Sleep Study(Polysomnography)
By
Hatem Ezz eldin Hassen MD Consultant of Phoniatrics KFHJ
DIAGNOSIS
History: Snoring
Obstructive episodes Arousals /nocturnal choking Excessive daytime sleepiness
Abnormal motor movements Morning headaches
Nasal obstruction Weight gain Drugs: alcohol intake
Cardiovascular symptoms Respiratory symptoms
Thyroid symptoms Social history
Examination General appearanceWeightHeightBlood pressureCraniofacial morphologyNasal airway
Tongue size ,Soft palate/uvula/tonsilsNasopharynx - adenoids / polyps / cyst / tumorHypopharynx-lingual tonsils/vallecula, epiglottic or supra-glottic cysts / tumourLarynx-vocal folds mobility
Investigations:
To assess the patient's general condition
To differentiate between simple snoring and sleep apnea and determine the presence, type and severity of any apneas or hypopneas and,
To assess the site of airway obstruction obstruction
Investigations Polysomnography Lateral cephalometry Naso-optic fibroscopy (Muller’s maneuver)
Sleep nasendoscopy Computed tomography (CT)
Magnetic resonance imaging (MRI)
Acoustic reflection technique Pharyngeal manometry Acoustic analysis of snoring sounds
*is the gold standard investigation in the diagnosis of OSAS and other forms of sleep related disorders.*multiple simultaneous recording of physiologic measures during sleep.
Polysomnography
PHYSIOLOGY OF SLEEP
Normal sleep entails a cyclical progression from non rapid eye movement sleep (N-REM) to rapid eye movement sleep (REM) with a periodicity of 90-120 minutes.
During N-REM sleep, subjects pass through 4 stages which represent progressively deeper sleep states.
During REM sleep, increased movements and EEG activity occurs with characteristic eye movements. Dreaming & Obstructive episodes are likely to occur during REM sleep
A normal young adult would spend 5 % of the night in stage 1, 45 % in stage 2, 15 % in stage 3, 10 % in stage 4, and 25 % in REM sleep (Baker, 1986).
PHYSIOLOGY OF SLEEP
Polysomnography
Electroencephalogram (EEG).
Submental electromyogram (EMG).
Electro – oculogram (EOG) : These three measurement are needed for
sleep staging and allow differentiation between sleep and wakefulness.
Oxygen saturation (PO2): by Modern pulse oximeters
Electrocardiogram (ECG) : To monitor apnea associated arrhythmias.
Nasal and oral airflow: airflow is usually detected using heat sensitive thermoisters. These are not able to
quantify airflow but simply detect its presence or absence. Absence of airflow for greater than 10 sec. Will be
counted as an apnea.
Chest and abdominal movement: patients wear an elasticized belt around the chest and abdomen into witch
are incorporated strain gauges that measure changes in circumference. This information allows differentiation
between central and obstructive apnea.
Anterior tibialis EMG: Allows the diagnosis of “periodic movements during sleep”
Sleeping position detector :
Sleep Lab
A: Central apnea B: Obstructive apnea
A
B
Polysomnography
Snoring: is a noise generated from the upper airway due to partial airway obstruction
An apnea: is the cessation of airflow at the nostrils and mouth for at least 10 seconds.
The apnea index (AI): is the number of apneas per hour of sleep. Hypopnea: a decrease in airflow associated with oxygen desaturation The apnea Hypopnea index (AHI): apneas + Hpopneas per hour of sleep The respiratory disturbance index (RDI): the total number of
obstructive apneas, hypopneas, and central apneas per hour. The sleep apnea syndrome (SAS): 30 or more apneic episodes during a 7-hour
period of sleep or an apnea index equals to or greater than 5.
The American sleep association grades sleep apnea as follows:
Mild: (AHI 5-15) Moderate: (AHI 5-30) Severe: (AHI >30).
Sleep Related Breathing Disorders - Definitions
Sleep Related Breathing Disorders - Definitions
Obstructive sleep apnea: The cessation of airflow in the presence of continued respiratory effort . Due to Upper airway obst.
Central sleep apnea: No flow of air at the nose or mouth associated with a cessation of all respiratory effort. These patients may or may not snore. Heart failure, frontal lobe damage or brain- stem lesions. Often no apparent cause, and it is thought to be related to instability of the respiratory control mechanisms.
Mixed apnea: this usually begins as a central apnea with no airflow or respiratory effort followed by increasingly forceful respiratory efforts again with no airflow until airway clears.
Obstructive apnea is more common than central apnea though any individual may demonstrate one or more of the above forms of apneas during a night's sleep.
Upper Airway Resistance Syndrome
Episodes of marked partial upper airway obstruction but, no complete obst. of the airway. They are able to maintain their oxygen saturation but need so much respiratory effort to overcome the partial obstruction that they induce frequent micro arousals
They usually have symptoms similar to those with OSA.
Treatment of UARS is similar to that of OSA; the use of CPAP usually is effective.
Main difference between UARS and OSA is the there is no hypoxia related to UARS.
