1. Obstructive Sleep Apnea
Annette Hulse, DO
Sep

2. Sleep Disordered Breathing
Snoring
Upper Airway Resistance Syndrome
Sleep apnea
Obstructive
Central
Mixed

3. Snoring
Loud/harsh during sleep, due to tissue vibration from the flow of air through membranous structures (the soft palate, uvula, and the pharyngeal walls) that do not have cartilaginous support
What determines the "stiffness" of the pharyngeal wall is not fully understood; the tissues are both distensable and collapsable

4. Snoring Any stage of sleep (most common in Stages 2,3,4)
Inhalation > exhalation
Worse with alcohol or other depressants
Worse with asthma, colds, congestion, allergies, smoking
More common with obesity or weight gain
~ 50% of all people snore at some point
Men (40%) > women (24%)
Men less likely to snore after age 70

5. Obstructive Sleep Apnea

6. Upper Airway Patency Structural Neuromuscular Craniofacial structure
Surrounding soft tissue (including adipose, tongue size, lateral pharyngeal walls)
Vascular structures (fluid displacement to lateral pharyngeal walls)
Neuromuscular
Including thoracic-upper airway link (caudal traction)

7. Sleep Stages
NREM (non-REM) sleep - consists of Stage 1 (transitional sleep), Stage 2 (light sleep), and Stage 3 and 4 (slow wave).
Most information about upper airway patency is primarily from NREM sleep due to difficulty of achieving REM sleep with invasive testing
REM sleep - also called Rapid Eye Movement sleep, is when the most vivid dreaming occurs.
Paralysis of skeletal muscles
Most people have higher AHI numbers in REM than non- REM (skeletal muscle paralysis during REM)

8. Prevalence of OSA Age 30 – 49 Age 50-70 Men 10% 17% Women 3% 9%
How many apneic events do you need to be diagnosed with OSA?

9. AHI: Apnea-Hypopnea Index
Apnea: stop breathing for 10 seconds or more
Hypopnea: at least a 30% decrease in airflow for 10 seconds or more (usually measured as 3% decrease in O2 Sat).
AHI = (apneas + hypopneas)/hours of sleep
Alternatively Respiratory Disturbance Index (RDI) may be reported; it includes not only apneas and hypopneas, but may also include other, more subtle, breathing irregularities

10. Gradations of OSA None/Minimal: AHI < 5 per hour
AHI 5-15 per hour – Mild OSA
AHI per hour – Moderate OSA
AHI ≥ 30 per hour – Severe OSA

11. Pathophysiology of OSA
Thought to be
Excessive arousals increase sympathetic drive
Hypoxias
Disruption of sleep architecture (REM vs. non-REM sleep) / sleep fragmentation
Risks (causation)
Daytime sleepiness (driving, operating machinery, attention to detail)
Increased cardiovascular risk – documented increase in HTN with severe OSA
Other risks uncertain (may include impaired glucose tolerance, stroke, pulmonary HTN)

12. Symptoms of OSA Morning headaches Difficulty concentrating
Daytime sleepiness
Memory loss
Nocturia
Snoring

13. Symptoms of OSA in Children
Snoring
Daytime sleepiness
Neurocognitive effects
ADHD, behavioral disorders, memory & learning, poor school performance, developmental delay, aggressive behavior
Enuresis
Tonsil & adenoid hypertrophy

14. OSA in Children More often during REM sleep
Smaller lung capacities  become more hypoxic and more hypercapnic
Typically do not awaken
Often mouth breathers, frequent URIs
Sleep in unusual positions, night sweats, morning headache

15. How Do We Diagnose Sleep Apnea?
“Sleep study” aka polysomnography

16. Polysomnography (PSG)
A sleep study measures sleep cycles and stages by recording:
Air flow in and out of lungs
The level of oxygen in your blood
Body position
Brain waves (EEG)
Breathing effort and rate
Electrical activity of muscles (EMG)
Eye movement (EOG)
Heart rate & EKG

20. Arousals
Any sudden change on Electroencephalographm EEG from a deeper sleep stage to a lighter sleep stage.
It may be related to an apnea, a hypopnea, a leg movement, or it may be "spontaneous”
Greater than 10 arousals per hour is abnormal

24. How is Sleep Apnea Treated?

25. Traditional Treatment
CPAP – nasal or oral
Treats SYMPTOMS

26. Oral Repositioning Devices
Oral devices reposition the mandible forward (anteriorly) to increase airway space behind the tongue; also may include tongue retaining device.

27. Surgery
Surgery may stiffen, remove or reposition tissues in and around your throat, including
Soft palate & uvula
Tonsils & adenoids
Tongue
Upper & lower jaw (MMA)
MMA ~ #35% “curative”

28. Ablation

29. Upper Airway Stimulation

30. Traditional Treatments --Children

31. Traditional Treatments for Children
Tonsillectomy & Adenoidectomy (rarely curative)
Rapid palatal expansion

32. Preferred Treatment Myofunctional therapy ~ 50% improvement in AHI +
Osteopathic Treatment
Functional dental appliance
CPAP if needed for symptom control

33. Osteopathic Considerations
Upper airway fluid retention decreases with better cranial/facial bone excursion with PRM
Hypopneas can be influenced by rib compliance and lung mechanics
Airway patency influenced by vascular fluid retention in pharyngeal areas (e.g., thoracic inlet, cervical lymphatics)
Diaphragm excursion a significant player in lung mechanics (C3- C5, phrenic nerve)
Address sympathetic tone
Note that CPAP will impede diaphragm excursion, rib compliance, and lung mechanics

34. Example of ALF in Sleep
Uses alternative to PSG that you can use with your patients from Sleepimage.com
N-REM sleep – more white area is better
REM sleep – more to the left is better

35. Baseline

36. Baseline

37. Baseline

38. With CPAP

39. With CPAP

40. With CPAP + ALF

41. REM-With CPAP

42. REM-With CPAP + ALF