Measure neck circumference  Mallampati score

5. 5

6. 6

7.  When abnormal breathing patterns disrupt
sleep, this is called sleep-disordered
breathing (SDB).
 There are different types which can occur in
one of several patterns.
7

8.  Also known as Sleep related breathing disorder ,
is a group of disorders characterized by
breathing difficulties while sleeping .
 Obstructive sleep apnea (OSA) is the most
common respiratory disorder of sleep .
 It is estimated that more than 18 million American
adults have obstructive sleep apnea .

9. Classification of SDB
 Chronic or habitual Snoring
 UARS-upper airway resistance Syndrome
 SDB characterized by Obstructive hypopneas
 OSAS- obstructive sleep apnea Syndrome
 CSA-central sleep apnea
 OHS-obesity Hypoventilation Syndrome

10.  Sleep disordered breathing (SDB) describes
a group of disorders characterized by:
Abnormal respiratory patterns (e.g. the
presence of apneas or hypopneas) or
Insufficient ventilation during sleep .
10

11.  An apnea is when a patient stops breathing
for 10 seconds or more, and wakes up just
enough to take a breath.
 In the 2007 AASM manual, apnea is defined
as the cessation of airflow in both the nasal
pressure transducer and oral thermistor for
10 or more seconds
11

12.  A hypopnea is when a patient doesn’t stop
breathing, but the patient’s breathing becomes
shallow (i.e., at least a 30% decrease in airflow)
for 10 seconds or more, with an associated with
at least a 4% oxygen desaturation or arousal.
12

14. Types of Sleep Disordered Breathing
 Apnea
– Cessation of airflow > 10 seconds
 Hypopnea
– Decreased airflow 30% from baseline
lasting > 10 seconds associated with > 4%
oxyhemoglobin desaturation

15.  Either way, sleep disordered breathing disrupts
the patient’s sleep pattern, night after night,
which not only makes the patient tired and
exhausted the next day, but may also put
excessive strain on the patient’s nervous
system and major organs .
15

16.  Sleep-disordered breathing is an umbrella
term for several chronic conditions in which
partial or complete cessation of breathing
occurs many times throughout the night,
resulting in daytime sleepiness or fatigue
that interferes with a person’s ability to
function and reduces quality of life.
16

17. Sleep Apnea is:
 Common
 Dangerous
 Easily recognized
 Treatable

18. Apnea Patterns
Obstructive Mixed Central
Airflow
Respiratory
effort

24.  An obstructive apnea is defined by the
absence of airflow despite persistent
ventilatory effort.
 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.
24

25.  A mixed apnea includes both central and
obstructive components, usually with an
initial central component followed by the
obstructive component.
25

26. 26

27.  OSA is the most common type of sleep-
disordered breathing (SDB)
 Obstructive Sleep Apnea (OSA) is the leading
cause of referral to sleep laboratories
worldwide, accounting for at least
75–80% of diagnoses .
27

28. 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

29. 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.

30. 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

31.  Despite being a common disease, OSAS is
underrecognized by most primary care
physicians in the United States
 An estimated 80% of Americans with OSAS
are not diagnosed
31

32.  OSA is a very important diagnosis for
physicians to consider because of its strong
association with and potential cause of the
most debilitating medical conditions.
32

33. 33

34.  What is sleep apnea
 The physiological consequences of the disorder
and how these lead to the presenting features.
 The clinical features and risk factors suggestive
of the presence of sleep apnea and
 Methods for making the diagnosis.
 Finally, we will discuss the treatment options
available for patients with sleep apnea.
34

35.  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.
WHAT IS OSA?

36.  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.

37. Alae nasi
Tensor palatini
Genioglossis
Geniohyoid
Thyrohyoid
Sternohyoid
Normal State

38. Sleep Apnea Event

39. Sleep Apnea Cycle
Ventilation
Apnea
Arousal
Sleep
Hypoxia
Sympathetic
activation
Reoxygenation

42. 42
Mechanism
 Sleep…
  Upper airway tone...
 Obstruction...
 Apnea…
  pO2, pCO2…

43. 43
Mechanism (cont.)
 …Arousal…
  Upper airway tone…
 Resumption of breathing…
 Hyperventilation…
 Return to sleep…
  Upper airway tone…
 This occurs HUNDREDS of times each night

44. 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

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

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

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

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

51. Consequences:
Excessive Daytime Sleepiness
 Increased motor vehicle crashes
 Increased work-related accidents
 Poor job performance
 Depression
 Family discord
 Decreased quality of life

52. Consequences: Cardiovascular
 Systemic hypertension
 Cardiac arrhythmias
 Cardiovascular disease
– Myocardial ischemia
– Congestive heart failure
 Cerebrovascular disease

53. 53

54. 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

55.  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).

