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Obstructive Sleep Apnea

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Last Update: December 11, 2022.

Continuing Education Activity

Obstructive sleep apnea (OSA) is characterized by episodes of complete collapse of the airway or partial collapse with an associated decrease in oxygen saturation or arousal from sleep. This disturbance results in fragmented, nonrestorative sleep. OSA has significant implications for cardiovascular health, mental illness, quality of life, and driving safety. This activity reviews the cause and pathophysiology of obstructive sleep apnea and highlights the role of the interprofessional team in its management.


  • Describe the pathophysiology of obstructive sleep apnea.
  • Review the presentation of a patient with obstructive sleep apnea.
  • Summarize the treatment options for obstructive sleep apnea.
  • Explain modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by obstructive sleep apnea.
Access free multiple choice questions on this topic.


Obstructive sleep apnea (OSA) is characterized by episodes of a complete (apnea) or partial collapse (hypopnea) of the upper airway with an associated decrease in oxygen saturation or arousal from sleep.[1] This disturbance results in fragmented, nonrestorative sleep. Other symptoms include loud, disruptive snoring, witnessed apneas during sleep, and excessive daytime sleepiness.[2][3][4] OSA has significant implications for cardiovascular health,[5] mental illness, quality of life, and driving safety.


Pharyngeal narrowing and closure during sleep is a complex phenomenon, and likely multiple factors play a role in the pathogenesis. Sleep-related reduced ventilatory drive and neuromuscular combined with anatomic risk factors are likely to play a significant role in upper airway obstruction during sleep.[1] The anatomic factors that promote pharyngeal narrowing include large neck circumference, soft tissue, bone, or vessels. [6] Many of these structures can lead to increased surrounding pressure of the upper airway resulting in pharyngeal collapsibility and/or insufficient space to accommodate the airflow in a portion of the upper airway during sleep. [7] In addition, the upper airway muscle tone plays a role as when it decreases, a repetitive total or partial airway collapse results. The most common cause of OSA in adults is obesity, male sex, and advancing age. [8] The severity of OSA decreases with age when adjusting for BMI. [9]  

Anatomic Factors

  • Micrognathia, retrognathia
  • Facial elongation
  • Mandibular hypoplasia
  • Adenoid and tonsillar hypertrophy
  • Inferior displacement of the hyoid

Nonanatomic Risk Factors

  • Central fat distribution
  • Obesity
  • Advanced age
  • Male gender
  • Supine sleeping position
  • Pregnancy[10]

Additional Factors

  • Alcohol use
  • Smoking
  • Use of sedatives and hypnotics

Associated Medical Disorders

  • Endocrine disorders (e.g., diabetes mellitus, metabolic syndrome, acromegaly, and hypothyroidism)[11][12]
  • Neurological disorders (e.g., stroke, spinal cord injury, and myasthenia gravis) [13][14]
  • Prader Willi syndrome[15]
  • Down Syndrome[16]
  • Congestive heart failure[17]
  • Atrial fibrillation [18]
  • Obesity hypoventilation syndrome (OHS)[19]

These relationships between OSA and various medical disorders are based mainly on observational studies and not necessarily randomized clinical trials. 


Obstructive sleep apnea is a common condition with significant adverse consequences.[20] OSA (using the definition of 5 or more events/ hour) affects almost 1 billion people globally [21], with 425 million adults aged 30-69 years having moderate to severe OSA (15 or more events/h).[22] In the United States, it has been reported that 25-30% of men and 9-17% of women meet the criteria for obstructive sleep apnea.[23][24] Prevalence is higher in Hispanic, Black, and Asian populations. Prevalence also increases with age, and when individuals reach 50 years of age or more, there are as many women as men who develop the disorder. The increasing prevalence of OSA is related to the rising rates of obesity ranging between 14% and 55%.[23] It has been reported that there is a genetic component as some risk factors, including obesity and upper airway soft tissue structure, are genetically inherited.[25]


Upper airway obstruction during sleep is often due to negative collapsing pressure during inspiration; however, progressive expiratory narrowing in the retro palatal area plays an important role.[26] The magnitude of upper airway narrowing during sleep is often related to body mass index, indicating that anatomical and neuromuscular factors contribute to airway obstruction.[27] To understand the mechanisms of OSA, it is helpful to use the concept of the pressure-flow relationship through collapsible tubes.[28] Additional information on risk factors is available in the etiology section. 

