Key references for pathophysiology and treatment of central sleep apnoea syndrome (CSAS)
| Reference | Summary | Comment |
|---|---|---|
| CPAP = continuous positive airway pressure; Pco2 = carbon dioxide tension; CSAS = central sleep apnoea syndrome; CHF = congestive heart failure. | ||
| Naughton et al83 | Controlled study with a CPAP treatment period of 1 month. Pressure: 10.2 (0.5) cm H2O. In a subgroup of 12 patients CPAP significantly reduced the frequency of apnoeas and hypopnoeas, increased the oxygen saturation and Pco2, and normalised minute volume during sleep | Comprehensive study suggesting CPAP as an additional treatment option for chronic heart failure patients |
| Naughton et al84 | Randomised controlled study with a CPAP treatment period of 3 months. Subjects: 12 patients in the control group (no CPAP) and 12 patients in the treatment group (10.1 (0.5) cm H2O). Significant improvements were found for the following parameters: apnoeas and hypopnoeas during sleep, arousals during sleep, left ventricular ejection fraction during wakefulness, symptoms of fatigue, and disease mastery | Extension of the study above, reaching good quality standards for clinical trials, and confirming CPAP as a beneficial treatment option for the CSAS |
| Javaheri85 | A one night CPAP treatment was performed in 29 patients with CHF. 16 responded to treatment, determined by a significant reduction in apnoeas, hypopnoeas, arousals, percentage of total sleep time below a saturation of 90%, and lowest saturation. 13 did not respond to CPAP Responders had a highly decreased frequency of premature ventricular contractions and couplets | Javaheri identified responders and a high proportion of non-responders in his study population. The results in responders are similar to the results in the studies above |
| Willson et al86 | Eleven patients were started on a 3 month home trial with nocturnal controlled nasal intermittent positive pressure ventilation (nIPPV). Ventilatory parameters were set in such a way that the Pco2 was maintained at or slightly below the patient's awake level. nIPPV abolished periodic breathing in all patients with a significant improvement in the sleep architecture, frequency of apnoeas and hypopnoeas, arousals, and a significant increase in left ventricular ejection fraction. Long term domiciliary usage of the device was poor; only 6 patients completed the 3 month trial | Volume controlled ventilation and slight hyperventilation does not seem to be an adequate treatment option for the majority of patients |
| Hanly et al87 | Nine patients were included in a randomised placebo controlled crossover study administering 2–3 l/min oxygen or compressed air for one night. Oxygen reduced Cheyne-Stokes respiration by 50%, mainly in stage 1 sleep, with no significant changes in the other sleep stages. The sleep architecture was improved, the same was found for apnoeas, hypopnoeas, and arousals | Low flow oxygen is effective in reducing apnoeas and hypopnoeas in patients with CHF, but its therapeutic benefit is much lower than CPAP |
| Andreas et al88 | Similar study design and results to Hanly's study, but exercise performance, measured as peak oxygen uptake, improved significantly in the 22 participants after 1 week of treatment with 4 l/min oxygen during sleep. Cognitive function improved as well, but no change was found in daytime symptoms | This is the only study evaluating exercise capacity, an important parameter for patients after treatment of central sleep apnoea |
| Franklin et al89 | Prospective intervention study of 20 patients, 16 with chronic heart failure. During one treatment night oxygen doses had been titrated individually, and in 17 of 20 patients the frequency, but not the duration, of central apnoeas was reduced significantly. The arousals were aalso reduced, but the effect on total sleep time and daytime sleepiness was very variable | The interindividual differences of the effect of oxygen was very variable in this study, despite an individual titration of oxygen flow. Oxygen eliminated some central apnoeas, whereas the majority of events remained unchanged |
| Xie et al90 | Six patients with idiopathic CSAS had been treated with 3% CO2 in their inhalation gas or with a full face mask, enlarging ventilatory dead space. Pco2 increased between 1.3 and 2.4 mm Hg and apnoeas and hypopnoeas were virtually eliminated | Hyperventilation below the threshold of apnoea plays a key role in central apnoeas. Increasing Pco2 in patients with CSAS seems to make these events less likely |