Sleep apnoea

Sleep apnoea

Problems in Practice SLEEP APNOEA K. PROWSE AND M. B. ALLEN Department of Respiratory Medicine, Road, Stoke-on-Trent, City General Hospital, Staffs...

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Problems in Practice

SLEEP APNOEA K. PROWSE AND M. B. ALLEN Department

of Respiratory Medicine, Road, Stoke-on-Trent,

City General Hospital, Staffs. ST4 6QG

Newcastle

INTRODUCTION Recognition of severe sleep apnoea, and in particular of the obstructive sleep apnoea syndrome (OSAS), is vital because the consequences to the patient, both physiological and socioeconomic, are potentially disastrous. The most prominent symptoms are excessive daytime sleepiness and loud snoring. The former is dangerous to those who drive or who operate machinery or who require intellectual activity and judgement at work, whilst the latter often leads to marital disharmony. Wide recognition of the condition is a relatively recent phenomenon but despite the wealth of reviews and literature on the subject, it is diagnosed infrequently outside specialist sleep centres and most physicians do not have access to the full facilities for detailed sleep studies (polysomnography). Recognition of sleep apnoea syndrome is of paramount importance to the patient, but the natural history of the condition, which has multiple origins, is not well understood, its prevalence is uncertain and the value of screening tests is not defined. Equally, the indications for treatment are not fully known and there is no clear consensus as to the best method of treatment for the different types of sleep apnoea. There is even less evidence for the longterm benefits of such treatment. Detailed discussion of sleep apnoea syndrome has been given in several excellent reviews published recently (l-5). This review is intended to present a general picture of sleep apnoea for the physician working in a district general hospital, aiming to help in its recognition and diagnosis, to indicate the place and value of referral to specialist centres and to discuss the present concepts of treatment. WHAT

IS SLEEP

APNOEA?

Sleep apnoea implies cessation of breathing during sleep and is defined as cessation of airflow at the nose and mouth for a period of more than 10 seconds. Sleep apnoea syndrome (SAS) is present when the number of such episodes exceeds 5-g/hour. The presence of apnoea is usually reported as the Apnoea Index (number of apnoeic episodes per hour of sleep). It is common practice to distinguish three types of apnoea. Central apnoea (Fig. 1) occurs as a result of failure of central respiratory drive, and breathing ceases in the absence of respiratory effort. Obstructive apnoea (Fig. 2) is seen more commonly. During sleep there is obstruction of the upper airways, so that airflow at the nose and mouth ceases but active respiratory movements continue and are usually Correspondence

to: Dr K. Prowse.

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Fig. 1. Central apnoea showing cessation of airflow and of abdominal and chest wall movement. T,

time (seconds); Saor, oxygen saturation by ear lobe oximeter; A, abdominal wall movement; C, chest wall movement; NA, nasal airflow; BA, buccal airflow. ECG, EEG, EOG and EMG have been omitted

So02

.,--/----

,



, ,

-_--. , -. ,--, ,‘.

__-VI

A

Fig. 2. Obstructive apnoea, showing cessation of nasal and buccal airflow with continuing respira-

tory movements. T, time in seconds; Saoz, oxygen saturation by ear lobe oximeter; A, abdominal movement; C, chest wall movement; NA, nasal airflow; BA, buccal airflow enhanced in an attempt to overcome the obstruction. In many patients both types of apnoea coexist, usually with one form dominant. In mixed apnoea there is usually an initial

central respiratory pause followed by obstructive ventilatory efforts. The most common, and clinically most important type of apnoea is obstructive, leading to the symptom complex and physiological changes of the obstructive sleep apnoea syndrome (OSAS). Severe symptoms may also occur as a result of repeated episodes of hypopnoea, sometimes with only a few episodes of frank apnoea. Not all patients who show episodes of obstructive apnoea have significant symptoms requiring treatment. Furthermore there is a considerable ‘grey area’ because sleep apnoea occurs in normal subjects. The prevalence of OSAS is dot known but estimates in different populations vary from 1 to 5%. As more is learned about the condition it has progressed from being a littleknown phenomenon to one of prime medical importance.

