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 · Apr 2009
Physiological response to increasing levels of neurally adjusted ventilatory assist (NAVA).
This study evaluated the response to increasing levels of neurally adjusted ventilatory assist (NAVA), a mode converting electrical activity of the diaphragm (EAdi) into pressure, regulated by a proportionality constant called the NAVA level. Fourteen rabbits were studied during baseline, resistive loading and ramp increases of the NAVA level. EAdi, airway (Paw) and esophageal pressure (Pes), Pes pressure time product (PTPes), breathing pattern, and blood gases were measured. ⋯ At this breakpoint, Pes, PTPes, EAdi, and P(a)(CO)(2) were similar to baseline. Further increase of the NAVA level reduced Pes, PTPes and EAdi without changes in ventilation. In conclusion, observing the trend in Paw during a ramp increase of the NAVA level allows determination of a level where the inspiratory effort matches unloaded conditions.
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Respir Physiol Neurobiol · Mar 2009
Clinical TrialThe compensatory responses to upper airway obstruction in normal subjects under propofol anesthesia.
Upper airway obstruction during sleep can trigger compensatory neuromuscular responses and/or prolong inspiration in order to maintain adequate minute ventilation. The aim of this study was to investigate the strength of these compensatory responses during upper airway obstruction during propofol anesthesia. We assessed respiratory timing and upper airway responses to decreases in nasal pressure in nine propofol anesthetized normal subjects under condition of decreased (passive) and increased (active) neuromuscular activity. ⋯ Compared to the passive condition, PCRIT decreased significantly (5.3 +/- 3.8 cm H2O, p < 0.05) and RUS increased (7.4 cm H2O ml-1 s, p < 0.05) in the active condition. The IDC increased progressively and comparably as decreased in both the passive and active conditions (p < 0.05). These findings imply that distinct compensatory mechanisms govern the modulation of respiratory pattern and pharyngeal patency during periods of airway obstruction under propofol anesthesia.