ACUTE AND CHRONIC CARDIOVASCULAR-RESPONSES TO SLEEP-DISORDERED BREATHING

Episodes of sleep disordered breathing are surprisingly common in asym ptomatic, middle-aged individuals. The majority of these events are hy popneas, rather than apneas. Even though these events cause rather mod est decreases in arterial oxygen saturation, they evoke substantial in creases in arterial pressure. In this population, mild to moderate sle ep disordered breathing is associated with elevated daytime blood pres sure. The mechanisms responsible for the acute and chronic cardiovascu lar effects of sleep disordered breathing are incompletely understood. Chemoreflex mechanisms appear to be more important than intrathoracic pressure changes in causing the acute elevation in arterial pressure that occurs after obstructive sleep apnea. Arousal from sleep may cont ribute to this presser response, either in an additive or synergistic manner. Relatively brief exposure to combined hypoxia and hypercapnia during wakefulness can produce an increase in sympathetic outflow to s keletal muscle that persists after return to room air breathing. This lingering post-asphyxic effect on sympathetic outflow may be the basis of chronically elevated sympathetic nervous system activity which acc ompanies sleep apnea syndrome and may contribute to sustained hyperten sion in these individuals.