Abstract

Dyspnea--the perception of respiratory discomfort--is a primary symptom of asthma. This review examines possible ways to link mechanisms, measurement and treatment that will increase our understanding of this condition. Functional neuroimaging methods have proven to be powerful tools that serve as advanced models of sensor motor brain function. Studies examining functional neuroimaging methods have revealed activation of distinct brain areas associated with increased dyspnea. Pulmonary hyperinflation has been proposed to influence the perception of dyspnea. The association of hyperinflation with minor levels of bronchoconstriction reflects the partition of the sensory effect of airway narrowing per se from that of the attendant elastic loading of the inspiratory muscles. There is evidence to suggest, however, that hyperinflation does not play an important role in the pathogenesis of exercise dyspnea as it does during induced bronchoconstriction. Decreased levels of perception of airway obstruction may be a risk factor associated with life-threatening asthma. A poor perceiver may be vulnerable to further hypoxia-induced suppression of respiratory sensation. Monitoring the response to bronchodilator therapy with formoterol and salbutamol in patients with acute or chronic asthma has resulted in significantly faster improvement in dyspnea, within 2 min. Regardless of the factors involved, much variability in dyspnea scores remains unexplained. Quantitative and qualitative assessment of the perception of dyspnea, symptom measurement and quality of life complement physiological measurements and contribute to our understanding of dyspnea in asthma.

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