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Clinical Investigations: OBESITY AND HYPOVENTILATION |

The Obesity-Hypoventilation Syndrome Revisited*: A Prospective Study of 34 Consecutive Cases FREE TO VIEW

Romain Kessler, MD, PhD; Ari Chaouat, MD; Philippe Schinkewitch, MD; Michèle Faller, MD; Simone Casel, MD; Jean Krieger, MD; Emmanuel Weitzenblum, MD, FCCP
Author and Funding Information

*From the Department of Pulmonology and Sleep Laboratory, University Hospital, Strasbourg, France,

Correspondence to: Romain Kessler, MD, PhD, Service de Pneumologie, Hôpital de Hautepierre, 67 200 Strasbourg, France; e-mail: Romain.Kessler@chru-strasbourg.fr



Chest. 2001;120(2):369-376. doi:10.1378/chest.120.2.369
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Study objectives: Obesity has many detrimental effects on the respiratory function and may lead to chronic hypoventilation in some patients, an association known as the obesity-hypoventilation syndrome (OHS). In many cases, patients with OHS also have sleep apneas. Hereafter, we describe several features of a cohort (n = 34) of patients with OHS and show the comparisons with a large cohort (n = 220) of patients with obstructive sleep apnea syndrome (OSAS). We compare also OHS patients with a group of patients with the association of OSAS and COPD, also known as “overlap” patients.

Design: Descriptive analysis of prospectively collected clinical data.

Setting: Respiratory care unit and sleep laboratory of university hospital.

Results: In OHS patients, OSAS was present in most of the cases (23 of 26 patients). However, in three patients, OHS was not associated with OSAS, showing that obesity per se may lead to chronic hypoventilation. As expected by definition, OHS patients had, on average the worst diurnal arterial blood gas measurements, compared to the other groups. For the OHS patients, the mean diurnal Pao2 was 59 ± 7 mm Hg, which was significantly different from the Pao2 of the OSAS patients (75 ± 10 mm Hg; p = 0,001) but also from the overlap patients (66 ± 10 mm Hg; p = 0.015). Pulmonary hypertension (ie, mean pulmonary artery pressure > 20 mm Hg) was more frequent in OHS patients than in “pure” OSAS patients (58% vs 9%; p = 0.001).

Conclusion: Patients with OSAS and chronic respiratory insufficiency had in most cases an associated OHS or COPD. Patients with OHS were older than patients with pure OSAS. They had mild-to-moderate degrees of restrictive ventilatory pattern due to obesity. Severe gas exchange impairment and pulmonary hypertension were quite frequent. The association of OHS and OSAS was the rule. However, in three patients, OHS was not associated with OSAS, suggesting that OHS is an autonomous disease.

Figures in this Article

The obstructive sleep apnea syndrome (OSAS) is rarely a cause of respiratory insufficiency. Conversely, daytime impaired gas exchange and pulmonary hypertension occur more frequently in patientswith the association of OSAS and COPD.1This association is usually referred to as the “overlap syndrome.” In addition, respiratory insufficiency and cor pulmonale are frequently observed in very severely obese patients, who were considered in the past as“ pickwickian” patients.2Some of the respiratory conditions of these patients were later described under the term obesity-hypoventilation syndrome (OHS).3 Surprisingly, little is known about the association of OSAS and OHS. For example, it is not clear from the literature which proportion of OHS patients has OSAS.

In this study, we report the features of 34 consecutive patients presenting with an OHS. We analyze clinical data, pulmonary function test results, and pulmonary hemodynamics and polysomnographic characteristics of these OHS patients and compare them with those of OSAS patients and with patients having the association of OSAS and COPD. Our aim was to determine which proportion of patients with OHS has pulmonary hypertension or OSAS.

We included in this study 34 patients who were consecutively admitted to our department between 1991 and 1997. These patients met the criteria for obesity-hypoventilation: (1) hypoventilation defined by a Pao2 < 70 mm Hg and a Paco2 > 45 mm Hg by diurnal blood gas analysis at rest, and (2) obesity with a body mass index (BMI)> 30 kg/m2.

