Breathless heart: only when the neck is deep in water?

Apnea severity is considered a risk marker and/or factor, because it contributes, via sympathetic activation and worsening of hemodynamics, to disease evolution, life-threatening arrhythmias, and fatal outcome. This was demonstrated in the presence of either central sleep apneas (CSA), with high values of the apnea-hypopnea index, or in central apneas during wakefulness. As an alternative interpretation, central apneas have been regarded as a compensatory response, because of positive physiological effects associated with the hyperpneic phase of the cycle, such as amelioration of gas exchange (for increased end-expiratory lung volume), desirable respiratory alkalosis, lytic effect on sympathetic activation, and improved bronchial patency. The pathophysiology of CSA in HF is complex; the main mechanism is identified to be an enhanced peripheral and/or central chemosensitivity, with apneas occurring after intense hyperventilation, due to hypoxia and/or hypercapnia. The circulatory delay between the lung and the chemoreceptors, as well as a reduction in either oxygen or carbon dioxide (CO2) lung stores may favor CSA maintenance. Finally, lung congestion may also increase ventilation instability via pulmonary J-receptors. A rational treatment would better counteract the pathophysiological triggers than targeting (sleep) apneas only. However, further comprehension of the complex interaction among the diverse, specific pathogenic mechanisms that lead to OSA and/or CSA may promote the identification of those needing a targeted treatment and the development of novel therapeutic strategies that could be tailored according to the diagnosed underlying mechanisms in the individual patient