CSA supplemental O2

The PSG findings are diagnostic of central sleep apnea (CSA); this can be a primary or secondary condition. Secondary causes include Cheyne-Stokes breathing (usually related to congestive heart failure or stroke), high altitude, and sedative-hypnotic use. In the absence of any of these abnormalities, the patient likely has primary (or idiopathic) CSA. This diagnosis requires PSG demonstrating a central event index of at least five per hour, in the absence of a Cheyne-Stokes breathing pattern, diurnal hypoventilation or another explanation for the findings (an alternate sleep pathology, medical disorder, or causal pharmacologic agent). This disorder is most often diagnosed in the middle-aged or elderly, and seems to be more common in men than women. Events are caused by a decrease in arterial CO2 levels below the apneic threshold during sleep, and is often associated with an elevated loop gain (a high ventilatory response to changes in CO2 levels). Because ventilatory control is more unstable during transitions into sleep, primary CSA is often seen more commonly in patients with frequent arousals. Affected patients may have an abnormally low CO2 level during the day, though this is unlikely to induce apnea during periods of wakefulness.

While CPAP is the preferred treatment for patients with CSA, most of the data for the use of this therapy comes from patients with CSA secondary to cardiac disease. It is thought to work in this population by minimizing airway narrowing during central apneas; such airway narrowing can lead to a greater negative airway pressure when breathing resumes, which can lead to ventilatory overshoot, subsequent hypocapnia, and repeated central events.

When CPAP fails to provide benefit, there are several other options that should be considered. Supplemental oxygen during sleep is a reasonable next step; it can be used on its own or as an adjunct to CPAP. Not only has this therapy been shown to decrease the degree of nocturnal hypoxemia, but it may also be associated with improvements in apnea hypopnea index (AHI) (choice D is correct). The mechanism for this improvement has not been elucidated, though some have theorized that it may be due to a decrease in CO2 chemosensitivity.

For patients with a normal ejection fraction, adaptive servo ventilation (ASV) can be considered, though this therapy is contraindicated in patients with an impaired ejection fraction (≤45%) based on the SERVE-HF randomized trial. ASV delivers a fixed level of expiratory pressure and a variable amount of pressure support during inspiration, as well as a backup respiratory rate.

Bilevel positive airway pressure (BPAP) can be an effective treatment for CSA when used in the spontaneous-timed (ST) mode, although it is typically used after both CPAP and oxygen therapy has failed. Unlike ASV, BPAP typically offers a fixed degree of inspiratory pressure support and thus can minimize hypopnea events. However, when used in the spontaneous mode without a backup rate, it will not ventilate the patient during periods of central apnea; indeed, the hyperventilation induced by a larger pressure support may actually exacerbate the frequency and duration of central apnea events. Therefore, BPAP should not be used without a backup rate in this population (choice B is incorrect).

Because the ventilatory response to CO2 is lower during REM sleep, primary CSA is usually significantly attenuated during REM (choice A is incorrect). In addition, because central events are more common during transitions into and out of sleep, low-dose sedative-hypnotic agents have been evaluated for primary CSA, and have been shown to reduce disease severity (choice C is incorrect), though there are no formal recommendations for use of this therapy at this time due to the relative paucity of data.1

Footnotes

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