Patients were excluded if the impairment of gas exchange could be explained by any other cause. Therefore, we excluded patients with COPD when they showed an obstructive ventilatory pattern (FEV1/vital capacity [VC] ≤ 60%) and patients with restrictive diseases (eg, kyphoscoliosis, diaphragmatic paralysis, and diffuse interstitial fibrosis), except when the restrictive ventilatory defect was exclusively the consequence of obesity.

We compared these patients with a series of OSAS patients, some of them (n = 30) exhibiting the association of OSAS and COPD (“overlap” patients) that we have recently published.4 In this series, OSAS patients were defined on the basis of a polysomnographic criterion of > 20 apneas and/or hypopneas per hour of sleep, of which> 80% were of the obstructive type. The association of OSAS and COPD defined overlap patients. The presence of COPD was defined by an obstructive spirographic pattern characterized by an FEV1/VC ratio ≤ 60%.,4

All the patients included in the present study were in a stable state at distance (minimum 6 weeks) from any acute exacerbation of the disease: pulmonary infection, acute bronchitis, or an episode of right-heart failure (with peripheral edema) or acute respiratory failure.

We performed conventional spirography with a 10-L, closed-circuit spirograph. Static lung volumes were measured by the helium dilution method. Normal values were those of the European Respiratory Society.5

We measured arterial blood gases while the patients were resting and sitting, and stability was confirmed over at least 1-month follow-up. Nocturnal oximetric data were computed from a night oximetry (Biox 3700; Ohmeda; Louisville, CO) performed separately from the polysomnography.

Right-heart catheterization was performed as previously described.6 Briefly, the hemodynamic measurements were always done while the patient was awake and in the supine position. We used either small-diameter, floated Grandjean 4F catheters (Plastimed; Saint-Leu-la-Forêt, France) or Swan-Ganz 5F catheters (Edwards Lab; Anasco, PR). The catheters were introduced percutaneously into an antecubital or a femoral vein. Cardiac output was calculated according to Fick’s equation applied to oxygen during steady-state conditions. Oxygen uptake was measured by an open-circuit system (Oxycon; Minjardt, The Netherlands).

Polysomnography was performed as described elsewhere.7 Briefly, the polygraphic sleep recording included standard EEG and electro-oculographic studies and electromyographic recording of chin muscles. Breathing during sleep was analyzed with a Fleisch pneumotachograph (Godart; Statham Instruments; Oxnard, CA) attached to a soft facial mask and by means of either thoracic and abdominal strain gauges or an esophageal balloon. Transcutaneous oxygen saturation was recorded with a pulse oximeter (Biox III; Ohmeda, Louisville, CO). Hypopneas were defined as a 50% decrease in tidal volume from its value during quiet wakefulness, for at least 10 s, without a major change in respiratory rate.

Only six patients were excluded from the study. Three patients had a combined restrictive and obstructive ventilatory pattern, two patients had unilateral diaphragm paralysis, and one patient had dorsal kyphosis.

Statistical Analysis

All data were expressed as mean ± SD. We compared the group of OHS patients (n = 34) with the group of overlap patients (n = 30) and with the group of “pure” OSAS patients (n = 220). We used one-way analysis of variance (ANOVA) for comparisons of parametric variables. To determine which groups were different from each other, we performed post hoc tests using the Bonferroni pairwise procedure. Nonparametric tests were used for qualitative variables (Kruskal-Wallis). To assess the role of confounding variables, we selected also a group of 32 patients from the large group of patients with pure OSAS, who matched in regards to age, gender, and BMI with the OHS patients.

Among the 34 patients with OHS, mean age was 61 ± 11 years; 9 patients were women. The average BMI was 40 ± 8 kg/m2, indicating severe obesity. Seventeen of 34 patients were smokers. While 13 patients were ex-smokers, 4 patients still continued smoking. Smoking duration was, on average, 35 ± 25 pack-years. Seven patients complained of chronic bronchitis. Half of the patients had been hospitalized for one or more times in an ICU before definitive diagnosis was made, and eight patients had been intubated and received mechanical ventilation in the past.

All OHS patients claimed having dyspnea on exertion at the time of diagnosis, and all of them reported progressive worsening of this condition during the past years. Associated diseases were common. Diabetes mellitus was present in 30% of the patients, systemic hypertension in 41%, and cardiac abnormalities were observed by echography in 50% of the patients.

