Understanding Pulmonary Diseases Trends and Evidences

Sleep Workshop Facilitators

Lily Y. Lao, MD Joseph Hope G. Cal, MD Teresita Celestina S. Fuentes, MD Emeraldee L. Garcia, RPSGT Nanette G. Deyro, RPSGT

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

uman

Sleep Medicine Workshop

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

What is sleep?
Reversible behavioral state of perceptual disengagement from and unresponsiveness to the environment Complex amalgam of behavioral processes physiological and

Carskadon and Dement

STAGES OF SLEEP

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

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

Non-REM
Stage III NREM
15-20% of sleep time; deep sleep delta waves 20% of the epoch

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

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

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

SLEEP ARCHITECTURE

SLEEP RELATED APNEA

(Apnea 10 sec. & 5/hr of sleep)

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 OSA
ATS, 1989

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

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

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 the same consequences

Mixed Apnea

Hypopnea
Reduced airflow, usually for more than 10 seconds Many labs require at least a 50% reduction in flow; 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

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

Assess sleepiness

Score > 10

indicates excessive sleepiness

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

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
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
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)

Differential Diagnosis of Excessive Sleepiness

Insufficient sleep syndrome Restless legs syndrome Narcolepsy Kleine Levin Syndrome Medications with sleepiness as side effects

Insufficient Sleep Syndrome

No specific abnormality in their sleep but simply 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

Restless Legs Syndrome

Abnormal sensations in their legs that typically appear in the evening Sensations can make sleep difficult Exacerbated by
Iron deficiency By inactivity

Common renal dialysis and pregnancy

Narcolepsy
Third decades of life Four cardinal features:
Marked daytime sleepiness Cataplexy
Suden onset of muscle atonia, in REM sleep

Hypnagogic or Hypnopomic Hallucination

Vivid dreams during wakefulness

Sleep Paralysis
Wake up from sleep unable to move Emerging from REM sleep and REM-associated atonia has not been switched ff

Kleine-Levin Syndrome
Adolescents Intermittent episodes of intense hypersomnia
Last for days and may sleep for 20 hours/day

Markedly increased appetite during the episodes

Obesity

PHYSICAL FINDINGS IN OSAS

BMI (>25) neck circumference
large edematous uvula low hanging soft palate large tonsils & adenoids retrognathia micrognathia hypertension cardiac arrhythmias evidence of CHF

In some patients

LABORATORY ASSESSMENT OF OSAS

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 Test

to document objectively excessive sleepiness pathologic sleepiness mean sleep latency less < 5 minutes

LABORATORY ASSESSMENT OF OSAS

Imaging Studies
CT Scan & MRI to measure cross sectional areas of upper airway & to assess maxillomandibular deficiencies

Pulmonary Function Test

to exclude intrinsic bronchopulmonary disease

Other Test
ECG test for hypothyroidism

SMOKING AND OSAS

Prevalence = 35% Stimulant effects of nicotine stimulates upper airway musculature & upper airway resistance Nightly nicotine withdrawal can sleep instability
- Kashyap. Sleep and Breathing, 2001

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

PATHOPHYSIOLOGICAL EFFECTS OF OSA ON THE CV SYSTEM

Acute Effects
myocardial oxygen delivery myocardial oxygen demand
arousals from sleep Sympathetic NS activation in LV afterload heart rate
negative intrathoracic pressure BP

intermittent hypoxia decrease cardiac output

nocturnal myocardial ischemia nocturnal pulmonary edema cardiac arrhythmias

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

platelet aggregability and blood caogulability

LV hypertrophy LV dysfunction and failure

- Leung et al. AJRCCM 2001

OSA & HYPERTENSION

Related to intermittent hypoxemia & sympathetic NS activation Hypoxia
potent vasoconstrictor activity of adrenal glands, renal sympathetic & ReninAngiotension system

HPN refractory to maximal medical therapy, 87% have OSA Correction of OSA BP to baseline levels within 1-4 weeks
- Leung. AJRCCM 2001

 The

single

most

important

laboratory

technique for assessment of sleep and its disorders

POLYSOMNOGRAPHY
Method of identifying and evaluating sleepstate and several physiologic variable during sleep
ATS 1989

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

What does Polysomnography measure?

