Sleep Apnea

Sleep apnea is a disorder in which breathing briefly stops several times (for periods of 10 seconds or longer) during sleep. Affected people may not be aware of any problem during the night, but may be sleepy during the day, with poor memory and concentration.

Severe sleep apnea is potentially serious; it may lead to hypertension, heart failure, myocardial infarction (heart attack), or stroke. Obstructive sleep apnea is the most common form. It may affect anyone, but more often occurs in middle-aged men, especially those who are overweight.

The most common cause is over-relaxation of the muscles of the soft palate; another possible cause is enlarged tonsils or adenoids.These problems cause obstruction of the airway,and result in snoring. If complete blockage occurs, breathing stops. This triggers the brain to restart breathing; the person may gasp and wake briefly.

In central sleep apnea, breathing stops because the chest muscles and diaphragm muscle temporarily cease to work, probably due to a disturbance in the brain’s control of breathing.

Causes include paralysis of the diaphragm and disorders of the brainstem (the part of the brain that controls breathing). Snoring is not a main feature.

Overweight people may find that losing weight helps. (In contrast, alcohol and sleeping drugs aggravate sleep apnea.)

In one treatment, air from a compressor is forced into the airway via a mask worn over the nose. Night-time artificial ventilation may be needed.

Tonsillectomy, adenoidectomy, or surgery on the soft palate may be performed.

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Sleep apnea in adults - technical

Sleep apnea in more detail - overview - technical

The number of patients diagnosed with obstructive sleep apnea/ hypopnea syndrome (OSAHS) is increasing, and therefore the requirement to provide sleep services for such patients is also increasing. In a cash-limited healthcare system it is important for sleep physicians to have a pragmatic and evidence-based approach to OSAHS to be able to diagnose symptomatic OSAHS accurately in conjunction with a sleep study; to identify those patients most likely to benefit from continuous positive airways pressure (CPAP) treatment; to identify those who would benefit from alternative treatment, such as a mandibular advancement device; and to determine the simplest and most effective way to initiate and continue CPAP therapy for the patient.


Obstructive sleep apnea/hypopnea syndrome (OSAHS) is a common disorder, in which upper airway resistance increases during sleep. This increased resistance is due to upper airway dilator muscle relaxation and airway narrowing, causing inspiratory flow limitation, snoring, hypoventilation, and ultimately complete obstruction, that is, apnea. In response to this obstruction, respiratory effort increases and pharyngeal dilator muscles are activated in order to defend the airway. If this fails to solve the problem, a return to the awake/semi-awake state occurs, and this finally terminates the apnea. This cycle is repeated, often hundreds of times each night. These cycles are associated with profound autonomic and cardiovascular changes, with systolic blood pressure falls of often 450mmHg due to the frustrated inspiratory efforts, and rises of 480mmHg with each arousal. These may directly damage the arterial system, but the evidence is unclear. Sleep fragmentation caused by the recurrent arousals is thought to be the main cause of the daytime sleepiness associated with OSAHS.

Population studies have estimated the prevalence of OSAHS to be 2–4% of adult men and 1–2% of women. It is still underdiagnosed, although awareness amongst health professionals and the general public is increasing. As the number of people, particularly in the Western world, who are overweight continues to rise, OSAHS will increase in prevalence with increasing demands on sleep services.

Investigation of OSAHS

Sleep studies are performed primarily to diagnose and quantify the severity of sleep-disordered breathing. Along with a clinical assessment, they can also be used to evaluate whether a patient’s daytime symptoms of sleepiness are likely to be attributable to arousals and sleep fragmentation that result from an obstructed upper airway.

Sleep studies have evolved over time as the understanding of the pathology of OSAHS has progressed, with different techniques of direct and indirect measurement being developed. The way in which OSAHS is investigated and diagnosed varies among centers. The minimum standards required to diagnose OSAHS are contentious. Traditionally polysomnography with EEG/EMG/EOG channels has been used to diagnose sleep-disordered breathing, and to initiate its treatment. There is no evidence that this complicated and expensive system of diagnosis and treatment is any more valid than simplified systems. Sleep centers increasingly have to review their investigative techniques to determine the most appropriate way of providing a pragmatic and evidence- based sleep service, with accurate, efficient, and cost-effective diagnosis and treatment. It needs to be appreciated that there is a difference between what can be studied and what should be studied in practical terms. Crucially, it is important for countries to work together towards the evidence-based minimums that are required for the accurate diagnosis of OSAHS.

