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Key questions on obstructive sleep apnoea

Posted on: 17 Jan 2019

Learning Objectives

This module brings you the latest in diagnosing and managing sleep apnoea, including:

  • The difference between apnoea and hypopnoea
  • Using and interpreting the Epworth sleepiness scale
  • The role of sleep studies and home pulse oximetry
  • Intra-oral devices vs CPAP for treating obstructive sleep apnoea

Dr Himender Makker is a consultant in respiratory and sleep medicine at University College London Hospital. Dr Rory McDermott is a specialist registrar in respiratory medicine.

Apnoea and hypopnoea are terms used to define cessation or reduction in oral or nasal airflow respectively. Apnoea is a complete cessation of airflow for 10 seconds or more, often associated with oxygen desaturation. Hypopnoea is a reduction in airflow for 10 seconds or more. However, criteria for hypopnoea vary among different sleep laboratories – reduction in airflow varies from 30% to 50% and an associated 4% reduction in oxygen saturation may be required to classify a reduction in airflow as hypopnoea. The widely accepted definition of hypopnoea is 50% or more reduction in airflow associated with 4% oxygen desaturation.1

Both apnoea and hypopnoea occur during sleep and may disturb sleep – oxygen desaturation is worse in apnoea than hypopnoea. Apnoea and hypopnoea are mostly due to upper airway obstruction (obstructive sleep apnoea – can’t breathe) or rarely due to loss of respiratory neural drive (central sleep apnoea – won’t breathe).

The diagnosis of obstructive sleep apnoea rests on the measuring number of apnoea and hypopnoea incidents on an overnight sleep study. The number of apnoea and hypopnoea incidents per hour known as apnoea hypopnoea index (AHI) is a standard measure for diagnosis and estimation of the severity of obstructive sleep apnoea. An AHI of >5 is required for the diagnosis of obstructive sleep apnoea. An AHI of 5-14 is mild, 15-30 moderate and >30 severe obstructive sleep apnoea.

A 4% oxygen desaturation dip from the baseline saturation is accepted as a surrogate marker for apnoea and hypopnoea. It is used to calculate the oxygen desaturation index, but it cannot differentiate between central or obstructive sleep apnoea and normal dip rate does not exclude sleep apnoea.

Fatigue and tiredness are extremely common symptoms among the population. Many people accept these symptoms as a part of their lifestyle and they are often ignored by health professionals, even when they present to health services. It is not uncommon for people to report fatigue and tiredness when they are actually sleepy. Sleepiness during the daytime should be explored further by establishing with the patient if it is intruding into their social life, affecting work or driving or simply asking them to complete an Epworth sleepiness scale (ESS) questionnaire. Excessive daytime sleepiness can be due to insufficient sleep or disturbed sleep. Obstructive sleep apnoea is one of the common causes of disturbed sleep and excessive daytime sleepiness. Patients have disturbed and unrefreshing sleep despite more than eight hours in bed. They snore extremely loudly and wake from sleep either for no apparent reason, to pass urine or gasping or choking for breath. Nocturia and frequency due to disturbed sleep can be falsely attributed to benign prostatic enlargement or diabetes. The mechanism of this is thought to be atrial dilatation leading to release of atrial natriuretic peptide and resultant inhibition of the renin-angiotensin axis.

Similarly, nocturnal choking is reported as waking up with panic attacks, palpitations and profuse sweating. Snoring is almost ubiquitous in obstructive sleep apnoea and is caused by turbulent airflow in the upper airways. Snoring in obstructive sleep apnoea is often loud and intrusive, however, snoring in the absence of other features of obstructive sleep apnoea, termed simple snoring, is unlikely to be of significance.

