Although weight loss is a common problem in chronic obstructive pulmonary disease (COPD), the precise cause of malnutrition in COPD patients is not known. The purpose of this study was to measure and compare resting energy expenditure (REE) in stable undernourished and adequately nourished COPD. REE was measured in normal, adequately nourished, and undernourished COPD patients by indirect calorimetry and then compared to predicted basal metabolic rate (BMR) calculated from the Harris-Benedict equation. We found that measured REE, compared to predicted, was significantly higher in the undernourished group, (1.15 +/- 0.02) and compared to the adequately nourished COPD (0.99 +/- 0.03) and normal groups (0.93 +/- 0.02) (p less than 0.0001). We conclude that there is a hypermetabolic state in stable malnourished COPD patients which may be a factor in weight loss. This elevated REE also needs to be taken into account when determining caloric requirements for COPD patients.

The respiratory inductance plethysmograph (RIP) has recently gained popularity in both the research and clinical arenas for measuring tidal volume (VT) and changes in functional residual capacity (delta FRC). It is important however, to define the likelihood that individual RIP measurements of VT and delta FRC would be acceptably accurate (+/- 10%) for clinical and investigational purposes in spontaneously breathing individuals on continuous positive airway pressure (CPAP). Additionally, RIP accuracy has not been compared in these regards after calibration by two commonly employed techniques, the least squares (LSQ) and the quantitative diagnostic calibration (QDC) methods. We compared RIP with pneumotachographic (PTH) measurements of delta FRC and VT during spontaneous mouth breathing on 0-10 cmH2O CPAP. Comparisons were made after RIP calibration with both the LSQ (6 subjects) and QDC (7 subjects) methods. Measurements of delta FRC by RIPLSQ and RIPQDC were highly correlated with PTH measurements (r = 0.94 +/- 0.04 and r = 0.98 +/- 0.01 (SE), respectively). However, only an average of 30% of RIPQDC determinations per subject and 31.4% of RIPLSQ determinations per subject were accurate to +/- 10% of PTH values. An average of 55.2% (QDC) and 68.8% (LSQ) of VT determinations per subject were accurate to +/- 10% of PTH values. We conclude that in normal subjects, over a large number of determinations, RIP values for delta FRC and VT at elevated end-expiratory lung volume correlate well with PTH values. However, regardless of whether QDC or LSQ calibration is used, only about one-third of individual RIP determinations of delta FRC and one-half of two-thirds of VT measurements will be sufficiently accurate for clinical and investigational use.

The available clinical information to date does not support the hypothesis that tissue oxygen debt is the primary cause of the wasting process in the chronic obstructive pulmonary disease (COPD) patient population. However, this should not deter the ‘believers’ of the hypothesis from further investigation. The information outlined above supports the need for reconsideration of this clinical problem. Tissue oxygen requirements and utilization is a complex interplay of multiple variables. Likewise, the assessment of nutritional status in the setting of oxygen therapy is complicated by shifts in body fluid compartments independent of changes in the fat-free mass (FFM). Utilization of newer techniques will be required to resolve the contribution of low tissue oxygenation to the wasting process. The continued development of noninvasive methods for the assessment of tissue metabolism, cardiac function, and tissue energy requirements will allow investigators to further clarify the relationship between tissue oxygenation and metabolism in patients with COPD. Clinical trials designed to examine this issue must recognize the multiple effects of oxygen on all aspects of nutrient utilization, including caloric intake, needs, and tissue delivery. Failure to address all aspects of this system will lead to continued debate regarding the etiology of weight loss in the COPD patient population.