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SLEEP AND BREATHING: Jean-Pierre Laaban, Edmond Chailleux for the Observatory Group of ANTADIR Daytime Hypercapnia in Adult Patients With Obstructive Sleep Apnea Syndrome in France, Before Initiating Nocturnal Nasal Continuous Positive Airway Pressure Therapy Chest 2005; 127: 710-715 [Abstract] [Full text] [PDF]

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Obesity Hypoventilation Syndrome: More than Just Obesity !

TAPAS BANDYOPADHYAY   (3 July 2005)

The role of OSA in daytime hypercapnia

Onofrio Resta, Pierluigi Carratù MD   (12 July 2005)

Obesity Hypoventilation Syndrome: More than Just Obesity ! 3 July 2005
TAPAS BANDYOPADHYAY, Pulmonary/Critical Care Saint Francis Hospital and Medical Center Send letter to journal: Re: Obesity Hypoventilation Syndrome: More than Just Obesity ! bpdk{at}msn.com TAPAS BANDYOPADHYAY	I read with great interest the article by Jean Pierre Laaban et.al. in Chest, March 2005 (1). The authors describe a large series of patients with obstructive sleep apnea (OSA) and daytime hypercapnia. The article cast some light on the intriguing disorder, the obesity hypoventilation syndrome (OHS). The patient population chosen in the study was somewhat skewed because by definition, all had OSA. As a central disorder in both OSA and OHS is probably some form of disordered ventilation, it is possible that the incidence of daytime hypercapnia is relatively high in this study. It was interesting to find that the prevalence of daytime hypercapnia increased with increasing body weight in this study. Prior studies differ as to the linear association between body weight and daytime hypercapnia. Akashiba and colleagues reported a study on 143 male patients with OSA. The BMI did not correlate well with daytime PCO2 (2). An ongoing study at our institution is evaluating the prevalence of daytime hypercapnia in morbidly obese subjects under evaluation for Bariatric surgery. Of interest was the low prevalence of daytime hypercapnia in subjects with morbid obesity (BMI > 40 kg/m2) with a poor correlation between the BMI and PCO2 (3). It is well known that many obese subjects do not suffer from obstructive sleep apnea (4) and even fewer have daytime hypercapnia when causes such as significant COPD are excluded. There has been a poor correlation between the AHI (Apnea Hypopnea Index) and BMI. It is likely that key factors other than obesity are involved in the pathogenesis of chronic hypoventilation and daytime hypercapnia. Interesting postulates are respiratory muscle fatigue, diminished ventilatory response to a respiratory load and resistance to circulating mediators like leptin. The important fact to realize is that we do not have accurate clinical predictors of hypercapnia in obese subjects. We should be considering the OHS more often, especially in subjects who are overweight, have obstructive sleep apnea and suffer respiratory complications. Simple and easily available tests like an arterial blood gas evaluation and spirometry may suffice for a diagnosis. Subjects with obesity hypoventilation syndrome tend to develop respiratory complications commonly and it is not uncommon to see such subjects being inappropriately treated for asthma and COPD in the absence of significant airway obstruction (5). More such studies will be needed to answer key questions on the obesity hypoventilation syndrome. It will of interest to see if the study subjects of Laaban and Chailleux have resolution of hypercapnia with the regular use of CPAP if controlled for weight loss. It is also important to screen for pulmonary hypertension in subjects with OHS because of the significant and often prolonged drop in oxygen saturation observed during sleep. Tapas Bandyopadhyay, MD, FCCP Saint Francis Hospital and Medical Center, Hartford CT 06105, e-mail:bpdk@msn.com References: 1. J Labin, E Chailleux. Daytime Hypercapnia in Adult Patients with Obstructive Sleep Apnea Syndrome in France, Before Initiating Nocturnal Nasal Continuous Positive Airway Pressure Therapy: Chest 2005; 127:710- 715. 2. Akashiba T, Kawahara S, Kosaka N. Determinants of chronic hypercapnia in Japanese men with Obstructive Sleep Apnea. Chest 2002; 121: 415-421. 3. T Bishop, SA Shaikh, C Barba, T Bandyopadhyay. Obesity Hypoventilation Syndrome: A New Look: Proceedings of the American Thoracic Society. Vol. 2 (2005). 4. Vgontzas AN, Tan TL, Bixler EO et al. Sleep apnea and sleep disruption in obese patients. Arch Intern Med. 1994; 154(15): 1705-11. 5. Kessler R, Chaout A, Schinkewitch P et al. The obesity-hypoventilation syndrome revisited: a prospective study of 43 consecutive cases. Chest 2001; 120:369-376.
The role of OSA in daytime hypercapnia 12 July 2005