History and Physical

Patients with suspected OSA usually present with excessive daytime sleepiness, loud snoring, gasping, choking, or breathing cessation while sleeping that a bed partner witnessed. Excessive daytime sleepiness is one of the most common symptoms. However, the majority of patients are asymptomatic.[24] Many patients only report daytime fatigue with or without other associated symptoms. Therefore, the distinction between sleepiness and fatigue should be objectively assessed. Epworth Sleepiness Scale (ESS) [29] can be used to quantitatively evaluate the severity of sleepiness. The ESS score ranges from 0 to 24, and more than 9 points indicate the presence of excessive daytime sleepiness and require additional assessment. A fatigue severity scale can also assess the severity of fatigue symptoms.[30] Using both ESS and FSS is usually helpful as sleepiness, and fatigue symptoms could be present concomitantly. Other symptoms vary from morning headaches [31] and self-reported insomnia [32] to nocturia.[33] Symptoms of sleep-onset insomnia and sleep maintenance insomnia were reported most by women.[34]

The STOP-BANG questionnaire is one of the most widely accepted screening tools for OSA.[35]

  • Snoring: Do you snore loudly (louder than talking or loud enough to be heard through closed doors)?
  • Tired: Do you often feel tired, fatigued, or sleepy during the daytime?
  • Observed: Has anyone observed you stop breathing during your sleep?
  • Blood pressure: Do you have or are you being treated for high blood pressure?
  • BMI: BMI ≥ 35 kg/m2
  • Age: age > 50 yrs
  • Neck circumference: Neck circumference >40 cm
  • Gender: Gender male 

Use STOP-BANG to decide if high probability of moderate-severe disease. High risk if ‘YES’ to ≥ 3 items Low risk if ‘YES’ to < 3 items Items.

Obesity is the most common finding in individuals with OSA. Other physical findings are large neck circumference (17 inches or 43 cm in males and 16 inches or 40.5 cm), crowded oropharynx (Mallampati 3 to 4), retrognathia, micrognathia, tonsilar hypertrophy, low-lying palate, overjet, and a large tongue. However, after adjusting for body weight and neck size, only lateral narrowing is an independent predictor of OSA.[36]


Any adult patient with unexplained daytime or sleep-related symptoms such as excessive sleepiness, fatigue, or unrefreshing sleep should be evaluated for sleep apnea. However, universal screening for OSA is not recommended in asymptomatic patients except for those who are at risk of occupational hazards such as driving or those who are pilots.[37] [38] In addition, due to the high prevalence of OSA and disease burden, patients with specific comorbidities such as refractory atrial fibrillation, resistant hypertension, and a history of stroke can be screened for sleep apnea regardless of symptoms.[39] 

Nighttime in-laboratory Level 1 polysomnography (PSG) is the gold standard test for the diagnosis of obstructive sleep apnea. During the test, patients are monitored with EEG leads, pulse oximetry, temperature and pressure sensors to detect nasal and oral airflow, respiratory impedance plethysmography belts around the chest and abdomen to detect motion, an ECG lead, and EMG sensors to detect muscle contraction in the chin, chest, and legs (as depicted in the polygraph). 

