Sleep Apnea-Hypopnea Syndrome

Original Editor - Eric Rousseau

Top Contributors - Eric Rousseau, Kim Jackson, Laura Ritchie and Adam Vallely Farrell  


Sleep apnea-hypopnea syndrome (SAHS) is divided into two categories. First, it can be linked with a complete or partial obstruction of the upper airway (UA) during sleep. This is known as obstructive sleep apnea-hypopnea syndrome (OSAHS). Then, it may also be consistent with central neurological respiratory abnormalities, causing the central sleep apnea syndrome (CSAS). Although some knowledge of sleep-disordered breathing goes as far back as ancient times, it was Charles Dickens in 1836, which drew up the first clinical presentation of OSAHS, without knowing it, by the detailed description of a character [1]. The first physicians to recognize the syndrome in 1956 suggested Pickwick syndrome as nomenclature [2], in honour of the novella containing the character described by Dickens, Posthumous Papers of Pickwick Club.

Definition and Prevalence

An apnea is defined as an interruption of airflow for a period of at least 10 seconds [3]. Hypopnea for its part is less well defined but can be considered an incomplete but significant decrease in flow associated with desaturation [4], arousal [5], or both [6]. The severity of SAHS is established according to the total amount of apneas and hypopneas per hour during sleep. In fact, there are several indexes but the apnea-hypopnea index (AHI), in which apneas and hypopneas are grouped, is most often used as both event types seem to have the same consequences [4]. Mild SAHS ranges from 5 to 15 events per hour of sleep, moderate OSAHS falls in the range of 15–30 events per hour of sleep, and severe SAHS would be a patient having over 30 events per hour of sleep [7]. When strictly an AHI greater than 5 is considered, the prevalence of OSAHS can then reach 24% for men and 9% for women [8]. However, when we take into account the presence of sleepiness, we then obtain a prevalence of 4% for men and 2% for women [3]. CSAS for their part are much less frequent than OSAHS [7].

Signs and Symptoms

Loss of ventilation during sleep will usually result in excessive daytime sleepiness, which can cause drowsiness and accidents, such as when sleep occurs while driving. In addition, sleep apnea subjects are regularly habitual snorers. But snoring is far from being specific to OSAHS since about 60% of adult men are habitual snorers [9]. Snoring and apnea events during the night might be witnessed by others and affects not only the apneic subject, but also the entourage. Other symptoms may include headaches, irritability, night sweats, attention deficit, memory loss, decreased libido, and depression [7]. In addition, by reducing the partial pressure of oxygen in the blood and causing oxygen desaturation, the resulting hypoxemia may be responsible for arterial hypertension [10] and the emergence of other chronic cardiovascular disorders [7], mediated by the sympathetic nervous system through increased adrenergic tone in the daytime [1].


The diagnosis is based on polysomnographic study (PSG), which includes electroencephalogram, electrocardiogram, oximetry, and recordings of the respiratory rate, respiratory sounds, thoracoabdominal movements and movements of the subject [7]. Thus, the PSG readings will ensure the quantification of the number of events per hour and the associated desaturation [2]. At the same time, sleep stages and micro-awakenings will be also described and measurement of respiratory efforts will qualify obstructive or central apnea, according to the absence or presence of these efforts, since the latter is a reflection of obstruction [3]. It is important to note that the central or obstructive nature of the episodes of apnea and hypopnea can also be mixed.

In addition to PSG, the diagnosis is also based on a careful history. One must be aware of the risk factors that have been well recognized: male, older age, being overweight, alcohol consumption, and certain anatomical factors inducing an anatomically smaller pharynx [6]. In addition, there are also a few other risk factors whose effect is controversial like smoking, nasal obstruction, ethnicity, genetic component, endocrine diseases, and the action of some drugs [7]. There are also some questionnaires such as the Epworth scale that are regularly used, aimed to objectively quantify daytime sleepiness [4]. Finally, the body mass index is also regularly used to quantify obesity but most of the time the neck circumference will be favoured [5].


Let's start by saying that the pharynx, in opposition to the larynx and trachea, is not a rigid tube, so as to allow some non-respiratory functions such as swallowing and vocalization. In fact, to model the mechanical behaviour of the pharynx, it is common to assimilate it with a physical model of the collapsible tube, known as the Starling resistor [6]. When there is an inspiratory drive originating from the upper respiratory control centres, a nervous impulse volley is travelling down in the phrenic nerves, resulting in a contraction of the diaphragm. This contraction, which induces a negative endopharyngeal pressure, added to the weight of the tissues surrounding the pharynx, tends to induce the closure of UA, especially at the oropharyngeal and velopharyngeal levels [7].

