Current central sleep apnea treatment options

There are treatment options for CSA, but as CSA has a number of causes it is important to identify the underlying cause to guide treatment.


Given that oxygen saturation levels fall during night-time apneic events, it is reasonable to assume that giving supplemental oxygen would maintain oxygen levels in the normal range. Certainly, supplemental oxygen has been shown to reduce the AHI by 37–85% in stable HFrEF with CSA (Randerath et al., 2017). However, while oxygen therapy may reduce CSA, hypoxia and left ventricular ejection fraction, in heart failure, the currently available evidence does not support its use long-term (Randerath et al., 2017).


Acetazolamide is a mild diuretic agent that causes metabolic acidosis. It was hypothesised to reduce the likelihood of developing CSA by shifting the apneic threshold of PaCO2 to a lower level. In a single, double-blind study, acetazolamide showed improvement in subjective sleep quality and decreased both the respiratory events and nocturnal oxygen desaturation. However, it did not show any improvement in left ventricular ejection fraction or in the objective measurement of sleep quality (Javaheri et al., 2016). Acetazolamide has been shown to be effective therapy in primary central sleep apnea and Cheyne-Stokes breathing in patients with heart failure and in the treatment of high-altitude periodic breathing, but it is not recommended currently (Bekfani & Abraham, 2016).

Continuous positive airway pressure

Findings from short-term clinical trials have shown that CPAP can alleviate CSA, improve LVEF and quality of life (Randerath et al., 2017). However, there has only been one long-term, multi-centre clinical trial of CPAP in HRrEF and CSA. This Canadian trial reduced the AHI by 53% but with residual CSA persisting in 43% of the patients (Bradley et al., 2005). CPAP is minimally effective in CSA and is a more suitable treatment for obstructive sleep apnea.

Adaptive servo-ventilation

Adaptive servo-ventilation (ASV) devices have been specifically designed to treat CSA (Baillieul et al., 2019). ASV therapy differs from CPAP or BPAP by providing dynamic (i.e. breath-by-breath) adjustment of inspiratory pressure support (IPS) and utilising an auto-backup rate to normalise breathing rate relative to a predetermined target (Aurora et al., 2016). These devices (figure 21) continually measure either minute ventilation or peak airflow amplitude and they use algorithms to target a specific level of ventilation which is achieved using just enough positive airway pressure (Javaheri et al., 2014). Res Med ASV devices use a three-minute moving average to monitor and determine an appropriate target minute ventilation, set to 90% of their most recent minute ventilation (Aurora et al., 2016). Philips Respironics ASV device utilises inspiratory flow as the primary variable to identify and respond to sleep-related breathing disorders (SRBD). In the absence of SRBD, the algorithm identifies and responds to obstructive sleep disordered breathing events as they occur by increasing the expiratory positive airway pressure (EPAP). During periods of airway stability, the algorithm will proactively assess the airway to minimise pressure while maintaining upper airway patency (Aurora et al., 2016).

An example of ASV (Philips DreamStation BiPAP AutoSV)

Figure 21. An example of ASV (Philips DreamStation BiPAP AutoSV).

Studies have demonstrated that ASV is superior to CPAP therapy for controlling the number of CSA events, improving sleep architecture and daytime hypersomnolence, particularly for Cheyne-Stokes breathing (Philippe et al., 2006; Allam et al., 2007). Indeed, in one study, both ASV and CPAP decreased the apnea-hypopnea index (AHI), but only ASV completely corrected Cheyne-Stokes breathing by attaining an AHI below 10/h (Philippe et al., 2006). ASV treatment guidelines do not recommend ASV in patients with CSA related to heart failure with reduced ejection fraction (HFrEF) (Aurora et al., 2016). This is because the SERVE-HF clinical trial showed that ASV was associated with increased all-cause and cardiovascular mortality (Cowie et al., 2015). However, some aspects of the SERVE-HF trial were controversial and there was low compliance with the ASV treatment (Baillieul et al., 2019).

While the Philips ASV device is not specifically indicated for the treatment of patients with heart failure, recent publications have demonstrated that, during PSG (acutely) as well as over the longer term (up to 12 months), ASV reduces the total apnea hypopnea index, and central apnea index to clinically acceptable levels in patients with heart failure (Lee-Chiong et al., 2015). Indeed, The European Task Force on Central Sleep Apnoea recommends that ASV can be used in CPAP non-responders with symptomatic central sleep apnoea and left ventricular ejection fraction (LVEF) > 45% but not in predominant CSA and LVEF ≤45% (Randerath et al., 2017). That being said, there may be some patients with HFrEF that will respond well to ASV.

Visit the Sleep and Breathing conference 2019 section to learn more about the encouraging compliance data in the ADVENT-HF trial. Dr Elisa Perger describes the effects of ASV on mortality and morbidity in patients with CSA, OSA and heart failure.

A treatment algorithm for the different types of CSA has been suggested (figure 22).

Proposed decision algorithm for CSA treatment

Figure 22. Proposed decision algorithm for CSA treatment (adapted from Randerath et al., 2017).
AHI, apnea-hypopnea index; ASV, adaptive servo-ventilation; CPAP, continuous positive airway pressure; CSA, central sleep apnea; LVEF, left ventricular ejection fraction; NIV, non-invasive ventilation; OSA, obstructive sleep apnea; QoL, quality of life.