Pulmonary Medicine

Obesity and Respiratory Function

What every physician needs to know:

Obesity is recognized as a significant and 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.

Classification:

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 overweightas a BMI of 25 -29.9 kg/m2, obese as a BMI from 30 – 39.9 kg/m2, and extreme or morbid obesity as a BMI of 40 or greater.

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 percent 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.

Chronic Obstructive Airways Disease

Obesity makes the breathing of patients with chronic obstructive pulmonary disease (COPD) worse. 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 differs.

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 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, although 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.

Asthma

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 development 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.

Respiratory Failure

Obesity has been shown to increase the duration of mechanical ventilation and to result in longer stays in the intensive care unit by 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.

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

Not applicable.

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

Not applicable.

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

Not applicable.

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 sleep apnea 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 chronic obstructive pulmonary disease (COPD).

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

Not applicable.

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 rib cage and 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.

Spirometry

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 the same 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?

Not applicable.

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

Not applicable.

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.

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

Not applicable.

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

Not applicable.

What’s the evidence?

Parameswaran, K, Todd, DC, Soth, M. "Altered respiratory physiology in obesity". Can Respir J. vol. 13. 2006. pp. 203-210.

(A comprehensive review of the impact of obesity on lung function.)

Salome, CM, King, GG, Berend, N. "Physiology of obesity and effects on lung function". J Appl Physiol. vol. 108. 2010. pp. 206-211.

(A detailed discussion of the impact of obesity on lung mechanics and flow rates.)

Rapoport, DM, Garay, SM, Epstein, M, Goldring, RM. "Hypercapnia in the obstructive sleep apnea syndrome: a reevaluation of the Pickwician Syndrome". Chest. vol. 89. 1986. pp. 627-635.

(This study examined the relationship between OHS and OSA in eight patients. Treatment of sleep apnea by a tracheostomy in seven patients and nasal CPAP in one patient corrected hypercapnia in four of the patients. Those four were thought to have a mechanical reason for their hypercapnia that was relieved with removal of pharyngeal obstruction during sleep. The patients with persistent hypercapnia were thought to have blunted ventilatory responses to hypercapnia.)

Swinburn, CR, Cooper, BG, Mould, H, Corris, PA, Gibson, GJ. "Adverse effect of additional weight on exercise against gravity in patients with chronic obstructive airways disease". Thorax. vol. 44. 1989. pp. 716-720.

(Adding weights to patients with COPD worsened the uphill exercise performance because of the impact of the increased weight on ventilation and oxygen consumption. The authors concluded that modest weight loss might benefit patients with COPD. However, their conclusions are flawed because the addition of weight in this study did not replicate the distribution of fat in an obese patient and because the weight was added acutely.)

Guenette, JA, Jensen, D, O' Donnell, DE. "Respiratory function and the obesity paradox". Curr Opin Clin Nutr Metab Care. vol. 13. 2010. pp. 618-624.

(This comprehensive review article demonstrates the impact of obesity on lung function in patients with COPD. The authors conclude that obese patients with COPD do not appear to have a disadvantage during exercise compared with patients with COPD who are of normal weight.)

Sava, F, Laviolette, L, Bernard, S. "The impact of obesity on walking and cycling performance and response to pulmonary rehabilitation in COPD". BMC Pulmonary Medicine. vol. 10. 2010. pp. 55.

(In this study of 261 patients with COPD, baseline and post-rehabilitation pulmonary function, six-minute-walk testing, and endurance time during a constant work rate exercise were compared among normal weight, overweight, and obese individuals. Walking, but not cycling, performance was worse in the obese group. Weight did not influence the magnitude of improvement after pulmonary rehabilitation.)

Flaherman, V, Rutherford, GW. "A meta-analysis of the effect of high weight on asthma". Arch Dis Child. vol. 91. 2006. pp. 334-339.

(This meta-analysis of the literature demonstrates that high body weight, either at birth or later in childhood, increases the risk for later development of asthma.)

Litonjua, AA, Sparrow, D, Celedon, JC, DeMolles, D, Weiss, ST. "Association of body mass index with the development of methacholine airway hyperresponsiveness in men: the Normative Aging Study". Thorax. vol. 57. 2002. pp. 581-585.

(Both low BMI and high BMI are associated with development of bronchial hyper-responsiveness.)

Pakhale, S, Doucette, S, Vandemhee, K. "A comparison of obese and nonobese people with asthma: exploring an asthma-obesity interaction". Chest. vol. 137. 2010. pp. 1316-1323.

(This study of 496 subjects demonstrated that obese patients with asthma have lower lung function and more co-morbidities than do asthmatics of normal weight.)
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