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.