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University Hospital Marqués de Valdecilla, University of Cantabria, Santander, Spain
Correspondence to: Rafael Golpe, MD, Rúa do Ensino, 1-3 D, 32002 Orense, Spain; e-mail: rafa898{at}separ.es
To the Editor:
We read with interest the article by Akashiba et al (February 2002),1 which reported on their study of the determinants of chronic hypercapnia in patients with obstructive sleep apnea syndrome (OSAS). We have recently conducted a study to assess the prevalence and mechanisms of diurnal hypercapnia in patients with OSAS, and we think that our results support the findings of Akashiba et al.
We retrospectively studied the records of 175 consecutive patients in whom OSAS had been diagnosed in our center. All patients underwent anthropometric evaluations and forced spirometry using a bell spirometer with a water seal. Diurnal arterial blood gas sampling while breathing room air was obtained from the radial artery. Polysomnography was performed and interpreted following standardized procedures. Patients with an apnea-hypopnea index (AHI) 
10 received a diagnosis of OSAS. COPD was diagnosed in patients with FEV1 values < 80% of the predicted value and FEV1/FVC ratios < 70%. For analyzing the data, we first classified the patients into the following two groups: those with diurnal PaCO2 46 mm Hg (ie, hypercapnic OSAS [H-OSAS]); and those with PaCO2 < 46 mm Hg (ie, normocapnic OSAS [N-OSAS]). The main characteristics for both groups were compared, using unpaired t tests and 
2 tests, when applicable. As a second step, correlations among diurnal PaCO2 and spirometric parameters (ie, FEV1, FVC, and FEV1/FVC ratio), gasometric parameters (ie, PaO2, PaCO2, and pH), polysomnographic parameters (ie, AHI), demographic parameters (ie, age), and anthropometric parameters (ie, body mass index [BMI]) were searched for all patients, using the Pearson correlation coefficient. Finally, multiple regression analysis was performed, introducing diurnal PaCO2 as the dependent variable and those parameters that previously had been found to correlate with PaCO2 using the Pearson correlation coefficient, as independent variables. The results were expressed as the mean ± SD, unless otherwise indicated.
One hundred seventy-five patients were studied (156 men and 19 women). AHI was 42 ± 24 kg/m2. Thirteen patients (7%) were morbidly obese (BMI, 40 kg/m2), 22 patients (13%) had COPD, and 24 patients (14%) had diurnal hypercapnia. H-OSAS and N-OSAS differed significantly in FEV1 (64 ± 26% predicted vs 96 ± 20% predicted, respectively; p < 0.0001), FVC (70 ± 23% predicted vs 101 ± 16% predicted, respectively; p < 0.0001), BMI (35 ± 7 vs 31 ± 5 kg/m2, respectively; p = 0.002), and the percentages of patients who were morbidly obese (21% vs 4%, respectively; p = 0.0068). There were no differences between both groups regarding age, sex, FEV1/FVC ratio, AHI, or the percentage of patients with COPD. Using the Pearson correlation coefficient, PaCO2 correlated with PaO2 (r = 0.22; p < 0.0001), FEV1 (r = -0.41; p < 0.0001), FVC (r = -0.46; p < 0.0001), and BMI (r = 0.24; p < 0.0015). PaCO2 did not correlate with age or FEV1/FVC. Correlation with AHI was weak but almost significant (r = 0.14; p = 0.053), so we decided to include AHI in the multiple regression analysis. Only FVC was found to correlate independently with PaCO2 in multiple regression analysis (p = 0.0075).
