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Sleep Apnea Learning Zone

Obstructive & Positional Obstructive Sleep Apnea

Read time: 40 mins
Last updated:12th Mar 2020

Obstructive sleep apnea (OSA)

Obstructive sleep apnea (OSA) is the most common sleep-related breathing disorder. OSA is characterised by recurrent obstruction of the pharyngeal airway during sleep, resulting in reduced (hypopnea) or complete cessation (apnea) of airflow despite ongoing breathing efforts. These disruptions to breathing lead to intermittent oxygen desaturation, sleep disturbance, and sympathetic activation (Strollo et al., 1996). Consequences of OSA include excessive daytime sleepiness, fatigue, reduced quality of life, increased risk of traffic and occupational accidents and increased risk of developing cardiovascular disease. When patients experience most of their apneic events in the supine sleep position, the term of positional obstructive sleep apnea (POSA) is used.

Visit different sections within the Obstructive Sleep Apnea Learning Zone to find out more about the epidemiology, pathophysiology, symptoms and diagnosis and current treatment options.

Obstructive sleep apnea epidemiology

Before we discuss the epidemiology, let us consider what obstructive sleep apnea (OSA) actually looks like.

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Figure 1. Polysomnographic tracings of obstructive sleep apnea (adapted from Eckert & Malhotra, 2008).
EMGgg, Electromyogram of the genioglossus muscle (intramuscular); EMGsub, EMG of the submental muscle (surface); EEG, electroencephalogram (C3–A2); Pepi, pressure at the level of the epiglottis; Flow, airflow measured via nasal mask and pneumotachograph; SaO2,  arterial blood oxygen saturation measured via pulse oximetry at the finger. 

Figure 1 shows evidence of snoring on the flow tracing preceding the apneic event during which oxygen saturation progressively falls. In this example, despite a lowered arousal threshold and progressive increases in EMGgg activity throughout the obstructive event, airflow was not able to be restored without an arousal (awakening) (Eckert & Malhotra, 2008). Learn more about the events that lead to OSA in the pathophysiology section.

OSA is the most common type of sleep apnea which occurs in about 10% of the adult population (Young et al., 2002). OSA occurs two to three times more often in older adults and is twice as common in men as in women (Table 1).

Table 1. Incidence of obstructive sleep apnea in adults (Peppard et al., 2013).

table 1.png


Many patients are unaware that their breathing is affected during sleep and it has been estimated that 12–18 million persons in the United States are untreated (Young et al., 2009).

Positional obstructive sleep apnea

Positional obstructive sleep apnea (POSA) is a distinct subset of OSA. It is a condition in which most of the apneic events occur when a patient lies on their back. POSA can often be avoided by sleeping on one’s side (van Maanen et al., 2014) and there are a number of ways of avoiding sleeping in the supine position, some being more attractive than others.

back to back with a tennis ball.png


However, POSA is not simply about avoiding sleeping in a supine position and its prevalence is underestimated. Approximately 56% of patients with OSA are known to suffer from POSA (Oksenburg et al., 1997) and it appears to vary with apnea severity. One study showed that 49.5% of patients with an AHI of 5–15/hour had POSA, whereas for patients with an AHI of 15–30/hour or >30/hour the figures were 19.4% and 6.5%, respectively.

Some patients have exclusive POSA (ePOSA), where their apnea-hypopnea index (AHI) normalises in non-supine positions (Cartwright et al., 1984). In a large population-based study of 1,719 subjects (HypnoLaus), 71% of subjects had OSA. POSA was present in 53% of all subjects and in 75% of OSA subjects. ePOSA was present in 26% of all subjects and in 36% of OSA subjects (Heinzer et al., 2018).

Visit the Sleep and Breathing conference 2019 section where Dr Raphaël Heinzer gives more details about POSA and ePOSA epidemiology and the HypnoLaus study.


Who gets obstructive sleep apnea?

OSA is mainly due to an anatomically small pharyngeal airway and so risk factors are conditions that reduce the size of the resting pharynx or increase airway collapsibility (Veasey & Rosen, 2019).

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Figure 2. Risk factors for obstructive sleep apnea (Punjabi 2008; Mayo Clinic, 2019).


We have already highlighted that gender and age are important risk factors for OSA but there are several other risk factors that should be considered.

