The document provides an extensive overview of sleep, detailing its stages, biological rhythms, and the importance of sleep for health. It discusses sleep disorders, particularly obstructive sleep apnea (OSA), its prevalence, risk factors, symptoms, and diagnosis methods, as well as available treatments including behavioral changes, medical therapies, and surgical options. Additionally, it highlights the cardiovascular risks associated with OSA and the impact of sleep disorders on overall well-being.

1. Dr Debashees nanda
M.S (E.N.T)
M.K.C.G Medical college
Berhampur

2. What is sleep?
A state of (1) sustained immobility in a (2)
characteristic posture accompanied by (3) reduced
responsivity to external stimuli;

3. The Biological Rhythms of Sleep
About every 90 or 100 minutes we
pass through 5 stages of sleep.
Throughout the five stages, our brain
waves continually fluctuate, thus
defining each distinctive stage.

4. The Circadian Rhythm
Our biological clock that is genetically
programmed to regulate physiological responses
within a 24 – 25 hour period.
Refers to circa=approximately and
dias=day.

5. Please don’t fall asleep
during the power point!!

6. Light Sleep -Stage 1
Body movement decreases
Spontaneous Waking may occur (when you feel like
you are falling out of bed)

7. Intermediate Sleep - Stage 2
Officially asleep
Your brain waves slow down with some bursts of
brain activity called ‘Sleep Spindles’
half of your sleep in this stage.
Helps refresh body
Sleep Talking can occur during this and all future sleep stages.Sleep Talking can occur during this and all future sleep stages.

8. Deep Sleep – Stage 3 -4
Deep sleep sets in – hard to wake up
brain waves become large and slow
Your breathing becomes rhythmic, and your muscles
remain relaxed.
Most Restorative stage (reparative hormones
released)
30-40 min first and shorter later

9. Deep Sleep – Stage 3 -4
Towards the end of stage 4, children may wet beds,
adults may sleep walk, etc…
Interestingly, even though you are in deep
sleep, your brain will still process the
meaning of certain stimuli!!

10. REM Sleep - Rapid Eye Movement
Nearly an hour after you fall asleep, you begin to
descend back through the stages of sleep.
During sleep you go stages 1,2,3,4,3,2 then…
You then enter what is known as REM Sleep!
REM –This stage only lasts about 10 minutes. (20 – 30
minutes later in night)

11. REM Sleep - Rapid Eye Movement
heart rate rises
breathing becomes rapid
every 30 seconds or so, your eyes rapidly move
around.
motor cortex is still active, but your brainstem blocks any
messages.
This leaves your muscles so relaxed that you are
essentially paralyzed.
Thus, you are not easily awakened.

13. How Much Sleep Do I Need?
Infants
20 hours
 50% REM
Children/Adolescents
10 hours
 25-30% REM
Bed Later, Up Later
Adults
8 hours
 20% or less REM
Elderly
6 hours
Bed Later, Up Earlier

14. (3) Areas of the brain involved in sleep
i) Hypothalamus
Studied the
brains of those
who had died
from the virus
encephalitis
lethargica
- Victims who had difficulty sleeping:
Damage to anterior region
- Victims who had difficulty staying awake
Damage to posterior region
Constantin von Economo
Confirmed in lesion
studies with animals
(Saper et al., 2001)

15. ii) Reticular System
(3) Areas of the brain involved in sleep
- Bremer (1936)
Cerveau isole transection = slow-wave
sleep pattern
Encephale isole transection = Normal
sleep-wake cycle
Thus, “wakefulness” area = somewhere
in-between the two
- Mouzzi & Morgan (1949)
Stimulation of the reticular formation of
sleeping cats woke them up.

16. (2) Theories of Sleep - Analysis
Effects of sleep deprivation - Humans
- REM sleep deprivation
- Preventing REM sleep makes the
body want it more. (Webb & Agnew,
1967)
- Deprivation of REM sleep causes a
transient rebound. (Brunner et al
1990)
- No cognitive or emotional effects
however.

17. (2) Theories of Sleep - Analysis
Effects of sleep deprivation - Animals
- After several days, experimental rats
died
- But, post-mortem revealed swollen
adrenal glands, gastric ulcers and
internal bleeding
- Result a consequence of stress and
physical damage??

