1. Obstructive Sleep Apnea and Obesity Hypoventilation Syndrome
Luai A. Al-Husseini,M.D, FCCP, DABSM
Diplomat, American Board of Internal Medicine
Diplomat, American Board of Pulmonary Medicine
Diplomat, American Board of Critical Care Medicine
Diplomat, American board of Sleep Medicine

2. Contents Definition Pathogenesis Pathophysiology Clinical Features
Treatment

3. History Charles Dickens – The Pickwick Papers
William Osler - Pickwickian Syndrome 1918
Guilleminault - OSAS
Fujita - UPPP
Sullivan - CPAP

4. Sleep Disordered Breathing (Obstructive Sleep Apnea)
Repetitive episodes of partial or complete upper airway obstruction during sleep, associated with hypoxemia, snoring, daytime sleepiness
Common
2-4% of children
4 to 9% of adults
>20% of the elderly
Even higher in African American, Asian and Hispanics
source: Atlanta Institute for ENT

5. Definition 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.

6. Sleep-disordered breathing: A spectrum of abnormality

7. Young T et al. N Engl J Med 1993;328:1230-1235.
Proportion of Men and Women Who Reported Hypersomnolence, According to Category of Sleep-Disordered Breathing.
85% men
Prevalence :
AHI > 5
Men 24% , Women 9%
AHI > 5 PLUS Daytime Sleepiness
Men4%, Women 2%
Recent studies:
AHI %
<
>
>5 and ESS
Figure 2. Proportion of Men and Women Who Reported Hypersomnolence, According to Category of Sleep-Disordered Breathing.
Young T et al. N Engl J Med 1993;328:

8. Epidemiology 85% men Prevalence - 2% in women, 4% in men
two thirds are obese
elderly
African-American

9. Obstructive Sleep Apnea

10. Normal Airway Response To Sleep

11. Why Obstruction Occurs During Sleep
Supine position
Control of breathing during normal non-rapid eye movement sleep
Lack of “wakefulness” drive
Minute volume decreases about 16%
PaCO2 increases 4-6 mmHg
SaO2 decreases as much as 2%
Decreased tone of pharyngeal muscles
Depressed reflexes, including pharyngeal dilator
Depressed response to hypoxia in men
REM sleep decreases tone of intercostal and accessory muscles, less effect on diaphragm; depression of minute volume, increase in CO2 not as great, depression of response to hypoxia greater

12. Airway Size In OSAS: CT Scan
Soft Palate
Uvula
Tongue Base
Baseline awake
Obstructive sleep apnea
CPAP asleep

13. Tongue Volume (Fat) in OSAS
Patients with OSAS had significantly greater tongue volumes, tongue fat and percentage of tongue fat than obese controls without sleep apnea, with increased fat toward the base of the tongue in the retroglossal region.
The apneic tongue is much larger and there is increased tongue fat deposition throughout the apneic tongue.

14. Sites of Airway Narrowing
18%
82%
Slide 14
Level 2
Slide 87
Airway closure during sleep is usually a diffuse process which limits the effectiveness of site-specific surgery. Morrison and colleagues used sleep endoscopy to show that only 18% of the patients in their study had airway closure limited to the palate alone.83 The rest of the patients demonstrated multiple sites of airway collapse. As a result, a single surgery may not be sufficient to eliminate sleep apnea.
83. Morrison DL, Launois SH, Isono S, Feroah TR, Whitelaw WA, Remmers JE. Pharyngeal narrowing and closing pressures in patients with obstructive sleep apnea. Am Rev Respir Dis 1993;148(3):
Adapted from Morrison DL et al. Am Rev Respir Dis 1993;148.
87. Morrison DL, Launois SH, Isono S, Feroah TR, Whitelaw WA, Remmers JE. Pharyngeal narrowing and closing pressures in the patients with obstructive sleep apnea. Am Rev Respir Dis 1993;148(3):

15. Obesity and OSA
About 70% of those with OSA are obese (Malhotra et al 2002)
Prevalence of OSA in obese men and women is about 40% (Young et al 2002)
Higher BMI associated with higher prevalence
BMI>30: 26% with AHI>15, 60% with AHI>5
BMI>40: 33% with AHI>15, 98% with AHI>5
(Valencia-flores 2000)

