1. OBSTRUCTIVE SLEEP APNEA
Helen Gidey, MD
Emory Johns Creek Hospital
March 13, 2008

2. 2006 American Academy of Sleep Medicine

3. WHAT IS OSA?

4. OSA IS :
Common
Dangerous
Easily recognized
Treatable

5. WHAT IS OSA?
Sleep disorder characterized by recurrent episodes of narrowing or collapse of pharyngeal airway during sleep despite ongoing breathing efforts.
These often lead to
Acute derangements in blood gas disturbances
Surges of sympathetic activation
Periodic arousal from sleep (fragmented sleep)

7. PATENT Vs COLLAPSED AIRWAY
2006 American Academy of Sleep medicine

8. WHAT IS OSA? Episodes of complete or partial collapse of airway are
translated to # of apnea and hypopnea events (AHI).
Apnea = cessation of airflow > 10 seconds
Hypopnea = Decreased airflow > 10 seconds associated with:
Arousal
Oxyhemoglobin desaturation

9. WHY DOES THIS MATTER? Excessive daytime somnolence
Impaired cognitive performance
Poor quality of life
Increased risk of MVA
Adverse cardiovascular outcomes
Pulmonary hypertension
(?DM/metabolic syndrome)

10. EPIDEMIOLOGY Disease prevalence = 2 – 4 % of US adult population
Higher in population subsets
1980’s = morbidity associated with OSA became more widely appreciated
Majority of cases still undiagnosed
 PCP = increase knowledge
= recognize risk factors
= identify affected individuals

11. WHAT ARE THE RISK FACTORS ?

12. RISK FACTORS Obesity Age Sex Race Craniofacial anatomy
Smoking and etoh consumption

13. OBESITY Strongest risk factor for OSA
Present in > 60% of patients referred for
a diagnostic sleep evaluation
Wisconsin Sleep Cohort Study
A one standard deviation difference in BMI was associated with a 4-fold increase in disease prevalence

14. Obesity Alters upper airway mechanics during sleep
Increased parapharyngeal fat deposition:
neck circumference: > 17” males
> 16” females
With subsequent:
 smaller upper airway
 increase the collapsibility of the pharyngeal airway

15. obesity
2. Changes in neural compensatory mechanisms that maintain airway patency:  diminished protective reflexes which otherwise would increase upper airway dilator muscle activity to maintain airway patency

16. obesity
3. waist circumference Fat deposition around the abdomen produces  reduced lung volumes (functional residual capacity) which can lead to loss of caudal traction on the upper airway  low lung volumes are associated with diminished oxygen stores

18. AGE Mechanisms proposed: Anatomic susceptibility
Preferential deposition of fat in the
parapharyngeal area
Changes in the body structures around the pharynx
Deterioration of protective reflex mechanisms

19. Risk Factor: Age % with AHI > 5 Slide 19 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):

20. GENDER  MALE GENDER Increased neck and waist circumference
Pharyngeal airway length
? Women not reporting the classic symptoms
? Differential response of bed partner to symptoms
of obstructive breathing during sleep
? Healthcare providers have lower index of suspicion
for considering OSA in men than women

21. CRANIOFACIAL ANATOMY Mandibular body length Retrognathia
Tonsilar hypertrophy
Enlarged tongue or soft palate
Inferiorly positioned hyoid bone
Maxillary and mandibular retro position
Decreased posterior airway space

22. SMOKING
Adjusted Odds Ratio for Sleep Apnea (AHI > 15) in Former & Current Smokers vs Nonsmokers
Odds Ratio
(Adjusted for age,
race, sex, BMI)
Slide 22
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)

23. Other risk factors Alcohol consumption Sedatives (benzodiazepines)
 reduce nerve output to compensatory dilator
muscles
 increase OSA severity in patients with preexisting syndrome.

24. DIAGNOSIS

25. DIAGNOSIS
Combined assessment of clinical features and objective sleep study data.
The gold standard: overnight polysomnogram
The Polysomnogram (PSG):
Provides detailed information on sleep state and
respiratory and gas exchange abnormalities.

26. PSG
Simultaneous recordings of multiple physiological signals during sleep.
Electroencephalogram (EEG)
Electrooculogram (EOG)
Electromyogram (EMG)
Electrocardiogram (ECG)
Oronasal airflow
Chest wall effort
Snore microphone
Oxyhemoglobin saturation

28. PSG Recurrent episodes of complete or partial collapse of
the upper airway are recorded as apnea or hypopnea
events.
 Apnea = complete cessation of airflow
for at least 10 seconds
 Hypopnea = 25 – 50% reduction in oronasal airflow associated with desaturation or an arousal from sleep.

