Chemosensitivity in chronic heart failure.

Abstract

Augmented peripheral and central chemoreceptor sensitivity has recently been demonstrated in both experimental and clinical settings of chronic heart failure (CHF). As a result of the effects of chemoreflexes on the respiratory, circulatory and neurohormonal systems, changes in their activity may account for several pathophysiological features of CHF--predominantly augmented ventilation, abnormal cyclic respiratory pattern and sympathetic overactivity. Although the precise underlying mechanisms are not known, a heightened chemoreflex drive may constitute an ominous sign in CHF. Patients with abnormally elevated chemosensitivity demonstrate an augmented ventilatory response to exercise, a severely impaired autonomic regulation and suppression of baroreceptor function, and a higher prevalence of ventricular arrhythmias. All these factors may unfavorably influence the prognosis of CHF. In fact, we have recently confirmed in a group of patients with advanced CHF that high peripheral chemosensitivity is an independent predictor of death. New therapies are needed in CHF to improve prognosis and quality of life. Drugs, such as opiates, and oxygen administration have been shown to suppress chemosensitivity, which may further favorably influence exercise tolerance and modify periodic breathing in CHF patients. Treatment strategies targeted at peripheral and central chemoreceptors may be a promising option for further evaluation.