The current main types of sleep study are discussed below.


Polysomnography was first used for the diagnosis of sleep disorders by neurologists and neurophysiologists, who were the first physicians to be involved in the investigation and diagnosis of the sleepy patient. Techniques used for the investigation of patients with neurological disorders were adapted for sleepy patients. Electrophysiological signals derived from the electroencephalogram (EEG), electro-oculogram (EOG), and electromyelogram (EMG) were used to determine sleep onset, sleep stage and duration, as well as sleep fragmentation, arousals and, more recently, microarousals. Simple signal transducers, such as oronasal thermistors and ribcage/abdominal mercury strain gauges, were added to document irregular breathing. The obstructive apneas were counted and the apnea index per hour of sleep invented and defined. Oximetry was added later. Polysomnography became established as the standard method of investigation of sleep patients, against which other techniques were judged. It has not, however, been properly validated as a tool to measure the actual pathological process resulting from reduced upper airway patency with sleep onset, and many of the variables measured may not be the best, or only, way to determine sleep, wakefulness, or arousals. There is no evidence that the diagnosis and management of OSAHS requires full polysomnography and it is not indicated for the vast majority of patients. The complexity and cost of polysomnography has limited its usefulness as the demands on sleep services increase; it is time-consuming and labor-intensive to set up and analyze, and is considerably more expensive than simpler techniques of monitoring. The equipment and the expertise required are not widely available.

Limited Sleep Studies

This term encompasses those sleep studies that do not record EEG/EOG/EMG. These simplified tests have evolved and been shown to be at least as good as polysomnography for the diagnosis of continuous positive airways pressure (CPAP)-responsive OSAHS. They can produce apnea–hypopnea indices, or respiratory disturbance indices, similar to those obtained by full polysomnography, but may also provide more sophisticated derivatives. Commonly, some or all of the following are monitored: oximetry, snoring, body movement, heart rate, oronasal airflow, chest and abdominal movements, and leg movements. Arousals are inferred from respiratory signals and autonomic indices such as rises in heart rate, blood pressure, or pulse transit time. Estimates of sleep onset, sleep duration, and awake time can be determined from body movements, measured with actigraphy, video, or other devices.

Many, even more limited, sleep study systems that vary in the number of recorded channels have been devised for home use. These can be applied by the patient at home, following suitable instruction from the sleep technician or physician. Most commonly they do not include measures of EEG/EMG/EOG. They are relatively cheap and do not require patients to spend a night in a hospital bed. However, they can be difficult to set up correctly, particularly for people living on their own or who cannot follow instructions easily, and this may lead to sufficient data loss to preclude a confident diagnosis.

Overnight Oximetry Alone

Portable recording oximeters are now often used to perform sleep studies, usually in the patient’s own home. Tracings of all-night oximetry and pulse rate are obtained (see Figure 1). Algorithms count the number of hypoxic dips and, by inference, respiratory events. In those patients with symptoms suggestive of OSAHS and a baseline SaO2 of greater than 92%, more than 15 44% SaO2 dips per hour allows a confident diagnosis of OSAHS. Recurrent pulse rate rises are usually indicative of recurrent arousal and help in the analysis. A visual review of the overnight tracings is always recommended, particularly for negative studies, to ensure the characteristic subtle SaO2 dipping of OSAHS is not missed (for example, when many of the SaO2 dips do not quite reach the 4% threshold for counting). Oximetry alone is clearly a limited study, but can be successfully used, with appropriate expertise, to identify severe cases of OSAHS (see Figure 2) thus allowing rapid referral for continuous positive airways pressure (CPAP) treatment.

