Am. J. Respir. Crit. Care Med., Volume 158, Number 6, December 1998, 1876-1882

Ventilatory and Cardiovascular Responses to Inspired He-O₂ during Exercise in Chronic Obstructive Pulmonary Disease

DAVID A. OELBERG, ROBERT M. KACMAREK, PAUL P. PAPPAGIANOPOULOS, LEO C. GINNS, and DAVID M. SYSTROM

Pulmonary and Critical Care Unit and Respiratory Care Services, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts

Blunted maximum cardiac output and systemic O₂ extraction could constitute primary limits to exercise in severe chronic obstructive pulmonary disease (COPD) or they could simply reflect cessation of exercise because of abnormal pulmonary mechanics. To determine which is the case, eight consecutive patients with severe COPD (FEV₁ = 0.56 ± 0.04 L, mean ± SEM), five of whom had 1-antiprotease deficiency, performed two incremental cycling tests while breathing N₂-O₂ or He-O₂. Expired gases and E were measured, and radial and pulmonary arterial blood was simultaneously sampled each minute. Peak exercise E was higher with He-O₂ than with N₂-O₂ (25.5 ± 2.2 versus 19.3 ± 1.5 L/min, p = 0.002) and Pa_CO2 was lower (42 ± 2 versus 46 ± 2 mm Hg, p = 0.0003). O₂max improved only modestly (594 ± 75 versus 514 ± 54 ml/min, p = 0.04), and was accompanied by an increase in peak exercise Ca_O2 (18.7 ± 0.9 versus 17.6 ± 0.9 ml/dl, p = 0.02). Peak Fick cardiac output was decreased (39 ± 3% pred) and Cv_O2 was elevated (130 ± 10% pred), and neither improved with He-O₂ (p > 0.05 for each). Abnormal peak exercise cardiac output and systemic O₂ extraction in severe COPD cannot be fully accounted for by limiting pulmonary mechanics and may contribute to exercise intolerance.

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