Objectives

1. Identify and understand the respiratory disturbances associated with obesity.
2. Understand the differences between the respiratory manifestations of simple obesity (SO) vs obesity hypoventilation syndrome (OHS).
3. Learn the abnormal pulmonary function test results associated with obesity.
4. Learn the physiologic basis of exercise intolerance in obese people.
5. Identify the challenges associated with critical illness in obese patients.

Abbreviations

BMI = body mass index; DVT = deep venous thrombosis; ERV = expiratory reserve volume; MVV = maximal voluntary ventilation; OHS = obesity hypoventilation syndrome; OSA = obstructive sleep apnea; PE = pulmonary embolism; SO = simple obesity; TLC = total lung capacity; Ve = minute ventilation; Vt = tidal volume; VTE = venous thromboembolism; V/Q = ventilation/perfusion

Obesity is a condition in which a person has excess body weight relative to other people of the same gender and height. Excess weight generally relates predominantly to excess body fat and, to a lesser degree, increased fat-free mass and excess body water. The degree of obesity is commonly expressed in terms of body mass index (BMI) (expressed as kg/m²). A BMI up to 25 kg/m² is considered normal, and 25 to 29 kg/m² is considered overweight. Mild to moderate obesity occurs when the BMI is in the range of 29 to 40 kg/m² . People with a BMI of > 40 kg/m² are considered morbidly obese. Obesity is a major public health problem that has reached epidemic proportion in the United States. The prevalence of people who are overweight and obese has risen dramatically in the United States from 1960 to 2000. The most recent National Health Examination Survey (1999-2000) showed the prevalences of people who are overweight (BMI = 25 to 29 kg/m² ) and obese (BMI >30 kg/m² ) to be 64.5% and 30%, respectively.¹ Alarmingly, the prevalence of morbid obesity has risen threefold between 1999 and 2000.²

Obesity is a major cause of morbidity due to the increased risks of insulin resistance and diabetes mellitus, hypertension, hyperlipidemia, atherosclerosis (including coronary artery disease and stroke), gallbladder and liver disease, gout, and several forms of cancer.^3-6 It also increases the difficulty of performing diagnostic tests and the risk of several complications among patients with critical illness. Moreover, obesity leads to impaired health-related quality of life⁷ and is associated with increased mortality.^8,9 Severely obese men (BMI >45 kg/m² ) have up to a 22% reduction in life expectancy.¹⁰ The medical complications related to obesity incur a huge economic burden of approximately $70 to 100 billion annually (~8.4% of the national healthcare expenditure).^11,12

In addition, obesity, particularly morbid obesity, is associated with a wide range of respiratory disturbances (Table 1). Obesity leads to alterations of respiratory mechanics, airflow resistance, breathing pattern, and respiratory drive and impaired gas exchange, with associated abnormal results found in pulmonary function testing. Moreover, obesity is a common cause of impaired exercise capacity and sleep-disordered breathing (obstructive sleep apnea [OSA] and alveolar hypoventilation). A small subgroup of morbidly obese people develop chronic daytime hypercarbia and hypoxia in the absence of parenchymal lung disease. Such people are considered to have obesity hypoventilation syndrome (OHS). Obese people without these disturbances are considered to have "simple obesity" (SO). This article will review the effects of obesity on the respiratory system and highlight selected aspects of providing care for obese patients with critical illness in the ICU.

Effect of Obesity on Respiratory Mechanics/Compliance

Obesity leads to reductions in lung, chest wall, and total respiratory system compliance, especially among people with OHS (Table 2).^13-15 Lung compliance is reduced due to increased pulmonary blood volume and closure of dependent airways.¹⁶ Chest wall compliance is thought to be reduced because of the excess elastic load posed by excess weight on the thorax and abdomen, as well as by an enhanced threshold load, wherein a greater (more negative) pleural pressure must be generated by the respiratory muscles to initiate airflow.^13-16 However, the chest wall compliance may be normal, or near normal, among people with simple, even morbid, obesity, irrespective of BMI.¹⁷ Thus, additional mechanisms may contribute to abnormal chest wall compliance among people with OHS.

