Patients with chronic obstructive pulmonary disease (COPD) markedly increase their pulmonary artery wedge pressure on mild exercise even though they have no overt left heart disease and no increase in the esophageal pressure (as a reflection of mean intrathoracic pressure). We wondered if lung distension due to gas trapping during the hyperpnea of exercise might cause the wedge pressure to rise by increasing juxtacardiac pressures above esophageal pressures. If this were so, then (1) tachypnea alone, without exercise, should cause the FRC and intracardiac pressures to increase in patients with COPD, (2) there should be an increase in FRC associated with the rise in wedge pressure on exercise, and (3) these changes should not occur in patients without COPD. We studied 39 patients with COPD (Ppa = 21 +/- 6 mm Hg [mean +/- SD], FEV1 [% predicted] = 39 +/- 16) and 13 control patients with similar pulmonary artery pressures but no airflow obstruction (Ppa = 22 +/- 20 mm Hg, FEV1 [% predicted] = 110 +/- 24). In those with COPD, light exercise raised the FRC by 0.5 +/- 0.5 L. Tachypnea alone, at the rate present during exercise, raised the FRC by 0.6 +/- 0.4 L and there was a 10% increase in left lower lobe area on lateral chest X-ray. Wedge, right atrial, and pulmonary artery pressures rose together during tachypnea with and without exercise. By contrast, in the control patients without COPD, the right atrial pressure change on exercise did not reflect that of the left atrium in extent or direction.(ABSTRACT TRUNCATED AT 250 WORDS)