Excess Ventilation in Chronic Obstructive Pulmonary Disease-Heart Failure Overlap. Implications for Dyspnea and Exercise Intolerance.

RATIONALE

An increased ventilatory response to exertional metabolic demand (high [Formula: see text]e/[Formula: see text]co relationship) is a common finding in patients with coexistent chronic obstructive pulmonary disease and heart failure.

OBJECTIVES

We aimed to determine the mechanisms underlying high [Formula: see text]e/[Formula: see text]co and its impact on operating lung volumes, dyspnea, and exercise tolerance in these patients.

METHODS

Twenty-two ex-smokers with combined chronic obstructive pulmonary disease and heart failure with reduced left ventricular ejection fraction undertook, after careful treatment optimization, a progressive cycle exercise test with capillary (c) blood gas collection.

MEASUREMENTS AND MAIN RESULTS

Regardless of the chosen metric (increased [Formula: see text]e-[Formula: see text]co slope, [Formula: see text]e/[Formula: see text]co nadir, or end-exercise [Formula: see text]e/[Formula: see text]co), ventilatory inefficiency was closely related to Pc (r values from -0.80 to -0.84; P < 0.001) but not dead space/tidal volume ratio. Ten patients consistently maintained exercise Pc less than or equal to 35 mm Hg (hypocapnia). These patients had particularly poor ventilatory efficiency compared with patients without hypocapnia (P < 0.05). Despite the lack of between-group differences in spirometry, lung volumes, and left ventricular ejection fraction, patients with hypocapnia had lower resting Pa and lung diffusing capacity (P < 0.01). Excessive ventilatory response in this group was associated with higher exertional Pc. The group with hypocapnia, however, had worse mechanical inspiratory constraints and higher dyspnea scores for a given work rate leading to poorer exercise tolerance compared with their counterparts (P < 0.05).

CONCLUSIONS

Heightened neural drive promoting a ventilatory response beyond that required to overcome an increased "wasted" ventilation led to hypocapnia and poor exercise ventilatory efficiency in chronic obstructive pulmonary disease-heart failure overlap. Excessive ventilation led to better arterial oxygenation but at the expense of earlier critical mechanical constraints and intolerable dyspnea.