Respiratory System Resistance

Total respiratory system resistance is elevated in obese subjects (Table 2). People with SO and OHS have approximately 30% and 100% increases in respiratory resistance during inspiration, respectively. Of note, the lung resistance in OHS is similar to that in SO, but the chest wall and total respiratory resistance are greater in OHS than in SO.^14,15 The increase in respiratory system resistance in obese people likely relates to increased resistance at the level of the small, rather than large, airways (due to reduced lung volume).¹⁶ As such, the FEV₁ /FVC ratio remains normal (in the absence of concomitant obstructive lung disease).¹⁶ Respiratory resistance increases further in the supine position, as compared to upright body position, possibly due to mass loading of the supralaryngeal airway by fat and increased intrapulmonary blood flow leading to further airway narrowing.^15,16,18 Reduced functional residual capacity (FRC) may also contribute to the increased resistance in the supine position.¹⁶

Respiratory Drive/Breathing Pattern

The majority of obese patients are eucapnic. However, as noted above, a small subset of people has chronically elevated Paco₂ (those with OHS). While both groups of patients have altered breathing patterns, they differ in the nature of the abnormal patterns noted. Eucapnic obese people have a 25 to 40% higher respiratory rate than normal,¹³ while maintaining normal tidal volume ( Vt ) both at rest and during exercise.^16,19 These changes, resulting from a normal to increased respiratory drive,¹³ lead to an increased resting minute ventilation (Ve ) and likely occur in an   effort to compensate for the increased load on the respiratory muscles. Eucapnia is also maintained, in part, by increased neural drive to the respiratory muscles (as assessed by mouth occlusion pressure) and possibly by increased ventilatory responsiveness to hypoxia.¹⁹ Eucapnic obese people also have altered central breath timing (with decreased expiratory time), perhaps, in part, related to altered respiratory system compliance. Patients with SO demonstrate reduced ventilatory responsiveness to CO₂ compared with non-obese people.

In comparison to eucapnic obese people, those with OHS (and resting daytime hypercarbia) have 25% greater respiratory rate and 25% lower Vt.^20,21 The reduction in Vt may contribute to impaired alveolar ventilation. Abnormal ventilatory control/drive, as a cause of this altered breathing pattern in people with OHS, is suggested by blunted mouth occlusion pressure responses to CO₂¹⁶ and by the ability to correct Paco₂ during a voluntary hyperventilation maneuver (suggesting patients are not hypoventilating, as a result of impaired chest wall mechanics or respiratory muscle function). In general, people with OHS have a greater magnitude of impairment in ventilatory responsiveness to CO₂ than those with SO. In contrast to eucapnic obese patients, they also have impaired ventilatory responses to hypoxia.²²

Respiratory Muscle Strength and Endurance

Inspiratory and expiratory muscle strength may be mildly impaired among obese people with OHS.¹⁴ The basis for this is not fully clear given the regular "training stimulus" of the increased mass load during breathing, but it may relate to fatty infiltration of the muscle and diaphragmatic over-stretching. Respiratory muscle endurance, as measured by a maximal voluntary ventilation (MVV) maneuver, is also reduced among obese patients.

Impairments in Gas Exchange

The nature of gas exchange impairment in obesity depends on the severity of the obesity and on whether the patient has SO or OHS (Table 3). Individuals with mild to moderate obesity may have normal Paco₂ .¹⁶ Persons with severe SO may have mildly reduced Paco₂ and widened alveolar-arterial oxygen difference (Paco₂-Paco₂).^16,23 These disturbances are much more severe in people with OHS, and those with OHS have daytime, as well as nocturnal, hypoxemia.²⁴ In both clinical variants of obesity, hypoxemia, when present, results from ventilation/perfusion (V/Q) mismatch and shunting in areas of the lung (especially the dependent, basilar regions) that are atelectatic and have increased airway closure but remain well perfused.^23,25 Persons with OHS have even higher shunt fraction (£ 40% of cardiac output) and lower V/Q ratios compared to those with SO.²⁶ Hypoventilation contributes to hypoxemia in people with OHS.²⁷ Obesity-related hypoxemia becomes more exaggerated in the supine position, when FRC is further reduced.¹⁴ By definition, Paco₂ is normal among people with SO and is elevated among people with OHS. Both blunted respiratory drive and increased work of breathing likely contribute to the hypercapnia in OHS.²⁸ In the presence of an extreme increase in respiratory work, hypoventilation and tolerance of a higher Paco₂ may be a more efficient way to breathe. The set point of the CNS chemoreceptors may then adjust to a higher Paco₂, with resultant decrease in respiratory drive. Several additional factors, including OSA, small upper airway caliber, and obesity itself, may also contribute to the pathogenesis of OHS.^16,28