PolysomnogramAfter complete sleep study the following
information is scored:
Lights out Sleep Latency – from lights out to onset of
sleep Sleep Stages
Non-REM – N1, N2, N3 REM
Sleep Efficiency – percentage of time asleep Respiratory Events Leg Movements Arousals Heart Rhythms Snoring intensity Lights on Quality of patient’s sleep compared to baseline
Scoring Respiratory Events
Apnea – when all of the following criteria are met1) There is a drop in the peak thermal sensor
excursion by >90% of baseline2) The duration of the event lasts at least 10
seconds3) At least 90% of the event’s duration meets the
amplitude criteria for apnea4) Classified as: obstructive, central, or mixed
based on respiratory effort
Hypopnea – when all of the following are met1) The nasal pressure signal excursion drops by
30% of baseline2) The duration of this drop occurs for a period of
at least 10 seconds3) There is a 4% desaturation from pre-event
baseline4) At least 90% of the event’s duration meets the
amplitude criteria
The AASM Manual for the Scoring of Sleep and Associated Events, 2007
Hypercapnic CSAImpaired Central Drive ("Won’t Breathe"):
1-Tumors or trauma-induced lesions to brainstem
2-congenital central hypoventilation syndrome (Ondine curse)
3-opioid-induced CSA
4 -OHS Impaired Respiratory Motor Control ("Can’t
Breathe")
1-myasthenia gravis
2-amyotrophic lateral sclerosis
3-post-polio syndrome 4-myopathies
5-Chest wall syndromes such as kyphoscoliosis
PSG Indications: Nonrespiratory Disorders
A PSG preceding an MSLT is indicated for evaluation of suspected narcolepsy or to help differentiate narcolepsy from idiopathic hypersomnia.
PSG is indicated for evaluation of suspected periodic limb movement disorder but NOT the restless legs syndrome (RLS; a clinical diagnosis).
A PSG is indicated to evaluate (1) nocturnal behavior possibly due to seizures, (2)atypical parasomnia behavior (frequent episodes each night ,stereotypic behavior, or behavior unusual for age), (3) nocturnal behavior/parasomnia that has resulted in injury to the patient or others
Portable Monitoring for OSA in Adults
Types of Monitoring Devices
Type 1 – in sleep center, attended, overnight polysomnogram
Type 2 – record same variables as type 1, unattended (at home)
Type 3 – evaluate four physiologic parameters – not sleep
respiratory movement and airflowheart ratearterial oxygen saturations(snoring), (position)
Type 4 – evaluate one or two parameters (saturation and airflow)
Approach to Reading the PSG
Before the PSG is read, a review of the clinical history with special attention to symptoms of sleep apnea, narcolepsy, RLS, and medications is very useful.
The presence of underlying lung disease may help explain a low awake arterial oxygen saturation (SaO2) or low baseline sleeping SaO2.
A clinical history of pacemaker insertion or known atrial fibrillation is also very helpful in providing a useful interpretation of ECG findings.
All digital PSG systems have a view that shows graphical summary information of the entire night. It is often useful to look at the big picture before going through the data in smaller time windows.
Tips for the clinician:
• The clinician should recognize that many patients with significant OSA do not complain of daytime sleepiness.
• A history of snoring and gasping would suggest a PSG is indicated.
• It should also be noted that some patients with OSA complain of insomnia.
• A PSG for PAP titration is the standard procedure to select a level of pressure for treatment.
• The titration can be performed on a separate night after
a diagnostic PSG or during the second part of the night during a split (partial night) study.
POLYSOMNOGRAPHY
Indications of Split Study: (1) AHI > 40 /hr with at least 2 hours of
monitoring, (2) AHI of 20 to 40 with special clinical
circumstances such as severe desaturation or arrhythmia thought due to OSA
(3) at least 3 hours remain for the PSG titration.
Indications of PSG Repeat: Time for CPAP titration is < 3 hours If the patient is being treated on CPAP and is
NOT doing well, a repeat PSG study on CPAP is indicated.
PSG is also indicated if a patient on CPAP gains > 10% of body weight to determine whether the pressure is adequate.
DD of OSAS Dyspnea due to pulmonary edema Idiopathic hypersomnia Nocturnal panic attacks Obesity-hypoventilation syndrome (pickwickian
syndrome Simple snoring Asthma Chronic Obstructive Pulmonary Disease Depression Gastroesophageal Reflux Disease Hypothyroidism Narcolepsy Periodic Limb Movement Disorder
Narcolepsy
Classic tetrad of 1- excessive daytime sleepiness (EDS), 2- cataplexy, 3- hypnagogic hallucinations, 4- sleep paralysis. Narcolepsy is thought to result from genetic predisposition, abnormal neurotransmitter functioning and sensitivity, and abnormal immune modulation. Diagnosis The combination of an overnight polysomnogram (PSG) & a multiple sleep latency test (MSLT) showing sleep latency 8 minutes or less and 2 or more sleep-onset random eye movement (REM) periods strong suggests narcolepsy An alternative criterion is a cerebrospinal fluid hypocretin level of 110 pg/mL or less.
Restless Legs Syndrome
Periodic leg movements of sleep [PLMS]).
