sleep 2012 revised

7/30/2019 Sleep 2012 Revised

1/154

UnderstandingPulmonary

Diseases

Trends and

Evidences


2/154

Sleep Workshop FacilitatorsLily Y. Lao, MD

Joseph Hope G. Cal, MD

Teresita Celestina S. Fuentes, MD

Emeraldee L. Garcia, RPSGT

Nanette G. Deyro, RPSGT


3/154

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


4/154


5/154


6/154


7/154


8/154

uman

Sleep Medicine Workshop

6th Biennial Symposium: Understanding Pulmonary DiseasesTrends and EvidencesSeptember 11-12, 2008 Crowne Plaza Hotel


9/154

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


10/154

STAGES OF SLEEP


11/154

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


12/154

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


13/154

Non-REM

Stage III NREM

15-20% of sleep time; deep sleep

delta waves 20% of the epoch


14/154

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


15/154

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


16/154

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


17/154

SLEEP ARCHITECTURE


18/154

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)


19/154

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


20/154

Obstructive Apnea


21/154

Central Apnea


seconds

Without abdominal and/or thoracic effort

May be terminated by an arousal and/or


Very different type syndrome than OSA;chemo-receptor irregularities


22/154

Central Apnea


23/154

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


24/154

Mixed Apnea


25/154

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



26/154

Hypopnea


27/154


28/154


29/154


30/154

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


31/154

Assess sleepiness

Score > 10

indicates

excessive

sleepiness


32/154

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


33/154

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


34/154

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


35/154

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)


36/154

Differential Diagnosis of Excessive Sleepiness

Insufficient sleep syndrome

Restless legs syndrome

NarcolepsyKleineLevin Syndrome

Medications with sleepiness as side effects


37/154

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


38/154

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


39/154


40/154

Kleine-Levin Syndrome

Adolescents

Intermittent episodes of intense hypersomniaLast for days and may sleep for 20 hours/day

Markedly increased appetite during the

episodes


41/154

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


42/154

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


43/154


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


44/154

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


45/154

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


46/154


47/154

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


48/154


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


49/154

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


50/154

The single most important laboratory

technique for assessment of sleep and its

disorders


51/154

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


52/154

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


53/154

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


54/154

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


55/154

How is a sleep study performed?


56/154

Patient Hook-up: EEG


57/154

EEG Electrode Application


58/154


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


59/154



60/154



61/154

EOG Electrode Application

Record eye movement

activity

Vicinity of right and left

outer canthus


62/154


63/154

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)


64/154

Chin EMG Application

Mental-submental

derivation

Electrode placed directly

over chin, referenced toelectrode placed 2-3 cm

off midline, slightly

below jawbone


65/154

ECG Electrode Application

Single-channel ECG

Electrodes over right

clavicle and lower left

thorax


66/154

Leg EMG Electrode Application

Anterior tibialis muscles

of each leg

Less precise than scalpand facial derivations


67/154

Respiratory Transducers

Respiratory tracings

represent indirect,

qualitative measures of

respiratory airflow and

effort

Thermal airflow sensors

Nasal cannula pressure

transducers


68/154


69/154

Oximetry

Pulse oximeter connected to polysomnograph

Periodically check readings with a regular

pulse oximeter


70/154

Snoring Monitoring

Monitored by placing a microphone on the

patients neck


71/154

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


72/154

Reading and Interpretation


73/154

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


74/154

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


75/154

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


76/154

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)


77/154

Obstructive Apnea


seconds

With abdominal and/or thoracic effort Usually terminated by an arousal and/or


Obstructive Apnea


78/154

Obstructive Apnea

l


79/154

Central Apnea


seconds

Without abdominal and/or thoracic effort May be terminated by an arousal and/or


Very different type syndrome than OSA;chemo-receptor irregularities

Central Apnea


80/154

Central Apnea

i d


81/154

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


82/154

Mixed Apnea

H


83/154

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


Hypopnea


84/154

Hypopnea

S i D fi iti


85/154

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


86/154

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


87/154

PLMS

PLMS


88/154

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


89/154

Respiratory Related Arousal

Cli i l E t P t


90/154

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


91/154

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


92/154

Obstructed Airway

OSA with closed upper airways


93/154

pp y

Snoring with partially close upper airway


94/154

Snoring with partially close upper airway

Effects of CPAP


95/154

Effects of CPAP

CPAP: opening of the upper airway


96/154


97/154

Before CPAP Titration
http://www.cpap.com/productpage/OptiLife-Nasal-Pillow-CPAP-Mask.html


98/154

Before CPAP Titration

After CPAP Titration


99/154

After CPAP Titration


100/154

Nasal Mask CPAP


101/154

Nasal Mask CPAP

Full face Mask


102/154

Full-face Mask

Chin Straps


103/154

Chin Straps

CPAP Machine


104/154

CPAP Machine

Supplemental Oxygen Therapy in Sleep


105/154

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


106/154

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


107/154

Laugh and the world

laughs with you,

snore and you sleep

alone.Anthony Burgess

English novelist, cr i tic


108/154


109/154


110/154


111/154


112/154


113/154


114/154


115/154


116/154


117/154


118/154


119/154


120/154


121/154

Thank You


122/154

PATHOGENESIS OSAS


123/154

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



124/154


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


125/154

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


126/154

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)


127/154

PHYSICAL FINDINGS IN OSASObesity

BMI (>25) neck circumference

In some patientslarge edematous uvula

low hanging soft palatelarge tonsils & adenoidsretrognathiamicrognathiahypertensioncardiac arrhythmiasevidence of CHF



128/154

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



129/154

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


130/154

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


131/154

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


CV SYSTEM


132/154

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


CV SYSTEM


133/154

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


134/154

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


OSA & STROKE


135/154

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



136/154

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


OSA & CHF


137/154

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



138/154


139/154


140/154


141/154


142/154

Indications for Cardiopulmonary

Sleep Studies


143/154

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


144/154

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


145/154

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)




146/154

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)




147/154

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




148/154

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.



149/154



150/154

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)




151/154

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)




152/154

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)




153/154

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)


Oral Appliances for OSA


154/154

sleep 2012 revised

Documents