Continuous positive airway pressure (CPAP), or fixedpressure CPAP, was the first modality described and still the most widely used. This modality delivers the same
pressure to the patient during both inspiration and expiration and remains unchanged throughout the night.

Bilevel positive pressure (BIPAP) provides the ability to independently adjust the inspiratory (IPAP) and expiratory (EPAP) pressure such that the pressure delivered during exhalation is lower than that delivered during inhalation (5). Several studies have confirmed the effectiveness of BIPAP in the treatment of OSA in adults (6, 7, 8, 9).

Most BIPAP devices are used in one of two modes: spontaneous (S-mode) or spontaneous-timed (ST-mode). In S-mode, IPAP is delivered in response to a patient “trigger.” In ST-mode, the patient may trigger the delivery of IPAP; in addition, the physician may set the device so that IPAP is delivered at prescribed intervals if a spontaneously triggered breath does not occur within that interval. This backup respiratory rate provided in the ST-mode is not commonly employed in the treatment of classic OSA but may be beneficial in selected patient groups with more complex sleep-disordered breathing, such as those with neuromuscular disorders, chest wall deformities, or congestive heart failure (CHF) with Cheyne-Stokes breathing.

The pressure required to maintain airflow and control of breathing may vary throughout the night, as well as from night to night, and may be dependent on patient factors such as sleep staging, body position, and alcohol consumption. In autotitrating devices, the physician sets a prescribed pressure range, allowing the delivered pressure to vary throughout the night in order to meet the patient’s changing pressure requirements in real time. Autotitrating devices employ computer algorithms to detect changes in airflow and adjust the delivered pressure accordingly. Autotitrating devices are available in both autotitrating continuous positive airway pressure (APAP) and autotitrating BIPAP (auto bilevel) forms.

One theoretical advantage of autotitrating technology is the reduction in the overall cumulative pressure exposure during the night and subsequent improvement in patient comfort and compliance. Compared to fixed CPAP, studies of APAP show similar effectiveness on both symptomatic and polysomnographic measures and a small (2 cm H₂O) average reduction in pressure. On an individual basis, some patients strongly prefer APAP over traditional fixed CPAP or BIPAP. The literature has not yet supported an improvement in adherence with autotitrating devices compared to fixed-pressure devices in CPAP naïve patients (10, 11).

CPAP has been shown to improve both subjective and objective measures of OSA. On polysomnography, proper CPAP titration is associated with improved sleep continuity and architecture. During the first night of treatment, some patients may manifest an unusually large percentage of rapid eye movement (REM) sleep (“REM rebound”) as a result of sudden reversal of the airway obstruction and associated chronic sleep deprivation. CPAP often has a beneficial impact on other nocturnal aspects of OSA, including treatment of snoring, decreased nocturnal awakenings, and a reduction in nocturia (17, 18, 19, 20, 21, 22).

In studies of patients with OSA and hypersomnia, treatment of CPAP is associated with a reduction in daytime sleepiness and improvement in neurocognitive function and quality of life measures (23, 24). The effect of CPAP on objective metrics of sleep propensity during the day (e.g., multiple sleep latency test [MSLT] or maintenance of wakefulness test) is less clear, with only some studies showing an effect and a less compelling impact in patients with mild OSA (17, 23, 25). Nevertheless, despite some controversy with regard to the sleep laboratory results, the data on motor vehicle collisions, one of the most important public health risks associated with OSA, are much more convincing. A number of studies employing driving simulators have demonstrated improved performance
following initiation of CPAP therapy (26, 27, 28). Similarly, a comparison of the number of accidents per driver per year over the 3 years before and following CPAP therapy in OSA patients demonstrated a notable reduction, reaching levels that were comparable to those in individuals without OSA (Fig. 136.3) (29).

Numerous studies have shown that OSA is associated with cardiovascular disease and that successful PAP therapy results in reduced cardiovascular mortality (30, 31, 32). In a prospective cohort from the Sleep Heart Health Study, investigators showed that sleep-disordered breathing is associated with increased overall mortality as well as mortality specifically due to coronary artery disease, particularly in those patients with severe OSA (AHI greater than 30) (Fig. 136.4) (31). A large observational study showed that men with severe OSA have an increased rate of both fatal and nonfatal cardiovascular events (32). Furthermore, treatment with PAP effectively lowered this cardiovascular risk (Fig. 136.5). Finally, Peker et al. (33) assessed incident cardiovascular events in middle-aged men with OSA over 7 years and noted that the incidence of cardiovascular events in patients who were adequately treated (by PAP, uvulopalatopharyngoplasty, or oral appliances) was about 7% in contrast to about 57% in patients who were inadequately treated.

Cardiac rhythm disturbances are common in OSA patients, and the favorable response of arrhythmias to CPAP therapy, especially in the absence of structural heart disease, reinforces the linkage between OSA and rhythm
disturbances (34, 35, 36, 37, 38, 39). A recent randomized controlled trial reported that, after 1 month, CPAP therapy reduces the frequency of premature ventricular beats by nearly 60% in OSA patients with heart failure compared to patients who are not receiving CPAP, in whom there was no significant change (39).

Studies also support the improvement in left ventricular function after initiation of PAP therapy for patients with OSA and heart failure (40). The mechanisms by which PAP may improve cardiac function in OSA patients with heart failure include relief of sleep-related hypoxemia, elimination of cyclic increases in left ventricular afterload, reduction in sympathetic nervous system activation, and reduced inflammation.

Epidemiologic studies have provided compelling evidence that OSA is associated with increased risk for systemic HTN (41, 42, 43, 44, 45, 46). Sleep apnea has been identified by the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure as a risk factor for HTN (47). Although it is plausible that PAP therapy would ameliorate diurnal HTN by eliminating intermittent hypoxic exposure and sympathetic nervous system activation and improving sleep continuity, the literature provides conflicting data in this regard (48, 49, 50, 51).

Using a randomized, placebo-controlled design to compare ambulatory blood pressure on CPAP and sham CPAP in subjectively sleepy OSA patients, Pepperell et al. (52) observed a small but significantly greater reduction in mean blood pressure during sleep in the active CPAP-treated group. Although small, the reduction in blood pressure in the active CPAP group would have a notable public health impact on cardiovascular risk. Conversely, there are a number of well-designed studies of groups of OSA patients either with or without subjective sleepiness, and with HTN, that have failed to demonstrate a significant reduction in blood pressure with PAP therapy (53, 54, 55). In summary, it is evident that further research is required to define the effect of PAP on HTN in OSA patients.

The association between sleep-disordered breathing, including OSA, and increased risk for stroke is increasingly recognized. Data from the Wisconsin Sleep Cohort indicate that, even after adjusting for age, gender, smoking, HTN, alcohol use, and body mass index (BMI), sleep-disordered breathing is associated with increased risk for prevalent stroke (56). Further, there is increasing awareness of the association between OSA, abnormal glycemic control, type 2 diabetes mellitus, and other features of the metabolic syndrome (57). Further studies are required to determine if PAP therapy of OSA reduces risk for incident stroke and improves insulin sensitivity and glycemic control.