Sleep apnea syndrome

SLEEP APNEA SYNDROMES
The mysteries of sleep have intrigued man for centuries, it has only been within last three decades that we have begun to understand physiology and physiopatology of this state that occupies a considerable portion of our lives. It was developped a better understanding of specific sleep disorders and their realationship to common medical problems seen during wakefulness. Hypertension (both systemic and pulmonary), cardiac arrythmias, headaches, and depression are just a few of the clinical entities that have recently been associated with sleep-related The physician often focuses on the management of the secondary effects without A common example is the middle-aged male presenting with vague complaints Physical examination reveals only mild hypertension. Paradoxally, most patients with sleep apnea syndromes do not realize that they Sleep apnea syndromes are a group of disorders characterized by periodic cessation of respiration and nocturnal sleep arousals. An apneic episode is defined as a cessation of airflow at the nose and mouth lasting longer than 10s. The diagnosis of sleep apnea syndrome is entertained when 30 or more episodes occur during 6 hours of sleep. The severity of the syndrome is usually quantitated by the apnea index (number
of apneic periods per sleep hour) and hypopnea index (number of hypopneic events per
SLEEP PHYSIOLOGY
Although the etiology of the human need to sleep is not understood, the mechanics of the sleep experience have been well drfined. Contrary to what used to be thought, sleep is not a simple homogenous state, but is composed of five stages that alternate in a cyclical pattern approximately every 90 REM sleep occupies about 20% of each sleep cycle and is characterised by binoculary synchronous rapid eye movements as well as decreased postural muscle tone, elevated and variable heart and respiratory rates, incresed body temperature, and elevated systolic blood pressure. REM sleep is also the stage in which 80% of each cycle is composed of quiet non-REM (rapid eye movement) sleep, from the lightest stage I to the deepest stage IV. NREM is characterised by decreased neuronal activity. In SAS sleep architecture is completly destroyed. CLASSIFICATION OF SAS
1. OBSTRUCTIVE cessation of oronasal airflow despite persistent ventilatory effort. (oronasal airflow is blocked and diaphragmatic efforts continue) cessation of airflow and ventilatory effort. (both diaphragmatic and intercostal efforts cease) initial central, progressing to obstructive pattern. (periods of obstructive apnea follow periods of central apnea) The differences between these three types may seem subtle but are extremely important, especially for therapeutic considerations. OBSTRUCTIVE SLEEP APNEA
Obstructive sleep apnea (OSA) is defined by the occurence of episodic partial of complete occlusion of the upper airway (usually at the level of the oropharynx) during sleep. These episodes may lead to the development of various mental or physical - 1% to `16% among adult men,
- 1% to 5% among adult women.
The aerodigestive tract is composed of both rigid and compliant structures. Abnormal anatomic and physiologic function of the structures from the nose to the larynx can result in suboptimal aerodigestive funtion and OSAS. With nasal obstruction, there is a large inspiratory pressure drop across the nose, leading to a high subatmospheric pressure at locations within the potentially collapsible There is a situation of disbalance between the dilating and collapsing forces at the pharyngeal level. During the inspiration, intraluminal pressure is negative (subatmospheric) and tends to produce pharyngeal collapse. This force is opposed by the distending action of the pharyngeal muscles, whose tone can decrease during sleep. - male gender (the classic patient with OSA is the male sex ,20:1 - male -female ratio) - obesity (particularly obesity of the upper body football player body habitus - stocky - certain endocrine disorders (hypothyroidism and acromegaly), - Prader-Willi syndrome (a congenital syndrome involving mental retardation, sexual infantilism, polyphagia with obesity, muscular hypotonia), - congenital craniophacial abnormalities (Pierre Robin syndrome). Common symptoms: (results of sleep deprination and hypoxemia)
(the bed partner often complains about disrupted sleep caused by the patient’s loud snoring, it’s often a long history of snoring, usually starting before age 21), (often manifested by falling asleep at inappropriate times - while talking, eating, or even during the physician’s interview; there may be a history of automobile accidents, caused by the patient’s falling asleep at the wheel, or the inability to maintain gainful employment because of suspected laziness), - personality changes (anxiety and depression become obvious), - morning headaches (headaches can be severe and persistent, causing further disruption - deterioration of intellectual functions, Consequences:
