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Idiopathic Central Sleep Apnea Syndrome (ICSAS) is much less common than Obstructive Sleep Apnea (OSA) and less well understood. These apneas follow abrupt increases in breathing and reductions in arterial CO2, suggesting that they arise from hyperventilation. The authors have evidence that patients with ICSAS, compared to normal controls, show chronic hyperventilation and low blood CO2 both asleep and awake. Also the patients have increased sensitivity of receptors to blood oxygen and carbon dioxide, suggesting that this may underlie their hyperventilation. They authors propose that, in central sleep apneics, chronic hyperventilation keeps arterial CO2 close to the threshold for apnea, and acute episodes of hyperventilation drive it below this threshold, resulting in central apneas.
If this is true, raising the patients' blood CO2 and maintaining it above the threshold should prevent central apneas. They did this by having patients breathe a Co2-enriched gas or breathe through a face mask with added dead space during sleep to increase the amount of rebreathed CO2.
The authors studied six male patients, ages 54-71, with Idiopathic Central Sleep Apnea Syndrome, defined as apneas and hypopneas occuring at least 10 times per hour during sleep, of which at least 75% were central, along with at least two other symptoms of sleep apnea such as excessive daytime sleepiness or nocturnal choking.
All these patients received routine lab polysomnography, with added measurement of esophageal pressure during the first night to determine apnea tpe. Central apneas were defined by absence of breathing for at least 10 secs without esophageal pressure swings or thoracoabdominal movements to indicate respiratory effort. Central hypopneas were defined by a 50% or greater reduction in breathing under similar conditions.
Studies were conducted on four consecutive nights in the sleep lab. The first night, a control night, subjects breathed room air without a face mask. The second night, patients went to sleep wearing a face mask, at first breathing room air but once entering stage 2 non_REM sleep with the occurrence of central apneas, the Co2-enriched gas was given for 1 hour, after which room air and the enriched gas were alternated at 1-hr intervals for the rest of the night. The concentration of CO2 was gradually increased if apneas persisted. The third night, patients received an enriched gas mixture slightly higher than the threshold found the night before for suppressing apneas (1.5-2.3% vs. 1.0-2.0%). The fourth night, only four subjects agreed to breathe through a face mask with added dead space, increased gradually to increase the amount of rebreathed carbon dioxide.
The six subjects ranged in age from 54 to 71, averaging 60; in Body Mass Index from 223 to 37, averaging 29 (i.e., all were slightly overweight); in Apnea Hypopnea Index from 28 to 79/hr, averaging 44; in Movement Arousals from 17 to 29/hr, averaging 23. While awake, they had normal levels of blood oxygen (71-101, averaging 84) and mildly low blood carbon dioxide (35-38, ave. 36). While asleep, they had mild oxygen desaturation (minima 80% to 92%, average 86% and low carbon dioxide (37 to 43%, ave. 40%). Apneas and hypopneas occurred mostly in stage 2 sleep (80% of the time) in association with "periodic breathing," defined as at least three consecutive cycles of overbreathing alternating with central apnea or hypopnea. Reductions in carbon dioxide level always preceded central apneas. An apneic threshold was found to be 0.29% lower than baseline CO2; CO2 never fell lower than this without causing an apnea/hypopnea.
Inhaling CO2-enriched gas increased blood carbon dioxide and reduced its variability. This abolished periodic breathing and desaturations as well as central apneas and hypopneas. As a result, the proportion of time spent in stable breathing during stage 2 sleep was longer, significantly less fragmented than when breathing room air. These improvements were due entirely to reduction s in central apneas and hypopneas, not to obstructive apneas or hypopneas, which occurred mainly in REM sleep. Breathing through added dead space had similar effects on blood carbon dioxide and stabilization of breathing during sleep.
The authors found their results quite consistent with their initial theory, which had evolved out of related previous research. They had shown a therapeutic effect on sleep apneas of increased blood CO2. They noted that a similar measure had been used to relieve central apneas associated with neurological or cardiac diseases and after tracheostomy for obstructive sleep apnea, though these treatments were brief and documentation was minimal. The authors concluded that their findings with added CO2 and added dead space "point to their potential as treatments for this disorder. More studies over longer time periods will be required to test the therapeutic potential of these approaches."
Small as this study was, involving only six patients and, at times, only four, I nevertheless am impressed enough by their findings to consider it important for all patients with central sleep apnea to be aware of this line of research, which seems quite likely to eventuate in therapeutic uses, perhaps sooner for those patients who carry some knowledge of the potential for this approach to convey to their doctors. I recall one study of one patients with central sleep apnea who responded much more poorly to BiPAP, which had the push-pull effect of hyperventilation, than with CPAP. So far, chat discussion, bulletin board postings, and even this website have relatively neglected central sleep apnea, leaving it in a somewhat "mysterious" position of unknown cause and treatment. Yet I am aware of people with central sleep apnea, which may not so infrequently occur along with obstructive sleep apnea.
The different response of the central and obstructive sleep apneas to these measures to increase carbon dioxide indicate the likelihood of fundamentally different mechanisms underlying the two disorders, and different treatments necessary to control them. The fact that the vast majority of sleep apneics have OSA should not lead us to ignore those unfortunate people who suffer, perhaps in addition, from central sleep apnea--or from restless legs, periodic leg movements or sleep, or narcolepsy, all of which can coexist with OSA.
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