Obstructive sleep apnoea
Snoring is defined as a rough rattling noise made on inspiration during sleep by vibration of the soft palate and the uvula. On inspiration, air on its way to the lungs travels by the tongue, soft palate, the uvula and the tonsils. In awake persons the muscles at the back of the throat tightens to hold these structures in place and prevents them from collapsing and vibrating in the airway. During sleep, the soft palate and uvula may vibrate causing the sounds of snoring. Snoring occurs nearly in a third of adults.
Sleep disordered breathing an overview:
This condition encompasses a spectrum of disorders with implications in many fields of medicine. The following are the spectrum in the order of increasing significance:
Upper airway resistance syndrome
Obstructive sleep apnea hypopnea syndrome
This is defined as a cessation of breathing for 10 seconds. In obstructive sleep apnea, the apneais accompanied by observed ventilatory effort (rise and fall of chest).
Sleep disordered breathing is represented by snoring. Rarely snoring could be totally benign, occuring as a consequence of a removable cause like nasal congestion, excessive fatigue, abnormal sleep position, CNS depressants etc.
It should be stressed that snoring indicates an underlying pathological change that is indeed more significant than the auditory annoyance of one's bed partner.
This is a respiratory sound, typically occurring during inspiration or expiration, and is generated in the upper airway during sleep. Simple snoring, noted by the bed partner has no clinical sequelae. These patients dont experience daytime somnolence. These patients usually benefit from weight reduction, positional modification during sleep or by using an oral appliance.
If a patient with snoring presents with comorbid hypertension / daytime excessive sleepiness then it is an indication for further investigation.
Also known as respiratory effort related arousal. This occurs when upper airway narrowing has led to an increased respiratory effort. This extra effort could stimulate arousal. This can be identified from the EEG of a polysomnagram. This is assumed to impact daytime sleepiness. When patients are noted to have several RERAs with clinically insignificant Apnoea-Hypopnoea index then Upper airway resistance syndrome (UARS) should be suspected.
Upper airways resistance syndrome indicates a middle ground between obstructive sleep apnea and primary snoring. Thesee patients dont have overt sleep apnoea and may not even snore, but still can't get a good night's sleep.
These patients may demonstrate anthropomorphic abnormalities with decreased posterior airspace with retrodisplacement of the tongue. Air flow is limited, but subsequent apnea / hypopnea is minor and dont cause concomitant oxygen desaturation.
This condition is also associated with esophageal pressure changes as per the sleep study conducted with esophageal pressure monitor. Daytime sleepiness is a consequence of disturbed, but not apneic sleep.
This is defined as a cessation of breathing for 10 seconds. In obstructive sleep apnoea, the apnea is accompanied by observed ventilatory effort (chest rise and fall). In central apnea no ventilatory effort is seen. Pure central apnea is rather rare.
A mixed apnea is a disordered breathing that begins as a disordered breathing event that begins as a central apnea and ends as an obstructive one.
Hypopnea episode is a partial reduction in ventilation with continued effort for at least 10 seconds. The criteria for hypopnea can vary between laboratories, a general definition is a reduction of 30% in airflow from baseline level plus a 4% or greater decrease in oxygen saturation.
AHI also kown as Respiratory disturbance index (RDI):
Also known as Apnoea-Hypopnea index is the cornerstone which helps to place a patient on the sleep apnoea spectrum. AHI is actually the sum of apneas plus hypopneas in 1 hour of sleep. The severity of apnea is not measured by AHI alone (other factors like clinical presentation, daytime sleepiness, hypoxemia, sleep fragmentation, and presence of arrhythmias should be taken into account).
Classification of OSA severity:
1. AHI of less than 5 is normal
2. AHI of 5-14 is classified as mild apnea
3. AHI of more than 30 is classified as severe apnea
Eventhough respiratory disturbance index is similar to AHI there are certain miunor differences. AHI measures total sleep time and averages the number of apneas and hypopneas per hour. RDI uses total recording time (which includes awake time in the sleep lab). RDI may also include RERA which AHI strictly excludes.
AHI does not factor the degree of oxygen desaturation or the number of arousals thoroughout the night.
Is defined as transient awakening from sleep as a result of apnoea or respiratory efforts.
It is the number of arousal events in one hour. Less than four is normal.
