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UnderstandingPulmonary
Diseases
Trends and
Evidences
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Sleep Workshop FacilitatorsLily Y. Lao, MD
Joseph Hope G. Cal, MD
Teresita Celestina S. Fuentes, MD
Emeraldee L. Garcia, RPSGT
Nanette G. Deyro, RPSGT
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Objectives:
provide both didactic and laboratory training
for interested personnel on the basics of
polysomnographic technology
recognize the basics of polysomnographic
monitoring, including EEG, respiration, body
movements, and how to score a sleep study
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uman
Sleep Medicine Workshop
6th Biennial Symposium: Understanding Pulmonary DiseasesTrends and EvidencesSeptember 11-12, 2008 Crowne Plaza Hotel
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What is sleep?
Reversible behavioral state of perceptual
disengagement from and unresponsiveness to
the environment
Complex amalgam of physiological and
behavioral processes
Carskadon and Dement
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STAGES OF SLEEP
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Non-REM Non-rapid eye movement
75-80% of sleep time in adult humans
Stage I NREM
2-5% of sleep time; lightest stage of sleep
alpha rhythm < 50% in an epoch
theta rhythm & beta waves appear EMG activity slightly
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Non-REM
Stage II NREM
45-55% of sleep time; intermediate sleep
begins after 10-12 minutes of Stage I NREM
sleep spindles, K complexes, delta waves < 20% lasts 30-60 mins
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Non-REM
Stage III NREM
15-20% of sleep time; deep sleep
delta waves 20% of the epoch
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REM
Rapid Eye Movement
20-25% of sleep time
1st REM noted 60-90mins after onset of NREM
sleep
EEG fast rhythms and delta waves
sawtooth appearance
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REM
Tonic Stage
desynchronized EEG, hypotonia & atonia of major
muscle groups
Phasic Stage
characterized by rapid eye moments in all directions
phasic swings in BP, HR, RR
frequently occur in early morning hours
Chokroverty 2000
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CYCLES OF SLEEP
Four or five 90-minute cycles of sequential stages
recur during the night
REM stage episodes increase in duration
Slow-wave sleep disappears beyond the second cycle
Infants: large REM sleep up to 2 years
Old: stage 3 diminishes or disappears, sleep
fragmentation REM : total sleep 25%
Nocturnal sleep fluctuates between 5-9 hrs
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SLEEP ARCHITECTURE
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SLEEP RELATED APNEA
Central Apnea
cessation of airflow with no respiratory effort
Obstructive sleep Apnea
cessation of airflow through the nose or mouthwith persistence of diaphragmatic & intercostalmuscle activities
Mixed Apnea
initial cessation of airflow with no respiratoryeffort followed by periods of upper airway OSA
ATS, 1989
(Apnea 10 sec. & 5/hr of sleep)
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Obstructive Apnea
Cessation of airflow, usually for more than 10
seconds
With abdominal and/or thoracic effort
Usually terminated by an arousal and/or
associated with a desaturation
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Obstructive Apnea
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Central Apnea
Cessation of airflow, usually for more than 10
seconds
Without abdominal and/or thoracic effort
May be terminated by an arousal and/or
associated with a desaturation
Very different type syndrome than OSA;chemo-receptor irregularities
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Central Apnea
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Mixed Apnea
Cessation of airflow >10 s (in adults) with
respiratory effort
Contains both central and obstructive
components, with each component lasting at least
one normal respiratory cycle
Typically leads to a desaturation and an arousal
Is really just a type of obstructive event with thesame consequences
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Mixed Apnea
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Hypopnea
Reduced airflow, usually for more than 10
seconds
Many labs require at least a 50% reduction inflow; however, more and more labs do not
require a specific % reduction, but look at the
SaO2 and EEG to affect the decision May be terminated by an arousal and/or
associated with a desaturation
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Hypopnea
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Sleep Apnea Syndrome
Based on Wisconsin Sleep Cohort minority of
subjects with evidence of sleep-disordered
breathing actually complain of excessive
daytime sleepiness