We defined three groups of patients. The first group consisted of the 34 patients with OHS without any consideration of the presence or absence of OSAS. The second group was composed of 30 patients with the association of COPD and OSAS (overlap patients). The last group included patients with an OSAS but without COPD and without OHS, so we call them pure OSAS. Only 23 of 34 patients with OHS underwent a complete set of investigations; some refused polysomnography and some refused right-heart catheterization. However, we found no significant differences in regards to demographics, lung function, or nocturnal oximetry data between those patients who underwent all investigations (n = 23) and the remainder (n = 11). So, we included all the 34 patients with OHS for the statistical analysis.

Table 1 shows that OHS patients and patients with COPD plus OSAS were generally older than the pure OSAS. As a mean, OHS patients were 8 years older than patients with pure OSAS (p < 0.05). The proportion of women was significantly higher in the OHS group compared to the two other groups (Table 1). Concerning the respiratory function data, the OHS patients showed a mild restrictive ventilatory pattern (Table 1) with a decreased total lung capacity (TLC; 78% of predicted). The VC was decreased at 79% of the predicted. The FEV1 was also decreased (70% of predicted) but mainly by a reduction of the lung volumes, since obstruction indexes such as the FEV1/VC ratio were in the normal range or only slightly decreased. However, approximately half of the patients had a FEV1/VC between 60% and 70%. So, it is possible that some patients with OHS exhibited minor airway obstruction, related to their smoking history. This pattern was completely different from that of patients with OSAS plus COPD who, by definition, demonstrated an obstructive ventilatory pattern with a FEV1, which was, as a mean, about half of the predicted value and a decreased (< 60%) mean FEV1/VC ratio (Table 1). Patients with pure OSAS had only mild impairment of results of pulmonary function tests; mean TLC was at 86 ± 11% of the predicted value.

The daytime arterial blood gas measures (Table 2 ) showed great differences among the three categories of patients. First of all, patients with pure OSAS had, on average, only mild abnormalities of blood gas levels, with slight hypoxemia and normocapnia. Secondly, the group of patients with OSAS plus COPD demonstrated a lower mean Pao2 and a significantly higher Paco2 (42 mm Hg as a mean). However, the range of the Paco2 values was large, since 27% of the patients showed Paco2 values> 45 mm Hg. Thirdly, the OHS patients had the worst gasometric values, with a mean Pao2 for the group of only 59 mm Hg and a mean Paco2 of 49 mm Hg. These values were significantly different compared to the two other groups (Table 2). Figure 1 shows the relationships of Paco2 and BMI for the three groups of patients. It appears that only four patients with pure OSAS had hypercapnia, whereas all patients with OHS had chronic hypercapnia (by definition) as well as 27% of patients with OSAS plus COPD. The nocturnal oximetric data confirmed also that the patients with OHS or with an association of OSAS plus COPD had worse oxygen nocturnal saturations than the patients with pure OSAS did. Only weak correlations were found between BMI and Paco2 either for the whole study population (r2 = 0.099; p = 0.001) or when considering each group separately (Fig 1). The patients with obesity-hypoventilation had the lowest mean nocturnal saturations (86 ± 5%) and spent more than half of the recording time with an oxygen saturation < 90% (Table 3 ).

The hemodynamic data as well show clearly that the patients with OHS or the association of OSAS plus COPD more frequently have pulmonary hypertension than their counterparts with pure OSAS (Table 3). Indeed, the group with OHS had the highest average mean pulmonary artery pressure (Ppa) value (23 ± 10 mm Hg) compared to the patients with OSAS plus COPD (20 ± 6 mm Hg). The patients with pure OSAS had a normal Ppa on average (15 ± 5 mm Hg). In the group with OHS, there were 17 of 29 patients (59%) with pulmonary hypertension defined by a Ppa ≥ 20 mm Hg. This figure was significantly different from that of patients with pure OSAS (19 of 220 patients with pulmonary hypertension, ie, 9%).