False-positive oximetry can occur with Cheyne– Stokes breathing, which also causes cyclical falls in SaO2 (e.g., heart failure, post stroke), and if there is a low awake baseline SaO2 (e.g., chronic obstructive pulmonary disease) where the nocturnal SaO2 oscillates considerably with only small actual PaO2 changes, due to the shape of the oxygen–hemoglobin dissociation curve. False-negative oximetry can occur in younger and thinner patients, who can have frequent apneas and arousals without detectable desaturations. Those with negative oximetry studies, but symptoms suggestive of OSAHS, should undergo further sleep study assessment. Oximetry, sound, video, chest and abdominal movements, body position, and leg movements are probably the most helpful conventional components of a sleep study to help diagnose OSAHS.

Other Tests

Objective tests for sleepiness, such as the maintenance of wakefulness test (MWT) or multiple sleep latency test (MSLT) can be performed, but these are more typically used in research studies. The correlations between both subjective and objective measures of sleepiness and indices of respiratory events or sleep disturbance on the sleep study tend to be poor. Furthermore, the correlation with actual daytime performance, such as driving accident rate, is even poorer.

Conditions Associated with OSAHS

OSAHS with excessive daytime sleepiness has been recognized increasingly to be associated with certain clinical conditions, either from the direct effects of apneas/hypopneas and hypoxia or from the sleep fragmentation. OSAHS is now recognized to be a cause of systemic hypertension, independent of obesity. The hypertension is likely to be due to increased day-time and night-time sympathetic nervous system activity caused by either the hypoxia and sleep fragmentation or both. The hypertension improves following effective treatment of the OSAHS. By extension, OSAHS may therefore be indirectly or directly related to vascular disease, including coronary heart disease, arrhythmias, heart failure, transient ischaemic attack (TIAs), and stroke; although controlled interventional studies to determine this have not yet been performed. The association of OSAHS with insulin resistance, also independent of obesity, has been demonstrated in some studies, although the mechanisms and the clinical relevance of this are still unclear. There is some evidence of cognitive dysfunction in people with untreated OSA (and possible residual decrements even after treatment), which may be due to nocturnal hypoxia or other effects of severe sleep fragmentation apart from sleepiness. This may be manifest as poor concentration, vigilance, or attention problems. It is well known that there is an increased risk of motor vehicle accidents in people with untreated OSA, which is up to seven times that in the general population. Both cognitive impairment and simulated steering performance (as a surrogate for driving ability) improve following therapeutic CPAP.

Treatment of OSAHS

In view of the increasing numbers of patients with OSAHS, the following questions should be asked regarding the use of CPAP: who will benefit the most from CPAP and are there better options for some patients?

CPAP treatment involves the delivery of air to the upper airway noninvasively, via a nose or full-face mask, at a pressure that maintains airway patency during sleep by means of ‘pneumatic splinting’. It is a well-established and effective therapy for OSAHS and, by eradicating the recurrent airway obstruction during sleep with its associated repeated arousals and sleep disturbance, abolishes daytime sleepiness.

CPAP remains the mainstay of treatment of people with significant symptomatic OSAHS. The best correlates of whether a patient is likely to have improved daytime sleepiness following a therapeutic CPAP trial are the number of 44% SaO2 dips per hour and the number of body movements (indicating arousals). There is considerable night-to-night variation in sleep study indices, which makes the use of thresholds to initiate treatment illogical. The sleep study needs to be interpreted to assess if there is sufficient evidence to explain the patient’s symptoms. If the severity of the OSAHS (and how much it may be affecting the patient) is unclear, then it is reasonable to undertake a diagnostic (as well as therapeutic) trial of CPAP, to determine whether the patient has sufficient clinical improvement to warrant continued treatment; giving rise to the concept of CPAPresponsive disease.

The initiation of CPAP therapy is an area of current development. Nasal CPAP has traditionally been initiated in hospital with overnight pressure titration. The optimal pressure at which the patient’s apneas, hypopneas, snoring, and arousals are largely abolished is established, as determined by polysomnography. The patient is then sent home on a fixed CPAP pressure. Recently, more expensive CPAP machines, capable of automatically titrating airway pressure, have been devised that continually adjust airway pressure in order to maintain airway patency. Self-titrating CPAP is well tolerated and improves OSA and sleep architecture in a manner comparable to manually adjusted CPAP. A technician is not required to be present overnight during the overnight titration CPAP. Currently, these machines are too expensive compared to fixed pressure machines for most health services to use them routinely in the long term. An alternative method of determining the required CPAP pressure is to use an algorithm that predicts the required pressure depending on neck circumference (or body mass index) and oxygen desaturation (or apnea–hypopnea index). This approach has been found to give comparable pressures and patient outcomes to self-titrating CPAP machines, and saves significant costs.

