title: Pharmacological treatment of exercise dyspnoea.
abstract: A better understanding of the mechanisms of dyspnoea improves the clinician's ability to treat patients with shortness of breath. Any intervention that: 1) reduces ventilatory demands; 2) reduces ventilatory impedance; or 3) improves inspiratory muscle function, may relieve dyspnoea. Reduced ventilatory demand may be obtained by reducing metabolic load. Supplemental oxygen during exercise reduces exertional breathlessness and improves exercise tolerance, the decrease in dyspnoea being proportional to decrease in minute ventilation. Reduced ventilatory demand may also be obtained by decreasing the central drive. Opiates have been shown to decrease minute ventilation at rest and during submaximal exercise. They can alter the central processing of neural signals within the central nervous system to reduce sensations associated with breathing. Contrastingly, no consistent improvement in dyspnoea (versus placebo) has been shown with anxolytics. Decreasing central drive may also be obtained by altering pulmonary afferent information. Interventions that alter transmittal of afferent information to the central controller, potentially reduce dyspnoea. Reduction of ventilatory impedance is obtained by administering B2, anticholinergics or theophylline. B2 and anticholinergics act by modulating the increase in operational lung volumes and the inspiratory muscle effort during exercise. The mechanism by which theophylline relieves dyspnoea is probably related to a mechanism other than its bronchodilation alone. Alterations in respiratory muscle function are currently being detected in patients with chronic obstructive pulmonary disease, due to alteration in respiratory muscle energy balance. Nutritional repletion may improve respiratory muscle function but uncertainty remains as to whether nutritional repletion may relieve dyspnoea. The cumulative benefit of interventions targeting the pathophysiologic mechanism of dyspnoea must be identified for optimum treatment of patients with shortness of breath.
authors.affiliation: Fondazione Don C. Gnocchi ONLUS (IRCCS), Via Imprunetana 124, 50020 Pozzolatico, Firenze, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Grazzini
authors.forename: L
authors.initials: L
authors.lastname: Stendardi
authors.forename: E
authors.initials: E
authors.lastname: Rosi
authors.forename: G
authors.initials: G
authors.lastname: Scano
mesh_terms: D014151:Anti-Anxiety Agents / Q000627:therapeutic use; D001993:Bronchodilator Agents / Q000627:therapeutic use; D018680:Cholinergic Antagonists / Q000627:therapeutic use; D004417:Dyspnea / Q000188:drug therapy* / Q000503:physiopathology*; D017079:Exercise Tolerance / Q000502:physiology; D006801:Humans; D010100:Oxygen / Q000502:physiology / Q000627:therapeutic use; D005082:Physical Exertion / Q000502:physiology*; D012132:Respiratory Muscles / Q000503:physiopathology
chemical_list: D014151:Anti-Anxiety Agents; D001993:Bronchodilator Agents; D018680:Cholinergic Antagonists; D010100:Oxygen