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Clinical Investigations: CONTROL OF BREATHING |

Ventilatory Drive at Rest and Perception of Exertional Dyspnea in Severe COPD*

Jose M. Marin, MD; Maria Montes de Oca, MD; John Rassulo; Bartolome R. Celli, MD, FCCP
Author and Funding Information

*From the Division of Pulmonary and Critical Care Medicine, St. Elizabeth’s Medical Center, Tufts University, Boston, MA.

Correspondence to: Bartolome R. Celli, MD, FCCP, Division of Pulmonary and Critical Care, St. Elizabeth’s Medical Center, 736 Cambridge St, Boston, MA 02135; e-mail: Bcelli@semc.org



Chest. 1999;115(5):1293-1300. doi:10.1378/chest.115.5.1293
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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 (ΔP0.1/Δ[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 andΔ P0.1/ΔPetco2. Again,Δ P0.1/ΔPetco2 was the only predictor for the change in dyspnea from rest to peak exercise (Δ 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.

Abbreviations: FRC = functional residual capacity; HR = heart rate; MVV = maximum voluntary ventilation; P0.1 = mouth occlusion pressure at 0.1 s after onset; Pdi = transdiaphragmatic pressure; Pdimax = maximal Pdi; Pemax = maximal expiratory mouth pressure; Petco2 = end-tidal Pco2; Pg = gastric pressure; Pgi = gastric pressure at end-inspiration; Pgimax = maximal inspiratory gastric pressure; Pimax = maximal inspiratory mouth pressure; Ppl = pleural pressure; Pplimax = maximal inspiratory pleural pressure; Ppli = pleural pressure at end-inspiration; TLC = total lung capacity; TTDI = diaphragmatic tension time index; V̇e = minute ventilation; V̇o2 = oxygen uptake; Vt = tidal volume

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