Flow chart f...
Figure. Flow chart f...
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Oral appliances (OAs) are an alternative therapy to PAP. OAs are devices that advance the mandible and tongue relative to the maxilla. This realignment increases the diameter of the posterior pharynx, preventing the airway collapse that leads to apneic events.3,18 OAs are indicated in patients who are not candidates for CPAP, do not respond to CPAP, fail CPAP or behavioral measures, or prefer OAs to CPAP. Although OAs have not been shown to be as effective as CPAP, they may be considered in patients with mild-to-moderate OSA.3,18

The two basic models of OAs are fixed and adjustable. Fixed OAs are molded to retain the mandible in a static position, whereas adjustable OAs are made with a screw-like mechanism that allows the mandible to be advanced to the point of maximal therapeutic benefit. The baseline AHI should steer the treatment recommendation for the appropriate type of OA.18 Fitting for an OA should be done by a dentist certified in sleep dentistry, as a thorough dental exam is necessary to ensure that patients are appropriate candidates for this type of device.18 In addition, after the patient has become acclimated to wearing the OA to the point of safest mandibular advancement, a repeat PSG done with the OA in place is recommended to ensure therapeutic efficacy.18

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Behavioral, surgical, and adjunctive treatments

Behavioral strategies for OSA management may include weight loss and positional therapy. Weight loss may decrease the AHI and decrease or eliminate the need for CPAP. It is therefore recommended for all overweight patients with a goal BMI of 25 or less.3,11 Positional therapy may be used in patients with a low AHI in a nonsupine position when compared to the AHI in a supine position. Because the area of the upper airway is decreased in the supine position, positional therapy uses a positioning device, such as an alarm or pillow, to prevent the patient from sleeping supinely.3 Both weight loss and positional therapy are generally used in conjunction with a primary OSA treatment, such as CPAP.3

A variety of upper airway surgical procedures can be considered as secondary treatment for OSA when the outcome of treatment with PAP or an OA is inadequate. Upper airway surgery (to correct obstructive anatomy or functional deficiencies that hinder other treatments) and bariatric surgery (to promote weight loss) may also be considered as adjunctive treatments. In addition, other adjunctive therapies, such as medication and supplemental oxygen, may be used in certain circumstances.3 Medication considerations may include eszopiclone and modafinil. Eszopiclone is a nonbenzodiazepine sedative-hypnotic that is commonly used to treat insomnia but can also be effective for short-term sleep disturbance related to initial acclimation to wearing CPAP, thus, improving machine use and treatment adherence.19 Common adverse reactions of this medication may include drowsiness, dizziness, headache, and dry mouth; more serious adverse reactions are abnormal thinking, amnestic behaviors, hallucinations, anxiety, and feelings of aggression or suicide. Modafinil is a wakefulness-producing medication that is indicated to treat residual sleepiness despite compliant CPAP use.3,20 Common adverse reactions of this medication may include headache, dizziness, insomnia, and gastrointestinal upset; more serious adverse reactions are chest pain, palpitations, severe skin rash or mouth sores, hallucinations, aggression, anxiety, or depression.

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Long-term management

OSA is a chronic disease that requires long-term management. Once therapy has been established, regular follow-up should occur annually and as needed to troubleshoot problems and assess adherence and treatment response, especially in patients with medical comorbidities.3 Untreated OSA has been linked to a variety of problems, including cardiovascular diseases and motor vehicle accidents; monitoring for these and other complications should occur (see Clinical and Functional outcomes associated with untreated OSA).3 Follow-up PSG or home-based sleep study is not indicated when symptoms resolve with CPAP treatment; however, a follow-up PSG or home-based sleep study is indicated to assess treatment response in these cases: from an OA or upper airway surgery, following substantial weight loss or weight gain, when there is inadequate treatment response, or when symptoms return despite a good initial treatment response.3,11

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Patient education

Education is an essential component in the management of patients with OSA and an important role of the NP (see Resources for further information about OSA). Initially, results of objective testing and treatment options should be reviewed with the patient. Discussion of treatment options should take into account disease severity, risk factors, associated medical conditions, and expectations. Once CPAP therapy is initiated, education should be provided on the function, care, and maintenance of home equipment, benefits of therapy, and potential problems. Additional elements of OSA education include pathophysiology, risk factors, natural history, and clinical consequences of OSA.3 Treatment adherence is influenced by patient attitudes and health beliefs.21 It is therefore important to explain both the short- and long-term effects of untreated OSA, including medical comorbidities and higher rates of vehicular accidents.

Patients must be educated on the importance of regular follow-up to assess CPAP adherence and address difficulties with machine use. Patient adherence with CPAP use will likely be the most frequent management challenge faced by the NP. Despite the fact that CPAP is the first-line treatment for OSA and has a known efficacy in the treatment of OSA, many patients either discontinue using it or do not use it as recommended.22 Addressing patient discomfort and reasons for not using the prescribed CPAP therapy shortly after setup of a home machine increases the likelihood of future adherence. Most patients determine their adherence with CPAP within the first week of treatment and some even as early as 3 days following the initiation of treatment.16,23 Early clinical intervention to promote long-term use is essential, as greater nightly usage leads to better clinical outcomes.16,23 In addition, education provided through cognitive behavioral therapy, along with supportive interventions that encourage CPAP use, has been shown to be effective in improving CPAP adherence.24,25 Involving the patient's social support system in the educational process may also be a helpful strategy to promote CPAP adherence.