The hypoxia resulting from numerous apneic periods causes many secondary effects. The hypoxia may be extreme with arterial oxygen tensions aproaching 20 to 30 mmHg. Despite the fact that each episode of hypoxia lasts only 15 to 20 seconds, the repetitive-nature of the apnea and its frequency result in prolonged hypoxic periods. Many patients have 300 to 400 apneic periods resulting in hypoxia during half of an average night’s sleep, which may have many adverse effects. - excessive daytime somnolence (may increase the risk of work-related and - arterial hypertension (50% of patients) (hypoxia, being a potent vasoconstrictor, results in reactive pulmonary and systemic hypertension; this may be initially transient, occuring only during sleep, yet persistent sleep apnea can result in sustained hypertension; the hypoxia is also a stimulus for production of erythropoietin, contributing to - cardiac arrythmias (48% to 75% of patients) (mediated by metabolic changes of the apnea - increased parasympathetic activity cause a - increased risk of coronary heart disease and - increased risk of heart failure (can result from the increased afterload and the incresed viscosity of - increased risk of cerebrovascular disease (the mechanism by which OSA may attribute to the development of cerebrovascular accidents is - history (the most important clues are uncovered by taking a careful history from both the patient and the patient’s bed partner) - physical examinaton (can be surprisingly unremarkabe; contrary to original reports about the syndrome, less than 10% of patients have typical Pickwickian features- alveolar hypoventilation with elevated carbon dioxide and reduced oxygen tensions, although many are obese; the degree of obesity correlates poorly with the degree of hypoventilation, there is a clear relationship between between excessweight, usually expressed as the body mass index - BMI - and the number of sleep related disturbances; one half to two thirds of patients with SAS have elevated systolic blood pressure; a minority of patients have related anatomic abnormalities: hypertrophy of the tonsils and adenoids in children and malformations of the jaw, such as retrognathia and relative micrognathia or a short, thick neck and jowls are occasionally noted. Acromegaly, goiter, and lymphoma may also cause airway obstuction) - direct observation of the patient during sleep -polysomnography (The polysomnograph is a multichannel recorder with capabilities for monitoring various physiologic parameters; the nocturnal or overninght polysomnogram is the diagnostic gold standard for OSA): (to determine the various stages of sleep), - detection of apnea - thermistor at the nose and mouth or - ENT examination to rule out any structural abnormality that might be causing the obstruction and could possible be corrected - depends on severity of symptoms, the clinical complications and side effects, and the - all patients with AHI over 20 should be treated - a multidisciplinary approach is necessary - weight reduction in obese patients (significant weight loss, however, is difficult to
achieve and only occasionally has a good result, it’s also very difficult to miantain), - avoidance od drugs and alcohol (there is well-proven influence of a number of drugs
on pharyngeal collapsibility - these include alcohol, hypnotics, sedatives, and opioid analgetics; alcohol and hypnotics do not cause obstructive sleep apnea, but rather - relief of nasal obstruction,
- avoidance of sleeping in in the supine posture (it is generally accepted that snoring
increases in intensity when patient lie on their back, rather than on the side or on the belly; we can distinguish also positional SAS), - oral appliances
(are prosthetic devices that either pull the tongue or the mandible forwards creating a prognathism, are used during the night, for sleeping) (in patients with macroglossia or micrognathia) anteriorly and thus reduce the airway obstruction) (the results are rather not so impressive) (have side-effects, such as excessive salivation or temporomandibular arthritis) (is proposed as an alternative for patients unable to tolerate other types of treatment - - nasopharyngeal tube (the idea is that a small bore latex tube, 3-7 mm external
diameter, is passed through the nose by the patient himself in the night; the tube is about 15 cm lenght, so that the tip of the tube rests a couple centimeters above the epiglottis; but few subjects are able to tolerate the nasopharyngeal tube for the whole night, it acts - drug therapy (medroxyprogesterone acetate, protryptiline [20-30mg at bedtime],
- nasal CPAP (continuous positive airway pressure)
(this therapeutic method involves connecting the subject to a blower delivering air at a predetermined positive pressure, that is continuously maintained throughout both phases the connection is generally performed via the nose, with a variety of nasal masks; the possitive pressure acts as a pneumatic splint opening up the occluded pharyngeal airway, and allowin the patient to breathe; the level of pressure required (5-15 cm H20 in most patients) must be individually determined, and must be high enough to eliminate snoring, hypopneas, apneas and sleeping fragmentation; the minimum level at which nasal CPAP must be used should a large variety of commercial nCPAP devices are now available on the market, with an extensive number of masks models for all sizes and forms of nose; the beneficial effects of nCPAP are rapid and spectacular, with almost complete disappearance of sleepiness and nocturia from the first night of therapy; the general rule is that treatment must be applied every night for an undetermined period - nasal BiPAP (bilevel positive airway pressure) (second-generation devices).
