Acute and chronic cardiovascular responses to sleep disordered breathing

Episodes of sleep disordered breathing are surprisingly common in asymptomatic, middle-aged individuals. The majority of these events are hypopneas, rather than apneas. Even though these events cause rather modest decreases in arterial oxygen saturation, they evoke substantial increases in arterial pressure. In this population, mild to moderate sleep disordered breathing is associated with elevated daytime blood pressure. The mechanisms responsible for the acute and chronic cardiovascular 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 contribute to this pressor 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 skeletal 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 accompanies sleep apnea syndrome and may contribute to sustained hypertension in these individuals.