Work of Breathing

The oxygen cost of breathing (oxygen consumed by the respiratory muscles per liter of ventilation, used as a surrogate for the energy cost of breathing) is increased several fold in severe obesity.²⁹ Overall, the work of breathing is increased for obese patients because of this high energy cost, as well as reduced lung compliance, increased respiratory resistance, and threshold inspiratory load from excess adipose tissue mass.^14,16,23 People with OSA also have elevated pharyngeal and nasopharyngeal resistance that correlates with BMI and may further increase the work of breathing. The work of breathing is estimated to be 60% greater than normal in people with SO and more than 250% greater than normal in those with OHS.

Pulmonary Function Tests

Pulmonary function test findings in obese people reflect the underlying physiologic alterations in respiratory mechanics and airflow resistance. The severity of the abnormal findings depends on both the magnitude of the obesity, as well as the distribution of body fat (central/truncal vs peripheral predominance) (Table 3). The pulmonary function test abnormality most frequently associated with obesity is a reduction in expiratory reserve volume (ERV). ERV is reduced because of mass loading with transmission of weight from the lower thorax and abdomen toward the lungs and upward displacement of the diaphragm. 30 ERV diminishes in proportion to the severity of obesity^13,31-33 and is particularly abnormal in the supine position.³⁰ Reductions in ERV are particularly large in people with OHS.¹³ FVC and FEV₁ are often reduced in proportion to each other in people with marked obesity, particularly individuals with OHS.³² VC and FRC may be reduced among those with severe SO, but total lung capacity (TLC) typically remains normal.³⁴ As such, abnormal findings in TLC should prompt consideration of an additional cause of lung volume impairment. Decrements in lung volume (including ERV, FRC, VC, and TLC) are greater among patients with OHS than with SO.^14,23 Inspiratory capacity (percent predicted) remains relatively normal, even in people with extreme obesity.³¹ Diffusing capacity also decreases in proportion to the degree of obesity.³¹

Body fat distribution, in part, determines the effect of obesity on pulmonary function. People with central, as opposed to peripheral, predominance of fat distribution have greater reductions in FVC, FEV₁, and TLC.^34,35 The MVV may also be reduced. The reduction in MVV occurs in proportion to the increase in BMI and to reductions in expiratory flow (FVC and FEV₁) and lung volume.³² The diffusing capacity for carbon monoxide is usually normal in people with SO and mildly reduced among those with OHS.^16,31 Interestingly, the majority of pulmonary function studies in obesity have included only men. Therefore, little is known about the relative effect of obesity on pulmonary function in women.

Exercise Intolerance

Maximal work rate and oxygen consumption and maximal exercise ventilation may be normal, or near normal, in young obese individuals. However, many obese people experience exercise intolerance. Obesity impairs exercise tolerance by several mechanisms (Table 4). Of note, the majority of studies on exercise and obesity have been conducted in people with SO. Resting metabolic rate is increased relative to lean body mass.³⁶ Obese people consume approximately 25% more oxygen than non-obese patients.¹³ This effect is more exaggerated during exercise. The high metabolic cost of performing relatively low-to-moderate amounts of work is thought to result primarily from the energy needed to move body mass.^36,37 Altered mechanics of the chest and abdomen contribute to the increased ventilatory work. In turn, the high metabolic cost of exercise leads to a higher heart rate and respiratory rate in peak exercise, such that individuals are functioning at a higher percentage of their ventilatory and cardiovascular reserve, even during submaximal exercise.³⁶ As such, obese people may develop decreased work capacity despite relative cardiovascular fitness. Of note, maximal oxygen consumption (Vo₂ max) (expressed as mL/kg body weight/min, is low in proportion to the percent of body fat,¹³ whereas Vo₂ max, expressed as ml/kg fat-free mass/min) is normal.¹⁴ The anaerobic threshold relative to body weight is reduced, as well.