Polysomnography could be performed in 26 of 34 OHS patients (Table 4 ). Only three patients had no OSAS, since their apnea-hypopnea index (AHI) was < 5/h. The remaining 23 patients had OSAS with an AHI of> 20/h of sleep. When comparing the polysomnographic data of the three groups of patients, only some mild differences could be demonstrated. First, the apnea index was not significantly different among the three groups. It was around 60/h of sleep. In the groups with OHS plus OSAS and OSAS plus COPD, the total number of events per hour of sleep (AHI) was higher than in pure OSAS (100 ± 35/h, 89 ± 37/h, and 73 ± 31/h, respectively) but the differences in means were not statistically significant, probably because of the huge dispersion of individual figures. The total sleep time, on average, was significantly lower in patients with OSAS plus OHS, but the dispersion of individual results was great (2.3 ± 2.4/h). The distribution of the sleep stages was not significantly different between the groups and showed mainly a shortage of stage 3 to stage 4 sleep and also of rapid eye movement sleep.

When comparing a group of patients with pure OSAS matched for age, BMI, and gender (n = 32) to the group of OHS patients (n = 34), the findings were not substantially different from the preceding results, except for the restrictive ventilatory pattern that reached a comparable extent for the two groups. The percent of predicted TLC was 78 ± 15% for the matched group of patients with pure OSAS compared to 78 ± 11% for the patients with OHS (not significant [NS]).

Our study highlights the impairment of gas exchange, which occurs in some patients with OSAS and an associated OHS or COPD. The deleterious effects on gas exchange of these associations can be observed even when the ventilatory defect is of mild-to-moderate degree, and would not induce per se respiratory insufficiency.

In a study published previously by our group,4 we examined patients with the association of OSAS plus COPD, and we showed that these patients had more gas exchange abnormalities and had more frequent pulmonary hypertension than OSAS patients without an associated COPD (patients with pure OSAS). In the present study, we have shown that patients with OHS, who have respiratory insufficiency by definition, also have the highest frequency of pulmonary hypertension, compared to OSAS plus COPD patients or to pure OSAS patients. By contrast, it appears that patients with pure OSAS have only a low risk of respiratory insufficiency and pulmonary hypertension, as shown by diurnal blood gas analysis, nocturnal oximetry, and right-heart catheterization. Indeed, if we consider the whole group of patients having OSAS proved by polysomnography (n = 265), approximately 17% (n = 45) had some features of an obstructive or a restrictive ventilatory defect. However, the restrictive ventilatory defect was mainly in relation to obesity, since patients with pure OSAS matched for BMI, age, and gender had the same degree of impairment of lung function test results. So in severely obese patients, usual lung function tests were not very helpful for the diagnosis of OHS.

The patients with OHS, who had the most severe arterial blood gas disturbances compared to the two other groups, also exhibited the most severe nocturnal oxygen desaturations. Therefore, it is not surprising that these patients also had pulmonary hypertension more frequently. Indeed, the major cause of secondary pulmonary hypertension is alveolar hypoxia. The presence of pulmonary hypertension with increased total pulmonary vascular resistances in 17 of 29 patients with OHS confirms that these patients suffered from profound and prolonged periods of hypoxia.8Numerous studies from our group and others9have shown that pulmonary hypertension is not only a marker of hypoxia over time but also a very potent prognostic factor. However, it is possible that in some patients with OHS, the pulmonary hypertension resulted from chronic left-heart failure, especially when cardiac echography demonstrated left ventricular hypertrophy, a common finding in severe obesity.1011

One could argue that our definition of OHS is controversial. Indeed, how can we relate the diurnal hypoventilation to obesity rather than to OSAS? It must be emphasized that OHS, ie, the respiratory consequence of morbid obesity, has received little attention in the medical literature since the first reports of the pickwickian syndrome and some elegant physiologic studies from Rochester and Enson3 and Lopata and Önal.12 But at the time of the study of Rochester and Enson,3 polysomnography was not available. In the more recent study of Lopata and Önal,12only three patients belonged to the group of OHS and all three patients had a significant number of obstructive sleep apneas. In the present study, we found 3 of 26 patients with OHS but without OSAS, demonstrating that obesity per se could lead to chronic hypoventilation. This figure is lower than the 25% of OHS patients without OSAS reported in the literature.13 Finally, the causal relationship between OSAS and OHS, which has been postulated, was not found in our three patients. However, a link between OSAS and OHS is not excluded. Indeed, the association of OHS plus OSAS was much more frequent than OHS without OSAS. In patients with OHS plus OSAS, the average proportion of obstructive apneas was 92 ± 10%. However, 12 patients out of 23 had variable amounts of central hypopneas (30 ± 12%), which corresponded to prolonged periods of hypoventilation.

