Chest
Volume 129, Issue 5, May 2006, Pages 1330-1336
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Original Research: Heart Failure
Closing Capacity and Gas Exchange in Chronic Heart Failure

https://doi.org/10.1378/chest.129.5.1330Get rights and content

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 (P0.1) 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 P0.1/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 P0.1, implying that there is a proportionately greater inspiratory effort per breath (P0.1/Pimax). These, together with the increased fR, are the only significant contributors to increases in the MRC dyspnea score.

Section snippets

Patients

The study was carried out in 20 stable ambulatory patients (18 men) with congestive heart failure due to cardiomyopathy (6 after ischemia) without pleural effusions. None had been hospitalized within 20 days preceding the study. None were current smokers, but nine patients were ex-smokers. All patients received therapy with diuretics (carvedilol, 15 patients; digitalis, 9 patients; oral anticoagulant therapy [dicumarol], 7 patients; and dobutamine IV, 1 patient). Within 1 month prior to

Results

Table 1 provides the anthropometric characteristics and baseline respiratory data for control subjects and CHF patients. In the control subjects, all baseline respiratory data were within normal limits; the MRC and Borg scores were zero, while the CHF patients exhibited slightly higher levels of MRC and Borg dyspnea scores.

In CHF patients, the FEV1/FVC ratio was within normal limits, while TLC and its subdivisions were reduced. This is also shown in Figure 1, where, for comparative purposes,

Discussion

The new findings of this study are that in CHF patients at rest (mostly in Weber class B and C), the following conditions prevail: (1) CC is not increased; (2) as a result of decreased FRC, however, airway closure with compromised pulmonary gas exchange is present during tidal breathing; (3) tidal FL is absent; (4) ventilation is increased as a result of increased fR with a concurrent decrease in Paco2; and (5) Pimax is decreased. Together with the concurrent increase in P0.1, this implies a

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