Obesity: Although slender people can also develop the disorder, obesity is the most significant risk factor for OSA (Shah & Roux, 2009). Increased adipose tissue around the upper airway (often causing a thick neck) may obstruct breathing or make the airway more prone to collapse during sleep. OSA has been reported in >40 % of patients with a body mass index (BMI) >30 and in 60% of patients with metabolic syndrome (Veasey & Rosen, 2019). Further, moderate to severe obesity is found in between 60 and 90% of people with OSA.

Narrowed airway: This can be associated with obesity, but a narrow airway due to bony structures (micrognathia) or enlarged tonsils or adenoids (particularly in children) can block the airway and lead to sleep apnea.

Menopause: The prevalence of OSA in females rises markedly after menopause- 47% to 67% of postmenopausal women have been found to have OSA. This may be because women tend to gain weight after menopause, but it is not likely to be the only factor (Jehan et al., 2016).

Genetic predisposition: Genetically inherited physical traits like face and skull shape, characteristics of the upper airway muscles, as well as body fat content and distribution can all contribute to sleep apnea.

Use of alcohol, sedatives or tranquilisers: Because these substances relax the muscles in the person’s throat, frequent use can lead to the disorder.

Smoking: Smoking can increase the amount of inflammation and fluid retention in the upper airway and smokers are more likely to develop OSA.

Nasal congestion: Allergies, a deviated septum and other issues that make it difficult to breathe through the nose may increase the risk of sleep apnea.

Medical comorbidity: OSA may contribute to the development of cardiovascular conditions, including hypertension, coronary artery disease, congestive heart failure, arrhythmia and stroke. There is also a high prevalence of sleep apnea in patients with type 2 diabetes.

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Obstructive sleep apnea pathophysiology

An obstructive sleep apnea (OSA) episode occurs when the soft tissues of the upper airway and tongue relax during sleep and block the flow of air into the lungs. These disruptions to breathing lead to intermittent blood gas disturbances (hypercapnia and hypoxemia) and are associated with increasing respiratory efforts and a brief awakening from sleep (arousal). Finally, pharyngeal activity is restored, the airway opens and hyperventilation occur in an attempt to recover oxygen and carbon dioxide levels and the patient fall back to sleep (figure 4). This does not happen during wakefulness as there is a protective mechanism which maintain the airway patency (Jyothi et al., 2019).

In severe cases disruptions to breathing can occur more than 100 times per hour, with each typically lasting 20–40 seconds, and these episodes reduce both deep NREM (non-rapid eye movement) and REM (rapid eye movement) sleep (Eckert & Malhotra, 2008).

SleepApnea_Fig4__5DF787DB-EB20-4D71-842A742CD15A7C34.png

Figure 4. Pathophysiology of obstructive sleep apnea (Jyothi et al., 2019).


Sleep apnea is a multifactorial disorder but typically involves some degree of upper airway anatomical impairment. In addition, upper airway muscle function, respiratory arousal threshold and ventilatory stability are also factors in the development of OSA (figures 4–8).

Anatomical impairment

SleepApnea_Fig5__FFAC723D-EB4A-4E90-983066421B71E660.png

Figure 5. Anatomical impairment (adapted from Carberry et al., 2018).


The pharynx is unique in that it lacks rigid or bony support and when collapse does occur it usually happens behind the soft palate or the oropharynx (from the tip of the soft pate to the epiglottis), or both. X-ray and CT imaging also show that patients with OSA may also have a reduced mandibular length, an inferiorly positioned hyoid bone, and may have mandibular repositioning all of which can compromise the upper airway (Fogel et al., 2004). There is a definite association between changes in lung volume and the size of the upper airway (Fogel et al., 2004) and it is thought that this effect is due to tracheal tug. As the lungs expand, the trachea is pulled downward which stiffens the upper airway making it less collapsible. The importance of this effect has not been fully established but it is suspected that sleep-induced reductions in lung volume can cause increased upper airway collapsibility in non-rapid eye movement (NREM) sleep in patients with OSA (Fogel et al., 2004).

Upper airway muscle function

Muscle tone decreases during sleep and is at its lowest during rapid eye movement (REM) sleep. As there are over 20 muscles in the upper airway, pharyngeal collapse is possible at one or multiple sites (figure 6).

SleepApnea_Fig6__62BB3A28-8FF4-46D5-A1F6C3022CB62C0D.png

Figure 6. Anatomy of the upper airway and important muscles controlling airway patency (adapted from Fogel et al., 2004).


The upper airways have complex neuronal patterns that differ between muscles and play a role in the maintenance of airway patency (figure 7).