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

57. Obstructive sleep apnea
(OSA)
 The primary causes of upper airway
obstruction are:
1. Lack of muscle tone during sleep
2. Excess tissue in the upper airway
3. The structure of the upper airway and jaw
57

58. Structures of the upper airway

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

61. Basic Concepts of OSA

62. 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

63. Fig. 4

64. 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%

65. • 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.

66. Sleep Apnea Risk Factors
 Obesity
 Increasing age
 Male gender
 Post-menopausal state
 Craniofacial/Upper Airway Soft Tissue
Anatomic Abnormalities
 Family history
 Alcohol or sedative use / sleeping pills
 Smoking
 Associated conditions e.g. Endocrinal
abnormalities

67. Risk Factors for OSA
 Obesity
 Obesity
 Obesity

68. BMI = W(kg)/H (m²)

71. Obesity
• Alters upper airway mechanics during sleep
1. Increased parapharyngeal fat deposition:
neck circumference: > 17” males
> 16” females
With subsequent:
Excessive fat deposition in the neck would
tend to narrow the pharyngeal cross-sectional
area smaller upper airway
 increase the collapsibility of the pharyngeal
airway

73.  The cardinal symptoms of sleep apnea
include the "3 S ’s":
1) Snoring when asleep
2) Sleepiness (excessive) when awake
3) Stopping breathing or struggling to
breathe when asleep ( S ignificant-other
report of sleep apnea episodes. )
73

74. 74

75. Clinical Manifestations
 Snoring**
 Witnessed Apneas by Bed
Partner
 Non-restorative Sleep**
 Restless Sleep
 Daytime Sleepiness**
 Waking up SOB/ Gasping
for Air
 Mood Changes
 Morning Headaches
 Vivid/Strange Dreams
 GERD
 Obesity
 Narrow/”Crowded”
Airway
 Large Neck
Circumference
 Cardiovascular Disease
 Cerebrovascular
Disease
 Cardiac Dysrhythmias

76. Not everyone who snores has sleep
apnea, but everyone with sleep apnea
snores.

77. 77

78. Is it just snoring or is it sleep
apnea?
 Not everyone who snores has sleep apnea,
and not everyone who has sleep apnea
snores. So how do you tell the difference
between normal snoring and a more serious
case of sleep apnea?
78

79.  The biggest telltale sign is how you feel
during the day.
 Normal snoring doesn’t interfere with the
quality of your sleep as much as sleep
apnea does, so you’re less likely to suffer
from extreme fatigue and sleepiness during
the day.
79

80.  It is very important that an attempt be made to
elicit information from the patient’s bed partner.
 The patient is often unaware of what occurs
during sleep and may not be aware of
symptoms such as snoring.
 A bed partner’s description of witnessed
apneas is highly suggestive of the presence of
sleep apnea.
80

81. Patients typically complain of daytime somnolence
with drowsiness, particularly during “passive
situations” such as after meals, while watching
television, or attending a lecture.
The hallmark daytime symptom of OSA is excessive
daytime sleepiness (EDS). EDS is thought to be
related to the fragmented and nonrestorative
sleep.
81

82. Assessing Daytime Sleepiness
 Often unrecognized by patient
– Ask family members
 Must ask specific questions
– Fatigue vs. sleepiness
– Auto crashes or near misses
– Sleep in inappropriate settings
 Work
 Social situations

84. 84

85. Epworth Sleepiness Scale:
Measures average sleep propensity (chance of dozing) over 8 common situations that almost
everyone encounters.
Situation Chance of Dozing
•Sitting and reading
•Watching T.V.
•Sitting inactive in a public place (i.e., theater, meeting)
•As a passenger in a car for 1 hour without a break
•Lying down to rest in the afternoon when circumstances
permit
•Sitting talking to someone
•Sitting quietly after lunch without alcohol
•In a car while stopped for a few minutes in traffic
Total
0-3
0-3
0-3
0-3
0-3
0-3
0-3
0-3
0-24 (0-10 normal)
3= High chance of dozing; 2=moderate; 1=slight; 0=never

