What every physician needs to know:

Obesity is recognized as a significant and rapidly increasing cause of morbidity and mortality around the world. This presentation reviews the significant impact that obesity has on pulmonary function, including testing, exercise, ventilatory control, and disease states. According to recent data, obesity is a common co-morbidity seen in many pulmonary disorders and clinicians should be aware of its implications.


The presence of obesity is defined by and categorized according to body mass index (BMI). BMI is calculated as weight in kilograms divided by the square of height in meters (kg/m2). The National Institute of Health defines overweight as a BMI of 25-29.9 kg/m2, obesity class I as a BMI of 30-34.9 kg/m2, obesity class II as a BMI of 35-39.9 kg/m2 , and obesity class III as a BMI of 40 and over.

Are you sure your patient has a lung disorder related to obesity? What should you expect to find?

Obese patients are often short of breath; in fact, dyspnea has been reported in nearly 80% of obese individuals. Deconditioning may be a contributing factor in some, but the fact that obesity affects breathing at rest and with exercise raises a question concerning how increased weight may impact other respiratory conditions. When obesity and pulmonary disorders coexist additional symptom burden is experienced by the patient often manifesting as decreased exercise capacity and worsened health status. New data suggests that both under- and over-diagnosis are common phenomena in obese individuals with pulmonary diseases and linked to worsened outcomes and over-treatment.

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Chronic Obstructive Airways Disease

Obesity is becoming a common COPD co-morbidity (higher prevalence of obesity in COPD than in general population) and may lead to more pronounced symptoms of dyspnea and exercise intolerance in COPD. In early studies that added weights to patients with COPD as they exercised, the additional weight had some effect on exercise performance, including mean ventilation and oxygen consumption. However, the addition of external weight to a patient with COPD should not be expected to have the same effect as naturally occurring weight gain does, since the weight distribution in the two circumstances differ.

Expiratory reserve volume (ERV) and functional residual capacity (FRC) continue to decrease as BMI increases in patients with obesity and COPD, a finding similar to that observed in obese patients without airflow obstruction. These same studies have shown a consistent reduction in lung hyperinflation and improvement in the inspiratory capacity. The FEV1/FVC ratio may be higher in these individuals as well.

The combination of obesity and COPD has not consistently been associated with increasing shortness of breath during exercise or with diminished exercise capacity compared to that of patients with COPD who are of normal weight, and this finding may be due to the type of exercise regimen employed in these research studies. Cycling performance has been shown to be independent of weight in patients with COPD in several studies. However, walking seems to be affected by obesity.

Obesity does not appear to impact the magnitude of improvement seen in COPD patients after completing pulmonary rehabilitation.

In the past few years several manuscripts were published to address rising challenges in diagnosis, management, and outcomes of COPD individuals with concomitant obesity. Studies confirmed that increased weight results in more frequent over-diagnosis of COPD. Inappropriate diagnosis leads to over-prescribed therapies resulting in more adverse events, no clinical improvement and overall worsened patient-related outcomes burdening individuals and healthcare systems. Interestingly, in one study, despite having better lung function, obese COPD individuals had more dyspnea and worsened quality of life when compared to normal weight COPD patients.

Increasing BMI is also associated with rising number of various co-morbidities. In COPDGene, a prospective large cohort study, worsened quality of life, reduced 6 minute walk distance, and increased dyspnea were observed in obese COPD individuals, even after adjustments were made for number of co-morbidities. Acute exacerbations of COPD have been linked to overall mortality, worsening lung function, and repeated events increasing overall COPD costs. Obese COPD individuals have higher odds of severe exacerbations and more frequent hospitalizations and emergency room visits underscoring the importance of healthy weight for patient-related outcomes in COPD.

Guidelines remain silent whether to recommend weight loss for obese COPD individuals. Pragmatic trials are on the way to answer this important question. In the meantime, a small prospective study confirmed clinically significant but short term improvements in BMI, exercise ability, and health status following combination of diet and resistance training. Importantly, skeletal muscle mass remained the same despite energy restriction, thus weight-loss associated sarcopenia was avoided.


