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Maastricht, the Netherlands
Dr. Wouters is Professor in Respiratory Medicine and Chairman, Department of Respiratory Medicine, University Hospital Maastricht.
Correspondence to: Emiel F. M. Wouters, MD, FCCP, Department of Respiratory Medicine, University Hospital Maastricht, Maastricht, the Netherlands; e-mail: e.wouters{at}lung.azm.nl
COPD is an irreversible disabling disease with increasing incidence worldwide. Patients with COPD frequently suffer in the end stage of the disease process from chronic hypercapnic respiratory failure (CHRF). Although high level of evidence has shown that adding noninvasive positive pressure ventilation (NIPPV) in addition to standard therapy with oxygen and medication is effective in the management of episodes of acute respiratory failure in patients with acute exacerbations of COPD,1 the role of NIPPV on long-term survival in CHRF is still a topic of controversy despite the wide application of NIPVV in chronic hypercapnic patients.23 Prognostic parameters have not been evaluated under these conditions, although patients are at high risk for readmission and life-threatening events. The study by Budweiser et al4 in this issue of CHEST (see page 1650) evaluated prognostic markers of long-term survival in patients with severe COPD and CHRF receiving NIPVV. The study comprised a 10-year observation period, a mean follow-up of 32 months, and included 188 patients treated with NIPVV. The study pointed out that nutritional status assessed by body mass index (BMI), hyperinflation, and base excess (BE) independently predicted mortality. A reduction of these risk factors after initiation of NIPVV (increase in BMI in patients with BMI < 25 kg/m2; a decrease of residual volume [RV]/total lung capacity [TLC] by 
4% in patients with RV/TLC 73% and a reduction in BE 50% if baseline BE is 9 mmol/L) was associated with improved survival.4
The study of Budweiser et al4 confirms the important role of nutritional status in COPD. Previous work5 in patients with COPD, largely treated with long-term home oxygen therapy, have demonstrated that male gender, older age, lower BMI, FEV1 percentage of predicted, PaO2, and PaCO2 were identified as independent negative prognostic factors. In another study6 based on the ANTADIR observatory, it was demonstrated that the effect of BMI on survival was independent of age, FEV1, PaO2 and sex. Lower BMI was also a powerful predictor of duration and rate of hospitalization.6 BMI in the study of Chailleux et al6 was significantly lower than in the study by Budweiser et al4: mean BMI, 23 kg/m2 vs 27.2 kg/m2. In the study by Chailleux et al,6 68.1% of the COPD patients had a BMI < 24 kg/m2. Studies78 have reported that body composition assessment provides information in addition to BMI in different categories of COPD and that fat-free mass corrected for body surface is an independent predictor of mortality irrespective of fat mass in COPD. It would be interesting to evaluate in future studies body composition besides BMI in patients with chronic respiratory failure because depletion in fat-free mass can be found even in patients with normal or high BMI.9 A BMI of 25 kg/m2, as used by Budweiser et al,4 was reported by Schols et al10 as a threshold value below which the mortality risk was clearly increased.
In a large prospective study11 cohort of persons of 50 to 71 years old, among all men and women, including smokers and those with preexisting disease, a U-shaped relation between current BMI and the risk of death was found, with the highest risk in the lowest and highest categories of BMI: a BMI between 23.5 kg/m2 and 24.9 kg/m2 was considered as the reference. These BMI cutoff values are markedly higher than arbitrarily defined in a multidimensional grading system for COPD.12 In accordance with the prospective data of Schols et al10 demonstrating that a gain in weight of 2 kg in depleted and nondepleted COPD patients was associated with an improvement of survival, Budweiser et al4 reported that an increase in body weight in patients with BMI < 25 kg/m2 resulted in an improved prognosis. Further studies have to explore minimally clinical important differences in BMI after intervention as well as the changes in body compartments after such interventions.
Hyperinflation is reported as a second independent predictor of mortality in this population treated with NIPVV.4 The possible value of hyperinflation in predicting survival is poorly explored. Two studies1012 using the percentage of normal inspiratory capacity (IC) and absolute IC failed to observe predictive capacity. However, by relating IC to TLC, a reflection of the functional reserve in COPD patients can be obtained. One study13 showed that hyperinflation expressed as the RV/TLC ratio was a powerful predictor of mortality in patients with COPD. Another study14 reported that the IC/TLC ratio is a good and independent predictor of all-cause and respiratory mortality; an IC/TLC threshold of 25% provided the best power. Budweiser et al4 used a cutoff value of RV/TLC 73%. Importantly, they could demonstrate that a reduction in RV/TLC by 4% in the most hyperinflated group resulted in a significant improvement of survival.4 Further studies in COPD are needed to explore beneficial effects of lung deflation on survival in COPD.
Budweiser et al4 also focused attention on the role of renal compensation in patients with persistently elevated carbon dioxide tension as a reduction in BE by > 42% was found as an independent predictor of mortality in patients showing BE 9 mmol/L.4 Renal compensatory mechanisms are frequently overlooked in patients with chronic respiratory failure. Hypercapnia leads to a fall in renal perfusion, and this vasoconstrictor mechanism withstands vasodilatory stimuli. The vasoconstriction and sodium retention can be considered as restoring processes of the intravascular volume and tissue perfusion as carbon dioxide acts as a potent vasodilator and lowers peripheral vascular resistance and increases arterial capacity. Reduction in hypercapnia will attenuate compensating mechanisms and improve fluid homeostasis in patients with CRHF.15
Comorbidity in COPD patients with CRHF is high, and overall prognosis is still poor, as illustrated by Budweiser et al.4 Besides discussion of physiologic variables, it will be important to realize that an effective management for these patients need to be centered on adequate management of symptoms and maintenance of a reasonable quality of life. Honoring the treatment preferences of these severely disabled patients is crucial to the provision of high-quality care. Understanding of patient preferences depends on the assessment of how they view the burden of treatment to its possible outcomes and the likelihood of these outcomes. Further studies on NIPVV in COPD patients with CRHF will contribute to a better provision of information to these patients. NIPVV needs to be embedded in the multidimensional end-of-life management of the patients with very disabling COPD.
Footnotes
The author has no conflict of interest to disclose.
References
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