16. OSA
Decreased physical activity, exercise performance, energy metabolism, motivation
Obesity

17. SDB with Aging

18. Risk Factor: Age % with AHI > 5 Slide 18 Level 2
The risk of developing sleep apnea increases with increasing age. This slide shows the results of a study which evaluated the prevalence of sleep-disordered breathing in a general middle aged adult population.6 The percentage of subjects with 5 or more apneas and hypopneas per hour of sleep increases with increasing age in both men and women.
Adapted from Young T et al. N Engl J Med 1993;328.
2006 American Academy of Sleep medicine
6. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;32(17):

19. Risk Factor: Family History
Likelihood of Sleep Apnea as Function of Family Prevalence
Odds Ratio
(Adjusted for age, race, sex,
BMI)
Slide 19
Level 2
Slide 33
A family history of sleep apnea increases an individual’s risk of developing sleep apnea. This study shows that the risk of developing sleep apnea increases as the number of family members with sleep apnea increases, to an almost 4 fold greater risk if 3 other relatives have sleep apnea.25
This familial aggregation is not explained entirely by familial similarities in BMI or neck circumference, suggesting other familial factors are important in increasing susceptibility to the disorder. However, this risk factor is not strong enough to warrant screening asymptomatic family members with sleep studies.
25. Redline S, Tishler PV, Tosteson TD, et al. The familial aggregation of obstructive sleep apnea. Am J Respir Crit Care Med 1995;151(3 Pt 1):682-7.
Relative Relatives Relatives
Adapted from Redline S et al. Am J Resp Crit Care Med 1995;151.
25. Redline S, Tishler PV, Tosteson TD, et al. The familial aggregation of obstructive sleep apnea. Am J Respir Crit Care Med 1995:151(3 Pt 1):

20. SMOKING
Adjusted Odds Ratio for Sleep Apnea (AHI > 15) in Former & Current Smokers vs Nonsmokers
Odds Ratio
(Adjusted for age,
race, sex, BMI)
Slide 20
Level 2
Cigarette smoking is also a risk factor for the development of sleep apnea. A longitudinal epidemiologic study showed that smokers are at an increased risk for developing sleep apnea when compared to nonsmokers. This slide shows that current smokers are at a greater risk than former smokers, and both are at greater risk than never-smokers for developing moderate-severity sleep apnea.27 This risk increases in a dose related manner, such that heavy smokers have a greater risk than light smokers. This risk from smoking is independent of sex, age and Body Mass Index (BMI).
Former Current
Smokers Smokers
Adapted from Wetter DW et al. Arch Intern Med 1994:154 ©1994 American Medical Association.
2006 American Academy of Sleep Medicine
27. Wetter DW, Young TB, Bidwell TR, Badr MS, Palta M. Smoking as a risk factor for sleep-disordered breathing. Arch Intern Med 1994;154(19)

21. Risk Factor: Sedatives
150
Phrenic Nerve
100
Peak Integrated activity
(% control)
Hypoglossal Nerve 50
Diazepam Injection
Slide 21
Level 2
Slide 34
Sedatives such as benzodiazepines have been shown to worsen sleep apnea in patients with pre-existing disease and to induce sleep apnea in individuals previously without the disorder.31, 32 These agents work by selectively reducing hypoglossal nerve output to the genioglossus muscle, one of the pharyngeal dilator muscles.
This slide shows the effect of injected diazepam on the output of the phrenic and hypoglossal nerves in a cat.33 There is a selective reduction in the hypoglossal nerve activity over time, while the phrenic nerve is spared. This reduction in neural output to the dilator muscle promotes collapse of the pharyngeal airspace. Sedatives may also increase the arousal threshold, prolonging apneas.34
31. Dolly FR, Block AJ. Effect of flurazepam on sleep-disordered breathing and nocturnal oxygen desaturation in asymptomatic subjects. Am J Med 1982;73(2):
32. Mendelson WB, Garnett D, Gillin JC. Flurazepam-induced sleep apnea syndrome in a patient with insomnia and mild sleep-related respiratory changes. J Nerv Ment Dis 1981;169(4):261-4.
33. Bonora M, St John WM, Bledsoe TA. Differential elevation by protriptyline and depression by diazepam of upper airway respiratory motor activity. Am Rev Respir Dis 1985;131(1):41-5.
34. Strollo PJ, Atwood CW, Sanders MH. Medical therapy for obstructive sleep apnea-hypopnea syndrome. In: Kryger M, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine. 4th ed. Philadelphia: Saunders; 2005.
Minutes after injection
Sanders MH. In: Principles and Practice of Sleep Medicine. Philadelphia: W.B. Saunders Company, 1994.
31. Dolly FR, Block AJ. Effect of flurazepam on sleep-disordered breathing and nocturnal oxygen desaturation in asymptomatic subjects. Am J Med 1982;73(2):
32. Mendelson WB, Garnett D, Gillin JC. Flurazepam-induced sleep apnea syndrome in a patient with insomnia and mild sleep-related respiratory changes. J Nerv Ment Dis 1981;169(4):
33. Bonora M, St. John WM, Bledsoe TA. Differential elevation by protriptyline and depression by diazepam of upper airway respiratory motor activity. Am Rev Respir Dis 1985;131(1):41-45.
34. Sanders MH. Medical therapy for sleep apnea. In: Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine, 2nd edition. Philadelphia: WB Saunders, 1994;

