Autonomic nervous system and obstructive sleep apnoa.

Understanding of the pathophysiology of obstructive sleep apnoea, a common yet relatively newly recognised condition, has advanced rapidly in recent y ears. This condition produces major acute haemodynamic changes and causal r elationships with arterial hypertension and cardiovascular morbidity have b een proposed. The role that the autonomic nervous system plays in mediating these cardiovascular changes has been the focus of intensive research acti vity and the development of new techniques in physiological monitoring, suc h as spectral analysis of heart rate variability, Finapres blood pressure m onitoring, measurement of muscle sympathetic nerve activity, radionuclide t ests and animal models of obstructive sleep apnoea have substantially incre ased the knowledge base. The acute haemodynamic changes ni-e associated wit h high levels of sympathetic discharge and with fluctuating parasympathetic activity. There are also chronic changes in baroreceptor and chemoreceptor reflexes associated with an increase in baseline daytime sympathetic activ ity and abnormal vagal reflex responses to voluntary respiratory manoeuvres . These acute autonomic changes appear to be provoked by a combination of s timuli triggered by hypoxaemia, upper airway responses, ventilatory changes and arousal. The mechanisms of the chronic autonomic changes ave less clea r; it is likely that recurrent hypoxaemia is important, but the roles of re current ventilatory stress and arousal are not clear. Normalising respirati on,vith CPAP therapy prevents the acute cardiovascular changes and reduces the acute sympathetic overactivity, and in compliant patients, restores abn ormal vagal responses to normal and reduces excess chronic sympathetic acti vity. Whether or not this produces a reduction in long term cardiovascular morbidity is riot established.