Onofrio Resta, MD Pulmonary, University of Bari, Pierluigi Carratù MD Send letter to journal: Re: The role of OSA in daytime hypercapnia oresta{at}pneumol.uniba.it Onofrio Resta, et al.	We read with great interest the study by Laaban JP and Chailleux E (March 2005),(1) investigating daytime hypercapnia (Paco(2) >/= 45 mm Hg) in patients with obstructive sleep apnoea (OSA), free of associated chronic obstructive pulmonary disease (COPD), with a wide range of Body Mass Index (BMI). The authors showed that patients with OSA, associated to daytime hypercapnia, have a significantly higher BMI than patients with OSA, but not hypercapnia, demonstrating that increased BMI is an independent predictive factor of daytime hypercapnia in a large group of obese patients. Furtermore, the authors demonstrated that Pao(2), BMI, FEV(1), and vital capacity (VC) can only explain <10% of Paco(2) variance, and that daytime hypercapnia was observed in 7% of patients with OSA not associated with obesity (BMI<30), suggesting that OSA itself may lead to hypercapnia. However, the role of sleep respiratory disturbance in the development of the hypercapnia is quite controversial. In fact, most of previous studies did not show a relationship between severity of OSA (expressed as index of apnoea-hypopnoea (AHI) and/or duration of events) and daytime hypercapnia, while nocturnal desaturation seems to play an important role in causing hypercapnia in OSA patients, as demonstrated by different articles,(2) including our study on a population of 219 obese patients with OSA but free of associated COPD.(3) However, few studies have evaluated this group of patients in terms of sleep hypoventilation (SH). We showed in a mixed population of 161 obese subjects (mean BMI 43.4±8.1) without COPD (29% with SH),(4) and in a population of 128 obese females (mean BMI 42.58±8.6) without COPD (21.8% with SH)(5), that SH was mostly associated to apnoeic or hypopnoeic events. In these patients, nocturnal desaturation, but not restrictive pulmonary pattern, plays a major role in establishing the Paco(2) level (34% of total variance). The relationship between diurnal Paco(2) and nocturnal desaturation is only partially obvious: it is well known that the severity of oxyhemoglobinic desaturations during sleep depends not only on the level of diurnal Sao(2) and Pao(2) but also on the nocturnal hypoventilation which may be present in these patients and may be independent of the diurnal level of Paco(2). Unfortunately, no further information is provided on nocturnal desaturation and/or sleep hypoventilation in the Laaban’s article in both, obese and not obese individuals. Interestingly, recent data found that in a population of mild obesity with OSA (mean BMI 32.2±0.8), circulating levels of leptin, an adipocyte-derived signaling factor that increases in accordance with BMI, were higher in hypercapnic patients with OSA than in eucapnic patients with OSA, in presence of similar BMI, % of pred VC, FEV(1)/VC % ratio, AHI, and visceral fat accumulation (VFA).(6) Furthermore, the same authors showed that in non obese individuals with OSA, sleep hypoxaemia (nocturnal average of Sao(2), and lowest Sao(2)) was correlated to serum leptin levels, but not to AHI, BMI and VFA.(7) The mechanical impairment of respiratory system due to obesity and/or COPD might be an important mechanism, but not the exclusive, in determining daytime hypercapnia in OSA. However, hypercapnia in non obeses and non COPD patients suggest that OSA itself may lead to daytime hypercapnia. Most likely, the characteristic features of OSA, such as chronic inflammation, metabolic failure, insulin resistance, nocturnal hypoxemia, and sleep fragmentation may play a crucial role in pathophysiological abnormalities of this subset of patients. References 1. Laaban JP, Chailleux E. Daytime hypercapnia in adult patients with obstructive sleep apnea syndrome in France, before initiating nocturnal nasal continuous positive airway pressure therapy.Chest. 2005 Mar;127(3):710-5. 2. Akashiba T, Kawahara S, Akahoshi T, et al. Relationship between quality of life and mood or depression in patients with severe obstructive sleep apnea syndrome.Chest. 2002 Sep;122(3):861-5 3. Resta O, Foschino Barbaro MP, Bonfitto P, et al. Hypercapnia in obstructive sleep apnoea syndrome.Neth J Med. 2000 Jun;56(6):215- 22 4. Resta O, Foschino-Barbaro MP, Legari G, et al. Sleep-related breathing disorders, loud snoring and excessive daytime sleepiness in obese subjects. Int J Obes Relat Metab Disord. 2001 May;25(5):669-75 5. Resta O, Foschino Barbaro MP, Carpagnano GE, et al. Diurnal PaCO2 tension in obese women: relationship with sleep disordered breathing. Int J Obes Relat Metab Disord. 2003 Dec;27(12):1453-8 6. Shimura R, Tatsumi K, Nakamura A, et al. Fat accumulation, leptin, and hypercapnia in obstructive sleep apnea-hypopnea syndrome. Chest. 2005 Feb;127(2):543-9. 7. Tatsumi K, Kasahara Y, Kurosu K, et al. Sleep oxygen desaturation and circulating leptin in obstructive sleep apnea-hypopnea syndrome.Chest. 2005 Mar;127(3):716-21.