22. Risk Factor: Alcohol Before Alcohol Slide 22 Blood Alcohol = 83 mg/dl
Phrenic
Hypoglossal
Blood Alcohol = 83 mg/dl
Phrenic
Hypoglossal
Slide 22
Level 2
Blood Alcohol = 134 mg/dl
Slide 35
Alcohol induces sleep apnea in individuals who snore, and worsens sleep apnea severity in patients with pre-existing disease.34 Alcohol selectively reduces the motor output of the hypoglossal nerve to the upper airway dilator muscles, promoting collapse of the pharyngeal airway, and can increase the arousal threshold, prolonging apneas. This slide shows the effect of increasing doses of ethanol on hypoglossal and phrenic nerve activity.35 Note the dose-related reduction in hypoglossal nerve activity.
34. Strollo PJ, Atwood CW, Sanders MH. Medical therapy for obstructive sleep apnea-hypopnea syndrome. In: Kryger M, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine. 4th ed. Philadelphia: Saunders; 2005.
35. Bonora M, Shields GI, Knuth SL, Bartlett D, Jr., St John WM. Selective depression by ethanol of upper airway respiratory motor activity in cats. Am Rev Respir Dis 1984;130(2):
Phrenic
Hypoglossal
Bonara M et al. Am Rev Respir Dis 1984;130 © American Lung Association.
34. Sanders MH. Medical therapy for sleep apnea. In Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine, 2nd edition. Philadelphia: WB Saunders, 1994:
33. Bonora M, Shields GI, Knuth SL, et al. Selective depression by ethanol of upper airway respiratory motor activity in cats. Am Rev Respir Dis 1984;130(2): Official Journal of the American Thoracic Society © American Lung Association.

23. Diagnosis
Clinical Features

24. DIAGNOSIS: CLINICAL FEATURES
Nocturnal symptoms
1. Snoring
– reflects the critical narrowing
- population survey: habitual snorers
25% of men, 15% of women
- prevalence increases with age (60%, 40%)
- the most frequent symptom of OSA
- absence makes OSA unlikely
(only 6% of patients with OSA did not report)

25. Clinical features
(nocturnal symptoms continued) 2. Witnessed apneas 3. Nocturnal choking or gasping - report of waking at night with a choking sensation; passes within a few seconds 4. Insomnia - sleep maintenance insomnia - (few have difficulty initiating sleep)

26. Clinical features Daytime symptoms 1. Excessive daytime sleepiness
- severity can be assessed
 subjectively = questionnaires
(Epworth Sleepiness Scale)
 objectively
MSLT = Multiple Sleep Latency Test
MWT = Maintenance of wakefulness Test
Osler Test

27. Clinical features (daytime symptoms) 2. fatigue 3. memory impairment
4. personality changes
5. morning headaches or nausea
6. depression

28. DIAGNOSIS American Academy of Sleep Medicine criterias:
A. Excessive daytime sleepiness that is not better explained by other factors
B. Two or more of the following that are not better explained by other factors:
choking during sleep; recurrent awakenings; unrefreshing sleep;
daytime fatigue; impaired concentration.
C. AHI (five or more obstructed breathing events per hour during sleep).

