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Supposedly, nasal continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP) are equally effective for obstructive apneas. CPAP has also been shown effective for some cases of central apnea. It is unclear how BiPAP affects central apnea. The authors report one case of central apnea where the two approaches had quite different effects.
This was a 57-year-old man who began snoring at age 40. He complained of 3 years of excessive daytime sleepiness. His body mass index was 27. His blood pressure was normal. His waking blood gases showed slightly low oxygen (74) but normal carbon dioxide (39). He had mild non-insulin-dependent diabetes but there was no indication of diabetic neuropathy. Pulmonary function tests were normal, without evidence of upper airway obstruction. Cephalometry showed no narrow pharynx or retracted lower jaw.
Standard overnight sleep studies were performed.On the second night, his Apnea Index was moderately high at 27/hr, comprising mainly central apneas (26/hr) and his Apnea/Hypopnea Index (56/hr) was vert high. His longest apnea lasted 38 seconds, and his arterial oxygen saturation fell as low as 69%. On another occasion, esophageal pressures were monitored to confirm the central nature of the apneas.
During waking, the response of his breathing was tested to lowered levels of oxygen and increased levels of carbon dioxide by adjusting the gas mixture he breathed, reducing oxygen saturation on the one hand to 80% and increasing carbon dioxide on the other hand to 65 mm Hg. He seemed to have an exaggerated sensitivity of breathing response to both low oxygen and high carbon dioxide.
CPAP as low as 6 cm H2O was found to markedly suppress central apneas, to an Apnea Index of 8-10 with a longest apnea of 21-24 seconds and lowest oxygen saturation of 89-92%. Higher pressure, up to 12, had more pronounced effects, reducing his Apnex Index to 0-4, his longest apnea to 0-12 secs, and his lowest oxygen saturation to 95-96%. His symptoms of excessive daytime sleepiness disappeared a few days after starting on CPAP.
Then, on two nights, he received alternating trials of CPAP and BiPAP for 10-30 minutes each during non-REM sleep. The BiPAP expiratory pressure was set at 2 cm H2O and the inspiratory pressure was randomly varied from 6 to 12 cm H2O in sequential trials. CPAP had its usual beneficial effect, but BiPAP had quite a different effect.
The lowest level of inspiratory BiPAP (6 cm H2O) left the central sleep apneas much as they were without treatment, with Apnea Index 15-27/hr, longest apnea 39-51 secs, and lowest oxygen saturation 71-78%. However, the higher levels of inspiratory BiPAP pressure (9 & 12 cm H2O) made the central apneas worse, Apnea Index increasing to 33-42, longest apnea to 63-69 seconds, and lowest oxygen saturation to 63-69%. BiPAP also reduced his carbon dioxide levels below those he had in the waking state.
The authors summarized these different affects by stating taht CPAP caused alveolar hypoventilation whereas BiPAP caused hyperventilation.
Six months later, the authors studied him overnight without CPAP but with inrpiration of gas enriched with carbon dioxide on three occasions. Without the enriched gas, his Apnea/Hypopnea Index was 32/hr; with it, his AHI went down to 7.3/hr.
The authors noted various proposed mechanisms by which CPAP might eliminate central apnea, such as stimulation of receptors to mechanical stretch in the pharynx leading to increased respiratory drive and "stiffen" the pharynx. On the other hand, there is other data to suggest that the beneficial effect of CPAP on central apneas comes from raising the blood level of carbon dioxide, which should stabilize respiration by constantly stimulating the respiratory drive. Their own data on this patient seem to support this mechanism. They believe that the underlying problem is one of increased sensitivity of receptors to carbon dioxide causing unstable respiratory drive, the central apneas being triggered by hyperventilation causing the patient to overshoot the apnea threshold carbon dioxide levels.
Regular viewers of this site may recall--and others may wish to refer to--a previous article reviewed here on the subject of central sleep apnea (Article #23). This article led in a similar direction, towards perceiving central sleep apneas as closely related to altered carbon dioxide sensitivity and hyperventilation. However, another article (Article #29) pointed to anatomical factors as well. Although the issue of what causes central sleep apnea seems still uncertain, what is most important is that inroads are being made into what has been viewed as a comparatively obscure condition, contrasted to obstructive sleep apnea. We should bear in mind that, while central sleep apneics may be in the minority, many more individuals have some combination of obstructive and central apneas. CPAP, it seems, may benefit both, but it is important to be aware of the possibility that BiPAP, supposedly an "improved" treatment, may benefit only the obstructive component and exacerbate the central component. Not only central sleep apneics, but also those with mixed obstructive-central apneas, may do worse on BiPAP for this reason. It would be interesting to examine sleep clinic polysomnography data for patients being tried on BiPAP who might have mixed apneas with an exacerbation of the central component, and follow up these patients if they continue on BiPAP for other reasons.
In my own research in psychopharmacology, I always found it far less interesting and instructive when a certain type of drug uniformly yielded beneficial effects on most patients, then when it had contrasting absent or countertherapeutic effects on certain patient groups. This uncommon situation spoke more the the underlying nature of the disorder than did the usual practice of extrapolating from the common neuropharmacological effects of a class of drugs to construct a biochemical theory about the illness they were used to treat.
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