Weight loss should also be advised in those patients with upper body obesity and a body mass index of greater than 26. Mandibular advancement devices can be effective in treating OSAHS, mainly in those who have milder disease, retrognathia, postural OSAHS, or in those who are intolerant of CPAP; but individual benefit is largely unpredictable. Drugs to increase respiratory drive during sleep, to suppress the rapid eye movement sleep often associated with more severe OSA, or to activate preferentially the upper airway dilator muscles have all been tried but have not been found to be sufficiently effective in the treatment of OSAHS. At present, excessive daytime sleepiness with OSAHS is the main indication for treatment, and improvement of the sleepiness is the outcome used to measure the success of treatment. As the evidence for other conditions being associated with OSAHS increases (e.g., vascular disease, diabetes), it is debated whether patients with OSA, but without excessive daytime sleepiness, should receive CPAP treatment to modify their associated conditions.

At present, there is not enough evidence to support or justify this. The small benefits in terms of blood pressure are more easily obtained with conventional antihypertensive therapy, which is supported by longer term data on vascular event rates. 


Read more: Sleep apnea in adults - technical

Further Reading

Bennett LS, Langford BA, Stradling JR, and Davies RJ (1998) Sleep fragmentation indices as predictors of daytime sleepiness and nCPAP responsiveness in obstructive sleep apnoea. American Journal of Respiratory and Critical Care Medicine 158: 778–786.

Chapman S, Robinson G, Stradling J, and West S (2005) Sleep apnoea. In: Oxford Handbook of Respiratory Medicine. Oxford University Press.

Choi S, Bennett LS, Mullins R, Davies RJ, and Stradling JR (2000) Which derivative from overnight oximetry best predicts symptomatic response to nCPAP in patients with obstructive sleep apnoea? Respiratory Medicine 94: 895–899.

Davies CWH, Crosby JH, Mullins RL, et al. (2000) Case-control study of 24 hour ambulatory blood pressure in patients with obstructive sleep apnoea and normal matched control subjects. Thorax 55: 736–740.

Ip MS, Lam B, Ng MM, et al. (2002) Obstructive sleep apnea is independently associated with insulin resistance. American Journal of Respiratory and Critical Care Medicine 165: 670–676.

Jenkinson C, Davies RJ, Mullins R, and Stradling JR (1999) Comparison of therapeutic and subtherapeutic nasal continuous positive airways pressure for obstructive sleep apnoea: a randomised prospective parallel trial. Lancet 353: 2100–2105.

Peppard PE, Young T, Palta M, and Skatrud J (2000) Prospective study of the association between sleep-disordered breathing and hypertension. New England Journal ofMedicine 342: 1378–1384.

Pepperell JCT, Ramdassingh-Dow S, Crosthwaite N, et al. (2002) Ambulatory blood pressure following therapeutic and sub-therapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised prospective parallel trial. Lancet 359: 204–210.

Punjabi NM, Sorkin JD, Katzel LI, et al. (2002) Sleep-disordered breathing and insulin resistance in middle-aged and overweight men. American Journal of Respiratory and Critical Care Medicine 165: 677–682.

Schmidt-Nowara W, Lowe AA, Wiegand L, et al. (1995) Oral appliances for the treatment of snoring and obstructive sleep apnea: a review. Sleep 18: 541–547.

Smith IE and Quinnell TG (2004) Pharmacotherapies for obstructive sleep apnea; where are we now? Drugs 64(13): 1385–1399.

Stradling JR, Hardinge M, Paxton J, and Smith D (2004) Relative accuracy of algorithm-based prescription of nasal CPAP in OSA. Respiratory Medicine 98: 152–154.

Stradling JR, Pepperell JCT, and Davies RJO (2001) Sleep apnoea and hypertension: proof at last? Thorax 56: 45–49.

Ward Flemons W, Littner MR, Rowley JA, et al. (2003) Home diagnosis of sleep apnea: a systematic review of the literature. Chest 124: 1543–1579.