Pathophysiology of Dyspnea in Chronic Obstructive Pulmonary Disease: A Roundtable

Abstract

Effective management of dyspnea in chronic obstructive pulmonary disease (COPD) requires a clearer understanding of its underlying mechanisms. This roundtable reviews what is currently known about the neurophysiology of dyspnea with the aim of applying this knowledge to the clinical setting. Dyspnea is not a single sensation, having multiple qualitative descriptors. Primary sources of dyspnea include: (1) inputs from multiple somatic proprioceptive and bronchopulmonary afferents, and (2) centrally generated signals related to inspiratory motor command output or effort. Respiratory disruption that causes a mismatch between medullary respiratory motor discharge and peripheral mechanosensor afferent feedback gives rise to a distressing urge to breathe which is independent of muscular effort. Recent brain imaging studies have shown increased limbic system activation in response to various dyspneogenic stimuli and emphasize the affective dimension of this symptom. All of these mechanisms are likely instrumental in exertional dyspnea causation in COPD. Increased central motor drive (and effort) is required to increase ventilation during activity because the inspiratory muscles become acutely overloaded and functionally weakened. Abnormal dynamic ventilatory mechanics and excessive chemostimulation during exercise also result in a widening disparity between escalating central neural drive and restricted thoracic volume displacement. This neuromechanical uncoupling may form the basis for the distressing sensation of unsatisfied inspiration. Interventions that alleviate dyspnea in COPD do so by improving ventilatory mechanics, reducing central neural drive, or both-thereby partially restoring neuromechanical coupling of the respiratory system. Self-management strategies address the affective aspect of dyspnea and are essential to successful treatment.

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“…The predominant diagnosis was people with COPD, the area in which most work has been done in breathlessness to date. [6,24] …”

Validity of a Self-administered Questionnaire Version of the Transition Dyspnea Index in Patients with COPD

“…It is the third leading cause of mortality worldwide and associated with significant individual and socioeconomic burden [1,3,4]. Dyspnea is the highly aversive cardinal symptom of COPD and causing significant reductions in patients activity levels and quality of life [1,5,6]. In fact, dyspnea is an important predictor of mortality in COPD with greater predictive value than spirometric lung function measures [7,8].…”

Tracheal occlusion modulates the gene expression profile of the medial thalamus in anesthetized rats

“…A sufficiently high load on the respiratory system results in the sensation of dyspnea, or breathlessness, which is one of the primary symptoms in pulmonary and cardiovascular diseases (40,44). It is one of the main symptoms that limits patients with obstructive pulmonary diseases, and it can also be considered one of the most important factors in determining the severity of the disease and the health-related quality of life (11).…”

“…Sensory information of breathing is continuously sent to the respiratory centers in the brain stem; minor changes in breathing are controlled by these centers without the activation of higher brain centers. When changes in respiratory information reach a certain threshold, then a gating-in process occurs, resulting in the cognitive awareness of breathing (2,44). The conscious awareness of breathing as in dyspnea requires the activation of higher brain centers (44).…”

“…When changes in respiratory information reach a certain threshold, then a gating-in process occurs, resulting in the cognitive awareness of breathing (2,44). The conscious awareness of breathing as in dyspnea requires the activation of higher brain centers (44).…”