29. Evaluation- physical exam
adenotonsillar hypertrophy
nasal obstruction
hypothyroidism
acromegaly
Down syndrome
micrognathia
retrognathia
obesity
vocal cord paralysis
H&N masses

30. Evaluation - physical exam
Nasal obstruction - turbinate hypertrophy, polyposis, septal deviation
oral cavity and oropharynx
redundant mucosa
beefy red
elongated uvula
macroglossia
AT hypertrophy

31. Complications of OSAS

32. Sleep Apnea Affects Many Aspects of Physical and Mental Health
Muscle
Insulin resistance
Brain
Cogniition and mood
stroke
Cancer
-Incidence
-Mortality
Inflammation
DIABETES
Liver
Insulin resistance
Pancreas
Abnormal insulin
Obstructive
Sleep
Apnea
Heart, Vessel,
Endothelium
Cardiovascular
disease
Pathologies in peripheral systems thought to be due, in part, to central circadian misalignment are indicated on the slide. These include cardiovascular disease, mood disorders, cognitive impairment, immune dysfunction, metabolic disorders, reproductive problems, and cancer among others.
GI tract
Peptic ulcer
Adipose
Obesity
Kidney
Nocturia
CRSD, circadian rhythm sleep disorder. Klerman EB. J Biol Rhythms. 2005;20(4): ; Young ME, Bray MS. Sleep Med. 2007;8(6):

34. All normotensive at baseline
AJRCCM 2002

35. Cardiometabolic Consequence Of OSA

36. Probability of CAD incidence estimated by Poisson model Start age 49 yrs, Systolic BP 133 mmHg and Sat. min 86%
Peker et al, ERJ 2006

37. The Relationship between Obstructive Sleep Apnea and Hypertension
Compared to those with AHI=0, the odds of having hypertension was 42% greater if AHI was 0.1-5, 2x greater if AHI was 5-15, and almost 3x greater if AHI was more than 15 per hour
Peppard et al. NEJM. 2000; 342:

38. Sympathetic System: Norepinephrine
24-hr urinary NE increased 45% in apneic (RDI>20) compared to non-apneic patients.
CPAP treatment lowered daytime plasma NE levels by 23%; Placebo had no effect on NE levels
Dimsdale et al, Sleep 1995;18:377-81

39. Prevalence of OSA in Stable outpatients with Heart Failure
Although beta-blockers and CRT therapy have both been shown to improve CSA, even with modern therapy and high beta-blocker use, CSA continues to have a high prevalence.

40. OSA and Abnormal Heart Rhythms: Atrial Fibrillation
Four times increased risk of AF in pts with OSA (AHI>30) (Sleep Heart Health Study 2006)
Onset of >75% of persistent Afib episodes in pts with OSA occur at night (8pm-8am)
A fib recurrence after cardioversion twice as high in untreated OSA
Observational review over 17 yrs suggests that nocturnal hypoxemia influences the onset of A fib
Postgrad Med J 2008; 84:15-22
Proc Am Thorac Soc 2008; 5:

41. J Am Coll Cardiol. 2007;49(5):565-571. doi:10.1016/j.jacc.2006.08.060
Obstructive Sleep Apnea, Obesity, and the Risk of Incident Atrial Fibrillation
Cumulative frequency curves for incident atrial fibrillation (AF) for subjects <65 years of age with and without obstructive sleep apnea (OSA) during an average 4.7 years of follow-up. p =
J Am Coll Cardiol. 2007;49(5): doi: /j.jacc

42. OSA and Strokes OSA is a risk factor for stroke
2 prospective cohort studies following 1022 and 1651 pts found a higher incidence of stroke in OSA
SLEEP, Vol. 30, No. 3, 2007

45. Community-based cohort
Sleep Apnea and 20-Year Follow-Up for All-Cause Mortality, Stroke, and Cancer Incidence and Mortality in the Busselton Health Study Cohort
Community-based cohort
400 residents of the Western Australian town of Busselton.
Moderate-severe OSA was significantly associated with all-cause mortality (HR = 4.2; 95% CI 1.9, 9.2), cancer mortality (3.4; 1.1, 10.2), incident cancer (2.5; 1.2, 5.0), and stroke (3.7; 1.2, 11.8)
Conclusions
Moderate-to-severe sleep apnea is independently associated with a large increased risk of all-cause mortality, incident stroke, and cancer incidence and mortality in this community-based sample.

46. Diagnosis

47. Diagnosis
Clinical: typical patient is male, 30-60y, snores, has daytime sleepiness, nocturnal choking or gasping, witnessed apneas during sleep, moderate obesity and large neck circumference and mild to moderate hypertension.
Women with OSA are postmenopausal, snoring is less frequent and daytime fatigue is more common than outright sleepiness.

