Closing Capacity and Gas Exchange in Chronic Heart Failure: Dyspnea

A possible explanation for the finding of increased central drive without a decrease in the VT would be the difference in operational length compensation of the diaphragm. Patients with CHF have smaller lungs and longer resting length of their diaphragms, which results in greater force generation for the same output during quiet breathing. This implies greater inspiratory effort with weaker inspiratory muscles, leading to an increased Borg dyspnea score at rest.
The resting values of P0 -/Plmax ratio and fR were also the only significant predictors of the level of MRC dyspnea. In fact, the P0 -/Plmax ratio (percentage) and the fR explained 61% of the variance in MRC score. This suggests that the increased inspiratory load and effort, as implied by higher than normal values for the P0 -/Plmax ratio and fR, is a cause of dyspnea in CHF patients.
Several studies in CHF patients have failed to demonstrate a direct relationship between dyspnea and cardiac function data such as pulmonary capillary wedge pressure. In the present study, neither MRC dyspnea score nor Borg dyspnea score at rest correlate with sPAP and ejection fraction. On the other hand, some previous studies have suggested increased inspiratory muscle load relative to inspiratory muscle capacity as a cause of dyspnea and exercise intolerance. further

Furthermore, McParland et al reported that in CHF patients Plmax as well as maximal expiratory pressure were reduced, both being significantly correlated with dyspnea during daily activities. The present results support the notion that inspiratory force and loading play a significant role in eliciting dyspnea, as shown by the significant relationship of the level of MRC score and the resting values of P0 /Plmax ratio (percentage) and fR (equation 1). However, the relationship of these resting measurements to the mechanisms of dyspnea during exercise remains to be elucidated in CHF patients. The absence of FL with the patient in the seated position is not surprising in CHF patients. FL was found in a small percentage of seated patients with acute heart failure.’ In contrast, FL is frequently observed in patients in the supine position, which is correlated to orthopnea and can be reversed by therapy. The ERV reduction secondary to FRC reduction (because of cardiomegaly and vascular engorgement) can decrease ERV predisposing the patient to FL.

In CHF patients, cardiac diameters and vascular engorgement would be smaller than in patients with acute heart failure, and this factor could explain why none of our CHF patients had FL in a sitting position.
In conclusion, the present results show that in CHF patients, relative to control subjects, the CC does not change while FRC decreases. Due to the decrease of FRC, most patients exhibit airway closure during tidal breathing with maldistribution of ventilation and impaired gas exchange within the lung (decreased PaC02 and increased P[A-a]O2). The impaired gas exchange is partly compensated by increased pulmonary ventilation, which is associated with increased inspiratory effort due to fR. Since Plmax is reduced, the association of increased inspiratory effort in the face of decreased potential force may explain the fact that CHF patients complain of dyspnea at rest (Borg score) and also exhibit chronic dyspnea (MRC score).

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