Other studies have specifically targeted the presence of hypercapnia in patients with severe OSA as a reason to justify short- or long-term treatment with modes enabled to deliver more aggressive ventilatory capability (13,16,17). In most cases these studies showed marked improvement in daytime PaCO2 levels with treatment of accompanying nocturnal hypoventilation with BPAP, which in some cases allowed resumption of CPAP treatment alone for satisfactory response to the underlying OSA. Patient adherence remained high in these patients (18).
In order to assess the reasons why a BPAP device was provided to a group of moderate-to-severe OSA patients, a study was done to investigate the frequency of BPAP prescription when CPAP was ineffective or not tolerated during titration (19). Of 286 consecutive adult patients referred to two sleep labs, 130 patients were enrolled and 105 (84% males) completed the study. A split-night (diagnostic and therapeutic) polysomnogram (PSG) was done, followed by another PSG with BPAP if CPAP was not tolerated, or failed to correct sleep-related breathing (SRB) abnormalities. There were 24 patients (23% overall) that received BPAP with the highest prevalence (11 of 17) in patients with OSA associated with OHS. The BPAP treated patients were more obese, hypercapnic, had severe SRB desaturations, and also had more obstruction, restriction, and hypoxia.
The prevalence and mechanism of hypercapnia in morbidly obese patients were investigated in a selected group of 285 patients presented to a sleep laboratory without other significant comorbid diseases. There were 89 morbidly obese patients (31.2%) who had a BMI > 40 kg/m2 and surprisingly 59.6% were predominately females (20). This group was further divided into three subgroups who were nor-mocapnic without OSA, normocapnic with OSA, and lastly hypercapnic (PaCO2 > 45 mmHg) with OSA. Their results showed that hypercapnia was found in 27% of the morbidly obese subjects (who were predominately males) but only in 11% of the nonmorbidly obese patients (P < 0.01). Several characteristics were more common in the patients with hypercapnia and OSA than patients with or without OSA including significantly more restriction based on a mean total lung capacity (% predicted) of 63.8% ± 16.4%, a higher respiratory disturbance index of 46.3 ± 26.9 events/hour, a longer total sleep time with SpO2 < 90% (TSTSpO2 < 90%) of 63.4 ± 33.9 minutes, and a lower rapid eye movement (REM) sleep at 9.5 ± 1.2%. Their conclusion about important factors associated with hypercapnia and OSA allowed them to construct a predictive model for diurnal hypercapnia: PaCO2 = -0.03 FVC %predicted - 0.05 FEV1 % predicted + 0.036 TSTSpO2 < 90% - PaO2 + 57.13 (r2 = 0.44).
Another small study investigated whether a variety of factors were associated with failure of CPAP therapy to resolve the apnea-hypopnea index (AHI) to < 5 or mean SaO2 > 90% (14). This study of 13 patients with OSA (Group A) over a 15-month period compared to an age- and AHI-matched control group (Group B) successfully treated by CPAP used logistic regression analysis to identify factors associated with initial failure to CPAP. The Group A versus Group B patients were significantly more obese (mean BMI = 44.2 kg/m2 vs. 31.2 kg/m2; P < 0.001), hypoxic at rest (P < 0.001), and at exercise (P < 0.005). Hypercapnia at rest (P < 0.001) and worsening during exercise was also more likely, and Group A patients also spent significantly (P < 0.0001) more time with oxygen saturation < 90%, which was the only factor independently associated with the initial failure of CPAP [odds ratio (OR) 1.13; 95% confidence interval (CI) 1.0-1.2]. The patients' awake blood gases proved that both daytime hypoxemia and hypercapnia improved significantly (P < 0.05) after three months of treatment with BPAP.
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