29. PSG Healthy individuals May experience apneas and hypopneas at sleep
onset or during REM sleep. But these last less
than ten seconds and do not recur.

30. PSG Sleep apnea severity index: AHI = apnea-hypopnea index
= # of apneas and hypopneas / hour of sleep
Mild: 5 – 15 events/hour of sleep
Moderate: 15 – 30 event/hour of sleep
Severe: > 30 events/hour of sleep

31. Apnea Patterns Obstructive Mixed Central Airflow Respiratory effort
There are three characteristic patterns of apnea.
An obstructive apnea is defined by the absence of airflow despite persistent ventilatory efforts, demonstrated by contraction of respiratory muscles such as the diaphragm.
A central apnea, in contrast, is the absence of airflow due to the lack of ventilatory effort. Since no effort is made to breathe, no airflow occurs.
A mixed apnea includes both central and obstructive components, usually with an initial central component followed by the obstructive component.
The clinical and pathological consequences of, and treatment for, mixed and obstructive apneas and hypopneas are the same, so we will refer to them together as sleep apnea. Clinically significant central apneas are less common and will not be discussed further in this presentation.
2006 American Academy of Sleep Medicine

32. Obstructive Apnea EEG Airflow Effort Effort Effort SaO2 Slide 32
Arousal
Airflow
Effort
(Rib Cage)
Effort
(Abdomen)
This slide depicts an obstructive apnea. The top channel shows the electroencephalogram (EEG) pattern of sleep. The next channel represents airflow. The next three channels show ventilatory effort by movements of the rib cage and abdomen and changes in esophageal pressure, all of which reflect contraction of respiratory muscles. The last channel indicates oxyhemoglobin saturation.
During an apnea, the upper airway collapses resulting in cessation of airflow. Ventilatory effort continues and increases in an attempt to overcome the obstruction, shown by the increase in esophageal pressure change. Rib cage and abdominal movements are in the opposite direction as a result of the diaphragm contracting against an occluded airway, forcing the abdominal wall to distend out and the chest wall to move inward.
The increasing efforts to breathe lead to an arousal from sleep, shown on the EEG, and results in opening of the airway and a resumption of normal breathing. The lack of airflow during the apnea also causes hypoxia, shown by the drop in oxyhemoglobin saturation.
Slide 32
Level 2
Effort
(Pes)
SaO2
10 sec
2006 American Academy of Sleep Medicine

33. Central Apnea EEG Airflow Effort Effort Effort SaO2 Slide 33 Arousal
(Rib Cage)
Effort
(Abdomen)
On this slide we see a central apnea. The top channel shows the EEG pattern associated with sleep; the next channel represents airflow; the lower channels indicate breathing efforts; and the last channel shows oxyhemoglobin saturation.
With sleep onset, both ventilatory effort – shown by the lack of a change in esophageal pressure – and airflow cease. With the resumption of ventilatory effort, airflow also resumes. Note that termination of the apnea is associated with arousal from sleep.
Slide 33
Level 2
Effort
(Pes)
SaO2
10 sec
2006 American Academy of Sleep Medicine

34. Obstructive Hypopnea EEG Airflow Effort Effort Effort SaO2 Slide 34
Arousal
Airflow
Effort
(Rib Cage)
Effort
(Abdomen)
This slide shows an obstructive hypopnea. During sleep, there is a partial obstruction of the upper airway which increases airway resistance and results in a reduction in airflow. This decrease in airflow occurs despite increased ventilatory effort, shown by the change in esophageal pressure. The rib cage and abdomen are moving in opposite or paradoxical movements, reflecting increased difficulty breathing against a partially closed airway.
The hypopnea may or may not cause a decrease in oxyhemoglobin saturation depending on the length of the hypopnea, the degree of reduction in airflow, and the baseline saturation level.
The increased ventilatory effort causes an arousal from sleep, which is associated with relief of the partial upper airway obstruction and resumption of normal airflow.
Slide 34
Level 2
Effort
(Pes)
SaO2
10 sec
2006 American Academy of Sleep Medicine

