Inspiratory resistance decreases limb blood flow in COPD patients with heart failure

Abstract

To the Editor: Chronic heart failure (CHF) with reduced left ventricular ejection fraction is a common and disabling comorbidity of chronic obstructive pulmonary disease (COPD) [1]. Understanding the mechanisms underlying exercise intolerance is paramount to providing a rationale to effectively rehabilitate the fast-growing population of patients with COPD plus CHF. The inspiratory muscles, in particular, are characteristically overloaded in COPD plus CHF, with greater elastic and resistive work of breathing. Moreover, these muscles might be functionally weakened as ventilation increases during exercise in patients with COPD [2]. It has been postulated that fatiguing contractions would stimulate diaphragmatic thinly myelinated group III and unmyelinated group IV fibres, thereby increasing limb sympathetic outflow and vascular resistance. The so-called respiratory muscle metaboreflex would then redirect blood flow from locomotor to respiratory muscles to avoid, or at least postpone, the impending failure of the “vital pump” [3, 4]. In this context, we previously found marked blood flow reduction to nonactive and active limbs during inspiratory resistive loading in CHF [5]. Work from our laboratory also showed improved peripheral muscle oxygen delivery after respiratory muscle unloading (under stable cardiac output and arterial oxygen content) in CHF-free COPD [6] and COPD-free CHF [7]. It is therefore conceivable that the coexistence of CHF would potentiate the respiratory muscle metaboreflex in patients with a primary diagnosis of COPD. After giving informed consent, 22 optimally treated patients with moderate-to-severe (Global Initiative for Chronic Obstructive Lung Disease stage II–III) COPD (10 with coexistent CHF, i.e. left ventricular ejection fraction <45% by echocardiography) and 10 age- and sex-matched controls underwent a ramp-incremental exercise test for …