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of obstructive sleep apnoea

Occlusion of the upper airways usually results when the tongue and soft palate move backwards and come into apposition with the posterior wall of the pharynx. The nasopharynx and oropharynx are both obstructed by this process. Apnoea with progressive asphyxia then occurs until the apnoea is terminated by a brief arousal from sleep. The patency of the upper airway is then restored, airflow resumes and the patient returns to sleep. This process is repeated many times during the course of a night. The airway occlusion follows the generation of intra-airways pressures below atmospheric pressure as a result of respiratory muscle activity. When this pressure exceeds the stabilizing forces produced by contraction of the dilator and abductor muscles of the oropharynx, passive collapse of the upper airways occurs. Anatomical and functional mechanisms lead to the development of this critical collapsing pressure, the most important being a small lumen in the upper airways and the reduction and instability of drive to the dilator and abductor muscles of the upper airways. The latter is characteristic of rapid eye movement (REM) sleep and light non-REM sleep. ‘Normal’ sleep apnoea

Changes in the overall control of breathing are well recognized during sleep, and many normal subjects show breathing irregularities ranging from apnoea to periodic (CheyneStokes) respiration (6). Such events are common in males of all ages, postmenopausal women and obese subjects and generally increase with age or after sedatives and alcohol. During pregnancy the frequency of such events is reduced. Whilst these events may not necessarily be normal it is doubtful that they require treatment. The apnoeic events may be central or obstructive in type, and in older men an Apnoea Index of about 5 is usually accepted as being within the normal range. Central apnoeic episodes lasting 10-20 seconds are common, especially during REM sleep. Whilst the apnoeic episodes appear to be of little physiological consequence in normal individuals they may be important in individuals with underlying chronic respiratory problems such as kyphoscoliosis or diaphragmatic weakness. If apnoea is associated with significant hypoxaemia it should be regarded as potentially important even in asymptomatic individuals and simple treatment advice given accordingly. ~ Does sleep apnoea matter?

When sleep apnoea is associated with a significant fall (>40/ 0 ) in arterial oxygen saturation (Sao,) there are important implications for the patient (Table I). The physiological Table I. Physiological consequences of

severe sleep apnoea Sleep fragmentation Hypoxaemia and reduced Sao, Pulmonary hypertension Congestive cardiac failure Cardiac arrhythmias Systemic hypertension

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consequences of repeated apnoea with its attendant hypoxaemia and reduced Sao, include pulmonary hypertension, congestive cardiac failure and systemic hypertension. Cardiac arrhythmias are common at the end of apnoeic episodes. There is often bradycardia (3035 beats/min) and occasionally this is profound with episodes of sinus arrest lasting l&20 seconds. Arrhythmias described include atria1 fibrillation, atria1 flutter, frequent premature ventricular ectopic beats and ventricular tachycardia and these may be responsible for the high incidence of sudden death at night in this condition. Recognition

of sleep apnoea

In the best traditions of medicine sleep apnoea will be recognized if the possibility of the diagnosis is considered and the correct questions are asked to elucidate symptoms. The common symptoms are summarized in Table II. The classic patient with OSAS is an Table II. Symptoms of obstructive sleep apnoea syndrome Nocturnal

Daytime

Excessive snoring Restless sleep Increased motor activity Insomnia Enuresis Hypnagogic hallucinations

Daytime somnolence Intellectual deterioration Morning ‘drunkenness’ Morning headaches Unrefreshing sleep Memory impairment Loss of sexual drive Dependent oedema

overweight, middle-aged male, although the condition can occur at any age and obesity is not necessarily present. The two dominant symptoms are excessive daytime sleepiness and loud snoring although the latter is infrequent in pure central apnoea. It is essential to take the history from the spouse or from other members of the family. Snoring occurs in more than half of the male population over the age of 40 years, but not all patients who snore have OSAS in which typically the snoring is so loud that the spouse moves to a separate bedroom. As the condition progresses, usually associated with weight gain, the pattern of snoring becomes irregular, alternating with periods of silence associated with vigorous breathing efforts. At the end of each apnoeic episode there may be a particularly loud and explosive snore often accompanied by marked restlessness, flailing of the limbs or thrashing around the bed. Many patients claim to sleep soundly but some are aware of the recurrent arousals and complain of insomnia associated with a choking sensation. On waking in the morning there may be a complaint that sleep has not been refreshing and many patients complain of disorientation and mental fogginess or a sensation of morning drunkenness. Morning headache is seen in about one-fifth of patients. Excessive daytime sleepiness is an important symptom. In mild cases it may be confined to situations conducive to sleep such as lectures or watching television but in severe cases uncontrollable sleep may occur either whilst driving or operating dangerous machinery, leading to accidents, or when lecturing or teaching. The main cause of the daytime sleepiness is

