J M Marin1, M Montes de Oca, J Rassulo, B R Celli. 1. Division of Pulmonary and Critical Care Medicine, St. Elizabeth's Medical Center, Tufts University, Boston, MA 02135, USA.
Abstract
BACKGROUND: The reasons for exertional dyspnea in severe COPD are not well established, but they are not solely related to the mechanical load. We tested the hypothesis that breathlessness may be determined, in part, by the response of an individual's central output. METHODS: In 26 patients with severe COPD (FEV1 < 50% predicted) and 22 matched control subjects, we assessed at rest the ventilatory and mouth occlusion pressure (P0.1) response to hyperoxic progressive hypercapnia. At rest and during a symptom-limited exercise test, routine cardiopulmonary variables were measured, and respiratory muscle function was evaluated using esophageal and gastric pressure. Dyspnea was assessed with a visual analog scale. RESULTS: Dyspnea with or without leg discomfort limited exercise in 73% of patients. Peak exercise dyspnea correlated only with dyspnea at rest (r = 0.5, p < 0.008) and P0.1 response to CO2 (deltaP0.1/delta[end-tidal PCO2]PETCO2) (r = 0.48, p = 0.02). Multiple regression analysis including resting and exercise data as independent variables revealed that 47% of the variance for dyspnea at peak exercise was explained by a model including dyspnea at rest and deltaP0.1/deltaPETCO2. Again, deltaP0.1/deltaPETCO2 was the only predictor for the change in dyspnea from rest to peak exercise (delta Dyspnea, r2 = 0.28, p = 0.005). There was no correlation between exercise dyspnea and any metabolic variable, pulmonary function, or respiratory muscle function test. CONCLUSION: In severe COPD, exertional dyspnea is not simply related to respiratory muscle load or mechanical impairment, but also to an individual's central motoneural output to the respiratory system.
BACKGROUND: The reasons for exertional dyspnea in severe COPD are not well established, but they are not solely related to the mechanical load. We tested the hypothesis that breathlessness may be determined, in part, by the response of an individual's central output. METHODS: In 26 patients with severe COPD (FEV1 < 50% predicted) and 22 matched control subjects, we assessed at rest the ventilatory and mouth occlusion pressure (P0.1) response to hyperoxic progressive hypercapnia. At rest and during a symptom-limited exercise test, routine cardiopulmonary variables were measured, and respiratory muscle function was evaluated using esophageal and gastric pressure. Dyspnea was assessed with a visual analog scale. RESULTS:Dyspnea with or without leg discomfort limited exercise in 73% of patients. Peak exercise dyspnea correlated only with dyspnea at rest (r = 0.5, p < 0.008) and P0.1 response to CO2 (deltaP0.1/delta[end-tidal PCO2]PETCO2) (r = 0.48, p = 0.02). Multiple regression analysis including resting and exercise data as independent variables revealed that 47% of the variance for dyspnea at peak exercise was explained by a model including dyspnea at rest and deltaP0.1/deltaPETCO2. Again, deltaP0.1/deltaPETCO2 was the only predictor for the change in dyspnea from rest to peak exercise (delta Dyspnea, r2 = 0.28, p = 0.005). There was no correlation between exercise dyspnea and any metabolic variable, pulmonary function, or respiratory muscle function test. CONCLUSION: In severe COPD, exertional dyspnea is not simply related to respiratory muscle load or mechanical impairment, but also to an individual's central motoneural output to the respiratory system.