Reserved for patients with excessively
sleepy more important clinical
consequence
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Assess sleepiness
Score > 10
indicates
excessive
sleepiness
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PATHOGENESIS OSAS
1. Neural factors
medullary respiratory neural output
2. Oropharygeal anatomic factors
tone of the upper airway dilator muscle during sleep
fat deposition in the region of pharynx & soft palate
abnormal facial features
narrow upper airway space adenotonsillar enlargement & craniofacial dysostosis
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RISK FACTORS FOR OSAS
Male gender
Menopausal women
Increasing age
Body Mass Index ( 25 = over wt; 30 = obese)
Increasing Neck Circumference (>17 inches men; >16inches in women)
Racial factors Alcohol
Smoking
Increasing drug use
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SYMPTOMS OF OSAS
Nocturnal symptoms during sleep loud snoring
choking during sleep
cessation of breathing
sitting up or fighting for breath abnormal motor activities
severe sleep disruption
gastroesophageal reflux causing heartburn
nocturia & nocturnal eneuresis
insomnia
excessive nocturnal sweating
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SYMPTOMS OF OSAS
Daytime Symptoms
excessive daytime somnolence
forgetfulness
personality changes
decreased libido & impotence in men
dryness of mouth on awakening
morning headache
automatic behavior with retrograde amnesia
hyperactivity (in children)
hearing impairment (in some patients)
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Differential Diagnosis of Excessive Sleepiness
Insufficient sleep syndrome
Restless legs syndrome
NarcolepsyKleineLevin Syndrome
Medications with sleepiness as side effects
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Insufficient Sleep Syndrome
No specific abnormality in their sleep butsimply do not sleep enough
American about 35% of population sleeping
< 6 hours/night Typically use an alarm clock
Affects glucose handling
Increase ghrelin stimulates appetite
Decrease leptin inhibits appetite
Risk for obesity
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Restless Legs Syndrome
Abnormal sensations in their legs thattypically appear in the evening
Sensations can make sleep difficult
Exacerbated by
Iron deficiency
By inactivity
Common renal dialysis and pregnancy
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Kleine-Levin Syndrome
Adolescents
Intermittent episodes of intense hypersomniaLast for days and may sleep for 20 hours/day
Markedly increased appetite during the
episodes
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PHYSICAL FINDINGS IN OSASObesity BMI (>25) neck circumference
In some patients
large edematous uvulalow hanging soft palatelarge tonsils & adenoidsretrognathiamicrognathia
hypertensioncardiac arrhythmiasevidence of CHF
LABORATORY ASSESSMENT OF
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LABORATORY ASSESSMENT OFOSAS
Overnight PSG
Characteristic PSG findings:
recurrent episodes of apneas & hypopneas, mostly
obstructive & mixed O2 desaturation followed by arousals & resumption of
breathing
AHI or RDI > 5
Multiple Sleep Latency Testto document objectively excessive sleepiness
pathologic sleepiness mean sleep latency less < 5minutes
LABORATORY ASSESSMENT OF
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LABORATORY ASSESSMENT OFOSAS
Imaging Studies
CT Scan & MRI to measure cross sectional areas ofupper airway & to assess maxillomandibular
deficiencies
Pulmonary Function Test
to exclude intrinsic bronchopulmonary disease
Other Test
ECG
test for hypothyroidism
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SMOKING AND OSAS
Prevalence = 35%
Stimulant effects of nicotine stimulates
upper airway musculature & upper airwayresistance
Nightly nicotine withdrawal can sleep
instability
- Kashyap. Sleep and Breathing, 2001
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CONSEQUENCES OF OSAS
Short Term Consequences
impairment of quality of life
traffic & work-related accidents
Long Term Consequences prevalence of hypertension
strong relationship between snoring, MI & stroke
association between supratentorial & infratentorial infarctions, TIA,
snoring & sleep apnea
Neurophsychological evidence of cognitive dysfunction
congestive heart failure
cardiac arrhythmia
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PATHOPHYSIOLOGICAL EFFECTS OF OSA ON THE
CV SYSTEM
Acute Effects myocardial oxygen delivery
intermittent hypoxia
decrease cardiac output
myocardial oxygen demand arousals from sleep
Sympathetic NS activation
in LV afterload negative intrathoracic pressure
BP
heart rate
nocturnal myocardial ischemia
nocturnal pulmonary edema
cardiac arrhythmias
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PATHOPHYSIOLOGICAL EFFECTS OF OSA ON THE
CV SYSTEM
Chronic Effects Autonomic CV derangements