This behaviour of UA to collapse is countered by the phasic contraction of airway dilator muscles, which precedes the diaphragmatic contraction by a few milliseconds [8]. The only structures able to help maintain a certain calibre of the pharyngeal lumen are the UA muscles, especially the genioglossus muscle, resulting in a delicate balance between the compressive forces and the pharynx dilators [8]. In the presence of OSAHS, the compressive forces on the pharynx exceed those that tend to dilate the UA, although the tonic activity of the muscles of the UA at rest is exaggerated in comparison with healthy subjects, both during awakening and sleep. This is generally interpreted as a neuromuscular compensation, but the actual compensation is obviously insufficient to counter the obstructive force [9]. The transpharyngeal pressure at which the UA are closed is called critical closing pressure (Pcrit). Pcrit is negative in normal subjects, that is less than the atmospheric pressure but becomes less negative in non-apneic snorers and positive in apneic subjects.

These obstructive forces can be of different sources. First, it might be related to anatomical features, such as enlarged tonsils, retrognathia and nasal obstruction [10]. Obesity is also an extremely important anatomical factor, possibly by increasing the mass of adipose tissue around the pharynx [3]. Second, there is a significant decrease of muscle control during REM sleep by loss of metabolic control, exacerbated by alcohol or hypnotics, causing a decrease in tonic and phasic activity of skeletal muscle associated with sleep, particularly affecting the muscles of the UA, with preservation of diaphragmatic activity [1]. Then, weakness of the respiratory muscles may also contribute to compressive forces in the case of muscular hypotonia or secondary to adverse mechanical conditions, as in the case of chronic obstructive pulmonary disease [2]. In addition, metabolic and mechanical stimuli will influence the activity of pharyngeal dilator muscles. More specifically, the mechanical stimuli consist of reflex activation of stabilizing muscles to UA negative pressure. This reflex activation decreases during sleep. Finally, these factors will also be amplified by the sleeping position of the subject, specifically the supine position that may contribute to pushing the tongue against the posterior pharyngeal wall [3].

The reason why men are more affected than women is not yet fully understood, but it has been suggested that there is a higher pharyngeal resistance in men with deficient activity of pharyngeal dilator muscles. There also appears to have a protective effect of female sex hormones, resulting in a lower AHI when postmenopausal women are treated with hormone therapy, and also a lower AHI during the luteal phase compared with the follicular phase of the menstrual cycle [3].

During the episodes of obstructive apnea during sleep, increased inspiratory efforts, not oxygen desaturation, will cause micro-awakenings, allowing respiratory control centres to send a drive command to the UA muscles. This will result in a rapid increase of the pharyngeal diameter, causing the sudden and characteristic entry of air which is frequently reported by input environment. This same cycle is repeated again and again during sleep. Micro-awakenings will also fragment sleep and be involved in the reported daytime sleepiness [7]. In addition, as previously mentioned, by reducing the partial pressure of oxygen in the blood and causing oxygen desaturation, the resulting hypoxemia can cause high blood pressure [10] and the appearance of other chronic cardiovascular disorders [7]. The sympathetic nervous system is largely responsible for this through the increased adrenergic tone in the daytime [1].

It was also noted that the apneic subjects demonstrate signs of inflammation in the mucosa and submucosa, in addition to interstitial and inter-fascicular fibrosis, and a greater proportion of type II muscle fibres than type I. However, since these changes are visible in both the apneic and the simpler snorer, they are seen as a consequence of repeated trauma secondary to airway tissue vibrations during sleep, especially because of snoring, rather than a cause. However, these effects may, in turn, be a contributing factor to sleep apnea by changing the tissue characteristics of the UA. For example, stiffness of the uvula was observed in vivo in patients with sleep apnea. It might, therefore, represent a vicious circle [4].

It looks like inflammation is present locally in the mucosa of OSAHS patients, but also systemically. More specifically, cytokines and C-reactive protein are elevated in OSAHS patients and those molecules have been found to be linked to sleepiness, fatigue and the development of cardiovascular and metabolic disorders [5].

Concerning the central events, they are caused by a decrease or instability of the central ventilatory drive. Any disease affecting the central nervous system in the area related to the control of breathing may cause CSAS. Central apnea may be isolated or in connection with Cheyne-Stokes, with periods of hyper or hypoventilation. Unlike obstructive apnea, it occurs mostly in the non-REM sleep stage [6].