86. Daytime Sleepiness

87. This is a self-administered scale in which the
patient rates his/her probability of doze off (0–3)
in eight different situations typical of daily life
The scale therefore may vary from 0 to 24 and
scores > 10 are compatible with EDS- reflect
an abnormally high level of sleepiness
 A patient with a score exceeding 18 should
probably be directed to a sleep specialist.
87

88.  Patients need to be specifically asked
about the presence of daytime sleepiness.
 They often don’t recognize they are sleepy
since the problem has been present for a
prolonged period of time and they have
changed their lifestyles gradually to
compensate for it.
88

89. Physical Examination
 The general physical examination is frequently
normal in patients with OSA, other than the
presence of obesity, an enlarged neck
circumference, and hypertension
 Perform an evaluation of the upper airway in
all patients, but particularly in nonobese adults
with symptoms consistent with OSA.
89

90. Diagnosis: Physical Examination
 Upper body obesity / thick neck
> 17” males
> 16” females
 Hypertension
 Obvious upper airway abnormality

91. Exam: Tonsillar Hypertrophy
Shepard JW Jr et al. Mayo Clin Proc 1990;65.
Oropharynx With Tonsillar
Hypertrophy
Normal Oropharynx

92. Exam: Oropharynx
Patient With the Crowded Oropharynx

93. Exam: Oropharynx
Class I
Class III
Class II
Class IV

96.  On average, the risk of OSA increases more
than two-fold for every 1-point increase in the
Mallampati Scale: a Mallampati IV patient has
an eight-fold risk of OSA.
 Such a strong association suggests that if a high
Mallampati score is noted during a routine
examination, inquiring further about snoring
and ES symptoms may be warranted
96

97. Physical Examination
Guilleminault C et al. Sleep Apnea Syndromes. New York: Alan R. Liss, 1978.
Structural Abnormalities

99. Chung – Toronto Western Hospital Curr Opin Anaesthesiol 22:405–411
Identification of Patients with OSA

100. Diagnosis
 The diagnostic process is guided by
understanding who to screen or refer for
polysomnography (PSG).
 The STOP-BANG inventory is a simple, office-
based screening tool that combines symptoms,
historical information, and physical examination
results to recognize individuals at high risk of
OSA.
10
0

101. Chung – University of Toronto Anesthesiology 2008; 108:812–21

102. STOP BANG
S – Snoring, loudly, heard through a closed door
T – Tiredness, during daytime
O – Observed, witnessed apneic episodes
P – Pressure, hypertension
B – BMI, > 35
A – Age, > 50 yr
N – Neck Circumference, > 40 cm
G – Gender, Male
Chung – University of Toronto Anesthesiology 2008; 108:812–21

103. 10
3

106. OSAHS: diagnostic criteria
(1. or 2.) and 3.
AASM, Sleep, 1999:22:667-89.

107. A. At least one of the following applies:
1. The patient complains of unintentional sleep episodes during wakefulness,
daytime sleepiness, unrefreshing sleep, fatigue, or insomnia.
2. The patient wakes holding his/her breath, gasping, or choking.
3. The bed partner reports loud snoring or breathing interruptions during the
patient's sleep.
B. Polysomnographic recording shows the following:
1. Five or more scoreable respiratory events occur per hour. These events
can include any combination of obstructive apneas, hypopneas, or
respiratory-associated arousals.
2. There is evidence of respiratory effort during all or a portion of each
respiratory event.
C. This disorder is not better explained by another sleep, medical, or psychiatric
disorder, substance abuse, or medication.
D. Associated features: snoring, obesity, systemic hypertension, pulmonary
hypertension, congestive heart failure, sleep fragmentation, recurrent
awakening from sleep, sleep-related cardiac dysrhythmias, nocturnal anginaM
gastroesophageal reflux, impaired quality of life, impaired concentration,
diabetes, metabolic syndrome
The individual must fulfill A, B, and C AASM International Classification, 2005
Diagnostic Criteria for OSAHS

