Begin at 5 cm H20 IPAP 2.5 cm H20 EPAP

If nonapneic desaturation

If nonapneic desaturation

If nonapneic desaturation

If nonapneic desaturation

Increase IPAP in 2.5 cm H20 stages

FIGURE 2 Algorithm for adjustment of inspiratory positive airway pressure and expiratory positive airway pressure during the trial of nasal bilevel positive airway pressure (BiPAPĀ®). Source: From Ref. 9.

is more effective in splinting the pharynx open than BPAP in patients with OS A. Another study of 10 selected patients with OSA requiring > 10 cm H2O of CPAP failed to show optimal resolution of SDB at any level of IPAP until a critical level of EPAP was achieved indicating a clear need to select an adequate EPAP level (11).

An alternative approach to BPAP titration has been to optimize all SDB events with CPAP and then to reduce both the EPAP and IPAP as allowed taking advantage of the natural hysteresis that occurs during a typical CPAP titration episode. In one study, a small but significant reduction in the optimal CPAP level occurred when a downward titration followed an initial titration procedure (12).


The importance of recognizing and addressing the differences in respiratory system loading that occurs during the inspiratory phase in specific subtypes of patients has helped guide which patients might best be considered for BPAP as well. The impact of obesity on the mechanical loading of the respiratory system, neuromuscular control, and the pathogenesis of apnea and related hypoventilation has been known for many years. This issue was more precisely studied in three groups of severely obese patients, who were eucapnic obese without OSA (O), eucapnic obese with OSA (OSA), or hypercapnic obese with sleep apnea (OH), and were compared to nonobese volunteers (NO) who were subjected to abdominal mass loading (13). This was assessed with diaphragmatic electromyogram (EMGdi), a measure of muscle activation, and mouth occlusion pressure (P0.15), an assessment of mechanical drive, during CO2 stimulation. The authors showed that P0.15 responses were decreased in OSA and OH but the EMGdi responses did not differ from the control subjects. However, when the NO control subjects were subjected to mass loading, the EMGdi and P0.15 responses increased. Their findings showed that both OSA and OH patients did not develop the expected increase in respiratory muscle response for a given level of activation and the impaired mass load compensation predisposes obese patients to develop hypercapnia. These kinds of observations may help explain why the early BiPAP study focused on patients with a mean body mass index (BMI) of 57.4 kg/m2 even though they were normocapnic and why severe obesity has emerged as an independent predictor of failed CPAP therapy (9,14).

The unloading of inspiratory muscle activity with BPAP measured as diaphragmatic pressure time product was studied in 18 obese subjects with a BMI > 40 kg/m2 including five healthy controls with simple obesity (SO), seven patients with OSA, and six with obesity-hypoventilation syndrome (OHS) (15). Although the overall ventilation as measured by end-tidal carbon dioxide with BPAP was not changed in SO and OSA, it was decreased in OHS, while the inspiratory muscle activity was reduced by at least 40% in all groups. The authors concluded that BPAP may be particularly effective for improving ventilation in patients with OHS by unloading the inspiratory muscles.

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