Scoring respiratory events in adults rely on 4 channels: [40] 

  1. Oronasal thermal sensor 
  2. Nasal air pressure transducer 
  3. Inductance plethysmography (esophageal manometry or pressure catheter may be used instead) 
  4. Pulse oximetry 

*A snoring monitor is a required channel but is not used in scoring any respiratory events 

According to the American Academy of Sleep Medicine (AASM), hypopnea can be defined based on one of two criteria. It can either be a reduction in airflow of at least 30% for more than 10 seconds associated with at least 4% oxygen desaturation (Medicare criteria) or a reduction in airflow of at least 30% for more than 10 seconds associated with at least 3% oxygen desaturation or an arousal from sleep on EEG (Recommended  AASM criteria).[41] 

Scoring apnea requires both of the following criteria to be met:

  • A. Drop in the peak signal excursion by ≥90% of pre-event baseline flow
  • B. Duration of the drop in flow is ≥10 seconds.
    • Apneas usually further are classified based on effort (RIP signals):
    • Obstructive apnea, if there is increased effort throughout the entire apnea
    • Central apnea, if there is no effort throughout the entire apnea

Mixed apnea occurs if there is no effort in the first part and there is an effort in the second part of the apnea (See polygraph).

Home sleep tests (HST) or portable monitoring (PM) have gained popularity due to their relative accessibility and lower cost. PM, however, should be used with specific rules and procedures based on the AASM unattended PM task force guidelines, which outlined the following criteria [42]:

  1. At a minimum, PM must record airflow, respiratory effort, and blood oxygenation.
  2. The airflow, effort, and oximetric biosensors conventionally used for in-laboratory PSG should be used in PM.
  3. PM testing must be performed under the auspices of an AASM-accredited comprehensive sleep medicine program with written policies and procedures.
  4. An experienced sleep technologist/technician must apply the sensors or directly educate patients in sensor application.
  5. The PM device must allow for the display of raw data with the capability of manual scoring or editing of automated scoring by a qualified sleep technician/technologist.
  6. A board-certified sleep specialist, or an individual who fulfills the eligibility criteria for the sleep medicine certification examination, must review the raw data from PM using scoring criteria consistent with current published AASM standards.[41] Under the conditions specified above, PM may be used for unattended studies in the patient's home.
  7. A follow-up visit to review test results should be performed for all patients undergoing PM.
  8. In patients with a high pretest probability of moderate to severe OSA, negative or technically inadequate PM tests should prompt in-laboratory polysomnography.

Unattended PM and HST are appropriate for adults with a high pretest probability for sleep apnea and no significant medical comorbidities (advanced congestive heart failure, chronic obstructive pulmonary disease, and neurologic disorders). These are level III sleep tests consisting of pulse oximetry, heart rate monitoring, temperature and pressure sensors to detect nasal and oral airflow, resistance belts around the chest and abdomen to detect motion, and a sensor to detect body position. Moderate and severe sleep apnea is detected on these tests, but due to the chance of underestimating the apnea-hypopnea index (AHI) relative to the total recording time (which may be longer than the total sleep time measured in an in-lab study), mild sleep apnea may go undiagnosed, and a repeat in-lab study may be needed. A proposed algorithm for the appropriate use of PM and in-lab PSG is outlined in the figure below.   

One of the main limitations of HST is that the majority of studies rely on total recording time (TRT) as the denominator instead of total sleep time (TST) in the calculation of AHI as there are no EEG sensors to differentiate sleep from wake. It is estimated that using TRT can result in an underestimation of AHI by at least 20%. [43] In order to differentiate indices of respiratory events generated by HST (without recorded sleep), the AASM recommended the use of the term Respiratory Event Index (REI). Both apnea-hypopnea index and REI are the average number of obstructive events per hour (during sleep or recording time, respectively).

While most PM devices include flow sensors, other technologies use an alternative method without flow such as peripheral arterial tonometry (called PAT) to identify sleep-disordered breathing events. The OSA severity obtained using PAT devices is called pAHI and is reported to provide similar indices to PSG-derived AHI.[44]

The severity of OSA in adults is based on AHI, REI, or pAHI as follows:

  • Mild: 5 to 15 events per hour
  • Moderate: >15 to 30 events per hour
  • Severe: greater than 30 events per hour

The burden of disease in mild OSA is controversial and based on associated clinical sequelae (such as excessive daytime sleepiness, sleep maintenance insomnia, and cognitive dysfunction).[45]

