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Definition: The American Thoracic Society consensus statement defines dyspnea as a “subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors and may induce secondary physiological and behavioral responses.” Dyspnea, a symptom, can be perceived only by the person experiencing it and, therefore, must be self-reported. In contrast, signs of increased work of breathing, such as tachypnea, accessory muscle use, and intercostal retraction, can be measured and reported by clinicians.

Epidemiology: Dyspnea is a common, and it has been reported that up to one half of inpatients and one quarter of ambulatory patients experience dyspnea, with a prevalence of 9–13% in the community that increases to as high as 37% for adults aged ≥70 years. Dyspnea is a frequent cause for emergency room visits, accounting for as many as 3–4 million visits per year. Furthermore, it is increasingly appreciated that the degree of dyspnea may better predict outcomes in chronic obstructive pulmonary disease (COPD) than does the forced expiratory volume in 1 s (FEV1), and formal measures of dyspnea have been incorporated into the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017 COPD severity assessment guidelines. Dyspnea may also predict outcomes in other chronic heart and lung diseases as well. Dyspnea can arise from a diverse array of pulmonary, cardiac, and neurologic underlying causes, and elucidation of particular symptoms may point toward a specific etiology and/or mechanism driving dyspnea (although additional diagnostic testing is often required as will be further discussed below).


The mechanisms underlying dyspnea are complex, as it can arise from different contributory respiratory sensations. While a large body of research has increased our understanding of mechanisms underlying particular respiratory sensations such as “chest tightness” or “air hunger” it is likely that a given disease state might produce the sensation of dyspnea via more than one underlying mechanism. Dyspnea can arise from a variety of pathways, including generation of afferent signals from the respiratory system to the central nervous system (CNS), efferent signals from the CNS to the respiratory muscles, and particularly when there is a mismatch in the integrative signaling between these two pathways, termed “efferent-reafferent mismatch” (Fig. 33-1).


Signalling pathways underlying dyspnea. Dyspnea arises from a range of sensory inputs, many of which lead to distinct descriptive phrases used by patients (shown in quotes in the figure). The sensation of respiratory effort likely arises from signals transmitted from the motor cortex to the sensory cortex (green arrow) when outgoing motor commands are sent to the ventilatory muscles (efferent signals, blue arrow). Motor output from the brain stem (blue arrow) may also be accompanied by signals transmitted to the sensory cortex and contribute to the sensation of effort (dotted green arrow). ...

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