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probably related to the excessive fragmentation of sleep but other factors may be involved because the severity of the symptom varies even in patients with equivalent degrees of sleep apnoea and sleep disruptions. The resulting intellectual deterioration, impairment of memory and poor judgement have important socioeconomic consequences for those with professional responsibilities or business commitments. In addition to the symptoms described above more general changes in personality may occur with mental instability, irritability and short temper. About’s third of patients complain of nocturia. Less common symptoms include impotence, loss of sexual drive, enuresis and hypnagogic hallucinations. The presenting symptoms may sometimes relate to sustained pulmonary hypertension which leads to right heart failure in about l&15% of patients with obstructive sleep apnoea syndrome. In some the pulmonary artery pressure may return to normal during the day, an important point for the investigator. Systemic hypertension is seen frequently and is present in more than 50%‘of patients with OSAS. At risk groups The wide array of symptoms in the sleep apnoea syndrome means that the condition may present to many medical specialties. Identifiable groups at risk are: 1. Obese adults. 2. Children: especially those with enlarged tonsils, nasal problems or craniofacial deformities. 3. Elderly subjects. 4. Chronic pulmonary disease: including chronic airflow obstruction, asthma, cystic fibrosis and diaphragmatic paralysis. 5. Upper airways disease, e.g. rhinitis, nasal polypi or nasal septal deviation. 6. Heart disease. 7. Neurological conditions: the differential diagnosis of excessive sleepiness includes narcolepsy, depression, drug abuse and nocturnal myoclonus. 8. Endocrine disorders, e.g. acromegaly and myxoedema. 9. Musculoskeletal disorders, e.g. kyphoscoliosis, muscular dystrophy and Shy-Drager syndrome. CHRONIC

OBSTRUCTIVE

PULMONARY

DISEASE

Patients with chronic obstructive pulmonary disease (chronic airflow obstruction) are often hypoxaemic and it is well recognized that during sleep, especially REM sleep, there may be large falls in arterial oxygen saturation (Sao,) (7). Any patient who has a reduced Sao, when awake is likely to show severe arterial oxygen desaturation during REM sleep because further falls in Pao, occur on the steep part of the O2 dissociation curve. The increasing use of ear oximeters has shown that large falls in Saoz may occur in subjects who have a normal waking Sao,, and these falls may be associated with disturbed sleep cycles, pulmonary hypertension and systemic hypertension. Only about lO-15% of patients with chronic obstructive pulmonary disease also have frank sleep apnoea syndrome although there is disagreement in the reported incidence largely due to the differing criteria used in the diagnosis of apnoea.

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OF SLEEP

APNOEA

The aims of investigation are to confirm or refute the diagnosis of sleep apnoea, to assess the severity of the physiological consequences of apnoea and to determine the type of apnoea present and hence the appropriate treatment. The diagnostic procedure of choice is a full sleep study (polysomnography) but facilities for this are not available in most district general hospitals and such investigations are confined to a few specialist centres. Important clues to the’diagnosis may be obtained from the physical examination of the patient in the light of the relevant history. Physical abnormalities such as obesity, receding jaw, large tongue or enlarged tonsils may point to the diagnosis. The blood count may show otherwise unexplained polycythaemia. In most patients except those with chest wall deformity or chronic obstructive lung disease, routine lung function tests are normal but the flow-volume loop may suggest obstruction of the upper airways. Simple screening techniques

The most useful simple screening technique is the overnight recording of Sao, using an ear oximeter. As one is looking for marked falls, the fact that such instruments are not accurate at Sao, >50% does not matter. Transcutaneous Pao, measurements have been used but are less reliable in adults, with longer response times and problems with skin burns. Modern oximeters have in-built storage facilities allowing easy display of Sao, levels. A simple recording will show whether significant falls in Sao2 occur during sleep. When such falls are seen (Fig. 3) significant apnoea or hypopnoea may be present but of course the occurrence of hypoxaemia may be due to other causes and the finding lends support to the