sympathetic NS activation
HR variability
impaired barroreflex control of HR systemic HPN
Myocardial Effects LV hypertrophy
LV dysfunction and failure
platelet aggregability and blood caogulability
- Leung et al. AJRCCM 2001
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OSA & HYPERTENSION
Related to intermittent hypoxemia & sympathetic NSactivation
Hypoxia
potent vasoconstrictor activity of adrenal glands, renal sympathetic & Renin-
Angiotension system
HPN refractory to maximal medical therapy, 87% have
OSA Correction of OSA BP to baseline levels within 1-4
weeks
- Leung. AJRCCM 2001
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The single most important laboratory
technique for assessment of sleep and its
disorders
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POLYSOMNOGRAPHY
Method of identifying and evaluating sleep-
state and several physiologic variable during
sleep
A multi-parametric test that is used to
study/record in detail all the biophysiological
changes that occur in the human body when
the person is asleep
ATS 1989
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What does Polysomnography measure?
It monitors the multiple physiological characteristics
simultaneously during sleep at night.
It allows assessment of sleep stages and wakefulness,
respiration, cardio-circulatory functions and body
movements.
It monitors physiological or pathological events in sleep.
When Is Sleep Laboratory
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When Is Sleep Laboratory
Evaluation in Order?
Serious excessive daytime sleepiness with no known
medical cause and not relieved by 2 weeks of significant
increase of time in bed Snoring with interrupted breathing or periodic limb
movements
Nocturnal seizures
Hauri et al. Sleep Disorders, 1992
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What is monitored in PSG?
Electroencephalogram (EEG)
Electrooculogram (EOG)
Chin electromyogram (EMG)
Electrocardiogram (ECG)
Nasal and/or oral airflow
Breathing effort (chest and
abdomen)
Oximetry
Leg electromyogram (EMG)
Body position
Snoring sensors
Continuous audio/video
monitoring & behavior
observation
AASM Practice Parameters for Indications for Polysomnography 2005
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How is a sleep study performed?
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Patient Hook-up: EEG
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EEG Electrode Application
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EEG Electrode Application
International 10/20 System
4 anatomical landmarks
Nasion
Inion
Right pre-auricular point
Left pre-auricular point
Cleansing of site
Collodion or EEG electrode paste
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EEG Electrode Application
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EEG Electrode Application
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EOG Electrode Application
Record eye movement
activity
Vicinity of right and left
outer canthus
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Several varieties of eye movements are
recorded and may assist/facilitate in sleep
staging
Waking eye movement (WEMs)
Slow eye movements (SEMs)
Rapid eye movements (REMs)
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Chin EMG Application
Mental-submental
derivation
Electrode placed directly
over chin, referenced toelectrode placed 2-3 cm
off midline, slightly
below jawbone
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ECG Electrode Application
Single-channel ECG
Electrodes over right
clavicle and lower left
thorax
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Leg EMG Electrode Application
Anterior tibialis muscles
of each leg
Less precise than scalpand facial derivations
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Respiratory Transducers
Respiratory tracings
represent indirect,
qualitative measures of
respiratory airflow and
effort
Thermal airflow sensors
Nasal cannula pressure
transducers
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Oximetry
Pulse oximeter connected to polysomnograph
Periodically check readings with a regular
pulse oximeter
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Snoring Monitoring
Monitored by placing a microphone on the
patients neck
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Technical Filter Settings
Low Frequency
Filter
High Frequency
Filter
EEG 0.3 Hz 35 Hz
EOG 0.3 Hz 35 Hz
ECG 0.3 Hz 70 Hz
EMG 10 Hz 100 Hz
Snoring 10 Hz 100 Hz
Respiration 0.1 Hz 15 Hz
AASM 2007
Reading and Interpretation
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Reading and Interpretation
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PSG FEATURES OF WAKE (W)
EEG Characteristics EOG EMG
Alpha rhythm (frequency: 8-13 Hz) over the
occipital region with eye closure, attenuating
with eye opening.