An uncomfortable sense of dyspnea, resulting from the above disturbances, often leads to a relatively sedentary lifestyle. Thus, deconditioning also often contributes to exercise intolerance. V/Q matching and arterial oxygenation often actually increase in obese patients during exercise because of increased depth of breathing.³⁶ The slopes of heart rate, BP, Ve, Vt, respiratory rate, dead space (Vd/ Vt ), and diffusing capacity responses to exercise of young, otherwise healthy, obese patients are similar to non-obese individuals, and the respiratory exchange ratio (Vo₂/Vco₂) remains normal except at the start of exercise, when transient hypoventilation may take place.³⁶

Cardiovascular factors also commonly limit the exercise tolerance of obese patients. Patients with chronic hypoxemia and/or sleep-disordered breathing may have pulmonary hypertension, with resulting impaired right and/or left ventricle stroke volume responses to exercise.^36,38 Diastolic dysfunction associated with hypertension, cardiac ischemia, claudication, and microvascular disease (eg, associated with diabetes mellitus) may also diminish exercise capacity. Finally, musculoskeletal disturbances, such as impaired mechanical efficiency of walking and pain (eg, due to arthritis) and altered breathing pattern related to anxiety, commonly limit exercise.³⁶ Collectively, these causes of impaired exercise often lead to impaired functional capacity, with diminished ability of the severely obese person to work and/or participate in recreational and/or social activities. Severely obese people may have difficulty performing activities of daily living.

Sleep-Disordered Breathing

A full review of the pathogenesis and management of sleep-disordered breathing is beyond the scope of this review but has been discussed elsewhere.^13,16,39,40 In brief, OSA is extremely common in the obese population, affecting up to 50% of obese men.¹³ Obesity is the most common factor predisposing to the development of OSA and is present in 60 to 90% of people with this disorder.¹⁶ Obesity and large neck circumference (>43 cm) predisposes to small retropharyngeal opening space and, in turn, correlates highly with sleep apnea.⁴⁰ Increased fat in and around the pharynx, as well as abdominal and chest wall fat, contribute to the risk of OSA in obese individuals.¹⁶ The majority of people with OHS have OSA.^16,41,42 Those with OHS also have alveolar hypoventilation with daytime hypercarbia and hypoxia that worsens during sleep.^24,41,42 Untreated OSA is associated with increased mortality.⁴⁰ Physiologic consequences of OSA and OHS include neuropsychiatric disturbances relating to sleep deprivation, as well as cardiac arrhythmias, pulmonary hypertension and cor pulmonale, systemic hypertension and coronary artery disease, congestive heart failure, polycythemia, and stroke.^{16,23,39,40,43} Existing therapies for OSA include positive airway pressure, oral appliances, surgical interventions (including the correction of anatomic abnormal findings, such as micrognathia or enlarged tonsils and uvulopalatopharyngoplasty), body sleep position training, and tracheostomy.^13,16,40 Bilevel pressure ventilation is usually needed to maintain effective ventilation and gas exchange among people with concomitant nocturnal alveolar hypoventilation and OSA. Lifestyle changes, such as weight loss, avoidance of sedative medications and alcohol, and maintenance of proper sleep hygiene, are also useful interventions.⁴⁰ Occult hypothyroidism should be excluded.

Deep Venous Thrombosis and Pulmonary Embolism

Obesity is a major independent risk factor for venous thromboembolism (VTE).^44,45 The risk of pulmonary embolism (PE) rises as   BMI increases.⁴⁰ Thromboembolism is particularly common among postoperative patients.^44,45 Immobility and reduction in fibrinolysis are mechanisms proposed to account for this increased risk. Therefore, prophylaxis against VTE is crucial in the obese patient. Unfractionated heparin, low molecular weight heparin, and pneumatic compression are all options for deep venous thrombosis (DVT) prophylaxis. However, the optimal strategy for the use of these methods is not well established among obese people and warrants further study. In particular, it is not clear that conventional subcutaneous dosing of heparin is sufficient to reduce DVT/PE risk to a comparable degree, as for non-obese individuals. The risk of VTE may be particularly high for hospitalized obese patients, especially those with critical illness who are immobilized by require prolonged mechanical ventilation.

Aspiration

The incidence of aspiration is higher among obese patients, as compared with non-obese patients.⁴⁴ Higher volumes of gastric fluid, a high incidence of gastroesophageal reflux, and increased intraabdominal pressure are thought to account for the increased risk of aspiration.