(within 24 to 48 hours following this procedure, hypersomnolence and nocturnal arrythmias usually disappear; within a fews months, most patients become normotensive and have reversal of their depression, intellectual teterioration, and virtually all other associated abnormalities; the therapeutic effect is dramatic, often producing a complete change in the patient’s life, which is described as miraculous) - in the past: permanent tracheostomy (within 24 to 48 hours following this procedure,
hypersomnolence and nocturnal arrythmias usually disappear; it was a gold standard for OSA; currently is reserved for severe OSA that does not respond to other forms of Noncompliance
- compliance rate - 77% to 89%
- reasons:
- general discomfort,
- mucosal irritation and epistaxis,
- nasal obstruction,
- feelings of bloatedness due to
- claustrophobia.
air swallowing,
- skin irritation
- air soreness.
- surgical treatment
- UPPP - (the objective is to remove excess or redundant soft tissue of the oropharynx while preserving palatal function; included in the resection are the uvula, part of the muscular portion of the soft palatea and redundant palatal-pillar - transpalatal advancement pharyngoplasty (mandibular-hyoid Three objectives of the treatment:
1. alleviation of symptoms,
2. decrease in morbidity,
3. decrease in mortality
It has been difficult to estimate the mortality of OSAS because various treatment modalities, including nCPAP, tracheotomy, and multiple upper airway procedures, have However, in a study of 385 patients, Hi et al. reported a significantly increased mortality among those with an apnea index greater than 20 as compared with OSAS In another study patients treated that underwent tracheotomy despite the fact that the conservatively managed group had lower mean apnea indexes than the tracheotomized group. After 11 years of follow-up, a statistically significant difference in survival favoring the tracheotomised groups has been reported. Thus, there exists considerable evidence that untreated OSA is associated with increased mortality. SLEEP APNEA SYNDROMES
DIFFERENTIAL DIAGNOSIS
The differential diagnosis, like a disease, is multidisciplinary hypersomnolence (excessive daytime sleepiness)
- periodic leg movements during sleep (nocturnal myoclonus characterised by frequent
leg-jerking during the night that can lead to poor-quality sleep) - narcolepsy, (1.sleep attacks during the day; 2.cataplexy, sudden muscle weakness;
3.hypnogogic hallucinations, the sudden transition from wakefulness to
dreaming (rapid-eye-movement) sleep, causing difficulty distinguishing the dream from reality; 4.sleep paralysis (the loss of muscle strength
normally associated with sleep being extended into the waking state). - chronic fatigue syndrome,
- nonrestorative sleep syndromes,
- alcohol or drug dependence,
- acromegaly,
- hyperthyroidism,
- myotonic dystrophy,
- depressing or hysterical episodes.
THE OVERLAP SYNDROME
- chronic bronchitis and emphysema (with the blue and bloated pattern) combined with - thus it seems reasonable that in a chronic bronchitis who has persistent airways obstruction, daytime hypoxemia, and obesity, that a sleep apnea syndrome be excluded by a step study before providing long term domiciliary oxygen therapy; whereas, in patients who are not obese and give no history to suspect such a condition, this is not necessary before instituiting this expensive treatment; Administration of oxygen to such patients with this overlap syndrome may cause a further rise in pCO2 whereus this is probably a safe procedure to adopt in those who only have chronic bronchitis or emphysema with nocturnal sleep desaturation alone. CENTRAL SLEEP APNEA
Pathogenesis:
- transient abolition of central drive to the ventilatory muscles; the resulting apnea leads
to a primary sequence of events similar to those of OSA - central apneas seem to have a purely neurologic bases; most studies to date implicate a gross impairment of respiratory center chemosensitivity; - damage to the respiratory neurons may follow infectious, vascular, or neoplastic 1. Defects in metabolic control system or respiratory muscles 2. Transient instabilities in central respiratory drive 3. Inhibition of central respiratory drive by upper airway reflexes Clinical features:
- many healthy individuals demonstrate a small number of central apneas during sleep
(particulary at sleep onset and in REM sleep); - recurrent respiratory failure, polycythemia, pulmonary hypertension, right-sided heart - poorly sleeping, morning headache, daytime fatigue and sleepiness. Diagnosis:
- obesity and hypertension are less prominent in CSA than in OSA, - key observation: recurrent apneas that are not accompanied by respiratory effort. Treatment:
- drug therapy - acetazolamid (a carbonic anhydrase inhibitor that stimulates
- low-flow oxygen.
