..

4. Obstructive Sleep Apnea
A Serious Epidemic

11. • Obstructive sleep apnea (OSA)—also referred to as
obstructive sleep apnea-hypopnea (OSAH)—is a
sleep disorder that involves cessation or significant
decrease in airflow in the presence of breathing
effort.
• OSA is characterized by repetitive episodes of
complete (apnea) or partial (hypopnea) upper airway
obstruction during sleep.
WHAT IS OSA?

12. 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

13. • By definition , apnea is defined as a total cessation
of breathing for 10 seconds or more.
• In OSA , this can happen anywhere from a few
times every hour to over 100 times every hour.
• Hypopnea is restricted breathing with greater than
30% chest wall movement decrease and blood
oxygen drop of more than 4% for 10 seconds or
more.

14. Measures of Sleep Apnea Frequency
• Apnea Index
– # apneas per hour of sleep
• Apnea / Hypopnea Index (AHI)
– # apneas + hypopneas per hour
of sleep

15. Diagnosis
• Clinical Manifestations
• AHI (Apnea Hypopnea Index)
– Normal: 0-5 events/hr
– Mild: 6-15 events/hr***
– Moderate: 16-30 events/hr
– Severe: > 30
***Must have clinical symptoms of OSA

16. Apnea / Hypopnea Index (AHI)
The total combinations of apneas and hypopneas
for the entire night divided by the total number of
hours one sleeps gives us the apnea/hypopnea
index or the AHI.

17. OSA
• Obstructive Sleep Apnea
– Cessation of airflow for 10 seconds
– Usually associated with 4% oxygen desaturation
• Obstructive Sleep hypopnea
– Decrease of 30–50% in airflow for 10 seconds
– May be associated with 4% oxygen desaturation
OSA syndrome
AHI ≥ 5
+
Symptom

18. Suggestion of sleep apnea
Snoring
Witnessed apnea, gasping
Obesity (esp. neck circumference)
Hypertension
Excessive daytime sleepness
Family history
Previous tonsillectomy
Non-restorative sleep
AHI ≥ 5+
OSA
syndrome

19. √ If the sleep study shows apnoeas and
hypopnoeas occurring at a rate of more than
five times per hour of sleep and is
accompanied by excessive daytime
sleepiness, a clinical diagnosis of obstructive
sleep apnoea-hypopnoea syndrome (OSAHS)
can be made

20. Sleep Apnea-hypopnoea syndrome
Abnormal
Breathing
Event
Oxygen
Desaturation
Daytime
Sleepiness
Apneas +
Hypopneas (AHI) 
5 per hour
Arousal/ Sleep
Fragmentation
Vascular
Consequences

21. Clinical Consequences
Cardiovascular
Complications
Morbidity
Mortality
Sleep Fragmentation
Hypoxia/ Hypercapnia
Excessive Daytime
Sleepiness
Sleep Apnea

22. Alae nasi
Tensor palatini
Genioglossis
Geniohyoid
Thyrohyoid
Sternohyoid
Adv Physiol Educ 32: 196–202, 2008Levitsky – LSU
Normal State

23. Upper airway anatomy
Sites of obstruction during
sleep apnea
Laryngopharynx
Hard Palate
Soft Palate
Nasopharynx
Hyoid bone
Larynx
Epiglottis Oropharynx
Tongue
Tongue
Obstructive Sleep Apnea

24. Adv Physiol Educ 32: 196–202, 2008Levitsky – LSU
Sleep Apnea Event

25. Pathophysiology of Sleep Apnea
Awake: Small airway + neuromuscular compensation
Loss of neuromuscular
compensation
+
Decreased pharyngeal
muscle activity
Sleep Onset
Hyperventilate: correct
hypoxia & hypercapnia
Airway opens
Airway
collapses
Pharyngeal muscle
activity restored
Apnea Arousal from
sleep
Hypoxia &
Hypercapnia
Increased
ventilatory effort

26. • Airflow cessations or reductions produce arousals,
fragmented sleep, reductions in blood
oxyhemoglobin saturation, and fluctuations in
blood pressure and heart rate
• OSA is the most common type of sleep-disordered
breathing (SDB) and is characterized by recurrent
episodes of upper airway collapse during sleep.
These episodes are associated with recurrent
oxyhemoglobin desaturations and arousals from
sleep.

