Heart failure and Cheyne-Stokes respiration E.Daskalopoulou-Vlachoyianni

Cheyne-Stokes respiration is reported in 30-40% of patients with severe heart failure. Its presence complicates clinical presentations with day-time somnolence, insomnia and additional complaints of profound fatigue and dyspnea; moreover, it has an adverse effect on the course of heart failure due to the activation of the sympathetic nervous system and the increase in the afterload of the left ventricle of the heart. The trigger for Cheyne-Stokes breathing is the stimulation of vagal receptors by lung congestion leading to hyperventilation and a fall in PaCO2 below the threshold for the maintenance of the respiratory drive. Variations in PaCO2 levels as a result of activation of central and, mainly, peripheral chemoreceptors, entail significant instability in the respiratory and, consequently, cardiovascular function. Cheyne-Stokes respiration is easy to identify, provided that clinical suspicion is high. A variety of pharmacological agents (theophylline, benzodiazepines) have been used for its treatment with poor results; on the other hand, oxygen therapy which reduces to some extent episodes of apnea/hyperventilation, and non-invasive mechanical ventilation (CPAP, Bilevel ASV) had the most encouraging outcomes.