Central sleep apnea (CSA) associated with Cheyne-Stokes respiration is observed during stages 1 and 2 sleep in approximately 30% of patients with congestive heart failure (CHF), and is characterized by typical waxing and waning hyperventilation interspersed with central apneas or hypopneas. It has been shown that hyperventilation results from acquired changes in ventilatory responses to hyper-capnia and hypoxia within a few weeks in experimentally induced CHF, and probably relates to changes in carotid body nitric oxide or elevated catecholamines. Moreover CSA severity can be attenuated in humans by the introduction of anti-heart failure therapy and improvement in heart function over several weeks. The responsible mechanisms for altered respiratory control are thought to relate to sympathoexcitation, circulatory delay, and possibly pulmonary congestion with vagal afferent stimulation. http://cheap-asthma-inhalers.com/
Whether normalization of heart function should lead to complete abolition of CSA has not been shown. Early case reports suggested normalization of heart function with transplantation led to complete abolition of CSA or the development of obstructive sleep apnea (OSA).> However, CSA persisting within a few days after heart transplantation has also been reported; more recently, a series of patients was reported in which CSA persisted 3 to 9 weeks following successful heart transplantation in approximately 20% of 29 patients with CHF and CSA despite normal heart allograft function. Those authors postulated that respiratory control centers may have been permanently altered in those patients with persistent CSA. However, no such study has assessed whether CSA persists after the initial peri-transplant period (ie, > 6 months) with normalization of allograft function. The aim of this study was to test the hypothesis that normalization of heart function, and associated attenuation of sympathetic activity, would lead to abolition of CSA.