108. Diagnosis
 Polysomnography (PSG) is considered the
gold standard diagnostic test for obstructive
sleep apnea (OSA)
 During Polysomnography (PSG) , the patient
sleeps while connected to a variety of
monitoring devices that record physiologic
variables
10
8

109. Polysomnography

110.  Overnight full polysomnography (PSG) is
considered the gold standard method for
diagnosis and classification of OSA severity.
 PSG involves the measurement of multiple
physiological parameters while the patient
sleeps in the sleep laboratory .
11
0

111.  Routine laboratory tests, are usually not
helpful in OSA unless a specific indication is
present.
 Pulmonary function tests are not indicated
to make a diagnosis of, or treatment plan
for, OSA alone..
11
1

112. Polysomnography
 EOG - Electrooculogram
 EEG - Electroencephalogram
 EMG - Electromyogram
 ECG - Electrocardiogram
 Tracheal noise
 Nasal and oral airflow
 Thoracic and abdominal respiratory effort
 Pulse oximetry

113. AASM standards and guidelines for
diagnostic polysomnography
 Sleep stages are recorded via an
electroencephalogram, electro-oculogram, and
chin electromyogram
 Heart rhythm is monitored with a single-lead
electrocardiogram
 Leg movements are recorded via an anterior
tibialis electromyogram
11
3

114.  Breathing is monitored, including airflow at the
nose and mouth (using both a thermal sensor
and a nasal pressure transducer), effort (using
inductance plethysmography), and oxygen
saturation
 The breathing pattern is analyzed for the
presence of apneas and hypopneas
11
4
AASM standards and guidelines for
diagnostic polysomnography

115. Standard Polysomnography
 EEG, EOG, EMG
 ECG
 Airflow
 Chest/abd, bands
 Pulse oximetry
 Left/right leg EMG
Presence/stage of sleep
Cardiac rate/rhythm
Apnea/hypopnea
Respiratory effort
Arterial oxygen sat
Leg movements (PLMs)

116. 11
6
Diagnosis-definitive
 Nocturnal Polysomnograph
– EEG
– Electromyelograph
 Chin
–  activity during REM
 Limbs
– checks non-respiratory causes of arousal
– Electro-oculogram
 Detects REM

117. Hank Morgan/ Rainbow

118. 11
8
DDx (cont.)
– Nasal/oral airflow
– Thoracic/abdominal movement
– Oxygen saturation
– Cardiac rate & rhythm
– Body position

119. Overnight PSG

120. Diagnosis of OSA
There are currently two major methods to
diagnose OSA:
 Overnight full polysomnography or Full in-lab
PSG
 Portable monitoring (PM) or Limited-Channel
Testing (LCT) device.
12
0

121. What Test Should be Used?
 In-laboratory full night polysomnography
– Split night studies
 Home diagnostic systems
– Oximetry to full polysomnography

122. 12
2
Split studies
 Part 1 – Definitive diagnosis
 Part 2 – Optimal CPAP level

123. Polysomnography (PSG)
Neurological
 EEG
 EOG
 EMG
Cardio-Respiratory
 Snoring
 Thoraco-
abdominal
movements
 Airflow
 Oximetry
Type 3
Type 4
Ref: Clinical guidelines for unattended PM in the diagnosis of OSA in adult
patients. J Clin Sleep Med 2007; 3:737–747
Type 1,2

124. 12
4

125. Portable monitoring (PM) or Limited-
Channel Testing (LCT) device.
= Home sleep testing (HST)
12
5

126. PSG vs. HST
The home sleep test measures the same 5 essential
channels for diagnosing OSA as the lab PSG. Other PSG
measurements apply to non-OSA clinical evaluations.
STANDARD IN LAB SLEEP STUDY
Airflow
Breathing Efforts
Blood Oxygen
Heart Activity
Snoring
Brain Waves
Eye Movements
Chin Movements
Leg Movements
Unusual Behavior
Body Position
Sleep Architecture
IN LAB SLEEP STUDY
Must record at least
12 channels of
information if a
AASM-accredited
center
IN HOME OSA
STUDY
HST captures only
what is necessary
for OSA diagnosis
Airflow
Breathing Efforts
Blood Oxygen
Heart Activity
Snoring
$$$ $
OSAOtherMetrics
> 90% of All Sleep Disorders Diagnosed Are OSA