35. Polysomnography in OSA
Polysomnogram
Polysomnography in OSA
Slide 35
Level 2
This figure demonstrates a page from a standard multi-channel all-night polysomnogram. Sleep stage is determined using the electroencephalogram (EEG), the electrooculogram (EOG), and the electromyogram (EMG). The lower series of channels measures respiratory parameters and are used to detect sleep apnea. They represent nasal-oral airflow, chest and abdominal wall motion, and arterial oxygen saturation. Additional parameters measured can include the electrocardiogram (EKG) and leg movement. Such a recording allows for a careful assessment of all desired variables over the course of an entire night, providing a relatively complete picture of the events occurring during sleep.
2006 American Academy of Sleep Medicine
52. American Thoracic Society. Indications and standards for cardiopulmonary sleep studies. Am Rev Respir Dis 1989;139(2):

36. PSG Duration of the diagnostic study should be at least six hours.
split-night studies
First half = diagnosis
Second half = initiation of CPAP therapy
(when obvious OSAS is present)

37. Diagnosis
Clinical Features

39. 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)

40. 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)

42. 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

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

44. 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).

45. UpToDate

46. OSA AND MEDICAL COMORBIDITY

48. CARDIOVASCULAR RISK Stressors arise from
Hypoxemia
Reoxygenation
Changes in intrathoracic pressure
CNS arousals
Stimulation of sympathetic nervous system
Acute peripheral vasoconstriction  elev BP
persist even in waking hours  elev BP

49. Mean arterial pressure during wakefulness and sleep
in subjects enrolled in Wisconsin Sleep Cohort Study.
Subjects with polysomnographically demonstrated sleep
apnea had higher blood pressures than either snorers
without apnea or non-snoring individuals. Redrawn from Hia,
KM, Young, TB, Bidwell, T, et al. Ann Intern Med 1994; 120:382.
(UpToDate)

50. Cardiovascular Risk HTN  Most studies suggest that OSA contributes
to systemic HTN
 Treatment of OSA may improve systemic HTN
(Consider this especially in the patient with risk
factors and clinical features of OSA, and the
HTN has been difficult to treat)

51. Cardiovascular Risk Cardiac arrhythmias
- bradycardia (increase vagal tone with hypoxemia)
- asystole
- atrial fibrillation
- NSVT
- ectopic ventricular beats
(bigeminy, trigeminy)

52. PULMONARY HYPERTENSION
Hypoxia results in pulmonary vasoconstriction
Autoregulatory mechanism in order to eliminate
V/Q mismatch
 in time may cause vasculature remodeling
 result in PH (PAP > 25mmg Hg)
Clinical Classification of Pulmonary Hypertension
Identifies OSA in the category of respiratory
Disorders associated with PH.

53. OSA and medical co morbidity
Conflicting data, but possible association of OSA
with:
 CVA
 Heart Failure
 DM

54. Other Comorbidities: MVA
Accident / driver / 5 yrs
Shown here is data comparing the automobile accident rate in sleep apnea patients with matched controls and with all Virginia drivers. The accident incidence was seven-fold greater in patients with sleep apnea than in matched controls without the disorder. The percentage of individuals with one or more crashes was also greater in the patients with apnea (13%) than in the controls (6%). The automobile crash rate for sleep apnea patients was 2.6 times the crash rate of all licensed drivers in Virginia.9 The risk of automobile accidents is related to severity of disease, with the highest rates seen in patients with severe apnea.12
Slide 54
Level 2
Adapted from Findley LJ et al. Am Rev Respir Dis 1988;138.
2006 American Academy of Sleep Medicine
9. Findley LJ, Unverzagt ME, Suratt PM. Automobile accidents involving patients with obstructive sleep apnea. Am Rev Respir Dis 1988;138(2):
12. Findley L, Fabrizo M, Thommi G, Suratt PM. Severity of sleep apnea and automobile crashes. N Engl J Med 1989;320(13):

55. Consequences: Excessive Daytime Sleepiness
Increased motor vehicle crashes
Increased work-related accidents
Poor job performance
Depression
Family discord
Decreased quality of life
The repetitive arousals which terminate the apneic episodes cause multiple awakenings each night. The patients are usually not aware of these events because they are brief. However, they cause disruption of the restorative effect of sleep. As a result, patients often wake up unrefreshed and sleepy. They complain of sleepiness during the day despite what should be adequate (and sometimes excessive) amounts of time in bed. This daytime sleepiness can have significant consequences.
It has been shown that patients with sleep apnea have an increased incidence of motor vehicle crashes9 and work related accidents, poor job performance, depression, family discord, and overall decreased quality of life.10,11
9. Findley LU, Unverzagt ME, Suratt PM. Automobile accidents involving patients with obstructive sleep apnea. Am Rev Respir Dis 1988;138(2):
10. Roth T, Roehrs TA, Conway WA. Behavioral morbidity of apnea. Sem Respir Med 1998;9:
11. Strohl KP, Redline S. Recognition of obstructive sleep apnea. Am J Respir Crit Care Med 1996;154(2 Pt 1):

56. TREATMENT
Objective = consequences discussed
Modality

57. 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):

58. 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.