Loud disruptive snoring and recurrent obstructive apnoea can lead to vibration injury/inflammation to upper airway mucosa reported as a dry (rather than sore) throat on waking up in morning. In addition to excessive daytime sleepiness, many patients with obstructive sleep apnoea have impaired concentration and memory and are irritable, anxious or depressed affecting their quality of life.2

The ESS is a quick and simple questionnaire for quantifying subjective daytime sleepiness. It can be undertaken in a waiting room environment or online. It is an eight item questionnaire in which patients score the likelihood of falling asleep (0-3 points for each item, with a score of 0 indicating no likelihood and 3 indicating a high likelihood). A total score of >10 out of 24 is considered to be indicative of excessive daytime somnolence. In addition to the total score, it is worth checking the likelihood score for each situation. A high chance of falling asleep when stopped at a traffic light is probably more significant than falling asleep while watching television. Overall, sleepiness intruding into work or driving is more relevant than sleepiness during social activities. In fact, ESS situations start from checking chances of falling asleep during passive, physical and mental states, such as sitting and resting to active situation like sitting and taking to someone.

ESS measures daytime sleepiness but is not specific for obstructive sleep apnoea and does not take into account the patient’s clinical narrative. A high ESS (>10) is seen in 10% of the population. As such, a history of intrusive somnolence should be sought to avoid unnecessary onward referral.  Scoring systems, for example, the STOP-BANG or the more complicated Berlin questionnaires, include added information such as the presence of witnessed apnoea and snoring and have a more relevant role in screening for obstructive sleep apnoea.

Results should be interpreted with caution as underestimation of somnolence is a well recognised pitfall of the scale due to patient avoidance of situations where they readily fall asleep. Furthermore, inter-observer variability is a well documented failing of the ESS. Finally, ESS score does not correlate well with severity of obstructive sleep apnoea (AHI) as patients with severe sleep apnoea may have a normal ESS score.

Most good predictors of obstructive sleep apnoea are located in the head and neck area. A simple routine of checking neck for size, chin for mandibular size and shape and inspection of oral cavity for tongue, uvula, tonsil enlargement and overall oral size is helpful.2

An increase in collar size (>17 inches/43 cm) is a good predictor of obstructive sleep apnoea. Obesity is the main reason for an increase in neck size. Excessive deposition of visceral fat in para-pharyngeal area narrows upper airway and increases risk of obstructive sleep apnoea. Neck obesity is more common in obese men than obese women, which may in part account for the higher risk of sleep apnoea seen in males. It is worth knowing that an increase in neck size due to muscle bulk in bodybuilders also increases risk of obstructive sleep apnoea.

Although, a stereotypical phenotype of obstructive sleep apnoea is that of a middle age obese man, it is equally common among the non-obese population across a different age spectrum and multiple ethnic groups. This is mainly due to craniofacial features, such as micro and retrognathia.

An inspection of the oral cavity for soft tissue enlargement causing a crowded and narrow oral passage is extremely useful. A large tongue indicated by teeth marks on the sides, a swollen and elongated uvula touching the back of the tongue and tonsils meeting in the middle are tell tail markers of snoring and sleep apnoea. An overall assessment oral cavity size using the Mallampati scoring system (grade 3 and 4) is a good predictor of obstructive sleep apnoea.

Many of the above physical examination features are seen in syndromic patients – such as Down’s syndrome, acromegaly and Marfan’s and individuals with these conditions should be routinely screened for obstructive sleep apnoea. Subclinical hypothyroidism as a possible risk factor and cause of daytime fatigue should be excluded by checking T4 and TSH.

Research over the last 20 years has established a clear causal link between obstructive sleep apnoea and cardiovascular diseases and metabolic problems. Patients with hypertension, particularly refractory and resistant hypertension and diabetes, have a much higher prevalence of obstructive sleep apnoea than the general population and should be considered for screening sleep studies.

Currently, we are diagnosing and treating only a small proportion (20%) of obstructive sleep apnoea patients. This is mainly due to a low index of suspicion in patients presenting with non-specific symptoms of poor sleep and daytime tiredness or not screening the high risk population. Short supply and under-resourced sleep services in the NHS are a poor excuse.

