Elevated O2 cost of ventilation contributes to tissue wasting in COPD.

BACKGROUND AND OBJECTIVES

Thirty to 50% of all COPD patients experience tissue wasting that may be caused by hypermetabolism, but the cause of the perturbed metabolic state is unclear. We hypothesized that the elevated O2 cost of ventilation (O2 COV) may be a contributing factor. All of the data are presented as means (+/-SEM). Ten hypoxemic (a PaO2 of 54+/-3 mm Hg) stable COPD patients (an FEV1/FVC ratio of 42+/-4%) and five healthy control subjects were studied. The patients were divided into two groups based on nutritional status. Group 1 (n = 6) was malnourished (a body mass index [BMI] of 17.6+/-0.7 kg/m2), and group 2 (n = 4) was normally nourished (a BMI of 26.0+/-3 kg/m2). The O2 COV was determined by measuring the change in the oxygen consumption (VO2) and the minute ventilation (VE) caused by CO2-induced hyperventilation.

RESULTS AND CONCLUSIONS

Group 1 had an elevated O2 COV when compared to group 2 and the control group, respectively: 16.4+/-1.0 vs 9.7+/-1.0 and 2.4+/-0.2 mL O2/L of VE (p < 0.05). The VO2 at rest was higher for group 1 than for group 2 and the control group, respectively: 4.5+/-0.3 vs 3.1+/-0.5 and 3.4+/-0.2 mL/kg/min (p < 0.05). The resting energy expenditure (REE) % predicted for group 1 was also higher than group 2 and the control group, respectively: 125+/-3% vs 87+/-7% and 97+/-2% (p < 0.05). Significant correlations were observed that implicate the increased O2 COV as a cause of tissue wasting: O2 COV vs BMI (r = -0.79; p = 0.007), O2 COV vs REE % predicted (r = 0.66; p = 0.039), and REE % predicted vs BMI (r = -0.83; p = 0.003). The O2 COV was also correlated with lung function: FEV1/FVC vs O2 COV (r = -0.84; p = 0.002). We conclude that in these COPD patients the O2 COV is associated with an increased metabolic rate which, in turn adversely affects the nutritional status.