Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · May 2009
Editorial ReviewMechanisms of activity-related dyspnea in pulmonary diseases.
Progressive activity-related dyspnea dominates the clinical presentation of patients afflicted by chronic obstructive and restrictive lung diseases. This symptom invariably leads to activity limitation, global skeletal muscle deconditioning and an impoverished quality of life. The effective management of exertional dyspnea remains an elusive goal but our understanding of the nature and mechanisms of this distressing symptom continues to grow. ⋯ Reductionist experimental approaches that attempt to partition, or isolate, the contribution of central and multiple peripheral sensory afferent systems to activity-induced dyspnea have met with limited success. Integrative approaches which explore the possible neurophysiological mechanisms involved in the two dominant qualitative descriptors of activity-related dyspnea in both diseases may prove to be more fruitful. In this review, we present a hypothetical model for exertional dyspnea that is based on current neurophysiological constructs that have been rigorously developed to explain the origins of perceptions of "effort," "air hunger" and the accompanying affective "distress" response.
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Dyspnea, or the uncomfortable awareness of respiratory distress, is a common symptom experienced by most people at some point during their lifetime. It is commonly encountered in individuals with pulmonary disease, such as chronic obstructive pulmonary disease (COPD), but can also be seen in healthy individuals after strenuous exercise, at altitude or in response to psychological stress. Dyspnea is a multifactorial sensation involving the brainstem, cortex, and limbic system, as well as mechanoreceptors, irritant receptors and chemoreceptors. ⋯ They stimulate the respiratory control system in response to hypoxia and/or hypercapnia, and the resultant increase respiratory motor output can be consciously perceived as unpleasant. They also can induce the sensation of dyspnea through an as yet undetermined mechanism-potentially via direct ascending connections to the limbic system and cortex. The goal of this article is to briefly review how changes in blood gases reach conscious awareness and how chemoreceptors are involved in dyspnea.
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Respir Physiol Neurobiol · May 2009
Editorial ReviewPathophysiology of dyspnea evaluated by breath-holding test: studies of furosemide treatment.
Breath-holding is one of the most powerful methods to induce the dyspneic sensation, and the breath-holding test gives us much information on the onset and endurance of dyspnea. In conscious subjects, immediately after the start of breath-holding at functional residual capacity (FRC), there is a certain period of no particular respiratory sensation lasting for 20-30s, which is designated "no respiratory sensation period". This period is terminated by the onset of dyspnea and followed by a progressive increase in the intensity of dyspnea until the breaking point of breath-holding. ⋯ Alleviation of dyspnea with inhaled furosemide in conscious subjects is also consistent with the result of animal studies in which inhaled furosemide suppresses the escape behavior in the lightly anesthetized condition. The purpose of this article is to emphasize the usefulness of breath-holding test as a tool for evaluation of dyspnea. Furthermore, the possible mechanisms of alleviation of dyspnea with inhaled furosemide are highlighted.