Multiple sleep latency test or nap study:
Patient is given 4-5 scheduled naps usually in the daytime. Latency period from wakefulness to the onset of sleep and rolling eye movement sleep are measured. This test is performed when narcolepsy is suspected or daytime sleepiness is evaluated objectively.
Mechanism of snoring:
During the muscles of pharynx are relaxed and cause partial obstruction. Breathing against obstruction causes vibrations of soft palate, tonsillar pillars and tongue base producing the sound. Sound intensity could be as high as 90dB.
Snoring could be primary (without association with OSA). Primary snoring is not associated with excessive daytime sleepiness and has apnoea-hypnoea index of less than 5.
Causes of snoring:
1. Adenotonsillar enlargement (common in children)
2. Deviated nasal septum
3. Turbinate hypertrophy
4. Nasal valve collapse
5. Nasal polypi / tumors
6. Elongated soft palate
7. Elongated uvula
8. Tonsillar enlargement
11. Laryngeal stenosis
12. Omega shaped epiglottis
13. Obesity with a thick neck
14. Use of alcohol, sedatives and hypnotics
Sites of snoring:
Sites affected in snoring could be soft palate, tonsillar pillars or hypopharynx. The site could vary from patient to patient and even in the same patient multiple sites can be involved.
Physiology of sleep:
Normal healthy adult sleeps for 7-8 hours a day. Sleep is known to occur in two phases i.e. non-REM and REM. These two phases occur in semiregular cycles, each cycle lasting for about 90-120 mins. There are thus three to four cycles of sleep.
This is also known as non rapid eyemovement sleep. It constitutes about 80% of sleep time.
This involves transition from wakefulness to sleep. It constitutes 2-5% of sleep. EEG shows decrease of alpha and increase of theta waves. There is loss of muscle tone. A person can be easily aroused from this stage.
This stage is characterized by sleep spindles or 'K' complexes and decrease in muscle tone. It constitutes about 50% of sleep
This stage forms 3% of sleep andd is characterised by delta waves. It is deep sleep.
This forms 10% of sleep characterized by delta waves. It is deep and most restful sleep.
This forms 20-25% of total sleep. This is characterized by rapid eye movements, increased autonomic activity with erratic cardiac and respiratory movements. Dreaming occurs in this stage, muscular activity is decreased.
Obstructive sleep apnea syndrome:
This is defined as a chronic respiratory sleep disorder typified by recurrent episodes of partial or complete upper airway obstruction during sleep that cause cessation of airflow in the presence of respiratory effort. These episodes cause repeated arousals and fragmented sleep and could be due to various anatomic and physiologic dysfunctions.
1. Restless sleep and snoring (this is observed in nearly 90% of these patients)
2. Sleep disruptions
4. Esophageal reflux
6. Heavy sweating
Day time symptoms:
1. Excessive daytime somnolence. This symptom is observved in 70% of patients. Motor vehicle accidents are a significant concern in patients with OSA.
2. Morning headaches
3. Sexual dysfunction
4. Hearing loss
5. Automatic behavior
6. Short term memory loss
7. Hypnogenic hallucinations
Patient's bed partner gives more reliable information than the patient. History should include snoring during sleep, restless disturbed sleep, gasping, choking or apnoeic events and sweating.
In the daytime there is history of excessive sleepiness and fatigue as measured by Epworth sleepiness scale, irritability, morning headaches, memory loss and impotence. The body position of the patient during sleep should also be elicited, intake for alcohol, and sedatives should be sought.
Epworth sleepiness scale:
Situation Score (0-3)
Sitting & reading
Sitting inactive in a public place
Passenger in a car for 1 hour
Lying down to rest in the afternoon
Sitting and talking to someone
Sitting quietly after a lunch without alcohol
Sitting in a car while stopped in traffic for a few minutes
0 - Never doze off
1 - Slight chance of dozing off
2 - Moderate chance of dozing off
3 - High chance of dozing off
Examination should include:
Body mass index:
This is calculated by dividing the body weight in kilograms by height in meters squared.
18.5-24.9 - Normal BMI
25-29% - Overweight
30-34.9 - Obese
Obese patients should be advised to reduce their body weight.
Neck circumference at the level of cricothyroid membrane is measured. Collar size should not be more than 42 cm in males ad 37.5 cm in females.