It monitors the multiple physiological characteristics

simultaneously during sleep at night.

It allows assessment of sleep stages and wakefulness, respiration, movements. It monitors physiological or pathological events in sleep. cardio-circulatory functions and body

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

What is monitored in PSG?

Electroencephalogram (EEG) Oximetry

Electrooculogram (EOG)
Chin electromyogram (EMG) Electrocardiogram (ECG)

Leg electromyogram (EMG)

Body position Snoring sensors

Nasal and/or oral airflow Breathing effort (chest and abdomen)

Continuous audio/video monitoring & behavior observation

AASM Practice Parameters for Indications for Polysomnography 2005

How is a sleep study performed?

Patient Hook-up: EEG

EEG Electrode Application

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

EEG Electrode Application

EEG Electrode Application

EOG Electrode Application

Record eye movement activity Vicinity of right and left outer canthus

 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)

Chin EMG Application

Mental-submental derivation Electrode placed directly over chin, referenced to electrode placed 2-3 cm off midline, slightly below jawbone

ECG Electrode Application

Single-channel ECG Electrodes over right clavicle and lower left thorax

Leg EMG Electrode Application

Anterior tibialis muscles of each leg Less precise than scalp and facial derivations

Respiratory Transducers
Respiratory tracings represent indirect, qualitative measures of respiratory airflow and effort
Thermal airflow sensors Nasal cannula pressure transducers

Oximetry
Pulse oximeter connected to polysomnograph Periodically check readings with a regular pulse oximeter

Snoring Monitoring
Monitored by placing a microphone on the patients neck

Technical Filter Settings

Low Frequency Filter 0.3 Hz 0.3 Hz 0.3 Hz High Frequency Filter 35 Hz 35 Hz 70 Hz

EEG EOG ECG

EMG Snoring Respiration

10 Hz 10 Hz 0.1 Hz

100 Hz 100 Hz 15 Hz
AASM 2007

Reading and Interpretation

PSG FEATURES OF WAKE (W)

EEG Characteristics
Alpha rhythm (frequency: 8-13 Hz) over the

EOG

EMG

Eye blinks; REMs Elevated chin

occipital region with eye closure, attenuating with eye opening.

EMG tone activity

PSG FEATURES OF NREM SLEEP

Stage
N1

EEG Characteristics
Low voltage mixed frequency

EOG
SEMs

EMG
Tonic EMG

(LVMF) background activity (4-7Hz)

Vertex waves (biphasic sharp transients, maximal centrally)

activity, less
than in the awake state

N2

LVMF background activity

Sleep spindles (distinct waves,

No EMs

Low level
tonic EMG

11-16 Hz, > 0.5s long); K-complexes

(biphasic vertex waves, > 0.5s long) N3 High voltage slow wave (HVS) No EMs

activity
Low level

activity: 0.5-2 Hz, > 75mV

amplitude over frontal regions

Tonic EMG
activity

PSG FEATURES OF REM SLEEP

EEG Characteristics LVMF background activity
Sawtooth waves: 2-6 Hz Usually occurring with phasic REMs

EOG Phasic REMs

(occur with bursts of phasic EMG)

EMG Low chin

EMG tone activity

SLEEP RELATED APNEA

(Apnea 10 sec. & 5/hr of sleep)

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 OSA
ATS, 1989

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

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

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 the same consequences

Mixed Apnea

Hypopnea
Reduced airflow, usually for more than 10 seconds Many labs require at least a 50% reduction in flow; 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

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 Limb movements

Scored only during sleep when > 50% of an epoch is obscured by movement artifact 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 in sleep only when there are > 4 limb movements in sequence occurring > 5s but < 90s apart.

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 <50%) associated with > 4% oxygen desaturation

PLMS

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

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 combined apneas 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 nonperiodic limb movements per hour of TST

Clinical Event Parameters

Spontaneous arousal index: number of arousals that occur which are not associated with any other clinical event Arousal index (AI): number of all arousals per hour of 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.