Fig. 3. Overnight sleep

trace of Sao,, showing normal resting Sao, with large falls occurring

during REM

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probable diagnosis but does not prove it. Conversely a negative finding of no fall in Sao, makes the diagnosis unlikely. Simple oximetry alone is not an adequate test because it does not indicate the type of apnoea, nor its relationship to stage of sleep. Some patients with significant apnoea will be missed and it does not provide the basis for definitive treatment. Positive findings on the oximeter trace should therefore only provide a strong stimulus for further investigations, if necessary by referral to a sleep laboratory. Simple oximetry may be supplemented by observation of the patient during sleep, if possible by video recording. Techniques of tape recording laryngeal sounds have proved useful although again not diagnostic. This can be done with a simple tape recorder or by recording from a microphone placed over the larynx. Cyclical fluctuations in heart rate, or abnormality of heart rhythm may be shown by overnight Holter cardiac monitoring. This test again must be interpreted with caution because there are other causes of cardiac arrhythmia, and many patients with sleep apnoea do not show gross changes in heart rate and will be missed by this screening technique. Where EEG facilities are available, daytime studies with ‘nap’ recordings or the multiple sleep latency test may provide useful information. Nap studies can be carried out in the afternoon, after a fairly large lunch, but information is limited because the pattern of sleep differs from that seen overnight and a negative test does not exclude sleep apnoea. The place of simple screening tests has yet to be clarified. Their interpretation, sensitivity and specificity is not yet determined. However, they can be performed in most district general hospitals and may prove important pointers to the diagnosis. The firm diagnosis of OSAS, therefore, requires a more detailed investigation in the form of polysomnography.

When to refer

When the diagnosis of sleep apnoea syndrome is suspected on the basis of history or screening tests, the patient should be referred to a centre with specialist sleep study facilities. Polysomnography involves the measurement during overnight sleep of a number of physiological variables which will usually include Sao,, thoracic and abdominal muscle movement, airflow at the nose and mouth, and heart rate. Conventionally such studies also involve recording of EEG, submental EMG and eye movements (EOG) which allow analysis of total sleep time and its distribution among the different sleep stages as well as giving an indication of sleep fragmentation due to arousals. Study of airflow identifies the presence of apnoea whilst recording of thoracic wall and abdominal muscle activity usually permits distinction between central and obstructive apnoea, although some subjects with obstructive apnoea may show muscle activity which is detectable only by an intraoesophageal balloon study so that the distinction is not absolute. Monitoring of the Sao, (Fig. 4) and heart rate gives an assessment of the consequences of the apnoea. Polysomnographic studies, therefore, will lead to a definitive diagnosis, or equally important for some patients, may exclude the diagnosis. In our experience, and that of other sleep laboratories, the occurrence of significant symptoms is usually related to the finding of more than 15-20 episodes of apnoea or hypopnoea per hour of sleep. If subjects are symptomatic with a lower Apnoea Index, other diagnoses, e.g. narcolepsy, must be considered especially when the main symptom is excessive daytime somnolence.

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Oxygen

Patient

Saturation

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Plot

-90

A OS/OS/S5

S, 02 Baseline Time

CHEST:

90.0%

desat .

24.9%

s,

66.4%

Lowest

02

-80 -70 -60 aI

E i= -50 dp

-40 -30 -20 -10

60

70

80

90

%SaO2

Fig. 4. Computerized plot of overnight Sao?in a patient with obstructive sleep apnoea, showing the different percentages of sleep time spent at different levels of Sao?.The vertical line demarcates the significant fall in Saoz (>4%). In this patient about 40% of total sleep time was spent with a significantly low Sao2 ENT assessment Full assessment by an ENT surgeon with experience of the condition is important in all patients with obstructive sleep apnoea. Unless the subject is examined lying down, narrowing of the oropharyngeal airway may be missed. In patients who are obese or who have short thick necks, general narrowing of the oropharynx may be found. Important positive findings include receding jaw, macroglossia, large tonsils, pendulous soft palate or redundant mucosal folds in the pharynx, and these may indicate a role for surgical treatment. In addition nasal obstruction, whether from rhinitis, polypi or anatomical deformity, may produce central or obstructive apnoea. Even in normal subjects nasal occlusion has been shown to increase the number of sleep-related respiratory abnormalities (8). Full assessment may involve radiography, cephalometry, CAT scanning and fluoroscopy. WHEN

IS TREATMENT

REQUIRED?

