Heart, lungs, and muscle interplay in worsening activity-related breathlessness in advanced cardiopulmonary disease.

Abstract

Activity-related breathlessness is a key determinant of poor quality of life in patients with advanced cardiorespiratory disease. Accordingly, palliative care has assumed a prominent role in their care. The severity of breathlessness depends on a complex combination of negative cardiopulmonary interactions and increased afferent stimulation from systemic sources. We review recent data exposing the seeds and consequences of these abnormalities in combined heart failure and chronic obstructive pulmonary disease (COPD). The drive to breathe increases ('excessive breathing') secondary to an enlarged dead space and hypoxemia (largely COPD-related) and heightened afferent stimuli, for example, sympathetic overexcitation, muscle ergorreceptor activation, and anaerobic metabolism (largely heart failure-related). Increased ventilatory drive might not be fully translated into the expected lung-chest wall displacement because of the mechanical derangements brought by COPD ('inappropriate breathing'). The latter abnormalities, in turn, negatively affect the central hemodynamics which are already compromised by heart failure. Physical activity then decreases, worsening muscle atrophy and dysfunction. Beyond the imperative of optimal pharmacological treatment of each disease, strategies to lessen ventilation (e.g., walking aids, oxygen, opiates and anxiolytics, and cardiopulmonary rehabilitation) and improve mechanics (heliox, noninvasive ventilation, and inspiratory muscle training) might mitigate the burden of this devastating symptom in advanced heart failure-COPD.