Obstructed Airway

OSA with closed upper airways

Snoring with partially close upper airway

Effects of CPAP

CPAP: opening of the upper airway

Before CPAP Titration

After CPAP Titration

Nasal Mask CPAP

Full-face Mask

Chin Straps

CPAP Machine

Supplemental Oxygen Therapy in Sleep 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 and supplemental 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 signs of CO2 retention are present
the patient is unable to tolerate nasal PAP therapy & is experiencing significant desaturation with respiratory events

PRECAUTIONS for Suplemental 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 to breathe

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

Laugh and the world laughs with you, snore and you sleep alone.
Anthony Burgess English novelist, critic

Thank You

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

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
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
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)

Obesity

PHYSICAL FINDINGS IN OSAS

BMI (>25) neck circumference
large edematous uvula low hanging soft palate large tonsils & adenoids retrognathia micrognathia hypertension cardiac arrhythmias evidence of CHF

In some patients

LABORATORY ASSESSMENT OF OSAS

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 Test

to document objectively excessive sleepiness pathologic sleepiness mean sleep latency less < 5 minutes

LABORATORY ASSESSMENT OF OSAS

Imaging Studies
CT Scan & MRI to measure cross sectional areas of upper airway & to assess maxillomandibular deficiencies

Pulmonary Function Test

to exclude intrinsic bronchopulmonary disease

Other Test
ECG test for hypothyroidism

SMOKING AND OSAS

Prevalence = 35% Stimulant effects of nicotine stimulates upper airway musculature & upper airway resistance Nightly nicotine withdrawal can sleep instability
- Kashyap. Sleep and Breathing, 2001

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

PATHOPHYSIOLOGICAL EFFECTS OF OSA ON THE CV SYSTEM

Acute Effects
myocardial oxygen delivery myocardial oxygen demand
arousals from sleep Sympathetic NS activation in LV afterload heart rate
negative intrathoracic pressure BP

intermittent hypoxia decrease cardiac output

nocturnal myocardial ischemia nocturnal pulmonary edema cardiac arrhythmias

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

platelet aggregability and blood caogulability

LV hypertrophy LV dysfunction and failure

- Leung et al. AJRCCM 2001

OSA & HYPERTENSION

Related to intermittent hypoxemia & sympathetic NS activation Hypoxia
potent vasoconstrictor activity of adrenal glands, renal sympathetic & ReninAngiotension system

HPN refractory to maximal medical therapy, 87% have OSA Correction of OSA BP to baseline levels within 1-4 weeks
- Leung. AJRCCM 2001

OSA & STROKE

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

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

Mechanisms:
systemic hypertension ischemia & reduced contractility due to hypoxia cardiac myocytes injury due to cathecolamine stimulation CPAP for 1 month dramatic improvement in LVEF (37 to 49%) & cardiac functional status

- Leung. AJRCCM 2001

Indications for Cardiopulmonary 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

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

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)
AASM Practice Parameters for Indications for Polysomnography 2005

Indications for Polysomnography

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)

AASM Practice Parameters for Indications for Polysomnography 2005

Indications for Polysomnography

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

AASM Practice Parameters for Indications for Polysomnography 2005

Indications for Polysomnography

Follow-up polysomnography is routinely indicated for the assessment 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.

AASM Practice Parameters for Indications for Polysomnography 2005

Indications for Polysomnography

Follow-up polysomnography or a cardiorespiratory (Type 3) sleep study is not routinely indicated in patients treated with CPAP whose symptoms continue to be resolved with CPAP treatment. (Option)

AASM Practice Parameters for Indications for Polysomnography 2005

Indications for Polysomnography

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)

AASM Practice Parameters for Indications for Polysomnography 2005

Indications for Polysomnography

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)

AASM Practice Parameters for Indications for Polysomnography 2005

Indications for Polysomnography

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)

AASM Practice Parameters for Indications for Polysomnography 2005

Indications for Polysomnography

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 a reasonable suspicion that OSA or CSA are present. (Guideline)

AASM Practice Parameters for Indications for Polysomnography 2005

Oral Appliances for OSA