Anesthesia and Perioperative Considerations

Obesity poses an increased risk of complications related to anesthesia and various types of surgery. First, gas exchange disturbances, such as hypoxia and hypercarbia, may be exaggerated during anesthesia^44,46 and in the early postoperative period.^47,48 Second, the incidence of postoperative pulmonary complications, such as VTE, aspiration pneumonia, atelectasis, worsened gas exchange, and respiratory failure, is greater among obese patients.^44,45,47 Rose and colleagues⁴⁹ reported a twofold increased risk of acute postoperative respiratory complications in obese patients compared with non-obese patients. Postoperative respiratory complications are particularly likely among obese patients who have undergone thoracic or upper abdominal incision.⁴⁴ Indeed, obesity in patients has been associated with a higher mortality in studies of liver transplantation,⁴⁷ lung transplantation,⁴⁴ and survivors of blunt trauma.⁴⁷

Recommendations for perioperative management, considered particularly important for obese individuals, include the following: preoperative spirometry to assess risk of postoperative respiratory complications,⁴⁵ perioperative administration of a histamine-2 receptor blocker or other agent to minimize gastric acidity,⁴⁴ aggressive DVT prophylaxis (consider use of adjusted dose subcutaneous heparin with monitoring of the partial thromboplastin time),⁴⁴ maintenance of the head at an angle of ≥ 45% upright, careful attention to pulmonary secretion clearance techniques (eg, incentive spirometry, chest physical therapy, use of nebulizers where needed to assist secretion clearance, and assisted/controlled coughing), early mobilization, and minimized use of medications with potential to suppress respiration.

Additional Considerations in the Critically Ill Obese Patient

As noted, obesity increases the risk of several medical conditions in patients, such as diabetes, cardiac disease, and disturbances of respiration that may increase the risk of and contribute to critical illness. In addition, when critical illness is present, obesity poses particular challenges to the implementation of routine patient care.

Logistic and Technical Difficulties

Obese patients may not be able to undergo certain important diagnostic (particularly radiographic) procedures if they exceed the weight limits of the necessary equipment.⁴⁵ Moreover, results from radiographic studies may be of limited quality due to excess fatty tissue in patients. These logistic difficulties can hinder the speed and accuracy of establishing important diagnoses for such patients. Also, peripheral venous access may be difficult to obtain due to the obscuring of insertion landmarks by fatty tissue. This can lead to increased use of central venous catheters and an increased number of skin puncture attempts to establish vascular access.^45,47 The increased difficulty establishing vascular access leads to an extended duration of indwelling central venous catheters, and, in turn, may lead to an increased risk of infection.^45,47 Doppler ultrasonography may be useful to establish venous access and reduce risk of associated complications in obese patients.⁴⁵

Fluid Management

The management of fluid intake may be extremely challenging due to the presence of cardiac and respiratory disturbances.^45,46 Severely obese persons, particularly those with sleep-disordered breathing, may have coexisting impairments in left ventricular contractility and ejection fraction, systemic hypertension, diastolic dysfunction, and pulmonary hypertension that make it difficult to establish and maintain optimal fluid balance and renal function.⁴⁵ The risk of cardiac arrhythmias is increased.^45,46 A physical exam may be less reliable in the detection of volume status in obese patients. The cuff used to measure systolic BP must be sufficiently large to assure an adequate reading. Invasive (arterial line) monitoring of BP may be required, especially in hemodynamically unstable patients.

Pharmacokinetics

The physiologic changes associated with obesity can lead to alterations in the distribution, metabolism, protein binding, and clearance of many medications.⁴⁵ The nature and magnitude of such changes depends on the degree of obesity, presence of comorbid (eg, renal or hepatic) disease, and the medication in question. As such, it is often difficult to dose medications appropriately. To avoid drug toxicity, ideal, as opposed to actual, body weight may be preferable as a reference for medication dosing in many instances. It is important to consider the tendency of medications to accumulate in fat stores.^45,47 Finally, creatinine clearance estimates, calculated by conventional formulas, may correlate poorly to measured creatinine clearance in obese persons with impaired renal function.⁴⁵ Medications used commonly in the ICU, that must be dosed cautiously (preferably with the assistance of a pharmacist) in obese patients, include benzodiazepines, propofol, aminophylline, digoxin, corticosteroids, and verapamil.⁴⁵

Nutritional Requirements

Obese patients often have excess breakdown of protein relative to fat utilization during critical illness.⁴⁵ As such, care must be undertaken to maintain protein and calorie supplementation to maintain satisfactory nitrogen balance,⁴⁵ despite the patient's obesity. Loss of fat-free mass during critical illness can lead to significant impairment of physical functioning over time. When available, indirect calorimetry may be the preferred means of establishing protein and calorie requirements in the obese patient.⁴⁵

