Ventilatory and cardiovascular responses to inspired He-O-2 during exercise in chronic obstructive pulmonary disease

Blunted maximum cardiac output and systemic OZ extraction could constitute primary limits to exercise in severe chronic obstructive pulmonary disease (COPD) or they could simply reflect cessation of exercise because of abnorm al pulmonary mechanics. To determine which is the case, eight consecutive p atients with severe COPD (FEV1 = 0.56 +/- 0.04 L, mean +/- SEM), five of wh om had alpha 1-antiprotease deficiency, performed two incremental cycling t ests while breathing N-2-O-2 or He-O-2. Expired gases and (V) over dotE wer e measured, and radial and pulmonary arterial blood was simultaneously samp led each minute. Peak exercise (V) over dotE was higher with He-O-2 than wi th N-2-O-2 (25.5 +/- 2.2 versus 19.3 +/- 1.5 L/min, p = 0.002) and Pa-CO2 w as lower (42 +/- 2 versus 46 +/- 2 mm Hg, p = 0.0003). (V) over dot O(2)max improved only modestly (594 +/- 75 versus 514 +/- 54 ml/min, p = 0.04), an d was accompanied by an increase in peak exercise Ca-O2 (18.7 +/- 0.9 versu s 17.6 +/- 0.9 ml/dl, p = 0.02). Peak Fick cardiac output was decreased (39 +/- 3% pred) and C (V) over bar(O2), was elevated (130 +/- 10% pred), and neither improved with He-OZ (p > 0.05 for each). Abnormal peak exercise car diac output and systemic O-2 extraction in severe COPD cannot be fully acco unted for by limiting pulmonary mechanics and may contribute to exercise In tolerance.