PLMS are characterized by involuntary, forceful dorsiflexion of the foot lasting 0.5-5 seconds and occurring every 20-40 seconds throughout sleep.
excessive daytime somnolence sleep disturbances, daytime fatigue, and
involuntary, repetitive, periodic, jerking limb movements (either while the patient is asleep or while he or she is awake and at rest). A positive family history also aids in the diagnosis of RLS, especially in children.
Thank You
Polysomnography
Measurements Pulse ox, EEG, EOG, ECG, EMG,
oral/nasal airflow, respiratory effort, limb/body movements
Definitions Apnea – lack of ventilation for ≥10 sec with
signs of arousal Hypopnea – decrease in respiratory
movement with a drop in O2 sat or with signs of arousal
AHI or RDI =(Apneas + Hypopneas)/hours of sleep
Important parameters RDI Lowest O2 saturation Number of desaturations below 90% Length of time below 90%
Medical Management
CPAP Pressure must be
individually titrated Compliance is as
low as 50%Air leakage, eustachian tube dysfunction, noise, mask discomfort, claustrophobia
PORTABLE MONITORING (HOME SLEEP TESTING, OUT OF CENTER SLEEP
TESTING) The tests are not always performed in the
home ;hence, the terms HST or PM are not ideal but are used in much of the literature on this subject.
In the past, PM has been used to diagnose OSA in settings in which access to PSG is limited or delayed.
The original classification used “level I, II, III, and IV” to refer to different classes of monitoring but currently the terminology is “type 1, 2, 3, and 4.”
The Centers for Medicare and Medicaid Services (CMS) has a different classification for monitoring The CMS terminology defines the respiratory disturbance index (RDI) as the total number of apneas and hypopneas per hour of monitoring time. Therefore, the index determined by PM (no EEG) would be an RDI using the CMS definition. CMS also refers to PM as HST.
Medical Management
BiPAP Useful when > 6 cm H2O
difference in inspiratory and expiratory pressures
No objective evidence demonstrates improved compliance over CPAP
Portable Monitoring for OSA in Adults
Limitations of Type 3 devices
Apnea Hypopnea Index – abnormal breathing events by recording time as sleep can not be recorded
Unless the patient was sleeping the entire recording time, the AHI calculated by a portable monitor will likely be lower than an attended polysomnogram
Can not distinguish sleep stages
Friedman algorithm for treatment
Mild (AHI 5-15) Symptomless: behavior modification Symptoms: behavior, device, consider
surgery Moderate (AHI 15-30)
Symptomless: behavior, device Symptoms: device, consider surgery for
device failures Severe (AHI >30)
Device, consider surgery as adjunct, refer for bariatric surgery BMI>40, consider tracheostomy
Sleep disordered breathing (SDB) is characterized by repetitive episodes of diminished and cessation of breathing during nocturnal sleep (Block et al, 1980).
The spectrum of SDB ranges from chronic snoring and upper airway resistance syndrome to obstructive sleep apnea (Guilleminault et al., 1991).
Grades of Sleep Apnea Severity
The severity of OSA was determined by the (AHI)
Mild: AHI 5-15 Moderate: AHI 15-30 Severe: AHI greater than 30
Obstructive Sleep Apnea
Respiratory Disturbance Index (RDI) – no longer used
apneas, hypopneas, respiratory related arousals
Apnea-Hypopnea Index (AHI) total number of respiratory events /
hours of sleep
Severity of OSA defined by the AHI:
< 5 – not sleep apnea5 – 15 – MILD15 – 30 – MODERATE
> 30 – SEVERE
Diagnosis of the site of upper airway obstruction:
Muller’s Maneuver Sleep endoscopy Fluoroscopy Manometry Cephalometrics Dynamic CT scanning and MRI
scanning Mallampati Airway Classification Friedman Classification
The report can include a measure of the sleep onset time (latency) and the proportion of sleep time spent in each of the sleep stages.Obstructive sleep apnea is characterized by absence of airflow at the nose and mouth despite the presence of respiratory effort (thoracic and abdominal). is caused by a structural narrowing of the upper airway that becomes manifest when muscular tone diminishes during sleepcentral sleep apnea, the patient’s airway is normal, but airflow is absent because of an absence of respiratory effort. Central apnea is caused by a neurological defect in the control of respiration, such as with bulbar poliomyelitis, degenerative neurological diseases, intracranial neoplasm, brain stem infarction, narcotic or sedative overdose, bilateral cervical cordotomy,Mixed apnea is diagnosed when elements of central control and obstruction are both found to be contributing to the apnea. It is generally classified with the predominating element. However, in many cases of advanced obstructive sleep apnea, a central element is notable
Sleep Disordered Breathing Primary snoring
RDI < 5 No daytime sleepiness
Upper airway resistance syndrome (UARS) RDI < 5 Arousal Index > 5
Obstructive sleep apnea syndrome (OSAS) RDI > 5 O2 desaturation < 90%
Obesity hypoventilation syndrome (Pickwickian) BMI >30 kg/m2
Daytime hypercapnia w/ PaCO2 ≥ 45mmHg Sleep disordered breathing