Hyperinflation and the (Passive) Chest Wall

Frederic G. Hoppin Jr.

Departments of Medicine, Memorial Hospital of Rhode Island and Brown University, Pawtucket, Rhode Island

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Cassart and colleagues have previously shown that the configuration of the passive chest wall is similar in normal and chronically hyperinflated subjects at the same (absolute) lung volume (1). In this month's Journal (pp. 1171-1175), they report a similar conclusion for the effects of lung volume reduction surgery (LVRS) (2). I will give some background on the critical role of operating lung volumes in ventilatory failure, summarize the main findings of this pair of articles, and comment on the importance of confirming their results during active inspiration.

There are compelling reasons for disciplined attention to the role of lung volume: (1) Lung function and chest wall function are each strongly volume dependent. It is therefore completely meaningless ever to consider either intrinsic functions of the lung (e.g., lung recoil or maximal expiratory flow rate) or of the chest wall (e.g., peak or maximum sustainable inspiratory pressures, or efficiency) without specifying the pertinent volumes; (2) the lung and chest wall are wedded for life, for better or worse, in sickness or in health by volume; (3) most parameters of ventilatory performance reflect this linkage. FEV₁, for example, falls with impairment of either the lung's expiratory capability or the chest wall's inspiratory capability; and (4) the interaction of lung and chest wall is central to ventilatory failure in emphysema. Primary changes in the lung impair maximal expiratory flow, increasing operating volumes, which, in turn, puts the chest wall at a marked disadvantage, decreasing its inspiratory strength, endurance, and efficiency (3). LVRS improves ventilatory function by the same paradigm, in reverse (4).

In the earlier study, Cassart and colleagues obtained computer-assisted tomograms (CATs) over a range of volumes in normal and chronically hyperinflated subjects (1). The total area of the diaphragm (A_di) and the area of the diaphragm apposed to the inside of the rib cage (A_ap) fell as lung volume increased from FRC to TLC, and the area of the dome of the diaphragm changed little (A_do). These findings are consistent with shortening and descent of the diaphragm and relatively unchanged transverse dimensions of the rib cage. The most interesting finding is that the data appear to fall along a continuous line for both groups, that is, diaphragm dimensions of hyperinflated subjects are similar to those of normal subjects at the same (absolute) lung volumes or lie on a projection of that line at the higher volumes of which those subjects are capable. One can reach a corresponding conclusion from these diaphragm data about the other part of the chest wall, namely the rib cage. Chronic hyperinflation does not increase the anteroposterior and lateral rib cage dimensions at a given (absolute) lung volume. If it had done so, then the diaphragm would lie higher in the chest and A_di and A_ap would be larger at that volume, and that was not the finding. The current report extends these observations to LVRS (2). The pre- and postsurgery data fall nicely in line with the earlier study. A_di and A_ap were low at FRC and TLC before surgery, as expected, and increased at three months post-LVRS, consistent simply with the observed reductions in these operating volumes. The combined message of these two studies, then, is that chronic hyperinflation increases and LVRS can subsequently decrease operating lung volumes, but neither chronic hyperinflation nor LVRS changes intrinsic chest wall configurationat least as measured under these passive conditions.

More relevant, but as yet unexplored in this context, is the configuration of the active chest wall. The subjects in these studies were instructed to relax against a closed glottis during acquisition of the CATs (5). In the normal subject, however, inspiratory effort changes chest wall configuration at a given (absolute) volume, particularly at high volumes (6), and thickens and by implication shortens the diaphragm (F. D. McCool, personal observation with ultrasound). It is the active, not the passive, configuration that is relevant to inspiratory function (through muscle length and mechanical advanage), and it seems plausible that the active configurations of normal and hyperinflated subjects differ at the same (absolute) lung volumes, unlike their passive configurations (1, 2). In particular, chronic hyperinflation might induce behavioral or structural adaptations of the rib cage muscles so that the rib cage was elevated at a given (absolute) lung volume, stretching the diaphragm muscle to a functionally more favorable length and improving its mechanical advantage by increasing A_ap.

The authors also report on a related index of configuration, namely curvature of the diaphragm. LVRS increases curvature somewhat at the lower, post-LVRS TLC, but little or none at the lower post-LVRS FRC. One might anticipate such findings for the passive condition, where the curvature is strongly influenced by the shapes and locations of the adjoining thoracic and abdominal viscera (7). Active inspiration, however, might well change that curvature.

There is a particularly sensitive configurational issue, as the authors note, at very high volumes. As lung volume increases, inspiratory strength falls progressively because of muscle shortening and reduction in the effect of abdominal pressure on the rib cage through A_ap. When the lung margin reaches the bottom of the costophrenic sulcus, that is, when A_ap is obliterated, an angle develops between the diaphragm and the inside of the thoracoabdominal cavity, and this introduces a new configurational factor. On geometric grounds, any further descent of the diaphragm requires that the angle open up and that overall curvature decrease. This configuration decreases the effectiveness of diaphragm tension, as can be concluded either from the piston model, which now must include the cosine of that increasing angle, or equivalently from the LaPlace relationship, which now sees the decrease in overall curvature. This critical change of configuration may represent a relatively catastrophic transition in the development of volume-related ventilatory failure and conversely in its relief by LVRS.

It will be important to confirm the reported findings (that normal, chronically hyperinflated, and post-LVRS subjects have the same relationship of chest wall configuration with absolute lung volume), and to look carefully at the critical configurational transition at very high lung volumes during active inspiration.

	References

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1. Cassart M, Pettiaux N, Gevenois PA, Paiva M, Estenne M. Effect of chronic hyperinflation on diaphragm length and surface area. Am J Respir Crit Care Med 1997; 156: 504-508 [Abstract/Free Full Text].

2. Cassart M, Hamacher J, Verbandt Y, Wildermuth S, Ritscher D, Russi EW, de Francquen P, Capello M, Weder W, Estenne M. Effects of lung volume reduction surgery for emphysema on diaphragm dimensions and configuration. Am J Respir Crit Care Med 2001; 163: 1171-1175 [Abstract/Free Full Text].

3. McCool FD, Tzelepis GE, Leith DE, Hoppin FG Jr.. Oxygen cost of breathing during fatiguing inspiratory resistive loads. J Appl Physiol 1989; 66: 2045-2055 [Abstract/Free Full Text].

4. Hoppin FG Jr.. Theoretical basis for improvement following reduction pneumoplasty in emphysema. Am J Respir Crit Care Med 1997; 155: 520-525 [Abstract].

5. Pettiaux N, Cassart M, Paiva M, Estenne M. Three-dimensional reconstruction of human diaphragm with the use of spiral computed tomography. J Appl Physiol 1997; 82: 998-1002 [Abstract/Free Full Text].

6. Konno K, Mead J. Measurement of the separate volume changes of rib cage and abdomen during breathing. J Appl Physiol 1967; 22: 407-422 [Free Full Text].

7. Braun NMT, Arora NS, Rochester DF. Force-length relationship of the normal human diaphragm. J Appl Physiol Respir Environ Exercise Physiol 1982; 53: 405-412 [Abstract/Free Full Text].