The association of asthma and obesity is complicated. Many studies have demonstrated that overweight children are at increased risk for developing asthma. Postulated underlying mechanisms include dietary effects, gastro-esophageal reflux, atopy, hormonal influences, biological activity of obese tissue, and the impact of obesity on airway mechanics.

Being overweight or obese is associated with a dose-dependent increase in the odds of incident asthma in both women and men. The Normative Aging Study demonstrated that a high BMI is associated with the development of airway hyper-responsiveness. This finding may not be a unique feature of obesity, since the same study also demonstrated that a low BMI is associated with the subsequent development of bronchial hyper-responsiveness. In addition, there does not appear to be an increased rate of methacholine-induced bronchial hyper-reactivity in obese individuals who do not have asthma compared with subjects of normal weight.

Obesity affects asthma control. One study has shown less effective control of asthma in obese asthmatics compared with asthmatics of normal weight despite similar expiratory flow rates and response to bronchodilators in the two groups. Obese asthmatics also have a greater sensation of dyspnea.

Weight loss in obese severe asthmatics has been shown to improve asthma outcomes. Current literature is available on both non-surgical and surgical weight loss approaches and their effect on outcomes in obese asthma individuals.

A randomized controlled trial has evaluated the role of a weight-loss program, exercise program, and a combination of both in obese asthma individuals. Data revealed that addition of exercise to a short-term weight-loss program was the most useful approach in achieving clinical control of asthma in this group of patients. Long-term effects of these interventions have yet to be evaluated and validated in subsequent studies.

Likewise, bariatric surgery has been shown to result in weight loss and improved asthma control. Significant positive changes to quality of life, control of asthma, and improved pulmonary function testing were reported. Importantly, these changes persisted for 5 years following surgical intervention, the longest follow-up available to date.

Respiratory Failure

Obesity has been shown to increase the duration of mechanical ventilation and result in longer stays in the ICU in patients who require mechanical ventilatory support. Despite these findings, the mortality rate does not appear to be increased in mechanically ventilated obese patients compared with non-obese patients.

Proper positioning of the obese patient may be helpful in improving ventilatory parameters. For example, putting the patient in reverse Trendelenburg, thereby displacing the abdominal contents away from the diaphragm, has been shown to increase tidal volume and decrease spontaneous respiratory rate.

Some studies have suggested that higher levels of positive end-expiratory pressure (PEEP) may also be helpful in opening areas of atelectasis at the lung bases. The level of PEEP may be increased to maximize oxygenation without negatively impacting hemodynamics.

Much of the respiratory failure morbidity and mortality has been attributed to acute respiratory distress syndrome (ARDS) and acute lung injury (ALI). Significant improvements in ARDS/ALI mortality have been seen due to implementation of mechanical ventilation protocols (high PEEP + low tidal volumes) based on data from randomized clinical trials performed by the ARDS Network. With time, it had been observed that perhaps obese individuals have a more frequent incidence of ARDS/ALI. Observational studies and meta-analyses have confirmed that obesity is associated with increased risk of ARDS/ALI. On the contrary, the 30- and 90-day mortality has been reportedly better in obese patients with ARDS/ALI. The nature of this association remains a conundrum but has been attributed to the “obesity paradox” well-described in the literature.

Beware: there are other diseases that can mimic a lung disorder related to obesity.

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How and/or why did the patient develop a lung disorder related to obesity?

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Which individuals are at greatest risk of developing a lung disorder related to obesity?

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What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?

Arterial Blood Gas Measurements

Mild hypoxemia and an increase in the alveolar-arterial oxygen gradient are typical in obese individuals, even in the presence of a normal PaCO2. This finding is probably related to an alteration in the distribution of ventilation and perfusion in the lungs. In upright individuals of normal weight, perfusion and ventilation are distributed primarily to the bases.