SLEEP APNEA SYNDROMES
DEFINITION
Sleep apnea syndromes are a group of disorders characterized by periodic cessation of respiration and nocturnal sleep arousals. An apneic episode is defined as a cessation of airflow at the nose and mouth lasting longer than 10s. The diagnosis of sleep apnea syndrome is entertained when 30 or more episodes occur during 6 hours of sleep. The severity of the syndrome is usually quantitated by the apnea index (number
of apneic periods per sleep hour) and hypopnea index (number of hypopneic events per
SLEEP STAGES
CLASSIFICATION
1. OBSTRUCTIVE cessation of oronasal airflow despite persistent ventilatory effort. cessation of airflow and ventilatory effort. initial central, progressing to obstructive pattern. OBSTRUCTIVE SLEEP APNEA
Obstructive sleep apnea (OSA) is defined by the occurence of episodic partial of complete occlusion of the upper airway (usually at the level of the oropharynx) during sleep. These episodes may lead to the development of various mental or physical - 1% to `16% among adult men,
- 1% to 5% among adult women.
RISK FACTORS
- obesity (particularly obesity of the upper body), - certain endocrine disorders (hypothyroidism and acromegaly), - Prader-Willi syndrome (a congenital syndrome involving mental retardation, sexual infantilism, polyphagia with obesity, muscular hypotonia), - congenital craniophacial abnormalities (Pierre Robin syndrome). Common symptoms:
- deterioration of intellectual functions, Consequences:
- excessive daytime somnolence (may increase the risk of work-related and motor - arterial hypertension (50% of patients), - cardiac arrythmias (48% to 75% of patients) - increased risk of coronary heart disease and - increased risk of cerebrovascular disease, DIAGNOSIS
- direct observation of the patient during sleep - detection of apnea - thermistor at the nose and mouth or - avoidance of sleeping in in the supine posture, - oral appliances (in patients with macroglossia or micrognathia) (pull the tongue anteriorly and thus reduce the airway obstruction), - drug therapy (medroxyprogesterone acetate, protryptiline [20-30mg at bedtime], - nasal CPAP (continuous positive airway pressure) - nasal BPAP (bilevel positive airway pressure) (second-generation devices). - UPPP - (the objective is to remove excess or redundant soft tissue of the oropharynx while preserving palatal function). - transpalatal advancement pharyngoplasty (mandibular-hyoid advancement, DIFFERENTIAL DIAGNOSIS
- periodic leg movements during sleep (nocturnal myoclonus characterised by frequent
leg-jerking during the night that can lead to poor-quality sleep) - narcolepsy, (1.sleep attacks during the day; 2.cataplexy, sudden muscle weakness;
3.hypnogogic hallucinations, the sudden transition from wakefulness to
dreaming (rapid-eye-movement) sleep, causing difficulty distinguishing the dream from reality; 4.sleep paralysis (the loss of muscle strength
normally associated with sleep being extended into the waking state). - chronic fatigue syndrome,
- nonrestorative sleep syndromes.
THE OVERLAP SYNDROME
- chronic bronchitis and emphysema (with the blue and bloated pattern) combined with CENTRAL SLEEP APNEA
Pathogenesis:
- transient abolition of central drive to the ventilatory muscles; the resulting apnea leads
to a primary sequence of events similar to those of OSA 1. Defects in metabolic control system or respiratory muscles 2. Transient instabilities in central respiratory drive 3. Inhibition of central respiratory drive by upper airway reflexes Clinical features:
- many healthy individuals demonstrate a small number of central apneas during sleep
(particulary at sleep onset and in REM sleep); - recurrent respiratory failure, polycythemia, pulmonary hypertension, right-sided heart - poorly sleeping, morning headache, daytime fatigue and sleepiness. Diagnosis:
- obesity and hypertension are less prominent in CSA than in OSA, - key observation: recurrent apneas that are not accompanied by respiratory effort. Treatment:
- drug therapy - acetazolamid (a carbonic anhydrase inhibitor that stimulates
- low-flow oxygen.
SLEEP APNEA SYNDROMES
DEFINITION
Sleep apnea syndromes are a group of disorders
characterized by periodic cessation of respiration and
nocturnal sleep arousals.