27. The primary problem in the sleep apnea patient is
the presence of an anatomically small pharyngeal
airway.
To prevent airway collapse during wakefulness, the
action of the airway dilator muscles is augmented –
a neuromuscular compensation for the small airway.
With sleep onset, there is a loss of the upper airway
reflex which drives this neuromuscular
compensation. As a result, dilator muscle
activity falls, the pharynx closes and the apnea
begins.

28. During the apnea, hypoxia and hypercapnia
develop, leading to increasing ventilatory effort.
Once this effort reaches a threshold level, the
patient arouses. Pharyngeal muscle activity is
restored, and the airway opens.
The patient then hyperventilates to correct the
blood gas derangements, returns to sleep, and the
cycle begins again.

29. http:// im.knuh.or.kr
Sequences

32. http:// im.knuh.or.kr
Cardiovascular
Complications
Neuro-cognitive
Complications
Significant Co-morbidities
HTN
CAD
Stroke
CHF

34. OSA Increases Co-Morbid Health Risks
• OSA is an independent risk factor for HTN & Type II DM
Obesity
Depression
40%
Diabetes
50%
CHF
50%
50%
Stroke
50%
Hypertension
35%
Wolk et al 2003 Javaheri et al 1999,
Somers et al 2007
Einhorn ADA 2005
Sjostrom et al 2004Sandberg et al 2008Smith et al 2002,
Schroder et al 2005
• Left undiagnosed, OSA increases risk of stroke by 2X, risk of fatal
cardiovascular events by 5X, and risk of serious vehicular accidents
%DiseaseCo-morbiditywithOSA
= With OSA
Sources: Yaggi et al, NEJM 2005; Young et al, Sleep 2008; Teran-Santos, NEJM 1999

35. American Journal of Kidney Diseases
Sleep Disturbances as Nontraditional Risk Factors for Development and
Progression of CKD
Nicolas F. Turek, BA, Ana C. Ricardo, MD, MPH, James P. Lash, MD
Nov 18, 2012 Authors & Disclosures Am J Kidney Dis. 2012;60(5):823-
833. © 2012 The National Kidney Foundation

36. Sleep Apnea is:
• Common
• Dangerous
• Easily recognized
• Treatable

38. • OSA associated with excessive daytime
sleepiness (EDS) is commonly called obstructive
sleep apnea syndrome (OSAS)—also referred to
as obstructive sleep apnea-hypopnea syndrome
(OSAHS).
• Despite being a common disease, OSAS is under
recognized by most primary care physicians in the
United States; an estimated 80% of Americans
with OSAS are not diagnosed.

39. • Although recognition of this disorder has increased
during the past few decades, data indicate that
most individuals affected remain undiagnosed.
• The gap in screening, identification, and effective
management of this disorder at the primary care
level is vast

40. • Identification of at-risk individuals for this
potentially serious condition continues to pose a
challenge.
• Underrecognition of presenting symptoms by
physcians, and by patients, may be one
contributing factor for improper identification and
management of OSA.

42. Incidence of Obstructive Sleep Apnea
• OSAHS is a common disorder occurring in 4% of
men and 2% of women.
• It is estimated that 18 million Americans suffer
from OSA
• OSA is found across all age groups, both sexes,
all socioeconomic classes and ethnic groups
• Most common in obese middle-aged men and
obese postmenopausal women

43. • Snoring is very common in the community,
occurring regularly in more than 30% of the adult
population.
• While OSA has been demonstrated in 24% of
adult males and 9% of women
• OSAHS has a prevalence of 4% in middle-aged
adult males and 2% in adult females; higher in
elderly.