48. Standard Polysomnography
EEG, EOG, EMG Presence/Stage
EKG Cardiac rate/rhythm
Airflow Apnea/hypopnea
Chest/Abd bands Respiratory effort
Pulse oximetry Arterial oxygen sat
Left/right leg EMG PLMS

51. OSA Severity Based on “cut-offs” of frequency of apneas and hypopneas
-Mild : 5-15 events per hour
-Moderate: > events per hour
-Severe: >30 events per hour
Additional Measures
-Degree of nocturnal hypoxemia
-Extent of sleep fragmentation

52. Limitations of Polysomnography
Requires an overnight stay in sleep lab
Time consuming
Labor intensive
Costly
Limited access in some regions
“First Night effect”

53. OSA - Implications
Symptoms generally more severe in patients with more severe disease
However, symptoms do not always correlate with AHI (eg UARS)
AHI does not always correlate with hypoxemia

54. Treatment

55. Treatment Behavioral modification pharmacotherapy orthodontic devices
continuous positive airway pressure

56. BEHAVIORAL METHODS Weight loss Avoid alcohol and sedatives
Avoid sleep deprivation
Avoid supine sleep position
Stop smoking
A variety of behavioral interventions are available to modify sleep apnea. Where appropriate, weight loss should be encouraged.59 Alcohol and sedatives should be avoided as they induce instability and promote collapsibility of the upper airway during sleep.34 Sleep deprivation also leads to upper airway instability during sleep, increasing the likelihood of collapse.60 Avoiding the supine position may modify the severity of the apnea in patients with position-dependent sleep apnea.61 Finally, smoking cessation should be encouraged since data suggests that smoking is an independent risk factor for sleep apnea.27
59. Smith PL, Gold AR, Meyers DA, Haponik EF, Bleecker ER. Weight loss in mildly to moderately obese patients with obstructive sleep apnea. Ann Intern Med 1985;103(6 PT 1):
34. Sanders MH. Medical Therapy for sleep apnea. In: Kryger MH, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine, 2nd edition. Philadelphia: WB Saunders, 1994;
60. Neilly JB, Kribbs NB, Maislin G, Pack AI. Effects of selective sleep deprivation on ventilation during recovery sleep in normal humans. J Appl Physiol 1992;72(1):
61. Cartwright R, Ristanovic R, Diaz F, Caldarelli D, Alder G. A comparative study of treatments for positional sleep apnea. SLEEP 1991;14(6):
27. Wetter DW, Young DB, Bidwell TR, Badr MS, Palta M. Smoking as a risk factor for sleep-disordered breathing. Arch Intern Med 1994;154(19):

57. WEIGHT LOSS Remains a highly effective method
10 – 15 % reduction in weight can lead to an approximately 50 % reduction in sleep apnea severity in moderately obese male patients.

58. Weight Loss and Sleep Apnea6 5 4 3
Mean Change in AHI, Events/hr 2 1 -1 -2 -3 -4
Slide 60
This slide depicts the relationship between weight change and apnea severity. In this study 694 randomly selected individuals were evaluated at four year intervals for sleep-disordered breathing to determine the longitudinal association between weight change and sleep apnea. A decrease in weight reduced the severity of the sleep apnea, with a 10% weight loss predicting a 26% drop in AHI. Conversely, a 10% gain in weight predicted a 32% increase in the AHI. This indicates that even a modest degree of weight loss can have a significant impact on apnea severity and that weight control can be an effective method for managing sleep apnea.50
50. Peppard PE, Young T, Palta M, Dempsey J, Skatrud J. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA 2000;284(23):
-20 to <-10%
-10 to <-5%
-5% to <+5
+5 to +10%
+10% to +20
Change in Body Weight
Adapted from Peppard PE et al. JAMA 2000;284.

