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The Obesity Hypoventilation Syndrome

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The Obesity Hypoventilation Syndrome Review Articles The Obesity Hypoventilation Syndrome Mark Anthony Powers MD Introduction Obesity and Pulmonary Function Compliance and Resistance Work of Breathing and CO2 Production Central Respiratory Drive Sleep Apnea and Obesity Hypoventilation Syndrome Leptin Treatment Summary We only need to look around us to see that we are in an epidemic of obesity and obesity-related medical problems. The obesity hypoventilation syndrome is a disorder in which an obese person with normal lungs chronically hypoventilates. Obesity impairs ventilatory mechanics, increases the work of breathing and carbon dioxide production, results in respiratory muscle dysfunction, and reduces ventilatory response to hypercapnia. Sleep-disordered breathing is present in most patients with the obesity hypoventilation syndrome. When noninvasive ventilation can be successfully in- troduced, hypoventilation can usually be corrected. Weight loss is the desirable long-term treatment for the obesity hypoventilation syndrome. This paper concisely overviews the physiologic factors that lead to the obesity hypoventilation syndrome and discusses therapies for it. Key words: obesity hypoventilation syndrome, OHS, Pickwickian syndrome, simple obesity, ventilatory drive, compliance, airways resistance, work of breathing, respiratory muscle endurance, sleep apnea syndrome, noninvasive positive-pressure ventilation. [Respir Care 2008;53(12):1723–1730. © 2008 Daedalus Enterprises] Introduction obese, defined as having a body mass index (BMI) in excess of 30 kg/m2, and two thirds are overweight (BMI Those who requested “Super Size Me” in the 1990s 25–30 kg/m2) or obese.1 Excess weight is associated with were more likely than not granted their wish. That phrase multiple health problems and with a shorter life expect- sold billions of burgers, fries, and sweet drinks. Recent ancy. A 20-year-old white male with a BMI of 45 kg/m2 data from the Centers for Disease Control and Prevention can expect to live 12 years less than a lean white male with reveal that one third of the United States population is now a BMI of 18–25 kg/m2. A 20-year-old African-American male with a BMI of 45 kg/m2 can expect to live 20 years less than if he were lean.2 Mark Anthony Powers MD is affiliated with the Duke Asthma, Allergy, Charles Dickens’s 1837 description of “a wonderfully and Airway Center, Duke University Medical Center, Durham, North fat boy” who seemed to fall asleep in the middle of knock- Carolina. ing on a door,3 gave birth to the label “Pickwickian syn- The author reports no conflicts of interest related to the content of this drome” for a patient described by Burwell et al in 1956. paper. Their patient fell asleep with a full house of aces over Correspondence: Mark Anthony Powers MD, Duke Asthma, Allergy, kings in his weekly poker game and was then finally con- and Airway Center, Duke University Medical Center, 4309 Medical Park vinced to check into the hospital. His findings included Drive, Suite 100, Durham NC 27704. E-mail: [email protected]. obesity, hypersomnolence, periodic respirations, polycy- RESPIRATORY CARE • DECEMBER 2008 VOL 53 NO 12 1723 THE OBESITY HYPOVENTILATION SYNDROME themia, hypoxemia, hypercapnia (P 73 mm Hg), fea- may be modest, the marked decline in ERV results in tidal aCO2 tures of cor pulmonale, ventilatory impairment, and re- respirations near RV, where airway caliber is narrowest. duced hypercapnic drive, which corrected with weight loss. Central obesity (excess weight located mostly in the His P was 37 mm Hg after an 18-kg weight loss.4 Ͼ aCO2 abdomen and a waist-to-hip ratio of 0.95) has more The obesity hypoventilation syndrome (OHS) is defined impact on pulmonary function than when excess weight is Ͼ 2 as obesity (BMI 30 kg/m ) with hypoventilation (PaCO distributed more around the hips (waist-to-hip ratio Ͼ 2 45 mm) without another coexisting pulmonary, chest- Ͻ 0.95).9 wall, or neuromuscular condition contributing to ventila- The diffusion capacity of the lung for carbon monoxide tory impairment. Simple obesity is defined as obesity with- consists of contributions from the alveolar membrane and out hypoventilation. Though BMI has been used to define capillary volume of the pulmonary circulation. Some obese obesity, body-fat percentage may be a more accurate mea- patients have an increase in diffusion capacity of the lung sure of obesity. BMI correlates more closely with body fat for carbon monoxide from an elevation of capillary vol- percentage (measured with bioelectric impedance) in men ume associated with an increase in blood volume and car- (r ϭ 0.89) than in women (r ϭ 0.80).5 Most of the medical diac output.10 Cardiac output and stroke