Helen Gidey, MD

Emory Johns Creek Hospital

March 13, 2008
2006 American Academy of Sleep Medicine
WHAT IS OSA?
OSA IS :

Common

Dangerous

Easily recognized

Treatable
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)
www.sleepdoctor.com
PATENT Vs COLLAPSED AIRWAY

2006 American Academy of Sleep medicine

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
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)
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
RISK FACTORS
Obesity
Age
Sex
Race
Craniofacial anatomy
Smoking and etoh consumption
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
Obesity
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
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
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
www.obesityinamerica.org
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

 Risk Factor: Age
35

30

25

% with 20
AHI > 5 Female
15
Male
10

0
30-39 Yrs 40-49 Yrs 50-60 Yrs

Adapted from Young T et al.

N Engl J Med 1993;328. 2006 American Academy of Sleep medicine
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
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
 SMOKING
Adjusted Odds Ratio for Sleep Apnea (AHI > 15)
in Former & Current Smokers vs Nonsmokers

Odds Ratio
3

(Adjusted for age, 2

race, sex, BMI)
1

0
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
Other risk factors
Alcohol consumption
Sedatives (benzodiazepines)

 reduce nerve output to compensatory dilator

muscles
 increase OSA severity in patients with
preexisting syndrome.
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.
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
www.tmjsleepcenter.com
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.
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.
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
 Obstructive Mixed Central

Airflow

Respiratory
effort

2006 American Academy of Sleep Medicine

 EEG
Arousal

Airflow

Effort
(Rib Cage)

Effort
(Abdomen)

Effort
(Pes)

SaO2
10 sec

2006 American Academy of Sleep Medicine

 EEG
Arousal

Airflow

Effort
(Rib Cage)

Effort
(Abdomen)

Effort
(Pes)

SaO2
10 sec

2006 American Academy of Sleep Medicine

 EEG
Arousal

Airflow

Effort
(Rib Cage)

Effort
(Abdomen)

Effort
(Pes)

SaO2
10 sec

2006 American Academy of Sleep Medicine

Polysomnography in OSA

2006 American Academy of Sleep Medicine

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)
Clinical Features
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)
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)
www.apnea.com
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
Clinical features
(daytime symptoms)
2. fatigue
3. memory impairment
4. personality changes
5. morning headaches or nausea
6. depression
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).
UpToDate
www.dentonsleepdisorderlab.com
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
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)
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)
Cardiovascular Risk
Cardiac arrhythmias
- bradycardia (increase vagal tone with hypoxemia)
- asystole
- atrial fibrillation
- NSVT
- ectopic ventricular beats
(bigeminy, trigeminy)
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.
OSA and medical co morbidity
Conflicting data, but possible association of OSA
with:
 CVA
 Heart Failure
 DM
 Other Comorbidities: MVA
Accident / driver / 5 yrs

0.45
0.4
0.35
0.3
0.25
0.2
0.15
0.1
0.05
0
No Apnea Sleep Apnea All Drivers

Adapted from Findley LJ et al. Am Rev Respir Dis 1988;138.

2006 American Academy of Sleep Medicine
Consequences:
Excessive Daytime Sleepiness
Increased motor vehicle crashes
Increased work-related accidents
Poor job performance
Depression
Family discord
Decreased quality of life
• Objective = consequences discussed
• Modality
BEHAVIORAL METHODS
Weight loss

Avoid alcohol and sedatives

Avoid sleep deprivation

Avoid supine sleep position

Stop smoking
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.
2006 American Academy of Sleep Medicine
MEDICAL Rx

Positive Pressure Therapy

* CPAP
* Bi-PAP
Surgical
2006 American Academy of Sleep Medicine
2006 American Academy of Sleep Medicine
CPAP
Has been shown to objectively:
Decrease MVA
Decrease blood pressure
Decrease day time sleepiness
Problems:
Mask discomfort
Patient acceptance
Claustrophobia
aerophagia
2006 American Academy of Sleep Medicine
SURGICAL METHODS
Reconstruct upper airway
Uvulopalatopharyngoplasty (UPPP)
Laser-assisted uvulopalatopharyngoplasty (LAUP)
Radiofrequency tissue volume reduction
Genioglossal advancement
Nasal reconstruction
Tonsillectomy

Bypass upper airway

Tracheostomy
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
2006 American Academy of Sleep Medicine
Otherwise snore
and this will
happen to you….

Or sleep alone….

www.corbett.com.au
REFERENCES
 2006 American Academy of Sleep Medicine
 Eckert, D, et al. “Pathophysiology of Adult Obstructive Sleep Apnea” American Thoracic
Society. Vol 5. pp 144-153, 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 154-160, 2008
 Punjabi, N. M. “The Epidemiology of Adult Obstructive Sleep Apnea” American
Thoracic Society. Vol 5.pp 136-143, 2008
 Schwartz, A, et al. “Obesity and Obstructive Sleep Apnea” American Thoracic Society.
Vol 5. pp 185 – 192, 2008
 UpToDate.com