The prevalence of diurnal hypercapnia in our patients was similar to that found in other studies and was somewhat lower than the findings of Akashiba et al. Our results suggest that the main mechanism promoting chronic alveolar hypoventilation in patients with OSAS is the presence of restrictive ventilatory defects. Several reports2 have emphasized the association between chronic hypoventilation and heavier weight in patients with OSAS. Although BMI in our study was different in patients with H-OSAS and N-OSAS, and correlated with PaCO2, it was not found to be an independent predictor of hypercapnia in multiple regression analysis. This suggests (in agreement with the findings of Akashiba et al) that the association between both parameters is related to impaired ventilatory mechanics in patients who are overweight, because FVC and BMI correlated significantly in our patients (r = -0.29; p = 0.0001). In agreement with Akashiba et al, we did not find a clear association between ventilatory obstruction and PaCO2 in our patients, unlike the findings of previously reported studies.3 However, forced spirometry may be relatively insensitive to detecting obstructive ventilatory obstructions if it is not combined with other lung function testing methods, such as whole-body plethysmography or gas dilution methods. Therefore, we cannot definitively exclude a role for airways obstruction in the development of alveolar hypoventilation in our patients. Our results also agree with Akashiba et al in not showing a clear association between AHI and chronic hypercapnia. The findings of previous reports regarding this question have been conflicting. We found interesting the association in the study by Akashiba et al between mean arterial oxygen saturation during sleep and PaCO2. Resta et al4 noted that, while AHI was similar for patients with H-OSAS and N-OSAS, patients with hypercapnia had more severe nocturnal oxyhemoglobin desaturations. Chan et al5 studied patients with overlap syndrome and found that the group with diurnal hypercapnia had no higher apnea indexes, but these patients had lower average levels of arterial oxygen saturation during sleep than did normocapnia patients. These observations suggest that the degree of desaturation during apneas, rather than the number of apneas, is more important for the development of diurnal hypercapnia. Some patients with primary alveolar hypoventilation syndrome and central sleep apnea respond favorably to nocturnal oxygen administration, which suggests that cerebral hypoxia during sleep can be an aggravating factor for hypoventilation disorders.6 PaCO2 elevation during apneas also might contribute, impairing the ventilatory response to increased PaCO2.
In conclusion, we have found that chronic hypercapnia in patients with OSAS is associated mainly with restrictive ventilatory defects that seem to be caused by obesity, although it is unlikely that this is the only promoting factor for hypoventilation. We did not find an influence of the severity of the sleep-related respiratory disturbances, as measured by the AHI, in the development of diurnal hypercapnia. We agree with Akashiba et al in their suggestion that nocturnal hypoxia and impaired ventilatory response to hypoxia and hypercapnia may play an important role in the development of chronic alveolar hypoventilation in these patients.
References
Nihon University School of Medicine, Tokyo, Japan
Correspondence to: Tsuneto Akashiba, MD, First Department of Internal Medicine, Nihon University School of Medicine, 30-1, Oyaguchi Kamimachi, Itabashi-Ku, Tokyo, Japan 173-8610
To the Editor:
We are pleased that Drs. Golpe, Jimenez, and Carpizo found our article1 of interest and that they had similar findings in their study. Although the study subjects were slightly different—Caucasian and Asian, more obese and less obese, with and without women, and with and without COPD—the conclusion is similar, that restrictive ventilatory impairment plays an important role in the development of diurnal hypercapnia in patients with obstructive sleep apnea syndrome (OSAS). Their study confirms our hypothesis, that restrictive pulmonary impairment is more important than obstructive disorders which, in previous studies,2 3 were thought to play a major role in development of diurnal hypercapnia in patients with OSAS. This restrictive pulmonary impairment may be induced by chest-wall abnormality and/or by respiratory muscle fatigue in patients with OSAS, and it may be a cause of "can’t breathe," described in the review by Martin and Sanders,4 in patients with obesity-hypoventilation syndrome.
However, in our study, oxygen desaturation during sleep was a more important factor than restrictive pulmonary impairment in the development of daytime hypercapnia. On stepwise multiple regression analysis, partial r2 of the mean arterial oxygen saturation (SaO2) during sleep and percent of vital capacity for daytime PaCO2 were 0.2770 and 0.1554, respectively. These results indicated that 27% and 15% of total variance in daytime PaCO2 were independently accounted for the mean SaO2 and percent vital capacity. The editorial in CHEST by Gozal5 has sophisticatedly interpreted our findings as being indicative of close interactions between a ventilatory debt incurred during obstructive sleep apnea-disturbed sleep and intrinsic individual factors associated with respiratory drive and gas exchanges. Because Golpe, Jiménez, and Carpizo did not show the degree of oxygen desaturation during sleep, we cannot comment on the contribution of desaturation during sleep to the development of chronic hypercapnia in patients with OSAS in their study. As Gozal pointed out,5 breath-by-breath measurements of CO2 and O2 levels during sleep and daytime may provide important insights in pathophysiology of daytime hypercapnia in patients with OSAS.
We are grateful to the authors for demonstrating the importance of restrictive pulmonary impairment in the development of daytime hypercapnuia, even in Caucasian patients with OSAS.
References
This article has been cited by other articles:
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  B. Mokhlesi and A. Tulaimat Recent Advances in Obesity Hypoventilation Syndrome Chest, October 1, 2007; 132(4): 1322 - 1336. [Abstract] [Full Text] [PDF]
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