Sympathovagal balance changes in sleep breathing disorders

Abstract

SummaryThe autonomic nervous system (ANS) plays a leading role in controlling visceral functions and it is well known that the increase of sympathetic activity underlies most of cardiovascular diseases such as hypertension, heart failure, myocardial infarction and arrhythmias. On the other hand parasympathetic activity acts as protective factor against the above mentioned conditions. Sleep breathing disorders (SBD) are commonly divided in three syndromes: obstructive sleep apnoea syndrome, central sleep apnoea syndrome and Cheyne-Stokes breathing syndrome, the latter two both characterized by cyclic non-obstructive breathing patterns. Cheyne-Stokes Respiration is a form of periodic breathing characterized by a crescendo-decrescendo pattern of ventilation with (CSR-CSA) or without (CSR) central apnoea. Obstructive sleep apnea (OSA) is significantly associated with increased cardiovascular morbidity and mortality. OSA exerts strong modulatory effects on the autonomic nervous system through a number of mechanisms including central respiratory-cardiac coupling in the brain stem, chemo-reflex stimulation, baro-reflexes, and reflexes relating to lung inflation. EEG arousals, often related to apnea termination, also represent the final way of autonomic activation. CSR is common among patients with congestive heart failure, being present in 30-40% of the two largest reported. If CSR "per se" promotes an increase of sympathetic outflow during sleep is not really known.Several lines of argument would support the hypothesis that CSR may be a compensatory mechanism for severe HF.