1. Amy S Jordan, David G McSharry, Atul Malhotra Lancet 2014; 383: 736–47

2. Introduction

3. Obstructive sleep apnea (OSA) - disorder of repetitive pharyngeal collapse during sleep complete collapse : apnea partial collapse : hypopnea - Oxygen desaturation, hypercapnea, sleep fragmentation - Cardiovascular, metabolic, neurocognitive effects - Associated with obesity - 4% in middle-aged men (20% in high-income coutries) 2% in middle-aged women (10% in high-income coutries)

4. Diagnosis and definition

5. Symptoms of Obstructive sleep apnea (OSA) - Snoring - Witnessed apneas - Waking up with a choking sensation - Excessive sleepiness - Non-restorative sleep - Difficulty initiating or maintaining sleep - Fatigue or tiredness - Morning headache

6. Diagnosis and definition Overnight polysomnography (in a lab) - Measure apnea-hypopnea index (number of apneas plus hypopneas per h of sleep) 1) Electroencephalogram 2) Left and right electro-oculogram 3) Chin electromogram  sleep-wake state 4) Respiratory inductance plethysmography bands – thorax 5) Respiratory inductance plethysmography bands – abdomen  Respiratory effort measurement 6) Nasal air pressure 7) Thermal air sensor 8) Arterial oxygen saturation  Airflow monitoring 9) Electromyography of the anterior tibialis  Limb movement that might alter sleep stage or respiration 10) Body position

10. Diagnosis and definition Home diagnosis and management - Polysomnography is usually definitive, but expensive, and time consuming. - Home-based diagnosis and treatment are no worse than laboratory diagnosis and treatment for some patients. - Home testing could be not appropriate for patients with lung disease, heart failure, or neuromuscular disease.

11. Pathophysiology and risk factors

12. Upper airway anatomy - Craniofacial structure - Body fat  Increased likelihood of pharyngeal collapse

14. Pathophysiology and risk factors Instability of respiratory control system Central respiratory output ↓ (low central respiratory drive)  Low upper airway dilator muscle activity  High airway resistance  Airway collapse

15. Pathophysiology and risk factors Low arousal threshold (from sleep) Arousal  Hyperventilation  Low CO2 concentration in blood below the chemical apnea thresthold 1) Central apnea 2) Low upper airway dilator muscle activity  collapse non-myorelaxant sedatives ?

16. Pathophysiology and risk factors Low lung volume The cross-sectional area of the upper airway ∝ lung volume Lung volume ↑ : mediastinal structures are pulled caudally  Stiffening and dilation of the pharyngeal airway Lung volume ↑ : increased stores of O2 and CO2  Buffering the blood gases from changes in ventilation

17. Pathophysiology and risk factors Poor upper airway muscle function Adequate contration ↓ -Fatigue -Neural injury -Myopathy

18. Pathophysiology and risk factors Fluid retention and shift of fluid overnight from the legs to neck - Edema can affect airway mechanics - Heart failure, ESRD, hypertension : states of excess extra-cellular fluid volume  Diuretics Male : more central fat distribution Obestiy : fat deposited around upper airway structure decreased lung volume Age, monopause, smoking

19. Consequences

20. CPAP 1) Reduce BP (2-3 mmHg) : reductions in surge in nocturnal blood pressure associated with OSA 2) Daytime sleepiness 3) Severity of OSA 4) Decreased incidence of both fatal and non-fatal cardiovascular event (although, this relation is unproven)

21. Consequences Diabetes mellitus - 87% of obese patients with type 2 diabetes had clinically important OSA. - Diabetes can lead to neuromyopathy, which might impair reflexes in the upper airway, increasing the likelihood of OSA. - counter-regulatory hormones during obstructive apnoea, glycaemic control might be worse in patients with diabetes.  most data show no major improvement in glycaemic control with treatment of OSA. - Effects on vascular function

22. Management

23. Nasal CPAP - TOC for adult OSA - pharyngeal intraluminal pressure > surrounding pressure - Increased end-expiratory lung volume  stabilise the upper airway through caudal traction - Adherence : 60~70%

24. Management

25. Oral device

26. Management Surgery 1. Uvulopalatopharyngoplasty 2. Maxilla-mandibular advancement 3. Tracheostomy 4. Hypoglossal nerve stimulation

27. Management Conservative management 1. Avoidance of depressants (Alcohol) 2. Sleeping for 7-8 h per night 3. Avoidance of a supine posture 4. Weight loss through diet and exercise 5. Neuromuscular exercise 6. Modafinil (stimulants)

28. Management Central apnea after using CPAP - Central apneas develop in roughly 10% of patients who start treatment with continuous positive airway pressure. - These central apnoeas resolve spontaneously with ongoing continuous positive airway pressure treatment. - Treatment-emergent central apnoeas seem to have no effect on outcomes or long-term adherence.

29. Prevention

30. Weight loss (though diet and exercise) a 10 kg reduction in bodyweight can yield a reduction in apnoea– hypopnoea index of roughly five events per h. Although bariatric surgery is highly effective at causing weight loss, long-term elimination of apnoea varies. avoidance of cigarettes, alcohol, and other myorelaxant drugs

31. Future directions

33. Ondine’s Curse