In obese individuals, perfusion is also greatest at the bases, but ventilation may be decreased at the bases because of limitations in chest wall and diaphragm movement, leading to basilar closure of small airways and atelectasis and redistribution of ventilation to the upper parts of the lungs. The change may lead to an imbalance between ventilation and perfusion. Hypoxemia results from the ventilation-perfusion mismatch and shunt.

Most obese patients do not have elevated levels of carbon dioxide, but hypercapnia may occur in some; such patients are frequently hypoxemic when arterial blood gas testing is done. The term “obesity hypoventilation syndrome” (OHS) has been coined for obese individuals with baseline hypercapnia and hypoxemia. Initially, development of OHS was thought to be due to fat distribution that made it difficult for the patient to ventilate. However, no data are available that demonstrate a relationship between hypercapnia and either BMI or body fat distribution.

One mechanism for development of hypercapnia in individuals with OHS may be a decrease in the ventilatory responsiveness to carbon dioxide. Another may be related to the obstructive sleep apnea (OSA) frequently seen in patients with OHS. In patients of normal weight with OSA and obese patients with OSA, oxygen levels fall and carbon dioxide levels increase during an obstructive apnea. With arousal from sleep, the pharyngeal muscles are activated, the pharynx opens, and air rushes in under pressure, creating a loud snoring sound. Subsequent breaths in afflicted individuals are generally large breaths that re-establish normal oxygen and carbon dioxide levels. Morbidly obese patients with OSA may be mechanically unable to take breaths sufficiently deep to normalize the carbon dioxide level, leading to sustained carbon dioxide elevation during the daytime.

Another co-morbid condition that may lead to persistent hypercapnia in patients with OSA is COPD.

What imaging studies will be helpful in making or excluding the diagnosis of a lung disorder related to obesity?

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What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of a lung disorder related to obesity?

Lung Volume Measurements

The lung volume measurement most affected in obesity is the expiratory reserve volume (ERV). With the exception of ERV, lung volumes are generally well preserved in those with mild or moderate obesity. However, as the level of obesity increases, the resting level of breathing may be altered, and functional residual capacity (FRC) may be reduced. Residual volume (RV) is typically preserved, and total lung capacity (TLC) is usually in the lower range of normal.

The effect of obesity on lung volumes is most likely due to adipose tissue around the ribcage, abdomen, and in the visceral cavity. The simplest explanation for the observed findings is that the diaphragm is displaced into the chest by the enlarged abdomen, directly affecting lung volume and diaphragm movement.

The decrement in lung volumes appears to be greater in those individuals who have been obese for a longer period of time.


The forced vital capacity (FVC) and forced expiratory volume in one-second (FEV1) have been shown to decrease with increasing obesity. The effect is comparatively small, and both FEV1 and FVC tend to remain within the normal range.

Expiratory flow rates decrease with increasing weight, but the decrease is proportional to the decrease in lung volume. Evidence that obesity causes bronchial obstruction is lacking. FEV1/FVC is generally preserved and may actually increase, indicating that both FEV1 and FVC are affected by obesity to a similar degree.

Diffusing Capacity

The diffusing capacity (DLCO) is generally normal in obesity, since the interface of alveoli and capillaries (the “alveolar capillary membrane”) is intact. Some studies suggest that the DLCO may even be increased in those individuals with morbid obesity, perhaps secondary to increased pulmonary blood volume.

What diagnostic procedures will be helpful in making or excluding the diagnosis of a lung disorder related to obesity?

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What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of a lung disorder related to obesity?

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If you decide the patient has a lung disorder related to obesity, how should the patient be managed?

Weight loss is the key intervention in managing patients with obesity-related lung dysfunction. Bariatric surgery induced weight loss has been shown to improve patient-related outcomes in asthma both short- and long-term. Studies including randomized trials evaluating weight-loss programs, exercise interventions or both have been conducted in asthma reporting good short-term results. Prospective single arm studies have been completed to investigate intentional weight loss in COPD and outcomes with good short-term results have been reported. Larger pragmatic trials are currently underway to provide better evidence-based guidelines.

What is the prognosis for patients managed in the recommended ways?

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What other considerations exist for patients with a lung disorder related to obesity?

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