Sleep Apnea-Hypopnea Syndrome

Introduction[edit | edit source]

Sleep apnea-hypopnea syndrome (SAHS) is divided into two categories.

  1. Obstructive sleep apnea-hypopnea syndrome (OSAHS): a complete or partial obstruction of the upper airway (UA) during sleep.
  2. Central sleep apnea syndrome (CSAS): Central neurological respiratory abnormalities causing the central sleep apnea syndrome (CSAS).[1]

Definition[edit | edit source]

  • Apnea: an interruption of airflow for a period of at least 10 seconds [2].
  • Hypopnea: an incomplete but significant decrease in flow associated with desaturation [3], arousal [4], or both [5].

The severity of SAHS is established according to the total amount of apneas and hypopneas per hour during sleep.

Index for severity: Apnea-hypopnea index (AHI), most often used [3].

  • 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
  • Severe SAHS would be a patient having over 30 events per hour of sleep [6].

Prevalence[edit | edit source]

When strictly an AHI greater than 5 is considered, the prevalence of OSAHS can then reach 24% for men and 9% for women [7]. However, when we take into account the presence of sleepiness, we then obtain a prevalence of 4% for men and 2% for women [2]. CSAS for their part are much less frequent than OSAHS [6].

Signs and Symptoms[edit | edit source]

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.

  • Sleep apnea subjects are regularly habitual snorers (snoring is far from being specific to OSAHS since about 60% of adult men are habitual snorers) [8].
  • 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 [6].

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 [9] 
  • Emergence of other chronic cardiovascular disorders [6](mediated by the sympathetic nervous system through increased adrenergic tone in the daytime) [1].

Diagnosis[edit | edit source]

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 [6].

  • PSG readings will ensure the quantification of the number of events per hour and the associated desaturation [10].
  • The 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 [2].
  • 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.

  • Risk factors: male, older age, being overweight, alcohol consumption, and certain anatomical factors inducing an anatomically smaller pharynx [5].
  • Other risk factors: smoking, nasal obstruction, ethnicity, genetic component, endocrine diseases, and the action of some drugs [6].

There are also some questionnaires such as the Epworth scale that are regularly used, aimed to objectively quantify daytime sleepiness [3].

Body mass index is also regularly used to quantify obesity but most of the time the neck circumference is favoured [4].

Pathophysiology[edit | edit source]

Muscle tone decreases during sleep and is lowest during REM sleep. An episode of apnea in obstructive sleep apnea is caused by at least 90% anterior to a posterior collapse of the airway for more than 10 seconds. A hypopnea is characterized by at least 30% reduction in airflow for more than 10 seconds associated with an oxygen desaturation or arousal on electroencephalogram (EEG).

The majority of patients with OSA have upper airway obstruction either at the level of the tongue or the soft palate. Other anatomical factors that contribute to OSA include enlarged tonsils, large volume of the tongue, abnormal maxilla position, length of the soft palate and a decrease in the cross sectional area of the upper airways.

The apneic episodes tend to occur in clusters with oxygen desaturation[11].

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 [5].

Clinical Aspects[edit | edit source]

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 [6]. 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 [6].

Treatments[edit | edit source]

See here also

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 [7]. 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 [5]. 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 [8]. 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 [9]. 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 [10].

Another approach gaining interest is using exercises to treat the OSAHS. Didgeridoo playing already has been shown to improve significantly the AHI [2] and another study revealed that playing a double reed musical wind instrument is associated with a lower risk of OSAHS [3]. Oropharyngeal exercises [4] and speech therapy [5] 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 [6] and the increase of UA muscles endurance, which were shown to be more prone to fatigue [7].

Conclusion[edit | edit source]

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.

References[edit | edit source]

  1. 1.0 1.1 1.2 Dickens C. The posthumerous papers of the Pickwick Club. Chapman and Hall, London, 1836.
  2. 2.0 2.1 2.2 2.3 Guillemineault C, Tilkian A, Dement WC. The sleep apnea syndromes. Annu Rev Med 1976;27:465-484.
  3. 3.0 3.1 3.2 3.3 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.
  4. 4.0 4.1 4.2 Thorpy MJ. Handbook of sleep disorders. Marcel Dekker. Inc, New York, 1990.
  5. 5.0 5.1 5.2 5.3 5.4 Berry DTR, Phillips BA. Sleep-disordered breathing in the ederly: review and methodology comment. Clin Psych Rev 1988;8:101-120
  6. 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 6.8 Weitzenblum E, Racineux JL. Syndrome d’apnées obstructives du sommeil. 2e édition. Masson, Paris, 2004.
  7. 7.0 7.1 7.2 Young T et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328:1230-1235
  8. 8.0 8.1 Maltais F, Carrier Y, Cormier Y, Series F. Cephalometric measurements in snorers, non-snorers, and patients with sleep apnea. Thorax 1991;46:419-423.
  9. 9.0 9.1 Pankow W et al. Influence of sleep apnea on 24-hour blood pressure. Chest 1997;112:1253-1258.
  10. 10.0 10.1 Burwell CS, Robin ED, Whaley RD, Bickelmann AG. Extreme obesity associated with alveolar hypoventilation: A pickwickian syndrome. Am J Med 1956;21:811-818.
  11. Slowik JM, Collen JF. Obstructive Sleep Apnea.(2019)Available from:https://www.ncbi.nlm.nih.gov/books/NBK459252/ (last accessed 5.10.2020)