44. Prevalence in Middle Aged Adults
% Men % Women
AHI ≥ 5
AHI ≥ 5 + daytime somnolence
24 9
4 2
AHI = Apnea Hypopnea Index
Symptomatic OSA (OSA with EDS)present in 4% of
middle aged men and 2% of women

46. Prevalence of Sleep Apnea
Sleep apnea is a common disorder.
0
5
10
15
20
25
AHI > 5 SAS Asthma
Male
Female
U.S. Pop
30-60 year olds
Percent of
Population
Adapted from Young T et al. N Engl J Med 1993;328.

47. OSA is a Largely Undiagnosed
Epidemic
• 18 million suffer (prevalence similar to Diabetes)
• 85% have not been diagnosed
Diabetes and OSA Prevalence is Similar
Diabetes OSA
Undiagnosed
Diagnosed
Millions of
Americans
(Adults)
10
20
Young 2002, 1997

48. Curr Opin Anaesthesiol 22:405–411
Epidemiology
• OSAHS Affects between 2 and 4% of US middle-
aged population
• 11% of shiftworkers have OSA
• Prevalence of OSA increases with age and body
weight
• An estimated 85% of people with OSA are
undiagnosed!
Chung – Toronto Western Hospital

49. Epidemiology
• Current Environment
– OSA prevalence and importance
– 4-7% adults affected
– Men:women =10:1
– 80-90% undiagnosed
– Most affected age 40-70 with an
Increase in prevalence by 7-20% ages
35-60
--Perimenopausal/menopausal women
more affected and is offset by ERT
therefore gender difference is offset
by age.
--Can affect children
33% of adults
are at risk for
OSA

50. • 1980’s = morbidity associated with OSA became
more widely appreciated
• Majority of cases still undiagnosed
 PCP = increase knowledge
= recognize risk factors
= identify affected individuals
Epidemiology

52. Biomechanics of the upper airway:
Changing concepts in the pathogenesis
of obstructive sleep apnea
S.M. Susarla, R.J. Thomas, Z.R. Abramson and L.B. Kaban
International Journal of Oral and Maxillofacial Surgery
Volume 39, Issue 12, Pages 1149-1159 (December 2010)

53. Fig. 2
Source: International Journal of Oral and Maxillofacial Surgery 2010; 39:1149-1159 (DOI:10.1016/j.ijom.2010.09.007 )

54. 28/05/2015

55. Structures of the upper airway

56. Anatomy of the Upper Airway

57. Pathophysiology of SDB
A continuum in the collapse of the airway
•Anatomic (secondary cause)
Fatty deposition in the airway
Retrognathia
Soft tissue excess
Upper airway blockage
•Neuromuscular (primary cause)
Autorotation of the mandible (functional
retrognathia)
Tongue
Pharyngeal dilator muscles

58. Most of apneic episodes occur within the pharynx, due to
the deformation of soft tissue (tongue, soft-palate).

59. Upper Airways

60. Most of apneic episodes occur within the pharynx, due to
the deformation of soft tissue (tongue, soft-palate).

61. Anatomical representation of the upper airway and the important muscles controlling airway
patency.
Fogel R B et al. Thorax 2004;59:159-163
Copyright © BMJ Publishing Group Ltd & British Thoracic Society. All rights reserved.

62. • Obstructive sleep apnea is a common disorder
characterized by repetitive episodes of pharyngeal
(upper) airway collapse or narrowing during sleep
• In people with OSA, pharyngeal muscles relax
during sleep and gradually allow the pharynx to
collapse.
• The level of pharyngeal collapse varies between
patients, but most often occurs at the
velopharyngeal level and/or retroglossal level.