Endotracheal Intubation and Mechanical Ventilation

It is difficult to secure a protected airway during endotracheal intubation in some obese individuals. Factors associated with difficult intubations include large neck circumference, limited neck mobility, small oropharyngeal opening, and difficulty with mouth opening.^45,50 As noted earlier, the supine position may also compromise gas exchange. End-tidal CO₂ monitoring may be inaccurate to detect proper tube placement in obese patients with widened Paco₂-Paco₂.⁴⁴ Critical care providers and anesthetists must be aware of these factors and be prepared to intubate the patient under direct visualization (fiberoptically) if needed.

Careful consideration must also be given to the choice of ventilator settings. A greater amount of mechanical work is required to ventilate obese patients with reduced lung and/or chest wall compliance,⁴⁷ and airway pressures may be increased. The Vt should be chosen based on ideal, rather than actual, body weight, to avoid excess alveolar distension and the potential for high airway pressures and barotraumas.^44,47 Positive end-expiratory pressure is often useful to recruit atelectatic alveoli and improve oxygenation. Importantly, obesity can lead to a longer time supported by mechanical ventilation and difficulty with liberation of the patient from the ventilator,⁴⁷ due to the increased work of breathing associated with the disturbances in respiratory mechanics, airways resistance, respiratory muscle function, cardiac function, and gas exchange.^46,47 Optimal approaches to weaning morbidly obese patients from mechanical ventilation have not been established.

Overall Outcomes Mortality Related to Critical Illness

Obesity is associated with longer lengths of mechanical ventilation support⁴⁷ and ICU and/or hospital stay,^47,51,52 which can lead to increased health-care costs.⁵² Conflicting data exist regarding the effect of obesity on mortality following critical illness. One retrospective study reported an overall mortality of 30% for morbidly obese persons, as compared to 17% for non-obese persons.⁴⁷ However, other studies have failed to demonstrate greater ICU mortality in obese patients.^51,52 This issue requires further clarification in prospective studies, along with clarification of whether there may be subgroups of obese patients who are at particular high risk. Such knowledge could prompt targeted intervention strategies designed to improve patient outcomes.

Benefits of Weight Loss

Weight loss leads to improvements in several of the metabolic and vascular disturbances associated with obesity.⁵³ Likewise, the respiratory disturbances related to obesity improve with weight reduction achieved by control of dietary intake, exercise, and/or by surgical gastroplasty. Specifically, weight loss can lead to improvements in oxygenation, and for people with OHS, in hypercarbia, as well.^13,14  Weight loss can also lead to improvements in lung volumezs,^13,14,54,55 respiratory muscle function,⁵⁴ exercise tolerance and gas exchange during exercise,⁵⁶ and sleep quality and gas exchange during sleep and a reduction of   daytime sleepiness.^{13,14,23,40,57} Thus, successful weight loss intervention strategies have the potential to significantly reduce morbidity and mortality related to obesity. Structured dietary and/or exercise programs, including pulmonary rehabilitation programs, should be considered for patients with obesity and respiratory disturbances. Consultation with a cardiologist may be needed to formulate a safe exercise prescription. Oxygen saturation should be maintained > 90% during exercise, particularly for patients with pulmonary hypertension, to prevent arrhythmias and exercise-induced increases in pulmonary artery pressure that may lead to syncope and circulatory collapse.

Conclusions

Obesity is a major cause of morbidity and mortality. Disturbances of respiratory function, including reduced respiratory system compliance, increased small airways resistance, impaired respiratory muscle function, increased work of breathing, impaired gas exchange, exercise intolerance, sleep-disordered breathing, and increased risks of VTE and aspiration are common, particularly among severely obese patients. These changes can occur independent of any underlying parenchymal lung disease and contribute significantly to functional disability, impaired quality of life, and mortality. Obesity also complicates the care of critically ill and perioperative patients. Weight loss can significantly decrease the risk and severity of obesity-related respiratory disturbances. Obese individuals with respiratory disturbances should be considered for inclusion in a structured rehabilitation program with dietary, behavioral, and exercise components (such as a pulmonary or cardiac rehabilitation program) in an effort to improve functional capacity and quality of life and to reduce the risk of developing pulmonary hypertension and cardiorespiratory failure.

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