Since none of the clinical features on its own are sensitive or specific enough to predict obstructive sleep apnoea, two good questionnaires, STOP-BANG and Berlin, were developed and are available for screening general and high risk populations. These questionnaires have much better sensitivity and specificity. These are in routine use for screening obstructive sleep apnoea in high risk populations, such as bariatric service. These questionnaires, particularly STOP-BANG that is easier to use and interpret, should be used in primary care.3

Home pulse oximetry is cheap and easy to perform but requires careful and considered interpretation. A positive sleep study is helpful, but a negative sleep study does not exclude obstructive sleep apnoea. It has reduced sensitivity, particularly in younger non-obese patients who can have frequent apnoea without oxygen desaturation. On the other hand, patients with co-existent pulmonary disease may register desaturations due to reduced respiratory drive during sleep (false positive and low specificity). Finally, diagnosis relies on single channel recording and increases chances of technical failure.2

Multichannel sleep recording system is required to exclude a diagnosis of sleep apnoea. These devices record nasal airflow, snoring levels, patient position, oximetry, pulse rate and chest and abdominal wall movement. These provide a much more detailed assessment of sleeping patterns and allow alternative diagnoses of upper airways resistance syndrome and central sleep apnoea syndrome.2

Patients with more complex or primary sleep disorders (narcolepsy, REM sleep disorders etc.) require polysomnography that includes EEG monitoring. This remains the most detailed and informative sleep study, but the cost implications and requirement of overnight admission are the major limiting factors.

Obstructive sleep apnoea and excessive daytime somnolence can be exacerbated by sedative medications and the need for these should be reviewed at the earliest opportunity. This is particularly important in patients who are on sedating types of anxiolytics and antidepressants.

Alcohol is also a muscle relaxant and can precipitate apnoeas in snorers and worsen existing apnoeas. Alcohol before sleep worsens sleep apnoea during first few hours of sleep, and avoidance before sleep can improve sleep apnoea control.

Obstructive sleep apnoea is worse in the supine body sleep position, and positioning devices that prevent patients from lying on their back can reduce apnoeic episodes. However, these are often uncomfortable or impracticable.

Weight loss through pure dietary measure is less effective than weight loss from a combination of diet and exercise. Improvement of upper airway muscle tone through cardiopulmonary exercise or specific upper airway muscle exercise, such as singing or playing the trumpet, can improve obstructive sleep apnoea.

Lifestyle measures serve as useful adjuncts, but the primary therapy for obstructive sleep apnoea remains continuous positive airway pressure devices (CPAP).4

Professional (vocational) drivers and heavy machinery operators who are excessively sleepy during the daytime (high ESS) or have a history of near misses or accidents should be promptly referred to prevent driving or work-related accidents.

Patients with metabolic syndromes (hypertension, diabetes, hyperlipidaemia) have a much higher prevalence of obstructive sleep apnoea than the general population and obstructive sleep apnoea adds to cardiovascular risks. Diagnosis and treatment of obstructive sleep apnoea can reduce the risk of cardiovascular disease.5

Similarly, patients with craniofacial abnormalities or syndromes such as Down’s syndrome are known to have a high risk of obstructive sleep apnoea. Treatment of obstructive sleep apnoea improves quality of life in these patients.

Morbidly obese patients, particularly those who have low daytime oxygen saturations, are likely to have nocturnal hypoventilation associated with obstructed sleep apnoea (obesity hypoventilation syndrome). These patients are at risk of developing acute ventilatory failure, requiring hospital admission and acute non-invasive ventilation (NIV). They carry chances of increased morbidity and mortality. Treating obesity hypoventilation syndrome with nocturnal oxygen, CPAP or domiciliary NIV can prevent the above problems.