A diminished ventilatory response to hypoxia and hypercapnia being acquired as a result of OSAS seems unlikely since no correlation was observed between Paco2 and AHI and in general between Paco2 and features of severity of OSAS, as found by several groups.1416 However, no significant correlation was found between Paco2 and weight indexes such as BMI, either when considering the whole group of patients or when considering only patients with OHS. Like us, some authors found no correlation between weight and Paco2,17 whereas some others did.14,1819 Similarly, there was no strong correlation between BMI and lung volumes such as VC or TLC.2021 It must be emphasized that conventional spirography might not be the best way to explore the consequences of obesity on the respiratory system. Indeed, it has been demonstrated that lowered chest wall compliance and a decreased strength of inspiratory muscles together with a restrictive pattern were common in patients with OHS3 and were probably the best predictors of hypercapnia. An increased incidence of female subjects (9 of 34 patients in our study) in the group of OHS patients compared to the group of patients with OSAS alone was also reported in the literature.13 This fact may be related to the impact of menopause on hormone-related respiratory drive, but also to the increased susceptibility of nocturnal disordered breathing in postmenopausal women.22Progesterone (and possibly estrogen) might protect women from sleep-disordered breathing during their reproductive years. It has been demonstrated that progesterone increases the muscle activity of upper airways, especially the activity of the genioglossus muscle. Female hormones, together with other factors (genetics, obesity) might also explain anatomic and structural differences in upper airways that were demonstrated between men and women.23

Beside this effect of female hormones, protecting women from OSAS, progesterone is also known as a respiratory stimulant, increasing the ventilatory drive. So, in postmenopausal women, one could expect an increased frequency of OSAS but also a decrease of the ventilatory drive, unmasking hypoventilation in severe obesity. Interactions between decreased sex hormone levels and obesity could explain, at least partially, a higher female to male ratio in our group of patients with OHS compared to patients with OSAS alone.

Considering the three groups of patients (n = 284), all hypercapnic patients but 4 belonged either to the OSAS plus COPD group or to the OHS group. So, hypercapnia was a pertinent discriminating factor between patients having OSAS alone or patients having OSAS associated with OHS or COPD. Nevertheless, four patients with OSAS but without COPD and without significant obesity showed hypercapnia. It is not excluded that in rare cases, some patients with severe OSAS might have daytime hypercapnia, especially in the case of excessive daytime sleepiness.24Apneas or hypopneas may cause only acute rises of carbon dioxide, but in the case of a normal lung function and a normal ventilatory drive, no excessive daytime accumulation of carbon dioxide should appear. On the contrary, in the case of a patient with OSAS and an impaired ventilatory function or an impaired ventilatory drive or both, persistent hypercapnia may occur. Some articles2526 have shown that hypercapnic patients with an OSAS have a decreased ventilatory response to hypercapnia but a normal response to hypoxia. Whether this abnormal ventilatory response to hypercapnia is the cause or the consequence of chronic hypercapnia remains unknown. Some human studies suggested that the diminished ventilatory responses were probably acquired. One argument in favor of this hypothesis is that the chemosensitivity of normal family members of hypercapnic patients with OSAS was not found predictive of patients’ hypercapnia.27Another argument of an acquired diminished response to hypercapnia is the improvement of the ventilatory response after treatment by tracheostomy or nasal continuous positive airway pressure ventilation.2830 However, even after efficient treatment of the OSAS, hypercapnia may persist, whatever the correction of the ventilatory response to carbon dioxide may be. Rapoport et al31observed persistent hypoventilation during wakefulness in half of their obese patients, in spite of treatment. The mechanisms that link obesity and hypoventilation are unknown, but are thought to imply a depressed central control of the ventilatory drive. Hence the Prader-Willi syndrome (PWS), the most common genetic disorder leading to obesity, is associated with sleep-disordered breathing. Arens and colleagues32 have shown that in obese PWS patients, the hypercapnic ventilatory responses were blunted compared to nonobese PWS patients or to obese control subjects. Moreover, isocapnic hypoxic ventilatory responses were absent or severely reduced in PWS patients compared to obese control subjects.

