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Disordered Breathing during Sleep: Discussion Paper

Normal unmedicated human sleep is characterized by electroencephalogram (EEG), continuously recorded throughout the night, into four stages, and a fifth of rapid eye movement sleep (REM) which occurs with increasing frequency and duration as the night progresses. During REM sleep, breathing is irregular and physiological control mechanisms are disturbed when compared with their activity during wakefulness. Thus, even in normal healthy subjects, minute ventilation is decreased in REM sleep, as are both hypoxic and CO2 drives for breathing (Douglas et al. 1982). In the Rayne Laboratory of the Department of Respiratory Medicine at the University of Edinburgh, studies have been carried out on breathing patterns (by respiratory inductive plethysmography), ear oxygen saturation (Hewlett Packard Ear Oximeter), air flow at nose and mouth, and EEG continuously throughout the night in subjects sleeping in a quiet, darkened, air-conditioned and sound-proofed room. Particular attention has been paid to sleep hypoxaemia, as shown as episodes when the ear oxygen saturation (reflecting the arterial saturation) falls by at least 10% from the preexisting values during stable sleep, in subjects who are older, have sleep apnoea syndromes, and with chronic bronchitis and emphysema. In normal, young, healthy subjects ear oxygen saturation changes little from resting values (95-98%) throughout a normal night's sleep. However, as age advances, particularly over the age of 55, episodes of transient hypoxaemia with falls in arterial oxygen saturation to below 75% occur with increasing frequency in both men and women, who are nonetheless otherwise healthy. These falls are usually associated with hypoventilation and irregular breathing in REM sleep, and such REM-associated hypoxaemic episodes must therefore, be regarded as normal in healthy subjects over 55 years of age. In sleep apnoea syndromes, breathing ceases recurrently for periods of 10 seconds or longer, many times in each hour of sleep (Guilleminault & Dement 1978). In pbstructive apnoea, chest wall movement continues whereas oral nasal air flow ceases due to transient obstruction of the upper airway. This is almost certainly due to failure of inspiratory contraction of the genioglossus muscle during these episodes (Remmers et al. 1978). Symptoms include snoring, enuresis and other abnormal behaviour during sleep, coupled with daytime sleepiness, and often with intellectual deterioration and personality changes. Morning headaches may be combined with mild systemic hypertension. Most series show that over 50% of such patients are obese, and they characteristically have reduced sleep latency, falling asleep very rapidly. Cardiac arrhythmias, and pulmonary hypertension particularly during the episodes, can be associated with the obesity and disturbance of sleep; patients with the established condition clearly have an increased threat to life, and death during episodes of daytime sleepiness from accidents, or at night, is well recognized. Obstructive sleep apnoea is now realized to be a common concomitant of the 'alveolar hypoventilation syndrome', where obesity and central cyanosis with secondary polycythaemia have long been recognized. Differential diagnosis includes other causes of upper airway narrowing (enlarged tonsils, myxoedema, acromegaly, congenital malformations, etc.) which compound the airway obstruction caused by failure of genioglossus inspiratory contraction, musculoskeletal disorders, neuromuscular disorders including cerebrovascular accidents and, in particular, cerebellar artery occlusive disease and secondary polycythaemia. Diagnostic