Obstructive sleep apnoea

Approach to pt with Obstructive sleep apnoea

1. Obstructive Sleep Apnoea Dr Muntasir Mansur MD Phase-A Resident ( Pulmonology ) Dhaka Medical College Hospital

2. NORMAL SLEEP The average human sleep need is 8 hours ( Range: 4-10 hrs) Sleep is divided into REM sleep Non-REM sleep

3. Sleep stages

4. Sleep stages: contd

5. Factors that drive sleep Circadian forces Homeostatic forces: A sleep deficit elicits a compensatory increase in intensity and duration of sleep, while excessive sleep reduces sleep propensity Neuro -hormonal forces: (+)Growth hormone via GHRH, (-) release of corticotropin releasing hormone Socio-cultural forces

6. Shorter sleep duration: an important health risk factor Sleeping ≤ 6 hours per night – higher risk of hypertension Sleeping ≤ 5 hours per night – high risk of coronary events Sleeping 7-8 hours – leading to a healthy life

7. Sleep Apnoea

8. Sleep Apnoea Sleep apnea is the intermittent cessation of airflow at the nose and mouth during sleep. Apneas of at least 10 s duration are important but in most cases the apneas last 20-30 s and can last as long as 2-3 min. Sleep apnea is a leading cause of daytime sleepiness and contributes to CVS disorders . Prevalence: 2% in middle-aged women and 4% in middle-aged men

9. Sleep Apnoea - contd Sleep apneas are divided into: Central sleep apnea : neural drive to all respiratory muscles is abolished Obstructive sleep apnea : airflow ceases despite continuing respiratory drive because of occlusion of the oropharyngeal airway.

10. Obstructive Sleep Apnoea

11. Introduction OSA is a sleep disorder that involve cessation or significant decrease in airflow in the presence of breathing effort It is the most common type of sleep disordered breathing and is characterized by recurrent episodes of upper airway collapse during sleep, usually at level of soft palate .

12. Aetiology Inspiration results in negative pressure within the pharynx During wakefulness, upper airway dilating muscles, including palatoglossus and genioglossus , contract actively during inspiration to preserve airway patency. During sleep - muscle tone declines , impairing the ability of these muscles to maintain pharyngeal patency In some patients – a combination of an anatomically narrow palatopharynx and underactivity of the dilating muscles during sleep results in inspiratory airway obstruction

13. Aetiology - contd Incomplete obstruction causes turbulent flow resulting in snoring More severe obstruction triggers increased inspiratory effort and transiently wakes the patient, allowing dilating muscle to re-open the airway These awakenings are so brief that patients have no recollection of them After a series of loud deep breaths the patients rapidly returns to sleep, snores and becomes apneic once more

14. Aetiology - contd The cycles of apnoea and awakening may repeat itself many hundred times per night & results in severe sleep fragmentation and secondary variations in blood pressure which predisposes over time to cardiovascular diseases

15. Risk factors Obesity, especially BMI >35 kg/m 2 Family history of obstructive sleep apnea Retrognathia Treatment-resistant hypertension CHF, atrial fibrillation, stroke Type 2 diabetes

16. Symptoms Witnessed episodes of apnea Loud, frequent, bothersome snoring Choking/gasping during sleep Excessive daytime sleepiness Unrefreshing sleep , sleep fragmentation Insomnia Nocturia Morning headaches Decreased concentration

17. Complications DAYTIME SLEEPINESS EFFECTS ON Heart AND CIRCULATION Hypertension Coronary artery disease Heart failure Atrial fibrillation stroke PSYCHOLOGICAL EFFECTS Depression Worsen nightmare Post traumatic stress disorder

18. Complications : cont EFFECTS IN INFANTS AND CHILDREN Failure to Thrive Attention Deficits and Hyperactivity OTHER ADVERSE EFFECTS ON HEALTH Diabetes Obesity Pulmonary hypertension Headaches High-risk pregnancies (GDM,PIH) EFFECTS ON BED PARTNER Disruption of the patient's bed-partner’s sleep quality

19. Assessment of daytime sleepiness A quantitative assessment of daytime sleepiness can be obtained by questionaire named Epworth sleepiness scale

20. Epworth sleepiness scale Normal subjects averages 5.9 (SD 2.2) Patients with severe obstructive sleep apnoea average 16.0 (SD 4.4)

