Pathophysiologic and therapeutic implications of sleep apnea in congestive heart failure.
Obstructive and central sleep apnea are common in patients with congestive heart failure (CHF). These sleep-related breathing disorders are characterized by two pathophysiologic features that could have important implications for disease progression in CHF: sympathetic nervous system activation, and adverse changes in cardiac loading conditions. In patients with obstructive sleep apnea, blood pressure is frequently elevated as a result of excessive sympathetic nervous system activity elicited by the combination of apnea, hypoxia, and arousals from sleep. The generation of exaggerated negative intrathoracic pressure during obstructive apneas further increases left ventricular afterload, reduces cardiac output, and may promote the progression of pump failure. Increased afterload and hypoxia can also predispose such patients to myocardial ischemia and arrhythmias. In patients with CHF, abolition of coexisting obstructive sleep apnea by nasal continuous positive airway pressure improves left ventricular function. Central sleep apnea (i.e., Cheyne-Stokes respiration) is also characterized by apnea, hypoxia, and increased sympathetic nervous system activity and, when present in CHF, is associated with increased risk of death. Recent medium-term trials involving small numbers of patients have demonstrated that nocturnally applied continuous positive airway pressure in patients with CHF and central sleep apnea alleviates central sleep apnea, improves left ventricular function, reduces sympathetic nervous system activity and improves symptoms of CHF. These studies emphasize the importance of considering obstructive and central sleep apnea in the differential diagnosis of conditions that could contribute to the development or progression of CHF. They also suggest that continuous positive airway pressure is a promising nonpharmacologic adjunctive therapy for patients with CHF and coexisting sleep-related breathing disturbances that warrants further investigation.
Department of Medicine of the Toronto Hospital, Ontario, Canada.
T D
TD
Bradley
J S
JS
Floras
D018450:Disease Progression; D004569:Electroencephalography; D004576:Electromyography; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D006439:Hemodynamics; D006801:Humans; D012307:Risk Factors; D012891:Sleep Apnea Syndromes / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D013564:Sympathetic Nervous System / Q000503:physiopathology