Eye blinks; REMs Elevated chin
EMG tone
activity
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Stage EEG Characteristics EOG EMGN1 Low voltage mixed frequency
(LVMF) background activity (4-7Hz)
Vertex waves (biphasic sharp
transients, maximal centrally)
SEMs Tonic EMG
activity, less
than in the
awake stateN2 LVMF background activity
Sleep spindles (distinct waves,
11-16 Hz, > 0.5s long); K-complexes
(biphasic vertex waves, > 0.5s long)
No EMs Low level
tonic EMG
activity
N3 High voltage slow wave (HVS)
activity: 0.5-2 Hz, > 75mV
amplitude over frontal regions
No EMs Low level
Tonic EMG
activity
PSG FEATURES OF NREM SLEEP
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EEG Characteristics EOG EMG
LVMF background activity
Sawtooth waves: 2-6 Hz
Usually occurring with
phasic REMs
Phasic REMs
(occur with bursts
of phasic EMG)
Low chin
EMG tone
activity
PSG FEATURES OF REM SLEEP
SLEEP RELATED APNEA
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SLEEP RELATED APNEA
Central Apnea
cessation of airflow with no respiratory effort
Obstructive sleep Apnea
cessation of airflow through the nose or mouth
with persistence of diaphragmatic & intercostal
muscle activities
Mixed Apnea initial cessation of airflow with no respiratory
effort followed by periods of upper airway OSAATS, 1989
(Apnea 10 sec. & 5/hr of sleep)
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Obstructive Apnea
Cessation of airflow, usually for more than 10
seconds
With abdominal and/or thoracic effort Usually terminated by an arousal and/or
associated with a desaturation
Obstructive Apnea
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Obstructive Apnea
l
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Central Apnea
Cessation of airflow, usually for more than 10
seconds
Without abdominal and/or thoracic effort May be terminated by an arousal and/or
associated with a desaturation
Very different type syndrome than OSA;chemo-receptor irregularities
Central Apnea
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Central Apnea
i d
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Mixed Apnea
Cessation of airflow >10 s (in adults) with
respiratory effort
Contains both central and obstructive
components, with each component lasting at leastone normal respiratory cycle
Typically leads to a desaturation and an arousal
Is really just a type of obstructive event with thesame consequences
Mixed Apnea
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Mixed Apnea
H
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Hypopnea
Reduced airflow, usually for more than 10
seconds
Many labs require at least a 50% reduction inflow; however, more and more labs do not
require a specific % reduction, but look at the
SaO2 and EEG to affect the decision
May be terminated by an arousal and/or
associated with a desaturation
Hypopnea
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Hypopnea
S i D fi iti
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Scoring Definitions:
Arousal An abrupt EEG frequency shift ( or frequency or >16 Hz, not including spindle frequency)
> 3s long, preceded by > 10s of sleep
Movement
time
Scored only during sleep when > 50% of an epoch is
obscured by movement artifactLimb
movements
An increase in the EMG activity lasting 0.5 to 5s with
an amplitude > 25% of the burst of EMG activity
recorded during bio-calibration.
