Competition for Intrathoracic Space Reduces Lung Capacity in Patients With Chronic Heart Failure: Discussion
These authors also suggest that, due to the increase in cardiac size, diffusion capacity of the lung suffers adversely, primarily as a consequence of a reduction in membrane diffusion as opposed to pulmonary capillary blood volume. Although moderate but significant correlations were observed between the cardiothoracic index and various components of pulmonary function, these findings may be underestimated for a number of reasons.
For instance, these authors only examined these relationships based on a one-dimensional measure of the thorax and heart. Also, they did not report data on the pulmonary thoracic index or other radio-graphically determined lung measurements. Thus, it is difficult to extrapolate these findings to true cardiac or lung volumes in relation to the volume of the thoracic cavity. The present investigation sought to expand this previous work and to gain a better understanding of the actual changes in cardiac volume in patients with stable chronic heart failure according to disease severity. In addition, we determined the impact that changes in cardiac volume have on lung volume using a three-dimensional volumetric analysis. Our results show a close association between the increase in cardiac volume and the loss of lung volume within a closed thoracic cavity, consistent with the restrictive pulmonary function pattern typically observed in heart failure patients. read
Although not specifically examined in the present study, the increase in heart size and reduction in lung volumes likely contribute to the rapid and shallow breathing patterns often observed in this population, particularly during exercise.- This type of pattern may subsequently play a role in limiting exercise tolerance. Work by Nanas et al suggested that inspiratory capacity (IC) was the best predictor of functional capacity in patients with chronic heart failure. Therefore, restrictive lung changes would lead to a high elastic load to inspiration and likely result in a reduced IC. Our data do suggest that this reduction in IC could simply be related to the direct relationship between loss of lung volume secondary to increased heart size and disease severity.
Interestingly, absolute diaphragm volume was significantly elevated in both heart failure groups as compared to control subjects, although only a difference between the patients with more severe chronic heart failure and control subjects was demonstrated when diaphragm volume was examined as a percentage of TTCV. These differences may be attributed to type II muscle fiber atrophy or a change in the motor unit recruitment during contraction associated with the disease.