63. Basic Concepts of OSA

64. Why does OSA occur?
• Upper airway tone is decreased during sleep,
especially in REM
• Collapse/obstruction of the upper airway during
sleep causes obstruction & apnea
-
-
-
-
-
Nares /hard palate
Pharynx
Larynx / trachea

65. Pathogenesis of OSA
White; AJRCCM 2005

66. During wakefulness, airway patency is protected
by pharyngeal muscle tone. With sleep there is a
loss of muscle tone predisposing to partial or
complete upper airway obstruction, particularly in
those with already narrow, compliant upper
airways.
In sleep, the changes are particularly evident in
rapid eye movement (REM) sleep, when the loss
of muscle tone can be profound.

67. Where partial or complete obstruction occurs, the
event is terminated by arousal, which is usually
brief (<15 s), as a result of the accompanying
return of muscle tone.
Once patency is restored, sleep resumes, and
along with it the tendency to obstruct again.
These cyclical obstructions terminated by arousals
provide the pathophysiological basis of OSA .

68. Pharyngeal airway
• Patency depends on balance of forces that tend to
collapse(negative intraluminal pressure and
extraluminal pressure) and the contraction of
dilator muscles
• Transmural press(Ptm)=Plumen –Ptissue
• Closing pressure is Ptm at which the pharynx
collapses
• Pcritical – at which airflow ceases completely
• Normal: –8 cm H2O OSA: > 0 cm H2O

70. Different models can be used to explain behavior of
the upper airway, including
1. The "balance of forces" Inspiratory negative
pressure and extraluminal positive pressure tend
to promote pharyngeal collapse.
Upper airway dilator muscles and increased lung
volume , airway suction pressure during
inspiration tend to maintain pharyngeal patency.
2. The Starling resistor mechanical model.

71. Factors influencing pharyngeal collapsibility.
Source: International Journal of Oral and Maxillofacial Surgery 2010; 39:1149-1159 (DOI:10.1016/j.ijom.2010.09.007 )
Copyright © 2010 International Association of Oral and Maxillofacial Surgeons Terms and Conditions

72. Factors influencing pharyngeal collapsibility
• Airway patency is promoted by pharyngeal dilator
activity and, to a lesser extent, caudal traction on
the airway due to lung expansion.
• Airway collapse is due to negative intra-luminal
pressure during inspiration and inward pressure
from extra-luminal factors, such as adipose tissue
within the pharyngeal walls.
• If collapsing pressures exceed dilating pressures,
the airway collapses and obstruction ensues

73. Fig. 4
International Journal of Oral and Maxillofacial Surgery
2010)
Starling resistor model of the pharyngeal airway. The pressure required to keep
the airway patent (Pcrit) is a function of the pressure upstream to the collapsing
segment (PUS).

74. • The morphologic structure of the upper airway is
important in the maintenance of the patent airway
during sleep and wakefulness.
• The nasal passage has a bony architecture with
the cartilaginous larynx and extra thoracic trachea,
which helps produce a conduit for inspiration and
expiration of air during sleep and wakeful state.

75. • The pharynx lacks a strong structural support, and
thus potentially collapsible, remains a potential
zone for the interruption of airflow.
• The three anatomic segments of the pharynx
(nasopharynx, oropharynx, hypopharynx), are
liable to collapse resulting in obstruction to airflow
during sleep (obstructive sleep apnea).

76. • The Starling resistor model of upper airway. The
airway is represented by a tube with a collapsible
segment (pharynx) between two rigid segments
with fixed diameters, resistances and pressures
(nasal and trachel segments).
• The airway collapses when the pressure
surrounding the airway becomes greater than the
pressure within the airway (Pcrit).