SleepApnea_Fig7__AD4D3912-7E18-4263-A0537F53B232128B.png

Figure 7. Upper airway muscle function (adapted from Carberry et al., 2018).
Blue tracings represent the desired response and navy tracings represent impairment. EMG, genioglossus electromyography; MTA, 100 ms moving time average of the rectified raw EMG signal; OSA, obstructive sleep apnea.


These groups of neurones within the brainstem are known to have different firing patterns according to the respiratory cycle (Fogel et al., 2004; Osman et al., 2018). For example, the genioglossus (the largest pharyngeal dilator muscle located at the base of the tongue), has six different patterns of input from the brain and ~30% of patients with OSA have poor genioglossus muscle responsiveness to airway narrowing during sleep. The control of the different upper airway muscles is therefore believed to contribute to OSA pathogenesis and can drive airway narrowing during sleep (Osman et al., 2018).

Respiratory instability

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Positional sleep apnea pathophysiology

POSA is associated with increased waist-to-hip ratio in men (Heinzer et al., 2018). This suggests that abdominal obesity in men may induce POSA by pulling up the diaphragm in the supine position, which in turn decreases the tension exerted on the pharyngeal walls through the mediastinum, favouring pharyngeal collapse (Heinzer et al., 2018). In addition, lung volume also plays a role in POSA as a higher positive airway pressure is required to keep the airway open when lung volume is reduced (Heinzer et al., 2005).

Visit the Sleep and Breathing conference 2019 section to learn more about the pathophysiology of POSA. Dr Raphaël Heinzer describes in more detail the effects of obesity, lung volume, upper airway size and head position.

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Obstructive sleep apnea symptoms and diagnosis

Obstructive sleep apnea symptoms

Sleep apnea is insidious, and patients are often unaware of their associated symptoms. As a result, it often goes undiagnosed or is first noticed by others due to habitual loud snoring combined with daytime sleepiness.

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Figure 10. Night-time and daytime symptoms of OSA (Veasey & Rosen, 2019).

Obstructive sleep apnea diagnosis

If OSA is suspected, the clinical approach to diagnosis should begin with an assessment of the likelihood of disease, the symptoms present and any relevant coexisting conditions (Veasey & Rosen, 2019). There are several steps that should be taken along the diagnostic pathway:

1. Carry out a sleep test/questionnaire

Getting patients to answer a sleep questionnaire, possibly with the help of their partner, is an important first stage to ascertain if sleep apnea could in fact be a problem. The Epworth Sleepiness Scale is also often used to determine the likelihood of a patient’s dozing in different settings as an indicator of inadequate restorative night-time sleep. The scores range from 0‒24, with more than 10 being indicative of excessive sleepiness. Specific to OSA is the STOP-BANG score:

S - snoring

T - tired

O - observed apnea

P - blood pressure

B - BMI over 35

A - older than 50 years old

N - large neck size

G - gender male

If there are ≥3 positive answers, the patient is considered at high risk of sleep apnea. Alternatively, the Berlin questionnaire can be used to evaluate the presence, loudness and frequency of snoring, apneas, daytime sleepiness, hypertension and obesity to help predict a high or low likelihood of sleep apneas (Slowik & Collen, 2019). It should be noted, however, that not every patient with OSA perceives sleepiness or has been informed of their snoring (Veasey & Rosen, 2019).

2. Refer the patient to a sleep specialist

A sleep specialist will be able to determine the best screening or diagnostic test. Polysomnography (PSG) is the gold standard for diagnosing sleep disordered breathing in a sleep laboratory. During a PSG study, both neurophysiological and respiratory parameters are measured such as brain wave activity (electroencephalogram, EEG), cardiac activity (electrocardiogram, ECG), eye movements (electro-occulogram, EOG) or chin activity, nasal and oral airflow, respiratory efforts, body position, oxygen saturation, snoring and leg movements. PSG interpretation, made by the sleep physician or a qualified sleep technician, will help to quantify sleep time, differentiate sleep stages, assess sleep fragmentation and evaluate the sleep disordered breathing severity by measuring the apnea hypopnea index (AHI) or the respiratory disturbance index (RDI) (Ibáñez et al., 2018).

sleeping man.jpeg

Apnea is defined as complete obstruction (airflow reduction by more than 90%) of the upper airways lasting for at least 10 seconds.

Hypopnea is defined as airflow restriction of more than 30% for at least 10 seconds, with at least a 3% oxygen desaturation and/or an arousal (AASM, 2013).

Disease severity is assessed by measuring the AHI which represents the number of apneas and hypopneas per hour of sleep (table 2).