Weight loss is an important strategy for OSA management, so overweight and obese patients with OSA should be counseled about losing weight. Good sleep hygiene—including a regular schedule that allows for 7 to 8 hours of total sleep time and a nonsupine sleep position—should also be discussed.3,20 In addition, education regarding risk factor modification, such as smoking cessation, avoiding alcohol, and medication effects, should be provided. Lastly, patients should be informed of the increased incidence of motor vehicle accidents that is associated with OSA and strongly encouraged to avoid drowsy driving.3

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Moving forward

OSA is a common chronic disorder that results from recurrent collapse of the upper airway during sleep. It is often underrecognized and underdiagnosed, and, left untreated, is associated with a variety of problems, including cardiovascular diseases and motor vehicle accidents. It is important for the NP to understand the risk factors, medical conditions, and symptomatology associated with OSA in addition to following current guidelines for the diagnosis and management of the disorder. Improvements in recognition, diagnosis, and management are necessary to address the substantial morbidity and increased mortality that make OSA a significant public health concern.

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Clinical and functional outcomes associated with untreated OSA

* Hypertension

* Stroke

* Cardiac dysrhythmias

* Coronary artery disease

* Heart failure

* Insulin resistance

* Depression

* Poor social or interpersonal functioning

* Memory impairment

* Concentration difficulty

* Decreased work productivity

* Increased risk of motor vehicle accidents

Sources: McNicholas WT, Bonsigore MR; Management Committee of EU COST ACTION B26. Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities. Eur Respir J. 2007;29(1):156-178.

Engleman HM, Douglas NJ. Sleep. 4: Sleepiness, cognitive function, and quality of life in obstructive sleep apnoea/hypopnoea syndrome. Thorax. 2004;59(7):618-622.

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Resources for further information about OSA

* American Academy of Sleep Medicine (www.aasmnet.org)

* American Board of Sleep Medicine (www.absm.org)

* American Sleep Apnea Association (www.sleepapnea.org)

* National Sleep Foundation (www.sleepfoundation.org)

* Sleep Education (www.sleepeducation.com)

* Sleep Research Society (www.sleepresearchsociety.org)

* National Center on Sleep Disorders Research (www.nhlbi.nih.gov/sleep)

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REFERENCES

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7. Engleman HM, Douglas NJ.Sleep 4: Sleepiness, cognitive function, and quality of life in obstructive sleep apnoea/hypopnoea syndrome. Thorax. 2004;59(7):618–622.

8. Hatipoglu U, Rubinstein I.Inflammation and obstructive sleep apnea syndrome pathogenesis: a working hypothesis. Respiration. 2003;70(6):665–671.

9. McNicholas WT, Bonsigore MR;Management Committee of EU Cost Action B26. Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities. Eur Respir J. 2007;29(1):156–178.

10. Coughlin SR, Mawdsley L, Mugarza JA, Calverley PM, Wilding JP.Obstructive sleep apnoea is independently associated with an increased prevalence of metabolic syndrome. Eur Heart J. 2004;25(9):735–741.

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15. Sawyer A, Weaver TE.Sleep related breathing disorders. In: Redeker N, McEnany GP, eds. Sleep Disorders and Sleep Promotion in Nursing Practice. New York, NY: ; 2011:95–120.

16. Budhiraja R, Parthasarathy S, Drake CL, et al.Early CPAP use identifies subsequent adherence to CPAP therapy. Sleep. 2007;30(3):320–324.

17. Aloia MS, Knoepke CE, Lee-Chiong T.The new local coverage determination criteria for adherence to positive airway pressure treatment: testing the limits. Chest. 2010;138(4):875–879.

18. Lettieri CJ, Paolino N, Eliasson AH, Shah AA, Holley AB.Comparison of adjustable and fixed oral appliances for the treatment of obstructive sleep apnea. J Clin Sleep Med. 2011;7(5):439–445.

19. Lettieri CJ, Shah AA, Holley AB, Kelly WF, Chang AS, Roop SA;CPAP Promotion and Prognosis-The Army Sleep Apnea Program Trial. Effects of a short course of eszopiclone on continuous positive airway pressure adherence: a randomized trial. Ann Intern Med. 2009;151(10):696–702.

20. Morgenthaler TI, Kapen S, Lee-Chiong T, et al.Practice parameters for the medical therapy of obstructive sleep apnea. Sleep. 2006;29(8):1031–1035.

21. Catcheside PG.Predictors of continuous positive airway pressure adherence. F1000 Med Rep. 2010;2.

22. Aloia MS, Arnedt JT, Stanchina M, Millman RP.How early in treatment is PAP adherence established? Revisiting night-to-night variability. Behav Sleep Med. 2007;5(3):229–240.

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24. Richards D, Bartlett DJ, Wong K, Malouff J, Grunstein RR.Increased adherence to CPAP with a group cognitive behavioral treatment intervention: a randomized trial. Sleep. 2007;30(5):635–640.

25. Smith I, Nadig V, Lasserson TJ.Educational, supportive and behavioural interventions to improve usage of continuous positive airway pressure machines for adults with obstructive sleep apnoea. Cochrane Database Syst Rev. 2009(2):CD007736.

Keywords:

obstructive sleep apnea; sleep apnea; sleep-disordered breathing

© 2013 Lippincott Williams & Wilkins, Inc.

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