18. Measurement of Sleep
Three principle measures of sleep:
(i) Electro-encephalogram (Head)
(ii) Electro-oculogram (Eye)
(iii) Electro-myogram (Neck)

19. 20 percent of adult population have some form of sleep
disorder.
TYPES
Respiratory-
•Obstructive sleep apnea/hypopnea
•Central sleep apnea/hypopnea
•Cheyne stokes breathing
•Sleep hypoventilation
Non Respiratory-
• Narcolepsy
• Periodic limb movement disorder
• Idiopathic hypersomnia

20. WHAT IS OSA?

21. OSA IS :
Common
Dangerous
Easily recognized
Treatable

22. www.sleepdoctor.com

23. 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

24. 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)

25. Pathophysiology of OSA
Airway size:

26. Pathophysiology of OSA
Sites of
Obstruction:
Obstruction
tends to
propagate

27. Pathophysiology of OSA
Sites of Obstruction:

29. Pathophysiology of OSA
Tests to determine site of obstruction:
Muller’s Maneuver
-After a forced expiration, an attempt at inspiration is made
with closed mouth and nose, whereby the negative pressure in
the chest and lungs is made very subatmospheric; the reverse of
Valsalva maneuver.
Sleep endoscopy
Fluoroscopy
Manometry
Cephalometrics
Dynamic CT scanning and MRI scanning

30. 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
 Concern = increase knowledge
= recognize risk factors
= identify affected individuals

31. RISK FACTORS
Obesity
Age
Sex
Race
Craniofacial anatomy
Smoking and alcohol consumption

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

33. 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

34. 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

35. AGE
Anatomic susceptibility
Preferential deposition of fat in the
parapharyngeal area
Changes in the body structures around the pharynx
Deterioration of protective reflex mechanisms

36. Risk Factor: Age
0
5
10
15
20
25
30
35
30-39 Yrs 40-49 Yrs 50-60 Yrs
Female
Male
% with
AHI > 5
Adapted from Young T et al.
N Engl J Med 1993;328. 2006 American Academy of Sleep medicine

37. GENDER
 MALE GENDER
Increased neck and waist circumference
? Women not reporting the classic symptoms
? Healthcare providers have lower index of suspicion
for considering OSA in women than men.

38. 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

39. SMOKING
0
1
2
3
4
5
Adjusted Odds Ratio for Sleep Apnea (AHI > 15)
in Former & Current Smokers vs Nonsmokers
Adapted from Wetter DW et al. Arch Intern Med 1994:154 ©1994 American Medical Association.
Former Current
Smokers Smokers
(Adjusted for age,
race, sex, BMI)
Odds Ratio
2006 American Academy of Sleep Medicine

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

41. 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.

42. 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

43. 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.
Study should be atleast for 6 hours.
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.

44. 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

45. EEG
10 sec
Arousal
Airflow
Effort
(Pes)
SaO2
Effort
(Abdomen)
Effort
(Rib Cage)
2006 American Academy of Sleep Medicine

46. 10 sec
Arousal
EEG
Airflow
Effort
(Pes)
SaO2
Effort
(Abdomen)
Effort
(Rib Cage)
2006 American Academy of Sleep Medicine

47. 2006 American Academy of Sleep Medicine

49. 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)

50. 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)

51. 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

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

54. 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).

55. www.dentonsleepdisorderlab.com

56. 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

57. 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.

58. Cardiovascular Risk
HTN
 Most studies suggest that OSA contributes
to systemic HTN
 Treatment of OSA may improve systemic HTN.
Cardiac arrhythmias
- bradycardia (increase vagal tone with hypoxemia)
- asystole
- atrial fibrillation
- ectopic ventricular beats
(bigeminy, trigeminy)

59. 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)

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

61. Other Comorbidities: MVA
0
0.05
0.1
0.15
0.2
0.25
0.3
0.35
0.4
0.45
No Apnea Sleep Apnea All Drivers
Accident / driver / 5 yrs
Adapted from Findley LJ et al. Am Rev Respir Dis 1988;138.
2006 American Academy of Sleep Medicine

62. • Objective = consequences discussed
• Modality

63. TREATMENTTREATMENT
BEHAVIORAL METHODS
Weight loss
Avoid alcohol and sedatives
Avoid sleep deprivation
Avoid supine sleep position
Stop smoking

64. 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.