Recent studies challenged however the traditional definition and scoring criteria of OSA in adults due to its limitations in capturing the pathophysiological impact in individual patients.[21] Different metrics have been proposed to increase precision in diagnosing individuals with OSA.[46] These metrics include hypoxic burden, [47] nocturnal heart rate changes, [48] total sleep time with SpO2 <90% (TST90), [49] duration of obstructive events, [50] sleep arousal burden, [51] and even Genetics. [52][53] 

Treatment / Management

The treatment of OSA is a multi-pronged approach and should be individualized to each patient. While treatment of moderate to severe OSA has been shown to improve clinical outcomes [54], there is limited or inconsistent evidence about the impact of therapy of mild OSA on neurocognition, mood, vehicle accidents, cardiovascular events, stroke, and arrhythmias.[45]

Lifestyle Changes and Treating Underlying Medical Conditions

The importance of weight loss should be emphasized in OSA patients with overweight and obesity.[55][56] Although weight loss is recommended and can often decrease the severity of obstructive sleep apnea, it is not usually curative. Patients should be educated on the impact of sleep duration and their health and prioritize getting at least 7 to 8 hours of sleep per night. [57] Patients should be counseled to avoid alcohol, benzodiazepines, opiates, and some antidepressants, which may worsen their condition. For all patients, it is important to address any concomitant nasal obstruction with nasal steroids for allergic rhinitis or surgically for nasal valve collapse. For patients with lung or heart disease (such as asthma or heart failure), it is very important to optimize the treatment of these disorders.

Positional Therapy

OSA that is more prominent in the supine position can be treated with a positioning device to keep a patient on their side can be an option. [58][59]

Positive Airway Pressure (PAP) Therapy

Continuous positive airway pressure (PAP) is the most effective treatment for adults.[60] Bilevel PAP (BPAP) is also better tolerated by patients who require higher pressure settings (greater than 15 cm H2O). However, despite the high efficacy of PAP in eliminating respiratory events, its effectiveness is dampened by the decreased use of treatment during sleep and inadequate adherence. Adherence to PAP among patients with OSA remains a great challenge as nearly half of patients do not adequately adhere to treatment after the first month.[61] The American Thoracic Society published a recent statement on PAP adherence tracking systems and the optimal monitoring strategies and outcome measures in adults. [62] It is important to standardize the PAP adherence report not only the number of hours used more than 4 hours per night (>70% of nights) but also the amount of mask leak and residual apnea and hypopnea index. However, what is the optimal goal in adherence to OSA treatment? Recent studies are looking at the utility of telemedicine adherence interventions, remote monitoring of CPAP,[63] and more interactive features with individual patients and their families have shown to increase CPAP adherence rates.[64][65][66]

Several studies have reported conflicting findings when assessing the effect of PAP therapy on cardiovascular outcomes in patients with OSA.[46] In a recent randomized control trial, CPAP use for a minimum of one year in patients with Acute Coronary Syndrome (ACS) and OSA (ISAACC) without excessive daytime sleepiness did not lower the incidence of cardiovascular events (defined as cardiac-related death or one or more of the following outcomes: acute myocardial infarction, non-fatal stroke, hospital admission for heart failure, and new hospitalizations for unstable angina or transient ischaemic attack).[67] The adherence to PAP therapy was low (2.78 h/night), and follow-up was not long enough, which are significant limitations of this study. In another observational cohort study with long-term follow-up, PAP use was associated with lower all-cause mortality among patients with severe OSA around years 6–7 of follow-up.[68] In a more recent study, patients with coronary artery disease and OSA without excessive sleepiness who exhibited higher changes in heart rate benefited more from CPAP therapy.[69]