Table 2. Apnea-hypopnea index (AHI) classification (Veasey & Rosen, 2019, American Sleep Apnea Association, 2017).

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Current obstructive sleep apnea treatment options

Treatment is recommended for all patients with an AHI or respiratory-event index of ≥15 events per hour or 5–14 events per hour with symptoms of sleepiness, impaired cognition, mood disturbance or insomnia or with pre-existing conditions such as hypertension, ischaemic heart disease or a history of stroke (Veasey & Rosen, 2019).

Studies have shown evidence for body weight as an important factor in determining the evolution of sleep apnea. In the Sleep Heart Health Study, compared with a stable weight over treatment follow-up, men with a weight gain more than 10 kg had a 5.2-fold increase in AHI. For a comparable gain in weight, women had a 2.5-fold risk of AHI increase (Punjabi et al., 2008). Although weight loss is recommended (ELF, 2019) and known to decrease severity of OSA, it is commonly difficult to achieve and sustain.

There is no medication available for the treatment of OSA. Attempts to develop pharmacotherapy to increase upper airway muscle activity or target the respiratory arousal threshold or loop gain have been, and continue to be, evaluated (Osman et al., 2018).

Continuous positive airway pressure

Continuous positive airway pressure (CPAP) is the gold standard therapy to prevent upper airway collapse and reduce OSA severity. CPAP applies positive pressure to the patients’ upper airway using a nasal (figure 12) or oronasal mask (figure 13).

An example of a nasal mask supplying continuous positive airway pressure wisp.jpg

Figure 12. An example of a nasal mask supplying continuous positive airway pressure (CPAP) (Philips DreamWear Wisp).

An example of a nasal mask supplying continuous positive airway pressure.jpg

Figure 13. An example of a Full Face mask supplying continuous positive airway pressure (CPAP) (Philips DreamWear FullFace mask).

There is convincing evidence that CPAP treatment can reduce AHI to <5 events per hour in most patients and alleviate daytime and nighttime symptoms such as sleepiness, fatigue, intellectual impairment, restlessness and restless sleep (Veasey & Rosen, 2019).

Studies have shown that CPAP:

  • markedly improves self-perception and vitality (Siccoli et al., 2008)
  • reduces fatigue and daytime sleepiness (Tomfohr et al., 2011)
  • reduces risk of motor vehicle accidents (MVA) (George et al., 2001)
  • lowers 24-hour systolic blood pressure by 4 mm Hg (Faccenda et al., 2001)

While the effects of CPAP for cardiovascular events in obstructive sleep apnea are unclear, it is widely recognised that CPAP can result in near complete resolution of symptoms only if the patient is adherent (NICE, 2018; Slowik & Collen, 2017; Patil et al., 2019).

CPAP compliance

CPAP does require patient cooperation to position the mask correctly and adhere to the therapy and compliance is estimated to be around 75% of patients using it for >4 hours per night for >70% of nights (Veasey & Rosen, 2019).

For patients who can’t tolerate high pressure, bilevel positive airway pressure (BPAP) is an alternative to CPAP. A bilevel machine delivers a low expiratory pressure during exhalation and a higher inspiratory pressure during inhalation.

Alternative options for patients with mild OSA who decline or are unable to use CPAP may be to use an oral appliance, positional therapy or surgical correction. Referrals within the sleep centre are often made if this is the case.

Oral appliances

These are custom-made devices inserted into the mouth to generally advance the mandible to help enlarge the upper airway. Intra-oral devices are appropriate for patients who snore or have mild to moderate OSA with normal daytime alertness. Oral appliance therapy is associated with clinically relevant decreases in the AHI (Vecchierini et al., 2016). However, adverse events such as tooth pain, changes in tooth position resulting in a different occlusion and articulation, or temporomandibular dysfunction can limit adherence to this therapy (Doff MH et al., 2012; 2013). They are not generally as effective as CPAP in reducing the AHI, but compliance is generally better (Phillips et al., 2013).

Positional therapy

For OSA with a strong positional component (POSA), alternatives include the use of specific treatments designed to avoid the supine sleeping position. A small lightweight positional therapy device that emits gentle vibrations can be used to remind the patient not to sleep on their back (figure 14). In a randomised, prospective, multicenter trial in patients with mild to moderate POSA, compliance with the sleep position trainer device was high and efficacy of this therapy was maintained over 12 months (de Ruiter et al., 2018).

Sleep position trainer devices have been shown to reduce AHI score by 46–69%(van Maanen et al., 2013; de Ruiter et al., 2018).

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