Sleep-related breathing disorders, including
obstructive sleep apnea (OSA) and
Cheyne-Stokes respiration with
central sleep apnea (CSR-CSA), commonly occur in patients with
congestive heart failure (CHF). In this setting they can have adverse pathophysiologic effects on the cardiovascular system. OSA may lead to development or progression of left ventricular (
LV) dysfunction by increasing LV afterload through the combined effects of elevations in systemic blood pressure and a generation of exaggerated negative intrathoracic pressure, and by activating the sympathetic nervous system through the influence of
hypoxia and arousals from sleep. Abolition of OSA by
continuous positive airway pressure (CPAP) can improve cardiac function in patients with CHF. In contrast to OSA, CSR-CSA is likely a consequence rather than a cause of CHF. Here, pulmonary congestion causes
hyperventilation by stimulating pulmonary
irritant receptors. This leads to reductions in PaCO2 below the apneic threshold during sleep, precipitating posthyperventilatory
central apneas. CSR-CSA is associated with increased mortality in CHF, probably because of sympathetic nervous system activation caused by recurrent
apnea-induced
hypoxia and arousals from sleep. Treatment of CSR-CSA by supplemental O2,
theophylline, and CPAP can alleviate
central apneas. Of these treatments, however, only CPAP has been shown to improve cardiac function and symptoms of
heart failure. We conclude that effective treatments of OSA and CSR-CSA may prove to be useful adjuncts to the standard pharmacologic
therapy of patients with CHF.