Animal models suggest an inherited mechanism. In the genetically obese mice (ob/ob), alveolar hypoventilation could be related to the lack of a protein, the leptin, which is the product of the ob gene.33Moreover, the administration of leptin restored the ventilatory responses to hypercapnia, independently of weight or carbon dioxide production.34 It must be emphasized that in the majority of obese humans, except in rare cases of congenital obesity, the plasmatic levels of leptin are increased. However, it is supposed that some obese patients develop a state of resistance against leptin, which could be similar to the resistance against insulin.

Our study has some limitations. Particularly, it is possible that the OHS group represents a subset of severely obese OSAS patients with delayed diagnosis. Indeed in our series, the OHS patients were significantly older than patients with pure OSAS. At the moment of the diagnosis, about half of them had been hospitalized for acute respiratory insufficiency one time or more in the past. Moreover, dyspnea on exertion was often present for many years before clinical diagnosis. It is possible that psychological factors related to morbid obesity may predispose these patients to underestimate or even to be unaware of their disease or medical condition for a long time.35 This behavior may also explain why we were unable to perform all the investigations in the patients with OHS: 25% refused polysomnography and 20% refused right-heart catheterization.

It would have been interesting to compare patients with OHS but without OSAS to OHS patients with OSAS. Unfortunately we found only three patients with OHS but without OSAS, so statistical comparisons were not possible.

In conclusion, patients with an OSAS seldom had chronic respiratory insufficiency. Gas exchange impairment was related in most cases to the association of COPD or was attributed to OHS. Patients with OHS, like patients with the association of OSAS plus COPD, exhibited many features of poor prognosis, such as severe hypoxemia, hypercapnia, and pulmonary hypertension. The association of OHS with OSAS was the rule. However, in three patients, OHS was not associated with OSAS, suggesting that OHS was an autonomous disease. Since a significant proportion of patients (17% in our study) with OSAS also had either airway obstruction or gas exchange impairment, pulmonary function tests and daytime blood gas measurements should be performed particularly in current or ex-smokers and in the case of a low baseline saturation before polysomnography.

Abbreviations: AHI = apnea-hypopnea index; ANOVA = analysis of variance; BMI = body mass index; NS = not significant; OHS = obesity-hypoventilation syndrome; OSAS = obstructive sleep apnea syndrome; Ppa = pulmonary artery pressure; PWS = Prader-Willi syndrome; TLC = total lung capacity; VC = vital capacity

Table Graphic Jump Location
Table 1. Anthropometric Data and Pulmonary Function Data *
* 

Data are expressed as mean ± SD. The statistical results between groups are those of the Bonferroni’s test performed after ANOVA. RV = residual volume.

 

p values of comparisons between OHS and pure OSAS patients.

 

p values of comparisons between pure OSAS patients and OSAS plus COPD.

§ 

p values of comparisons between OHS and OSAS plus COPD.

Table Graphic Jump Location
Table 2. Arterial Blood Gases and Nocturnal Oximetry *
* 

Data are expressed as mean ± SD. The statistical results between groups are those of the Bonferroni’s test performed after ANOVA. Sao2 = mean nocturnal oxygen transcutaneous saturation; tSao2 < 90 = percentage of nighttime with Sao2 < 90%.

 

p values of comparisons between OHS and pure OSAS patients.

 

p values of comparisons between pure OSAS patients and OSAS plus COPD.

§ 

p values of comparisons between OHS and OSAS plus COPD.

 

Daytime values.

