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 characterized 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 (E)-CO₂ output CO₂) intercept, E-CO₂ slope, peak E/CO₂ ratio and peak PETCO₂. Multiple logistic regression analysis revealed that CO₂ intercept ≤ 3.5 L/minute [odds ratios (95% CI) = 7.69 (2.61–22.65), P < 0.001] plus E-CO₂ slope ≥ 34 [2.18 (0.73–6.50), P = 0.14] or peak E/CO₂ 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 overlapping. 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.

KEYWORDS:

• Carbon dioxide
• cardiopulmonary exercise testing
• dyspnoea
• exertion
• gas exchange