Complete head and neck examination:
Examination should look out for tonsillar hypertrophy, retrognathia, macroglossia, elongated soft palate and uvula, base of tongue tumors, septal deviation, nasal polypi, turbinate hypertrophy and nasal valve collapse. Nasopharynx and larynx should also be examined.
This should be performed in all suspected patients with OSA. A flexible endoscope is passed through nose and the patient is asked to inspire vigorously with nose and mouth completely closed. Collapse of soft tissues at the level of tongue base and just above the soft palate should be looked out for. Level of pharyngeal obstruction can be elicited.
Hypertension, congestive cardiac failure, pedal oedema, truncal obesity and any sign of hypothyroidism.
Should be taken for craniofacial anomalies and tongue base obstruction.
This investigation is the corner stone of diagnosis and evaluation of OSA. Polysomnographys is an overnight study that records a multitude of physiologic factors, which includes:
Individual patient studies are performed in a sleep lab wherre the state, quality of sleep in each stage, and the apnea-hypopnea index can be determined.
The following studies need to be performed:
EEG - To assess the brain waves
EMG - To assess the muscle tone
EOG - To assess eye movements
Measurement of airflow, chest and abdominal efforts - To assess respiratory effort
ECG - To assess heart rate rhythm and activity
Pulse oximetry - To assess oxygen saturation
Sleep apnea worsens during REM sleep when the muscle tone of hypopharyngeal and oropharyngeal musculature are at their lowest resulting in an upper airway collapse. Airway obstruction, oxygen desaturation and in severe cases carbondioxide retention can cause arousals from sleep.
Polysomnography can differentiate between primary snoring, pure OSA and central sleep apnoea.
Split night polysomnography:
In this study the first part of the night is used in usual polysomnography while the second part of night is used in titration of pressures for continuous positive airway pressure. This procedure is not recommended because episodes of sleep apnoea occur more often in second hald of night and are thus missed. Titration of pressures for CPAP should ideally be done on a second night.
Physiologic changes of sleep affect multiple systems including CVS, CNS, RS, GI, Thermoregulatory and Endocrine systems.
CVS changes are controlled by autonomic nervous system. Generally vagal tone increases and sympathetic input decreases throughout the night causing the below stated changes:
1. Heart rate and blood pressure decreases during NREM sleep.
2. Further decreases in HR and BP occurs during tonic REM sleep.
3. HR and BP increase during phasic REM
4. Cardiac dysrhythmias may diminish / disappear during sleep, premature ventricular contractions increase during REM sleep.
1. Blood flow to the brain increases during sleep and is higher during REM sleep
2. Intracranial pressure and temperature increase during REM sleep and decrease during NREM sleep. These differences indicates variations in the metabolic activity of the brain.
1. Respiration becomes fully involuntary
2. Ventilatory control becomes manily driven by carbondioxide levels. The partial pressure of carbondioxide rises by 4 mm of Hg during sleep. In a healthy person this increase is physiologic; but however in a patient wiht lung disease, this increase may result in significant oxygen desaturation. Chemical responses to hypoxia and hypercapnia decrease in NREM and decrease still further in REM sleep. This is the reason why OSA is most severe during REM sleep.
3. Decrease in tidal volume causing overall decrease in ventilation
4. In NREM sleep, respiratory rate, tidal volume, and minute ventilation decrease, leading to an increase in end-tidal carbondioxide and a decrease in oxygen saturation.
5. During REM sleep, respiration may be rapid and irregular
6. Upper airway resistance increases by up to 7 times that of waking levels, Muscle tone is lost, especially in the intercostal and pharyngeal muscles; however the diaphragm maintains its tone
7. Mucociliary clearance of alveolar oxygen tension and arterial oxygen tension decreases. The decrease in Pao2 is normally less than 2%.
8. Patients with sleep disturbances experience arousals due to laboured breathing. The exact stimulus for arousal is unknown, but mechanoreceptors in the upper / lower airway or the diaphragm may be responsible.