Clinical Aspects

Subjects will usually consult due to excessive daytime sleepiness, excessive snoring, or as episodes of apnea have been reported by the entourage. Excessive sleepiness and snoring are not specific to OSAHS, hence the need to establish the diagnosis with the PSG. Moreover, the reverse is also true, that is to say, a subject may have an AHI indicative of the presence of OSAHS, but without any symptoms [7]. In these circumstances, treatment can still be considered as a preventive measure according to the severity of the disease since the significant cardiovascular adverse side effects attributed to OSAHS. Although it does not seem unanimous, it has been reported that mortality increases significantly when the AHI is greater than 20 [7].


Since 1981, the recommended treatment for OSAHS is continuous positive airway pressure ventilation (CPAP), which keeps the airway open by pushing air into the respiratory system [8]. Although very effective, it is unfortunately not always well-tolerated. After 5 years of usage, only 50% will still be using it. Note that for CSAS, the bilevel positive airway pressure ventilation (BPAP) is sometimes used [6]. As an alternative to CPAP, there are mandibular advancement devices (MAD), which tries to push the mandible forward in order to increase the calibre of the UA. However, even among the patients who tolerate well the device, MAD systems provide benefits in approximately only 50% of patients and is usually more effective with mild to moderate severity sleep apnea [9]. There is also an approach using hypoglossal nerve neurostimulation, but it is still under study, requires invasive surgery, and is very expensive for the moment [10]. Finally, when craniofacial anatomical features are obviously causative in the pathophysiology of a specific subject, then a surgery executed by an otorhinolaryngology might be indicated [1].

In parallel to those treatment procedures, as obesity is a known risk factor to OSAHS, it is often proposed to lose weight. As needed, the input of a dietician might be of interest. Aerobic activities are often recommended as a safe way to lose weight. It has also been suggested that physical activity could improve the inflammatory profile in patients with OSAHS [2].

Another approach gaining interest is using exercises to treat the OSAHS. Didgeridoo playing already has been shown to improve significantly the AHI [3] and another study revealed that playing a double reed musical wind instrument is associated with a lower risk of OSAHS [4]. Oropharyngeal exercises [5] and speech therapy [6] also demonstrated the beneficial effects of rehabilitation. More studies are necessary to determine to best exercises paradigms but it seems like a very promising avenue. There are discussions on the plausibility of upper airway remodelling as an outcome of orofacial exercise [7] and the increase of UA muscles endurance, which were shown to be more prone to fatigue [8].


OSAHS is a therapeutic challenge. There are many treatment options but some patients cannot tolerate these actual therapeutic approaches or do not have the desired results. Thereby, more studies are necessary but current evidence brings physical therapy and exercises in the front row in the treatment arsenal for sleep apnea.


  1. 1.0 1.1 1.2 1.3 1.4 Dickens C. The posthumerous papers of the Pickwick Club. Chapman and Hall, London, 1836.
  2. 2.0 2.1 2.2 2.3 Burwell CS, Robin ED, Whaley RD, Bickelmann AG. Extreme obesity associated with alveolar hypoventilation: A pickwickian syndrome. Am J Med 1956;21:811-818.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Guillemineault C, Tilkian A, Dement WC. The sleep apnea syndromes. Annu Rev Med 1976;27:465-484.
  4. 4.0 4.1 4.2 4.3 4.4 Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000;342:1378-1834.
  5. 5.0 5.1 5.2 5.3 Thorpy MJ. Handbook of sleep disorders. Marcel Dekker. Inc, New York, 1990.
  6. 6.0 6.1 6.2 6.3 6.4 6.5 Berry DTR, Phillips BA. Sleep-disordered breathing in the ederly: review and methodology comment. Clin Psych Rev 1988;8:101-120
  7. 7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 7.11 Weitzenblum E, Racineux JL. Syndrome d’apnées obstructives du sommeil. 2e édition. Masson, Paris, 2004.
  8. 8.0 8.1 8.2 8.3 8.4 Young T et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328:1230-1235
  9. 9.0 9.1 9.2 Maltais F, Carrier Y, Cormier Y, Series F. Cephalometric measurements in snorers, non-snorers, and patients with sleep apnea. Thorax 1991;46:419-423.
  10. 10.0 10.1 10.2 10.3 Pankow W et al. Influence of sleep apnea on 24-hour blood pressure. Chest 1997;112:1253-1258.