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. MEDICAL Rx
Positive Pressure Therapy
* CPAP
* Bi-PAP
Surgical

61. Positive Airway Pressure
This slide depicts the therapeutic effect of continuous positive airway pressure (CPAP). In the panel on the left, you can see upper airway closure in an untreated sleep apnea patient. Note that the airway closure is diffuse, involving both the palate and the base of the tongue. In the second panel, CPAP is applied and the airway is splinted open by the positive pressure.
2006 American Academy of Sleep Medicine
69. Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. Lancet 1981;1(8225):

62. CPAP
This slide depicts a patient sleeping while using a positive airway pressure system. These devices are highly portable, fit on a nightstand, and can easily be transported outside of the home.
2006 American Academy of Sleep Medicine

63. CPAP Has been shown to objectively: Problems: Decrease MVA
Decrease blood pressure
Decrease day time sleepiness
Problems:
Mask discomfort
Patient acceptance
Claustrophobia
aerophagia

64. Uvulopalatopharyngoplasty (UPPP)
This slide depicts the uvulopalatopharyngoplasty (UPPP) surgical technique.
The panel on the left depicts the preoperative upper airway, demonstrating a long soft palate and the presence of palatine tonsils. The incision site is marked with the dotted line.
The panel on the right depicts the postoperative oropharynx, with amputation of the uvula, bilateral palatine tonsillectomy, and trimming and suturing together of the anterior and posterior tonsillar pillars.
2006 American Academy of Sleep Medicine
89. Fujita S, Conway W, Zorick F, Roth T. Surgical correction of anatomic abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1981;89(6):

65. SURGICAL METHODS Reconstruct upper airway Bypass upper airway
Uvulopalatopharyngoplasty (UPPP)
Laser-assisted uvulopalatopharyngoplasty (LAUP)
Radiofrequency tissue volume reduction
Genioglossal advancement
Nasal reconstruction
Tonsillectomy
Bypass upper airway
Tracheostomy
Several surgical alternatives have been developed for the treatment of sleep apnea. These treatments fall in two basic categories: upper airway reconstruction or bypassing of the upper airway. At present time tracheostomy, which bypasses the entire upper airway, is used only in life threatening situations or when all other therapies have failed.85
Treatments which involve upper airway reconstruction include:
uvulopalatopharyngoplasty (UPPP)
laser-assisted uvulopalatopharyngoplasty (LAUP)
radiofrequency tissue volume reduction (also called somnoplasty)
genioglossal advancement (GA)
maxillomandibular advancement (MMA)
nasal surgery
tonsillectomy
These are site-specific surgeries, attempts to surgically correct the site of airway collapse.86
85. Standards of Practice Committee of the American Sleep Disorders Association. Practice parameters for the treatment of obstructive sleep apnea in adults: efficacy of surgical modifications of the upper airway. SLEEP 1996;19(2):
86. Powell NB, Guilleminault C, Riley RW. Surgical therapy of obstructive sleep apnea. In: Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine, 2nd edition. Philadelphia: WB Saunders, 1994:

66. PRIMARY CARE MANAGEMENT
Recognize the prevalence
Identify affected patients based on risk factors and symptoms
Counsel on behavioral changes
Refer to specialist
Monitor symptoms and compliance during Rx

67. Sleep Apnea
2006 American Academy of Sleep Medicine

68. Otherwise snore and this will happen to you….
Or sleep alone….

69. REFERENCES 2006 American Academy of Sleep Medicine
Eckert, D, et al. “Pathophysiology of Adult Obstructive Sleep Apnea” American Thoracic Society. Vol 5. pp , 2008
Golbin, J, et al. “Obstructive Sleep Apnea, Cardiovascular Disease, and Pulmonary Hypertension.” American Thoracic Society. Vol 5. pp 20o– 206, 2008
McNicholas, W, et al. “Diagnosis of Obstructive Sleep Apnea in Adults” American Thoracic Society. Vol 5. pp , 2008
Punjabi, N. M. “The Epidemiology of Adult Obstructive Sleep Apnea” American Thoracic Society. Vol 5.pp , 2008
Schwartz, A, et al. “Obesity and Obstructive Sleep Apnea” American Thoracic Society. Vol 5. pp 185 – 192, 2008
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