An apneic episode is defined as a cessation of airflow at
the nose and mouth lasting longer than 10s. The diagnosis of
sleep apnea syndrome is entertained when 30 or more
episodes occur during 6 hours of sleep.
The severity of the syndrome is usually quantitated by the apnea
index (number of apneic periods per sleep hour) and hypopnea index
(number of hypopneic events per hour). SLEEP STAGES
1. Active sleep (REM)
2. Quiet sleep (NREM)
CLASSIFICATION
1. OBSTRUCTIVE cessation of oronasal airflow despite
persistent ventilatory effort.
2.CENTRAL
cessation of airflow and ventilatory
initial central, progressing to obstructive
pattern.
OBSTRUCTIVE SLEEP APNEA
Obstructive sleep apnea (OSA) is defined by the occurence of episodic partial of complete occlusion of the upper airway (usually at the level of the oropharynx) during sleep. These episodes may lead to the development of various mental or - 1% to `16% among adult men,
- 1% to 5% among adult women.
- obesity (particularly obesity of the upper body), - certain endocrine disorders (hypothyroidism and acromegaly), - Prader-Willi syndrome (a congenital syndrome involving mental sexual infantilism, polyphagia with obesity, muscular - congenital craniophacial abnormalities (Pierre Robin syndrome). Common symptoms:
- deterioration of intellectual functions, Consequences:
- excessive daytime somnolence (may increase the risk of work-related motor vehicle accidents, mental deficits) - cardiovascular consequences - arterial hypertension (50% of patients), - increased risk of coronary heart disease - increased risk of cerebrovascular disease, DIAGNOSIS
- direct observation of the patient during sleep - detection of apnea - thermistor at the nose and mouth or - avoidance of sleeping in in the supine posture, - oral appliances (in patients with macroglossia or micrognathia) (pull the tongue anteriorly and thus reduce the airway - drug therapy (medroxyprogesterone acetate, protryptiline [20- - nasal CPAP (continuous positive airway pressure)
- nasal BPAP (bilevel positive airway pressure) (second-
generation devices).
- surgical treatment
- UPPP - (the objective is to remove excess or redundant soft tissue of the oropharynx while preserving palatal - transpalatal advancement pharyngoplasty (mandibular- hyoid advancement, maxillmandibular advancement). Three objectives of the treatment:
1. alleviation of symptoms,
2. decrease in morbidity,
3. decrease in mortality
Noncompliance (CPAP - treatment)
- compliance rate - 77% to 89%
- reasons:
- general discomfort,
- mucosal irritation and epistaxis,
- nasal obstruction,
- feelings of bloatedness due to air swallowing,
- claustrophobia,
- skin irritation
- air soreness.
SLEEP APNEA SYNDROMES
DIFFERENTIAL DIAGNOSIS
hypersomnolence
- periodic leg movements during sleep (nocturnal myoclonus
characterised by frequent leg-jerking during the night that can lead to poor- - narcolepsy,
1.sleep attacks during the day;
2.cataplexy, sudden muscle weakness;
3.hypnogogic hallucinations, the sudden transition from
wakefulness to dreaming (rapid-eye-movement) sleep, causing difficulty distinguishing the dream 4.sleep paralysis (the loss of muscle strength normally
associated with sleep being extended into the - chronic fatigue syndrome,
- nonrestorative sleep syndromes.
THE OVERLAP SYNDROME
- chronic bronchitis and emphysema (with the blue and bloated pattern) combined with an obstructive sleep apnea syndrome CENTRAL SLEEP APNEA
Pathogenesis:
- transient abolition of central drive to the ventilatory muscles; the
resulting apnea leads to a primary sequence of events similar to those of 1. Defects in metabolic control system or respiratory muscles 2. Transient instabilities in central respiratory drive 3. Inhibition of central respiratory drive by upper airway reflexes Clinical features:
- many healthy individuals demonstrate a small number of central apneas
during sleep (particulary at sleep onset and in REM sleep); - recurrent respiratory failure, polycythemia, pulmonary hypertension, - poorly sleeping, morning headache, daytime fatigue and sleepiness. Diagnosis:
- obesity and hypertension are less prominent in CSA than in OSA, - key observation: recurrent apneas that are not accompanied by respiratory Treatment:
- drug therapy - acetazolamid (a carbonic anhydrase inhibitor that
- low-flow oxygen.

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