CSA-CSR is characterized by a crescendo-decrescendo pattern of 20-30 second hyperventilation followed by 10- 40 second hypopneas or apneas during exercise, wakefulness or stages 1 and 2 non-rapid eye movement sleep (1,2). CSA-CSR is associated with elevated pulmonary capillary wedge pressure, ventricular dilatation, atrial fibrillation, and increased central and peripheral chemosensitivity to arterial C02 levels (1).
In contrast to obstructive sleep apnea whose detrimental impact is widely accepted, CSA-CSA has not consistently been shown to be associated with higher mortality rates, with some even arguing for its beneficial effects in HF by providing intrinsic positive end-expiratory pressure (PEEP), augmented stroke volume, avoidance of hypercapnic acidosis, attenuated sympathetic activity, bronchodilation and cyclic respiratory muscle rest, akin to those seen with episodic CPAP (2). This is an interesting way of looking at CSA-CSR, underscoring the importance of addressing the underlying problem (e.g. HF) rather than the symptoms alone.
1. Rosen D, Roux FJ, Shah N. Sleep and breathing in congestive heart failure. Clin Chest Med 2014, 35: 521–534. https://www.ncbi.nlm.nih.gov/pubmed/25156768
2. Naughton MT. Cheyne-Stokes respiration: friend or foe. Thorax 2012;67:357-360. http://thorax.bmj.com/content/thoraxjnl/67/4/357.full.pdf