Once the diagnosis of sleep apnoea has been made the clinical decision is whether to treat and, if so, how? The natural history of mild sleep apnoea is not known but the condition

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may progress depending upon the major causative factors. Moderate cases with daytime somnolence and/or intellectual deterioration probably progress without treatment but again the rate of progression is uncertain. If symptoms do not warrant immediate treatment these patients should be reviewed regularly at least in terms of symptoms. Patients with severe obstructive sleep apnoea syndrome, as shown by severe somnolence, daytime respiratory failure or hypercapnia, have a poor prognosis, death resulting from the physiological consequences of the repeated hypoxaemia. From the literature it seems likely that these patients have a prognosis untreated of not more than l-2 years. In the present state of knowledge treatment should be undertaken if any of the following conditions are present: 1. Symptoms:

excessive sleepiness, intellectual deterioration, depression, endangered occupation. 2. Findings: Apnoea Index ~15, pulmonary hypertension, hypercapnia, polycythaemia. A summary of treatment

morning

drunkenness,

significant

arrhythmias,

is given in Table III.

Table III. Treatment of sleep apnoea syndrome General Treat underlying medical conditions Local surgery to nose or tonsils Weight reduction Avoid sedatives and alcohol Specific Effective

Uncertain or doubtful

Central Acetozolamide Nocturnal O2 Tracheostomy Ventilation at night CPAP

Obstructive Protriptyline

Clomipramine Medroxy progesterone Naloxone Theophylline Almitrine

Nocturnal OZ Theophylline Almitrine

Medroxy progesterone CPAP UVPPP Tracheostomy

Treatment of central sleep apnoea

Although less common than obstructive apnoea, central apnoea is more difficult to treat (9). When features of obstructive apnoea coexist treatment directed at that condition will often ameliorate central apnoea. In moderately affected patients the first step is to treat any associated conditions such as nasal obstruction or congestive cardiac failure. Specific treatment with acetazolamide (250 mg four times daily) reduces the frequency of central apnoea for periods of l-2 weeks but its long-term use is less successful, the side-effect of paraesthesiae limits tolerance of the drug and its use may lead to the development of obstructive apnoea. Reports of the use

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of other drugs are mainly anecdotal and there have been few systematic studies. Little benefit has been reported with theophylline, naloxone or medroxyprogesterone. The use of supplemental oxygen at night has been shown to reduce or abolish central sleep apnoea. Although the mechanism is uncertain it is certainly worth trying but the response should be monitored carefully. Diaphragmatic pacing has been tried in some subjects and is occasionally helpful. Severely affected patients require more aggressive therapy usually involving mechanical ventilation possibly through a tracheostomy or by a negative-pressure (cuirrass) ventilator. The recently reported technique of using mechanical ventilation in conjunction with CPAP (continuous positive airways pressure) offers hope for the long-term management of such patients because it is better tolerated and avoids the potential complications of tracheostomy. Treatment of obstructive sleep apnoea

The available form of treatment may be divided into four groups-simple measures, medical, surgical and mechanical. Simple measures are effective in many patients with mild or moderate symptoms. After the exclusion or treatment of underlying medical disorders, such as acromegaly or myxoedema, the first line of treatment is weight reduction. About a third of patients are able to lose weight with consequent improvement in symptoms and reduction in apnoea and hypoxaemia. It is worth noting, however, that not all patients who fail to lose weight fail because of poor compliance with dietary instructions. Some patients who have not lost weight on stringent diets may do so subsequently when medical treatment is begun. It is important to avoid alcohol or sedatives in the evening or at night as there is abundant evidence that both may exacerbate the condition. Medical treatment. The most effective therapeutic agents seem to be the tricyclic antidepressants, of which the most frequently used is protriptyline in doses varying from 5-30 mg daily. The drug appears to act by increasing the tone of the upper airway muscles and by altering sleep state with a reduction in REM sleep. The long-term benefit of such medication has yet to be proven. In our series of 48 patients with OSAS, 27 have shown sustained benefit during follow-up for l-8 years but eight deteriorated after a good initial response. The remaining 19 patients either obtained no benefit or stopped the drug because of anticholinergic side-effects. Medoxyprogesterone (MPA) has been of value in a small number of patients but its use is limited by the unacceptable hormonal side-effects in males. Other drugs such as theophylline or almitrine seem to confer no benefit. Supplemental nocturnal oxygen has been used in the treatment of obstructive sleep apnoea (10) but does not affect or alter the underlying mechanical condition and may be counterproductive in those with hypercapnia. Its use should not detract from treatment of the underlying disorder. Surgical treatment. The most popular surgical approach is uvulopalatopharyngoplasty (UVPPP), the aim of which is to increase the size of the oropharyngeal lumen by excising redundant tissue. Snoring is improved by this procedure but although nocturnal oxygenation may be increased the effects on apnoea are less predictable. When improvement in apnoea occurs’it may be maintained for more than a year in about 60% of patients (11).

