Exercise ventilation in COPD: influence of systolic heart failure

Abstract

Systolic heart failure is a common and disabling co-morbidity of chronic obstructive pulmonary disease (COPD) which may increase exercise ventilation due to heightened neural drive and/or impaired pulmonary gas exchange efficiency. The influence of heart failure on exercise ventilation, however, remains poorly char acterized in COPD. In a prospective study, 98 patients with moderate to very severe COPD [41 with coexisting heart failure; ‘overlap’(left ventricular ejection fraction < 50%)] underwent an incremental cardiopulmonary exercise test (CPET). Compared to COPD, overlap had lower peak exercise capacity despite higher FEV1 . Overlap showed lower operating lung volumes, greater ventilatory inefficiency and larger decrements in end-tidal CO2 (PETCO2) (P < 0.05). These results were consistent with those found in FEV1 -matched patients. Larger areas under receiver operating characteristic curves to discriminate overlap from COPD were found for ventilation (VE)-CO ˙ 2 output VCO ˙ 2) intercept, VE- ˙ VCO ˙ 2 slope, peak VE/ ˙ VCO ˙ 2 ratio and peak PETCO2. Mul tiple logistic regression analysis revealed that VE- ˙ VCO ˙ 2 intercept 3.5 L/minute [odds ratios (95% CI) = 7.69 (2.61–22.65), P < 0.001] plus VE- ˙ VCO ˙ 2 slope 34 [2.18 (0.73–6.50), P = 0.14] or peak VE/ ˙ VCO ˙ 2 ratio 37 [5.35 (1.96–14.59), P = 0.001] plus peak PETCO2 31 mmHg [5.73 (1.42–23.15), P = 0.01] were indicative of overlap ping. Heart failure increases the ventilatory response to metabolic demand in COPD. Variables reflecting excessive ventilation might prove useful to assist clinical interpretation of CPET responses in COPD patients presenting heart failure as co-morbidity.