| Mechanism of augmented exercise hyperpnea in chronic heart failure and dead space loading. | |
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MedLine Citation:
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PMID: 23274121 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Patients with chronic heart failure (CHF) suffer increased physiological VD/VT (dead-space-to-tidal-volume ratio) primarily due to increased pulmonary ventilation/perfusion mismatch, yet they demonstrate compensatory augmentation of total ventilation such that arterial [Formula: see text] ( [Formula: see text] ) remains remarkably normal from rest to moderate exercise. This paradoxical effect suggests that the control law governing isocapnic exercise ventilatory response is not merely determined by metabolic CO(2) production ( [Formula: see text] ) per se but is responsive to an apparent (real-feel) metabolic CO(2) load ( [Formula: see text] ) that also incorporates the adverse effect of physiological VD/VT on pulmonary CO(2) elimination. By contrast, healthy individuals subjected to dead space loading with increased series VD/VT also experience augmented ventilation at rest and during exercise as with increased alveolar VD/VT in CHF, but the resultant response is hypercapnic instead of eucapnic, as with CO(2) breathing. The ventilatory effects of dead space loading are therefore similar to those of increased alveolar VD/VT and CO(2) breathing combined. These observations are consistent with the hypothesis that the increased series VD/VT in dead space loading adds to [Formula: see text] as with increased alveolar VD/VT in CHF, but this is through rebreathing of CO(2) in dead space gas thus creating a virtual (illusory) airway CO(2) load within each inspiration, as opposed to a true airway CO(2) load during CO(2) breathing that clogs the mechanism for CO(2) elimination through pulmonary ventilation. Thus, the respiratory chemosensing mechanism at the controller may be responsive to putative drive signals mediated by within-breath [Formula: see text] oscillations independent of breath-to-breath fluctuations of the mean [Formula: see text] level. |
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Authors:
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Chi-Sang Poon; Chung Tin |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-12-25 |
Journal Detail:
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Title: Respiratory physiology & neurobiology Volume: - ISSN: 1878-1519 ISO Abbreviation: Respir Physiol Neurobiol Publication Date: 2012 Dec |
Date Detail:
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Created Date: 2012-12-31 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101140022 Medline TA: Respir Physiol Neurobiol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2012. Published by Elsevier B.V. |
Affiliation:
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Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Electronic address: cpoon@mit.edu. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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