1. Gastric acid secretion generally increases during sleep and peaks during REM sleep
2. Swallowing and esophageal motility deceases during sleep
Thermoregulatory system changes:
1. During REM sleep thermoregulation and perspiration are absent. Body becomes cold blooded.
2. Overall body temperature decreases during sleep
Endocrine system changes:
1. Growth hormone levels peak during early hours of sleep and gradually deline
2. Prolactin levels are affected by sleep and increase during both nocturnal and daytime sleep
3. TSH levels tend to decrease during sleep coinciding with the decreased metabolic needs off the body during sleep.
4. Melatonin and cortisol levels are affected by circadian rhythms but not by sleep itself.
Risk factors of sleep apnoea:
1. Obesity - 10% increase in weight is associated with 6 fold risk of developing sleep disordered breathing.
2. Sex - OSA affects men commonly. The incidence in women increases after menopause
3. Obstruction - Upper airway may be obstructed at any level. Mallampati classification scale can be used to help in classifying this category
4. Neck circumferance - A neck circumference of more than 43 cm is a predictor for an increased apnea-hypopnea index
5. Pulmonary disease - COPD and restrictive / neuromuscular diseases of lungs can cause airway problems
6. CNS depressents like alcohol and sleeping pills cause more relaxed airway with propensity to collapse
7. Tobacco use
9. Acromegaly (due to macroglossia)
10. Supine position during sleep
11. Cranofacial anomalies and previous trauma that affects upper airway function / patency
Apnoea clusters and oxygen desaturation:
OSA are often known to occur in clusters. Oxygen desaturation occurs with each apnea. The end of the apnea sequence typically ends with a brief (less than 3 seconds) EEG arousal. In patients with severe OSA, the cluster of apnoeas occurs throughout sleep. The desaturation from the first apnoea is typically associated with a higher desaturation percentagge change than subsequent apneas in the series.
1. Life style changes - Patients with mild disease and minimal symptoms can be treated with weight loss and dietary restrictions.
2. Alcohol use should be avoided
3. Smoking to be avoided
4. Positional therapy - Patient should sleep on the side as supine position may cause obstructive apnoea. A rubber ball can be fixed to the back of shirt to prevent the patient from assuming supine position.
5. Intraoral devices- These devices alter the postion of the mandible / tongue to open the airway and relieve snoring and sleep apnoea. Mandible advancement device keeps the mandible forward while tongue retaining device keeps tongue in anterior position during sleep. Mandibular advancement device is useful in retrognathic patients.
6. CPAP - Provides peneumatic splint to airway and increases its calibre. Optimal airway pressure for the device to open the airway is determined during sleep study and is usually keptat 5-20 cm of water. About 40% of patients find the use of CPAP device cumbersome and difficult to carry with them when travelling.
If CPAP is not tolerated, a BiPAP (bilevel positive airway pressure) device can be used. It delivers positive pressure at two fixed levels - a higher inspiratory and a lower expiratory pressure.
Is indicated for failed conservative therapy.
This is the gold standard of treatment but is not acceptedd socially because of its complications
Advancement genioplasty with hyoid suspension
Tongue base radiofrequency ablation
Maxillomandibular advancement osteotomy
Static & dynamic factors involved in the pathophysiology of sleep disorders:
Both statis & dynamic factors are involved in the development of OSA. Static factors include:
1. Surface adhesive forces
2. Neck & jaw posture
3. Tracheal tug
4. Gravity - Gravitational forces can be felt simply by tilting the head back to where the retropositionof the tongue and soft palate reduces the pharyngeal space.
Any anatomic feature that decreases the size of pharynx (eg. retrognathia) increases the chance of development of OSA. For most patients OSA worsens in the supine sleeping position.
An important static factor that has been found in patients with OSA is the reduced diameter of the pharyngeal airway in wakeefulness in OSA patients compared with that of non-OSA patients. In the absence of craniofaial abnormalities, the soft palate, tongue, parapharyngeal fat pads, and lateral pharyngeal walls are enlarged in OSA patients.
1. Nasal / Pharyngeal airway resistance
2. Bernoulli effect
3. Dynamic adherence
Bernoulli effect plays an important role (dynamic) in OSA pathophysiology. According to this effect, when the airflow velosity increases at the site of stricture in the airway, the pressure on the lateral wall decreases causing airway collapse in that region. This effect is exaggerated in areas where the airway is most compliant. This effect helps partially to explain whey obese patients (with excessive fat deposition) around the neck are most likely to have OSA.
The cross sectional area of the airway in patients with OSA is smaller that that of people without OSA.