This document provides an overview of obstructive sleep apnea (OSA), including its pathophysiology, symptoms, diagnosis via polysomnography, treatment options such as CPAP, oral appliances, surgery, and lifestyle changes, and potential health consequences if left untreated. OSA is caused by physical blockage of the upper airway during sleep, which can be due to excess soft tissue or structural abnormalities. Diagnosis requires an overnight sleep study to measure respiratory disturbances, oxygen levels, and sleep stages. Treatment aims to eliminate snoring and breathing pauses through devices like CPAP or procedures to enlarge the airway. Untreated OSA has been linked to cardiovascular disease, strokes, and traffic accidents due to daytime sleepiness

1. OBSTRUCTIVE SLEEP APNEA
MANAGEMENT CONCEPTS
BY
DENISE WATTS, BSRC, CRT, RPSGT, RST
UTMB SLEEP DISORDER CENTER
dmwatts@utmb.edu

2. Pathophysiology of OSA
 Physical blockage
 Upper Airway
Closure
 Continued
respiratory
effort

3. Pathophysiology
Physical Characteristics
 Enlarged Tongue
 Nasal Obstruction
 Enlarged Soft Palate
 Large/Floppy Epiglottis
 Narrow oropharynx
 Tonsillar hypertrophy

4. Pathophysiology
Physical Characteristics
Elongated and Edemaous Uvula
 Softpalate is exposed to recurrent vibratory trauma,
ie. Snoring, and high negative inspiratory pressure
 Lengthening of the uvula due to stretching
 Thickening of the uvula caused by edema
 Increase airway resistance

5. Pathophysiology
Physical Characteristics
 Retrognathia-receeding chin
 Craniofacial Deformities
 Increased BMI-Obesity, Morbid Obesity
 Neck Circumference
 Male: 16-17 inches in diameter
 Female: 14-15 inches in diameter
 Measurement taken around the cricothyroid membrane

6. Pathophysiology
Physical Characteristics
Mallampati Score
Class 1: Full visibility of tonsils, uvula and soft
palate
Class 2: Visibility of hard and soft palate, upper
portion of tonsils and uvula
Class 3: Soft and hard palate and base of the
uvula are visible
Class 4: Only Hard Palate visible

8. Pathophysiology of OSA
Symptoms
 EDS-Excessive Daytime Sleepiness
 Measured by the Epworth Sleepiness Scale
 Morning Headaches
 Lack of oxygen
 Cognitive impairment
 Lack of oxygen
 Snoring, gasping, snorts, choking
 Hypercapnia cause arousals

10. Pathophysiology of OSA
History
 Mouth breathing
 Fatigue
 Depression
 Drowsy driving
 One in fifteen MVAs
 Males over 40
 Witnessed apneas
 Bed partner’s input

12. Sleep Study
 OSA can only be diagnosed with a polysomnogram
 Must have a physician referral
 Diagnose a wide spectrum of pulmonary and
nonpulmonary disorders of sleep
 Periodic Limb movement Disorder
 Involuntary limb movements which cause frequent arousal
which lead to EDS
 REM Behavior Disorder
 Electromyographic (EMG) atonia with elaborate motor
activity associated with dream mentation

13. Sleep Studies
Diagnostic
 Evaluation of sleep
Therapeutic
 CPAP/BiPAP treatment for OSA
Split Study
 Patient meets OSA qualifications within 2 hours of
sleep time at which time CPAP titration is initiated
 TDC patients
 Medicare patients and certain insurance companies

14. Sleep Study Parameters
 EEG
 Stages of sleep
 10/20 system of measurement
 Eyes
 Stages of sleep
 Slow rolling eye movement
 REM
 Chin
 Muscle atonia during REM
 Nasal/Oral Airflow
 SaO2
 Snoring

15. Sleep Study Parameters
 Thoracic Effort
 Abdominal Effort
 Legs
 Periodic limb movement disorder
 EKG
 Bradycardia
 Tachycardia
 dysrhythmias
 Epoch
 30 seconds of data per page

16. Respiratory Events, Arousals & Desats
Respiratory Events
Obstructive
 Apnea
 Hypopnea
 RERA-Respiratory effort related apnea
 Mixed Apnea
Neurological
 Central Apnea
 AHI= Apnea Hypopnea Index
 Total Apneas + Hypopneas per hour of sleep
 RDI=Respiratory Disturbance Index
 Total Apneas + Hypopneas + RERA’s per hour of sleep
 RDI or AHI
 5 - 15 = mild
 16 - 29 = moderate
 > 30 = severe

17. Respiratory Events, Arousals & Desats
Cortical Arousal
 Brain disturbance caused by respiratory events, leg movements,
body movement ie. Changing positions, coughing, etc.
 Sleep fragmentation
 Hypoxia to hypercapnia
Desaturation
 Must be at least either 3% or 4% depending of the patient’s
insurance or lack of insurance

18. Obstructive
 At least a 10 second cessation of airflow despite
continuous ventilatory effort.
 Episodes occur repeatedly through out the night
 May or may not be associated with an
oxyhemaglobin desaturation of at least 3% or 4%
 May or may not be associated with a cortical arousal
 May or may not be accompanied by snoring
 May be REM (rapid eye movement) related
 May be positional