Periodic limb movements sequence are scored insleep only when there are > 4 limb movements in
sequence occurring > 5s but < 90s apart.
S i D fi iti
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Scoring Definitions:
Apnoea Absence of or > 90% decrease in airflow compared to
baseline lasting > 10s
Classified as central, obstructive or mixed apnea
Hypopnoea Any of the following respiratory events lasting >10s
are scored:
> 50% reduction of airflow
> 30% reduction of airflow (but 4% oxygen desaturation
PLMS
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PLMS
PLMS
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PLMS
Repetitive (at least 4) episodes of muscle contraction(0.5-5 s duration), typically separated by 20-40
seconds, but not more than 90 seconds (120 seconds
in some laboratories)
Arousals sometimes associated with the movements
Positive diagnosis if > 5 per hour of sleep
Movements may be determined to be not clinically
significant if not associated with arousals
Respiratory Related Arousal
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Respiratory Related Arousal
Cli i l E t P t
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Clinical Event Parameters
Apnea index (AI): number of apneas per hour of TST
Hypopnea index (HI): number of hypopneas per
hour of TST
Apnea/hypopnea index (AHI): number of combinedapneas and hypopneas per hour of TST
Periodic limb movement index (PLMI): number of
periodic limb movements in sleep per hour of TST
Isolated limb movements index: number of non-
periodic limb movements per hour of TST
Cli i l E t P t
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Clinical Event Parameters
Spontaneous arousal index: number of arousals thatoccur which are not associated with any other
clinical event
Arousal index (AI): number of all arousals per hourof TST
Periodic limb movement arousal index (PLMAI):
number of periodic limb movements associated with
arousal in sleep per hour of TST Mean Heart rate: the average heart rate during the
PSG evaluation which can also be reported by sleep
state, REM, non-REM, and wake.
Obstr cted Air a
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Obstructed Airway
OSA with closed upper airways
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pp y
Snoring with partially close upper airway
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Snoring with partially close upper airway
Effects of CPAP
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Effects of CPAP
CPAP: opening of the upper airway
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Before CPAP Titration
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Before CPAP Titration
After CPAP Titration
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After CPAP Titration
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Nasal Mask CPAP
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Nasal Mask CPAP
Full face Mask
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Full-face Mask
Chin Straps
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Chin Straps
CPAP Machine
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CPAP Machine
Supplemental Oxygen Therapy in Sleep
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Study
Supplemental oxygen therapy should be instituted upon
receipt of a physician order under specific circumstances :
the patient is currently under treatment of a physician andsupplemental oxygen therapy is prescribed
the patient is undergoing a PSG study for titration of nasal PAP therapy
& is still experiencing desaturation, per facility protocol, after reaching
optimal PAP level to eliminate respiratory events & arousals & no signsof CO2 retention are present
the patient is unable to tolerate nasal PAP therapy & is experiencing
significant desaturation with respiratory events
PRECAUTIONS for Suplemental
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Oxygen Therapy:
In patients with chronic obstructive pulmonary
disease, adding supplemental oxygen may lead to
an increase in PaCO2 and
changes in hypoxic drive, which impairs the drive tobreathe
Fire hazard is increased with the use of oxygen in the
sleep disorders facility
Power outage can lead to inability to use the oxygen
concentrator and adequate back up should be in
place
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Laugh and the world
laughs with you,
snore and you sleep
alone.Anthony Burgess
English novelist, cr i tic
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Thank You
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PATHOGENESIS OSAS
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PATHOGENESIS OSAS
