Closing Capacity and Gas Exchange in Chronic Heart Failure: CC and Gas Exchange

Closing Capacity and Gas Exchange in Chronic Heart Failure: CC and Gas ExchangeThere also was no significant difference in CC between CHF patients and control subjects, indicating that in our CHF patients there was “no premature airway closure.” In fact, in CHF patients the CC was actually smaller than that in control subjects, although not significantly. This may reflect the fact that pulmonary fibrosis and/or vascular engorgement- may render the peripheral airways more resistant to collapse. In line with the findings of Collins et al, however, in most of our patients (13 of 20) the CC exceeded the FRC (ie, during tidal breathing there was cyclic opening and closing of peripheral airways with a concurrent maldistribution of ventilation and a risk of mechanical injury to the peripheral airways). As a result of this maldistribution of ventilation, Pa02 decreased and P(A-a)O2 increased (Table 4). review

The AN2 was increased in CHF patients, providing further evidence for the presence of pulmonary mixing inhomogeneity. It is not clear whether the increased AN2 resulted from the enhancement of the gravity-dependent inhomogeneity within the lung or was an expression of the local differences in elastic properties of the alveolar walls. In CHF patients with chronic pulmonary hypertension and edema, the pulmonary capillary and tissue membranes undergo remodeling, which may result in changes in elastic properties. The remodeling at the level of alveolar-capillary membranes could also contribute to decreased Dlco (Table 1). In fact, in CHF patients there is a reduced alveolar-capillary diffusion transfer, which is inversely related to pulmonary vascular resistance. This may explain the fact that in our CHF patients the values of Dlco normalized for VA (and Dlco/VA ratio) remained significantly lower than those in the control subjects. In line with previous reports, VE was increased in CHF patients with a concurrent decrease in PaC02. The increase in VE was due entirely to increased fR since the VT was the same in CHF patients and control subjects.

In line with the findings of Ambrosino et al the Ti/Ttot ratio was the same in CHF patients as in control subjects, whereas the inspiratory drive, as reflected by P01 and the Vt/Ti ratio, was significantly higher in CHF patients. The mechanisms for the increased inspiratory drive in CHF patients are poorly understood. It is of interest, however, to note that, despite the increased P0 1 and Vt/Ti ratio and the decreased Plmax the CHF patients exhibited a normal Vt at rest. In CHF patients, lung compliance is decreased due to congestion or fibrosis, and, under these conditions, the respiratory muscles usually try to conserve energy by decreasing VT and increasing fR.

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