What Interventions Are Effective for Managing Dyspnea in COPD?

Mechanisms of Dyspnea

Numerous peripheral and central neural receptors and pathways contribute to the experience of dyspnea. Like pain, dyspnea is a multidimensional and complex symptom. Two primary components have been proposed: one related to sensory aspects (e.g., intensity, spatial, temporal awareness) and the other related to affective aspects. Based on neuroimaging studies, the affective component of dyspnea, similar to pain, is thought to be processed in central limbic structures and the insular cortex, cingulate gyrus, and amygdala.

Normally, individuals are unaware of the act of breathing. Respiratory drive, generated at the level of the brainstem, produces the motor output that results in breathing. Ventilation is monitored and automatically adjusted in response to many afferent sensory inputs integrated centrally, including those coming from receptors in the chest wall, lung parenchyma, upper and lower airways, and chemoreceptors. The conscious awareness of breathing and dyspnea occurs when there is an imbalance between the level of neural respiratory drive and resultant ventilation (i.e., neuromechanical dissociation). Respiratory sensation is further modulated by affective state (e.g., anxiety, depression), endogenous opioids, and activity of other sensory modalities (e.g., distractive stimuli).

There are several mechanisms of dyspnea in COPD. Neuromechanical factors likely predominate over chemoreceptor stimulation, except during acute events resulting in worsened hypoxemia or hypercapnia. COPD is characterized by persistent inflammation and remodeling of airways, lung parenchyma, and vasculature. The pathophysiology of COPD is characterized by partially reversible expiratory airflow limitation and lung hyperinflation. This is due to small airway collapse during expiration from loss of tethering parenchymal lung attachments (emphysema) and small airway obstruction from excess mucus, airway inflammation, and remodeling (chronic bronchitis) combined with reduced driving pressure for expiratory airflow from a loss of elastic recoil (emphysema). As a result, lung emptying is incomplete. End-expiratory lung volume is usually increased at rest and further dynamically increases with increased ventilation, such as during exertion, anxiety, or panic attacks. Hyperinflation (increased end-expiratory lung volume) increases work and oxygen costs of breathing (increased threshold and elastic loads) while causing functional inspiratory muscle weakness (resulting from abnormal chest geometry and respiratory muscle shortening) and possibly negatively affecting cardiac performance. Emphysema is also associated with increased physiological dead space (e.g., areas of ventilation that lack vascular perfusion). Ultimately, neuromechanical dissociation and associated dyspnea occur as a result of increased respiratory neuromuscular output and effort in the face of reduced respiratory response (e.g., low tidal volume, elevated carbon dioxide level).

COPD is not only a lung disease; it is also associated with important systemic manifestations that can further contribute to exercise intolerance and dyspnea, particularly at advanced stages of the disease. Systemic inflammation, malnutrition, inactivity, inadequate levels of anabolic hormones, and medication side effects are all factors that can lead to skeletal muscle wasting, cachexia, and reduced aerobic capacity. During exertion, excess carbon dioxide production results from anaerobic metabolism and lactic acid production by exercising skeletal muscles resulting in a need for increased ventilatory drive, and resultant dyspnea for those with severe disease.