65. 2006 American Academy of Sleep Medicine

66. MEDICAL Rx
Positive Pressure Therapy
* CPAP
* Bi-PAP
-pressurized air delivered at two alternating
levels. The inspiratory positive airway pressure is
higher and supports a breath as it is taken in.
Conversely, the expiratory positive airway pressure is
a lower pressure that allows you to breathe out. These
pressures are preset and alternate just like your
breathing pattern.

67. 2006 American Academy of Sleep Medicine

68. 2006 American Academy of Sleep Medicine

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

72. Nonsurgical Management
Oral appliance
Mandibular
advancement device
Tongue retaining
device

73. SURGICAL METHODS
Reconstruct upper airway
Uvulopalatopharyngoplasty (UPPP)
Laser-assisted uvulopalatopharyngoplasty (LAUP)
Radiofrequency tissue volume reduction
Genioglossal advancement
Nasal reconstruction
Tonsillectomy
Bypass upper airway
Tracheostomy

74. Surgical Management
Algorithms
Friedman et al
developed a staging
system for type of
operation:

75. Surgical Management
Algorithms:
Friedman et
al:

76. Surgical Management
 Tracheostomy
 Primary treatment modality
 Once placed, uncommon to decannulate
Thatcher GW. Maisel RH. The long-term evaluation of tracheostomy in the
management of severe obstructive sleep apnea. [Journal Article] Laryngoscope.
113(2):201-4, 2003 Feb.

77. Surgical Management
Nasal Surgery
Limited efficacy when used alone
Verse et al 2002 showed 15.8% success rate when used
alone in patients with OSA and day-time nasal
congestion with snoring (RDI<20 and 50% reduction)
Adenoidectomy

78. Surgical Management
Uvulopalatopharyngoplasty

79. 2006 American Academy of Sleep Medicine

80. Surgical Management
Uvulopalatopharyngoplasty
The most commonly performed surgery for OSA
Severity of disease is poor outcome predictor
Levin and Becker (1994) up to 80% initial
success decreased to 46% success rate at 12
months
Friedman et al showed a success rate of 80% at 6
months in carefully selected patients
Friedman M, Ibrahim H, Bass L. Clinical staging for
sleep-disordered breathing. Otolaryngol Head Neck
Surg 2002; 127: 13–21.

81. Surgical Management
UP3
Complications
Minor
 Transient VPI
 Hemorrhage<1%
Major
 NP stenosis
 VPI

82. Surgical Management
Cahali, 2003 proposed
the Lateral
Pharyngoplasty for
patients with
significant lateral
narrowing:
Cahali MB. Lateral pharyngoplasty: a new
treatment for obstructive sleep apnea
hypopnea syndrome. Laryngoscope.
113(11):1961-8, 2003 Nov.

83. Surgical Management
Lateral Pharyngoplasty

84. Surgical Management
Laser Assisted
Uvulopalatoplasty
High initial success rate
for snoring
Rates decrease, as for
UP3 at twelve months
Performed awake

86. Surgical Management
Radiofrequency
Ablation – Fischer et
al 2003
Radiofrequency device is inserted
into various parts of palate, tonsils
and tongue base at various thermal
energies

87. Surgical Management
Tongue Base Procedures
Lingual Tonsillectomy
 may be useful in patients with hypertrophy, but usually in
conjunction with other procedures

88. Surgical Management
Tongue Base Procedures
 Lingualplasty
 Chabolle, et al success
rate of 77% (RDI<20,
50% reduction) in 22
patients in conjunction
with UPPP
 Complication rate of
25% - bleeding, altered
taste, odynophagia,
edema
 Can be combined with
epiglottectomy

90. Surgical Management
Mandibular
Procedures
Genioglossus
Advancement
 Rarely performed
alone
 Increases rate of
efficacy of other
procedures
 Transient incisor
paresthesia

91. Surgical Management
Lingual
Suspension:

92. Surgical Management
 Lingual
Suspension:

93. Surgical Management
Hyoid Myotomy and
Suspension
Advances hyoid bone
anteriorly and inferiorly
Advances epiglottis and
base of tongue.

94. Surgical Management
Maxillary-Mandibular Advancement
Severe disease
Failure with more conservative measures
Midface, palate, and mandible advanced
anteriorly
Limited by ability to stabilize the segments and
aesthetic facial changes

95. Surgical Management
Maxillary-Mandibular
Advancement
Performed in
conjunction with oral
surgeons

96. 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

97. 2006 American Academy of Sleep Medicine

98. Otherwise snore
and this will
happen to you….
Or sleep alone….
www.corbett.com.au