1. Neural factors
medullary respiratory neural output
2. Oropharygeal anatomic factors
tone of the upper airway dilator muscle during sleep
fat deposition in the region of pharynx & soft palate
abnormal facial features
narrow upper airway space
adenotonsillar enlargement & craniofacial dysostosis
RISK FACTORS FOR OSAS
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RISK FACTORS FOR OSAS
Male gender
Menopausal women
Increasing age
Body Mass Index ( 25 = over wt; 30 = obese) Increasing Neck Circumference (>17 inches men; >16
inches in women)
Racial factors
Alcohol
Smoking
Increasing drug use
SYMPTOMS OF OSAS
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SYMPTOMS OF OSAS
Nocturnal symptoms during sleep loud snoring
choking during sleep
cessation of breathing
sitting up or fighting for breath abnormal motor activities
severe sleep disruption
gastroesophageal reflux causing heartburn
nocturia & nocturnal eneuresis
insomnia
excessive nocturnal sweating
SYMPTOMS OF OSAS
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SYMPTOMS OF OSAS
Daytime Symptoms
excessive daytime somnolence
forgetfulness
personality changesdecreased libido & impotence in men
dryness of mouth on awakening
morning headache
automatic behavior with retrograde amnesia
hyperactivity (in children)
hearing impairment (in some patients)
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PHYSICAL FINDINGS IN OSASObesity
BMI (>25) neck circumference
In some patientslarge edematous uvula
low hanging soft palatelarge tonsils & adenoidsretrognathiamicrognathiahypertensioncardiac arrhythmiasevidence of CHF
LABORATORY ASSESSMENT OFOSAS
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OSAS
Overnight PSGCharacteristic PSG findings:
recurrent episodes of apneas & hypopneas, mostlyobstructive & mixed
O2 desaturation followed by arousals & resumption ofbreathing
AHI or RDI > 5
Multiple Sleep Latency Test
to document objectively excessive sleepiness
pathologic sleepiness mean sleep latency less < 5minutes
LABORATORY ASSESSMENT OFOSAS
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OSAS
Imaging Studies
CT Scan & MRI to measure cross sectional areas ofupper airway & to assess maxillomandibular
deficiencies Pulmonary Function Test
to exclude intrinsic bronchopulmonary disease
Other Test
ECG
test for hypothyroidism
SMOKING AND OSAS
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SMOKING AND OSAS
Prevalence = 35%
Stimulant effects of nicotine stimulates
upper airway musculature &
upper airwayresistance
Nightly nicotine withdrawal can sleep
instability
- Kashyap. Sleep and Breathing, 2001
CONSEQUENCES OF OSAS
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Q
Short Term Consequences impairment of quality of life
traffic & work-related accidents
Long Term Consequences
prevalence of hypertension
strong relationship between snoring, MI & stroke
association between supratentorial & infratentorial infarctions, TIA,
snoring & sleep apnea
Neurophsychological evidence of cognitive dysfunctioncongestive heart failure
cardiac arrhythmia
PATHOPHYSIOLOGICAL EFFECTS OF OSA ON THE
CV SYSTEM
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CV SYSTEM Acute Effects
myocardial oxygen delivery intermittent hypoxia
decrease cardiac output
myocardial oxygen demand arousals from sleep
Sympathetic NS activation
in LV afterload negative intrathoracic pressure
BP
heart rate
nocturnal myocardial ischemia
nocturnal pulmonary edema cardiac arrhythmias
PATHOPHYSIOLOGICAL EFFECTS OF OSA ON THE
CV SYSTEM
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CV SYSTEM
Chronic Effects Autonomic CV derangements
sympathetic NS activation
HR variability
impaired barroreflex control of HR
systemic HPN
Myocardial Effects LV hypertrophy
LV dysfunction and failure
platelet aggregability and blood caogulability
- Leung et al. AJRCCM 2001
OSA & HYPERTENSION
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Related to intermittent hypoxemia & sympathetic NSactivation
Hypoxia
potent vasoconstrictor
activity of adrenal glands, renal sympathetic & Renin-Angiotension system
HPN refractory to maximal medical therapy, 87% haveOSA
Correction of OSA BP to baseline levels within 1-4weeks
- Leung. AJRCCM 2001
OSA & STROKE
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In patients with stroke sleep apnea reported to
occur in 43-91%
Obstructive apnea significant decline in cerebral
blood flow Abrupt & marked alterations in blood flow velocity
associated with alternating obstructive apnea &
hyperpnea
alteration in shear forces
acceleration of atherosclerosis
- Leung. AJRCCM 2001