Figure Jump LinkFigure 1. Relationship between BMI and Paco2 in patients with OHS (top), the association of OSAS and COPD (middle), and pure OSAS (bottom). The horizontal line indicates the level of Paco2 (45 mm Hg), above which patients are hypercapnic.Grahic Jump Location
Table Graphic Jump Location
Table 3. Pulmonary Hemodynamics *
* 

Data are expressed as mean ± SD unless otherwise indicated. The statistical results between groups are those of the Bonferroni’s test performed after ANOVA. PVR = total pulmonary vascular resistance; PH = pulmonary hypertension, ie, Ppa > 20 mm Hg.

 

p values of comparisons between OHS and pure OSAS patients.

 

p values of comparisons between pure OSAS patients and OSAS plus COPD.

§ 

p values of comparisons between OHS and OSAS plus COPD.

Table Graphic Jump Location
Table 4. Polysomnographic Data *
* 

Data are expressed as mean ± SD. The statistical results between groups are those of the Bonferroni’s test performed after ANOVA. AI = apnea index; TST = total sleep time; REM = rapid eye movement.

 

p values of comparisons between OHS and pure OSAS patients.

 

p values of comparisons between pure OSAS patients and OSAS plus COPD.

§ 

p values of comparisons between OHS and OSAS plus COPD.

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Arens, R, Gozal, D, Omlin, KJ, et al Hypoxic and hypercapnic ventilatory responses in Prader-Willi syndrome.J Appl Physiol1994;77,2224-2230. [PubMed]
 
Tankersley, C, Kleeberger, S, Russ, B, et al Modified control of breathing in genetically obese (ob/ob) mice.J Appl Physiol1996;81,716-723. [PubMed]
 
O’Donnell, CP, Schaub, CD, Haines, AS, et al Leptin prevents respiratory depression in obesity.Am J Respir Crit Care Med1999;159,1477-1484. [PubMed]
 
Van Gemert, WG, Severeijns, RM, Greve, JW, et al Psychological functioning of morbidly obese patients after surgical treatment.Int J Obes Relat Metab Disord1998;22,393-398. [PubMed]
 

Figures

Figure Jump LinkFigure 1. Relationship between BMI and Paco2 in patients with OHS (top), the association of OSAS and COPD (middle), and pure OSAS (bottom). The horizontal line indicates the level of Paco2 (45 mm Hg), above which patients are hypercapnic.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1. Anthropometric Data and Pulmonary Function Data *
* 

Data are expressed as mean ± SD. The statistical results between groups are those of the Bonferroni’s test performed after ANOVA. RV = residual volume.

 

p values of comparisons between OHS and pure OSAS patients.

 

p values of comparisons between pure OSAS patients and OSAS plus COPD.

§ 

p values of comparisons between OHS and OSAS plus COPD.

Table Graphic Jump Location
Table 2. Arterial Blood Gases and Nocturnal Oximetry *
* 

Data are expressed as mean ± SD. The statistical results between groups are those of the Bonferroni’s test performed after ANOVA. Sao2 = mean nocturnal oxygen transcutaneous saturation; tSao2 < 90 = percentage of nighttime with Sao2 < 90%.

 

p values of comparisons between OHS and pure OSAS patients.

 

p values of comparisons between pure OSAS patients and OSAS plus COPD.

§ 

p values of comparisons between OHS and OSAS plus COPD.

 

Daytime values.

Table Graphic Jump Location
Table 3. Pulmonary Hemodynamics *
* 

Data are expressed as mean ± SD unless otherwise indicated. The statistical results between groups are those of the Bonferroni’s test performed after ANOVA. PVR = total pulmonary vascular resistance; PH = pulmonary hypertension, ie, Ppa > 20 mm Hg.

 

p values of comparisons between OHS and pure OSAS patients.

 

p values of comparisons between pure OSAS patients and OSAS plus COPD.

§ 

p values of comparisons between OHS and OSAS plus COPD.

Table Graphic Jump Location
Table 4. Polysomnographic Data *
* 

Data are expressed as mean ± SD. The statistical results between groups are those of the Bonferroni’s test performed after ANOVA. AI = apnea index; TST = total sleep time; REM = rapid eye movement.

 

p values of comparisons between OHS and pure OSAS patients.

 

p values of comparisons between pure OSAS patients and OSAS plus COPD.

§ 

p values of comparisons between OHS and OSAS plus COPD.

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