I agree with SleepRider, this CSR looks real.
Let's work on trying to minimize this, IMHO it is likely significant.
It is likely that an ASV is in your future, but we need to work with what you have.
Just to supplement info here. You have 2.45 hours of CSR (assuming the machine correctly captured all of it) over 29 % of the 8.33 hr night with a net CAI of over 5.
The above qualifies for a diagnosis of CSR. (But that is up to your doctor)
Some of the article is outright scary.
Etiology
Cheyne-Stokes respiration is a specific form of periodic breathing (waxing and waning amplitude of flow or tidal volume) characterized by a crescendo-decrescendo pattern of respiration between central apneas or central hypopneas. The American Academy of Sleep Medicine (AASM) recommends to score a respiratory event as Cheyne-Stokes breathing if both of the following criteria are met:
- There are episodes of at least three consecutive central apneas and/or central hypopneas separated by a crescendo and decrescendo change in breathing amplitude with a cycle length of at least 40 seconds (typically 45 to 90 seconds).
- There are five or more central apneas and/or central hypopneas per hour associated with the crescendo/decrescendo breathing pattern recorded over a minimum of two hours of monitoring.
https://www.ncbi.nlm.nih.gov/books/NBK448165/
Unlike obstructive sleep apnea (OSA) which can be the cause of heart failure, Cheyne-Stokes respiration is believed to be a result of heart failure. The presence of Cheyne-Stokes respiration in patients with heart failure also predicts worse outcomes and increases the risk of sudden cardiac death. Despite increasing recognition and growing knowledge, Cheyne-Stokes respiration remains elusive, and patients have very limited treatment options.
Treatment / Management
The main cornerstone of management of Cheyne-Stokes respiration is optimizing the treatment for the trigger factor, congestive heart failure (CHF), or stroke. The American Academy of Sleep Medicine recommends that positive airway pressure should be considered for all patients with central sleep apnea. The two main modalities of noninvasive treatment for Cheyne-Stokes respiration are continuous positive airway pressure (CPAP) and adaptive servo-ventilation (ASV).[8][9][10][9]
CPAP delivers continuous positive pressure and has several mechanisms of actions. The positive pressure keeps the upper airway splinted during the central apnea, leading to stabilization of respiratory drives and improvement in oxygenation and ejection fraction. The positive pressure will also reduce the preload by reducing the venous blood flow to the right atrium and afterload by increasing the intrathoracic pressure, thereby improving the ejection fraction. In a clinical trial, CPAP therapy in patients with Cheyne-Stokes respiration showed improvement in nocturnal desaturation, Left ventricular function and six-minute walk distance, but there was no improvement in survival.
Adaptive servo-ventilation is the newer modality of noninvasive treatment which is effective and well tolerated by patients. This mode of noninvasive ventilation can counteract hyperventilation during the hyperpnea phase and prevent hypoventilation during the apnea phase. It delivers constant continuous pressure and can recognize apnea or hypopnea and adjust pressure support with backup ventilation if needed to deliver preset tidal volume. During the hyperventilation phase, the pressure support is reduced, depending on the patient to prevent large tidal volume. Adaptive servo-ventilation is more effective than conventional noninvasive ventilation therapies like continuous positive airway pressure and bilevel positive airway pressure therapy and has been shown to improve the functional class, cardiac functions, exercise capacity and brain natriuretic peptide (BNP) levels. However, in a recent large clinical trial involving patients with systolic heart failure and Cheyne-Stokes respiration breathing, the addition of adaptive servo-ventilation to guideline-based medical therapy did not improve outcome and increased the risk of cardiovascular death.