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OSA & ISCHEMIC HEART DISEASE
Ischemic episodes related to O2 desaturation &
post-apneic surges in HR & BP CPAP frequency of ST depression & relief of
nocturnal angina
- Leung. AJRCCM 2001
OSA & CHF
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Mechanisms:
systemic hypertension
ischemia & reduced contractility due to hypoxia
cardiac myocytes injury due to cathecolaminestimulation
CPAP for 1 month dramatic improvement in LVEF (37to 49%) & cardiac functional status
- Leung. AJRCCM 2001
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Indications for Cardiopulmonary
Sleep Studies
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Sleep Studies
COPD patients with awake PaO2 > 55mmHg but with
cor pulmonale
Patients with restrictive ventilatory impairment
secondary to chest wall and neuromuscular
disturbances and complicated by chronic
hypoventilation, polycythemia, pulmonary
hypertension, disturbed sleep, daytime somnolence
and fatigue
ATS 1989
Indications for Cardiopulmonary
Sleep Studies
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Sleep Studies
Patients with disturbances of respiratory control
whose awake PaO2 > 45mmHg or with complications
Snoring and obesity
Patients with excessive daytime sleepiness
Patients with nocturnal cyclic bradytachyarrhythmia,
nocturnal abnormalities of atrioventricular
conduction and ventricular ectopy during sleep
ATS 1989
Indications for Polysomnography
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Polysomnography is routinely indicated for the
diagnosis of sleep related breathing disorders.
(Standard)
Polysomnography is indicated for positive airway
pressure (PAP) titration in patients with sleep related
breathing disorders. (Standard)
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A preoperative clinical evaluation that includes
polysomnography or an attended cardiorespiratory
(Type 3) sleep study is routinely indicated to evaluate
for the presence of obstructive sleep apnea in
patients before they undergo upper airway surgery
for snoring or obstructive sleep apnea. (Standard)
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Follow-up polysomnography or an attended cardiorespiratory(Type 3) sleep study is routinely indicated for the assessment
of treatment results in the following circumstances:
(Standard)
After good clinical response to oral appliance treatment in patients
with moderate to severe OSA
After surgical treatment of patients with moderate to severe OSA
After surgical or dental treatment of patients with SRBDs whose
symptoms return despite a good initial response to treatment
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Follow-up polysomnography is routinely indicated for theassessment of treatment results in the following
circumstances: (Standard)
After substantial weight loss (e.g., 10% of body weight) has occurred in
patients on CPAP for treatment of SRBDs After substantial weight gain (e.g., 10% of body weight) has occurred
in patients previously treated with CPAP successfully, who are again
symptomatic despite the continued use of CPAP
When clinical response is insufficient or when symptoms return
despite a good initial response to treatment with CPAP.
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Indications for Polysomnography
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Patients with systolic or diastolic heart failure should
undergo polysomnography if they have nocturnal
symptoms suggestive of sleep related breathing
disorders (disturbed sleep, nocturnal dyspnea,snoring) or if they remain symptomatic despite
optimal medical management of congestive heart
failure. (Standard)
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Patients with coronary artery disease should be
evaluated for symptoms and signs of sleep apnea. If
there is suspicion of sleep apnea, the patients should
undergo a sleep study. (Guideline)
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Patients with history of stroke or transient ischemic
attacks should be evaluated for symptoms and signs
of sleep apnea. If there is suspicion of sleep apnea,
the patients should undergo a sleep study. (Option)
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Patients referred for evaluation of significant
tachyarrhythmias or bradyarrhythmias should be
questioned about symptoms of sleep apnea. A sleep
study is indicated if questioning results in areasonable suspicion that OSA or CSA are present.
(Guideline)
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Oral Appliances for OSA
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