127.  Due to financial considerations, PM is
becoming increasingly common in the USA
and has been used with reasonable
success worldwide.
 There are three types of PMs Type II–IV, in
the order of decreasing measurements of
sleep and respiratory variables
12
7

128.  level 3 portable monitors have the largest
body of supportive evidence for use in
diagnosing OSA.
 In general, level 3 monitors are best used to
confirm the diagnosis of OSA rather than to
rule it out.
12
8

129.  In carefully selected patients (generally
those with a high pretest probability of
disease and without comorbidities), patients
with a home-based approach had similar
clinical outcomes to those patients studied
in the laboratory (PSG).
12
9

130. Clinical Probability of OSAS
 Ambulatory diagnostic-therapeutic approach
requires accurate identification of probable
cases of OSAS
1) Sleepy snorer by Epworth Sleepiness Score
2) Sleep Apnea Clinical Score (SACS) based on
snoring, witnessed episodes of apnea, neck
circumference, and systemic hypertension

131. Clinical Probability of OSAS
1. “Sleepy Snorer” by Epworth Sleepiness Score
2. Sleep Apnea Clinical Score (SACS)
Ref: Likelihood ratios for a sleep apnea clinical
prediction rule. AJRCCM 1994;150:1279-85.

132. Outcomes of Home-Based Diagnosis
and Treatment of Obstructive Sleep
Apnea
Chest 2010; 138: 257-263
 Home testing and autoCPAP resulted in the
same results in sleepiness, adherence, blood
pressure and QoL as in-lab testing.
 “It is really not about the technology; it is
about the initial and then chronic care of the
patient….” (Dr N Collop, editorial)

133.  Apnoea-hypopnoea index (AHI)= number
of apnea/hypopnea per hour of sleep
 AHI<5 Normal
 AHI 5-15 Mild OSA
 AHI 15-30 Moderate OSA
 AHI >30 Severe OSA
Severity Grading of OSAS

134. Setting Up CPAP
 When initiating CPAP, there are numerous
options available.
 The current standard is to perform a single
overnight polysomnogram while the patient
is monitored so the attendant can increase
CPAP levels to progressively eliminate
disordered breathing events.
13
4

135. Titration
 The appropriate pressure that can resolve the
upper airway obstruction is classically derived
by a CPAP titration polysomnogram
 The current gold standard is a full-night-
monitored CPAP titration in a sleep laboratory.
 However, split night studies, autotitrating PAP
devices, and other empiric methods of initiating
CPAP are also available.
13
5

136.  Some studies are “split,” i.e., in a patient
with severe OSA that meets the preset
criteria for severity, the CPAP titration is
initiated after at least 2 h of a diagnostic
study.
13
6

137.  The CPAP is generally initiated at a setting of
5 cm of water after appropriate
measurement of the facial area and mask
fit.
 The CPAP setting is gradually titrated in
increments of 1–2 cm of water at a time.
13
7

138.  The titration is guided by resolution of snoring,
resolution or substantial improvement in airflow
pattern and apneas and hyponeas as well as
tolerance by the patient.
 Central apneas are sometimes seen with CPAP
titration. These are usually self-limited.
13
8

139. Auto Titration
 With increasing demand for services and
difficulties associated with access to sleep
laboratories and costs, there has been
interest in performing out of sleep center
titrations utilizing autotitrating PAP
machines.
13
9

140.  In selected patient groups without serious
comorbidities, these devices may be
adequate.
 Autotitrating PAP (APAP) has been
advocated as an alternative to traditional
CPAP titration.
14
0

141.  Two groups of patients in whom autotitrating
PAP may not be appropriate include
1. Patients with serious cardiopulmonary
illness
2. Patients with obesity hypoventilation
syndrome.
14
1

142. AASM recommendations for
APAP use
 APAP devices are not recommended to
diagnose OSA
 APAP devices are not currently
recommended for split-night titration
14
2

143.  At this time, APAP cannot be recommended
as first-line therapy in all patients with OSA
14
3

144. Summary
 Magnitude of OSA and paucity of sleep labs needs
simplified approaches for physicians
 Enough evidence now exists that simple ambulatory
diagnostic–therapeutic strategies have equivalent
clinical outcome in cases with high pretest probability
 Patients who have a low probability, have co-morbidities
or have difficulties during ambulatory management
should be referred to a sleep centre for detailed
evaluation/in-laboratory attended full PSG and further
management

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