Document Detail


Mechanism of augmented exercise hyperpnea in chronic heart failure and dead space loading.
MedLine Citation:
PMID:  23274121     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Patients with chronic heart failure (CHF) suffer increased alveolar VD/VT (dead-space-to-tidal-volume ratio), yet they demonstrate augmented pulmonary 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 exercise hyperpnea is not merely determined by metabolic CO2 production ( [Formula: see text] ) per se but is responsive to an apparent (real-feel) metabolic CO2 load ( [Formula: see text] ) that also incorporates the adverse effect of physiological VD/VT on pulmonary CO2 elimination. By contrast, healthy individuals subjected to dead space loading 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 CO2 breathing. The ventilatory effects of dead space loading are therefore similar to those of increased alveolar VD/VT and CO2 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 CO2 in dead space gas thus creating a virtual (illusory) airway CO2 load within each inspiration, as opposed to a true airway CO2 load during CO2 breathing that clogs the mechanism for CO2 elimination through pulmonary ventilation. Thus, the chemosensing mechanism at the respiratory 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. Skeletal muscle afferents feedback, while important for early-phase exercise cardioventilatory dynamics, appears inconsequential for late-phase exercise hyperpnea.
Authors:
Chi-Sang Poon; Chung Tin
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2012-12-27
Journal Detail:
Title:  Respiratory physiology & neurobiology     Volume:  186     ISSN:  1878-1519     ISO Abbreviation:  Respir Physiol Neurobiol     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-03-18     Completed Date:  2013-09-06     Revised Date:  2014-03-07    
Medline Journal Info:
Nlm Unique ID:  101140022     Medline TA:  Respir Physiol Neurobiol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  114-30     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier B.V. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Carbon Dioxide / physiology
Exercise / physiology*
Heart Failure / physiopathology*
Humans
Hypercapnia / physiopathology*
Pulmonary Gas Exchange / physiology
Pulmonary Ventilation / physiology
Respiratory Dead Space / physiology*
Grant Support
ID/Acronym/Agency:
HL067966/HL/NHLBI NIH HHS; R01 HL067966/HL/NHLBI NIH HHS; RC1 RR028241/RR/NCRR NIH HHS; RR028241/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
142M471B3J/Carbon Dioxide
Comments/Corrections
Comment In:
Respir Physiol Neurobiol. 2013 Oct 1;189(1):203-10   [PMID:  23851107 ]

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