LAUSR

In cardiopulmonary medicine, residual exertional dyspnea (RED) can be defined by the persistence of limiting breathlessness in a patient who is already under the best available therapy for the underlying heart and/or lung disease. RED is a challenge to the pulmonologist because the patient (and the referring physician) assumes that the "lung doctor" should invariably provide a successful plan to fight the symptom. After presenting a simplified framework to understand the neurobiological underpinnings of dyspnea in cardiorespiratory disease, I discuss the seeds of RED associated with 1) increased metabolic cost of work, 2) increased inspiratory constraints, 3) diaphragm dysfunction, 4) impaired right ventricle preload, 5) increased central and/or peripheral chemosensitivity, 6) increased physiological dead space, 7) increased pulmonary venous and/or high left ventricle filling pressures, 8) impaired chronotropic response to exertion, and 9) increased activation of the cortical-limbic circuits. I finalize by outlining the following two common coexistence of diseases in which these multiple mechanisms interact to produce severe RED: chronic obstructive pulmonary disease-heart failure with reduced ejection fraction and chronic pulmonary fibrosis-emphysema. RED exposes the important limitations of the current reductionist approach focused only on the (over)treatment of the poorly reversible cardiopulmonary disease(s). Conversely, recognizing the existence of RED sets the stage for a more holistic approach toward one of the most devastating symptoms known to man.