HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:
Guest Access | Sign In via User Name/Password

This Article Full Text Free Full Text (PDF) Free Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Torchio, R. Articles by Milic-Emili, J. Search for Related Content PubMed PubMed Citation Articles by Torchio, R. Articles by Milic-Emili, J.

Closing Capacity and Gas Exchange in Chronic Heart Failure^*

^* From the Fisiopatologia Respiratoria (Drs. Torchio, Gulotta, Perboni, and Guglielmo), Ospedale San Luigi Gonzaga, Orbassano, Turin, Italy; the Department of Cardiology (Drs. Greco-Lucchina and Montagna), Ospedale San Luigi Gonzaga, Orbassano, Turin, Italy; and Meakins-Christies Laboratories (Dr. Milic-Emili), McGill University, Montreal, QC, Canada.

Correspondence to: Roberto Torchio, MD, Fisiopatologia Respiratoria, Ospedale San Luigi Gonzaga, I-10043 Orbassano, Torino, Italy; e-mail r.torchio{at}inrete.it

Abstract

Background: Although it is commonly assumed that pulmonary congestion and edema in patients with chronic heart failure (CHF) promotes peripheral airway closure, closing capacity (CC) has not been measured in CHF patients.

Purpose: To measure CC and the presence or absence of airway closure and expiratory flow limitation (FL) during resting breathing in CHF patients.

Methods: In 20 CHF patients and 20 control subjects, we assessed CC, FL, spirometry, blood gas levels, control of breathing, breathing pattern, and dyspnea.

Results: The patients exhibited a mild restrictive pattern, but the CC was not significantly different from that in control subjects. Nevertheless, airway closure during tidal breathing (ie, CC greater than functional residual capacity [FRC]) was present in most patients but was absent in all control subjects. As a result of the maldistribution of ventilation and the concurrent impairment of gas exchange, the mean (± SD) alveolar-arterial oxygen pressure difference increased significantly in CHF patients (4.3 ± 1.2 vs 2.7 ± 0.5 kPa, respectively; p < 0.001) and correlated with systolic pulmonary artery pressure (r = 0.49; p < 0.03). Tidal FL is absent in CHF patients. Mouth occlusion pressure 100 ms after onset of inspiratory effort (P_0.1) as a percentage of maximal inspiratory pressure (PImax) together with ventilation were increased in CHF patients (p < 0.01 and p < 0.005, respectively). The increase in ventilation was due entirely to increased respiratory frequency (fR) with a concurrent decrease in PaCO₂. Chronic dyspnea (scored with the Medical Research Council [MRC] scale) correlated (r² = 0.61; p < 0.001) with fR and P_0.1/PImax.

Conclusions: In CHF patients at rest, CC is not increased, but, as a result of decreased FRC, airway closure during tidal breathing is present, promoting the maldistribution of ventilation, ventilation-perfusion mismatch, and impaired gas exchange. The ventilation is increased as result of increased fR, and PImax is decreased with a concurrent increase in P_0.1, implying that there is a proportionately greater inspiratory effort per breath (P_0.1/PImax₎. These, together with the increased fR, are the only significant contributors to increases in the MRC dyspnea score.

Key Words: closing volume • hypocapnia • hypoxemia • maximal inspiratory pressure • peripheral airway closure