Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/58169
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dc.contributor.authorRocha, Alcides [UNIFESP]
dc.contributor.authorArbex, Flavio F. [UNIFESP]
dc.contributor.authorSperandio, Priscilla A. [UNIFESP]
dc.contributor.authorSouza, Aline [UNIFESP]
dc.contributor.authorBiazzim, Ligia [UNIFESP]
dc.contributor.authorMancuso, Frederico [UNIFESP]
dc.contributor.authorBerton, Danilo C.
dc.contributor.authorHochhegger, Bruno
dc.contributor.authorAlencar, Maria Clara N. [UNIFESP]
dc.contributor.authorNery, Luiz E. [UNIFESP]
dc.contributor.authorO'Donnell, Denis E.
dc.contributor.authorNeder, J. Alberto
dc.date.accessioned2020-09-01T13:21:17Z-
dc.date.available2020-09-01T13:21:17Z-
dc.date.issued2017
dc.identifierhttp://dx.doi.org/10.1164/rccm.201704-0675OC
dc.identifier.citationAmerican Journal Of Respiratory And Critical Care Medicine. New York, v. 196, n. 10, p. 1264-1274, 2017.
dc.identifier.issn1073-449X
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/58169-
dc.description.abstractRationale: An increased ventilatory response to exertional metabolic demand (high V-E/V-CO2 relationship) is a common finding in patients with coexistent chronic obstructive pulmonary disease and heart failure. Objectives: We aimed to determine the mechanisms underlying high V-E/V-CO2 and its impact on operating lung volumes, dyspnea, and exercise tolerance in these patients. Methods: Twenty-two ex-smokers with combined chronic obstructive pulmonary disease and heart failure with reduced left ventricular ejection fraction undertook, after careful treatment optimization, a progressive cycle exercise test with capillary (c) blood gas collection. Measurements and Main Results: Regardless of the chosen metric (increased V-E-V-CO2 slope, V-E/V-CO2 nadir, or end-exercise V-E/V-CO2), ventilatory inefficiency was closely related to Pc-CO2 (r values from -0.80 to -0.84; P < 0.001) but not dead space/tidal volume ratio. Ten patients consistently maintained exercise Pc-CO2 less than or equal to 35 mm Hg (hypocapnia). These patients had particularly poor ventilatory efficiency compared with patients without hypocapnia (P < 0.05). Despite the lack of between-group differences in spirometry, lung volumes, and left ventricular ejection fraction, patients with hypocapnia had lower resting Pa-CO2 and lung diffusing capacity (P < 0.01). Excessive ventilatory response in this group was associated with higher exertional Pc-O2. The group with hypocapnia, however, had worse mechanical inspiratory constraints and higher dyspnea scores for a given work rate leading to poorer exercise tolerance compared with their counterparts (P < 0.05). Conclusions: Heightened neural drive promoting a ventilatory response beyond that required to overcome an increased "wasted" ventilation led to hypocapnia and poor exercise ventilatory efficiency in chronic obstructive pulmonary disease-heart failure overlap. Excessive ventilation led to better arterial oxygenation but at the expense of earlier critical mechanical constraints and intolerable dyspnea.en
dc.description.sponsorshipQueen's University
dc.description.sponsorshipCapes, Brazil
dc.description.sponsorshipSoutheastern Ontario Academic Medical Association, Canada
dc.format.extent1264-1274
dc.language.isoeng
dc.publisherAmer Thoracic Soc
dc.relation.ispartofAmerican Journal Of Respiratory And Critical Care Medicine
dc.rightsAcesso aberto
dc.subjectventilationen
dc.subjectexerciseen
dc.subjectchronic obstructive pulmonary diseaseen
dc.subjectcardiopulmonary exercise testen
dc.titleExcess Ventilation in Chronic Obstructive Pulmonary Disease-Heart Failure Overlap Implications for Dyspnea and Exercise Intoleranceen
dc.typeArtigo
dc.description.affiliationUniv Fed Sao Paulo, Pulm Funct & Clin Exercise Physiol Unit, Div Respirol, Sao Paulo, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Div Cardiol, Sao Paulo, Brazil
dc.description.affiliationUniv Fed Rio Grande do Sul, Div Respirol, Porto Alegre, RS, Brazil
dc.description.affiliationFed Univ Hlth Sci, Med Imaging Res Lab, Porto Alegre, RS, Brazil
dc.description.affiliationQueens Univ, Resp Invest Unit, Kingston, ON, Canada
dc.description.affiliationUnifespUniv Fed Sao Paulo, Pulm Funct & Clin Exercise Physiol Unit, Div Respirol, Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Div Cardiol, Sao Paulo, Brazil
dc.identifier.doi10.1164/rccm.201704-0675OC
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000415216500012
dc.coverageNew York
dc.citation.volume196
dc.citation.issue10
Appears in Collections:Artigo

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