Oxygen transport and oxygen consumption during supplemental oxygen administration in patients with chronic obstructive pulmonary disease.

PURPOSE

Oxygen consumption (VO2) is independent of oxygen delivery (DO2) above a critical level of DO2. VO2 may become dependent on DO2 when oxygen demand exceeds oxygen supply. We studied DO2 VO2, and exercise capacity in 12 stable, ambulatory patients with chronic obstructive pulmonary disease (COPD) receiving ambient air and 26% oxygen to ascertain whether VO2 is dependent on DO2 in this patient sample.

PATIENTS AND METHODS

An exercise protocol consisting of a symptom-limited, low-level treadmill test with progressive increments in workload was performed twice, once with patients breathing ambient air and once with patients breathing 26% oxygen. Expired gas, arterial and mixed venous blood values, and recordings of systemic and pulmonary artery pressures were obtained after a 10-minute period of rest (while standing) and during the last minute of each three-minute exercise level.

RESULTS

Five patients had an increase in exercise capacity, defined as an increase in the maximal VO2 greater than 25%, using supplemental oxygen. In these patients, oxygen delivery increased from 10.9 +/- 3.4 to 13.8 +/- 4.7 mL/minute/kg (p = 0.008) at rest and from 16.2 +/- 5.0 to 24.7 +/- 2.7 mL/minute/kg (p = 0.046) during exercise with supplemental oxygen administration. VO2 increased from 0.329 +/- 0.065 to 0.436 +/- 0.109 L/minute (p = 0.029) at rest and from 0.776 +/- 0.275 to 1.119 +/- 0.482 L/minute (p = 0.048) during exercise. Three of these five patients had an arterial oxygen pressure greater than 55 mm Hg at rest. Seven patients had little or no increase in exercise capacity with supplemental oxygen. This patient group had no increase in VO2 at rest. The DO2 failed to increase at rest despite an increase in arterial oxygen content because of a reduction in cardiac output.

CONCLUSION

These data demonstrate that DO2 may fail to increase in some patients with COPD and resting or exertional hypoxemia when supplemental oxygen is administered because of a reduction in cardiac output; that patients who fail to increase their DO2 are less likely to increase exercise capacity; and that some stable, ambulatory patients with COPD who do not qualify for supplemental oxygen at rest by current standards may have inadequate DO2 to meet physiologic needs.