Oral Appliance

For patients unable or unwilling to use CPAP or those who will be unable to access electricity reliably, custom-fitted and titrated oral appliances or mandibular advancements devices (MAD) can be used to bring the lower jaw forward and relieve airway obstruction (See picture). This typically works best for candidates with appropriate dentition and mild to moderate sleep apnea. In a randomized clinical trial on 126 patients with moderate-severe OSA,[70] 24-hour mean arterial pressure was similar between CPAP and MAD after 1-month of therapy. MAD was superior to CPAP for improving quality of life measures. More recently, another RCT demonstrated similar long-term improvement in self-reported neurobehavioral outcomes during a 10-year follow-up.[71] The American Academy of Sleep Medicine (AASM) and the American Academy of Dental Sleep Medicine (AADSM) developed guidelines for using MAD in patients with OSA.[72] The AASM/AADSM guidelines recommend the following: 

  1. Oral appliances can be considered rather than no treatment for adult patients with snoring (without OSA) or those with OSA who do not tolerate CPAP therapy or prefer alternate treatment.
  2. When a sleep physician prescribes oral appliance therapy for an adult patient with obstructive sleep apnea.
  3. A qualified dentist should use a custom, titratable appliance.
  4. A follow-up with a qualified dentist after oral appliance therapy is initiated in adult patients with OSA to assess for dental-related side effects.
  5. A follow-up with sleep testing to confirm treatment efficacy.

Surgical Treatments

Uvulopalatopharyngoplasty (UPPP) surgically removes the uvula and tissue from the soft palate to create more space in the oropharynx.[73] This is sometimes done in conjunction with a tonsillectomy and adenoidectomy. Nevertheless, the long-term efficacy of UPPP is very limited, with less than 50% of patients having a significant increase in AHI after the first year.[74] 

Maxillomandibular advancement (MMA) requires both the upper and lower jaws to be detached and surgically advanced anteriorly to increase space in the oropharynx.[75] This is best for patients with retrognathia and is less successful in older patients or those with larger neck circumferences. More recently, drug-induced sleep endoscopy (DISE) has been used for preoperative planning to identify multiple levels of obstruction in these patients and candidacy for surgical treatment such as MMA and hypoglossal nerve stimulator.[76] This allows surgeons to address any nasal, soft palate, and hypopharyngeal obstructions that may be present during a single surgery.[77]

A newer option is the implantable hypoglossal nerve stimulator (HNS), usually unilateral, although bilateral implantation has been recently reported.[78] It works by stimulating the genioglossus (upper airway dilator muscle) during apneas resulting in tongue protrusion and relief of the obstruction.[79] HNS effectively reduces AHI (median AHI score at 12 months decreased by 68%, from 29.3 events per hour to 9.0 events per hour) and improves sleepiness symptoms in those with moderate to severe OSA that is not tolerating PAP treatment.[80] Adverse events reported short- and long-term following HNS is not very common. In one study, 134 adverse events were reported from 132 patient reports over five years.[81] The most common adverse events reported after HNS are tongue abrasion (11.0%), pain (6.2%), and device malfunction (3-6%).[79] 

The eligibility criteria for HNS adopted from the original randomized trial include the following characteristics:[80]

  • Adults >18 years of age
  • Moderate to severe OSA (AHI between 20 to 50 with less than 25% central or mixed apneas)
  • Inability to tolerate CPAP
  • No complete concentric collapse at the palate on drug-induced sleep endoscopy

Exclusion criteria for HNS include the following:

  • BMI > 32.0 kg/m2.
  • Neuromuscular disease.
  • Hypoglossal-nerve palsy.
  • Severe restrictive or obstructive pulmonary disease.
  • Moderate-to-severe pulmonary arterial hypertension.
  • Severe valvular heart disease.
  • Heart failure, New York Heart Association class III or IV.
  • Recent myocardial infarction or severe cardiac arrhythmias (within the past 6 months).
  • Persistent uncontrolled hypertension despite medication use.
  • Active psychiatric disease and coexisting nonrespiratory sleep disorders.

In extreme cases, OSA can also be treated with a tracheostomy to bypass the oropharyngeal obstruction. This management option is also best addressed at academic or specialty sleep centers that are experienced in treating patients with tracheostomy. Such patients will encounter numerous challenges with home care, durable medical equipment, and family/partner education on tracheostomy management. Many patients with severe OSA requiring tracheostomy have comorbidities. 