20. Hypopnea
 Decrease in airflow of at least 30% along with
continued respiratory effort
 Must be at least 10 seconds
 Must have at least a 3% or 4% desaturation
 May or may not have an arousal
RERA-Respiratory Effort-Related Arousal
 Increased respiratory effort with decrease airflow
 Must be at least 10 seconds
 Must have an arousal
 Must not have a desaturation

22. Mixed Apnea
 Has both a cortical and respiratory aspect
 Begins with a central portion lasting at least 25% of
entire respiratory event which is then followed by an
increase in respiratory effort (respiratory muscles)
which is the obstructed aspect.
Central Apnea
 Complete cessation of airflow and respiratory effort
 Must at least 10 seconds
 May or may not have an arousal
 May or may not have a desaturation of at least 3% or
4%
 Cheyne-Stokes
 CHF

25. PAP Treatments
CPAP
 First line of treatment
 Titrate until all OSA’s, snoring and arousals are
eliminated
BiPAP
 Central apneas
 Reached maximum CPAP pressure
 Must meet insurance qualification to be covered

26. CPAP Side Effects
 Discomfort
 Bloating
 Irritation
 Occasional Rhinorrhea
 Congestion
 Nasal/Oral dryness
 Add humidification
Claustrophobia
 Nasal prongs
 Full face mask
 RAMP
 Gradual increase to prescribed pressure

27. Treatment Options
 Oral Appliance
 Mild Sleep Apnea
 May still require CPAP
 ENT Surgery
 Mild sleep apnea
 May still require CPAP
 Tracheotomy
 Severe sleep apnea, life-threatening

28. ORAL DEVICES
 Mandibular advancement device (MAD)
 Most widely used dental device for sleep apnea. It is similar
in appearance to a sports mouth guard. MAD forces the
lower jaw forward and down slightly, which keeps the
airway open.
 Tongue retraining device (TRD)
 Splint that holds the tongue in place to keep the airway as
open as possible

29. Maxillomandibular Advancement

30. Surgical Management
 UPPP- Uvulopharyngopalatoplasty
 Rhinological procedures
 Tongue base suspension/reduction
 Hyoid suspension
 Maxillomandibular advancement
 Bariatric-RDI can drop 50%
 Tracheotomy

31. Palatal Reduction
Uvulopharyngopalatoplasty (UPPP)
 Corrects oropharynx obstruction
 Most common procedure
 Trim excess palatal length and
uvula
 Often combined with
tonsillectomy
* Success = RDI reduction of ≥50%

32. Tongue Base Suspension/Reduction
Suspension
 Sutures attach to screw at inner
mandible
 Reduces tongue collapse
 Variable success 20-82%
Reduction
 Tissue reduction from heat
generated by radiofrequency
 Multiple office based treatments
 Promising success rate 60-85%

33. Behavioral Treatment
 Avoid Alcohol
 Reduces upper airway muscle tone
 Increases the frequency of abnormal breathing
 Delays arousals
 Weight Loss
 Avoid sedative hypnotics, ie. Benzodiazepines
 Positional Apneas-Supine
 Train to sleep in the lateral recumbent position
 Attach an uncomfortable object to the back
 Tennis ball sewn into pajamas

34. Behavioral Treatment
 Sleep Hygiene
 Have a set bed time
 Have a bed time routine
 NO Television
 Light and noise
 Trigger wake-brain thinks it’s supposed to be daytime/wake
 Dark room
 Cool temperature
 Cell phones off/vibrate
 Shift workers
 Wear earplugs
 Blackout curtains

35. Treatment Goals
 Establish normal nocturnal oxygenation and ventilation
 Eliminate snoring
 Eliminate sleep fragmentation caused by excessive
arousals

36. Treatment Goals
Treatment should be based on the effect of the
sleep disorder on daytime symptoms and
cardiovascular function as well as the absolute
number of respiratory episodes
 Look at the whole picture

37. Pathophysiological Consequences
 Heart Disease
 Atrial Fibrillation
 Right and Left Ventricular Failure
 Nocturnal Dysrhythmias
 Bradycardia
 During apneic episode
 Tachycardia
 After apneic episode
 Compensates for decrease blood flow

38. Pathophysiological Consequences
 Cerebrovascular disease
 Chronic exposure contributes to neuronal destruction
 Early deterioration in neurological status
 Delirium
 Stroke
 Recurrent hypoxemia
 Decrease in cerebral blood flow
 Increase in intracranial pressure
 Desaturations affects all organs/tissues
 Trickle down effect

39. Pathophysiological Consequences
 CAD
 Myocardial Infarct
 Vascular Disease
 Systemic HTN
 Pulmonary HTN

40. Consequence of OSA
Motor Vehicle Accidents
 Sleep fragmentation
 EDS
 Impaired cognition/delayed reaction time
 Accident rate is 7X higher than that of the general
driving population
Occupational Accidents

42. Bibliography
Courson,MS4, Andrew and Vicente Resto, MD, PhD, FACS.
“Surgical Management of Obstructive Sleep Apnea in
Adults.”University of Texas Medical Branch, Department of
Otolaryngology, Grand Rounds Presentation. 4 Sept. 2009
Rowley, MD., James A. “Obstructive Sleep Apnea-Hypopnea
Syndrome.”emedician from WedMD. Apr 2,
2009.http://emedicine.medscape.com/article/302773-print
“Sleep Apnea”. Wikipedia.