59. SLEEP POSITION TRAINING
Lying in the supine position results in a decrease in the size of the pharynx because of the effects of gravity.66,67 As a result, some people experience sleep apnea only when sleeping on their backs, while others may experience a worsening of the severity of their apnea when supine. These patients may benefit from sleep-position training, which is designed to prevent sleeping in the supine position.61 This slide illustrates the use of a tennis ball sewn into the back of a night shirt as a means of training the patient to avoid the supine position and sleep in the lateral recumbent position.
The presence of a position-dependent breathing disturbance should be demonstrated before initiating this form of treatment. Positional dependence is less common in obese patients with severe disease. Changing position may convert severe apneas to milder forms of the disease such as hypopneas without changing the degree of sleep fragmentation.68 In these settings, positional therapy may not be sufficient and should be carefully monitored for effectiveness.
2006 American Academy of Sleep Medicine
66. Fouke JM, Strohl KP. Effect of position and lung volume on upper airway geometry. J Appl Physiol 1987;63(1):
67. Pevernagie DA, Stanson AW, Sheedy PF, Daniels BK, Shepard JW Jr. Effects of body position on the upper airway of patients with obstructive sleep apnea. Am J Respir Crit Care Med 1995;152(1):
61. Cartwright R, Ristanovic R, Diaz F, Caldarelli D, Alder G. A comparative study of treatments for positional sleep apnea. SLEEP 1991;14(6):
68. Pevernagie DA, Shepard JW Jr. Relations between sleep stage, posture and effective nasal CPAP levels in OSA. SLEEP 1992;15(2):

60. Treatment - CPAP 100% effective titrate pressure
poor compliance %

62. CPAP for OSA: Benefits Improved cognitive function
Improved quality of life
Reduced daytime sleepiness
Reduced risk of automobile accidents
Reduced health care costs
Reduced blood pressure
Reduced cardiac arrhythmias
Improved glucose tolerance
Reduced mortality rate
Reversal of impotence

63. Mean percentage days CPAP used
CPAP Compliance
Mean percentage days CPAP used
Slide 63
Level 2
Slide 72
Kribbs and colleagues69 objectively evaluated the pattern of patient CPAP use by installing covert time and pressure monitors in the CPAP devices. This graph shows how often patients used their CPAP for varying lengths of time. The height of the 20 minute column shows that patients tried to use their CPAP most nights (70%). The patients succeeded in using their CPAP 4 hours or more a night about 55% of the time. Patients were able to use their CPAP all night only 20% of the time. Compliance over time was stable, with use at 3 months the same as use after 1 month.
69. Kribbs NB, Pack AI, Kline LR, et al. Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea. Am Rev Respir Dis 1993;147(4):
Time CPAP used
Adapted from Kribbs NB et al. Am Rev Respir Dis 1993;147.
75. Kribbs NB, Pack AI, Kline LR, et al. Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea. Am Rev Respir Dis 1993;147:

64. Bi-level Positive Airway Pressure
Positive Pressure Therapy
CPAP
Bi-level 15 10
Pressure 5
Slide 64
Level 2
Insp
Flow
Slide 77
Bi-level positive airway pressure may improve acceptability of therapy to patients requiring high pressure levels or those who complain of difficulty exhaling against the positive pressure. Bi-level devices allow the application of different pressure levels during inspiration and expiration. This slide shows the difference in the way positive pressure is delivered by the 2 modalities.74
With CPAP, positive pressure is delivered at the same level during inspiration and expiration. Bi-level therapy takes advantage of the differences in pressure in the upper airway during phases of respiration. During inspiration, negative intrathoracic pressure creates a pressure gradient which causes the pressure in the upper airway to be negative, promoting collapse of the airway.
During expiration, the gradient reverses, pressure in the upper airway increases, and the forces promoting airway collapse are reduced. As a result, less pressure is required to keep the airway open during expiration than during inspiration. Bi-level devices allow independent adjustment of pressure levels during respiration, permitting the patient to breathe out against a lower positive pressure.
74. Sanders MH, Kern N. Obstructive sleep apnea treated by independently adjusted inspiratory and expiratory positive airway pressures via nasal mask. Physiologic and clinical implications. Chest 1990;98(2):
Exp
80. Sanders MH, Kern N. Obstructive sleep apnea treated by independently adjusted inspiratory and expiratory positive airway pressures via nasal mask. Physiologic and clinical implications. Chest 1990;98(2):

65. Autotitrating CPAP (Ayas N, Sleep 2004)
Most commonly, increases pressure to eliminate vibration of palate and soft tissue.
Now costs about the same as “straight” CPAP.
May improve compliance.
Results in lower pressure over all.
Can obviate the need for in-lab titration, in many cases.
Is supplanting in-lab titration