volume increased literature uses BMI to define levels of obesity. Increasing with BMI by 0.08 L/min and 1.35 mL for each 1 kg/m2 BMI predicts an increased likelihood of OHS. Nowbar of et al found that 33 (27%) of 121 hospitalized patients with BMI in a series of 700 consecutive patients without cor- 11 BMI 35–49 kg/m2 had OHS, and 14 (48%) of 29 with onary disease reported by Stelfox et al. BMI Ͼ 50 kg/m2 had OHS.6 Compared to patients with simple obesity, patients with Compliance and Resistance OHS visit their physicians more than twice as often, have more than twice the yearly medical fees, and have signif- icantly more hospital days per year. Hospital days were Elastance of the respiratory system is the sum of lung reduced from 7.9 d/y before diagnosis to 2.5 d/y after and chest-wall (including diaphragm) elastance. Compli- diagnosis and treatment of OHS in Berg et al’s review of ance is the inverse of elastance and measures the change in health-care utilization in patients with this disorder.7 Hos- volume from an applied pressure. Naimark and Cherniack pitalized patients with OHS had a subsequent one-year found the compliance of the respiratory system (Crs)tobe mortality rate of approximately 20% in Nowbar et al’s 119 mL/cm H2O in seated lean subjects, and 52 mL/cm H2O series, which is more than twice the mortality rate of hos- in seated obese subjects. Crs declined further, to 43 mL/ 6 pitalized patients with simple obesity. cm H2O, in the supine position in the obese subjects, but did not change in the supine position in the lean subjects. Obesity and Pulmonary Function Most of the Crs reduction was from reduced chest-wall compliance with obesity. Lung compliance was also re- Obesity affects respiratory mechanics. Pulmonary func- duced.12 Explanations for reduced lung compliance include tion tests are frequently performed with obese patients an expanded capillary blood volume, or respiring with who have respiratory symptoms or are being considered portions of the lungs below the lower inflection point (of for surgical procedures. The predicted values for interpret- the pressure-volume curve), where lung compliance is re- ing pulmonary function tests use age and height and are duced. Abdominal surgery further lowers compliance. Pe- based on a nonsmoking population studied in leaner times. losi et al found C (measured postoperatively on mechan- We then must determine if the “abnormal” results in an rs ical ventilation) to be 34 mL/cm H O in postoperative obese patient’s pulmonary function tests are from obesity 2 obese patients, versus 62 mL/cm H O in lean patients.13 or a lung disorder. 2 Airways are at their maximum caliber at TLC and are Patients with mild obesity (BMI 30–35 kg/m2) have significantly lower forced vital capacity (FVC), total lung narrowest at RV. Tidal breathing at low FRC causes the capacity (TLC), and residual volume (RV) than lean sub- obese to respire with greater airways resistance (Raw). Zerah jects (Fig. 1). Functional residual capacity (FRC) is the et al found the Raw to be 56% higher in subjects with a 2 volume at which tidal breathing occurs and is determined mean BMI of 46 kg/m than in those with a mean BMI of 2 by a balance of the lungs’ tendency to collapse (elasticity) 27 kg/m . The higher Raw was related to the decrease in and the chest wall’s tendency to expand. FRC is signifi- FRC (r ϭ 0.7, P Ͻ .001). The total resistance of the cantly reduced, even in overweight subjects (BMI 25– respiratory system is the sum of chest-wall resistance and 2 30 kg/m ). The decline in FVC, TLC, and RV is linear, Raw, and is measured with forced oscillation. Further in- and the decline in FRC and expiratory reserve volume crease in respiratory-system resistance (beyond the increase (ERV ϭ FRC – RV) is exponential with increasing BMI in Raw) occurs with increasing obesity, which reflects in- (see Fig. 1).8 Though the reductions in FVC, TLC, and RV creased chest-wall resistance.14 1724 RESPIRATORY CARE • DECEMBER 2008 VOL 53 NO 12 THE OBESITY HYPOVENTILATION SYNDROME (% predicted) FRC (% predicted) VC (% predicted) LCO D 20 30 40 50 60 70 20 30 40 50 60 70 20 30 40 50 60 70 Body Mass Index (kg/m2) Body Mass Index (kg/m2) Body Mass Index (kg/m2) ERV (% predicted) RV (% predicted) TLC (% predicted) 20 30 40 50 60 70 20 30 40 50 60 70 20 30 40 50 60 70 2 Body Mass Index (kg/m2) Body Mass Index (kg/m2) Body Mass Index (kg/m ) Fig. 1. Changes in pulmonary function measurements with increasing body mass index (BMI). Forced vital capacity (FVC), total lung capacity (TLC), and residual volume (RV) decline linearly. Functional residual capacity (FRC) and expiratory reserve volume (ERV) decline exponentially. The diffusion capacity of the lung for carbon monoxide (DLCO) tends to increase with increased pulmonary capillary blood volume.
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