77. Starling resistor model of the upper airway with a collapsible (pharyngeal) segment between two rigid
tubes (nasal and tracheal).
Hillman D R et al. Br. J. Anaesth. 2003;91:31-39
©2003 by Oxford University Press

79. We can distinguish the following situations:
1. “Rigid”tube and free flow:
When the pressure inside the tube is much higher, than
the outside pressure and the pressure upstream is
greater, than the critical pressure.
2. Partially collapsible tube and vibration:
When the pressure inside the tube is close to outside
pressure and upstream pressure is greater than the
critical pressure.
3. Very collapsible tube and choked flow:
When the pressure inside the tube is much lower than
outside pressure and upstream pressure is less than the
critical pressure.

81. The pathophysiology of OSA
is complex.
• The main factors are interact to produce the
clinical state, OSA :
1. Abnormal anatomy, structural abnormalities
2. Increased collapsibility of the upper airway,
3. Defective airway reflexes.
• All the factors may not be present in one particular
patient. Furthermore, the predominant factor is likely
to vary from patient to patient

82. OSA Pathophysiology
•UAW obstruction at level of tongue/palate
Size of UAW lumen is a balance
between
- Tendency of pharynx to collapse
during inspiration
- Dilating forces (pharyngeal muscles)

83. What else contributes?
• Muscle collapse or weakness
–Alcohol
–Sleeping pills
–Sedatives or muscle relaxants
–Weight gain
–Deeper sleep, with more relaxed muscles

84. • The primary problem in the sleep apnea patient is
the presence of an anatomically small pharyngeal
airway.
• Structural compromise may be due to anatomic
disturbances such as tonsillar hypertrophy,
retrognathia and macroglossia.
• In the majority there is only reduction in airway
size which can be described as “crowding”
Structural abnormalities

87. Structural abnormalities
• Oropharyngeal airway may predispose to closure (
short neck)
• Obesity may contribute to reduction in upper
airway size by  fat deposition in the soft tissues
of the pharynx or by compressing the pharynx by
superficial fat masses in the neck.
• The airway may also have high compliance –
“floppy” and be prone to collapse.

88. • In general, people with OSA have an anatomically
narrow upper airway (e.g., due to obesity or
anatomical variation), and a narrow airway is more
prone to collapse.
• During wakefulness, people with OSA reflexively
compensate for their more collapsible airway with
increased airway dilator muscle activity.
• During sleep, however, their airway dilator muscle
activity is decreased and airway collapse can
result from negative airway pressure at the
beginning of inspiration and/or the absence of
substantial positive airway pressure at the end of
expiration.

89. Pathogenesis
• Occlusion of the oropharyngeal airway results in
progressive asphyxia until there is a brief arousal
from sleep, whereupon airway patency is restored
and airflow resumes.
• The patient then returns to sleep and the process
is repeated, up to 300-400 x per night – sleep
becomes fragmented.

90. Collapse of the pharyngeal airway can block
airflow or significantly restrict airflow (hypopnea),
both of which can cause oxyhemoglobin
desaturation.
• An episode of apnea or hypopnea is terminated by
a brief arousal or a lighter stage of sleep,
accompanied by activation of the upper airway
dilator muscles and restoration of airway patency.
• This cycle occurs repeatedly throughout the night,
commonly resulting in daytime hypersomnolence,

91. • The largest upper airway dilator muscle is the
genioglossus muscle, which is one of several
different muscles in the tongue that facilitate
multiple purposes including speech, swallowing
and breathing.
• The genioglossus muscle causes tongue
protrusion and stiffening of the anterior pharyngeal
wall.
• In people with OSA, the neuromuscular activity of
the genioglossus muscle falls markedly at sleep

92. DILATOR MUS

93. • The genioglossus, tensor palatini and the hyoid
muscles play major roles in maintaining a patent
airway.
• The genioglossus pulls the tongue forward and
opposes pharyngeal collapse due to the
inspiratory negative airway pressure.

94. • in the awake subject, there is a phasic inspiratory
activation of upper airway muscles slightly before
diaphragmatic contraction, splinting upper airway
sufficiently to prevent its collapse.
• There is no single muscle implicated in the
maintenance of the pharyngeal apperture.