66. Supplemental Oxygen Not a primary treatment for sleep apnea
Does not improve daytime sleepiness
May prolong apneas
Reduces oxygen desaturation during apneas
Reduces arrhythmias
Slide 84
Supplemental oxygen is not a first-line therapy for sleep apnea78, but may be useful in patients who will not accept more definitive therapy but have severe nocturnal desaturation. Because collapse of the airway continues to occur, use of oxygen alone does not prevent the fragmentation of sleep caused by the recurrent sleep apnea events. As a result, there is no improvement in the symptoms of daytime sleepiness. Oxygen therapy may prolong apnea duration by increasing oxygen stores prior to the apneas, delaying one of the signals of arousal. The depth of oxyhemoglobin desaturation during the apneic events, however, may be decreased. The use of oxygen may reduce the frequency of dysrhythmias in patients who have dysrhythmias that are related to hypoxemia but should be used with caution in patients with obstructive lung disease and CO2 retention.
78. Morgenthaler TI, Kapen S, Lee-Chiong T, et al. Practice parameters for the medical therapy of obstructive sleep apnea. Sleep 2006;29(8):
83. Fletcher EC, Munafo DA. Role of nocturnal oxygen therapy in obstructive sleep apneas. When should it be used? Chest 1990;98(6):

67. Treatment - surgical
adenotonsillectomy - preferred treatment in children
tracheostomy - cure for OSAS
used for failure of more conservative treatment
life threatening cardiopulmonary complications
alternative techniques to lessen complications

68. Treatment - surgical Uvulopalatopharyngoplasty (UPPP)
excise excess tissue from free margin of soft palate
+/- tracheostomy
variable response - approximately 50%
+/- nasal surgery

69. Treatment - surgical laser midline glossectomy mandibular advancement
maxillary advancement - LeFort I osteotomy
hyoid suspension and inferior sagittal mandibular osteotomy
hyoid expansion

70. Enlarge the Bony Space- Other Surgeries
Genioglossus Advancement/ Hyoid Repositioning
Success ~80% (11-18mm)
Less effective with RDI >60
Maxillo-mandibular Advancement
Particularly useful in the setting of hypopharyngeal obstruction (Fujita 2 or 3)
Best results when performed following “Stage 1” surgery

72. Oral Appliances (Kushida C, Sleep 2006)
Indicated for patients with mild-to-moderate obstructive sleep apnea who
prefer oral appliances to CPAP
do not respond to CPAP
are not appropriate candidates for CPAP
fail treatment attempts with CPAP (Kushida Sleep 2006)
Not as effective as CPAP
Lower blood pressure 3-4 mmHg (Otsuka Sleep Breath 2006)
Outperformed surgery in the only head-to-head trial.
Preferred to CPAP in head-to-head trials.

73. Dental Appliances

74. ADJUSTABLE POSITIONER

75. Nasal EPAP – Provent® Nasal valves
Decreased AHI from 43 to 27, improved Epworth in a small group of CPAP “failure” patients (Walsh JK, Sleep Med 2011)
Reduced AHI by about 50% (compared with 10% for sham) in RCT of 250 people (Berry RB, Sleep 2011)

76. Hypoglossal nerve Stimulation For OSA

77. Obesity Hypoventilation Syndrome

78. Obesity Hypoventilation Syndrome

79. Complications of OHS CNS Upper Airway Metabolic Respiratory General
Cognitive Deficit
Decreased neuronal Drive
Upper Airway
OSA
Increased intubation risk
Metabolic
Central Obesity
Metabolic Syndrome
Chronic inflammation
Respiratory
Restrictive lung disease
Pulmonary Hypertension
Hypercapnia/Hypoxemia
CVS
Endothelial dysfunction
CAD
CHF
General
Peripheral edema
Decreased physical activity
Increased morbidity/mortality

80. Treatment of OHS Comprehensive and multidisciplinary approach
Immediate initiation of noninvasive positive airway pressure (PAP).
Lifestyle modifications for weight loss.
In advanced cases: Consider tracheostomy and bariatric surgery or medication for weight loss.
Oxygen should not be administered as a sole therapy for OHS.
Respiratory stimulants (ie, progestins and acetazolamide) in patients who continue to have serious alveolar hypoventilation despite PAP therapy and weight loss (minimally effective and are associated with adverse effects).
Abstain from alcohol and sedatives.

81. Conclusion

82. Conclusion Life threatening complications
Suboptimal treatment either due to poor response or limited compliance
Long-term therapy and follow-up.
Keep OHS in mind hen encountering an obese sleepy hypercapnic patient.

83. Thank You All