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The findings suggest that factors other than purely anatomical ones determine the presence of apnoea. UVPPP has an important place in the treatment of some patients with sleep apnoea but the criteria for selection require further elucidation. The ultimate surgical therapy for obstructive sleep apnoea syndrome is tracheostomy which bypasses the site of obstruction. As a definitive treatment it leaves much to be desired in terms of social factors and possible long-term complications. It should be reserved for extreme cases and is seldom required, although it may be used as a temporary procedure pending or during other upper airway surgery. Mechanical measures. Probably the most important advance in the home treatment of obstructive sleep apnoea syndrome was the introduction by Sullivan and colleagues of continuous positive airways pressure (CPAP) applied through a close-fitting nasal mask (12, 13). The positive pressure acts as a pneumatic splint for the airways, preventing obstruction and hence alleviating apnoea. When tested in the laboratory results were extremely impressive. Initial home management was disappointing largely because of difficulties in compliance caused by problems with the mask or the noise of the pressure generator. The recent introduction of better masks and quieter machinery has improved patient compliance. In most centres it is, therefore, the treatment of choice for obstructive sleep apnoea, which fails to respond to simple measures or medical therapy. The technique may be ineffective after UPPP.

THE

FUTURE

The importance of sleep apnoea as a serious medical condition is being recognized more widely but long-term studies are required to elucidate its prevalence and natural history, to identify and evaluate simple screening techniques and to assess long-term results of treatment. Effective and rational therapy is difficult in the present state of knowledge and little attention has been paid to the psychological and psychiatric disturbances resulting from the condition. REFERENCES 1. Bradley TD, Phillipson EA. Pathogenesis and pathophysiology of the obstructive sleep apnoea syndrome. Med Clins N Am 1985;69(6): 1169-85. 2. Cherniak NS. Sleep apnoea and its causes. J. Clin Invest 1984; 73: 1501-6. 3. Saunders NA, Sullivan CE, eds. Sleep and breathing. Lung biology in health and disease, Vo121.

New York: Marcel Dekker, 1984. 4. Edelman, NH, Santiago TV, eds. Breathing

disorders of sleep. Contemporary issues inpulmonary disease, Vol 5. New York: Churchill Livingstone, 1986. 5. Stradling JR, Phillipson EA. Breathing disorders during sleep. QJ Med New Series 58, 1986;

58(225):3-18. 6. Block AJ, Boysen PG, Wynne JW, et al. Sleep apnoea, hypopnoea and oxygen desaturation in normal subjects. New Engl J Med 1979; 300:513-17. 7. Douglas NJ, Calverley PMA, Leggett JE, et al. Transient hypoxaemia sleep in chronic bronchitis and emphysema. Lancet 1979$:1-4. 8. Zwillich CW, Pickett C, Hanson FN, et al. Disturbed sleep and prolonged apnoea during nasal obstruction in normal man. Am Rev Resp Dis 1981;124:158-60.

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9. White DP. Central sleep apnoea. Med Clins N Am 1983;69:1205-19. 10. Martin RJ, Sanders MH, Gray BA, et al. Acute and long-term ventilatory effects of hyperoxia in the adult sleep apnea syndrome. Am Rev Resp Dis 1982;125:175-80. 11. Conway W, Fujita S, Zorich F, et al. Uvulopalatopharyngoplasty: one year follow-up. Chest 1985;88:385-7. 12. Sullivan CE, Issa FG, Berthon-Jones M, et al. Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. Lancet 1981;i:862-5. 13. Sullivan CE, Issa FG, Berthon-Jones M, et al. Home treatment of obstructive sleep apnoea with continuous positive airways pressure applied through a nose-mask. Bull Eur Physiopath Resp 1984;20:49-54.