The above used to be the main problems with the older type of CPAP machine and masks which affected CPAP tolerance and compliance. There have been tremendous improvements in CPAP machine and mask designs to improve comfort and tolerance. The above side effects were mainly due to cold room air sucked in by the compressor pump and delivered to the upper airway via the nose. This caused irritation of nasal mucosa and CPAP (vasomotor) rhinitis. This can be easily prevented by built-in heated tubing and humidifiers attached to CPAP.  Rhinitis responds well to anticholinergic and corticosteroid nasal spray with temporary discontinuation of CPAP. ENT surgeons can easily sort-out persistent or recurrent rhinitis, sinusitis and significant epistaxis.6

The current main hindrances to CPAP compliance are psychological barriers – claustrophobia, appearance and absence of symptoms. Reassuring patients that sleeping quietly without snoring and obstructed breathing is more likely to be preferred by their bed partner than their looks can be helpful. Explanation that obstructive sleep apnoea is a risk factor for cardiovascular and metabolic problems and should be treated similar to hypertension and hyperlipidaemia should help to improve acceptance and compliance in asymptomatic patients. Claustrophobia can be difficult to manage, but a trial of smaller nasal cushion/pillow type to the mask may help. Others may need formal psychological support or CBT.

Oral advancement devices were first used at the start of the 20th century by Pierre Robin. By protruding the mandible, they stabilise the tongue and hyoid and improve the patency of the upper airway at the tongue base level. Boil and bite devices are readily available over the counter, while dentist fitted devices may provide superior results. Either way, the chosen device should be retentive, comfortable and adjustable. A recent trial has shown that semi-bespoke are better than simple boil and bite devices and are as good as dentist fitted device.

A mandibular advancement splint is not as effective as CPAP – it reduces the AHI by half compared to normalisation of AHI by CPAP. Mandibular advancement splints prevent upper airway collapse at the tongue base level only and may not work in patient with retropalatal or multiple levels upper airway obstruction. However, it is preferred over CPAP by most patients.7

In general, oral advancement devices should not be recommended for patients with severe obstructive sleep apnoea or significant nocturnal desaturation, where CPAP is more likely to reduce the AHI more effectively. However, it may be important to look past AHI alone in specific circumstances and there is sufficient evidence that oral advancement devices can provide an effective and well tolerated alternative to CPAP.

Driving when excessively tired is a criminal offence and any patient who falls asleep while driving is personally liable for any incidents. This principal holds for patients with sleep apnoea syndrome who describe daytime somnolence in conjunction with an abnormal sleep study. Such patients must inform the DVLA of their diagnosis and not drive until established on treatment that has improved their excessive daytime somnolence.

Patients who are free from sleepiness need not directly liaise with the DVLA, but should remain vigilant to any change in their clinical situation and should be strongly counselled to cease driving and seek re-assessment in such case.

For group 2 licences, driving will only be permitted again when satisfactory control of symptoms is achieved and confirmed by specialist opinion.

  1. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. Sleep 1999;22:667–89.
  2. Schlosshan D, Elliott MW. Sleep • 3: Clinical presentation and diagnosis of the obstructive sleep apnoea hypopnoea syndrome. Thorax 2004;59:347-352.
  3. Abrishami A, Khajehdehi A, Chung F. A systematic review of screening questionnaires for obstructive sleep apnea. Can J Anaesth. 2010 May;57(5):423-38.
  4. Shneerson J, Wright J. Lifestyle modification for obstructive sleep apnoea. Cochrane

Database Syst Rev. 2001;(1).

  1. Dewan NA, Nieto FJ, Somers VK. Intermittent hypoxemia and obstructive sleep apnoea: implications for comorbidities. Chest. 2015 Jan;147(1):266-74.
  2. Ward K, Hoare KJ, Gott M. What is known about the experiences of using CPAPfor obstructive sleep apnoea from the users’ perspective? A systematic integrative literature review. Sleep Med Rev. 2014 Aug;18(4):357-66.
  3. Marklund M, Verbraecken J, Randerath W. Non-CPAP therapies in obstructive sleep apnoea: mandibular advancement device therapy .European Respiratory Journal May 2012, 39 (5) 1241-1247;

Dr Himender Makker is a consultant in respiratory and sleep medicine at University College London Hospital and Dr Rory McDermott is a specialist registrar in respiratory medicine

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