Sleep-related breathing disorders * 7 Series

The previous reviews in this series have focused on the pathophysiology and treatment of obstructive sleep apnoea which is much the commonest sleep and breathing disorder. ' However, there is an increasing awareness that normal sleep physiology interacts with coexisting medical diseases to promote sleep disruption and daytime sleepiness.2 Sleep fragmentation induces more daytime tiredness than does simple sleep deprivation3 and can produce depression of the hypoxic and hypercapnic ventilatory responses, depression of upper airway dilatory muscle activity, and a reduction in the critical closing pressure within the pharynx.45 These changes become important when the upper airway is already compromised by disease for example, a large tongue in Down's syndrome6 orwhen unrelated pathology coexists with the medical problem as in chronic obsructive pulmonary disease (see below). In this case the additional problems are largely those associated with obstructive sleep apnoea and they can act to accelerate patient decline. Two further mechanisms operate singly or together with the unstable upper airway to produce sleep and breathing problems in medical illness. It is now accepted that both the hypercapnic and hypoxic ventilatory responses decline with the onset of sleep and become flatter still in stages 3/4 sleep.7'These adjustments probably represent a change in respiratory controller gain and are associated with a change in the carbon dioxide set point such that apnoea occurs during sleep at a higher carbon dioxide tension than during wakefulness.10 In normal subjects the Paco, during sleep is still well above the apnoeic threshold. However, if the Paco2 is reduced, as happens at altitude" or in some medical conditions such as congestive cardiac failure, then controller instability produces periodic breathing during sleep. These apnoeic events are entirely central, associated with an open glottis, and are not accompanied by increased respiratory efforts. TIhey differ from the reflex central apnoea described by Bradley et al where apnoeas are promoted by contact of the walls of the upper airway during a period of previous increased inspiratory effort. '2 Sometimes obstructive and central events can coexist in the same disease category as has recently been described in acromegaly. '3 Whilst most patients with acromegaly are predisposed to obstructive events by changes in the dimensions of their upper airways, some are relatively hypocapnic, particularly if they have high circulating levels of IgF and increased hypercapnic ventilatory drives. These subjects develop prolonged central apnoeas. Studies of this kind are likely to be extended to other conditions as the wider relevance of sleep disordered breathing is recognised. A final, less well understood problem is that of hypoventilation during sleep. Normal subjects show state-related falls in minute ventilation'4 which are probably central in origin. In addition, as sleep deepens the response to ventilatory loading is impaired,'5 as is load detection, at least in stage 2 sleep. '6 The effects of mass loading, whether due to obesity'7 or thoracic cage restriction, are to reduce ventilation further probably by an increase in thoracic impedance although detailed studies directly measuring ventilation in the latter condition are lacking. Nonetheless, assisted ventilation during the night by nasal intermittent positive pressure ventilation (NIPPV) does appear to produce significant changes in blood gas tensions and exercise performance over time, implying that such hypoventilation is clinically important. '819