Differential Diagnosis

  • Asthma
  • Central sleep apnea
  • Chronic obstructive pulmonary disease
  • Depression
  • Gastroesophageal reflux
  • Hypothyroidism
  • Narcolepsy
  • Periodic limb movement disorder


The short-term prognosis of OSA with treatment is good, but the long-term prognosis is guarded. The biggest problem is the lack of adherence to CPAP, as nearly 50% of patients stop using CPAP within the first month despite education.[82] Many patients have comorbidities and /or are at risk for adverse cardiac events and stroke. Hence those who do not use CPAP are at increased risk of cardiac and cerebral adverse events [83] in addition to higher annual healthcare-related expenses. [84] Further, OSA is also associated with pulmonary hypertension, hypercapnia, hypoxemia, and daytime sedation. In addition, these individuals have a high risk of motor vehicle accidents. The overall life expectancy of patients with OSA is lower than the general population. OSA is known to affect cardiac function, particularly in obese individuals. [85][86] CPAP treatment was recently found to improve left ventricular (LV) and right ventricular (RV) mechanics in patients with OSA. [87]


  • Hypertension
  • Myocardial infarction
  • Cerebrovascular accident
  • Depression
  • Sleeplessness related accidents

Deterrence and Patient Education

Weight loss should be encouraged in patients with OSA. They should be counseled to avoid alcohol, benzodiazepines, opiates, and some antidepressants, which may worsen their condition. Additionally, they should be made aware of the importance of proper sleep hygiene, getting enough sleep every night, and the risks of driving while sleepy. Adherence to CPAP use should be encouraged as well as how to clean and maintain the machine properly.

Enhancing Healthcare Team Outcomes

The management of patients with OSA is best accomplished with an interprofessional team that includes a sleep specialist, primary provider, cardiologist, otolaryngologist, dietitian, pulmonologist, and neurologist. There are many options to treat OSA, the primary one being CPAP. Unfortunately, compliance with CPAP remains low. Some patients may benefit from an oral or nasal device, but compliance remains an issue. Surgery is the last step and should only be considered after a thorough patient evaluation. Surgery does not cure the disorder, is expensive, and can be associated with severe complications. The prognosis for most patients with OSA is guarded. Until the patient starts to lose weight, most therapies have poor efficacy.

Review Questions

A polygraph depicting example of central and obstructive apnea


A polygraph depicting example of central and obstructive apnea. Contributed by Abdulghani Sankari, MD

A polygraph recording during sleep


A polygraph recording during sleep. The panel shows electroencephalogram (EEG), Electrooculogram (EOG), electrocardiogram (ECG), in addition to chin electromyogram (EMG) signals from the lower limbs and respiratory signals (C flow), chest and abdomen (more...)

A polygraph recording during sleep


A polygraph recording during sleep. The panel shows electroencephalogram (EEG), Electrooculogram (EOG), electrocardiogram (ECG), in addition to chin electromyogram (EMG) during 120 seconds window. Note the repetitive obstructive apnea (OA) with persistent (more...)

Clinical assessment of patients with suspected sleep apnea


Clinical assessment of patients with suspected sleep apnea. Contributed by Abdulghani Sankari, MD, PhD

The available types of sleep apnea testing from level I (in-lab PSG) to portable monitoring devices (level II, III and IV)


The available types of sleep apnea testing from level I (in-lab PSG) to portable monitoring devices (level II, III and IV). Note that only level II and III are acceptable for testing of OSA by the AASM guidelines. Contributed by Abdulghani Sankari, MD, (more...)


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Disclosure: Jennifer Slowik declares no relevant financial relationships with ineligible companies.

Disclosure: Abdulghani Sankari declares no relevant financial relationships with ineligible companies.

Disclosure: Jacob Collen declares no relevant financial relationships with ineligible companies.

Copyright © 2023, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK459252PMID: 29083619


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