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Am Fam Physician. 1999;59(5):1280-1282

Obesity often appears to affect respiratory function; however, few medical references include obesity as a cause of dyspnea. Obesity has been shown to reduce expiratory reserve volume and functional residual capacity because of alterations in chest wall mechanics. Obese persons may also experience exertional dyspnea because of the metabolic load placed on their gas transport system upon exertion. Despite these observations, obesity alone has not been shown to cause dyspnea in persons at rest. In an attempt to answer this question, Sahebjami conducted a prospective, open study to evaluate baseline dyspnea in otherwise “healthy” obese men and to see whether their pulmonary function test profiles differed from those of obese men without dyspnea.

All men seen during a three-month period at the Cincinnati Veterans Affairs Medical Center who had a body mass index (BMI) of 28 kg (61.6 lb) per m2 or greater were screened for the study. Patients were first asked to sit in a chair for 10 minutes on arrival at the clinic, and then to complete a written questionnaire that asked whether they had any difficulty breathing at rest and, if so, to quantify the degree of difficulty on a scale of zero to 10 (referred to as the Borg Scale Dyspnea Index [BSDI]). The men then underwent pulmonary function tests, including forced expiratory volume (FEV1) and forced vital capacity (FVC). Those with values greater than 80 percent of predicted value were screened further for potential entry to the study. Clinical records, including medical history and chest radiographs or electrocardiograms, were reviewed. Exclusion criteria included the presence of cardiopulmonary disease, malignancy, neuromuscular disorders, recent surgery or any serious systemic illness. Those who remained eligible then underwent extensive pulmonary function testing, including flow rates, lung volumes and single-breath carbon monoxide diffusing capacity (DLco). In addition, arterial blood gas samples were obtained from the radial artery of all patients at rest while breathing room air.

Twenty-three men met the criteria for the study. Of these, 15 reported dyspnea at rest (dyspneic group), and eight denied any shortness of breath at rest (nondyspneic group). Age and height of the men were similar in both groups. However, BMI, BSDI scores and body weights were significantly greater in the dyspneic group. In addition, 86.6 percent of men in the dyspneic group had a smoking history, compared with 62.5 percent of men in the nondyspneic group. Baseline arterial blood gas parameters did not differ between groups. FVC, FEV1 and FEV1/FVC ratio were within normal limits in both groups. In addition, lung volume and gas exchange patterns were similar between groups. FEV1, maximum voluntary ventilation and maximum static expiratory mouth pressure (Pemax) were significantly reduced in the group with dyspnea.

The author concludes that obesity alone, without the presence of underlying lung disease, can be a cause of dyspnea at rest in otherwise healthy men. In this study, obese patients with dyspnea weighed more, had lower Pemax levels and lower maximum voluntary ventilation than patients without dyspnea. These factors are most likely responsible for the sensation of dyspnea in these persons.

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