95. • The onset of sleep disturbs the functions of these
muscles. Upper airway resistance has been
repetitively shown to increase during sleep in
normal subjects which may be twice as in
wakefulness.
• Also during sleep, there is a reduction in the cross-
sectional area of the pharynx.
• A fall in the activity of the dilator muscles of the
pharynx has been proposed as the most likely
mechanism for the sleep induced decrease in
pharyngeal patency.

96. • The impaired activities of the dilator muscles result
in ineffective splinting of the upper airway, thus
increasing the transmission of the subatmospheric
intrathoracic pressure into the upper airway.
• The interplay of the impaired upper airway muscle
activity, the unopposed subatmospheric inspiratory
pressure due to the elevated upper airway
resistance provide a favourable ground for airway
collapse during sleep.

98. Sites of Airway Narrowing
Adapted from Morrison DL et al. Am Rev Respir Dis 1993;148.
Collapse at soft
palate only
Multiple sites of
collapse
18%
82%

99. •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.
• 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.

100. Pathophysiology of OSA

101. • The primary defect in OSAHS is an anatomically
small or collapsible pharyngeal airway.
• During wakefulness, neuromuscular compensatory
systems function to increase the activity of the
pharyngeal dilator muscles, thus preserving airway
patency.
• This reflex driven augmented muscle activity is
lost at sleep onset, and collapse of the pharyngeal
airway occurs.

102. • Closing of the upper airways can be caused by
various abnormalities, mainly mechanical,
anatomical and functional abnormalities.
• Sleep onset is marked by a decrease in muscle
tone, a physiologic reduction of muscle activity
also extended to the muscles of the pharynx.
• In stages III and IV NREM sleep and REM sleep,
muscles are more relaxed and muscle weakness
also affects the upper airway.

103. • In OSA Obstruction or collapse can occur at any
point of the pharynx. This process is more
pronounced during REM phase characterized by
an absolute relaxation of muscle tone.
• This decrease in muscle tone does not affect
equally all the involved muscles with respiratory
function.

104. • In NREM sleep stages the activity of the
intercostal muscles causes 60% of tidal volume.
• In REM, the responsible muscle for keeping the
tidal volume is the diaphragm exempt of the
muscular generalized atony.

105. • REM sleep is a very active sleep stage for our
brains – sometimes more active than Wake!
• REM, like other stages of sleep, is a biological
necessity. When we don’t get enough REM, our
brain will compensate by promoting REM
whenever possible. This is called REM Rebound
• REM rebound is the lengthening and increasing
frequency and depth of REM sleep which occurs
after periods of sleep deprivation. When people
have been prevented from experiencing REM,
they take less time than usual to attain the REM
state

106. • When a person has been deprived of REM sleep
for long enough they will not cycle through sleep
patterns as a well rested person would.
• These REM deprived patients will enter REM
sleep much more rapidly and will spend more time
in REM sleep over the course of the night as their
body attempts to "catch up" for the lost REM. This
expedited process of entering REM is called REM
rebound

107. • Collapse of the airway produces arousal which
restores the patency of the airway. However,
frequent arousals interrupt sleep and block REM
sleep.
• A progressive REM sleep debt results which
causes more frequent REM sleep onsets and
more frequent airway collapse. The clycle can be
broken by inflating the airway with CPAP
continuous Positive Airway Pressure.

108. The sleep apnea cycle:
Apnea
Pharyngeal
collapse
CO2 & O2  Arousal
REM deprivation by arousal
REM sleep debt
REM rebound
Reduced airway tone
at REM onset
Airway
restored

109. CONTINUOUS POSITIVE AIRWAY
PRESSURE (CPAP)
• Least invasive AND
most successful
treatment modality
for OSA
– Delivery of low levels
of continuous
pressure via a nasal
or oronasal interface
to “splint” open the
airway during sleep