21. Investigations Sleep Study - Polysonography Respiratory Measures - Apnea- Hypopnea index - SaO 2

22. What type of sleep study should be ordered? Polysomnography in the sleep laboratory Standard method for diagnosis and determining severity Assesses other sleep disorders Recommended: “full-night” sleep study Alternative: “Split-night” study Initial diagnostic recording Then positive airway pressure titration the same night

23. Respiratory events in OSA Apnea-hypopnea index (AHI) Episodes of apnea and hypopnea per hour of sleep Mild OSA: AHI ≥5 and <15/h Moderate OSA: AHI ≥15 and <30 Severe OSA: AHI ≥ 30 Apnea: airflow cessation ≥10 sec Hypopnea: airflow reduction ≥10 sec plus 3% - 4 % OxyHb desaturation or arousal from sleep

24. What other conditions should be considered? Chronic sleep deprivation disorder (shift-work disorder) Circadian rhythm disorder Depression and anxiety Hypothyroidism Obesity hypoventilation syndrome Central sleep apnea syndrome Congestive heart failure ( Cheyne -Stokes respiration ) Opiate-induced central sleep apnea

25. Treatment Counsel overweight patients about weight loss Treat any nasal congestion Advise alcohol avoidance close to bedtime Offer trial of therapy (CPAP: Continuous Positive Airway Pressure) if patient has Daytime sleepiness or frequent nocturnal awakenings Recent accident or near-miss attributable to sleepiness Mandibuler Advancement devices Surgical Interventions

26. R ole of weight loss and exercise Helps reduce severity and symptoms Recommend dietary modification Recommend regular exercise Bariatric surgery can reduce severity in morbidly obese

27. Role of CPAP Improves quality of life Improvement in cognitive function Decreases anxiety and depression Improvement in all sleep related symptoms including snoring , witnessed apnoeas , choking , nightmares , daytime hypersomnolence and nocturia .

28. CPAP prescription should include: Pressure setting Mask type and size Heated humidifier Associated supplies ( tube, filters, mask straps ) Educate patients on equipment, maintenance, care Also: on benefits of therapy and potential problems How should CPAP be initiated?

29. Factors that optimize patient adherence to CPAP therapy Early follow-up (within 1–2 weeks of therapy initiation) Support groups and bed partner support Cognitive behavioral therapy focused on CPAP Aid in therapy goal-setting Support in troubleshooting difficulties Heated humidification + nasal steroid for congestion Other PAP modes if patient has intolerance to pressure Short-term sedative hypnotic (for select patients only)

30. How should CPAP masks be chosen? No one mask type is superior to another Select mask to maximize patient comfort Oronasal (“full face”) masks Patients who sleep with their mouth open Nasal masks Better tolerated with claustrophobia Nasal pillows (sit under the nose and fit in the nares) Also better tolerated with claustrophobia Patients with unusual nasal bridge anatomy, facial hair, or absent dentition

31. Role of mandibular advancement devices Decrease airway collapsibility and enlarge upper airway Requires adequate dentition, may exacerbate TMJ Refer to experienced dentist Less effective than CPAP for normalizing the AHI Mild or moderate OSA : May be reasonable initial therapy Severe OSA: Not recommended as initial therapy Patients tend to accept better than CPAP Follow-up sleep study needed to document adequacy

32. Role of surgical intervention Uvulopalatopharyngoplasty (UPPP) Small reduction in symptoms Fewer than half of patients have reduction in severity Tonsillectomy , nasal septoplasty Increase CPAP tolerability + reduce snoring (not cure ) Maxillomandibular advancement Invasive procedure with prolonged postop recovery Cure rate >90%, particularly in nonobese with retrognathia Tracheostomy Cures OSA Can be used in life-threatening situations

33. How should treatment be monitored? Ensure CPAP use during all sleep sessions Assess symptom resolution Monitor side effects of CPAP Assess comorbid conditions associated with OSA Monitor remission due to weight loss or surgery Monitor remission in those with history drowsy driving If relapse occurs, investigate stepwise : Inadequate therapy adherence Problems with CPAP delivery Change in pressure needs Non-OSA sleep factors

34. Prognosis Reversals of symptoms and risks with successful treatment